ncRNA Symbol	ncRNA Category	Species	Disease Name	Sample	Dysfunction Pattern	Validated Method	Description	Clinical Application	Causality	Causal Description	PubMed ID
ARHGAP5-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Epigenetics( m6 A-modified)	qRT-PCR	Among these lncRNAs, we found that ARHGAP5-AS1 is the lncRNA with the highest levels of m6 A modification and significantly increased expression in HCC specimens.  METTL14 acts as the m6 A writer of ARHGAP5-AS1 and IGF2BP2 stabilises the lncRNA as its m6 A reader.We identified oncoprotein CSDE1 working as the interacting protein of the lncRNA and TRIM28 as the E3 ligase of CSDE1 in HCC. Interestingly, ARHGAP5-AS1 could attenuate interactions between CSDE1 and TRIM28, which prevents the degradation of CSDE1 via the ubiquitin-proteasome pathway. Elevated levels of CSDE1 coordinate oncogenic RNA regulons, promote translation of VIM and RAC1 and activate the ERK pathway, which contributes to HCC prognosis.		Yes	ARHGAP5-AS1 remarkably promotes malignant behaviours of HCC cells ex vivo and in vivo. 	36354136
HOTTIP	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(PTBP1/KHSRP )	qRT-PCR//RIP	Our data demonstrated HOTTIP was upregulated in OS tissues.  In mechanism, PTBP1 and KHSRP highly expressed in OS and HOTTIP was identified to interact with PTBP1 to promote KHSRP expression. Meanwhile, we found that overexpression of KHSRP or PTBP1, individually, can partially remove the repression of HOTTIP suppression for OS cell progression. 		Yes	HOTTIP knockdown resulted in a suppression of OS cell proliferation, invasion and migration, as well as a promotion of OS cell apoptosis, while HOTTIP overexpression exhibited opposite effects.	33475442
HOTTIP	LncRNA	Homo sapiens	Glioma	 SF268 cells	Interaction(miRNA-10b/Zeb1/Zeb2)	Transfection//Migration Assay//qRT-PCR//MTT//ELISA	lncRNA HOTTIP was found to be particularly elevated in SF268 cells and over-expression of HOTTIP in both A172 and LN229 remarkably increased their TMZ IC-50s, along with increased cell proliferation, migration, clonogenicity and markers of angiogenesis and metastasis. As a mechanism we observed increased expression of miRNA-10b and mesenchymal markers Zeb1/Zeb2 and reduced expression of E-cadherin in SF268 cells indicating a role of EMT in TMZ resistance. A172 and LN229 cells with overexpressed HOTTIP also had similarly induced EMT and the elevated miR-10b levels. Further, silencing of miR-10b in HOTTIP overexpressing cells as well as the SF268 cells reversed EMT with associated sensitization of all the tested cells to TMZ. 		Yes	lncRNA HOTTIP was found to be particularly elevated in SF268 cells and over-expression of HOTTIP in both A172 and LN229 remarkably increased their TMZ IC-50s, along with increased cell proliferation, migration, clonogenicity and markers of angiogenesis and metastasis. 	35402278
HOTTIP	LncRNA	Homo sapiens	Retinoblastoma	RB tissues and cells	Interaction(miR-101-3p/STC1 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//IHC	HOTTIP expression was promoted in RB tissues and cells. There were target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1. Inhibition of miR-101-3p or overexpression of STC1 reversed the effect of si-HOTTIP on the proliferation and apoptosis of RB cells. 		Yes	Downregulation of HOTTIP inhibited proliferation and promoted apoptosis of Y79 cells, while upregulation of HOTTIP promoted proliferation and inhibited apoptosis of HXO-RB-44 cells. 	33784880
HOTTIP	LncRNA	Homo sapiens	stomach carcinoma	cell lines MGC-803, HGC-27, SNU-1, and SGC-7901 	regulation[adsorbing miR-615-3p]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	" LncRNA HOTTIP was highly expressed in gastric carcinoma cell lines MGC-803, HGC-27, SNU-1, and SGC-7901 than in normal gastric mucosa cell line RGM-1.It affects cell proliferation and apoptosis in gastric carcinoma by adsorbing miR-615-3p via a sponge effect.
"		Yes	 After knockdown of lncRNA HOTTIP, the proliferation function of gastric carcinoma cells was markedly weakened, and the proportion of apoptotic cells increased. 	32633359
HOTTIP	LncRNA	Homo sapiens	Nasopharyngeal Neoplasms	NPC tissues	Interaction[Inhibiting miR-4301 ]	CCK8//qRT-PCR//Transwell Assay	HOTTIP expression was increased in NPC tissues.HOTTIP silencing suppressed the proliferation, cell cycle, migration, and invasion of NPC cells. 	Higher levels of HOTTIP are correlated with lower survival in NPC patients.	Yes	HOTTIP silencing suppressed the proliferation, cell cycle, migration, and invasion of NPC cells. 	30685769
HOTTIP	LncRNA	Homo sapiens	Arthritis, Rheumatoid	rheumatoid arthritis synovial fibroblasts	Interaction(miR-1908-5p/STAT3 axis)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//H&E Staining//ELISA	We found that HOTTIP was upregulated in rheumatoid arthritis synovial fibroblasts (RASFs).HOTTIP directly bound to miR-1908-5p and negatively modulated miR-1908-5p expression while positively regulating STAT3. 		Yes	 In addition, in vivo experiments demonstrated that overexpression of HOTTIP aggravated inflammation in RA mice, which was demonstrated by hematoxylin and eosin (HE) staining and the increased expression levels of CD4+ interleukin (IL)-17+, forkhead Box P3 (FOXP3) and retinoid-related orphan receptor gamma-t (RORγt)	34808131
HOTTIP	LncRNA	Homo sapiens	Mouth Neoplasms	oral cancer tissues	Interaction(miR-206)	qRT-PCR//Transfection//Wound Healing Assay//Transwell Assay	HOTTIP was abnormally increased in oral cancer. Besides, when HOTTIP was knocked down in oral cancer cell lines, miR-206-206 was remarkably up-regulated. Dual-luciferase reporter gene experiment confirmed the binding relationship between miR-206 and HOTTIP. 	At the same time, the survival analysis showed that the higher expression of HOTTIP was significantly correlated with a shorter overall survival. 	Yes	The results of cell functional experiments found that HOTTIP played a role in promoting tumor proliferation and migration in oral cancer cells. B	34268933
HOTTIP	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OTSCC tissues and cells	regulation[HMGA2-Mediated Wnt/β-Catenin Pathway]	qRT-PCR//MTT//Western Blot//Transwell Assay	HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients. HOTTIP knockdown restrained proliferation, migration, and invasion of OTSCC cells by miR-124-3p/HMGA2 axis through Wnt/β-catenin pathway.	HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients. 	Yes	Silencing HOTTIP impeded proliferation, migration, and invasion of OTSCC cells. Moreover, HOTTIP knockdown inhibited proliferation, migration, and invasion of OTSCC cells by targeting miR-124-3p.	31910357
HOTTIP	LncRNA	Homo sapiens	Lung Diseases	A549 cells and Lung tissues of mouse model 	Interaction(miR‑744‑5p/PTBP1 signaling axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//EdU Staining//IF	The results of the present study revealed that the proliferation and migration of A549 cells were both suppressed following the knockdown of HOTTIP. The lncRNA HOTTIP was found to target and downregulate the expression levels of miR‑744‑5p.  Furthermore, miR‑744‑5p targeted and downregulated the expression levels of PTBP1.		Yes	The knockdown of lncRNA HOTTIP expression also relieved the fibrosis of the lung tissues of mice.	34212978
HOTAIRM1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Regulation[miR-17-5p/ PTEN axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Microarray	 HOTAIRM1 and phosphatase and tensin homolog (PTEN) were both downregulated in GC, whereas miR-17-5p was upregulated.Moreover, the PI3K/AKT pathway was found activated in GC. HOTAIRM1 targeted miR-17-5p, whereas PTEN was the downstream target gene of miR-17-5p.		Yes	HOTAIRM1 suppressed proliferation and migration of GC cell line and induced their apoptosis, whereas miR-17-5p played the opposite role on GC cell line. HOTAIRM1 also postponed tumor growth in vivo and inhibited the PI3K/AKT pathway in GC.	30302796
HOTAIRM1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells and patients	Regulation(SYN2 )	qRT-PCR//Migration Assay//Cell Viability Assay//Western Blot	Results from univariate and multivariate Cox regression showed that SYN2, HOTAIRM1, BCAS1, and ALDOC were significantly associated with patient prognosis. Results from in vitro experiments showed that knockdown HOTAIRM1 expression promoted breast cancer cells proliferation, clone formation, and invasion. Up-regulation of HOTAIRM1 inhibited breast cancer cells proliferation, clone formation, and invasion.	Results from univariate and multivariate Cox regression showed that SYN2, HOTAIRM1, BCAS1, and ALDOC were significantly associated with patient prognosis.  Immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR) results showed that the expression levels of SYN2 and HOTAIRM1 were negatively correlated with BRCA stage, whereas those of BCAS1 and ALDOC were positively correlated with BRCA stage. 	Yes	Results from in vitro experiments showed that knockdown HOTAIRM1 expression promoted breast cancer cells proliferation, clone formation, and invasion. Up-regulation of HOTAIRM1 inhibited breast cancer cells proliferation, clone formation, and invasion.	35694102
HOTAIRM1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues cells or exosomes	Interaction(miR-498/ABCE1 axis)	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Invasion Assay//Transwell Assay	HOTAIRM1 expression was dramatically upregulated, whereas miR-498 expression was significantly downregulated in NSCLC tissues cells or exosomes as compared to control groups. Functionally, HOTAIRM1 functioned as a sponge of miR-498 and miR-498 targeted ABCE1. In addition, HOTAIRM1 silencing inhibited NSCLC growth in vivo by downregulating ABCE1 and upregulating miR-498 expression.		Yes	Mechanistically, HOTAIRM1 knockdown repressed cell viability, migration, invasion and glycolysis metabolism, whereas induced cell apoptosis in NSCLC; however, miR-498 inhibitor hindered these effects.	33537917
HOTAIRM1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Regulation[Wnt signaling pathway]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	Lower lncRNA HOTAIRM1 expressions were observed in the HCC tissues than those of the paracancerous tissues.HOTAIRM1, which was downregulated in HCC, might inhibit the proliferative ability and promote the apoptosis of HCC cells by suppressing the Wnt pathway, thereby inhibiting the progression of hepatocellular carcinoma.	 ROC curve indicated a high sensitivity and specificity of lncRNA HOTAIRM1 for HCC. PFS in HCC patients was correlated with tumor size and lncRNA HOTAIRM1 expression, whereas not correlated with age, sex, GGT, AFP, Child-Pugh grade, HBsAg, cirrhosis, number of tumors, micro-vessel metastasis, tumor differentiation, and TNM stage of HCC.	Yes	Overexpression of HOTAIRM1 led to decreased proliferative ability and increased apoptosis of HepG2 and HHCC cells. 	30070317
HOTAIRM1	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tumor tissues and cells	interaction[ARHGAP24 ,miR-106a-5p]	RNA Pull-Down//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 HOTAIRM1 expression was lowered in OC tumor tissues and cells.In conclusion, our study showed that HOTAIRM1 suppressed OC progression through derepression of ARHGAP24 by sponging miR-106a-5p. 	Decreased HOTAIRM1 expression was associated with advanced FIGO stages and lymphatic metastasis.	Yes	Up-regulation of HOTAIRM1 suppressed OC cell proliferation and invasion, and promoted apoptosis. 	31935390
HOTAIRM1	LncRNA	Homo sapiens	Ovarian Neoplasms	skov3 cell	Expression [highly expressed]	qRT-PCR//Western Blot	HOTAIRM1 was overexpressed in SKOV3 cells.		Yes	 Silencing of HOTAIRM1 alleviated cell proliferation, and increased cell apoptosis of SKOV3 cells. Moreover, siHOTAIRM1 significantly increased expression of pro-apoptotic agents, such as Bad and Bax, while it decreased expressions of Bid and Bcl-2 (anti-apoptotic agents). Also, silencing of HOTAIRM1 resulted in a suppressed expression of Wnt pathway-related proteins and also expression of its downstream target gene, matrix metalloproteinase 9(MMP9).	33939846
HOTAIRM1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Expression(highly expressed)	qRT-PCR//Colony Formation Assay//Western Blot	This study identified HOTAIRM1 as a novel significantly upregulated lncRNA in OSCC, which is strongly associated with unfavorable prognosis of OSCC.	This study identified HOTAIRM1 as a novel significantly upregulated lncRNA in OSCC, which is strongly associated with unfavorable prognosis of OSCC.Systematic bioinformatics analyses demonstrated that HOTAIRM1 was closely related to tumor stage, overall survival, genome instability, the tumor cell stemness, the tumor microenvironment, and immunocyte infiltration.	Yes	HOTAIRM1 plays a pivotal role in OSCC cell proliferation, and is mainly involved in the regulation of the cell cycle. In vitro, cell loss-functional experiments confirmed that HOTAIRM1 knockdown significantly inhibited the proliferation of OSCC cells, and arrested the cell cycle in G1 phase. At the molecular level, PCNA and CyclinD1 were obviously reduced after HOTAIRM1 knockdown. The expression of p53 and p21 was upregulated while CDK4 and CDK6 expression was decreased by HOTAIRM1 knockdown. In vivo, knocking down HOTAIRM1 significantly inhibited tumor growth, including the tumor size, weight, volume, angiogenesis, and hardness, monitored by ultrasonic imaging and magnetic resonance imaging	35087800
HOTAIRM1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	blood	Interaction[ targeting miR-148b ]	CCK8//qRT-PCR//Flow Cytometry	HOTAIRM1 expression was higher while miR-148b expression was lower in AML patients than in healthy controls.In summary, HOTAIRM1 was involved in the progression of AML through targeting miR-148b, shedding light on the biological function and molecular mechanism of HOTAIRM1 in AML.		Yes	HOTAIRM1 silencing and miR-148b overexpression both suppressed cell proliferation and induced apoptosis in AML cells. miR-148b was identified as a target of HOTAIRM1 in AML cells. Moreover, HOTAIRM1 knockdown inhibited proliferation and induced apoptosis in AML cells by negatively regulating miR-148b. 	35520918
HOTAIRM1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cells	Expression[highly expressed]	qRT-PCR//MTT//Colony Formation Assay//Western Blot	HOTAIRM1 expression was abnormally upregulated in PDAC tissues and cells when compared with the control samples, and was positively associated with the expression of KRAS gene mutation.		Yes	HOTAIRM1 knockdown attenuated cell proliferation by inducing cell cycle arrest at G0/G1 phase, promoted cell apoptosis, and inhibited cell migration in PDAC cells by regulating related-genes expression.	30613920
HOTAIRM1	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cells	Expression[highly expressed]	qRT-PCR//ChIP	HOTAIRM1 was abnormally up-regulated in GBM tissues and cells, and this up-regulation was correlated with grade malignancy in glioma patients.		Yes	HOTAIRM1 silencing caused tumor suppressive effects via inhibiting cell proliferation, migration and invasion, and inducing cell apoptosis. In vivo experiments showed knockdown of HOTAIRM1 lessened the tumor growth.	30376874
HOTAIRM1	LncRNA	Homo sapiens	Glioblastoma	GBM tissue samples and cells	interaction[SNAI2]	ChIP//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	HOTAIRM1 was significantly overexpressed in GBM tissues and cells. Our results indicate a positive feedback loop between HOTAIRM1 and SNAI2, and suggest that the lncRNA HOTAIRM1 is a potential biomarker and therapeutic target in GBM.		Yes	HOTAIRM1 knockdown significantly weakened the migration and invasion by GBM cells.	33323548
HOTTIP	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	blood,cell lines	Regulation[HOTTIP/microRNA-608/DDA1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	HOTTIP was highly expressed in AML-M5 patients than normal controls.HOTTIP expression was significantly up-regulated in AML cell lines U-937 and THP-1.Dual-luciferase reporter gene indicated that HOTTIP could bind to microRNA-608, which was lowly expressed in AML-M5 patients. Overexpression of microRNA-608 significantly inhibited the proliferative ability and cell cycle progression of U-937 and THP-1 cells. More importantly, microRNA-608 could partially reverse the regulatory effect of HOTTIP on AML cells. Meanwhile, DDA1 was verified as the target of microRNA-608. Subsequent experiments elucidated that DDA1 significantly accelerated the proliferation and cell cycle of AML cells. 		Yes	Up-regulation of HOTTIP remarkably promoted the proliferative potential and cell cycle progression of AML cells. 	31002141
HOTTIP	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction[c-Myc]	CCK8//qRT-PCR//Wound Healing Assay//Western Blot	HOTTIP was demonstrated to be upregulated in OS tissues and cell lines.HOTTIP promoted cell migration and invasion by upregulating c-Myc in OS. The positive feedback loop formed by HOTTIP and c-Myc may contribute to OS progression, and HOTTIP may act as a therapeutic target for OS.		Yes	knockdown of HOTTIP inhibited OS cell migration, invasion and EMT, and suppressed c-Myc expression. In addition, overexpression of c-Myc increased HOTTIP expression and enhanced OS cell migration and invasion.	31423232
HOTAIRM1	LncRNA	Homo sapiens	Thyroid Neoplasms	TC cells and tissues	interaction[HOTAIRM1/miR-148a/Wnt10 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The pronounced upregulated expression of HOTAIRM1 was evident in TC cells and tissues, and was associated with TNM stage and lymph node metastasis.Taken together, these results suggest that miR‑148a and Wnt10b are downstream effectors of the HOTAIRM1 signaling pathway in TC. This HOTAIRM1/miR‑148a/Wnt10 axis may thus be amenable to therapeutic targeting in order to improve disease outcomes in patients with TC.	The pronounced upregulated expression of HOTAIRM1 was evident in TC cells and tissues, and was associated with TNM stage and lymph node metastasis.	Yes	When HOTAIRM1 was knocked down, this inhibited the proliferative and invasive abilities of TPC?1 and BCPAP cells in vitro. 	33650656
HOTTIP	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	exosomes	Regulation( miR-19a-3p and miR-19b-3p/TLR5/NF-κB pathway)	CCK8//qRT-PCR	Accordingly, HOTTIP was found to be upregulated in M1-derived exosomes. A mechanism study further showed that M1 exosomes and HOTTIP activated the TLR5/NF-κB signaling pathway by competitively sponging miR-19a-3p and miR-19b-3p. Furthermore, cancer cells expressing HOTTIP were noted to induce the polarization of both local M1 and M2 macrophages; however, M1 exosomes were observed to reprogram local TAMs into M1 macrophages. 		Yes	 Therefore, the function of HOTTIP in cancer cells was explored, for which overexpression of HOTTIP was found to inhibit proliferation, migration and invasion but induced apoptosis of cancer cells in vitro. 	35210436
HOXA11-AS	LncRNA	Mus musculus	Parkinson Disease	SH-SY5Y neuronal and microglia	Interaction(FSTL1/NF-κB axis)	qRT-PCR//Luciferase Report Assay//Western Blot	Inhibition of HOXA11-AS protects mice against PD through repressing neuroinflammation and neuronal apoptosis through miR-124-3p-FSTL1-NF-κB axis.		Yes	Inhibition of HOXA11-AS protects mice against PD through repressing neuroinflammation and neuronal apoptosis through miR-124-3p-FSTL1-NF-κB axis.	33839699
HOXA11-AS	LncRNA	Mus musculus	Atherosclerosis	AS mice tissues, vascular endothelial cell	Interaction(miR-515-5p/ROCK1 axis)	Western Blot//Transfection//Flow Cytometry//RIP//qRT-PCR//MTT//Luciferase Report Assay	Our data showed that HOXA11-AS was significantly up-regulated (P < 0.001), whereas miR-515-5p was dramatically down-regulated in AS mice tissues (P < 0.001) and ox-LDL-treated HUVECs (P < 0.01). Luciferase assay and RIP results confirmed that miR-515-5p is directly bound to HOXA11-AS and ROCK1. HOXA11-AS promoted ox-LDL-induced HUVECs injury by directly inhibiting miR-515-5p from increasing ROCK1 expression and subsequently decreasing the expression and phosphorylation of eNOS. MiR-515-5p mimics could partially reverse the effects of HOXA11-AS knockdown.		Yes	 Ox-LDL could induce endothelial injuries by inhibiting cell proliferation (P < 0.001) and SOD synthesis (P < 0.001), promoting apoptosis (P < 0.01), ROS (P < 0.001), and MDA production (P < 0.001), increasing Bax (P < 0.001) and cleaved Caspase-3 (P < 0.001), and decreasing Bcl-2 (P < 0.001) and phosphorylated eNOS (P < 0.01). HOXA11-AS knockdown attenuated endothelial injuries via increasing eNOS phosphorylation. 	35578440
HOXA10-AS	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(lncRNA HOXA10-AS/miR-6509-5p/YBX1 signaling pathway )	IHC//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//H&E Staining//Colony Formation Assay//EdU Staining//Transwell Assay	 LncRNA HOXA10-AS is identified to be highly expressed in GC using the ENCORI database. The targets of HOXA10-AS included miR-6509-5p and Y-box binding protein 1 (YBX1). Specifically, HOXA10-AS downregulated miR-6509-5p in GC. An increase of miR-6509-5p inhibited GC cell growth. Meanwhile, miR-6509-5p interacted with YBX1 in GC. Together, lncRNA HOXA10-AS potentially acted as an oncogene through the lncRNA HOXA10-AS/miR-6509-5p/YBX1 signaling pathway in GC.	 Kaplan-Meier plot analysis indicated that the survival rate of the patient is associated with the expression of lncRNA HOXA10-AS.	Yes	Interference of HOXA10-AS inhibited GC cell proliferation, migration, and invasion as well as facilitated GC apoptosis. 	35521747
HOXA10-AS	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cells	Interaction(miR-582-3p/RAB31)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	 Briefly, HOXA10-AS was highly expressed in NPC cells. Further, HOXA10-AS could bind to miR-582-3p by acting as a competing endogenous RNA. Besides, Ras-related protein Rab-31 (RAB31) was proven as the target gene of miR-582-3p. Additionally, E2F transcription factor 1 (E2F1) acted as a transcription factor to activate HOXA10-AS expression. In the final rescue assays, we observed that the effect of HOXA10-AS depletion on NPC cell growth could be fully reversed by RAB31 overexpression or miR-582-3p inhibition. 		Yes	HOXA10-AS down-regulation restrained NPC cell proliferation and migration. 	35072529
HOXA10-AS	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer cell lines	Interaction( HOXA10-AS/miR-340-3p/HTR1D ceRNA axis)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 Lessened level of lncRNA HOXA10-AS reduced the sponging of miR-340-3p, resulting in an increase of miR-340-3p and a subsequent decrease of HTR1D to ultimately suppress the malignant biological behaviors of cancer. These data illustrated that the HOXA10-AS/miR-340-3p/HTR1D ceRNA axis acted a crucial part in the malignant biological behavior of pancreatic cancer in an AKT-dependent manner.		Yes	 Lessened level of lncRNA HOXA10-AS reduced the sponging of miR-340-3p, resulting in an increase of miR-340-3p and a subsequent decrease of HTR1D to ultimately suppress the malignant biological behaviors of cancer.	35813473
HOXA10-AS	LncRNA	Homo sapiens	Mouth Neoplasms	cancer cells	Regulation(TP63)	In Vivo Experiment//Wound Healing Assay//qRT-PCR//RIP//MTT//Colony Formation Assay//Transwell Assay	Recent transcriptomic profiling has recognized a tumor-biased expressed lncRNA, the HOXA10-AS transcript, whose expression is associated with patient survival.  In this study, we identify that HOXA10-AS serves as a modular scaffold for TP63 mRNA processing and that such involvement regulates cancer growth.	Recent transcriptomic profiling has recognized a tumor-biased expressed lncRNA, the HOXA10-AS transcript, whose expression is associated with patient survival. 	Yes	 Functional cell-based assays show that the HOXA10-AS transcript is essential in the regulation of oral cancer growth and metastasis. 	35858923
HOXA10-AS	LncRNA	Homo sapiens	Glioma	glioma cells	Regulation	Cell Proliferation Assay//qRT-PCR//RNA-seq//Flow Cytometry	In low-grade gliomas, HOXA10-AS activation is a robust marker of poor prognosis that complements IDH1/2 mutations, as validated in another retrospective cohort, and correlates with developmental pathways in tumor transcriptomes. Loss- and gain-of-function studies in patient-derived glioma cells, organoids, and xenograft models identify HOXA10-AS as a potent onco-lncRNA that regulates cell proliferation, contact inhibition, invasion, Hippo signaling, and mitotic and neuro-developmental pathways. 		Yes	Loss- and gain-of-function studies in patient-derived glioma cells, organoids, and xenograft models identify HOXA10-AS as a potent onco-lncRNA that regulates cell proliferation, contact inhibition, invasion, Hippo signaling, and mitotic and neuro-developmental pathways. 	34686327
HOXA10	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC stem cells and  tumor tissues	Interaction(microRNA-29a/MCL-1/phosphatidyl inositol 3-kinase/protein kinase B axis)	CCK8//qRT-PCR	HOXA10-AS and MCL-1 were highly expressed while miR-29a was poorly expressed in the collected tumor tissues and the extracted OSCC stem cells. In addition, HOXA-10-AS and MCL-1 were found to activate the phosphatidyl inositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway.	. High expression of HOXA10-AS and MCL-1, while poor expression of miR-29a was relevant to poor prognosis in patients. 	Yes	Silencing of HOXA10-AS suppressed proliferation and tumor sphere formation ability of stem cells, and it reduced growth and metastasis of tumors in animals. 	33831733
HOTTIP	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer stem cells 	regulation[miR-148a-3p/WNT1 pathway]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	In this study, we found that HOTTIP was markedly up-regulated in BCSCs and had a positive correlation with breast cancer progression.Our study is the first to report that HOTTIP regulates the CSC-like properties of BCSCs by as a molecular sponge for miR-148a-3p to increase WNT1 expression, offering a new target for breast cancer therapy.		Yes	 Functional studies revealed that overexpression of HOTTIP markedly promoted cell clonogenicity, increased the expression of the stem cell markers, OCT4 and SOX2, and decreased the expression of the differentiation markers, CK14 and CK18, in breast cancer cells.	32307830
HOTTIP	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[highly expressed]	qRT-PCR	Our results found that HOTTIP was upregulated in human primary CRC tissues.		Yes	 Knockdown of HOTTIP inhibited CRC cell proliferation, migration, and invasion.	31945724
HOTTIP	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[DKK1 ]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	Here, we found that HOTTIP level was significantly higher in CRC than in corresponding adjacent normal tissues.Mechanistic analyses indicated that HOTTIP regulates CRC cell metastasis partly through the downregulation of tumor suppressor DKK1 expression. Collectively, our results suggest that tumor expression of lncRNA HOTTIP plays an important role in CRC metastasis. HOTTIP may serve as a candidate biomarker in this disease.	Here, we found that HOTTIP level was significantly higher in CRC than in corresponding adjacent normal tissues, and patients with a larger tumor size, advanced pathological stage, or distant metastasis had higher HOTTIP expression.	Yes	Moreover, silencing HOTTIP expression by siRNA or shRNA could inhibit CRC cell migration and invasion in vitro and in vivo, whereas HOTTIP overexpression promoted cell metastasis, as documented in the SW480 cell lines. 	30229808
HOTTIP	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	patients with PTC	Expression[highly expressed]	qRT-PCR	PAPAS was downregulated, while the lncRNA HOXA transcript at the distal tip (HOTTIP) was upregulated in patients with PTC.	PAPAS expression level decreased, while HOTTIP expression level increased with the increase of clinical staging.	Yes	PAPAS overexpression led to the inhibition of cell proliferation, while HOTTIP overexpression increased proliferation of PTC cells, and HOTTIP overexpression decreased the effects of PAPAS overexpression. 	32194727
HOTTIP	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Regulation[PI3K/Akt/Atg13 signaling pathway]	Wound Healing Assay//qPCR//CCK8//Luciferase Report Assay//Transwell Assay	The results showed that HOTTIP expression was significantly upregulated in the RCC tissues and cell lines.Further research revealed that HOTTIP modification could affect RCC cell autophagy via the PI3K/Akt/Atg13 signaling pathway.	The results showed that HOTTIP expression was significantly upregulated in the RCC tissues and cell lines, and it was closely associated with TNM stage, histological grade, lymph node metastasis and patient prognosis. 	Yes	The in vitro and in vivo assays indicated that HOTTIP silencing inhibited RCC cell proliferation, migration and invasion and induced autophagy, and 3-MA (an autophagy inhibitor) reversed these effects. 	30511250
HOTTIP	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissue	Regulation[Wnt/β-catenin signaling]	qRT-PCR	 In the present study, our results observed that lncRNA HOTTIP expression levels were notably higher in ovarian cancer tissue samples compared to adjacent normal tissue samples. Furthermore, we demonstrated that inhibition of lncRNA HOTTIP suppressed Wnt/β-catenin signaling by downregulating β-catenin expression. Thus, these results suggest that aberrant HOTTIP expression level could serve as a promising biomarker for monitoring ovarian cancer and potential target of ovarian cancer treatment.	 Increased lncRNA HOTTIP expression levels were significantly associated with advanced FIGO stage and lymph node metastasis of ovarian cancer patients. Survival plots analysis results showed high lncRNA HOTTIP expression levels in ovarian cancer patients showed a poor prognosis compared to patients with low lncRNA HOTTIP expression levels. 	Yes	Function assays showed that lncRNA HOTTIP knockdown in ovarian cancer cells decreased cell proliferation and cell invasion capacities. 	30452402
HOTTIP	LncRNA	Homo sapiens	Ovarian Neoplasms		regulation[MEK/ERK pathway]	Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	In conclusion, HOTTIP was demonstrated to promote the proliferation, migration and invasion of OC cells by activating the MEK/ERK pathway.		Yes	The results demonstrated that knockdown of HOTTIP in OC cells significantly reduced the phosphorylation levels of MEK and ERK, inhibited the proliferation and invasion of OC cells and promoted their apoptosis.	33000231
HOTTIP	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cell lines and clinical tissues	regulation[miR-615-3p/SMARCE1 pathway]	qRT-PCR	 In this study, we demonstrated overexpression of HOTTIP in ovarian cancer cell lines and clinical tissues. In summary, lncRNA HOTTIP promotes the growth and metastatic phenotypes of ovarian cancer via regulating miR-615-3p/SMARCE1 pathway.	 Further, we showed that higher level of HOTTIP was associated with poor survival of ovarian cancer patients.	Yes	Notably, HOTTIP silencing restrained proliferation, migration, and invasiveness of ovarian carcinoma cells.	32783402
HOTTIP	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tissue samples and cell lines	Interaction(miR-148a-3p/AKT2 axis )	qRT-PCR//Colony Formation Assay//Western Blot	 The expression of HOTTIP was significantly upregulated in OC tissue samples and cell lines.  In addition, HOTTIP increased AKT2 expression by negatively regulating miR-148a-3p and then inhibited ASK1/JNK signaling. Further rescue experiments revealed that downregulation of miR-148a-3p and overexpression of AKT2 obviously diminished the effects of HOTTIP downregulation in OC cells. 		Yes	 The silencing of HOTTIP led to the inhibition of cell proliferation and NLRP1 inflammasome-mediated pyroptosis. 	33710684
HOTTIP	LncRNA	Homo sapiens	Ovarian Neoplasms	OCC tissues and cells	Interaction(HIF-1α )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//ELISA//Transwell Assay	HOTTIP was highly expressed in OCC. RNA pull-down indicated a direct interaction between HIF-1α and HOTTIP.		Yes	After HOTTIP knockdown, HIF-1α expression and VEGF concentration in OCC were decreased. Cell migration, invasion, and cell viability were decreased. Cell apoptosis rate and G0/G1 phase cells were increased. 	36699159
HOTTIP	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues,cell lines	Expression[highly expressed]	qRT-PCR	Furthermore, it was proved that HOTTIP was upregulated in HNSCC cell lines and cancerous tissues compared with corresponding normal cell lines and normal tissues. 		Yes	Functional assessment analysis revealed that HOTTIP might play a key role in the oncogenesis and progression of HNSCC.	31032351
HOTAIRM1	LncRNA	Homo sapiens	Glioblastoma	glioblastoma patients	Regulation(TGM2)	In Vivo Experiment//Western Blot//qRT-PCR//RNA-seq//Colony Formation Assay	 We identified HOTAIRM1 as a candidate lncRNA whose up-regulation is significantly associated with shorter survival of glioblastoma patients, independent from IDH mutation and MGMT promoter methylation.  HOTAIRM1 knock-down decreased expression of transglutaminase 2 (TGM2), a candidate protein implicated in mitochondrial function, and knock-down of TGM2 mimicked the phenotype of HOTAIRM1 down-regulation in glioblastoma cells. 		Yes	Glioblastoma cell line models uniformly showed reduced cell viability, decreased invasive growth and diminished colony formation capacity upon HOTAIRM1 down-regulation. Integrated proteogenomic analyses revealed impaired mitochondrial function and determination of reactive oxygen species (ROS) levels confirmed increased ROS levels upon HOTAIRM1 knock-down. 	34584066
HOTAIRM1	LncRNA	Homo sapiens	Thyroid Neoplasms	 PTC tissues	regulation[miR-144]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining	In this study, we identified a long noncoding RNA (lncRNA) HOTAIRM1, whose encoding gene was amplified and expression was upregulated in ATC compared with papillary thyroid cancer and normal thyroid. Altogether, these findings identified a genomic copy number amplified and highly expressed lncRNA HOTAIRM1, which exerted oncogenic roles via repressing miR-144 biogenesis in ATC. 		Yes	 Functional assays revealed that HOTAIRM1 promoted proliferation, inhibited apoptosis, and promoted migration and invasion of ATC cells in vitro, and promoted ATC tumour growth and metastasis in vivo.	32951513
HOTAIR	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-6888-3p/SYK )	CCK8//qRT-PCR//Western Blot	 We found that HOTAIR and SYK were highly expressed in OS, whereas miR-6888-3p expression was low. Mechanistically, these results suggest that the HOTAIR sponge, miR-6888-3p, regulates SYK expression. 		Yes	 In addition, downregulation of HOTAIR or SYK significantly inhibited the growth and migration of OS cells and the PI3K/AKT pathway, both in vitro and in vivo. Additionally, downregulation of miR-6888-3p promoted the proliferation and migration of OS cells and activated the PI3K/AKT pathway.	35435107
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	Regulation[miR-217/DACH1 signaling pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	HOTAIR was up-regulated and miR-217 was down-regulated in NSCLC cell lines.HOTAIR was up-regulated in NSCLC cell and regulates the proliferation, migration, invasion through the miR-217/DACH1 signaling pathway. It provides a novel potential treatment strategy for NSCLC.		Yes	 Silencing of HOTAIR significantly repressed cell proliferation and inhibited cell migration and invasion in H1299 and A549 cells by facilitating miR-217 expression.	30720199
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells and tissues	Interaction(CCL22)	qRT-PCR//Transwell Assay	 In conclusion, this study suggests that HOTAIR may promote proliferation, migration and invasion of the NSCLC cells by inhibiting CCL22 expression, which may play a key role in NSCLC cell immunity.		Yes	 In conclusion, this study suggests that HOTAIR may promote proliferation, migration and invasion of the NSCLC cells by inhibiting CCL22 expression, which may play a key role in NSCLC cell immunity.	35176085
HOTAIR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and the CRC cell lines	Regulation[p21]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 HOTAIR was found to be expressed at high levels, while p21 was determined to be at a low level among both the CRC tissues and the CRC cell lines.  The principal findings demonstrated that down-regulation of HOTAIR elicits an inhibitory effect on proliferation, invasion, and migration, while promoting the apoptosis of CRC cells through the up-regulation of p21. 	The expressions of HOTAIR and p21 were determined to be related to lymph node metastasis, tumor node metastasis, Dukes staging, distant metastases, histological types, and the degree of differentiation.	Yes	 Cells transfected with HOTAIR siRNA displayed inhibited rates of proliferation, invasion, and migration, as well as decreased cyclin E and CDK2, while apoptosis and p21 were increased.	29808247
HOTAIR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Interaction[recruiting EZH2]	qRT-PCR	 In this study, Hotair was found to be upregulated in colorectal cancer (CRC) cells and clinical specimens. In conclusion, Hotair mediated tumorigenesis via recruiting EZH2, which might shed light on the development of a novel therapeutic approach for patients with CRC.		Yes	Further investigation showed that knockdown of Hotair dramatically suppressed cell proliferation and colony formation, suggesting that Hotair may stimulate tumorigenesis of CRC.	30362162
HOTAIR	LncRNA	Homo sapiens	Colorectal Neoplasms	tissue and cell lines	Interaction(SNAIL/HNF4α )	CCK8//qRT-PCR//Western Blot	 HOTAIR was highly expressed in both tissue and cell lines of colorectal cancer, indicated a regulatory function in colorectal cancer.We further found that HOTAIR suppressed HNF4α via recruiting SNAIL, and the overexpression of HNF4α inhibited cell viability, migration, invasion and EMT of colorectal cancer cells. We demonstrated that HOTAIR regulates the level of HNF4α via recruiting SNAIL, knocking down HOTAIR repressed the cell viability and metestasis of colorectal cancer cell line in vitro, and suppressed the tomorgenesis and migration/invasion of colorectal cancer in vivo.		Yes	Knock-down of HOTAIR suppressed cell viability, migration, invasion and epithelial-mesenchymal transition (EMT) of colorectal cancer cells in vitro, and inhibited the growth and metastasis of colorectal tumor in nude mice.	33588137
HOTAIR	LncRNA	Homo sapiens	Colorectal Neoplasms	 tumor cell	Interaction(HOTAIR/miR-211-5p/FLT-1 axis )	RNA Pull-Down//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Invasion Assay//Transwell Assay	 We found that HOTAIR was highly expressed and predicted poor prognosis survival in CRC. Downregulation of HOTAIR repressed tumor malignant behaviors and cancer stemness. Mechanistically, HOTAIR facilitated the expression of the microRNA (miR)-211-5p target gene fms-like tyrosine kinase-1 (FLT-1), thereby modulating cancer stem cell (CSC) properties in CRC. We conclude that HOTAIR/miR-211-5p/FLT-1 axis contributes to CRC cancer stemness.	 We found that HOTAIR was highly expressed and predicted poor prognosis survival in CRC. 	Yes	Downregulation of HOTAIR repressed tumor malignant behaviors and cancer stemness. 	34470574
HOTAIR	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miR-203a-3p/ Wnt/β-catenin signaling )	qRT-PCR//Western Blot	 The expressions of HOTAIR were upregulated in CRC tissue tissues compared to adjacent control tissues. We also found HOTAIR was downregulated by miR-203a-3p in CRC cell lines. We also determined that β-catenin and GRG5 were inhibitory targets of miR-203a-3p, and that Wnt/β-catenin signaling was inhibited by both HOTAIR knockdown and miR-203a-3p overexpression. Significantly, we found that increased expression of miR-203a-3p is essential for cell proliferation repression, chemoresistance reduction, and Wnt/β-catenin signaling inhibition induced by HOTAIR knockdown.		Yes	 Both HOTAIR knockdown and miR-203a-3p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. 	29680837
HOTAIR	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Interaction[down-regulating miRNA-34a]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	QRT-PCR results showed that HOTAIR expression in colon cancer was significantly higher than that in normal tissues. QRT-PCR results showed that mRNA levels of miR-34a and HOTAIR in colon cancer tissues were negatively correlated. Besides, luciferase reporter gene assay revealed that overexpression of miR-34a significantly attenuated the luciferase activity of the wild-type HOTAIR vector group without attenuating the mutant HOTAIR vector group (p>0.05) In addition, the recovery experiment also found a mutual regulation between HOTAIR and miR-34a, together they could affect the malignant progression of colon cancer.	The incidence of distant metastasis was higher in patients with high expression of HOTAIR while their survival rate was lower than that of patients with low HOTAIR expression.	Yes	Meanwhile, cell proliferation, invasion as well as migration ability of the cells in HOTAIR knockdown group was significantly decreased than those in the negative control group.	31298326
HOTAIR	LncRNA	Homo sapiens	Colonic Neoplasms		Interaction[regulating IGF2BP2]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay//IF	We determined the expressions of HOTAIR, IGF2BP2, E-cadherin, and vimentin. Meanwhile, cell growth, cycle and apoptosis, migration, and invasion were assayed. LoVo cells were transplanted into nude mice, and tumor formation and microvessel density were evaluated. LncRNA HOTAIR positively regulated IGF2BP2. Besides, the expressions of HOTAIR and E-cadherin and the apoptosis were increased, while the expressions of IGF2BP2 and vimentin, the growth, invasion and migration of LoVo cells, the average tumor weight, and microvessel density value were decreased. Of importance, overexpressed IGF2BP2 could reverse the above impacts. 		Yes	Taken together, the current study indicates that silencing of HOTAIR could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing IGF2BP2 and the epithelial-mesenchymal transition.	30335892
HOTAIR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cells and tissues 	regulation[miR-488-5p/NUP205 Axis]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 It was demonstrated that high expression of HOTAIR in PTC cells (BCPAP) and tissues resulted in fast tumor growth and poor survival time of the PTC-bearing mice models.HOTAIR promoted the growth, migration, and invasion of papillary thyroid carcinoma mainly through regulating the miR-488-5p/NUP205 axis.		Yes	 Moreover, overexpression of HOTAIR leaded to markedly enhanced proliferation, migration, and invasion of BCPAP cells.	33107391
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	cell lines	Interaction(miR-126/EGFL7 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//IHC//Transwell Assay	These findings suggest that lncRNA HOTAIR regulate RCC angiogenesis through miR-126/EGFL7 axis and provide a new perspective on the molecular pathways of angiogenesis in RCC development, which might be potential therapeutic targets for RCC treatment.		Yes	HOTAIR knockdown and miR-126 overexpression suppressed the proliferation, migration, and angiogenesis of RCC cells. HOTAIR regulated EGFL7 expression by competitively binding to miR-126.HOTAIR significantly suppressed the RCC tumor progression and lung metastasis in vivo. 	33502949
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC cells	Expression(highly expressed)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	We found that the high expression of lncRNA HOTAIR in RCC is associated with poor prognosis. Moreover, HOTAIR and AR form a feedback loop to promote the expression of each other. Interestingly, we also found that in RCC, HOTAIR is associated with the Hedgehog pathway, especially GLI2, via bioinformatics analysis. Furthermore, HOTAIR promotes GLI2 expression in the presence of AR. Mechanistically, HOTAIR interacts with AR and they cooperatively bind to GLI2 promoter and increase its transcription activity.	We found that the high expression of lncRNA HOTAIR in RCC is associated with poor prognosis.	Yes	We further confirmed how HOTAIR-AR axis regulates GLI2 expression by analyzing its function in RCC cells and found that HOTAIR and AR synergistically enhanced the expression of GLI2 downstream genes, such as VEGFA, PDGFA, and cancer stem cell transcription factors, and promoted tumor angiogenesis and cancer stemness in RCC cells both in vitro and in tumor xenografts. 	33157157
HOTAIR	LncRNA	Homo sapiens	Osteoarthritis	cartilage tissues	regulation[inhibiting WIF-1 expression and activating Wnt pathway]	CCK8//qRT-PCR//Colony Formation Assay//Tunel	HOTAIR expression was greatly elevated in osteoarthritic compared to normal chondrocytes. Activation of Wnt/β-catenin signalling by HOTAIR through WIF-1 repression in osteoarthritic chondrocytes increases catabolic gene expression and promotes cartilage degradation.		Yes	 Silencing and over-expression of HOTAIR in SW1353 cells respectively reduced and increased the expression of genes associated with cartilage degradation in OA. 	32650720
HOTAIR	LncRNA	Homo sapiens	Osteoarthritis	OA cartilages and LPS-stimulated CHON-001 chondrocytes	Interaction(miR-1277-5p/SGTB axis)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//ELISA	 HOTAIR and SGTB were up-regulated, while miR-1277-5p was down-regulated in OA cartilages and LPS-stimulated CHON-001 chondrocytes.HOTAIR aggravated chondrocyte apoptosis and inflammation in OA via regulating miR-1277-5p/SGTB pathway.		Yes	HOTAIR depletion inhibited LPS-induced apoptosis and inflammation in chondrocytes. Moreover, down-regulation of HOTAIR attenuated LPS-triggered chondrocyte apoptosis and inflammation via sponging miR-1277-5p. Also, miR-1277-5p repressed LPS-induced chondrocyte apoptosis and inflammation by targeting SGTB. 	33721916
HOTAIR	LncRNA	Homo sapiens	Osteoarthritis	Chondrocytes	Interaction(miR-107/CXCL12 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	HOTAIR expression was enhanced, and miR-107 level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by HOTAIR silence, and restored by knockdown of miR-107.		Yes	HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect.	34183035
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		interaction[miR-122]	CCK8//qRT-PCR//ChIP//Western Blot	In this study, we found that HOTAIR was highly expressed whereas miR-122 was suppressed in HCC, and HOTAIR negatively regulated miR-122 expression in HCC cells. Mechanistically, a CpG island was located in the miR-122 promoter region. HOTAIR epigenetically suppressed miR-122 expression via DNMTs-mediated DNA methylation.		Yes	Furthermore, knockdown of HOTAIR dramatically inhibited HCC cell proliferation and induced cell cycle arrest in vitro and suppressed tumorigenicity in vivo by upregulating miR-122 expression.	30195653
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[HOTAIR/miR-214-3p/FLOT1 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	HOTAIR and FLOT1 expression were significantly up-regulated, whereas miR-214-3p was obviously down-regulated. Otherwise, HOTAIR regulated FLOT1 expression through targeting miR-214-3p in HCC cells. Simultaneously, low HOTAIR expression inhibited FLOT1 expression by up-regulating miR-214-3p, which suppressed tumor growth in vivo.		Yes	Also, down-regulation of HOTAIR and FLOT1 as well as up-regulation of miR-214-3p inhibited cell proliferation, invasion, and migration. Intriguingly, the effects of miR-214-3p overexpression on HCC cells were rescued by high expression of HOTAIR. 	31933720
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-526b-3p/DHX33 axis)	qRT-PCR	 The levels of HOTAIR and DHX33 were increased in HCC tissues and cells. Interestingly, miR-526b-3p could directly bind to HOTAIR, and DHX33 was a direct target of miR-526b-3p. Additionally, interference of HOTAIR restrained the tumor growth by upregulating miR-526b-3p and downregulating DHX33 in vivo.		Yes	Knockdown of either HOTAIR or DHX33 suppressed proliferation, migration and invasion but increased apoptosis in HCC cells. Moreover, DHX33 overexpression reversed the suppressive effect of HOTAIR knockdown on progression of HCC cells.	33843021
HOTAIR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue samples and cell lines	regulation[HOTAIR-miR-326-MTA2 axis]	qRT-PCR	Our results showed that HOTAIR was highly expressed both in OSCC tissue samples and cell lines compared with corresponding normal oral mucosa tissues and human oral keratinocytes.The HOTAIR-miR-326-MTA2 axis may contribute to a better understanding of OSCC pathogenesis and be a potential therapeutic target for OSCC.	Its overexpression was positively correlated with TNM (tumor-node-metastases) stage, histological grade, and regional lymph node metastasis. 	Yes	The knockdown of HOTAIR by short hairpin RNA significantly decreased the migration, invasion, and epithelial-mesenchymal transition of OSCC cells in vitro.	31995261
HOTAIR	LncRNA	Homo sapiens	pancreatic adenocarcinoma	tumor and adjacent healthy tissues	Interaction[upregulating HK2]	CCK8//qRT-PCR//Western Blot	the expression level of HOTAIR was significantly upregulated in tumor tissues compared with adjacent healthy tissues (P<0.05) in 46/51 patients. Therefore, it was concluded that the lncRNA HOTAIR may promote cancer cell energy metabolism in pancreatic adenocarcinoma by upregulating HK2.	 	Yes	HOTAIR and HK2 overexpression led to the promotion of tumor cell proliferation. HOTAIR overexpression increased lactate production, glucose uptake and ATP production.	31452722
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		interaction[miR-149-5p]	Flow Cytometry//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	 In summary, we find that HOTAIR can regulate HNRNPA1 expression through a ceRNA mechanism by sequester miR-149-5p, which post-transcriptionally targets HNRNPA1, thus promoting lung cancer progression.		Yes	LncRNA HOTAIR and HNRNPA1 are reported to play an oncogenic role in non-small cell lung cancer, and the overexpression of HNRNPA1 is shown to promote the proliferation of lung adenocarcinoma cells. 	33102210
HOTAIR	LncRNA	Homo sapiens	Breast Neoplasms	MCF-7 cells	Regulation(PI3K/AKT/mTOR signaling pathway)	CCK8	The results revealed that HOX antisense intergenic RNA knockdown can downregulate the expression of PI3K, AKT, and mTOR RNAs compared to negative control in MCF-7 cells. In addition, the proliferation of breast cancer cells was significantly reduced following the HOX antisense intergenic RNA silencing.		Yes	 In addition, the proliferation of breast cancer cells was significantly reduced following the HOX antisense intergenic RNA silencing.	35649067
HOTAIR	LncRNA	Homo sapiens	Breast Neoplasms	hepatocellular carcinoma cells	Interaction( miR-130a-3p/Suv39H1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 HOTAIR functioned as a ceRNA by sponging miR-130a-3p and subsequently promoted Suv39H1-mediated AKT/mTOR signaling. Suv39H1 restoration abolished the effects of HOTAIR knockdown on BC cell growth and metastasis. HOTAIR facilitated the Suv39H1-mediated AKT/mTOR pathway by acting as a molecular sponge of miR-130a-3p.		Yes	High HOTAIR expression facilitated BC cell growth and metastasis. 	35619625
HOTAIRM1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	regulation[HOTAIRM1/miR-107/TDG axis]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this study, we used quantitative reverse transcription PCR (qRT-PCR) to show that HOTAIRM1 was significantly downregulated in PTC tissues and low HOTAIRM1 expression levels were associated with lymph node metastasis and advanced TNM stage.  In conclusion, we validated HOTAIRM1 as a novel tumor-suppressor lncRNA in PTC and proposed that the HOTAIRM1/miR-107/TDG axis may serve as a therapeutic target for PTC.	In this study, we used quantitative reverse transcription PCR (qRT-PCR) to show that HOTAIRM1 was significantly downregulated in PTC tissues and low HOTAIRM1 expression levels were associated with lymph node metastasis and advanced TNM stage. 	Yes	Overexpression of HOTAIRM1 was found to inhibit PTC cell proliferation, invasion, and migration in vitro.	32269214
HOTAIRM1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	ADC tissues	regulation[miR-498/WWOX Axis]	CCK8//qRT-PCR//EdU Staining	HOTAIRM1 expression was considerably decreased in ADC tissues.HOTAIRM1 suppressed the proliferation and invasion of ADC cells via the modulation of miR-498/WWOX axis. 		Yes	 The knockdown of HOTAIRM1 promoted the cell cycle, growth, and invasion of ADC.	32606933
HOTAIRM1	LncRNA	Homo sapiens	Prostatic Neoplasms	cell lines	regulation[suppressing the Wnt pathway]	Flow Cytometry//qRT-PCR//MTT//Western Blot	HOTAIRM1 was overexpressed in PC3 cells compared with RWPE-1 cells.Overall, HOTAIRM1 silencing in PC3 cells inhibited the proliferative ability and promoted the apoptosis of PCa cells by suppressing the Wnt pathway, thereby inhibiting the progression of PCa.		Yes	Reducing HOTAIRM1 alleviated cell proliferation and increased apoptosis of PC3 cells so that the expression of pro-apoptotic agents such as Bad and Bax was significantly increased, while that of Bid and Bcl-2 (anti-apoptotic) was decreased.	33368390
HOTAIRM1	LncRNA	Homo sapiens	Thyroid Carcinoma, Anaplastic	ATC of papillary thyroid cancer 	Interaction(miR-144 / MET/AKT signalling)	In Vivo Experiment//Western Blot//qPCR//Luciferase Report Assay//Invasion Assay	In this study, we identified a long noncoding RNA (lncRNA) HOTAIRM1, whose encoding gene was amplified and expression was upregulated in ATC compared with papillary thyroid cancer and normal thyroid. HOTAIRM1 was found to bind ILF3, repress the binding between ILF3 and precursor miR-144 (pre-miR-144), block the effects of ILF3 on stabilizing pre-miR-144, and therefore downregulate pre-miR-144. Intriguingly, HOTAIRM1 was also found to directly bind primary miR-144 (pri-miR-144), repress the binding between pri-miR-144 and DROSHA, block the processing of pri-miR-144 by DROSHA, and therefore upregulate pri-miR-144 and downregulate pre-miR-144. 	Increased genomic copy number and expression of HOTAIRM1 were both correlated with poor survival of ATC patients.	Yes	Functional assays revealed that HOTAIRM1 promoted proliferation, inhibited apoptosis, and promoted migration and invasion of ATC cells in vitro, and promoted ATC tumour growth and metastasis in vivo. 	32951513
HOTAIRM1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Regulation[HOTAIRM1/HOXA1 Axis]	qRT-PCR//Western Blot	The expression levels of HOTAIRM1 and HOXA1 were significantly upregulated in type I EC tissues.Moreover, we identified that HOTAIRM1 acts as a regulator for the expression of the HOXA1 gene in type I EC cells. As an oncogene, HOXA1 silencing also caused suppressive effects on tumors by inhibiting cell proliferation, migration and invasion. In addition, we also confirmed the role of HOTAIRM1 and HOXA1 in promoting tumor growth in vivo.		Yes	 Knockdown of HOTAIRM1 significantly inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro, while the over-expression of HOTAIRM1 led to the opposite effects.	31853186
HOTAIRM1	LncRNA	Homo sapiens	Liver Neoplasms	cells	interaction[miR-125b]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 The expression level of RIZ1 and miR-125b was upregulated, and HOTAIRM1 was downregulated in liver cancer cells. For the first time, we found that RIZ1 was upregulated in liver cancer cells and RIZ1-mediated H3K9me1 enrichment on the HOTAIRM1 promoter regulated the growth and metastasis of liver cancer cells by targeting miR-125b, which could further accelerate tumor proliferation, migration and invasion. 		Yes	Transwell and CCK-8 assay showed that RIZ1 expression is associated with the proliferation, invasion and migration of liver cancer cells, silencing of RIZ1 inhibited cell proliferation, migration, and invasion in HEPG2 and HCC-LM3 cells.	32964965
Hotairm1	LncRNA	Mus musculus	Sepsis	a mouse model of sepsis	Regulation( Notch/Hes1 signaling)	RNA Pull-Down//Northern Blot//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Microarray//ELISA//ChIP	Using a mouse model of sepsis, we found that the long noncoding RNA HOTAIRM1 (HOXA transcript antisense RNA myeloid-specific 1) was highly expressed in mice during the late phase of sepsis. The upregulation of HOTAIRM1 was induced by Notch/Hes1 activation and, moreover, was critical for the formation of an immunosuppressive microenvironment. Further mechanistic studies identified HOXA1 as a key transcription factor targeted by HOTAIRM1 to regulate PD-L1 expression in lung alveolar epithelial cells. These results implicated that the Notch/Hes1/HOTAIRM1/HOXA1/PD-L1 axis was critical for sepsis-induced immunosuppression and could be a potential target for sepsis therapies.		Yes	HOTAIRM1 induced T cell exhaustion by increasing the percentage of PD-1+ T cells and regulatory T cells, accompanied by elevated PD-L1. Blockade of either Notch/Hes1 signaling or HOTAIRM1 inhibited T cell exhaustion in late sepsis, having alleviated lung injury and improved survival of mice. 	35022270
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues ,cell lines	Regulation[PI3K/ATK Signaling Pathway]	Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	The levels of HOTAIR and KLF12 were significantly upregulated and the level of miR-618 was strikingly downregulated in GC tissues and cells.miR-618 inhibited GC progression and PI3K/ATK signaling pathway by targeting KLF12. Mechanistically, HOTAIR modulated KLF12 expression by sponging miR-618 in GC cells.		Yes	 HOTAIR silencing blocked GC progression and PI3K/ATK signaling pathway by sponging miR-618 and also restrained xenograft tumor growth in vivo. 	31391030
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Regulation[miR-217-GPC5 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	We observed that Hotair was frequently up-regulated in GC tissues and cell lines, and high Hotair level was positively correlated with poor prognosis in GC patients. MiR-217 was decreased while GCP5 was increased in GC cells. Hotair negatively regulated the expression of miR-217 in GC while miR-217 targeted GCP5 to down-regulate its expression. Hotair promoted GC development by promoting GCP5 expression via sponging miR-217.		Yes	Knockdown of Hotair inhibited GC cells' viability, migration, invasion, Epithelial mesenchymal transition process. 	30557546
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[NF-κB pathway]	qRT-PCR	 The results showed that the expression of HOTAIR was higher in gastric cancer than in normal tissues, but reached the highest level in atrophic gastritis, suggesting that HOTAIR may be involved in the molecular process of nonresolving inflammation. Then tumor necrosis factor-α-induced protein-8 like-2 (TIPE2), a known gene associated with nonresolving inflammation, was overexpressed and the results showed that the promotion in TIPE2 expression triggered HOTAIR reduction, this result was further verified by microarray analysis and TIPE2 knockout mice. Subsequently, the data obtained from HOTAIR knockdown experiment showed that it significantly enhanced colony forming capability and inhibited p27 expression in AGS cells. Furthermore, deletion constructs and luciferase-based activity assays indicated that the -475 to -443bp region of HOTAIR promoter contained a crucial regulatory element. Transcription factor prediction with software TRANSFAC revealed that nuclear factor-κB signaling protein p65 had a binding site in this region and might have roles in HOTAIR expression. The binding of phosphor-p65 to HOTAIR promoter was verified by chromatin immunoprecipitation, and succeeding experiment results demonstrated that p65 reduction by p65 small interfering RNA and TIPE2 overexpression also decreased HOTAIR expression. Conclusively, our results suggest that HOTAIR was associated with nonresolving inflammation, and its expression is regulated by p65.		Yes	ubsequently, the data obtained from HOTAIR knockdown experiment showed that it significantly enhanced colony forming capability and inhibited p27 expression in AGS cells. 	30635945
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Regulation[miR-126/CXCR4 axis ]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay	HOTAIR was highly expressed in gastric cancer tissues and several gastric cancer cell lines. Our study demonstrated that high HOTAIR expression promote proliferation and metastasis in gastric cancer via miR-126/CXCR4 axis and downstream signaling pathways.		Yes	Overexpressed HOTAIR facilitated proliferation and metastasis in vitro while HOTAIR knockdown inhibit proliferation and metastasis. 	31517442
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines 	Expression[highly expressed]	qRT-PCR	 The expression levels of HOTAIR were significantly upregulated in GC tissues and cell lines. 	Increased HOTAIR was associated with tumor differentiation, lymph node and distant metastasis, and clinical stage. Furthermore, the area under the ROC curve (AUC) was up to 0.8416 (95 % CI=0.7661 to 0.9170, P<0.0001). The sensitivity and specificity were 66.67 and 87.04%, respectively. The correlation between HOTAIR expression and overall survival (OS) was statistically significant.	Yes	 In addition, knockdown of HOTAIR can inhibit GC cell growth and affect cell cycle distribution.	31281803
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	regulation[suppressing CCND1 and CCND2,stimulating miRNA-206]	Western Blot//ISH//Wound Healing Assay//Flow Cytometry//MTT//Transwell Assay	 HOTAIR expression significantly increased, and miRNA-206 expression significantly decreased in cancer tissues (p < .01 and p < .001, respectively);HOTAIR knockdown had antitumor effects by suppressing CCND1 and CCND2 expression by stimulating miRNA-206 in gastric cancer in vitro study.		Yes	HOTAIR knockdown suppressed cell viability, increased cell apoptosis by maintaining cells in the G1 phase, and inhibited cell invasion and migration by regulating miRNA-206 expression (p < .01 or p < .001).	33473276
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue	Expression[highly expressed]	CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	Meanwhile, the level of HOTAIR, H19, PVT1, and LINC00152 was upregulated.		Yes	 HOTAIR knockdown GC cells exhibited decreased migration, invasion, proliferation, and upregulated apoptosis, which released more miR-30a and -b into the exosomes.	32951010
HOTAIR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[miR-1277-5p,COL5A1]	qRT-PCR//Western Blot	We found that HOTAIR and COL5A1 were overexpressed in GC compared to normal controls, which predicted poor prognosis. HOTAIR regulates GC growth by sponging miR-1277-5p and upregulating COL5A1, and COL5A1-mediated GC cell proliferation may be mediated by effects on the tumor microenvironment, which provides novel targets for GC treatment.		Yes	HOTAIR/miR-1277-5p/COL5A1 axis in GC was demonstrated, and HOTAIR and COL5A1 were found to promote GC growth while miR-1277-5p exerted the reverse effects. 	32583079
HOTAIR	LncRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	regulation[miR-601/ZEB1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	HOTAIR was upregulated in BC tissues and cells, and its knockdown suppressed the proliferation, migration, invasion and the activity of AKT signaling pathway of BC cells.In short, this study demonstrated that HOTAIR promoted the proliferation, migration, invasion of BC through regulating the miR-601/ZEB1 axis, which provided a theoretical basis for the research on lncRNA-directed therapeutics in BC.		Yes	HOTAIR was upregulated in BC tissues and cells, and its knockdown suppressed the proliferation, migration, invasion and the activity of AKT signaling pathway of BC cells.	32694942
HOTAIR	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cells	Interaction(miR-129-5p/FZD7 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	HOTAIR and FZD7 were upregulated, while miR-129-5p was down-regulated in breast cancer tissues and cells. FZD7 restored the inhibition of miR-129-5p on breast cancer progression. Furthermore, HOTAIR was a sponge of miR-129-5p and FZD7 was a target of miR-129-5p.		Yes	Knockdown of miR-129-5p reversed the effect of HOTAIR knockdown on cell proliferation, migration, invasion and EMT. 	33104019
HOXA11-AS	LncRNA	Homo sapiens	Skin Neoplasms	 human skin cancer tissues and cell lines	Interaction(PI3K/AKT/mTOR signaling pathway)	Flow Cytometry//Transfection//Western Blot//Transwell Assay	The results showed significant (P < 0.05) upregulation of lncRNA HOXA11-AS transcript levels in human skin cancer tissues and cell lines.  Flow cytometry showed that HOXA11-AS knockdown triggered arrest of the A375 and HMCB cells at G2/M check point of cell cycle by inhibiting the expression of cyclin B1. Additionally, western blot analysis showed that HOXA11-AS knockdown resulted in the deactivation of PI3K/AKT/mTOR signaling pathway. 		Yes	knockdown of HOXA11-AS significantly (P < 0.05) inhibited the proliferation and colony formation of A375 and HMCB skin cancer cells. 	33442511
HOXA11-AS	LncRNA	Homo sapiens	Keloid	tissues and fibroblasts of keloid	Interaction(miR-182-5p on ZNF217)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qPCR//CCK8//Flow Cytometry//RIP//Luciferase Report Assay//Bioinformatics Analysis	HOXA11-AS was highly expressed in tissues and fibroblasts of keloid. Deficiency of HOXA11-AS blocked the proliferation and migration of keloid fibroblasts and induced fibroblast apoptosis. HOXA11-AS directly combined to miR-182-5p whose downregulation reversed the effects of HOXA11-AS knockdown. ZNF217 was a target of miR-182-5p, and HOXA11-AS indirectly promoted ZNF217 expression by binding to miR-182-5p. MiR-182-5p enrichment also blocked keloid fibroblast proliferation, survival and migration, while further ZNF217 overexpression abolished these effects. HOXA11-AS knockdown also hindered the growth of keloid in mouse models.		Yes	Deficiency of HOXA11-AS blocked the proliferation and migration of keloid fibroblasts and induced fibroblast apoptosis. HOXA11-AS directly combined to miR-182-5p whose downregulation reversed the effects of HOXA11-AS knockdown. ZNF217 was a target of miR-182-5p, and HOXA11-AS indirectly promoted ZNF217 expression by binding to miR-182-5p. MiR-182-5p enrichment also blocked keloid fibroblast proliferation, survival and migration, while further ZNF217 overexpression abolished these effects. HOXA11-AS knockdown also hindered the growth of keloid in mouse models.	35987744
HOXA11-AS	LncRNA	Homo sapiens	Keloid	 keloid tissues and keloid fibroblasts	Interaction(miR-205-5p-FOXM1 Pathway)	Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay	 HOXA11-AS and FOXM1 were significantly upregulated in keloid tissues and keloid fibroblasts, while miR-205-5p was downregulated. MiR-205-5p was targeted by HOXA11-AS, and its inhibition overturned the effects of HOXA11-AS knockdown. Moreover, FOXM1 was a target of miR-205-5p, and HOXA11-AS regulated the expression of FOXM1 by adsorbing miR-205-5p. 		Yes	HOXA11-AS knockdown or miR-205-5p enrichment inhibited proliferation, migration, invasion, ECM accumulation, and glycolysis but accelerated apoptosis of keloid fibroblasts. 	33261854
HOXB-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cancerous tissues	Regulation[p53 ]	Western Blot//Flow Cytometry//qRT-PCR//RIP//ChIP	The results of qRT-PCR showed that the expression of HOXB-AS3 was significantly higher in cancerous tissues of patients with hepatocellular carcinoma than in adjacent tissues.Highly expressed HOXB-AS3 was confirmed to promote the proliferation of hepatocellular carcinoma cells and inhibit apoptosis, and the mechanism was related to the regulation role of HOXB-AS3 in p53 expression by binding to DNMT1.		Yes	 Inhibition of HOXB-AS3 expression in liver cancer cells including Hep3B and LM3 could promote cell proliferation, inhibit cell apoptosis and induce cell cycle arrest in the G0/G1 phase. 	30402841
HOXB-AS3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction( IGF2BP2/c-Myc )	qRT-PCR//Colony Formation Assay//Western Blot	HOXB-AS3 was upregulated in OSCC tissues, in both TCGA database and in patients with OSCC recruited into the present study.HOXB-AS3 was also found to encode a protein that directly interacted with IGF2BP2 and thereby promoted the stability of c-myc. Taken together, the results from the present study indicated that increased HOXB-AS3 expression was associated with poor prognosis in OSCC. 	 HOXB-AS3 was associated with poor prognosis in OSCC. 	Yes	The proliferation and viability decreased in the 2 OSCC cell lines following knock down of HOXB-AS3.	34457052
HOXB-AS3	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues and cells	Interaction(miR-498-5p/ADAM9 axis)	qRT-PCR//IHC//Western Blot	HOXB-AS3 expression was upregulated in EC tissues and cells. A putative miR-498-5p binding site in HOXB-AS3 was verified. Inhibition of miR-498-5p rescued the effects of HOXB-AS3 knockdown on cell proliferation and apoptosis. Finally, ADAM9 was verified as a direct target gene of miR-498-5p.		Yes	EC cell proliferation and viability decreased significantly in HOXB-AS3 knockdown groups. 	34187214
HOXB-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Expression(highly expressed)	qRT-PCR	In the following study, HOXB-AS1 was unveiled to be highly expressed in HCC tissues as opposed to normal tissues.  In summary, this study highlights HOXB-AS1 as key upregulated lncRNA in HCC which being an oncogene can cause proliferation and metastasis of HCC cells. 	 Moreover, the data showed that expression levels of HOXB-AS1 contribute significantly to the patient's survival rates.	Yes	Silencing of HOXB-AS1 led to the loss of proliferation, migration, and invasiveness of HCC cells, namely Hep3B and Huh7. 	36045719
HOXB-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissue	regulation[Sponged miR-149-3p to Upregulate Wnt10b]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In this study, We found that HOXB-AS1 expression was significantly upregulated in EC tissue samples and was associated with shorter survival time.  In conclusion, our results indicated that HOXB-AS1 exerted oncogenic function as competing endogenous RNA (ceRNA) of miR-149-3p to release Wnt10b and activated Wnt/β-catenin pathway.	 In this study, We found that HOXB-AS1 expression was significantly upregulated in EC tissue samples and was associated with shorter survival time. 	Yes	 Furthermore, upregulation of HOXB-AS1 promoted proliferation, invasion, and migration of EC cell.	33073693
HOXB-AS1	LncRNA	Homo sapiens	Multiple Myeloma	cell lines	Regulation[HOXB-AS1/ELAVL1/FUT4 axis]	qRT-PCR	In this study, we unveiled that HOXB-AS1 was highly expressed in MM and loss-of-function assays certified that HOXB-AS1 obstruction suppressed MM cell proliferation, and stimulated cell apoptosis.In conclusion, the whole modulation mechanism of HOXB-AS1/ELAVL1/FUT4 axis in MM was validated in this study, which suggested that HOXB-AS1 might function as a powerful and promising therapeutic biomarker for the clinical treatment of patients with MM.		Yes	In this study, we unveiled that HOXB-AS1 was highly expressed in MM and loss-of-function assays certified that HOXB-AS1 obstruction suppressed MM cell proliferation, and stimulated cell apoptosis.	31886581
HOXB13	LncRNA	Homo sapiens	Glioblastoma	GBM tissues	Regulation[HOXB13/HOXC-AS3 signaling axis]	qRT-PCR	Through microarray and immunohistochemistry analyses, HOXB13 was highly expressed in GBM tissues.We believed that HOXB13/HOXC-AS3 signaling axis can be served as therapeutic targets for this highly aggressive cancer.		Yes	 GBM cells U87 and U251 overexpressing HOXB13 showed enhanced proliferation, migration, and invasion relative to the control cells, while knockdown of HOXB13 led to decreased cell proliferation, migration, and invasion abilities. 	31062400
HOXA-AS3	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues 	Interaction(miR-29a-3p/LTβR /NF-κB signaling)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//IF	GC cells and tissues exhibited significant HOXA-AS3 upregulation (P < 0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status. At a mechanistic level, we found that HOXA-AS3 was able to sequester miR-29a-3p, thereby regulating the expression of LTβR and modulating NF-κB signaling in GC.	GC cells and tissues exhibited significant HOXA-AS3 upregulation (P < 0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status.	Yes	 Knocking down HOXA-AS3 disrupted GC cell proliferation, migration, and invasion in vitro and tumor metastasis in vivo. 	33602223
HOXA-AS3	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC clinical samples and human CRC cell lines (SW480, SW620, HCT116, COLO205, and LOVO)	Interaction(miR-4319/SPNS2 axis)	CCK8//qRT-PCR//Western Blot	In this study, HOXA-AS3 was significantly over-expressed in CRC clinical samples and human CRC cell lines (SW480, SW620, HCT116, COLO205, and LOVO). The dual luciferase reporter assay suggested that HOXA-AS3 acted as a sponge of miR-4319, and miR-4319 further directly targeted SPNS2 for expression regulation. Besides, HOXA-AS3 was determined to mediate CRC cell proliferation and apoptosis via miR-4319/SPNS2 axis. 		Yes	The depletion of HOXA-AS3 remarkably inhibited cell proliferation, induced cell cycle arrest, and promoted cell apoptosis in CRC cell lines. Additionally, HOXA-AS3 knockdown was determined to facilitate miR-4319 expression and reduce expression level of sphingolipid transporter 2 (SPNS2) in CRC cell lines. 	34671931
HOXA-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues and cell lines	Regulation[MEK/ERK Signaling Pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In the present study, HOXA-AS3 was highly expressed in HCC tumor tissues and cell lines. Taken together, our study is the first to show the interaction of HOXA-AS3 with miR-29c in facilitating cell proliferation, metastasis, EMT process, and MEK/ERK signaling pathway in HCC.	High HOXA-AS3 expression was correlated with low survival of HCC patients. 	Yes	 Loss-of-function experiments showed that knockdown of HOXA-AS3 inhibited cell proliferation, migration, invasion, the epithelial-mesenchymal transition (EMT) process, and the mitogen-activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathway in HCC.	30963785
HOXA-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines	Interaction( miR-455-5p/PD-L1 Axis)	qRT-PCR	High HOXA-AS3 expression was observed in the HCC cell lines.  We also identified an miR-455-5p binding site in HOXA-AS3. By sponging miR-455-5p, HOXA-AS3 increased the expression of PD-L1. Additionally, both the inhibition of PD-L1 and overexpression of miR-455-5p reversed the effects on cell proliferation and invasion triggered by the overexpression of HOXA-AS3. 		Yes	 Furthermore, overexpression of HOXA-AS3 in HCC cells enhanced proliferation, migration, and invasion, regulated the cell cycle, and retarded apoptosis. 	34988230
HOXA-AS3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-218-5p/COL1A1/LPCAT1 axis)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Here, we found that the expression of lncRNA HOXA-AS3 was upregulated in OSCC tissues and cell lines compared with the para-cancerous tissues and normal human oral keratinocyte (NHOK), respectively. Further, the luciferase reporter assay showed that HOXA-AS3 was directly bound to miR-218-5p. Moreover, the expression of miR-218-5p was negatively regulated by HOXA-AS3, and miR-218-5p could inhibit the expression of collagen type I alpha1 (COL1A1) and lysophosphatidylcholine acyltransferase 1 (LPCAT1). 		Yes	 Inhibition of HOXA-AS3 significantly inhibited the proliferation and colony formation of OSCC cells. 	34698001
HOXA-AS3	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	tissues and cells 	Interaction(miR-29a-3p)	Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	HOXA-AS3 was elevated and miR-29a-3p was decreased in tissues and cells of cervical cancer patients. Bioinformatics analysis confirmed that HOXA-AS3 negatively regulates cervical cancer development by sponging miR-29a-3p.	 Knockdown of HOXA-AS3 could inhibit the progression of cervical cancer and was more conducive to patient survival.	Yes	 Knockdown of HOXA-AS3 could inhibit the progression of cervical cancer and was more conducive to patient survival.	35817473
HOXA-AS3	LncRNA	Homo sapiens	Glioblastoma	GBM cells	regulation[miR-455-5p/USP3 axis]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our results showed that lncRNA HOXA-AS3 was significantly up-regulated in GBM cells and could promote GBM cell proliferation, invasion and migration in vitro and in vivo. The newly identified HOXA-AS3/mir-455-5p/USP3 pathway offers important clues to understanding the key mechanisms underlying the action of lncRNA HOXA-AS3 in glioblastoma.	 HOXA-AS was found to be associated with poor survival prognosis in glioma patients. 	Yes	Our results showed that lncRNA HOXA-AS3 was significantly up-regulated in GBM cells and could promote GBM cell proliferation, invasion and migration in vitro and in vivo. 	32918360
HOXA-AS3	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cells and tissues	Interaction(miR-29c/CDK6 axis)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	HOXA-AS3 level was upregulated in PC, and its knockdown suppressed PC cells proliferation, whereas miR-29c antagonized the regulatory effect of HOXA-AS3 knockdown by directly binding to HOXA-AS3.Moreover, CDK6 was a target of miR-29c and miR-29c exerted anti-proliferation effects through inhibiting CDK6. 		Yes	HOXA-AS3 level was upregulated in PC, and its knockdown suppressed PC cells proliferation, whereas miR-29c antagonized the regulatory effect of HOXA-AS3 knockdown by directly binding to HOXA-AS3.	34659534
HOXA-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC  tissue	Interaction[microRNA-216a-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	In this experiment, qRT-PCR results revealed that HOXA-AS2 level in NSCLC tumor tissue specimens was remarkably higher than that in adjacent tissues. Subsequently, qRT-PCR verified that microRNA-216a-5p level was remarkably decreased in NSCLC tissues and negatively correlated with HOXA-AS2 expression. In addition, the result of the cell recovery experiment and Western blotting revealed that there might be a mutual regulation between HOXA-AS2 and microRNA-216a-5p, the two of which could jointly regulate the malignant progression of NSCLC.	Compared with those with low expression of HOXA-AS2, the patients with high expression had a higher incidence of distant metastases and a lower overall survival rate. 	Yes	The proliferative and metastasis abilities of the cells in the HOXA-AS2 overexpression group were remarkably increased when compared with the control group, while the opposite results were observed in HOXA-AS2 silence group.	31389597
HOXA-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[upregulating IGF2]	qRT-PCR//Wound Healing Assay//Transwell Assay	By comparing with the expression level in adjacent tissues, HOXA-AS2 expression was higher in NSCLC samples. In this work, HOXA-AS2 could enhance migratory and invasive abilities of NSCLC cells by upregulating IGF2, which might offer a potential therapeutic target for NSCLC.		Yes	Moreover, HOXA-AS2 knockdown inhibited invasion and migration of NSCLC cells and, conversely, HOXA-AS2 overexpression obtained the opposite results.	31210310
HOXA-AS2	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues,cell lines	Regulation[miR-125b/Smad2 axis ]	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Invasion Assay	Our results firstly demonstrated the upregulation of HOXA-AS2 in both bladder cancer cells and clinical bladder tumors.Furthermore, this study also identified miR-125b as a downstream target of HOXA-AS2 and revealed the downregulation of miR-125b by HOXA-AS2 as well as the involvement of HOXA-AS2/miR-125b/Smad2 interactions in the functional role of HOXA-AS2 in mediating the migration, invasion and stemness of bladder cancer cells.	Such upregulation was also positively correlated with the advanced stage, invasion and lymph node metastasis of bladder cancer as well as the expression of cancer stem cell marker OCT4 in patients.	Yes	Such upregulation was also positively correlated with the advanced stage, invasion and lymph node metastasis of bladder cancer as well as the expression of cancer stem cell marker OCT4 in patients.	30412716
HOXA-AS2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells and tissues	Interaction(miR-567/CDK8)	qRT-PCR//Western Blot	LncRNA HOXA-AS2 was up-regulated in OSCC cells and tissues with the expression of miR-567 decreased. In terms of the mechanism, we found that lncRNA HOXA-AS2 negatively regulates miR-567 expression via a direct interaction. We also observed that miR-567 directly targets the 3' UTR of CDK8. Moreover, silencing lncRNA HOXA-AS2 inhibited tumor growth with the expression of miR-567 increased and CDK8 decreased in vivo.	The tissue lncRNA HOXA-AS2 expression was found to positively correlate with the TNM stage and lymph node metastasis of OSCC patients. 	Yes	Functionally, overexpression of lncRNA HOXA-AS2 significantly promoted OSCC cell proliferation, while knockdown of lncRNA HOXA-AS2 significantly inhibited it. 	34267554
HOXA-AS2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells	Interaction(EZH2)	Western Blot//CCK8//qRT-PCR//Cell Cycle Assay//EdU Staining	Compared with HIOEC cells, HOXA-AS2 expression in OSCC cells was upregulated. In addition, HOXA-AS2 was predicted to directly target EZH2 and positively regulate EZH2 expression. EZH2 overexpression could reverse the inhibitory effect of HOXA-AS2 knockdown on the proliferation, migration, and invasion of Tca-8113 cells. 		Yes	HOXA-AS2 knockdown significantly inhibited Tca-8113 cell proliferation, blocked the cell cycle by arresting cells in the G0/G1 phase, promoted apoptosis, and suppressed migration and invasion. 	34519570
HOXB-AS3	LncRNA	Homo sapiens	Ovarian Neoplasms	 EOC tissues	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	HOXB-AS3 was abundantly expressed in EOC tissues, and higher levels of HOXB-AS3 in EOC patients were significantly associated with disease status and overall survival status. 	HOXB-AS3 was abundantly expressed in EOC tissues, and higher levels of HOXB-AS3 in EOC patients were significantly associated with disease status and overall survival status. EOC patients with high levels of HOXB-AS3 had strikingly shorter disease-free survival (DFS) and overall survival (OS) times than those with low levels. HOXB-AS3 also might as an independent prognostic factor. 	Yes	Further study revealed knockdown of HOXB-AS3 significantly inhibited the proliferation, invasion and migration of EOC cells. 	33148416
HOXB-AS3	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC patients	Interaction(miR-378a-3p/LDHA/ECAR)	qRT-PCR//Western Blot	HOXB-AS3 was abundantly expressed in EOC tissues, and higher levels of HOXB-AS3 in EOC patients were significantly associated with disease status and overall survival status.Mechanistic investigations suggested that knockdown of HOXB-AS3 could decrease lactate dehydrogenase A (LDHA) expression and the extracellular acidification rate (ECAR) by sponging miR-378a-3p.	HOXB-AS3 was abundantly expressed in EOC tissues, and higher levels of HOXB-AS3 in EOC patients were significantly associated with disease status and overall survival status. EOC patients with high levels of HOXB-AS3 had strikingly shorter disease-free survival (DFS) and overall survival (OS) times than those with low levels.	Yes	Further study revealed knockdown of HOXB-AS3 significantly inhibited the proliferation, invasion and migration of EOC cells. 	33148416
HOXB-AS3	LncRNA	Homo sapiens	Lung Neoplasms	NSCLC tissues and cells	regulation[ PI3K-AKT pathway]	qRT-PCR	 In the current research, we found HOXB-AS3 was obviously elevated in NSCLC tissues and cells.  Overall, we implied that HOXB-AS3 might provide a new perspective for lung cancer treatment via targeting PI3K/AKT.		Yes	Functional assays showed that inhibition of HOXB-AS3 was able to repress A549 and H1975 cell proliferation, cell colony formation ability and meanwhile, triggered cell apoptosis.	32039488
HOXD-AS2	LncRNA	Homo sapiens	Glioma	cell lines	Expression[highly expressed]	qRT-PCR	HOXD-AS2 was increased in glioma cells and it was associated with glioma grade and poor prognosis.	HOXD-AS2 was increased in glioma cells and it was associated with glioma grade and poor prognosis.	Yes	Loss of HOXD-AS2 can inhibit glioma cell growth by inducing cell-cycle G1 arrest in vitro.	30485495
HOXD-AS2	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Expression(highly expressed)	cell invasion assay//Migration Assay//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay	 The expression level of HOXD-AS2 gene in glioma was significantly higher than that in the normal brain tissue, which was related to the tumor grade. The level of HOXD-AS2 gene in patients with high-grade glioma was higher than that in patients with low-grade glioma.	 High expression of HOXD-AS2 gene was a risk factor for poor prognosis of glioma patients. 	Yes	Knocking down the expression of HOXD-AS2 in glioma cell line U251 arrested the cell cycle and reduced the cell proliferation. Furthermore, it could significantly reduce the migration ability of the cells but had no significant effect on the invasion.	36408341
HOXD-AS2	LncRNA	Homo sapiens	Glioblastoma	GBM patient tumor samples and GBM cell lines	Interaction(miR-3681-5p/MALT1 signaling pathway)	In Vivo Experiment//cell invasion assay//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//IHC	HOXD-AS2 was found to be significantly up-regulated in GBM tissues, which was further confirmed in GBM patient tumor samples and GBM cell lines. We further identified and validated miR-3681-5p as a target of HOXD-AS2, and miR-3681-5p was negatively regulated by HOXD-AS2. By negatively affecting miR-3681-5p, HOXD-AS2 could promote the expression of MALT1 to augment the aggressiveness of GBM cells. miR-3681-5p overexpression or MALT1 knockdown attenuated aggressiveness of GBM cells. 		Yes	Silencing HOXD-AS2 inhibited cell proliferation, migration and invasion, and promoted cell apoptosis. 	34802389
HOXC-AS3	LncRNA	Homo sapiens	Breast Neoplasms		Interaction[sponging miR-3922-5p]	Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay	HOXC-AS3 is aberrantly overexpressed in breast cancers especially the HER2 type.Our results demonstrated that miR-3922-5p was a direct target of HOXC-AS3, and PPP1R1A was a target of miR-3922-5p in breast cancer		Yes	 In addition, HOXC-AS3 regulates cell Invasion and migration both in vitro and in vivo. 	31797701
HOXC-AS3	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	interaction[binding to YBX1]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//ChIP	Based on public breast cancer expression data and using bioinformatics methods, we discovered significantly upregulated expression levels of HOXC-AS3 in diseased tissues.Further, mechanistic studies demonstrated the potential of HOXC-AS3 in the transcriptional activation of TK1 via its binding to YBX1. Furthermore, the silencing of TK1 reversed HOXC-AS3-mediated increase in breast cancer cell growth and migration. 	We verified this result in breast cancer samples and found that the expression of HOXC-AS3 was well correlated with the prognosis of breast cancer. 	Yes	In vitro and in vivo experimental evidence suggests that HOXC-AS3 has the potential to regulate tumorigenesis. 	33194034
HOXC-AS3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-96)	qRT-PCR//RNA Pull-Down//Transwell Assay	NSCLC tissues exhibited significantly increased expression levels of HOXC-AS3 and premature miR-96. HOXC-AS3 was localized to both nucleus and cytoplasm, and a direct interaction between HOXC-AS3 and premature miR-96 was observed. In NSCLC cells, HOXC-AS3 upregulated the expression of premature miR-96 but downregulated the expression of mature miR-96. 		Yes	HOXC-AS3 suppressed the role of miR-96 in inhibiting NSCLC cell invasion and migration.	35034519
HOXC-AS3	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	Interaction(miR-96)	CCK8//qRT-PCR//Western Blot	HOXC-AS3 was upregulated in OC, while mature miR-96 and miR-96 precursor were downregulated in OC. In OC cells, overexpression of HOXC-AS3 reduced the expression levels of mature miR-96, but not miR-96 precursor. In addition, overexpression of HOXC-AS3 attenuated the effects of overexpression of miR-96. HOXC-AS3 suppresses the formation of mature miR-96 in OC cells to promote cell proliferation.		Yes	Cell proliferation analysis showed that overexpression of HOXC-AS3 resulted in increased cell proliferation, while overexpression of miR-96 suppressed cell proliferation. 	33651311
HOXC-AS3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC specimens and cells	Interaction(HOXC-AS3/YBX1/HOXC8 axis )	In Vivo Experiment//Wound Healing Assay//CCK8//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 The levels of HOXC-AS3 and HOXC8 were increased in human NSCLC specimens and cells. HOXC-AS3 directly bound to YBX1 to suppress its ubiquitination mediated by MDM2. YBX1 bound to the HOXC8 promoter and enhanced its transcription. Knockdown of HOXC8 inhibited the effects of HOXC-AS3 overexpression on NSCLC. HOXC-AS3 promotes NSCLC growth and metastasis by stabilising YBX1 and thus increasing HOXC8 transcription. 		Yes	Knockdown of HOXC-AS3 suppressed NSCLC cell proliferation, migration and invasion, as well as tumour growth and metastasis in vivo. 	35387975
HOXC-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues	Interaction(HOXC13 )	qRT-PCR//IHC//RIP//Transwell Assay	We found that HOXC-AS2 was significantly up-regulated in NSCLC tissues. Taken together, HOXC-AS2 knockdown inhibited NSCLC cell proliferation and migration, as well as stimulated NSCLC cell apoptosis through regulation of HOXC13 expression.		Yes	HOXC-AS2 expression resulted in significant decreases in NSCLC cell proliferation, migration, and epithelial-mesenchymal transition (EMT) process marker proteins, simultaneously activated A549 and HCC827 cell apoptosis. 	33427025
HOXC-AS2	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	Interaction[HOXC-AS2/miR-876-5p/ZEB1]	qRT-PCR//Luciferase Report Assay//RIP	We found HOXC-AS2 was upregulated in glioma cells and tissues. Our results conclude that HOXC-AS2/miR-876-5p/ZEB1 constitutes a positive feedback loop to regulate EMT in GBM, providing a potential therapeutic target for glioma.		Yes	Depletion of HOXC-AS2 was associated with the inhibition of migration, invasion and EMT process in glioma cells. 	31571911
HOXC-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	regulation[Wnt/β-catenin signaling]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	lncRNA HOXC-AS1 expression is up-regulated in GC cells and a decrease of lncRNA HOXC-AS1 inhibited cell viability. HOXC-AS1 may promote the proliferation and the EMT process and inhibit apoptosis by binding eIF4AIII via Wnt/β-catenin signaling, which indicates that HOXC-AS1/eIF4AIII might be an axis that could be further used as a biomarker to help with the diagnosis of GC.		Yes	lncRNA HOXC-AS1 expression is up-regulated in GC cells and a decrease of lncRNA HOXC-AS1 inhibited cell viability. 	32307743
HOXC-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC cells	Interaction(miR-99a-3p/MMP8)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Therefore, we examined GC cells and tissues for the expression of HOXC-AS1 and correlated the expression levels with the disease specific survival of the patients, finding that HOXC-AS1 was overexpressed and probably had a tendency of leading to a poor prognosis.  After knockdown of HOXC-AS1, miR-99a-3p was clearly overexpressed in GC cells. In addition, matrix metalloproteinase 8 (MMP8) was shown to be combined with miR-99a-3p using TargetScan. Similar experiments, along with western blot, were conducted to validate the correlation between miR-99a-3p and MMP8. Finally, rescue experiments for CCK-8 were completed, disclosing that HOXC-AS1 promoted cell progression of GC through sponging miR-99a-3p followed by subsequent upregulation of MMP8.	Therefore, we examined GC cells and tissues for the expression of HOXC-AS1 and correlated the expression levels with the disease specific survival of the patients, finding that HOXC-AS1 was overexpressed and probably had a tendency of leading to a poor prognosis. 	Yes	The Cell Counting Kit-8 assay and colony formation assay were then performed under knockdown of HOXC-AS1, revealing that cell proliferation of GC was distinctly decreased. Afterwards, miR-99a-3p was predicted to bind with HOXC-AS1 by DIANA tools.	35884594
HOXC-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells	Interaction(IGF2BP2 )	RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	HOXC-AS1 is highly expressed in ESCC cells and plays oncogenic effects in vivo. qPCR showed the positive relationship between HOXC-AS1 and SIRT1 following HOXC-AS1 knockdown or overexpression. RNA-pulldown, mass spectrometry and RIP assay demonstrated that IGF2BP2 is an RBP downstream of HOXC-AS1. Then, RIP and qPCR showed that IGF2BP2 could bind to SIRT1 mRNA and knockdown IGF2BP2 resulted in decreased SIRT1 mRNA level. Finally, a series of rescue assay showed that the HOXC-AS1-IGF2BP2-SIRT1 axis can affect the function of ESCC.		Yes	HOXC-AS1 is highly expressed in ESCC cells and plays oncogenic effects in vivo. qPCR showed the positive relationship between HOXC-AS1 and SIRT1 following HOXC-AS1 knockdown or overexpression. 	36510377
HOXC-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC and in NPC cell lines	Interaction(miR-4651/FOXO6 )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The present study found that HOXC-AS1 was highly expressed in NPC and in NPC cell lines, suggesting a critical role of HOXC-AS1 in NPC progression. We found that HOXC-AS1 could sponge miR-4651 subsequently binding FOXO6 and inhibiting its expression. Therefore, HOXC-AS1/miR-4651/FOXO6 may form a competing endogenous RNA (ceRNA) network that promotes NPC progression.	 In addition, the abundance of HOXC-AS1 was negatively correlated with the prognosis of NPC.	Yes	 It could be observed that HOXC-AS1 knockdown decreases cell proliferation, migration and invasion, but induces cell apoptosis in NPC. 	34507637
HOXC9	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	LUAD tumor tissues and cell lines	Interaction(circCENPF/hsa-miR-184 axis )	cell invasion assay//Migration Assay//Proliferation Assay//migration assay//PCR//Cell Proliferation Assay//Invasion Assay//IF	 HOXC9 expression was increased in NSCLC and correlated with poor prognosis in lung adenocarcinoma. In addition, HOXC9 expression levels were significantly correlated with immune cell infiltration of tumors and biomarkers of immune cells.  Finally, the circCENPF/hsa-miR-184 axis was identified as the most promising upstream regulatory pathway of HOXC9 in lung adenocarcinoma.	 HOXC9 expression was increased in NSCLC and correlated with poor prognosis in lung adenocarcinoma.	Yes	 Overexpression of HOXC9 promoted NSCLC cell proliferation, migration, and invasion in vitro.	36272177
HOXC13-AS-201	LncRNA	Homo sapiens	Ameloblastoma	AB tissues	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Real-time qPCR confirmed that lncRNA ENST00000512916 was up-regulated in AB tissues. 		Yes	ENST00000512916 knockdown significantly inhibited cell proliferation, migration and the expression of CDK2/4/6 in AM-1 cells. Moreover, ENST00000512916 knockdown suppressed tumor growth in vivo. 	32110049
HOXC13-AS	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	Regulation[miR-497-5p/PTEN axis]	CCK8//qRT-PCR//Colony Formation Assay	It showed that HOXC13-AS was increased in breast cancer tissues compared with the adjacent normal tissues and upregulated HOXC13-AS promoted the growth of breast cancer cells. Hence, we conclude that HOXC13-AS, which is significantly upregulated in breast cancers, promoted cell proliferation through the suppressed miR-497-5p and further upregulated PTEN.		Yes	It showed that HOXC13-AS was increased in breast cancer tissues compared with the adjacent normal tissues and upregulated HOXC13-AS promoted the growth of breast cancer cells. 	31066051
HOXC13-AS	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	regulation[ miR-378g/HOXC13 axis]	Western Blot//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//EdU Staining//Transwell Assay	 In this study, GEPIA indicated that HOXC13-AS and its neighbor gene HOXC13 were upregulated in HNSC samples, and we consistently unveiled their upregulation in OSCC tissues and cell lines. In sum, our findings suggested that HOXC13-AS functioned as a ceRNA to accelerate the malignant behaviors of OSCC cells via miR-378g/HOXC13 axis, shedding a new light on the lncRNA-targeted treatment for OSCC.		Yes	Silencing HOXC13-AS abrogated OSCC cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT).	32763778
HOXBLINC	LncRNA	Mus musculus	Leukemia, Myeloid, Acute	HSPCs 	Regulation	In Vivo Experiment//colony Formation Assay//Flow Cytometry//qRT-PCR//RIP//RNA-seq//ChIP-seq//ChIP	Here, we show that the activation of HOXBLINC, a HOXB locus-associated long non-coding RNA (lncRNA), is a critical downstream mediator of NPM1c+-associated leukemic transcription program and leukemogenesis. Mechanistically, HoxBlinc binds to the promoter regions of NPM1c+ signature genes to control their activation in HoxBlincTg HSPCs, via MLL1 recruitment and promoter H3K4me3 modification.		Yes	 HOXBLINC loss attenuates NPM1c+-driven leukemogenesis by rectifying the signature of NPM1c+ leukemic transcription programs. Furthermore, overexpression of HoxBlinc (HoxBlincTg) in mice enhances HSC self-renewal and expands myelopoiesis, leading to the development of AML-like disease, reminiscent of the phenotypes seen in the Npm1 mutant knock-in (Npm1c/+) mice.  HoxBlincTg and Npm1c/+ HSPCs share significantly overlapped transcriptome and chromatin structure. 	33782403
HOXA-AS2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-520c-3p/SNX5 axis)	Western Blot//Tunel//CCK8//qRT-PCR//Transwell Assay	We found that HOXA-AS2 expression was remarkably upregulated in OSCC tissues and cell lines.  Our bioinformatics analysis found that HOXA-AS2 can target miR-520c-3p, which was confirmed by dual-luciferase reporter gene assay. The expression of HOXA-AS2 was found to be negatively associated with miR-520c-3p in OSCC tissues. Moreover, sorting nexin 5 (SNX5), a downstream target of miR-520c-3p, was inhibited by miR-520c-3p overexpression. SNX5 was also increased in OSCC tissues and cell lines. 	Additionally, we found that the higher expression of SNX5 was strongly associated with the tumor grade of OSCC patients in Oncomine database. 	Yes	 The downregulation of HOXA-AS2 inhibited cells proliferation, migration and invasion. Most importantly, the knockdown of HOXA-AS2 induced cells apoptosis by promoting autophagy by regulating SNX5.	36528556
HOXA-AS2	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues	interaction[miR-520c-3p ]	qRT-PCR//Luciferase Report Assay	We observed that HOXA-AS2 was up-regulated in OS tissues.HOXA-AS2 could negatively regulate the expression of miR-520c-3p in OS cells. 		Yes	In vitro experiments revealed that HOXA-AS2 knockdown significantly inhibited OS cells proliferation by promoting apoptosis and causing G1 arrest, whereas HOXA-AS2 overexpression promoted cell proliferation. 	30081707
HOXA-AS2	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction[miR-124-3p/E2F3]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	HOXA-AS2 expression was increased in OS tissues and cells and associated with poor survival of patients. HOXA-AS2 silence impeded OS progression possibly by functioning as a decoy of miR-124-3p to target E2F3, indicating novel evidence of HOXA-AS2 as a promising therapeutic target of OS.	HOXA-AS2 expression was increased in OS tissues and cells and associated with poor survival of patients. 	Yes	Knockdown of HOXA-AS2 inhibited cell viability, migration and invasion in OS cells.	31853184
HOXA-AS2	LncRNA	Homo sapiens	Parkinson Disease	PBMCs of PD patients	Interaction(PRC2/PGC-1α)	qRT-PCR//RNA Pull-Down	We found that HOXA-AS2 was upregulated in the PBMCs of PD patients and negatively associated with peroxisome proliferator-activated receptor gamma coactivator-1a (PGC-1α) expression.Mechanistic investigations demonstrated that HOXA-AS2 could directly interact with polycomb repressive complex 2 (PRC2) and modulate the histone methylation of the promoter of PGC-1α.		Yes	Moreover, HOXA-AS2 knockdown significantly repressed microglial M1 polarization and promoted M2 polarization by regulating PGC-1α expression. 	34511122
HOXA11-AS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-506-3p/Slug axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	RT?qPCR revealed that HOXA11?AS expression was increased, while that of miR?506?3p was decreased in HCC tissues and cells compared with that in adjacent non?tumor tissues and normal hepatic cells. Taken together, the present study demonstrates that HOXA11‑AS functions as an oncogene to promote the progression of HCC via the miR‑506‑3p/Slug axis, providing a therapeutic target for patients with HCC.		Yes	miR?506?3p downregulation reversed the inhibitory effects of HOXA11?AS deletion on cell proliferation, invasion and epithelial?mesenchymal transition (EMT), as shown by CCK?8 and Transwell assays, as well as western blot analysis.	32901858
HOXA11-AS	LncRNA	Homo sapiens	Ovarian Neoplasms	Ovarian cancer cells	Expression(highly expressed)	Western Blot//CCK8//qRT-PCR//Cell Cycle Assay//Transwell Assay	Ovarian cancer cells expressed HOXA11-AS substantially higher than normal cells, while cisplatin-resistant cells expressed HOXA11-AS significantly higher than ovarian cancer cells. 		Yes	HOXA11-AS knockdown was found to significantly inhibit cell viability, migration, and invasion of A2780 and OVCAR3 cells, and promote apoptosis by CCK-8 assay, transwell assay, cell cycle, and apoptosis assay, and promoted the sensitivity of A2780/DDP cells to cisplatin. It has been shown by the western blot test that HOXA11-AS knockdown increases the amount of cellular autophagy in cells.In contrast, adding the autophagy inhibitor 3-methyladenine (3-MA) to HOXA11-AS cells knocked down in vivo reduced its anti-tumor properties.	35706412
HOXA11-AS	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Regulation[HOXA11-AS/miR-98-5p/YBX2 axis]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	HOXA11-AS was highly expressed in OSCC tissues and cells.HOXA11-AS plays an active role in the progression of OSCC, and the discovery of HOXA11-AS/miR-98-5p/YBX2 axis provides new therapeutic targets for OSCC.		Yes	Knockdown of HOXA11-AS significantly reduced proliferation, migration, invasion and EMT, while promoted apoptosis of OSCC cells.	31731187
HOXA11-AS	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Regulation[miR-518a-3p/PDK1 axis]	qRT-PCR	qRT-PCR analysis indicated that HOXA11-AS expression was significantly upregulated in OSCC tissues.Taken together, our study demonstrates that HOXA11-AS/miR-518a-3p/PDK1 axis is an important regulator of OSCC progression and may serve as a potential therapeutic target in OSCC.		Yes	Functional studies revealed that HOXA11-AS significantly promotes cell proliferation, reduces the percentage of G0/G1 phase cells and enhances the cell invasion in OSCC.  In a mouse model of OSCC, HOXA11-AS overexpression promoted tumor growth, concomitant with reduced miR-518a-3p expression and increased PDK1 expression.	31139017
HOXA11-AS	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cell lines	Interaction[ sponging miR-125a-5p]	qRT-PCR	 It was found that HOXA11-AS expression levels in OS tissues and OS cell lines were higher than those in OS adjacent tissues and normal human osteoblast cell lines. Our study elucidated the role of a new HOXA11-AS/miR-125a-5p/Rab3D regulatory pathway in promoting OS metastasis.	 The higher expression level of HOXA11-AS was positively correlated with more severe clinical stage, distant metastasis and poor prognosis of OS.	Yes	Inhibition of HOXA11-AS expression could reduce metastasis and invasion of OS cell lines. 	31191012
HOXA11-AS	LncRNA	Homo sapiens	Glioma	glioma tissues 	interaction[miR-124-3p]	qRT-PCR	We found that LncRNA HOXA11-AS expression was markedly elevated in glioma tissues compared to normal brain tissues.In summary, the findings highlight the importance of LncRNA HOXA11-AS/miR-124-3p axis in the regulation of glioma progression. 	 The LncRNA HOXA11-AS expression in cases of high-grade glioma was significantly higher than that in cases of low-grade. Patients with high LncRNA HOXA11-AS expression had shorter OS time than those with low LncRNA HOXA11-AS expression. 	Yes	Moreover, silencing LncRNA HOXA11-AS inhibited cell proliferation, increased apoptosis, and inhibited invasion and migration of glioma cells.	30064227
HOXA11-AS	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction[upregulating microRNA-125a]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Results indicated that lncRNA HOXA11-AS was significantly increased in U251 cells and positively correlated with glioma World Health Organization (WHO) grade in glioma tissues. miR-125a inhibitor could partially reverse these effects of lncRNA HOXA11-AS silencing on U251 cells. In vivo assays also indicated that lncRNA HOXA11-AS inhibitor could inhibit glioma growth in vivo by regulating the expression of miR-125a. In conclusion, we revealed that lncRNA HOXA11-AS acted as an oncogene in glioma via interacting with miR-125a and considered that lncRNA HOXA11-AS was a potential therapeutic target for glioma.	Results indicated that lncRNA HOXA11-AS was significantly increased in U251 cells and positively correlated with glioma World Health Organization (WHO) grade in glioma tissues. 	Yes	lncRNA HOXA11-AS silencing could inhibit cell migration, invasion, proliferation, and promote apoptosis, while up-regulate the expression of caspase-3/8/9 and Bax, inhibit the expression of Bcl-2 and gab2 in U251 cells. 	31737190
HOXA11-AS	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[miR-130a-5p/HMGB2]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the current study, we demonstrated that the lncRNA HOXA11-AS was overexpressed in glioma.  Finally, we revealed that HOXA11-AS exerted its oncogenic effects by binding to miR-130a-5p, thereby neutralizing the suppressive effect of miR-130a-5p on HMGB2.	The overexpression of HOXA11-AS was correlated with advanced stages of glioma and poor prognosis. 	Yes	Downregulating HOXA11-AS expression significantly suppressed the proliferation, migration and invasion of glioma cells and increased their apoptosis. The growth of glioma cells in vitro was also suppressed by the downregulation of HOXA11-AS.	30657566
HOXA11-AS	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction(miR-124 Axis)	In Vivo Experiment//qRT-PCR//Cell Proliferation Assay//Luciferase Report Assay//Cell Apoptosis Assay//cell invasion assay	Here, HOXA11-AS was overexpressed and miR-124 was underexpressed in glioma. Expression of miR-124 was negatively related to that of HOXA11-AS. Expression of miR-124 was repressed by HOXA11-AS functioning as sponge. In addition, miR-124 knockdown partially abolished the inhibitory roles of HOXA11-AS downregulation in glioma cells. 		Yes	Silencing of HOXA11-AS suppressed cell proliferation, invasion, and promoted apoptosis in glioma cells in vitro. Moreover, inhibition of HOXA11-AS expression repressed glioma xenograft tumor growth. 	34117619
HOXA11-AS	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(Tpl2-MEK1/2-ERK1/2 pathway)	In Vivo Experiment//Wound Healing Assay//CCK8//qRT-PCR//IF//H&E Staining//IHC//EdU Staining//Transwell Assay	We found that HOXA11-AS was significantly upregulated in glioma, and was correlated with the poor prognosis of glioma patients. Mechanistically, HOXA11-AS acted as a molecular sponge for let-7b-5p in the cytoplasm, antagonizing its ability to repress the expression of CTHRC1, which activates the β-catenin/c-Myc pathway. In addition, c-Myc was involved in HOXA11-AS dysregulation via binding to its promoter region to form a self-activating loop.	We found that HOXA11-AS was significantly upregulated in glioma, and was correlated with the poor prognosis of glioma patients. 	Yes	 Ectopic expression of HOXA11-AS promoted the proliferation, migration, and invasion of glioma cells in vitro and in vivo. 	36351895
HOXA11-AS	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD	Interaction(microRNA-148b-3p/PKM2 axis)	Luciferase Report Assay//Bioinformatics Analysis	The expression of HOXA11-AS was markedly increased in LUAD, and was strongly associated with a poor prognosis. In addition, HOXA11-AS promoted proliferation and glycolysis in LUAD, and miR-148b-3p inhibited proliferation and glycolysis in LUAD. Mechanistically, HOXA11-AS positively regulated PKM2 expression by binding to miR-148b-3p, thereby promoting LUAD proliferation and glycolysis. In addition, HOXA11-AS inhibited LUAD xenograft growth and glycolysis via upregulation of miR-148b-3p expression and downregulation of PKM2 expression in vivo.	The expression of HOXA11-AS was markedly increased in LUAD, and was strongly associated with a poor prognosis.	Yes	Mechanistically, HOXA11-AS positively regulated PKM2 expression by binding to miR-148b-3p, thereby promoting LUAD proliferation and glycolysis. 	35924724
HOXA11-AS	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cancer tissues and cell lines	Interaction(Let-7c-5p/IGF2BP1 Axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	Upregulation of lncRNA HOXA11-AS was found in LUAD, and suppression of HOXA11-AS could suppress the proliferative ability of LUAD cells. The let-7c-5p was expressed to be downregulated, which played an inhibitory role in LUAD cell proliferation. Let-7c-5p was negatively regulated by HOXA11-AS.  HOXA11-AS promoted LUAD cell proliferation by targeting let-7c-5p/IGF2BP1, which could be potential molecular targets for LUAD.		Yes	HOXA11-AS promoted LUAD cell proliferation, while let-7c-5p had an inverse effect. Besides, IGF2BP1, regulated by let-7c-5p, had a positive relation with HOXA11-AS, while overexpression of IGF2BP1 could suppress the inhibition of silencing HOXA11-AS on LUAD cell proliferation. Experiments on mice confirmed that HOXA11-AS facilitated LUAD cell growth in vivo through regulating the let-7c-5p/IGF2BP1 axis	35368660
HOXA11-AS	LncRNA	Homo sapiens	Prostatic Neoplasms		regulation[miR-518b/ACTN4 axis ]	Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	HOXA11-AS in PCa cells was expressed at high levels.CTCF-induced upregulation of HOXA11-AS facilitates PCa progression via miR-518b/ACTN4 axis, providing a new target for PCa treatment.		Yes	Silenced HOXA11-AS in PCa cells could lead to a significant elevation in the abilities of cell proliferation and migration whereas a remarkable declination in cell apoptosis capability.	31971633
HOXA11-AS	LncRNA	Homo sapiens	Prostatic Neoplasms	cell lines	Expression(highly expressed)	qPCR//Luciferase Report Assay//Microarray	In this study, we found that homeobox A11 antisense RNA (HOXA11-AS), a highly expressed lncRNA in cell lines derived from prostate cancer bone metastases, promoted the cell invasion and proliferation of PC3 prostate cancer cells. These results suggest that prostate cancer HOXA11-AS and HOXB13 promote metastasis by regulation of CCL2/CCR2 cytokine and integrin signaling in autocrine and paracrine manners.		Yes	In this study, we found that homeobox A11 antisense RNA (HOXA11-AS), a highly expressed lncRNA in cell lines derived from prostate cancer bone metastases, promoted the cell invasion and proliferation of PC3 prostate cancer cells. 	33514011
HOXA11-AS	LncRNA	Homo sapiens	Prostatic Neoplasms	Pca tissues	Interaction(miR-24-3p/JPT1 axis)	In Vivo Experiment//RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	We revealed that HOXA11-AS was upregulated in PCa. Furthermore, we showed that HOXA11-AS1 serves as a competing endogenous RNA (ceRNA) to regulate Jupiter microtubule associated homolog 1 (JPT1) via sponging microRNA-24-3p (miR-24-3p). Functionally, the overexpression of miR-24-3p or knockdown of JPT1 could partially reverse the effects of HOXA11-AS overexpression on PCa cell behaviors.		Yes	 Silencing of HOXA11-AS significantly inhibited PCa cell proliferation, colony formation, invasion, and promoted apoptosis in vitro. On the contrary, forcing of HOXA11-AS expression caused opposite effects on cancer cell behaviors.	34337714
HOXA11-AS	LncRNA	Homo sapiens	skin melanoma	melanoma tissues 	Interaction(miR-152-3p/ITGA9 Axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	 HOXA11-AS and ITGA9 were up-regulated while miR-152-3p was down-regulated in melanoma. HOXA11-AS modulated proliferation, apoptosis, metastasis and EMT in melanoma cells by regulating miR-152-3p/ITGA9 axis in part.		Yes	 Knockdown of HOXA11-AS refrained cell proliferation, metastasis and epithelial-mesenchymal transition (EMT) but induced apoptosis in melanoma cells. 	33564267
HOXA11-AS	LncRNA	Homo sapiens	Demyelinating Diseases	keloid tissues	Regulation[ miR-124-3p/TGFβR1 axis]	Flow Cytometry//qRT-PCR//Tunel//Western Blot	We found that HOXA11-AS and TGFβR1 were significantly up-regulated, while miR-124-3p was down-regulated both in keloid tissues or fibroblasts than in normal skin tissues or fibroblasts. Taken together, our findings revealed that HOXA11-AS inhibits cell apoptosis and promotes angiogenesis through miR-124-3p/TGFβR1 axis, contributing to the progression of keloid formation, which might provide a novel target for keloid therapy.		Yes	 Functionally, high expression of HOXA11-AS essentially inhibited cell apoptosis and promoted fibroblast-induced angiogenesis. 	31878829
HOXA11-AS	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HSCC tumors	interaction[Sponging miR-155]	Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	The current study demonstrated that the expression of HOXA11-AS was significantly upregulated in HSCC tumors and was positively associated with lymph node metastasis.Furthermore, luciferase reporter gene assay combined with cellular functional experiments demonstrated that HOXA11-AS functioned as a molecular sponge for miR-155, and inhibition of miR-155 attenuated the suppressive effect of HOXA11-AS knockdown on the aggressive phenotype in HSCC.	The current study demonstrated that the expression of HOXA11-AS was significantly upregulated in HSCC tumors and was positively associated with lymph node metastasis.	Yes	Moreover, functional experiments revealed that HOXA11-AS knockdown suppressed the proliferation and migration potential in FaDu cells.	31987067
HOXA11-AS	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cells	Interaction(miR-155/C-Myc)	In Vivo Experiment//Wound Healing Assay//Transfection//qRT-PCR//MTT//RNA-seq//Cell Apoptosis Assay//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining//Transwell Assay	High-throughput sequencing data revealed that lncRNA HOXA11-AS was significantly downregulated in cells co-incubated with SM.Given the properties of HOXA11-AS as a miR-155 sponge, we further confirmed that SM upregulated the expression of miR-155 in FaDU cells. C-Myc is a transcription factor that regulates cell differentiation and apoptosis, whose mRNA is considered to be targeted by miR-155. We showed that c-Myc expression was downregulated by SM and accompanied by increased apoptosis, which was consistent with the findings of transcriptome sequencing. 		Yes	Further assays demonstrated that SM-induced downregulation of lncRNA HOXA11-AS showed important implications for apoptosis. Furthermore, SM administration suppressed xenograft tumor growth in a xenograft mouse model in vivo.	35903338
HOXA11-AS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[ binding to EZH2 ]	Western Blot//qRT-PCR//RIP//Transwell Assay//ChIP	And the higher expression level of HOXA11-AS in HCC patients indicated a lower 5-year survival rate.  We also demonstrated that HOXA11-AS could inhibit miR-124 expression by binding to EZH2. Furthermore, overexpression of miR-124 or knockdown EZH2 expression could reverse the HOXA11-AS-induced migration and invasion effects in HCC cells. In summary, the high HOXA11-AS expression in HCC patients is associated with the poor outcome. HOXA11-AS could inhibit miR-124 expression by binding to EZH2 and thus promoted the migration and invasion of HCC cells.	And the higher expression level of HOXA11-AS in HCC patients indicated a lower 5-year survival rate. 	Yes	 Knockdown of HOXA11-AS in HepG2 and Hep3B cells caused impaired cell invasion and migration abilities.upregulation of HOXA11-AS in MHCC-97H and BEL7402 cells displayed higher invasion and migration capabilities. 	31493246
HOXA11-AS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-3619-5p/SALL4 axis)	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	HOXA11-AS and SALL4 were upregulated while miR-3619-5p was downregulated in NSCLC tissues and cells. Moreover, miR-3619-5p could directly bind to HOXA11-AS and its inhibition attenuated the inhibitory effect of HOXA11-AS knockdown on progression of NSCLC cells. Furthermore, SALL4 was a direct target of miR-3619-5p and its overexpression reversed the anti-tumor role of miR-3619-5p in NSCLC cells. Besides, HOXA11-AS modulated SALL4 expression via sponging miR-3619-5p. Additionally, silencing HOXA11-AS inhibited tumor growth though upregulating miR-3619-5p and downregulating SALL4. 		Yes	HOXA11-AS knockdown suppressed cell proliferation, migration, invasion, and glycolysis but promoted apoptosis in NSCLC cells. 	34050851
HOXA11-AS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Regulation[microRNA-148a-3p/DNMT1 Regulatory Axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	HOXA11-AS expression was notably upregulated and miR-148a-3p expression was conspicuously downregulated in NSCLC tissues and cells. HOXA11-AS facilitated NSCLC tumorigenesis through miR-148a-3p/DNMT1 axis in vitro and in vivo, deepening our understanding of the molecular basis of HOXA11-AS in the development of NSCLC.		Yes	HOXA11-AS knockdown curbed NSCLC cell proliferation and promoted cell apoptosis through directly increasing miR-148a-3p expression.	31908486
HOXA-AS2	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Regulation[miR-15a-5p/HOXA3 Axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Using quantitative real-time polymerase chain reaction, HOXA-AS2 was found to be differentially expressed in PTC tissues and cell lines.Mechanistically, loss-of-function assays showed a positive correlation between HOXA3 and HOXA-AS2 expression. Subcellular fractionation assay results revealed abundant HOXA-AS2 expression in the cytoplasm of PTC cells. Additionally, FOXD2-AS1 was found to upregulate HOXA3 expression by binding to miR-15a-5p. Finally, rescue assays demonstrated the overall function of the HOXA-AS2/miR-15a-5p/HOXA3 axis in PTC progression. These findings will significantly contribute to further research and the development of more efficient treatments for thyroid cancer in the future.	Kaplan-Meier analysis indicated that the overall survival rate of patients with higher levels of HOXA-AS2 was lower than those with relatively lower levels. 	Yes	 Loss-of-function assays revealed that HOXA-AS2 knockdown inhibited PTC progression by inhibiting cellular proliferation, migration, and invasion and accelerating apoptosis.	30375256
HOXA-AS2	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML cell lines and tissues	regulation[suppressing LATS2]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Cycle Assay//ChIP	HOXA-AS2 was upregulated in AML cell lines and tissues, and the overexpression of HOXA-AS2 is negatively correlated with the survival of patients. Moreover, more in-depth mechanism studies showed that carcinogenicity of HOXA-AS2 exerted mainly through binding with the epigenetic inhibitor Enhancer of zeste homolog 2 (EZH2) and then inhibiting the expression of Large Tumor Suppressor 2 (LATS2). 	HOXA-AS2 was upregulated in AML cell lines and tissues, and the overexpression of HOXA-AS2 is negatively correlated with the survival of patients. 	Yes	Silencing HOXA-AS2 can inhibit the proliferation and induce differentiation of AML cells in vitro and in vivo. Overexpressing HOXA-AS2 showed the opposite result. 	33268767
HOXA-AS2	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients	regulation[SOX4/PI3K/AKT pathway ]	qRT-PCR	This study showed that HOXA-AS2 was overexpressed in AML patients.In conclusion, these findings suggest that HOXA-AS2 probably functions as an oncogene via SOX4/PI3K/AKT pathway and might be a useful biomarker for the prognostic prediction in AML patients, providing a potential therapeutic target for AML.	 In addition, the increased HOXA-AS2 expression was correlated with higher white blood cell and bone marrow blast counts, unfavorable karyotype classification, more measurable residual disease positivity, and earlier death. There was also a tendency toward inferior survival in patients with high HOXA-AS2 expression, and HOXA-AS2 was an independent prognostic factor among the normal-karyotype AMLs. 	Yes	Furthermore, the results of in vitro study showed that silencing HOXA-AS2 significantly inhibited the growth of leukemic cells by inducing G1/G0-phase arrest and apoptosis. 	32369230
HOXA-AS2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 tissues and cells of cervical cancer	Interaction(miR-509-3p/BTN3A1 axis)	In Vivo Experiment//Western Blot//Transfection//Tube Formation Assay//qRT-PCR//RIP//FISH//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	The HOXA-AS2 level was found high in tissues and cells of cervical cancer.Angiogenesis of HUVECs was restrained after silencing HOXA-AS2.  Additionally, HOXA-AS2 upregulated the BTN3A1 by interaction with miR-509-3p. 		Yes	HOXA-AS2 restrained cell proliferation, migration and invasion. BTN3A1 overexpression rescues the inhibitory effect of silenced HOXA-AS2 on cell phenotypes in cervical cancer. Moreover, xenograft tumour growth in mice was suppressed by HOXA-AS2 depletion and was facilitated by BTN3A1 overexpression.	34240204
HOXA-AS2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer cells	Interaction(Notch signaling pathway)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Co-IP//CCK8//qRT-PCR//RIP//FISH//IF//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our study first found that HOXA-AS2 expression was up-regulated in cervical cancer cells. Additionally, luciferase reporter assays were performed to confirm that HOXA-AS2 activated Notch signaling pathway via the mediation of independent recombination signal binding protein for JK (RBP-JK) activity. As we know, Notch intracellular domain (NICD) is associated with RBP-JK in the nucleus to promote target genes in the Notch pathway. Through RNA immunoprecipitation (RIP), RNA pull down, and fluorescent in situ hybridization (FISH) assays, we observed that HOXA-AS2 combined with NICD. 		Yes	 Then functional analysis including cell counting kit-8 (CCK-8), colony formation, transwell, and wound healing uncovered that reduction of HOXA-AS2 remarkably impeded cell proliferation and migration in cervical cancer. 	34076871
HOXA-AS2	LncRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Expression[Regulating RND3]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	HOXA-AS2 expression was increased in glioma tissues and cells.Mechanically, HOXA-AS2 epigenetically inhibited RND3 transcription by binding to EZH2. Moreover, overexpression of RND3 exerted similar tumor-suppressive effects to the depletion of HOXA-AS2. Furthermore, the anti-cancer effects induced by si-HOXA-AS2 were greatly reversed by silencing of RND3. Finally, knockdown of HOXA-AS2 impaired tumor growth in vivo possibly via increasing RND3 expression.	High HOXA-AS2 expression was associated with larger tumor size and advanced pathological stage.	Yes	Functionally, knockdown of HOXA-AS2 suppressed cell proliferation and invasion, and promoted apoptosis. 	31819475
HOXA-AS2	LncRNA	Homo sapiens	Glioma	glioma specimens and cells	Interaction(miR-302a/KDM2A/JAG1 axis)	In Vivo Experiment//Immunoblotting//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Microarray//ELISA//IHC//ChIP	We found aberrant upregulation of lncRNA HOXA-AS2, lysine demethylase 2A (KDM2A), and jagged 1 (JAG1) and a downregulation of microRNA-302a (miR-302a) in glioma specimens.  Next, RNA immunoprecipitation, chromatin immunoprecipitation, and dual-luciferase reporter gene assay demonstrated that lncRNA HOXA-AS2 upregulated KDM2A expression by preventing miR-302a from binding to its 3'untranslated region. 		Yes	 The functional experiments suggested that lncRNA HOXA-AS2 could promote regulatory T (Treg) cell proliferation and immune tolerance, which might be achieved through inhibition of miR-302a and activation of KDM2A/JAG1 axis.	35181676
HOXA-AS2	LncRNA	Homo sapiens	Glioma	Glioma Stem Cells (GSCs)	Expression(highly expressed)	qRT-PCR//RNA-seq//Cell Apoptosis Assay//Cell Proliferation Assay//ChIP-seq	We found that HOXA-AS2 is overexpressed only in aggressive (IDHwt) glioma and GSC lines. ShRNA-based depletion of HOXA-AS2 in GSCs decreased cell proliferation and altered the expression of several hundreds of genes. Integrative analysis revealed that these expression changes were not associated with changes in DNA methylation or chromatin signatures at the promoter of the majority of genes deregulated following HOXA-AS2 silencing in GSCs, suggesting a post-transcriptional regulation. In addition, transcription factor binding motif enrichment and correlation analyses indicated that HOXA-AS2 affects, directly or indirectly, the expression of key transcription factors implicated in GCS biology, including E2F8, E2F1, STAT1, and ATF3, thus contributing to GCS aggressiveness by promoting their proliferation and modulating the inflammation pathway.		Yes	Integrative analysis revealed that these expression changes were not associated with changes in DNA methylation or chromatin signatures at the promoter of the majority of genes deregulated following HOXA-AS2 silencing in GSCs, suggesting a post-transcriptional regulation.	35563134
HOXA-AS2	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC  tissues, cell lines	regulation[HOXA-AS2/miR-519/HIF-1α and/or HOXA-AS2/miR-519/PD-L1]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	HOXA-AS2 and HIF-1α were found to be significantly upregulated in NPC tumor tissues, as well as in NPC cell lines. In conclusion, the present study demonstrated that HOXA-AS2/miR-519/HIF-1α and/or HOXA-AS2/miR-519/PD-L1 may be a novel mechanism regulating the progression of NPC, which may facilitate the development of targeted clinical therapy.		Yes	The overexpression of HOXA-AS2 significantly enhanced NPC progression, including the cell proliferative, migratory and invasive abilities.	32973958
HOXA-AS2	LncRNA	Homo sapiens	Gallbladder Neoplasms	 gallbladder carcinoma tissues	Interaction(miR-6867/Hippo )	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The expression of HOXA-AS2 in gallbladder carcinoma tissues was significantly higher than that in adjacent tissues (p < 0.05). Through software prediction and fluorescein reporter gene detection, it was found that HOXA-AS2 has a binding site with miR-6867, and the two are negatively correlated, that is, the expression of miR-6867 is enhanced after the expression of HOXA-AS2 is downregulated. And the 3'UTR of YAP1 protein in the Hippo signaling pathway binds to miR-6867. Therefore, HOXA-AS2 may affect the expression of YAP1 protein by regulating miR-6867, thereby inhibiting the Hippo signaling pathway and promoting the proliferation and metastasis of gallbladder cancer cells. HOXA-AS2 is abnormally expressed in gallbladder cancer cells. 		Yes	Through cell proliferation and plate clone detection, it was found that silencing HOXA-AS2 inhibited cell proliferation and invasion. 	36299503
HOXA11-AS	LncRNA	Homo sapiens	Breast Neoplasms	 tumor tissues of 56 BC patients	Interaction(miR-125a-5p/TMPRSS4)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	HOXA11-AS was upregulated in tumor tissues of 56 BC patients compared to adjacent non-tumor tissues, with high levels being associated with worse overall survival. We identified miR-125a-5p as a target of HOXA11-AS, with miR-125a-5p inhibitors partially restoring the reduction of cell proliferation and metastasis induced by HOXA11-AS silencing. We also determined that miR-125a-5p targeted TMPRSS4 mRNA, with HOXA11-AS knockdown and miR-125a-5p mimics suppressing TMPRSS4. 	HOXA11-AS was upregulated in tumor tissues of 56 BC patients compared to adjacent non-tumor tissues, with high levels being associated with worse overall survival.	Yes	Silencing of HOXA11-AS inhibited the proliferation and metastasis of BC cells, leading to cell cycle arrest in G0/G1 and induction of apoptosis. 	35106863
HOXA-AS2	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cells	regulation[miR-509-3p/PBX3 axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In the present study, we discovered that HOXA-AS2 was highly expressed in PCa tissues and cells.Rescue experiments certified the facilitated role of HOXA-AS2-miR-509-3p-PBX3 axis in regulating the progress of PCa.		Yes	HOXA-AS2 depletion obviously influenced cell proliferation, migration, invasion, as well as epithelial-to-mesenchymal transition (EMT) progression. 	32519740
HOXA-AS2	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissues and cells	Interaction(miR-885-5p/KDM5B)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay	 HOXA-AS2 expression level was elevated in PCa tissues and cells. HOXA-AS2 competitively adsorbed miR-885-5p, thereby blocking the effect of HOXA-AS2 knockdown by the miR-885-5p inhibitor in PCa cells. Moreover, KDM5B, a target of miR-885-5p, neutralized the function of miR-885-5p in PCa cells.		Yes	 Silencing of HOXA-AS2 suppressed proliferation and migration and facilitated apoptosis in PCa cells. 	36404720
HOXA-AS2	LncRNA	Homo sapiens	Hepatoblastoma	HB tissues	Interaction(ARID1B/HOXA-AS2/HOXA3 axis)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//IHC//Invasion Assay	In our previous study, genome-wide analysis with a lncRNA microarray found that lncRNA HOXA-AS2 was up-regulated in HB. . In conclusion, HOXA-AS2 is significantly overexpressed in HB and the ARID1B/HOXA-AS2/HOXA3 axis plays a critical role in HB tumorigenesis and development. 		Yes	Our data revealed knockdown of HOXA-AS2 increased cell apoptosis and inhibited cell proliferation, migration and invasion in HB. Up-regulation of HOXA-AS2 promoted HB malignant biological behaviours. 	33683826
HOXA-AS2	LncRNA	Homo sapiens	Aortic Aneurysm, Thoracic	VSMCs, TAA tissues	Interaction(IGF2BP3/KIAA1522)	RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Apoptosis Assay//EdU Staining	 HOXA-AS2 was detected to have significantly high expression in TAA tissues and function as an oncogene to promote proliferation of VSMCs, while inhibiting cell apoptosis (Figure 1, **P < 0.01). HOXA-AS2 was unveiled to bind with miR-520d-3p (Figure 2, *P < 0.05, **P < 0.01) and further up-regulate KIAA1522 to facilitate the growth of VSMCs (Figure 3-4, *P < 0.05, **P < 0.01). HOXA-AS2 was also found to recruit IGF2BP3 to stabilize KIAA1522 mRNA (Figure 5, **P < 0.01). 		Yes	 HOXA-AS2 was detected to have significantly high expression in TAA tissues and function as an oncogene to promote proliferation of VSMCs, while inhibiting cell apoptosis (Figure 1, **P < 0.01). 	35730141
HOXA5	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Expression[highly expressed]	qRT-PCR//Western Blot	Consistent with these observations, expression of HOXA5 short RNA was upregulated in advanced colon cancer tissues.		Yes	 Ingenuity Pathway Analysis of differentially expressed genes between HOXA5 short RNA overexpressed and silenced HCT116 cells revealed that HOXA5 short RNA preferentially modified expression of epidermal growth factor (EGF) signal-related genes.	31159758
HOXA11-AS	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines,blood	Interaction[SRSF1 ]	CCK8//qRT-PCR//Western Blot//Transwell Assay	Up-regulation of HOXA11-AS was found in GC tissues, cell lines, and serum samples. HOXA11-AS promotes GC cell proliferation and invasion via SRSF1 and may function as a promising marker in GC.	In GC patients, decreased serum HOXA11-AS levels were negatively related with tumor size, TNM stage, and lymph node metastasis. The area under the receiver operating characteristic curve of serum HOXA11-AS in the diagnosis of GC was 0.924 (95%CI: 0.881-0.967; sensitivity, 0.787; specificity 0.978). Results of the Kaplan-Meier survival curves suggested the GC patients with a lower HOXA11-AS level having a better overall survival rate. 	Yes	HOXA11-AS promoted GC cell proliferation and invasion. 	31235999
HOXA11-AS	LncRNA	Homo sapiens	Stomach Neoplasms	plasma 	regulation[suppression of HOXA12-AS]	qRT-PCR	 LncRNA HOXA11-AS was upregulated in plasma of gastric cancer cells than in plasma of healthy controls and was inversely correlated with PTCSC3 in plasma of gastric cancer patients. 		Yes	PTCSC3 overexpression led to inhibited, while HOXA11-AS overexpression led to promoted migration and invasion of gastric cancer cells.	32368140
HOXA11-AS	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues 	Interaction( miR-124-3p)	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC//Invasion Assay//Transwell Assay	We found HOXA11-AS is up-regulated in GC tissues and can bind with miR-124-3p.  Meanwhile, we validated that HOXA11-AS promotes migration and invasion of GC cells via down-regulating miR-124-3p and up-regulating ITGB3 in vivo.		Yes	Through overexpression/knockdown experiments and function tests in vitro, we demonstrated HOXA11-AS can promote ITGB3 expression by sponging miR-124-3p, consequently enhance the proliferation, migration, and invasion of GC cells. 	34715856
HOTAIR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cell lines	Interaction[binding to miR-206]	Western Blot//Wound Healing Assay//CCK8//FISH//RIP//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	RT‐qPCR demonstrated that HOTAIR expression in HNSCC cells was higher than that in HIOEC cells (P < 0.05). HOTAIR regulated HNSCC cell biological functions by binding to miR-206 through STC2.		Yes	Downregulated HOTAIR or upregulated miR-206 suppressed HNSCC cell proliferation, invasion and migration. 	31297902
HOTAIR	LncRNA	Homo sapiens	Parkinson Disease	SH-SY5Y cells	Interaction(miR-221-3p)	Western Blot//qRT-PCR//RIP//MTT//ELISA	The results showed that HOTAIR was highly expressed, while miR-221-3p expression was decreased in PD model in vivo and in vitro.  In conclusion, HOTAIR attenuated the injury of SH-SY5Y cells induced by MPP+ via miR-221-3p/α-synuclein axis, suggesting the potential therapeutic value of HOTAIR in PD.		Yes	In SH-SY5Y cells treated with MPP+, the knockdown of HOTAIR increased cell viability and reduced cell apoptosis, the secretion of inflammatory cytokines and oxidative stress reaction, while HOTAIR overexpression led to opposite effects. 	35398161
Hpx-202	LncRNA	Rattus norvegicus	Spinal Cord Injuries	ASCI rats	Regulation(RAD21/VEGFA)	RNA Pull-Down//Western Blot//Transfection//Tunel//qRT-PCR//RIP//Luciferase Report Assay	The overexpression of LncRNA MIAT was conducive to the recovery of motor function in ASCI rats and repressed neuronal cell apoptosis and increased neuronal cell viability. Furthermore, the overexpression of LncRNA MIAT in PC12 cells upregulated RAD21 expression by repressing RAD21 protein degradation and further promoted VEGFA transcription to inhibit neuronal cell apoptosis, ultimately improved ASCI.		Yes	The overexpression of LncRNA MIAT was conducive to the recovery of motor function in ASCI rats and repressed neuronal cell apoptosis and increased neuronal cell viability. 	33741460
HCP5	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues	Interaction(MiR-106b-5p/p21 Axis)	In Vivo Experiment//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	Significant downregulation of HCP5 was detected in GC tissues. Consistently, overexpression of HCP5 came into an opposite effect. Moreover, we demonstrated that MEF2A could combine with the promoter region of HCP5 and thereby induce HCP5 transcription. Luciferase reporter assays revealed that HCP5 could compete with miR-106b-5p as a competing endogenous RNA (ceRNA) and upregulated p21 expression in GC.	Negative correlation was determined between HCP5 expression level and tumor size and overall survival in GC patients.	Yes	HCP5 depletion had a facilitating impact on proliferation, migration and invasion of GC cells. Consistently, overexpression of HCP5 came into an opposite effect.	33613117
HCP5	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissue	regulation[Down-Regulation of miR-320]	CCK8//qRT-PCR	We found that HCP5 was up-regulated in NSCLC and predicted the poor survival of NSCLC patients. Therefore, HCP5 may stimulate the proliferation of NSCLC cells by up-regulating survivin through the down-regulation of miR-320.	We found that HCP5 was up-regulated in NSCLC and predicted the poor survival of NSCLC patients. 	Yes	 Cell proliferation assay showed that HCP5 and survivin overexpression led to increased, while miR-320 overexpression led to decreased cell proliferation rate. 	32104093
HCP5	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Regulation(PI3K/AKT/mTOR signaling)	qRT-PCR//Western Blot	Our findings revealed that HCP5 expression was at a higher level in ESCC tissues and cells compared to that in control tissues and cells. Furthermore, we found that HCP5 bound with miR-139-5p to upregulate PDE4A via the competing endogenous RNA network in ESCC cells. Importantly, HCP5 was discovered to stimulate the PI3K/AKT/mTOR signaling by regulating the downstream target genes. 		Yes	Additionally, HCP5 promoted ESCC cellular activities by promoting proliferation, migration, invasion ability and stemness characteristics of ESCC cells as well as suppressing cell apoptosis. 	34190001
HCP5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Regulation[ HCP5/miR-139-5p/ZEB1 axis]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The expression level of HCP5 in CRC tissues was obviously higher compared to para-carcinoma tissues (P < 0.05). Moreover, overexpression HCP5 was found in CRC cell lines (GEO, HCT116, LOVO and SW620) compared to normal colon cell line (CCD-18CO) (P < 0.05).Overall, the present study indicated that HCP5 played a key regulator in CRC development and progression by targeting HCP5/miR-139-5p/ZEB1 axis, which may serve as a novel therapeutic target for CRC therapy.	HCP5 overexpression and of miR-139-5p downregulation were dramatically correlated with low TNM stage, poor differentiation, low tumor depth invasion in CRC patients (P < 0.05).	Yes	 Besides, HCP5 overexpression or ZEB1 knockdown repressed Snail family transcriptional repressor (SNAI) and vimentin expressions, upregulated E-cadherin expression, and inhibited cell proliferation and metastasis (P < 0.05). 	30899394
HCP5	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	regulation[miR-299-3p/PFN1/AKT Axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression of HCP5 had a higher level in colorectal cancer samples and cells by qRT-PCR, comparing with the normal colorectal tissues and human normal colon epithelial cell. The experiments and analyses support our hypothesis that knockdown of lncRNA HCP5 suppresses the progression of colorectal cancer by miR-299-3p/PFN1/AKT axis.		Yes	 It was revealed that knockdown of HCP5 inhibited viabilities, migration and invasion, while inducing apoptosis in SW480 and HCT-116 cells. 	32606965
HCP5	LncRNA	Homo sapiens	Carcinoma, Renal Cell	neoplasm tissues	regulation[miR-214-3p/MAPK1 axis]	qRT-PCR	qRT-PCR revealed that HCP5 was enhanced in neoplasm tissues of ccRCC patients and correlated with the metastatic characteristics of RCC.Mechanically, HCP5 inhibited the growth and metastasis of ccRCC cells by regulating miR-214-3p/MAPK1 axis.		Yes	Over-expression of HCP5 promoted the proliferation, migration and invasion of renal carcinoma cells. The deletion of HCP5 inhibited the proliferation, migration and invasion of RCC in vitro and the metastasis of RCC in vivo.	33380840
HCP5	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-29b-3p/DNMT3A/AKT axis)	CCK8//qRT-PCR//FISH//Western Blot	In the present study, we demonstrated that lncRNA HCP5 was overexpressed in HCC tissues and cell lines, and these findings were obvious even in metastatic and recurrent cases. Knockdown of HCP5 significantly alleviated cell growth, metastasis, and invasion both in vitro and in vivo through promoting apoptosis and by inactivating the epithelial-mesenchymal transition (EMT) progress.  Subsequently, DNMT3A was identified as a downstream regulatory factor of miR-29b-3p, and acted as a participated element of HCC progression by activating AKT phosphorylation. Taken together, our study elucidated for the first time that HCP5 plays a crucial role in HCC via the HCP5/miR-29b-3p/DNMT3A/AKT axis.		Yes	Moreover, miR-29b-3p has been identified as a negatively regulatory target gene of HCP5, and served as a tumor suppressor of HCC to prevent cell proliferation, migration, and invasion.	34148029
HCP5	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	regulation[lncRNAHCP5/microRNA-525-5p/PRC1 crosstalk ]	qRT-PCR//Luciferase Report Assay	 High expression of lncRNA HCP5 was found in OC tissues and cells. The study suggested that lncRNA HCP5 might promote malignant behaviors of OC cells through the miR-525-5p/PRC1 crosstalk and the Wnt/β-catenin pathway.		Yes	Silencing of lncRNA HCP5 led to a decrease in cell proliferation, invasion, migration and EMT process.	32511950
HCP5	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC samples and cells	interaction[Sponging miR-29b-3p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	The results revealed dysregulation of HCP5 and miR-29b-3p in BC samples and cells. The findings in this study supported that lncRNA HCP5 could promote cell invasion and migration by sponging miR-29b-3p in human BC.		Yes	HCP5 negatively regulated the expression of miR-29b-3p and enhanced cell viability, migration and invasion.	33235469
HCP5	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[miR-140-5p/SOX4 Axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Our results demonstrated that HCP5 expression was significantly increased in OSCC tissues and cell lines.  Mechanistically, we confirmed that HCP5 might serve as a competitive endogenous RNA (ceRNA) for miR-140-5p to alleviate the repression of its downstream target, SOX4, a master regulator of EMT. Furthermore, restoration of miR-140-5p expression diminished the oncogenic effects of HCP5 on OSCC cells.		Yes	 Our results demonstrated that HCP5 expression was significantly increased in OSCC tissues and cell lines. 	31849534
HCP5	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-101/EPHA7 )	qRT-PCR//Western Blot	HCP5 was up-regulated both in OS tissues and cell lines and high expression of HCP5 was associated to low survival in OS patients.miR-101 was targeted by HCP5 and its expression was decreased in OS. The inhibitor of miR-101 reversed the impact of HCP5 down-regulation on cell proliferation, apoptosis, and metastasis in OS. Ephrin receptor 7 (EPHA7) was proved to be a target of miR-101 and had ability to recover the effects of miR-101 inhibitor in OS. 	HCP5 was up-regulated both in OS tissues and cell lines and high expression of HCP5 was associated to low survival in OS patients.	Yes	Down-regulation of HCP5 inhibited cell proliferation, migration, and invasion, suggesting its carcinogenic role in OS. 	33439936
HCP5	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-29b-3p-LOXL2 axis)	CCK8//qRT-PCR	MiR-29b-3p expression was decreased and HCP5 and LOXL2 levels were increased in OS tissues and cell lines. Moreover, transfection with sh-HCP5-1 and sh-HCP5-2 suppressed the malignant biological behavior of OS cells. HCP5 directly targeted miR-29b-3p, and promoted OS proliferation, migration, and invasion via the miR-29b-3p/LOXL2 axis. 		Yes	MiR-29b-3p could directly act on LOXL2 and knockdown of LOXL2 restrained the proliferation, migration, and invasion of OS cells.	35899856
HCP5	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines 	Interaction(miR-216a-5p/CDC42 axis)	In Vivo Experiment//IHC//Western Blot//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	Besides, RT-qPCR and western blot assay revealed that elevated HCP5 suppressed miR-216a-5p expression and then up-regulated the expression of CDC42. In contrast, knocking down HCP5 resulted in increased expression of miR-216a-5p and then downregulated the expression of CDC42. 		Yes	 The results displayed that the overexpression of HCP5 promoted cervical cancer cell proliferation and migration in vitro, and the elevated HCP5 can also promote tumor growth in vivo. 	35399723
HCP5	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Interaction(miR-205/ VEGF-A)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	Results showed that HCP5 upregulation was found in glioma tissues and cell lines. miR-205 was downregulated in glioma cells. Knockdown of HCP5 led to miR-205 upregulation and VEGF-A downregulation. miR-205 overexpression exhibited the similar effects as HCP5 downregulation on cell viability and proliferation. And VEGF-A overexpression could reverse the effects of HCP5 downregulation on cell viability and proliferation, as well as tumor growth.	Patients with high HCP5 expression showed lower survival probability and shorter survival time.	Yes	HCP5 downregulation inhibited cell proliferation and migration and mitigated tumor growth. 	35769676
HCP5	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC tissues	Interaction(MicroRNA-128-3p/HCP5)	In Vivo Experiment//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	The increased level of HCP5 was observed in NPC tissues. The luciferase assay verified that HCP5 could bind with miR-128-3p. Furthermore, forced expression of miR-128-3p could prevent the function of HCP5 on NPC cells.		Yes	 Silencing of HCP5 prevented tumor progression in vitro and in vivo. 	35602292
HCP5	LncRNA	Homo sapiens	Multiple Myeloma	MM tissues	Interaction(miR-128-3p/Wnt/β-catenin/cyclin D1 signaling via PLAGL2)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//EdU Staining//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Bioinformatics Analysis	HCP5 was significantly increased in MM. HCP5 regulated PLAGL2 expression by sponging miR-128-3p. PLAGL2 overexpression effectively rescued cells from influences by sh-HCP5 on cell proliferative and apoptotic rates. Additionally, HCP5 knockdown significantly inhibited Wnt/β-catenin/cyclin D1 signaling, and these effects were eliminated by PLAGL2 overexpression.		Yes	HCP5 knockdown effectively thwarted the proliferative rate and cell cycle of MM cell lines and suppressed tumor growth. 	34331612
HCP5	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cells	regulation[miR-140-5p/CDK8 Axis]	CCK8//qRT-PCR//Transwell Assay	HCP5 and CDK8 were significantly upregulated in PC tissues and cells, opposite to the expression of miR-140-5p.Downregulation of HCP5 impeded PC progression by downregulating CDK8 via sponging miR-140-5p.		Yes	High expression of HCP5 contributed to the low survival rate and HCP5 silencing inhibited proliferation, migration, and invasion of PC cells in vitro. Simultaneously, in vivo experiments indicated that downregulation of HCP5 suppressed tumor growth. 	32407143
HCP5	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Regulation[miR-203/SNAI axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Moreover, HCP5 is overexpressed in tumor tissues of patients with LUAD, specifically in patients with EGFR and KRAS mutations and current smoker. Finally, we demonstrated that upregulation of HCP5 increases the expression of Snail and Slug by sponging the microRNA-203 (miR-203) and promoting epithelial-mesenchymal transition (EMT) in LUAD cells.	HCP5 high expression level is positively correlated with poor prognosis of patients with LUAD.	Yes	We found that HCP5 knockdown obviously inhibited the tumor growth and produced significantly smaller tumors compared with control mice (Figure ​(Figure44A-D).	31131047
HCP5	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues,cell lines	Interaction[sponging miR-219a-5p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//RNA-seq//IHC//Transwell Assay	We observed that HCP5 was upregulated in TNBC cell lines and specimens. RNA sequencing and antibody array suggested that HCP5 achieves its functions through regulating apoptosis pathway. Bioinformatics, luciferase and RIP experiments proved that both HCP5 and BIRC3 could competitively bind to miR-219a-5p. Increased BIRC3 and decreased miR-219a-5p were observed in TNBC tissues and cell lines. We then performed gain- and loss-of-function studies as well as rescue experiments in TNBC cells. The decrease of proliferation and migration due to HCP5 knockdown could be rescued when miR-219a-5p inhibitor or BIRC3 was transfected and vice versa. Our study suggested that lncRNA HCP5 promotes TNBC progression as a ceRNA to regulate BIRC3 by sponging miR-219a-5p. In a word, we revealed a new signaling pathway to mediate TNBC, and provided HCP5 as a new target for improving treatment of TNBC.		Yes	 HCP5 knockdown induced TNBC cell apoptosis, and inhibited cell proliferation and orthotopic xenograft tumor growth. 	31215169
HCP5	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC cell lines	Interaction(miR-216a-5p/ZEB1)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	 In this study, HCP5 expression levels were confirmed to be prominently raised in LSCC cell lines. Furthermore, miR-216a-5p was confirmed to sponge HCP5, and its expression was prominently downregulated in LSCC cell lines and upregulated in HCP5-silenced LSCC cell lines. miR-216a-5p overexpression downregulated the cell proliferation and migration and invasive ability of LSCC cells. Additionally, the protein level of zinc finger E-box binding homeobox 1 (ZEB1), one target gene of miR-216a-5p, was highly expressed in LSCC cell lines, and its expression level was downregulated by HCP5 knockdown and miR-216a-5p overexpression. 		Yes	 HCP5 knockdown reduced cell proliferation and migration and invasive ability of LSCC cell lines.	36248798
HCP5	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines	Interaction(DDX21)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Using RT-qPCR analysis, we found that lncRNA HCP5 was differentially expressed in GC cell lines. Mechanistically, RNA binding protein immunoprecipitation and dual luciferase reporter assay confirmed the interaction between lncRNA HCP5 and DDX21. The effects of lncRNA HCP5 overexpression the proliferation, migration and invasion of GC cells were partly rescued by DDX21 silencing. 		Yes	 CCK-8, wound healing and transwell assay indicated that the proliferation, migration and invasion of gastric cancer cells were inhibited by downregulation of lncRNA HCP5 and lncRNA HCP5 overexpression exhibited the opposite effects in gastric cancer cells. 	33505109
HCP5	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines	Interaction(miR-299-3p/SMAD5 axis)	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay	 In our study, lncRNA HCP5 was highly expressed in GC cell lines compared with normal gastric epithelial cell. Interestingly, SMAD5 is identified as the downstream target of miR-299-3p, and its expression was inhibited by miR-299-3p. 		Yes	 LncRNA HCP5 silencing inhibited AGS cells proliferation, migration, and invasion, while promoted cell apoptosis. Moreover, miR-299-3p downregulation could abolish the effect of HCP5 knockdown on cellular behaviors of AGS cells.	33371778
HCP5	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tissues and cells	regulation[miR-140-5p/IGF1R pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 The expression of HCP5 was significantly upregulated in ccRCC tissues and cells. Hence, the HCP5/miR-140-5p/IGF1R pathway might be a promising therapeutic target in ccRCC.	Moreover, patients with high HCP5 expression level had unfavorable overall survival (OS) and progression-free survival (PFS) compared to those with low HCP5 expression. 	Yes	 Additionally, HCP5 knockdown led to the prohibition of ccRCC cell proliferation, colony formation, migration, and invasion; the promotion of cell cycle arrest at G0-G1 and apoptosis in vitro; and the inhibition of tumor growth in vivo.	32271414
hcR1445	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC cells and tissues	Interaction(miR-576-5p/SFRP1 axis)	Flow Cytometry//RIP//Proliferation Assay//IF//PCR//IP//Transwell Assay	 hcR1445 level was declined in OC cells and tissues.  hcR1445 reduced cellular invasion, proliferation, and migration by blocking the ability of miR-576-5p to upregulate SFRP1 expression and consequently prohibit WNT/β-catenin signal transduction. hcR1445 upregulation suppressed OC growth, development, and intraperitoneal metastasis in vivo.		Yes	 hcR1445 reduced cellular invasion, proliferation, and migration by blocking the ability of miR-576-5p to upregulate SFRP1 expression and consequently prohibit WNT/β-catenin signal transduction. hcR1445 upregulation suppressed OC growth, development, and intraperitoneal metastasis in vivo.	36259450
HHIP-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(HHIP/CELF2)	CCK8//qRT-PCR//Transwell Assay//Western Blot	The results showed that HHIP-AS1 and HHIP levels are downregulated in NSCLC, and that low HHIP-AS1 and HHIP expression is associated with poor outcomes.  HHIP-AS1 enhances HHIP expression and stability, and this effect is mediated by CELF2. HHIP silencing attenuates the suppressive roles of HHIP-AS1 in proliferation, migration, and invasion.	The results showed that HHIP-AS1 and HHIP levels are downregulated in NSCLC, and that low HHIP-AS1 and HHIP expression is associated with poor outcomes. 	Yes	HHIP-AS1 overexpression represses cell proliferation, migration, and invasion in NSCLC. 	36374812
HGBC	LncRNA	Homo sapiens	Gallbladder Neoplasms	 GBC tissue,cell lines	Regulation[miR-502-3p/SET/AKT axis]	FISH//Luciferase Report Assay//RNA Pull-Down//RIP	We found that lncRNA-HGBC was upregulated in GBC and its upregulation could predict poor survival. LncRNA-HGBC specifically bound to RNA binding protein Hu Antigen R (HuR) that in turn stabilized lncRNA-HGBC. LncRNA-HGBC functioned as a competitive endogenous RNA to bind to miR-502-3p that inhibits target gene SET. Overexpression, knockdown or mutation of lncRNA-HGBC altered the inhibitory effects of miR-502-3p on SET expression and downstream activation of AKT. Clinically, lncRNA-HGBC expression was negatively correlated with miR-502-3p, but positively correlated with SET and HuR in GBC tissue.	We found that lncRNA-HGBC was upregulated in GBC and its upregulation could predict poor survival.	Yes	Overexpression or knockdown of lncRNA-HGBC in GBC cell lines resulted in increased or decreased, respectively, cell proliferation and invasion in vitro and in xenografted tumors.	31752906
HERH-4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	advanced HCC cells	Interaction(miR-29b/c /CCNA2)	qRT-PCR//Northern Blot//ChIP//FISH	 Two lncRNAs, the highly expressed lncRNA in recurrent HCC (HERH)-1 and HERH-4, were upregulated in the advanced HCC cells. HERH-4 acted as an miR-29b/c sponge to facilitate CCNA2 protein translation through a competing endogenous RNA (ceRNA) pathway.		Yes	HERH-1/4 enhanced proliferation and promoted DNA replication and G1-S transition during the cell cycle in HCC cells. 	34445994
HERH-1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	advanced HCC cells	Interaction(CREB1)	qRT-PCR//Northern Blot//ChIP//FISH	 Two lncRNAs, the highly expressed lncRNA in recurrent HCC (HERH)-1 and HERH-4, were upregulated in the advanced HCC cells. HERH-1 interacted with the transcription factor CREB1. CREB1 enhanced cyclin A2 (CCNA2) transcription, depending on HERH-1-CREB1 interaction. 		Yes	HERH-1/4 enhanced proliferation and promoted DNA replication and G1-S transition during the cell cycle in HCC cells. 	34445994
HEIH	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	Expression[highly expressed]	qRT-PCR//MTT//Tunel//Transwell Assay	Compared with Control group, the expression of lncRNA-HEIH rose significantly in GC tissues		Yes	Compared with those in si-NC group, the proliferation of HGC-27 cells was suppressed (p<0.05), while the apoptosis of HGC-27 cells was promoted (p<0.01) in si-HEIH group. (4) The invasion of HGC-27 cells was remarkably inhibited in Si-HEIH group than si-NC group (p<0.05).	33015781
HEIH	LncRNA	Homo sapiens	Stomach Neoplasms	 GC patients and MKN45 and AGC cells	Expression(highly expressed)	CCK8//qRT-PCR//Survival Analysis	The lncRNA-HEIH was highly expressed in both GC tissues and GC cell lines. 	Patients with high HEIH expression were associated with medium-high differentiation (p = 0.0058), distant metastasis (M, p = 0.0378), lymph node metastasis (N, p = 0.0083), and a deeper tumor invasion (T, p = 0.0204). The elevated expression levels of HEIH in GC patients were associated with a worse prognosis compared to GC patients with low HEIH expression. This finding was supported by the parameters overall survival (p = 3.3e-06), first progression (p = 0.00028), and postprogression (p = 1.5e-08). 	Yes	Downregulation of HEIH expression inhibited cell proliferation, enhanced oxaliplatin sensitivity, and induced the expression of p53 in MKN45 and AGC cells. 	33877891
HEIH	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Interaction[Wnt/β-catenin pathway]	qRT-PCR	The expression of HEIH was upregulated in breast cancer tissue samples and cell lines. Moreover, a negative relationship existed between HEIH and miR-200b, and HEIH regulated breast cancer development via regulating miR-200b. Pre-leukemia transcription factor 3 (PBX3) was verified as a functional target of miR-200b, and miR-200b regulated the malignant behaviors of breast cancer cells through targeting PBX3. Furthermore, suppression of HEIH inhibited the activation of Wnt/β-catenin pathway, which was remarkably reversed after suppression of HEIH and inhibition of miR-200b synchronously. Our results reveal that HEIH may contribute to breast cancer development via modulation of microRNA-200b/axis and inducing the activation of Wnt/β-catenin pathway. Further studies are still required to confirm our findings.		Yes	Suppression of HEIH inhibited cell viability, promoted cell apoptosis, and decreased migration and invasion in MDA-MB-231 cells. 	31526439
HEIH	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Cell Viability Assay//EdU Staining//Transwell Assay	The results indicated high expression levels of HEIH in human breast cancer tissues, and its expression was positively associated with malignancy status and poor disease prognosis.	The results indicated high expression levels of HEIH in human breast cancer tissues, and its expression was positively associated with malignancy status and poor disease prognosis.	Yes	 Following HEIH knockdown, the proliferative and metastatic activity of MDA?MB?231 cells was decreased, whereas the induction of cell apoptosis was increased.	32945377
HEIH	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Expression[highly expressed]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	In our study, we confirmed the elevated expression of HEIH in NSCLC tissues and cell lines compared with the normal ones. 		Yes	Moreover, overexpression of HEIH accelerated the cell migrating rate and increased the invasive cell number according to the results of a wound healing assay and transwell assay.	30230600
HEIH	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	regulation[miR-4458/PBX3]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 HEIH was confirmed to be upregulated in both ESCC tissues and cell lines. The present study clarified that HEIH regulated ESCC progression by suppressing miR-4458 and upregulating PBX3. 		Yes	Functionally, we noticed that depletion of HEIH restrained ESCC cell viability, and invasion capability. 	32449803
HEIH	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues,cell lines	regulation[miR-3619-5p/CTTNBP2 axis]	Western Blot//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay	Herein, HEIH expression was found to be up-regulated in ovarian cancer tissues (n = 25; twofold higher than normal tissues, P < 0.05) and cell lines (sixfold higher than normal ovarian epithelial cell line on average, P < 0.05), and high HEIH expression predicted poor prognosis (survival rate is about 25% after 40 mo; P < 0.05).	Herein, HEIH expression was found to be up-regulated in ovarian cancer tissues (n = 25; twofold higher than normal tissues, P < 0.05) and cell lines (sixfold higher than normal ovarian epithelial cell line on average, P < 0.05), and high HEIH expression predicted poor prognosis (survival rate is about 25% after 40 mo; P < 0.05).	Yes	Furthermore, we found that HEIH facilitated tumor growth in vivo by regulating CTTNBP2 expression (P < 0.05).	33110047
HEIH	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cell lines	Regulation[miR-4458/SOCS1 axis]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	In our study, we found that HEIH was overexpressed in TNBC tissues and cell lines compared with adjacent normal mammary tissues and normal mammary epithelial cell line, respectively.Furthermore, we observed that HEIH and miR-4458 had a high correlation score in TNBC tissues, and HEIH directly binds to miR-4458, and negatively regulates miR-4458 expression in TNBC cells.	Finally, we found that TNBC patients with tumor size ≥ 5 cm or advanced clinical stage had higher levels of HEIH expression than patients with tumor size < 5 cm or early clinical stage. 	Yes	The in vitro cell proliferation and apoptosis assays suggested down-regulation of HEIH inhibited TNBC cell proliferation and promoted apoptosis through regulating miR-4458/SOCS1 axis.	31456112
HEIH	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms		regulation[ miR-939-5p/NOS2/NO axis]	qRT-PCR	In contrast, HEIH was found to be markedly upregulated in TNBC patients and showed a modulatory role on miR-939-5p/NOS2/NO axis.		Yes	inally, knocking down of HEIH resulted in improvement of immunogenic profile of TNBC cells through inducing MICA/B and suppressing the immune checkpoint inhibitor PDL1. In the same context, knockdown of HEIH resulted in the alleviation of the immune-suppressive TME by repressing interleukin-10 and tumor necrosis factor-α levels.	33368266
HEIH	LncRNA	Homo sapiens	esophageal carcinoma	EC tissues 	regulation[upregulating microRNA-185 and downregulating KLK5]	RNA Pull-Down//Western Blot//ISH//qRT-PCR//FISH//Luciferase Report Assay//H&E Staining//IHC//EdU Staining//Transwell Assay	 Results from this study indicated that HEIH and KLK5 were elevated and miR-185 was declined in EC. Collectively, we reveal that HEIH depletion dampens EC progression by upregulating miR-185 and downregulating KLK5, which provides novel treatments for EC.	High HEIH and KLK5 indicated worse prognosis and high miR-185 suggested better prognosis of EC patients.	Yes	Depleting HEIH or restoring miR-185 suppressed the malignant phenotypes of EC cells, and delayed tumor growth in EC mice.	33223519
HEIH	LncRNA	Homo sapiens	Cholangiocarcinoma	CHOL tissues and cells	regulation[miR-98-5p/HECTD4]	qRT-PCR//Luciferase Report Assay//RIP	According to the results, HEIH expression was up-regulated in CHOL tissues and cells. In conclusion, HEIH promoted CHOL tumorigenesis and progression by miR-98-5p/HECTD4 axis, which opens up a new insight for CHOL therapeutics.		Yes	 Functionally, knockdown of HEIH attenuated cell proliferation, migration and invasion. 	32062383
HEIH	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tissues and cell lines	regulation[miR-194-5p/WEE1 Axis]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that HEIH was up-regulated in retinoblastoma tissues and cell lines.	Furthermore, high level of HEIH was associated with TNM stage, optic nerve invasion and choroidal invasion of patients with retinoblastoma. 	Yes	 Functional studies showed that HEIH knockdown significantly suppressed retinoblastoma cell proliferation, migration and invasion.	33262604
HEIH	LncRNA	Homo sapiens	stomach carcinoma	GC tumour tissues and matched para-tumour tissues	Interaction(miR-214-3p )	Western Blot//Transfection//qRT-PCR//Cell Proliferation Assay//Transwell Assay	The expression of HEIH in GC tissues was higher than in adjacent normal tissues. The expression of HEIH was upregulated in MKN-45, NCL-N87, KATO III cell lines compared within normal gastric epithelial cells. We also proved that miR-214-3p was the direct target of lncRNA HEIH, and that overexpression of miR-214-3p could reverse the effects of HEIH. 		Yes	Knockdown of lncRNA HEIH significantly decreased the number of migrated and invaded cells. Additionally, downregulation of HEIH could increase GC cell apoptosis compared with the non-specific control (NC) group. 	33226411
HECW1	CircRNA	Homo sapiens	Spinal Cord Injuries	 PC12 cells	Interaction(miR-3551-3p/LRRTM1 Axis)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//PCR	The expression of circ Hecw1, TNF-α, IL-6, and IL-1β in LPS-triggered PC12 cells and the expression of miR-3551-3p and IL-10 were significantly decreased.Our study revealed that circHecw1 regulates SCI neuronal cell inflammation imbalance by regulating the miR-3551-3p/LRRTM1 signaling.		Yes	Knockdown of circHecw1 promoted proliferation and inhibited apoptosis and reduction in the inflammatory cytokine expression. 	35699802
HDAC1	LncRNA	Homo sapiens	Multiple Myeloma	myeloma cells 	Interaction(Slug)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay	 In the present study, the expression of class I HDACs in myeloma cells and tissues was evaluated. Mechanistically, the results revealed that HDAC1 regulated the mRNA stability of Slug, while it had no effect on its transcription or nuclear export.		Yes	Targeted inhibition of HDAC1 suppressed the migration of myeloma cells. Of the assessed transcription factors, small interfering (si)‑HDAC1 decreased the expression of Slug.	34738621
HCP5	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues and cell lines	Interaction[miR‑4656 ]	CCK8//qRT-PCR//Western Blot	n the present study, we found the overexpressed expression of HCP5 in prostate cancer tissues and cell lines via RT‑qPCR analysis.Functional experiments demonstrated that HCP5 acted as a competing endogenous RNA (ceRNA) to sponge miR‑4656. Ectopic expression of HCP5 decreased the expression of miR‑4656 in prostate cancer cells. MiR‑4656 was found to be decreased in prostate cancer tissues and was negatively correlated with the expression of HCP5. Further luciferase reporter assay revealed that miR‑4656 was able to bind the 3'‑untranslated region (3'‑UTR) of the cell migration inducing hyaluronidase 1 (CEMIP) and suppressed the expression of CEMIP. Consistent with the negative regulation of miR‑4656 by HCP5, western blot analysis uncovered that overexpression of HCP5 upregulated the abundance of CEMIP in prostate cancer cells. The CCK‑8 assay showed that depletion of CEMIP significantly inhibited the HCP5‑promoted proliferation of prostate cancer cells. Collectively, our data provide a novel mechanism by which HCP5 regulates the progression of prostate cancer.	High expression of HCP5 was positively correlated with the metastasis of prostate cancer.	Yes	Downregulation of HCP5 inhibited the proliferation, colony formation and induced apoptosis of prostate cancer cells.	31746434
HCP5	LncRNA	Homo sapiens	Thyroid Carcinoma, Anaplastic	ATC tissues	Interaction[sponging miR-128-3p ]	qRT-PCR//MTT//RIP	Besides, HCP5 expression level was increased in ATC tissues when compared with adjacent normal tissues. MiR-128-3p was predicted to be a target gene of HCP5. The expression level of miR-128-3p was significantly decreased in ATC cells and tissues, as compared to Nthy-ori 3-1 cells and adjacent normal tissues, respectively. MiR-128-3p overexpression reduced ATC cell viability, and induced cell apoptosis. HCP5 directly bound to miR-128-3p and regulated the expression of miR-128-3p in ARO and SW1736 cells. Furthermore, the effects of HCP5 knockdown on ATC cell viability and apoptosis were attenuated by the inhibitor of miR-128-3p. These findings suggested that knockdown of HCP5 exerted anti-tumor effect via sponging miR-128-3p in ATC, which might provide a potential approach for the treatment of ATC.		Yes	Knockdown of HCP5 reduced cell viability, while elevated apoptotic rate and caspase-3/7 activity in ARO and SW1736 cells.	31102936
HOTAIR	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML tissues,cell lines	Interaction[HOXA5 ]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining//ChIP	 LncRNA HOTAIR was found to be upregulated in AML cells and tissues.Furthermore, HOTAIR was observed to recruit Dnmt3b and to increase HOXA5 promoter methylation. Moreover, silencing HOTAIR and upregulating HOXA5 were found to induce apoptosis and reduce proliferation of AML cells in vivo.		Yes	With silencing of HOTAIR and overexpression of HOXA5, AML cell proliferation was decreased while the apoptosis was induced.	31168296
HCG18	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction( miR-152-3p/RAB14 )	In Vivo Experiment//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 It was found that HCG18 expression was highly expressed in ccRCC tissues and cells, and patients with high expression of HCG18 had a short overall survival time.  In addition, miR-152-3p was confirmed as a downstream target of HCG18 and was inversely regulated by HCG18, and RAB14 was a target of miR-152-3p. Functional assays demonstrated that miR-152-3p silencing or RAB14 addition abolished the inhibitory effects of HCG18 knockdown on ccRCC progression.	 It was found that HCG18 expression was highly expressed in ccRCC tissues and cells, and patients with high expression of HCG18 had a short overall survival time. 	Yes	Moreover, HCG18 depletion attenuated ccRCC cell viability, migration and invasion.	33732021
HCG18	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LHSCC tissues	Interaction(miR‑133/FGFR1 )	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	HCG18 and FGFR1 were upregulated, but those of miR?133b were downregulated in LHSCC tissues.HCG18 could competitively bind with miR‑133b. Moreover, the miR‑133b inhibitor promoted cell viability, migration, invasion and the expression levels of Bcl‑2, p‑PI3K and p‑AKT, but inhibited the expression levels of p53 and Bax, which were abrogated by shHCG18. miR‑133b could competitively bind with FGFR1, and the miR‑133b mimic decreased the expression level of FGFR1 in transfected LHSCC cells. 		Yes	Short hairpin RNA (sh) HCG18 and miR?133b mimic inhibited LHSCC cell viability, while enhancing miR?133b expression. 	34878161
HCG18	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Regulation(miR-188-5p/FOXC1 Axis)	Western Blot//Transfection//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay	HCG18 expression was elevated in OS tissues, and enhanced HCG18 expression was related to metastasis. HCG18 silencing repressed the viability, migration and invasion of OS cells. Moreover, HCG18 interacted with miR-188-5p. MiR-188-5p up-regulation repressed cell viability, invasion and migration in OS cells. FOXC1, a known target of miR-188-5p, was negatively modulated by miR-188-5p. Furthermore, miR-188-5p inhibition or FOXC1 over-expression partially abolished the reduced of cell viability, invasion and migration mediated by HCG18 silencing in OS cell lines. This study revealed that HCG18 knockdown repressed the viability, invasion and migration of OS cells by targeting miR-188-5p and regulating FOXC1 expression. Thus, HCG18/ miR-188-5p/FOX may be a hopeful target for OS therapy.	HCG18 expression was related to metastasis.	Yes	HCG18 silencing repressed the viability, migration and invasion of OS cells. Moreover, HCG18 interacted with miR-188-5p. MiR-188-5p up-regulation repressed cell viability, invasion and migration in OS cells. 	34041718
HCG18	LncRNA	Mus musculus	Diabetic Neuropathies	DPN model and HG-induced macrophages	Interaction(miR-146a/TRAF6 axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//ELISA	LncRNA HCG18 was highly expressed in DPN model and HG-induced macrophages. In addition, miR-146a was identified as a target of lncRNA HCG18. Overexpression of miR-146a reversed the promoting effect of HCG18 on M1 macrophage polarization. Simultaneously, TRAF6 was a target gene of miR-146a TRAF6 expression was positively modulated by HCG18 and was negatively modulated by miR-146a. 		Yes	The levels of inflammatory factors (TNF-α, IL-1β, and IL-6) were elevated in DPN model. The expression of M1 markers (CD11c and iNOS) was visibly up-regulated in DPN model and was positively correlated with HCG18 expression.  LncRNA HCG18 facilitated M1 macrophage polarization.	32996080
HCG15	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(USF1-mediated ZNF641)	qRT-PCR	TCGA data revealed that HCG15 was markedly overexpressed and closely associated with the poor prognosis of HCC. Collectively, our study demonstrated that HCG15 was a new HIF-1 target gene and played a tumor-promoting role in HCC cells by enhancing USF1-mediated ZNF641 transcription.	TCGA data revealed that HCG15 was markedly overexpressed and closely associated with the poor prognosis of HCC. 	Yes	HCG15 knockdown prominently suppressed the migration, invasion and proliferation of Hep3B and Huh7 cells. HCG15 overexpression markedly enhanced the proliferation and mobility of Huh7 cells. 	35427894
HCG15	LncRNA	Homo sapiens	Myocardial Reperfusion Injury	cardiomyocyte	Regulation( NF-κB/p65 and p38 pathways)	In Vivo Experiment//Western Blot//qRT-PCR//RNA-seq//Cell Apoptosis Assay//ELISA	HCG15, one of the differentially expressed lncRNAs, was verified to have the highest correlation with cTnT by qRT-PCR, and it also contributed to the diagnosis of AMI by receiver operating characteristic (ROC) analysis. We also confirmed that HCG15 was mainly wrapped in exosomes from AC16 cardiomyocytes under hypoxia, which contributed to cardiomyocyte apoptosis, the release of inflammatory factors, and inhibition of cell proliferation via the activation of the NF-κB/p65 and p38 pathways, whereas suppressing the expression of HCG15exerted opposite effects.		Yes	. Upregulation of HCG15 expression facilitated cardiomyocyte apoptosis and inflammatory cytokine production and inhibited cell proliferation.  In addition, Overexpression of HCG15 aggravated cardiac IR injury in C57BL/6J mice. T	34707098
HCG11	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines	Regulation[miR-1276/CTNNB1 and Wnt signaling pathway]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	HCG11 was discovered highly expressed in GC tissues and cells. Overall, HCG11 accelerated proliferation and migration in GC through miR-1276/CTNNB1 and Wnt signaling pathway, revealing that HCG11 could be a brand new target for GC.		Yes	Depletion experiments were used to evaluate HCG11 silence on cell proliferation, migration and apoptosis.	31889902
HCG11	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(miR-942-5p/BRMS1 Axis)	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Results showed that LncRNA HCG11 was downregulated in GC cells.  In addition, lncRNA HCG11 was found to act as a molecular sponge of miR-942-5p. Furthermore, miR-942-5p promoted GC progression by suppressing lncRNA HCG11 expression. Besides that, BRMS1 was confirmed as a direct target of miR-942-5p. More importantly, breast cancer metastasis suppressor 1 (BRMS1) inhibited GC progression by upregulating lncRNA HCG11 and downregulating miR-942-5p. 		Yes	 Functionally, overexpression of HCG11 inhibited GC cell proliferation, migration, and invasion. 	34054958
HCG11	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-522-3p,SOCS5]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Downregulation of lncRNA HCG11 and upregulation of miR-522-3p were found in NSCLC tissues and cells, and abnormal expressions of lncRNA HCG11 and miR-522-3p were related to adverse clinical outcomes of NSCLC patients. LncRNA HCG11 inhibits cell viability, migration and invasion in NSCLC by functioning as a ceRNA of miR-522-3p to upregulate SOCS5.		Yes	 Functionally, lncRNA HCG11 inhibited cell viability, migration and invasion in NSCLC by downregulating miR-522-3p.	32844573
HCG11	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues 	Interaction(miR-875/SATB2 axis)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//IHC//Invasion Assay	 The present study showed that the expression levels of HCG11 were reduced in tumor tissues compared with adjacent normal tissues, and similar results were obtained in experiments using lung cancer cell lines. In conclusion, HCG11 was shown to suppress the malignant properties of NSCLC cells by targeting a miR‑875/SATB2 axis, and may therefore be a promising target for the treatment of NSCLC.	 Additionally, patients with high HCG11 expression had an increased survival rate compared with patients with low HCG11 expression. 	Yes	 Further studies have shown that overexpression of HCG11 inhibited NSCLC cell proliferation in vitro and in vivo.	34080031
HCG11	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Regulation[miR-26a-5p/ATG12 axis]	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Invasion Assay//Transwell Assay	The enrichment of HCG11 was enhanced in HCC tissues and cells and was negatively related to the prognosis of HCC patients. LncRNA HCG11 accelerated the proliferation, metastasis, and autophagy while impeded the apoptosis of HCC cells via HCG11/miR-26a-5p/ATG12 axis. HCG11 might be a potential therapeutic target for the treatment of HCC.		Yes	HCG11 interference suppressed the proliferation, metastasis, and autophagy while promoted the apoptosis of HCC cells. HCG11 promoted the growth of murine xenograft tumor and autophagy through miR-26a-5p/ATG12 axis in vivo.	31858580
HCG11	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and OC cell lines	regulation[modulating miR-144-3p/PBX3]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The upregulated of HCG11 was observed in OC tissues and OC cell lines.These data displayed that the knockdown of HCG11 prevented cell progression in OC by sponging miR-144-3p and downregulating PBX3. 		Yes	Functionally, the knockdown of HCG11 prevented cell viability of SKOV3 cells, while miR-144-3p inhibitor abrogated the suppressor on cell progression. Furthermore, PBX3 was verified to be a target gene of miR-144-3p. In addition, PBX3 knockdown prevented the cell progression of SKOV3 cells.	33215418
HCG11	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	Interaction( miR-1270/PTEN)	qRT-PCR//Bioinformatics Analysis//Western Blot	HCG11 was weakly expressed in ovarian cancer and functioned as a tumor suppressor in ovarian cancer by retarding cell proliferation, migration, and EMT. Besides, HCG11 could bind to miR-1270 and PTEN was a target gene of miR-1270. Mechanically, HCG11 competitively bound with miR-1270 to upregulate PTEN. From rescue experiments, HCG11 impeded AKT/mTOR pathway to retard ovarian cancer cell growth by miR-1270/PTEN.		Yes	HCG11 was weakly expressed in ovarian cancer and functioned as a tumor suppressor in ovarian cancer by retarding cell proliferation, migration, and EMT. 	35016264
HCG11	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cell	Interaction(miR-455-5p)	qRT-PCR//MTT//RIP	Knockdown of HCG11 increased OSCC cell proliferation, as indicated by enhanced cell vitalities over time, increased G1/S transition and Ki67 levels. Furthermore, lncRNA HCG11 was shown to negatively regulate miR-455-5p and miR-455-5p targeted PTPRS directly to affect its downstream indicators, which can further modulate OSCC cell proliferation and growth. 		Yes	Knockdown of HCG11 increased OSCC cell proliferation, as indicated by enhanced cell vitalities over time, increased G1/S transition and Ki67 levels.	33151000
HCG11	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(miR-942-5p/IGF2BP2  Axis)	qRT-PCR//RNA Pull-Down//RIP	Our data revealed that HCG11 expression is decreased in OS, which is a result of transcriptional repression of YY1. HCG11 can raise p27 Kip1 expression via binding to miR-942-5p and IGF2BP2, and p27 Kip1 acts as a key effector for HCG11 exerting biological functions.	 Low HCG11 level is closely associated with larger tumor size and shorter overall survival of OS patients. 	Yes	 HCG11 negatively regulates cell proliferation, cell cycle, DNA replication in vitro and tumor growth in vivo.	34518440
HCG11	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(miR-1245b-5p/PKP2 axis)	qRT-PCR//RIP	We found that the lncRNA HCG11 was significantly upregulated in OS.  In conclusion, the HCG11/miR-1245b-5p/PKP2 axis promotes OS expression by promoting cell proliferation, migration, and invasion, and inhibiting apoptosis.		Yes	LncRNA HCG11 silencing inhibits OS progression by repressing cell proliferation, migration, and invasion, and promoting cell apoptosis. 	34949159
HCG11	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	interaction[sponging miR-942-5p and targeting GFI1]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Long noncoding RNA HCG11 was downregulated in CC. Long noncoding RNA HCG11 increased the expression of GFI1 and suppressed cell proliferation and invasion by acting as a miR-942-5p sponge.		Yes	 Functional assays demonstrated that lncRNA HCG11 inhibited CC cell proliferation and invasion. Finally, the overexpression of lncRNA HCG11 suppressed the proliferation and metastasis of CC cells in vivo.	32794340
HCG11	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[miR-496/CPEB3 axis]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	 HCG11 was expressed at low level in glioma samples compared with normal samples.HCG11 was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging micro-496 to upregulate cytoplasmic polyadenylation element binding protein 3 (CPEB3). CEPB3 and miR-496 involved in HCG11-mediated glioma progression.		Yes	Overexpression of HCG11 efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis.	31310044
HCG11	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(miR-590-3p/CADM2 molecular axis)	Western Blot//Transfection//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU	 HCG11 expression was lower in glioma tissues compared with that in paracancerous tissues, and its expression level was negatively correlated with WHO tumor stage.In addition, compared with in astrocyte cell line, the expression of HCG11 was lower in glioma cells. Functional experiments showed that HCG11 inhibited glioma cells migration and proliferation, while miR-590-3p facilitated these processes. Acting as a competitive endogenous RNA, HCG11 adsorbed miR-590-3p and upregulated the expression of CADM2, the target gene of miR-590-3p.	 HCG11 expression was lower in glioma tissues compared with that in paracancerous tissues, and its expression level was negatively correlated with WHO tumor stage.	Yes	 Functional experiments showed that HCG11 inhibited glioma cells migration and proliferation, while miR-590-3p facilitated these processes. 	35279660
HCG11	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	Interaction(MicroRNA-144COX-2 axis)	qRT-PCR	 In general, down-regulation of long non-coding RNA-HCG11 can regulate the microRNA-144COX-2 axis in glioma, thus reducing the proliferation rate of glioma cells and improving the apoptosis rate of glioma cells. 		Yes	 In general, down-regulation of long non-coding RNA-HCG11 can regulate the microRNA-144COX-2 axis in glioma, thus reducing the proliferation rate of glioma cells and improving the apoptosis rate of glioma cells. 	35818213
HCG18	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction( miR-324-5p/CDK16 axis)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	HCG18 was highly expressed in melanoma tissues and cells.HCG18 was confirmed to be a sponge of miR-324-5p, and CDK16 might be a downstream gene of miR-324-5p. HCG18 was found to reverse the effect of miR-324-5p by upregulating CDK16 expression in melanoma cell proliferation, apoptosis, migration and invasion in vitro.	Besides, we found that HCG18 was closely correlated with thickness, TNM stage and metastasis. 	Yes	 Functional experiments discovered that HCG18 knockdown restrained cell proliferation, migration and invasion, while promoted cell apoptosis in melanoma cells.	35273726
HCG18	LncRNA	Homo sapiens	Prostatic Neoplasms	 PC cells	Interaction(miR-370-3p/DDX3X Axis)	RNA Pull-Down//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 According to the results, HCG18 was significantly up-regulated in PC cells and it facilitated cell proliferation, migration, and invasion in PC.  Furthermore, a series of mechanism experiments were carried out to verify the relationship among HCG18, miR-370-3p, and DEAD-box helicase 3 X-linked(DDX3X) in PC cells. In summary, our study showed that lncRNA HCG18 accelerated cell proliferation, invasion, and migration of PC via up-regulating DDX3X through sponging miR-370-3p, providing a novel finding about PC-related regulatory mechanism.		Yes	 According to the results, HCG18 was significantly up-regulated in PC cells and it facilitated cell proliferation, migration, and invasion in PC	34708395
HCP5	LncRNA	Homo sapiens	Rhinitis, Allergic	PBMCs, CD4+ T cells, Tregs, and nasal tissues of AR patients	Interaction(miR-16/ATXN2L axis)	Western Blot//Transection//qRT-PCR//Flow Cytometry//CCK8//Luciferase Report Assay//ELISA	 lncRNA HCP5 expression dramatically downregulated in PBMCs, CD4+ T cells, Tregs, and nasal tissues of AR patients, as well as in IL-13-treated NECs.HCP5 promoted Tregs differentiation and proliferation via targeting miR-16/ATXN2L axis. Additionally, HCP5 inhibited IL-13-induced GM-CSF, eotaxin, and MUC5AC production in NECs. HCP5 sponged miR-16 and negatively regulated its expression, and miR-16 targeted ATXN2L and inhibition of miR-16 suppressed IL-13-induced GM-CSF, eotaxin, and MUC5AC expression. HCP5/miR-16/ATXN2L axis mediated Tregs proliferation and functions in AR. Besides, the regulation of IL-13-induced dysfunction of NECs by lncRNA HCP5 depended on miR-16/ATXN2L in the inflammatory response of AR.		Yes	HCP5 promoted Tregs differentiation and proliferation via targeting miR-16/ATXN2L axis. 	35122570
HCG18	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissue and cell lines	Regulation[ miR-140/CCND1 and Hedgehog signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	We found that HCG18 expression was upregulated in both NPC specimens and cell lines.Mechanistically, HCG18 may directly bind to miR-140 and effectively act as a ceRNA for miR-140 to increase the expression of cyclin D1 (CCND1). In addition, HCG18 may contribute to NPC progression via modulating Wnt/β-catenin signaling and Hedgehog pathway.	Higher levels of HCG18 were associated with positive lymph node metastasis and poor prognosis of NPC patients. Importantly, the multivariate analysis confirmed that HCG18 was an independent risk factor for outcome. 	Yes	Functionally, the downregulation of HCG18 exhibited tumor-suppressive effects via the inhibition of cell proliferation and metastasis. 	31841193
HCP5	LncRNA	Homo sapiens	stomach carcinoma	GC tissues	interaction[miR-27b-3p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	We found that HCP5 was overexpressed in GC tissues. The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.	Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage.	Yes	 HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor.	32357145
HCP5	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	regulation[miR-186-5p/MAP3K2 signal axis]	qRT-PCR	We found that the HCP5 expression was up-regulated in NB tissues and cells.This study showed that lncRNA HCP5, as ceRNA, regulated MAP3K2 to promote NB progression through competitive binding of miR-186-5p. 		Yes	Down regulation of the HCP5 expression inhibited the proliferation of NB cells and the growth of subcutaneous transplanted tumor in nude mice. 	33189302
HCP5	LncRNA	Homo sapiens	Skin Neoplasms	CSCC cells	Regulation(STAT3/VEGFR2 pathway)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Tunel//CCK8//qRT-PCR//Flow Cytometry//Microarray//IHC//Transwell Assay	In conclusion, HCP5 may competitively bind to miR‑138‑5p to regulate EZH2 in CSCC cells, promoting autophagy and reducing apoptosis through the STAT3/VEGFR2 pathway. 		Yes	In conclusion, HCP5 may competitively bind to miR?138?5p to regulate EZH2 in CSCC cells, promoting autophagy and reducing apoptosis through the STAT3/VEGFR2 pathway. 	34195851
HCP5	LncRNA	Homo sapiens	skin melanoma	SKCM tissue	Interaction[sponging miR-12]	Western Blot//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	HCP5 level was decreased in SKCM tissue specimens compared to noncancerous counterparts.HCP5 overexpression decreased SKCM cell malignancy in vitro by upregulating RARRES3, possibly via sponging miR-1286.	Low expression of HCP5 was associated with SKCM patients' poor overall survival and disease progression.	Yes	HCP5 overexpression significantly reduced the malignancy of primary SKCM cells in vitro. 	31496735
HCG22	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues 	Interaction(miR-650)	qRT-PCR	Compared with that in adjacent tissues, the expression of HCG22 significantly decreased in OSCC tissues (P<0.05).  Compared with that in HOK cells, the expression of HCG22 was significantly lower in SCC-25, HN13, HSC-3, and CAL-27 cells (P<0.05). miR-650 mimics could reduce the luciferase activity of HCG22 wild-type plasmid cells (P<0.05), and the expression of miR-650 in SCC-25 and HSC-3 cells decreased after upregulation of HCG22 expression (P<0.05).	 Moreover, the prognostic survival of patients in the low-HCG22 expression group was significantly lower than that in the high-expression group (P<0.05). 	Yes	Upregulation of HCG22 expression could inhibit the proliferation, migration, invasion, and apoptosis of SCC-25 and HSC-3 cells, upregulatethe expression of E-cadherin, and downregulate the expression of N-cadherin and vimentin (P<0.05). 	34859625
HCG22	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	Regulation(Akt, mTOR, and Wnt/β-catenin pathways)	BrdU//qRT-PCR//Transwell Assay	We found that HCG22 was weakly expressed in OSCC cells. . In conclusion, HCG22 exerted anti-tumor property in OSCC by inhibiting the Akt, mTOR, and Wnt/β-catenin pathways.		Yes	HCG22 overexpression inhibited cell proliferation and invasion and induced apoptosis in OSCC cells. The levels of PCNA, Vimentin, and Bcl-2 were decreased and E-cadherin and Bax expression was elevated in OSCC cells after HCG22 overexpression. 	33649984
HCG22	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cell lines	Interaction(miR-425-5p )	CCK8//qRT-PCR//Western Blot	The results revealed that lncRNA HCG22 was expressed at low levels, while miR-425-5p was highly expressed in OSCC cell lines, based on bioinformatics analysis. Moreover, lncRNA HCG22 and miR-425-5p were found to have a direct targeted association, and lncRNA HCG22 inhibited cell proliferation, invasion and migration by targeting miR-425-5p. 		Yes	The overexpression of lncRNA HCG22 inhibited the proliferation, invasion and migration of OSCC cells. 	35222723
HCG18	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	interaction[binding to miR-197-3p]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay//ChIP	It was found that HCG18 was upregulated in GC samples, and the knockdown of HCG18 inhibited proliferative and migratory abilities in GC. HCG18 is upregulated in GC samples by E2F1 induction, which stimulates proliferative and migratory abilities in GC by binding to miR-197-3p.		Yes	It was found that HCG18 was upregulated in GC samples, and the knockdown of HCG18 inhibited proliferative and migratory abilities in GC. 	33090399
HCG18	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-152-3p,DNAJB12 ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 It was found that HCG18 was upregulated in GC tissues and cell lines, Our results demonstrated that HNF1A-induced HCG18 overexpression promoted GC progression by competitively binding with miR-152-3p and upregulating DNAJB12 expression. 	Patients with high HCG18 expression had a shorter overall survival time compared with those with low HCG18 expression. 	Yes	It was found that HCG18 was upregulated in GC tissues and cell lines, and knockdown of HCG18 inhibited the proliferation, migration, and invasion of GC cells.	32801777
HCG18	LncRNA	Homo sapiens	Stomach Neoplasms	GC specimens	regulation[miR-141-3p ]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	HCG18 was aberrantly up-regulated in GC tissues, and it indirectly regulated the activity of Hippo signaling through counteracting miR-141-3p expression.		Yes	Down-regulation of HCG18 inhibited viability, migration, and invasion of GC cells, while miR-141-3p transfection led to opposite effect.	32725768
HCG18	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-146a-5p/TRAF6)	IHC//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	HCG18 expression was increased in GC. Furthermore, HCG18 overexpression inhibited miR-146a-5p and upregulated TRAF6 and p65 expression. Altogether, HCG18 promotes GC progression via the miR-146a-5p/TRAF6 axis and could be a GC treatment target.		Yes	HCG18 overexpression significantly increased GC cell proliferation, invasion, and migration.  Finally, miR-146a-5p/TRAF6 was found to be involved in the role of HCG18 in GC progression in vivo. 	35240920
HCG18	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-370-3p/EGFR axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	HCG18 expression was up-regulated in GC tissues, and its high expression was closely associated with increased tumour size, advanced TNM stage, poor differentiation of tumour tissues and unfavourable prognosis of patients with GC.  Furthermore, HCG18 served as a miRNA sponge to repress miR-370-3p and indirectly up-regulated EGFR expression in GC cells.	HCG18 expression was up-regulated in GC tissues, and its high expression was closely associated with increased tumour size, advanced TNM stage, poor differentiation of tumour tissues and unfavourable prognosis of patients with GC. 	Yes	Additionally, HCG18 overexpression promoted the proliferation, migration and invasion of GC cells, and its knockdown suppressed the malignant phenotypes of GC cells. 	34618022
HCG18	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell	Interaction(miR-103a-3p/UBE2O/mTORC1/HIF-1α-Positive Feedback Loop)	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//Invasion Assay	In this study, we demonstrated that HCG18 is significantly upregulated in BC tissues and cells and that BC patients with high HCG18 expression tend to have poor prognosis. In terms of mechanism, we found that HCG18 positively regulated the expression of BC-related ubiquitin-conjugating enzyme E2O (UBE2O) by sponging miR-103a-3p, and our previous research verified that UBE2O could promote the malignant phenotypes of BC cells through the UBE2O/AMPKα2/mTORC1 axis. 	In this study, we demonstrated that HCG18 is significantly upregulated in BC tissues and cells and that BC patients with high HCG18 expression tend to have poor prognosis.	Yes	 In vitro assays indicated that HCG18 promotes BC cell proliferation and invasion and endows BC cells with cancer stemness properties. In vivo assays revealed that reducing HCG18 expression in the BC cell line MDA-MB-231 markedly decreased tumor growth and lung metastasis in xenograft mouse models. 	34976998
HCG18	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cell lines	regulation[HCG18/miR-1271/ MTDH/Wnt/β-catenin signalling]	qRT-PCR	Herein, we found that HCG18 expression was significantly upregulated in colorectal cancer tissues and cell lines.Overall, the results of our study demonstrate that HCG18 exerts a potential oncogenic function in colorectal cancer by enhancing MTDH/Wnt/β-catenin signalling via sponging of miR-1271, highlighting the importance of HCG18/miR-1271/ MTDH/Wnt/β-catenin signalling in the progression of colorectal cancer.		Yes	 Knockdown of HCG18 significantly inhibited the growth and invasion of colorectal cancer cells, while its overexpression had the opposite effect. 	31854468
HCG18	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-214-3p/CENPM axis]	Flow Cytometry//qRT-PCR//Wound Healing Assay//Colony Formation Assay	The results showed that HCG18 was highly expressed in HCC tissues. Therefore, those results suggested HCG18 functioned as an oncogene to promote the proliferation and migration of HCC cells via miR-214-3p/CENPM axis.		Yes	 HCG18 silencing inhibited the proliferation and migration while induced the apoptosis of HCC cells. 	32663252
HCG18	LncRNA	Homo sapiens	Ovarian Neoplasms	EOC tissues	Interaction(miR-29a/b/TRAF4/TRAF5/NF-κB pathway)	qRT-PCR//MTT//IHC	Abnormal expression of HCG18 and miR-29a/b was observed in EOC tissues.miR-29a/b mimics and TRAF4/5 knockdown exhibited effects similar to HCG18 knockdown. Further experiments suggested that HCG18 directly targets miR-29a/b and upregulates TRAF4/5 expression, which are inhibited by targeting miR-29a/b. Moreover, overexpression of TRAF4/5 antagonized the inhibitory effect of HCG18 knockdown, suggesting that they are involved in HCG18-mediated oncogenic effects. 		Yes	Knockdown of HCG18 using shRNA inhibited proliferation, migration, EMT and the proinflammatory pathway in EOC cells.  Silencing HCG18 reduced tumour size and levels of Ki67 and TRAF4/5 while increasing miR-29a/b levels in vivo.	34983361
HCG18	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 HNSCC patient tissues and cell lines	Interaction( cyclin D1)	qRT-PCR//RIP//Western Blot	 We observed that HCG18 was upregulated in HNSCC patient tissues and cell lines. We also found that HCG18 directly binds to the functional protein cyclin D1. Upregulated cyclin D1 reversed the inhibitory effects of HCG18 in HNSCC cell lines and activated the WNT pathway-related proteins (AXIN2, survivin, c-Myc, and β-catenin) simultaneously. Knockdown of cyclin D1 could accelerate the inhibitory effects of HCG18 and decrease the expression of AXIN2, survivin, c-Myc, and β-catenin. This indicated that lncRNA HCG18 might be involved in the tumorigenesis of HNSCC via the cyclin D1-WNT pathway. 		Yes	Furthermore, silencing of HCG18 significantly inhibited proliferation, migration, and invasion of HNSCC cells, whereas the opposite effects were detected in the HCG18-overexpressed group. 	35389764
HCG18	LncRNA	Homo sapiens	Osteosarcoma	OS tumor tissues and cell lines	Interaction(miR-34a/RUNX2 Pathway)	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	 HCG18 and RUNX2 were notably enhanced, whereas miR-34a was decreased in OS tumor tissues and cell lines. Furthermore, HCG18 directly bound to miR-34a, and miR-34a was confirm to be a negative regulator of RUNX2. Interestingly, the anti-tumor effects of HCG18 silencing were attenuated by miR-34a inhibitor and RUNX2 overexpression. 		Yes	 Functional experiments uncovered that HCG18 silencing significantly inhibited the capabilities of proliferation, migration, and invasion, while overexpression of HCG18 play the opposite roles.	36401685
HHIP-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[HHIP  ]	qRT-PCR	The expression levels of HHIP-AS1 were significantly decreased in HCC tissues.Taken together, our findings demonstrate that HHIP-AS1 represses HCC progression by promoting HHIP expression, and indicate that the use of HHIP-AS1 may offer a promising treatment for HCC patients.	Downregulation of HHIP-AS1 expression correlated with larger tumor size, metastasis, and advanced TNM stage, and also predicted worse overall survival rate of HCC patients.	Yes	Through performing overexpression and knockdown experiments, the biological function of HHIP-AS1 was identified to suppress HCC cell proliferation, migration and invasion, while promote apoptosis. 	31604528
HHIP‑AS1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	Interaction(miR‑153‑3p/PCDHGA9 axis)	CCK8//qRT-PCR//Transwell Assay	The results showed that the expression of HHIP?AS1 in lung cancer tissues was significantly lower than that in normal tissues (P<0.001). In conclusion, HHIP‑AS1 inhibits the EMT and stemness of lung cancer cells by regulating the miR‑153‑3p/PCDHGA9 axis. 		Yes	HHIP‑AS1 overexpression inhibited the proliferation, invasion and clonal formation of the A549 and NCI‑H1299 cells. 	34643245
HIF1A-AS2	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	SCLC cells	Regulation	qRT-PCR//Transfection//Cell Apoptosis Assay//Western Blot	The levels of HIF-1α and Beclin-1 were decreased in both cell lines by knockdown of HIF1A-AS2. MRP1 expression was decrease in H69AR cells.  In addition, CoCl2-induced hypoxic environment decreased in doxorubicin sensitivity of H69 cells, and knockdown of HIF1A-AS2 reversed this effect of hypoxia. Knockdown of HIF1A-AS2 increased drug sensitivity of SCLC cells in relation to autophagy.		Yes	Knockdown of HIF1A-AS2 increased doxorubicin sensitivity of SCLC cells and decreased autophagy. Knockdown of HIF1A-AS2 has also affected the expression of several genes that will increase drug sensitivity and inhibit autophagy in both cell lines.	34378101
HOTAIR	LncRNA	Homo sapiens	Skin Neoplasms	cell lines	Interaction[sponging miR-326]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	HOTAIR expression in CSCC cell lines exhibited an obvious elevation. Furthermore, HOTAIR competitively bound to miR-326, so as to positively modulate miR-326 expression.		Yes	Cell function analysis revealed that HOTAIR overexpression remarkably facilitated CSCC cell migration, proliferation and EMT process, which were impeded by down-regulation of HOTAIR.	31649487
HOTAIR	LncRNA	Homo sapiens	Pre-Eclampsia	PE placenta tissues	interaction[targeting miR-106]	RIP//qRT-PCR//EdU Staining//ChIP	 HOTAIR was up-regulated in PE placenta tissues, which repressed the proliferation, migration and invasion of trophoblast cells. High level of HOTAIR repressed the proliferation, migration and invasion of trophoblast cells through targeting miR-106 in an EZH2-dependent manner, which may provide new insights into the roles of HOTAIR and miR-106a as potential regulators in PE.		Yes	 HOTAIR was up-regulated in PE placenta tissues, which repressed the proliferation, migration and invasion of trophoblast cells. 	32320706
HOTAIR	LncRNA	Homo sapiens	Psoriasis	HaCaT cells	Interaction( lncRNA-HOTAIR/miR-126 axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	 IL-22 induced cell proliferation and suppressed apoptosis. However, HOTAIR-plasmid inhibited cell viability and induced apoptosis in IL-22-stimulated HaCaT cells. In addition, the western blotting results indicated that HOTAIR-plasmid increased cleaved caspase-3 expression and the cleaved caspase-3/caspase-3 ratio, whereas the HOTAIR-plasmid-mediated effects were reversed by miR-126 mimic. Collectively, the results of the present study demonstrated that the lncRNA-HOTAIR/miR-126 axis may be implicated in the regulation of psoriasis progression and may serve as a potential therapeutic target for psoriasis.		Yes	 IL-22 induced cell proliferation and suppressed apoptosis. However, HOTAIR-plasmid inhibited cell viability and induced apoptosis in IL-22-stimulated HaCaT cells. 	33747185
HOTAIR	LncRNA	Homo sapiens	Diabetic Retinopathy	 endothelial cells 	Expression [highly expressed]	In Vivo Experiment//FISH//Tube Formation Assay	Hyperglycemia significantly augmented HOTAIR expression in HRECs and promoted angiogenesis, oxidative damage, and mitochondrial aberrations. Similarly, vitreous humor and serum from proliferative DR patients and retinas from diabetic animals demonstrated increased HOTAIR expression compared to non-diabetic controls. 		Yes	HOTAIR knockdown protected against glucose-induced increases of angiogenic and diabetes-associated molecules in the retina. Mechanistically, we showed that HOTAIR exerts its capabilities by preventing oxidative stress and modulating epigenetic pathways involving histone methylation, histone acetylation, DNA methylation, and transcription factors.	33724292
HOTAIR	LncRNA	Homo sapiens	Sarcoma, Synovial	SS tissues	Interaction(microRNA-126/SDF-1)	cell invasion assay//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//IF	HOTAIR was expressed at high levels in SS tissues.. In contrast, miR-126 was expressed at low levels in SS tissues, and was negatively correlated with HOTAIR expression. Furthermore, HOTAIR knockdown increased miR-126 expression level and decreased the expression level of stromal cell-derived factor-1 (SDF-1) at the protein level. On the other hand, while miR-126-mimic decreased the protein expression level of SDF-1, miR-126-inhibitor increased its expression level in SW982 cells. 		Yes	HOTAIR knockdown in SW982 cells inhibited cellular proliferation in vitro, but also significantly increased the ratio of cells in the G1/G0 phase of the cell cycle, and decreased the ratio of cells in the G2/S phase.HOTAIR knockdown inhibited the invasion and migration of the SW982 cells, as observed in the Transwell and wound healing assays. 	33868482
HOTAIR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	HPV16-positive cervical cancer cells	Interaction(miR-214-3p/Wnt/β-catenin signal pathway)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Colony Formation Assay//RIP//MTT//RNA-seq//ChIP-seq//IHC	Our results showed that expression of HOTAIR was up-regulated, while that of miR-214-3p was down-regulated in HPV16-positive cervical cancer cells. HOTAIR could act as a ceRNA through binding to miR-214-3p, promote cell proliferation and inhibit the apoptosis of HPV16 positive cervical cancer. HOTAIR/miR-214-3p/Wnt/β-catenin signal pathway might played important regulated roles in HPV16 positive cervical cancer.		Yes	HOTAIR knockdown could significantly inhibited cell proliferate ability and promote cellular apoptosis, whereas the inhibition of miR-214-3p expression partially reversed such results. 	34320988
Hotair	LncRNA	Mus musculus	Breast Neoplasms	breast cancer cells	Regulation	qRT-PCR//RNA-seq//Invasion Assay	 We show that sustained high levels of HOTAIR over time increased breast metastatic capacity and invasiveness in breast cancer cells, promoting migration and subsequent metastasis to the lung. 		Yes	 We show that sustained high levels of HOTAIR over time increased breast metastatic capacity and invasiveness in breast cancer cells, promoting migration and subsequent metastasis to the lung. 	36579891
Hotair	LncRNA	Mus musculus	Osteoarthritis	 articular cartilage tissues 	regulation[miR-20b/PTEN axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	Results found that HOTAIR was significantly up-regulated in articular cartilage tissues of OA mice and IL-1β-induced chondrocytes, accompanied by down-regulation of miR-20b and increased expression of the phosphatase and tensin homolog (PTEN). HOTAIR can participate in OA by promoting chondrocyte apoptosis and ECM degradation, which may be related to its targeted regulation of miR-20b/PTEN axis.		Yes	HOTAIR silencing improved cartilage tissue damage in OA mice, and promoted the expression of collagen II and aggrecan in cartilage tissue, while inhibited the expression of matrix metalloproteinases (MMP)-13 and ADAMTS-5. Overexpression of HOTAIR inhibited the proliferation of IL-1β-induced chondrocytes and promoted apoptosis and extracellular matrix (ECM) degradation, whereas the effect of HOTAIR knockdown was reversed.	32315726
Hotair	LncRNA	Mus musculus	Parkinson Disease	brain tissue	Interaction[regulating miR-126-5p and RAB3IP]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting indicated that HOTAIR and RAB3IP increased while miR-126-5p decreased in PD cells and PD mice. 		Yes	Additionally, the CCK-8 assay and flow cytometric analysis indicated that the knockdown of HOTAIR and RAB3IP and the overexpression of miR-126-5p significantly increased cell proliferation and reduced apoptosis in PD cells.	30738012
Hotair	LncRNA	Mus musculus	Parkinson Disease	brain tissues,cell lines	regulation[miR-326/ELAVL1 Axis]	qRT-PCR//Luciferase Report Assay//RIP	 LncRNA HOTAIR was upregulated in PD mice and MPP induced SH-SY5Y cells.Collectively, HOTAIR silencing significantly inhibits neuronal damage through repressing NLRP3 mediated pyroptosis activation via regulation of miR-326/ELAVL1 axis in PD, which may contribute to a better understanding of PD pathogenesis and provide new treatment strategies for this disease.		Yes	Additionally, knockdown of HOTAIR notably attenuated the symptom of PD in vivo.	32968928
Hotair	LncRNA	Mus musculus	Sepsis	Monocytes 	Interaction[as a sponge of miR-211 to induce IL-6R expression]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	The expression of IFN-γ, IL-6, IL-17, TNF-α, IL-1β, IL-6R and HOTAIR was significantly upregulated in the septic mice, whereas miR-211 expression was downregulated.HOTAIR may promote the progression of sepsis by indirectly regulating the expression of IL-6R via miR-211.		Yes	HOTAIR overexpression and miR-211 knockdown significantly inhibited cellular proliferation and promoted monocyte apoptosis, whereas the overexpression of miR-211 exhibited the opposite effects in monocytes. 	31656541
Hotair	LncRNA	Mus musculus	Myocardial Reperfusion	myocardial tissues,cell line	interaction[binding SRSF1 with microRNA-126]	qRT-PCR//ELISA//Luciferase Report Assay	 LDH and CK-MB were significantly released in mice with myocardial IR. HOTAIR was upregulated, while microRNA-126 was downregulated in IR mice and H2O2-induced H9c2 cells. HOTAIR aggravates myocardial IR by competitively binding SRSF1 with microRNA-126.		Yes	Overexpression of HOTAIR stimulated proliferative ability, LDH release, and Caspase-3 activity in H2O2-induced H9c2 cells.	32964995
HOMER3-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(HOMER3/Wnt/β-catenin axis)	qRT-PCR//Western Blot//IHC//IF	 Here, we identified a lncRNA, HOMER3-AS1, which is over-expressed in HCC and correlated with poor survival of HCC patients. Mechanism investigations revealed that HOMER3-AS1 activated Wnt/β-catenin signaling via upregulating HOMER3. Functional rescue experiments revealed that HOMER3/Wnt/β-catenin axis mediated the roles of HOMER3-AS1 in promoting HCC cellular malignant phenotypes. 	 Here, we identified a lncRNA, HOMER3-AS1, which is over-expressed in HCC and correlated with poor survival of HCC patients.	Yes	HOMER3-AS1 promoted HCC cellular proliferation, migration, and invasion, and reduced HCC cellular apoptosis. Furthermore, HOMER3-AS1 promoted macrophages recruitment and M2-like polarization. In vivo, HOMER3-AS1 significantly facilitated HCC progression. 	34815380
HOMER1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	regulation[miR-1322/CXCL6 axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Notably, circ-HOMER1 was upregulated in both HCC cells and tissues.Furthermore, we found that circ-HOMER1 promoted HCC cell growth and aggressiveness by miR-1322/CXCL6 axis.	This aberrant expression pattern was closely correlated with larger tumor size, higher tumor-node-metastasis stage, and poorer prognosis for the patients with HCC. 	Yes	Moreover, silenced circ-HOMER1 inhibited cell proliferation, migration, and invasion concomitant with the promotion of apoptosis in HCC cells, and vice versa. 	32037619
HOMER1	LncRNA	Homo sapiens	Alzheimer Disease	AD female	Regulation	qRT-PCR//Western Blot	 First, we showed downregulation of HOMER1B/C and HOMER1A mRNA and hsa_circ_0006916 and hsa_circ_0073127 levels in AD female cases compared to controls by RT-qPCR.A positive correlation was observed between HOMER1B/C, HOMER1A mRNA, and hsa_circ_0073128 with HOMER1B/C protein only in females. 		Yes	SNHG5 silencing or miR-299 overexpression suppressed the proliferation of BC cell, arrested the cell cycle in the G1 cell phase, and decreased the glucose consumption and lactate production of BC cell. 	34502114
HNSCAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCs tissue and cells	Regulation(KRT80)	Western Blot//Wound Healing Assay//CCK8//RNA-seq//Colony Formation Assay	HNSC-associated transcript 1 (HNSCAT1, previously recognized as linc01269), was downregulated in tumor samples and advanced tumor stages and was also associated with favorable outcomes in HNSC. More importantly, through high-throughput transcriptome analysis (RNA-seq, in NODE database, OEZ007550), we identified KRT80, a tumor suppressor in HNSC, as the target of HNSCAT1. KRT80 expression was modulated by lncRNA HNSCAT1 and presented a positive correlation in tumor samples (R = 0.52, p < 0.001).		Yes	Overexpression of HNSCAT1 triggered treatment efficacy in HNSCs both in vivo and in vitro. 	35965679
HNRNPU	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC patients and cell lines	Interaction(MicroRNA 205-5p/AXIN2 Axis and Wnt/β-Catenin Signaling Pathway)	RNA Pull-Down//Western Blot//Transfection//Colony Formation Assay//Flow Cytometry//CCK8//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC		As revealed by Kaplan-Meier curve, CC cases showing low HNRNPU-AS1, high miR-205-5p, and low AXIN2 levels had the poorest prognosis.	Yes	AXIN2 reversed the CC cell proliferation-promoting, apoptosis-inhibiting, and Wnt/β-catenin signaling-activating behavior mediated by miR-205-5p or HNRNPU-AS1 knockout.	34309414
HNF1A-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tumors and cell lines	regulation[miRNA-20a-5p/TRIM32 Axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	Expression of HNF1A-AS1 and TRIM32 was upregulated and miR-20a-5p was downregulated in breast cancer tumors and cell lines. Knockdown of HNF1A-AS1 suppressed breast carcinogenesis presumably through targeting miR-20a-5p/TRIM32 axis, suggesting that HNF1A-AS1 might be a promising therapy target for breast cancer.		Yes	Deletion of HNF1A-AS1 induced cell apoptosis rate, but suppressed cell proliferation, EMT, migration, and invasion in MDA-MB-231 and MCF-7 cells. 	32319789
HOTAIR	LncRNA	Homo sapiens	Skin Neoplasms	CSCC, CSCC cell lines A431 or SCC13, A431- or SCC13-derived CSCC stem cells	Interaction(Sp1/miR-199a )	In Vivo Experiment//ChIP//Western Blot//Transfection//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//IF	 By measuring its expression using RT-qPCR in CSCC vs. normal tissues, as well as in CSCC cell lines A431 or SCC13, A431- or SCC13-derived CSCC stem cells (CSCSCs), and normal skin fibroblasts (HSFs), we detected higher expression of HOTAIR in CSCC than in normal tissues, in recurrent than in non-recurrent CSCC tissues, in CSCCs and CSCSCs than in HSFs, and particularly, in CSCSCs than in CSCCs. Mechanistically, HOTAIR directly interacted with and up-regulated Sp1. Sp1 then induced DNMT1-mediated promoter methylation and direct transcriptional repression of miR-199a-5p. Targeting Sp1 or DNMT1 further boosted the in vivo anti-tumor and anti-metastasis activities of targeting HOTAIR. 	Kaplan-Meier analysis suggested that higher expression of HOTAIR was positively correlated with worse overall survival of CSCC patients. 	Yes	 Functional assays on colony formation, EdU incorporation, sphere formation, western blot on stem-cell biomarkers, and in vivo models showed that HOTAIR was essential in maintaining multiple stem cell phenotypes of CSCSCs in vitro and in vivo xenograft growth as well as metastasis. 	34697449
HOTAIR	LncRNA	Homo sapiens	Non-alcoholic Fatty Liver Disease	NAFLD tissues	Interaction(miR-130b-3p/ROCK1 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Oil Red O Staining	 The level of HOTAIR was upregulated in NAFLD. Meanwhile, HOTAIR bound with miR-130b-3p, and ROCK1 was identified to be the direct target of miR-130b-3p. Moreover, miR-130b-3p mimics-caused lipid accumulation decrease was reversed by pcDNA3.1-ROCK1. 		Yes	Downregulation of HOTAIR reversed lipid accumulation in FFA-treated HepG2 cells and primary hepatocytes.	34774989
HIF1A-AS2	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 kidney carcinoma tissues	Interaction(miR-30a-5p/SOX4 axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//migration assay//Luciferase Report Assay//Cell Proliferation Assay//EdU Staining	HIF1A-AS2 was upregulated in kidney carcinoma tissues when compared with para-carcinoma tissues (P < 0.05).The HIF1A-AS2-miR-30a-5p-SOX4 axis was associated with the malignant progression and development of renal carcinoma. 	In addition, tumor size, tumor node mestastasis stage and differentiation were identified as being closely associated with HIF1A-AS2 expression (P < 0.05).	Yes	 Knockdown or overexpression of HIF1A-AS2 either restrained or promoted the malignant phenotype and WNT/β-catenin signaling in renal carcinoma cells (P < 0.05). MiR-30a-5p was downregulated in renal cancers and partially reversed HIF1A-AS2 functions in malignant renal tumor cells. HIF1A-AS2 acted as a microRNA sponge that actively regulated the relative expression of SOX4 in sponging miR-30a-5p and subsequently increased the malignant phenotypes of renal carcinomas. HIF1A-AS2 showed a carcinogenic effect and miR-30a-5p acted as an antagonist of the anti-oncogene effects in the pathogenesis of renal carcinomas.	33710813
HOTAIR	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive	COPD patient lungs and CSE-induced HPVEC	Interaction(DNMT1)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Microarray//Cell Proliferation Assay	 The expression levels of the HOTAIR were up-regulated in COPD patient lungs and CSE-induced HPVEC.  HPVEC apoptosis with down-regulated Bcl-2 expression, increased promoter methylation, DNMT1, Bax and Cleaved-caspase 3 expression was found in emphysema mouse model and CSE-induced HPVEC. DNMT1 was a target of HOTAIR and had a positive correlation with HOTAIR.		Yes	 Knockdown HOTAIR can attenuate cell apoptosis and emphysema via DNMT1 mediated hypermethylation of Bcl-2 promoter in mice. In vitro, HOTAIR can aggravate the apoptosis of CSE-exposed HPVEC. 	36527094
HOTAIR	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cell lines	Interaction( miR-34a /JAK2/STAT3 pathway)	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	HOTAIR was upregulated in CSCs following PDAC enrichment of PDAC.Conversely, miR-34a was downregulated and appeared to be a direct target of HOTAIR. Furthermore, HOTAIR activated the JAK2/STAT3 pathway through miR-34a, thereby promoting CSCs-like properties, invasion and migration of PDAC cells. 		Yes	Moreover, knocking down HOTAIR or overexpressing miR-34a significantly inhibited CSCs-like properties, invasion and migration of PDAC cells. In vivo experiments indicated that knocking down HOTAIR could inhibit the tumorigenicity of CFPAC-1 cells.	33737813
HOTAIR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Interaction[MAPK1]	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The results showed that the expression of lncRNA HOTAIR was significantly (p < 0.01) upregulated (up to 4.1-fold) in cervical cancer cell lines. 		Yes	Silencing of lncRNA HOTAIR expression resulted in inhibition of the proliferation of the DoTc2 cervical cancer cells via induction of apoptotic cell death. HOTAIR silencing also resulted in decrease of the migration and the invasive properties of the cervical cancer cells. 	32864005
HOTAIR	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Expression [highly expressed]	In Vivo Experiment//IHC//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//MTT//migration assay//H&E Staining//cell invasion assay//Colony Formation Assay//ChIP	LncRNA HOTAIR and EZH2 were highly expressed in NPC, and E-cadherin was lowly expressed.  HOTAIR recruited histone methylase EZH2 to mediate trimethylation of H3K27 and regulated E-cadherin expression.		Yes	Down-regulation of HOTAIR or EZH2 inhibited NPC cell progression and tumor growth.	33965547
HOTAIR	LncRNA	Homo sapiens	Glioblastoma	GBM cell lines	Regulation(upregulating H3K4me2 and downregulating H3K27me3)	In Vivo Experiment//Western Blot//H&E Staining//Flow Cytometry//qRT-PCR//IF//Microarray//Cell Proliferation Assay//IHC//ChIP	we found that the combination of AQB and GSK-LSD1 showed a powerful effect of inhibiting cell cycle processes by targeting CDKN1A, whereas apoptosis promoting effects of combination therapy were mediated by BBC3 in vitro. ChIP assays revealed that GSK-LSD1 and AQB regulate P21 and PUMA, respectively via upregulating H3K4me2 and downregulating H3K27me3.		Yes	Microarray analysis showed that AQB and GSK-LSD1 regulate cell cycle processes and induces apoptosis in GBM cell lines. 	34246782
HOTAIR	LncRNA	Homo sapiens	Glioblastoma	 glioma tissues	Interaction(miR-301a-3p/FOSL1)	Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	In this study, HOTAIR expression was found to be positively regulated by TRPM7, significantly upregulated in glioma tissues, and is a poor prognosis factor for glioma patients. Mechanistically, HOTAIR directly interacted with miR-301a-3p, and downregulation of miR-301a-3p efficiently reversed FOSL1 suppression induced by siRNA HOTAIR, which implied that HOTAIR positively regulated FOSL1 level through sponging miR-301a-3p and played an oncogenic role in glioma progression. In contrast to HOTAIR's role, miR-301a-3p alone served as a tumor suppressor to decrease glioma cell viability and migration/invasion. 		Yes	Moreover, reduced HOTAIR expression impeded the proliferation and invasion of glioma cells. 	35292358
HOTAIR	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues and cells	Interaction[sponging miR-17-5p]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	HOTAIR was significantly upregulated, while miR-17-5p was downregulated in thyroid cancer tissues and cells.MiR-17-5p was a target of HOTAIR and counter-regulated by HOTAIR. Introduction of miR-17-5p also inhibited the cell viability, migration and invasion in TPC-1 and FTC-133 cells. Moreover, introduction of miR-17-5p reversed knockdown of HOTAIR-mediated the suppression effects on the cell viability, migration and invasion in thyroid cancer cells.		Yes	Silencing HOTAIR significantly inhibited the cell viability, migration and invasion of TPC-1 and FTC-133 cells. Additionally, knockdown of HOTAIR inhibited thyroid cancer tumorigenesis in mice. 	31607138
HOTAIR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	cell lines 	Regulation(DLX1)	Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//Cell Proliferation Assay//IHC//ChIP	We observed HOTAIR was highly expressed in MDA-T32 cells but presents significantly decreased levels in MDA-T41 and K1 cells.  To explore novel HOTAIR downstream mechanisms, we analyzed TCGA transcriptome in PTC tissues and found DLX1 negatively correlated to HOTAIR, and its lower expression associated with reduced progression free survival. We further validated DLX1 gene was epigenetically suppressed by HOTAIR via performing chromatin immunoprecipitation. Moreover, IHC staining shows a significantly stepwise decrease of DLX1 protein from normal thyroid tissues to stage III PTC tissues.		Yes	 HOTAIR knockdown in MDA-T32 cells significantly suppressed proliferation, colony formation, migration with cell cycle retardation at G1 phase. On the contrary, HOTAIR overexpression in MDA-T41 cells dramatically enhanced proliferation, colony formation, migration with cell cycle driven toward S and G2/M phases. 	36494673
HOTAIR	LncRNA	Homo sapiens	Medulloblastoma	medulloblastoma tissues and cell lines	regulation[miR-1/miR-206-YY1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we found that HOTAIR and YY1 were up-regulated in medulloblastoma tissues and cell lines, and HOTAIR increased YY1 expression. These data indicate that HOTAIR promotes medulloblastoma progression via acting as a competing endogenous RNA (ceRNA) to regulate YY1 expression through binding to miR-1 and miR-206.		Yes	The functional experiments showed that HOTAIR knockdown suppressed medulloblastoma cell proliferation, tumor growth, migration and invasion, and promoted cell apoptosis via the modulation of the miR-1/miR-206-YY1 axis, as well as epithelial to mesenchymal transition (EMT).	31986414
HOTAIR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissue	Expression(highly expressed)	CCK8//qRT-PCR//Tunel//Cell Apoptosis Assay	qRT-PCR results showed that the expression of LncRNA Hotair in tumor tissue and serum of patients with non-small-cell lung cancer was significantly upregulated. These results show that the expression level of LncRNA Hotair of NSCLC cell lines can promote the invasion and migration of NSCLC, and its expression has a significant correlation with Lymph node metastasis, tumor size, and TNM stage.	Clinicopathological correlation analysis showed that the upregulation of LncRNA Hotair expression was closely related to lymph node metastasis and tumor lymph node metastasis (TNM) stage (P < 0.05). 	Yes	 The results showed that transfection of pcDNA3.1-Hotair could promote the expression of LncRNA Hotair in NSCLC, while transfection of Si-Hotair could reduce the expression level of LncRNA Hotair, hinder the migration and invasion of cancer cells, and promote cell apoptosis. 	34777731
HOTAIR	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissue samples and cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//Tunel//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The results showed that HOTAIR was highly expressed both in CCA tissue samples and cell lines compared with corresponding normal bile duct tissues and Human intrahepatic biliary epithelial cells (HIBEC).	Its overexpression was closely correlated with Tumor size, TNM stage and postoperative recurrence in CCA patients. Moreover, up-regulation of HOTAIR has correlation with prognosis in CCA patients. 	Yes	Knockdown of HOTAIR by siRNAs significantly decreased the migration and invasion but increased apoptosis of CCA cells in vitro.	30111807
HOTAIR	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cell lines (HuB28 and HuCCT1) 	regulation[miR-204-5p/HMGB1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	HOTAIR and HMGB1 were over-expressed, while miR-204-5p was lowly expressed in CCA tissues and cells.The restoration experiments showed that HOTAIR repressed cell apoptosis, autophagy and promoted cell proliferation via miR-204-5p/HMGB1 axis.		Yes	Additionally, HOTAIR silencing retarded the xenograft tumor growth by up-regulation of miR-204-5p and down-regulation of HMGB1.	32755793
HOTAIR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	blood	Interaction[PTCSC3 ]	qRT-PCR	 LncRNA HOTAIR was up-regulated in early stage LSCC patients and was significantly and inversely correlated with PTCSC3 in LSCC patients.Therefore, PTCSC3 may negatively interact with HOTAIR through STAT3 to inhibit LSCC cell proliferation.		Yes	 PTCSC3 overexpression mediated the inhibited, while HOTAIR overexpression mediated the promoted proliferation of LSCC cells.	31171714
HOTAIR	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid tumor tissues	Interaction(microRNA-761/PPME1)	Flow Cytometry//In Vivo Experiment//Luciferase Report Assay//Western Blot	HOTAIR was expressed to a significantly greater extent than miR-761 in thyroid tumor tissues (P < .001). miR-761 and PPME1 were negatively correlated (coef = -1.91, P < .001). HOTAIR competitively binds to miR-761 and miR-761 directly targets PPME1. 	 HOTAIR was highly correlated with TNM (χ 2 = 5.797, P = .016), tumor size (χ 2 = 7.955, P = .005) and lymphatic metastasis (χ 2 = 6.0, P = .014).	Yes	 HOTAIR promoted cell proliferation and inhibited cell apoptosis, whereas miR-761 did not. HOTAIR elevated and miR-761 suppressed PPME1 expression. HOTAIR expression appears to affect the survival time in vivo.	34195365
HOTAIR	LncRNA	Homo sapiens	Retinoblastoma	RB cell lines and Y79 and HXO-RB44 cells	Interaction(miR-20b-5p/RRM2/PI3K/AKT axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Bioinformatics Analysis	HOTAIR was elevated in RB cells relative to that in normal retinal cells and showed relatively high expression in Y79 and HXO-RB44 cells. sh-HOTAIR induced RB cell-cycle arrest, restrained proliferation, and strengthened apoptosis. HOTAIR functioned as the ceRNA of miR-20b-5p and targeted RRM2. RB cells had poorly-expressed miR-20b-5p and highly-expressed RRM2. miR-20b-5p downregulation or RRM2 overexpression facilitated RB cell-cycle and proliferation, suppressed apoptosis, and reversed the protective effect of sh-HOTAIR on RB. sh-HOTAIR reduced tumor growth and Ki67-positive cells in vivo and inactivated PI3K/AKT pathway.		Yes	HOTAIR functioned as the ceRNA of miR-20b-5p and targeted RRM2. RB cells had poorly-expressed miR-20b-5p and highly-expressed RRM2. miR-20b-5p downregulation or RRM2 overexpression facilitated RB cell-cycle and proliferation, suppressed apoptosis, and reversed the protective effect of sh-HOTAIR on RB.	35248107
HOTAIR	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues and cell lines 	interaction[miR-217]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	It was demonstrated that the expression of HOTAIR was upregulated in liver cancer tissues and 3 liver cancer cell lines (MHCC97H, HepG2 and Hep3B). Overall, HOTAIR contributes to the proliferation and growth of liver cancer via downregulation of miR-217.		Yes	Inhibition of HOTAIR with HOTAIR small interfering (si) RNA lentiviral vectors significantly suppressed the cell proliferation of HepG2 cells, and downregulated the protein expression levels of two proliferation markers, Ki67 and proliferating cell nuclear antigen (PCNA).	29849802
HOTAIR	LncRNA	Homo sapiens	Esophageal Neoplasms	oesophageal cancer tissues and adjacent normal tissues,cell lines(EC8712, EC8733, ECA109, EC9706 , EC8501 ,HEEC)	Interaction[regulate miR-204 and HOXC8 ]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The immunohistochemistry (Figure ​(Figure1E,F)1E,F) and RT‐qPCR (Figure ​(Figure1G)1G) results demonstrated that compared with the adjacent normal tissues, the positive expression rate of HOXC8 as well as the expression of HOTAIR was considerably elevated in the oesophageal cancer tissues, while the expression of miR‐204 was notably decreased. In summary, our results show that lncRNA HOTAIR could specifically bind to miR-204 as a competing endogenous RNA and regulate miR-204 and HOXC8.	 	Yes	Silenced HOTAIR or elevated miR-204 inhibited proliferation, migration and invasion, along with stimulated apoptosis of oesophageal cancer cells. 	31389660
HOTAIR	LncRNA	Homo sapiens	Diabetic Nephropathies	HMC	Interaction( miR-147a/WNT2B axis)	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining	 LncRNA HOTAIR could serve as a sponge of miR-147a. The inhibition effect of lncRNA HOTAIR silencing on the biological functions of HG-induced HMC could be reversed by miR-147a inhibitor. WNT2B was targeted by miR-147a, and its overexpression also overturned the suppressive effect of miR-147a on the proliferation, fibrosis, and oxidative stress of HG-induced HMC.		Yes	Our data showed that lncRNA HOTAIR knockdown could inhibit the proliferation, fibrosis, and oxidative stress in HG-induced HMC. 	35193668
HOTAIR	LncRNA	Homo sapiens	Endometriosis	ectopic endometrial tissues and cells	Interaction(miR-519b-3p/PRRG4 pathway)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	The qRT-PCR results showed that the average relative expression of LncRNA HOTAIR was much higher in ectopic endometrial tissues than in eutopic endometrial tissues. Bioinformatics analysis suggested that the downstream target genes of LncRNA HOTAIR were miR-519b-3p and Prrg4. Knockdown of LncRNA HOTAIR can reduce the up-regulation of Prrg4 by miR-519b-3p and then inhibit the invasion and migration ability of endometrial stromal cells.		Yes	 Scratch and transwell assays showed that the cell migration and invasion ability of LncRNA HOTAIR overexpression group was significantly higher than those in the control group. Conversely, the LncRNA HOTAIR knockdown group showed the opposite results.	36338672
HOTAIR	LncRNA	Homo sapiens	Arthritis, Rheumatoid	HFLSs	Interaction(miR-106b-5p/Smad7 axis)	Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	The qRT-PCR results indicated that the expression of lncRNA HOTAIR was markedly decreased and that of miR-106b-5p was markedly increased in HFLSs of RA. Smad7 was identified as a target gene of miR-106b-5p, and the effects of downregulation of miR-106b-5p on HFLSs could be abolished by silencing Smad7. We found that lncRNA HOTAIR was significantly downregulated in the HFLSs of patients with RA. Moreover, lncRNA HOTAIR influenced cell growth, migration, invasion, and apoptosis in HFLSs through the miR-106b-5p/Smad7 axis.		Yes	Cell proliferation, invasion, and migration of HFLSs were inhibited by lncRNA HOTAIR upregulation, and the expression of miR-106b-5p was negatively regulated by lncRNA HOTAIR in HFLSs. Apoptosis of HFLS cells was improved by the overexpression of lncRNA HOTAIR. All the effects of lncRNA HOTAIR upregulation on HFLSs were reversed after the overexpression of miR-106b-5p. 	36164683
HNF1A-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-124/MYO6]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	 In this study, we found that HNF1A-AS1 was upregulated in CRC tissues and cell lines. In this study, we first found that HNF1A-AS1 regulated cell migration, invasion and glycolysis via modulating miR-124/MYO6 in CRC cells.		Yes	Functional experiments determined that reduction of HNF1A-AS1 or promotion of miR-124 inhibited cell migration and invasion as well as glycolysis in CRC cells. 	32110048
HNF1A-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cell lines	interaction[PBX3]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ChIP	 HNF1A-AS1 and OTX1 were highly expressed in colon cancer.  Further, HNF1A-AS1 upregulated OTX1 to activate the ERK/MAPK pathway.		Yes	Silencing of HNF1A-AS1 inhibited angiogenesis of colon cancer in vivo and in vitro. 	32325080
HNF1A-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[ Notch signaling pathway ]	Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//MTT//Luciferase Report Assay//Colony Formation Assay//ChIP	The high expression of HNF1A-AS1 was examined in OSCC tissues and cell lines.Mechanically, HNF1A-AS1 was positively regulated by the transcription factor STAT3. Recently, Notch signaling pathway has been reported in human malignancies. In this study, we analyzed the correlation between HNF1A-AS1 and Notch signaling pathway. It was uncovered that the expression of Notch1 and Hes1 (the core factors of Notch signaling pathway) was negatively regulated by HNF1A-AS1 knockdown. Rescue assays further demonstrated the positive regulatory effects of HNF1A-AS1 on Notch signaling pathway in OSCC. In conclusion, upregulation of HNF1A-SA1 induced by transcription factor STAT3 promotes OSCC progression by activating Notch signaling pathway.		Yes	Results of loss-of-function assays demonstrated that silenced HNF1A-AS1 inhibited the proliferation, migration and epithelial-mesenchymal transition (EMT) of OSCC cells.	30404566
HNF1A-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-32-5p/HMGB1 Axis]	Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	 HNF1A-AS1 and HMGB1 were upregulated, while miR-32-5p was downregulated, in OS tissues and cells. Downregulation of HNF1A-AS1 blocked OS progression through the miR-32-5p/HMGB1 axis, which provides a possible target and prognostic biomarker for treatment of OS.		Yes	 Functionally, HNF1A-AS1 depletion induced apoptosis and impeded proliferation, migration, and invasion of OS cells. 	32706998
HIPK3	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 cell lines	regulation[ miR-485-3p/FGF2 axis]	colony Formation Assay//Western Blot//qRT-PCR//PCR//Colony Formation Assay//IF	This study confirmed that circHIPK3 was highly expressed in CC tissues.Overexpression of circHIPK3 triggered the upregulation of FGF2 expression while knockdown of circHIPK3 reduced FGF2 expression in CC cells, and the transfection of miR-485-3p mimics reversed the upregulation of FGF2 expression and enhanced malignant phenotypes in CC cells with overexpressed circHIPK3.		Yes	Overexpressed circHIPK3 could remarkably expedite the proliferation, migration and invasion of SiHa cells, and knocking down circHIPK3 could significantly impede the proliferation, migration and invasion of HeLa cells. 	33177072
HIPK3	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells and tissues	regulation[ circ-HIPK3/miR-338-3p/HIF-1α axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	circ-HIPK3 expression was significantly elevated in CC cells and tissues.Therefore, targeting circ-HIPK3/miR-338-3p/HIF-1α axis may be a novel therapeutic strategy for CC.		Yes	 circ-HIPK3 silence repressed growth and metastasis, while induced apoptosis in CC cells.	32021434
HIPK3	CircRNA	Homo sapiens	Prostatic Neoplasms	serum of PCa patients	Interaction(miR-212/BMI-1 pathway)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//IF//MTT//PCR//Transwell Assay	Exosomal circHIPK3 was increased in serum of PCa patients, and could discriminate PCa patients from normal volunteers. MiR-212 targeted BMI-1, and downregulated BMI-1 expression.Exosomal circHIPK3 knockdown inhibited PCa progression by regulating miR-212/BMI-1 axis, at least in part, offering a new insight into the molecular mechanism of PCa.		Yes	Depletion of exosomal circHIPK3 or overexpression of exosomal miR-212 reduced viability, migration and invasion, but promoted cell apoptosis in PCa cells, which was attenuated by miR-212 inhibition or BMI-1, respectively.  Exosomal circHIPK3 knockdown also suppressed tumor growth in vivo. 	34313249
HIPK3	LncRNA	Homo sapiens	Acute Kidney Injury	septic AKI patients and LPS-triggered HK2 cells	Interaction( microRNA-338/forkhead box A1 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA	 The results displayed that circHIPK3 expression was enhanced in septic AKI patients and LPS-triggered HK2 cells. Furthermore, circHIPK3 functioned as a molecular sponge for miR-338, and forkhead box A1 (FOXA1) was negatively regulated by miR-338. CircHIPK3 aggravated cell injury in LPS-treated HK2 via targeting miR-338, and FOXA1 addition overturned the suppressing impacts of miR-338-3p augmentation on LPS-activated HK2 cell damage. Finally, we demonstrated that circHIPK3 modulated LPS-induced cell damage via the miR-338/FOXA1 axis. 		Yes	Moreover, circHIPK3 interference expedited HK2 cell viability and attenuated apoptosis, inflammatory and oxidative damages following LPS stimulation.	35148669
Hipk3	CircRNA	Mus musculus	Diabetic Nephropathies	 renal tissues of mice with DN	Interaction( miR-185)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	Up-regulation of circHIPK3 was observed in the renal tissues of mice with DN. Similarly, circHIPK3 expression in rat mesangial cells increased significantly in a microenvironment of high glucose. Luciferase assay demonstrated that circHIPK3 can specifically sponge miR-185, and silencing of miR-185 can reverse the effects of knocking down circHIPK3 on cell proliferation and mRNA abundance of cyclin D1, PCNA, TGF-β1, Col. I, and FN in MCs.		Yes	A loss-of-function experiment indicated that down-regulation of circHIPK3 inhibited cell proliferation and significantly decreased mRNA abundance of cyclin D1, PCNA, TGF-β1, Col. I, and FN in MCs. 	32889056
Hipk3	CircRNA	Mus musculus	Spinal Cord Injuries	SCI rat models	regulation[ Circ-HIPK3/miR-558/DPYSL5 axis ]	RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay	In this study, circ-HIPK3 was found lowly expressed in SCI rat models and AGE1.HN and PC12 cells induced by 100uM of CoCl2. Circ-HIPK3/miR-558/DPYSL5 axis modulated the apoptosis of AGE1.HN and PC12 cells in SCI.		Yes	Meanwhile, inhibited circ-HIPK3 or overexpressed circ-HIPK3 could separately elevate or reduce the apoptosis of AGE1.HN and PC12 cells.	32247616
HIPK2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cancer tissues	Expression(highly expressed)	qRT-PCR	Circular RNA circ HIPK2 expressions were up-regulated in patients with non-small cell lung cancer, compared with paracancerous tissue. 	Circular RNA circ HIPK2 expressions in III-IV patients with non-small cell lung cancer were higher than those of I-II patients. Overall survival rate and disease-free survival rate of patients with high circ HIPK2 expression were lower than those of patients with low circ HIPK2 expression. 	Yes	Circ HIPK2 promoted cell proliferation of non-small cell lung cancer. MiR-485-5p is a target for circ HIPK2 in non-small cell lung cancer; it reduced cell proliferation and accelerated HSP90 Ubiquitination in non-small cell lung cancer.	35181624
HIF2PUT	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation(HIF-2a)	CCK8//qRT-PCR//Transwell Assay	 lncRNA HIF2PUT was downregulated in NSCLC tissues and cell lines.  Furthermore, they found that HIF2PUT plays role in cell proliferation and invasion in NSCLC through regulating HIF-2a. 	Moreover, low expression of HIF2PUT was significantly related to TNM stage (p = 0.045) and histological type (p = 0.025). 	Yes	The authors also indicated that HIF2PUT mainly expressed in cytoplasm and overexpression of HIF2PUT attenuates cell proliferation and invasion in NSCLC cells. 	34287062
HIF2PUT	LncRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction[regulating HIF2]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	LncRNA HIF2PUT and HIF-2α were downregulated in osteosarcoma cell lines.Increased HIF2PUT expression inhibited the enrichment of CD133 in osteosarcoma stem cells. There was a strong positive correlation between relative HIF2PUT level and relative HIF-2α level in the 30 paired osteosarcoma cancer tissues.		Yes	Wound healing and transwell assays showed that lncRNA overexpression inhibited osteosarcoma stem cell migration and invasion. 	30966832
HIF1A-AS2	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-429/PD-L1 Axis)	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	HIF1A-AS2 was elevated in GC tissues and cell lines.. Moreover, HIF1A-AS2 directly bound to miR-429 based on bioinformatics prediction and luciferase assay, and inhibition of miR-429 abolished the effects of HIF1A-AS2 knockdown on GC cells. Furthermore, miR-429 directly targeted PD-L1, and overexpression of miR-429 suppressed GC tumorigenesis via PD-L1. 		Yes	Functional experiments showed that HIF1A-AS2 knockdown inhibited GC cell proliferation, migration, and invasion in vitro, as well as hindered tumor growth in vivo. 	33555514
HIF1A-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-153-5p/S100A14 Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	HIF1A-AS2 expression was raised in NSCLC tissues and cell lines. The HIF1A-AS2/miR-153-5p/S100A14 axis plays a crucial role in promoting NSCLC progression.	High HIF1A-AS2 expression was related to poor prognosis. 	Yes	 HIF1A-AS2 knockdown decreased proliferation, migration and invasion while promoting apoptosis.	32922043
HIF1A-AS2	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues 	Expression[highly expressed]	qRT-PCR	 aHIF levels were increased in EOC tissues and were upregulated by hypoxia in EOC cells. 		Yes	 Functional data revealed that aHIF knockdown accelerated cell apoptosis under hypoxia and inhibited EOC tumorigenesis and tumor growth in vivo.	30588022
HIF1A-AS2	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Regulation[HIF1A-AS2-miR-33b-5p-SIRT6 axis]	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//IHC	In this study, we demonstrated that HIF1A-AS2 was overexpressed in OS tissues and cells.Taken together, a newly identified regulatory mechanism for the lncRNA HIF1A-AS2-miR-33b-5p-SIRT6 axis was systematically studied in OS, which could be a promising target for the treatment of OS.		Yes	Downregulation of HIF1A-AS2 significantly affects multiple biological functions in OS cells, including cell proliferation, cell cycle progression, cell apoptosis, cell migration, and cell invasiveness. 	31626739
HIF1A-AS2	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Interaction[as a sponge of miR-129-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	We showed that the expression of HIF1A-AS2 was upregulated in the osteosarcoma samples compared with the expression in noncancerous samples. In addition, overexpression of HIF1A-AS2 promoted cell proliferation, cell cycle progression and invasion of osteosarcoma cells through the modulation of miR-129-5p.	Moreover, patients with high HIF1A-AS2 expression had a shorter overall survival. 	Yes	Ectopic expression of HIF1A-AS2 enhanced osteosarcoma cell proliferation, cell cycle progression and invasion. 	31866584
HIF1A-AS2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	HPV- positive cervical cancer cells	Regulation(P53/caspase9/caspase3 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//EdU Staining//ChIP	HIF1A-AS2 was significantly increased in cervical cancer tissue, and in the HPV- positive cervical cancer cells.  In terms of mechanism, we found that HIF1A-AS2 was mediated by HPV16 E6 and regulated cell apoptosis via P53/caspase 9/caspase 3 axis.		Yes	 Further investigation showed that the inhibition of HIF1A-AS2 suppressed cell proliferation, migration, invasion, and induced apoptosis, while up-regulation of HIF1A-AS2 revealed opposite results. 	35728704
HIF1A-AS2	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues,cell lines	Expression[highly expressed]	qRT-PCR//Transwell Assay	In our results, HIF1A-AS2 was also found to be upregulated in TNBC tissues compared with non-TNBC tissues or adjacent normal tissues. Besides, HIF1A-AS2 expression was also elevated in TNBC cell lines compared with the normal breast epithelial cell line.	Moreover, high expression of HIF1A-AS2 was associated with lymph node metastasis, distant metastasis and unfavorable histological grade in TNBC patients. Survival analysis showed a TNBC patient with high HIF1A-AS2 expression had shorter overall survival than patients with low HIF1A-AS2 expression, and HIF1A-AS2 high expression acted as an independent poor prognostic factor for overall survival in TNBC patients.	Yes	The cell migration and invasion assays suggested inhibition of HIF1A-AS2 obviously depressed TNBC cell migration and invasion. 	30635931
HIF1A-AS2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	129 LUAD tissues and paired adjacent non-tumor tissues (n = 56) 	Interaction(miR-146b-5p/IL-6/STAT3 axis)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//IHC//Invasion Assay	Using clinical samples, we showed that HIF1A-AS2 was upregulated in LUAD specimens, predicting poorer overall survival and disease-free survival. RNA precipitation assays, western blotting, luciferase assays, and rescue experiments demonstrated that HIF1A-AS2 sponged microRNA-146b-5p (miR-146b-5p), promoting interleukin-6 (IL-6) expression, activating the IL-6/STAT3 pathway, and leading to LUAD progression.	Using clinical samples, we showed that HIF1A-AS2 was upregulated in LUAD specimens, predicting poorer overall survival and disease-free survival. miR-146b-5p and IL-6 levels were correlated with the prognosis of LUAD patients. 	Yes	HIF1A-AS2 silencing inhibited the proliferation, migration, and tumorigenesis of LUAD cells and therapeutic efficacy of osimertinib against tumor cells in vitro and in vivo.	34703647
HIF1A-AS2	LncRNA	Homo sapiens	Carcinoma, Renal Cell	kidney cancer tissues and ccRCC cells	regulation[miR-130a-5p/ERBB2 Pathway]	qRT-PCR//Luciferase Report Assay//Western Blot	HIF1A-AS2 was highly expressed in kidney cancer tissues and ccRCC cells.Our results indicated a critical role for the HIF1A-AS2-miR-130a-5p axis in renal carcinoma progression, which may act as a promising diagnostic biomarker and a pivotal therapeutic target for renal carcinoma cures.		Yes	Interference of HIF1A-AS2 in vivo hindered cell proliferation, invasion and migration while accelerated cell apoptosis.	33061459
HIPK3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues or cells	Interaction(micro RNA-124 or micro RNA-506/pyruvate dehydrogenase kinase 2 axis)	qRT-PCR	We found that circHIPK3 was upregulated in HCC patients and associated with clinical characteristics, while miR-124 and miR-506 were downregulated in HCC patients. Additionally, we proved that knock down of circHIPK3 remarkably suppressed the proliferation and invasion of HCC cells. Mechanistically, circHIPK3 directly bound to miR-124 or miR-506 and inhibited their expression, and PDK2 was a target gene of miR-124 or miR-506. Moreover, circHIPK3 overexpression reversed the inhibitory effect of miR-124 or miR-506 on HCC progression. miR-124 or miR-506 could also suppress tumorigenesis of HCC cells by PDK2. Furthermore, in vivo evidence confirmed that knock down of circHIPK3 inhibited tumor formation. We suggest that circHIPK3 can accelerate the proliferation and invasion of HCC cells by sponging miR-124 or miR-506 to upregulate PDK2, which is the underlying mechanism of circHIPK3-induced HCC progression.	We found that circHIPK3 was upregulated in HCC patients and associated with clinical characteristics, while miR-124 and miR-506 were downregulated in HCC patients	Yes	Additionally, we proved that knock down of circHIPK3 remarkably suppressed the proliferation and invasion of HCC cells. Mechanistically, circHIPK3 directly bound to miR-124 or miR-506 and inhibited their expression, and PDK2 was a target gene of miR-124 or miR-506. 	35212603
HIPK3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues，cell line（16HBE ，SPC-A1, A549, NCI-H1299, and NCI-H1650）	Interaction[miR-130a-3p-PTEN/p22]	CCK8//qRT-PCR	In the present study, the level of circRNA-HIPK3 were measured by Taq-man based quantitative real-time PCR (qRT-PCR) analysis in both NSCLC patient specimens and cells, which showed that circRNA-HIPK3 was Expression[Expression[up-expression]-expression]regulated in both NSCLC tissues and cell lines.In the present study, the level of circRNA-HIPK3 were measured by Taq-man based quantitative real-time PCR (qRT-PCR) analysis in both NSCLC patient specimens and cells, which showed that circRNA-HIPK3 was Expression[Expression[up-expression]-expression]regulated in both NSCLC tissues and cell lines.		Yes	 MiR-193a expression was increased by circHIPK3 silencing. We then showed that miR-149 interacts with FOXM1 by binding to the 3'-untranslated region (UTR). Further, ectopic overexpression of miR-149 by transfecting miR-149 mimics significantly inhibited growth, migration and invasion of HSCLCs, which was found to be mediated through FOXM1. Moreover, miR-149 overexpression decreases the viability and proliferation of HSCLCs. Therefore, our data suggest that circHIPK3 regulates the function of NSCLCs through miR-149-mediated FOXM1 expression regulation, potentially providing a novel insight into the pathogenesis of NSCLC.	31597523
HIST1H2AG-6	LncRNA	Homo sapiens	Diabetes Mellitus, Type 2	peripheral blood mononuclear cells	Regulation(lower expressed)	qRT-PCR	The microarray analysis revealed that there were 55 lncRNAs and 36 mRNAs differentially expressed in patients with T2DM compared with healthy controls. Notably, lnc-HIST1H2AG-6 was significantly upregulated and lnc-AIM1-3 was significantly downregulated in patients with T2DM, which was validated in a large-scale qRT-PCR examination (90 controls and 100 patients with T2DM). Spearman's rank correlation coefficient revealed that both lncRNAs were correlated with 36 differentially expressed mRNAs. Furthermore, functional enrichment (KEGG and GO) analysis demonstrated that the two lncRNA-related mRNAs might be involved in multiple biological functions, including cell programmed death, negative regulation of insulin receptor signal, and starch and sucrose metabolism. Multivariate logistic regression analysis revealed that lnc-HIST1H2AG-6 and lnc-AIM1-3 were significantly correlated with T2DM (OR = 5.791 and 0.071, respectively, both P = 0.000). Furthermore, the ROC curve showed that the expression of lnc-HIST1H2AG-6 and lnc-AIM1-3 might be used to differentiate patients with T2DM from healthy controls (area under the ROC curve = 0.664 and 0.769, respectively).		Yes	Notably, lnc-HIST1H2AG-6 was significantly upregulated and lnc-AIM1-3 was significantly downregulated in patients with T2DM, which was validated in a large-scale qRT-PCR examination (90 controls and 100 patients with T2DM). Spearman's rank correlation coefficient revealed that both lncRNAs were correlated with 36 differentially expressed mRNAs. Furthermore, functional enrichment (KEGG and GO) analysis demonstrated that the two lncRNA-related mRNAs might be involved in multiple biological functions, including cell programmed death, negative regulation of insulin receptor signal, and starch and sucrose metabolism. 	34092238
HMMR-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and HCC cells	Interaction(miR-147a/ARID3A axis)	qRT-PCR	LncRNA HMMR-AS1 was significantly up-regulated in HCC tissues and HCC cells and was related to the poor prognosis. Further study of the mechanism showed that HMMR-AS1 could competitively bind to miR-147a to prevent the degradation of ARID3A.		Yes	 Inhibiting the expression of HMMR-AS1 could significantly inhibit tumor growth in vitro and in vivo. 	35179300
HNF1A-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCC tumor tissues and cells	Interaction(miR-298/TCF4 axis)	qRT-PCR//RIP//Western Blot	 HNF1A-AS1 was overexpressed in ESCC tumor tissues and cells. miR-298 was validated as a direct target of HNF1A-AS1.  In conclusion, knockdown of HNF1A-AS1 could inhibit EMT and stemness by regulating the miR-298/TCF4 axis.		Yes	 sh-HNF1A-AS1 significantly inhibited EMT and stemness of ESCC cells.  Animal experiments showed that sh-HNF1A-AS1 significantly inhibited tumor growth and increased the level of miR-298 in tissues.	35188404
HNF1A-AS1	LncRNA	Homo sapiens	Glioma	cell lines	regulation[miR-32-5p/SOX4 axis]	Flow Cytometry//qRT-PCR//Transwell Assay//Western Blot	The results demonstrated that HNF1A-AS1 was predominantly highly expressed in glioma cell lines compared with nontumor glial epithelial cell, which was associated with the stimulation of transcription factor myelocytomatosis oncogene.HNF1A-AS1 exerted oncogenic property in glioma progression via upregulating miR-32-5p-mediated SOX4 expression, suggesting potential novel therapeutic target for future glioma treatment.		Yes	Knockdown of HNF1A-AS1 remarkably inhibited glioma cells proliferation, migration, and invasion, while accelerating cell apoptosis in vitro. 	33448691
HNF1A-AS1	LncRNA	Homo sapiens	Glioblastoma	 clinical samples	Interaction(miR-22-3p/ENO1 axis)	In Vivo Experiment//ChIP//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	 In the current study, we analyzed clinical samples to show that the HNF1A-AS1 expression is upregulated and associated with poor patient survival in GBM.  Mechanistically, the transcription factor EGR1 forced the HNF1A-AS1 expression by directly binding the promoter region of HNF1A-AS1. Furthermore, combined bioinformatics analysis with our mechanistic work, using luciferase reporter assays and RIP, we first demonstrated that HNF1A-AS1 functions as a competing endogenous RNA (ceRNA) with miR-22-3p to regulate ENO1 expression in GBM cells. HNF1A-AS1 directly binds to miR-22-3p and significantly inhibits miR-22-3p expression, while ENO1 expression was increased.	 In the current study, we analyzed clinical samples to show that the HNF1A-AS1 expression is upregulated and associated with poor patient survival in GBM. 	Yes	 Functional studies revealed that HNF1A-AS1 knockdown markedly inhibits malignant phenotypes of GBM cells, whereas overexpression of HNF1A-AS1 exerts opposite effect. 	34772911
HNF1A-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Interaction[targeting miR-149-5p/Cdk6]	qRT-PCR	In the current study, we found that HNF1A-AS1 was relatively upregulated in both NSCLC patient tissues and cell lines. miR-149-5p was then proved to be a novel target of HNF1A-AS1, whose expression was negatively correlated with HNF1A-AS1 in NSCLC patient tissues and cell lines. HNF1A-AS1 increased the expression of cyclin-dependent kinase 6 (Cdk6) via sponging with miR-149-5p. Gain- and loss-of-functional studies indicated that HNF1A-AS1 promoted NSCLC progression partially through inhibition of miR-363-3p and induction of Cdk6. Subcutaneous xenotransplanted tumor model confirmed that interference of HNF1A-AS1 suppressed the tumorigenic ability of NSCLC via upregulation of miR-149-5p and downregulation of Cdk6 in vivo. In conclusion, our findings clarified the biologic significance of the HNF1A-AS1/miR-149-5p/Cdk6 axis in NSCLC progression and provided novel evidence that HNF1A-AS1 may be a new potential therapeutic target for the treatment of NSCLC.		Yes	Functional studies established that overexpression of HNF1A-AS1 promoted cell proliferation, cell cycle, invasion, and migration of NSCLC cells in vitro. The promotion abilities of HNF1A-AS1 on NSCLC cell progression were suppressed via knockdown of HNF1A-AS1.	31243821
HNF1A-AS1	LncRNA	Homo sapiens	neuroendocrine carcinoma	gastric NENs tissues	Expression(lower expressed)	Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	HNF1A-AS1 expression was decreased in gastric NENs tissues (p < 0.01). Oncostatin M was identified as the downstream target of HNF1A-AS1. Inhibition of transforming growth factor-β activity inhibited HNF1A-AS1/Oncostatin M-mediated epithelial-mesenchymal transition. 		Yes	 Over-expression of HNF1A-AS1 suppressed cellular proliferation, migration and invasion. Knockdown of transcription factor 3 inhibited the expression of HNF1A-AS1 and promoted cellular migration and invasion. 	34037532
HNF1A-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(HNF1A-AS1/IGF2BP2/CCND1)	In Vivo Experiment//Transfection//Immunoblotting//Tube Formation Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Transwell Assay	Our results showed that HNF1A-AS1 was upregulated in CRC and associated with unfavorable prognosis. Bioinformatics prediction and further experiments proved that HNF1A-AS1 could promote CCND1 expression by suppressing PDCD4 or competitively sponging miR-93-5p. Meanwhile, METTL3 mediated HNF1A-AS1 m6A modification and affected its RNA stability. HNF1A-AS1/IGF2BP2/CCND1 may act as a complex to regulate the stability of CCND1.		Yes	HNF1A-AS1 promoted proliferation, migration and angiogenesis, accelerated cell cycle and reduced cell apoptosis in CRC. 	36230970
Hmrhl	LncRNA	Homo sapiens	Leukemia, Myelogenous, Chronic, BCR-ABL Positive	 K562 cell line	Expression [highly expressed]	Transfection//Migration Assay//qRT-PCR//FISH//RNA-seq//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Invasion Assay//Transwell Assay	Results indicate its high expression in CML patient samples as well as in K562 cell line.		Yes	Silencing experiments suggest role of Hmrhl in cell proliferation, migration & invasion. RNA-seq and ChiRP-seq data analysis further revealed its association with important biological processes, including perturbed expression of crucial TFs and cancer-related genes. 	34734184
HMMR-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues	Regulation[MiR-138/sirt6 axis]	Western Blot//ISH//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	HMMR-AS1 expression was significantly upregulated in LUAD tissues and was associated with larger tumor diameter, advanced TNM stage, lymph node metastasis, and shorter survival. Taken together, HMMR-AS1 is significantly over-expressed in LUAD, and HMMR-AS1-miR-138-sirt6 axis play a critical role in LUAD tumorigenesis. Our findings highlight an oncogenic role of HMMR-AS1 in LUAD.	HMMR-AS1 expression was significantly upregulated in LUAD tissues and was associated with larger tumor diameter, advanced TNM stage, lymph node metastasis, and shorter survival. 	Yes	 Knockdown of HMMR-AS1 induced apoptosis and growth arrest in vitro and inhibited tumorigenesis in mouse xenografts. 	31128573
HIT000218960	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues	Interaction[Expression[highly expressed]regulation of HMGA2]	CCK8//qRT-PCR//Western Blot	HIT000218960 and HMGA2 were highly expressed in GC tissues compared with in healthy tissues.	The HIT000218960 expression level was associated with tumor size, Tumor-Node-Metastasis staging and lymph node metastasis in patients with GC.	Yes	HIT000218960 silencing decreased the proliferative and migratory ability of HGC27 and NCI-N87 cells; however, HMGA2 overexpression partly reversed this inhibitory effect.	31186705
HMGN2P17	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
HMGA1-lnc	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor and matched non-malignant tissues from 36 LUAD patients 	Expression [highly expressed]	RNA-seq	We identified the lncRNA RP11.513I15.6, which we refer to as HMGA1-lnc, neighboring HMGA1 to be significantly downregulated in both LUAD cohorts. Conversely, we found HMGA1 significantly overexpressed in LUAD and anticorrelated with HMGA1-lnc.		Yes	 In vitro experiments demonstrated siRNA-mediated inhibition of HMGA1-lnc in immortalized non-malignant lung epithelial cells resulted in a significant increase in HMGA1 gene expression.	33505435
HLNC1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and cell lines	interaction[USP49]	qRT-PCR	We found that HLNC1 was markedly upregulated in HCC samples and cell lines.HLNC1-USP49 interaction dramatically destabilized USP49.		Yes	HLNC1 could promote viability and migration of HCC cells.	32691951
HLA-F-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[HLA-F-AS1/miR-330-3p/PFN1 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Expressions of HLA-F-AS1 and PFN1 were significantly up-regulated while miR-330-3p was significantly down-regulated in CRC tissues and cell lines.HLA-F-AS1 promoted CRC progression via regulating miR-330-3p/PFN1 axis.		Yes	Over-expressions of HLA-F-AS1 or transfection of miR-330-3p inhibitors could promote the proliferation, migration and invasion and block apoptosis of CRC cells, whereas knockdown of HLA-F-AS1 or transfection of miR-330-3p mimics led to the opposite effects.	31863778
HLA-F-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer tissues and cells	Interaction(miR-21-3p/PEG3 axis)	qRT-PCR//Western Blot	Among the ovarian cancer tissues and cells, the expressions of PEG3 and lncRNA HLA-F-AS1 were depleted while an elevated miR-21-3p expression was observed. MiR-21-3p targeted PEG3 3'UTR while HLA-F-AS1 targeted miR-21-3p. HLA-F-AS1 overexpression mitigated the enhancement brought about by miR-21-3p mimic on ovarian cancer cells' proliferation and migration. Meanwhile, PEG3 overexpression abrogated miR-21-3p mimic's function as an oncogene in the progression of ovarian cancer. 		Yes	HLA-F-AS1's overexpression attenuated ovarian cancer development in vivo and in vitro .	35276697
HLA-F-AS1	LncRNA	Homo sapiens	Glioblastoma	62 GBM tumors 	Interaction(lncRNA MEG3)	RNA Pull-Down//Transfection//qPCR//Cell Apoptosis Assay//Transwell Assay	HLA-F-AS1 was highly expressed, and MEG3 was downregulated in GBM. Overexpression of HLA-F-AS1 reduced the expression levels of MEG3 while overexpression of MEG3 did not alter the expression of HLA-F-AS1. 		Yes	HLA-F-AS1 increased cell migration and invasion, but decreased cell apoptosis. MEG3 played opposite roles and reduced the effects of HLA-F-AS1 on cell behaviors.	34934358
HLA-F-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-541-3p/TRABD)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Colony Formation Assay	Our findings demonstrated that HLA-F-AS1 expression was significantly upregulated in TNBC tissues and cells, and high level of HLA-F-AS1 indicated the poor prognosis of patients with TNBC. HLA-F-AS1. In addition, signal transducer and activator of transcription 3 (STAT3) transcriptionally induced HLA-F-AS1 upregulation in TNBC cells via interacting with HLA-F-AS1 promoter. Moreover, HLA-F-AS1 acted as the molecular sponge of microRNA 541-3p (miR-541-3p) to elevate TRABD (TraB domain containing) expression in TNBC cells. 	Our findings demonstrated that HLA-F-AS1 expression was significantly upregulated in TNBC tissues and cells, and high level of HLA-F-AS1 indicated the poor prognosis of patients with TNBC. 	Yes	HLA-F-AS1 promoted TNBC progression by facilitating cell proliferation and stemness maintenance and inhibiting cell cycle arrest at G0/G1 stage and apoptosis in vitro as well as inducing tumor growth in vivo.Rescue experiments confirmed that the decrease of cell proliferation and stemness characteristics under silenced HLA-F-AS1 was rescued by TRABD overexpression in TNBC cells. 	33618253
HIVEP2-DT	LncRNA	Homo sapiens	Osteoarthritis	damaged cartilage from patients with OA and in human articular chondrocytes	Interaction(DHX9/TAK1/NF-κB signaling)	RNA Pull-Down//ChIP//Western Blot//FISH//qRT-PCR//RIP//Luciferase Report Assay//IF	The abundance of PILA was increased in damaged cartilage from patients with OA and in human articular chondrocytes stimulated with the proinflammatory cytokine tumor necrosis factor (TNF).  PILA promoted PRMT1-mediated arginine methylation of DExH-box helicase 9 (DHX9), leading to an increase in the transcription of the gene encoding transforming growth factor β-activated kinase 1 (TAK1), an upstream activator of NF-κB signaling. Furthermore, intra-articular injection of an adenovirus vector encoding PILA triggered spontaneous cartilage loss and exacerbated posttraumatic OA in mice. 		Yes	 Knockdown of PILA inhibited TNF-induced NF-κB signaling, extracellular matrix catabolism, and apoptosis in chondrocytes, whereas ectopic expression of PILA promoted NF-κB signaling and matrix degradation. 	35609127
HOXD-AS2	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	interaction[targeting HOXD8 and activating PI3K/Akt signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Mechanistic studies revealed that HOXD-AS2 regulated the expression of its nearby gene HOXD8 and inhibited the activity of the PI3K/Akt signaling pathway.	The low expression of lncRNA HOXD-AS2 was associated with lymph node metastasis and tumor-node-metastasis stage in GC.	Yes	In vitro functional experiments demonstrated that overexpression of HOXD-AS2 inhibited GC cell progression.	33250958
hsa_circ_0001361	LncRNA	Rattus norvegicus	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(miR-525-5p/VMA21 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Circ_0001361 was up-regulated, while miR-525-5p was down-regulated in LUAD tissues and cells. Functional experiments demonstrated that circ_0001361 drove LUAD cell growth and metastasis. Mechanistically, circ_0001361 functioned as a sponge of miR-525-5p to up-regulate downstream target VMA21 level. MiR-525-5p/VMA21 axis was involved in circ_0001361-mediated malignant phenotypes of LUAD cells. Finally, inhibition of circ_0001361 restrained in vivo xenograft tumor growth via regulating miR-525-5p/VMA21 axis.		Yes	Functional experiments demonstrated that circ_0001361 drove LUAD cell growth and metastasis.	34507559
ELFN1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	cancer tissues and cell lines 	Interaction(MYC/ELFN1-AS1/EZH2/FOXP1/TPM1 )	qRT-PCR//Luciferase Report Assay//ChIP	ELFN1-AS1 was transcriptionally activated by MYC. Moreover, ELFN1-AS1 led to transcriptional silencing of tropomyosin 1 (TPM1) via recruiting enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and forkhead box P1 (FOXP1). Collectively, MYC-upregulated ELFN1-AS1 recruited EZH2 and FOXP1 to restrain TPM1 expression, thereby promoting colorectal cancer tumor growth.		Yes	 ELFN1-AS1 knockdown inhibited colorectal cancer tumor growth through restricting cell proliferation and facilitating cell apoptosis. 	35857351
LCIIAR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	Interaction( LCIIAR/hsa-miR184/SLC16A3/CDCP1 network)	Transfection//qRT-PCR//FISH//migration assay//Cell Proliferation Assay	 We show that increase LCIIAR expression correlated with poor clinical stage and adverse clinical outcomes and that could also serve as an independent unfavorable prognostic factor in patients with Lung Adenocarcinima.  We also demonstrated that the LCIIAR/hsa-miR184/SLC16A3/CDCP1 network regulates SLC16A3/CDCP1 overexpression in and is associated with poor prognosis in this tumour. 	 We show that increase LCIIAR expression correlated with poor clinical stage and adverse clinical outcomes and that could also serve as an independent unfavorable prognostic factor in patients with Lung Adenocarcinima. 	Yes	More importantly, we confirmed that silencing of LCIIAR expression significantly inhibits the proliferation, and migration abilities of these tumour cells. 	35860557
LCAT1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues	Regulation[LCAT1-miR-4715-5p-RAC1/PAK1 axis ]	RIP//Luciferase Report Assay	LCAT1 is an oncogene that is significantly upregulated in lung cancer tissues and associated with poor prognosis. LCAT1-miR-4715-5p-RAC1/PAK1 axis plays an important role in the progression of lung cancer. 	LCAT1 is an oncogene that is significantly upregulated in lung cancer tissues and associated with poor prognosis. 	Yes	 LCAT1 knockdown caused growth arrest and cell invasion in lung cancer cells in vitro, and inhibited tumorigenesis and metastasis in the mouse xenografts. 	31779616
LCAL1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues	Regulation[AMPK/mTOR/S6K axis ]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Colony Formation Assay	Recently, lung cancer-associated lncRNA 1 (LCAL1) has been identified to be overexpressed in lung cancer tissues. Our study revealed that overexpressed LCAL1 may induce aerobic glycolysis in lung cancer cells through AMPK/HIF1α axis, enhance protein synthesis through AMPK/mTOR/S6K axis, and suppress autophagic cell death through AMPK/ULK1 pathway.		Yes	while inhibiting LCAL1 expression has shown potential to inhibiting lung cancer growth.	30741368
LBX2‑AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	Regulation(miR‑491‑5p/S100A11 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//ELISA//Transwell Assay	The results showed that LBX2‑AS1 was upregulated both in colorectal cancer tissues and cells, which was distributed in the cytoplasm and nucleus of colorectal cancer cells. Clinically, high LBX2‑AS1 expression could be an independent prognostic factor for colorectal cancer. Furthermore, relative operating characteristic curve analysis showed that LBX2‑AS1 was a sensitive diagnostic marker for colorectal cancer. Highly expressed ELK1, as a transcription factor, could bind to the two conserved sites in the promoter region of LBX2‑AS1, thereby activating the transcription of LBX2‑AS1. Silencing LBX2‑AS1 markedly inhibited proliferative, migratory and invasive abilities of colorectal cancer cells. miR‑491‑5p expression was downregulated, while S100A11 expression was upregulated in colorectal cancer tissues and cells. Dual‑luciferase reporter assays confirmed that LBX2‑AS1 could block S100A11 degradation via competitively binding to miR‑491‑5p. Furthermore, LBX2‑AS1 overexpression could notably reverse the inhibitory effect of miR‑491‑5p on proliferation and invasion of colorectal cancer cells. Taken together, LBX2‑AS1 induced by transcription factor ELK1 may facilitate colorectal cancer cell proliferation and invasion via regulation of the miR‑491‑5p/S100A11 axis. Thus, LBX2‑AS1 could be an underlying prognostic and diagnostic marker for colorectal cancer.	Clinically, high LBX2‑AS1 expression could be an independent prognostic factor for colorectal cancer. Furthermore, relative operating characteristic curve analysis showed that LBX2‑AS1 was a sensitive diagnostic marker for colorectal cancer.	Yes	Dual‑luciferase reporter assays confirmed that LBX2‑AS1 could block S100A11 degradation via competitively binding to miR‑491‑5p.	34080639
LBX2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[LBX2-AS1/miR-4766-5p/CXCL5]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Transwell Assay	LBX2-AS1 was up-regulated in GC tissues and cells, and its knockdown suppressed proliferation, migration and invasion of GC cells. The LBX2-AS1/miR-4766-5p/CXCL5 regulatory axis provides a theoretical basis for the research on lncRNA-directed therapeutics in GC.		Yes	LBX2-AS1 was up-regulated in GC tissues and cells, and its knockdown suppressed proliferation, migration and invasion of GC cells. 	33061849
LBX2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[Notch signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//EdU Staining//Transwell Assay	We found that LBX2-AS1 was highly expressed in NSCLC tissues and cell lines.Mechanistic studies revealed that the suppression of LBX2-AS1 resulted in the reduced expressions of Notch1, p21, and Hes1, suggesting that LBX2-AS1 might promote the activation of the Notch pathway.	The increased levels of LBX2-AS1 were observed to be positively correlated with TNM stage, histological grade, and lymph node metastasis. Furthermore, the Kaplan-Meier survival curves indicated that patients with higher expressions of LBX2-AS1 had unfavorable overall survival.	Yes	Lost-of-functions assays revealed that the knockdown of LBX2-AS1 in H1299 and A549 cells inhibited cell proliferation, migration, and invasion.	31539129
LBX2-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction[ZEB1 and ZEB2]	qRT-PCR	Furtherly, dysregulation of LBX2-AS1 was identified in ESCC tissues with metastasis. Collectively, our data showed that ZEB1-induced upregulation of LBX2-AS1 promoted cell migration and EMT process in ESCC via enhancing the stability of ZEB1 and ZEB2.		Yes	 Loss-of function assays were conducted and revealed that LBX2-AS1 knockdown suppressed ESCC cell migration and epithelial-mesenchymal transition (EMT). 	30824187
LBX2-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Interaction(miR-627-5p/RAC1/PI3K/AKT pathway)	Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//IHC//Transwell Assay	. The results illustrated that LBX2-AS1 level was substantially increased in colon cancer tissues and was obviously correlated with the tumor volume and early distant metastasis of patients.  On the other hand, miR-627-5p, down-regulated in colon cancer tissues, was negatively associated with LBX2-AS1 expression. Functional experiments showed that miR-627-5p suppressed colon cancer growth. Mechanistically, LBX2-AS1, as an endogenous competitive RNA, targeted miR-627-5p and restrained its expression, while miR-627-5p targeted and negatively regulated the RAC1/PI3K/AKT axis. 		Yes	 Besides, overexpression of LBX2-AS1 remarkably boosted growth, proliferation, and metastasis and restrained apoptosis in colon cancer cells, whereas LBX2-AS1 knockdown produced the opposite effect.	35816228
LBX2-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian tissues	regulation[inhibiting miR-455-5p and miR-491-5p]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Colony Formation Assay	Ovarian cancer tissue specimens showed significant higher LBX2-AS1 expression levels that non-cancerous counterparts.This lncRNA increased the cell growth, survival, migration, invasion and tumour formation of ovarian cancer cells by inhibiting miR-455-5p and miR-491-5p, thus liberating the expression of E2F2 cancer-promoting gene.	High expression level of LBX2-AS1 was significantly associated with reduced overall survival of patients.	Yes	LBX2-AS1 knockdown significantly down-regulated the cell growth, colony formation, migration, invasion and tumour formation capacity of ovarian cancer cells and increased their apoptosis in vitro.	33342041
LBX2-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	regulation[miR-4784/KDM5C axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ChIP	 LBX2-AS1 expression was markedly increased in OC tissues and cell lines. This study proved that ELK1 activated-LBX2-AS1 aggravated the progression of OC by targeting the miR-4784/KDM5C axis, suggesting that LBX2-AS2 may be a promising diagnostic biomarker of OC.		Yes	Functionally, LBX2-AS1 silencing inhibited cell proliferation, migration and stemness but facilitated cell apoptosis in OC. Moreover, depletion of LBX2-AS1 suppressed tumor growth of OC in vivo.	33099720
LBX2-AS1	LncRNA	Homo sapiens	Glioma	 clinical glioma tissues	Interaction(Akt/GSK3β pathway)	Western Blot//Migration Assay//qRT-PCR//RNA-seq//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	 In this study, using online-available datasets combined with clinical glioma tissues collected, we found that LBX2-AS1 was significantly increased and negatively correlated with prognosis in glioma. RNA sequencing and western blot analysis confirmed that LBX2-AS1 regulates the Akt/GSK3β pathway.	 In this study, using online-available datasets combined with clinical glioma tissues collected, we found that LBX2-AS1 was significantly increased and negatively correlated with prognosis in glioma. 	Yes	In vitro functional assays such as CCK-8, Annexin V, transwell assay, and western blot analysis showed that silencing of LBX2-AS1 suppressed the proliferation, migration, and invasion of glioma cells and increased apoptosis. 	33637977
LBX2-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissue	Regulation(FSTL3 /TF RARα)	In Vivo Experiment//ChIP//Western Blot//Transfection//Wound Healing Assay//CCK8//FISH//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//IHC//Bioinformatics Analysis//Transwell Assay	Bioinformatics analysis indicated that lncRNA LBX2-AS1, RARα, FSTL3 were remarkably fostered in thyroid cancer tissue, and LBX2-AS1 was evidently correlated with clinical features.  The LncMAP triplet prediction showed that LBX2-AS1 recruited TF RARα to modulate FSTL3. RIP assay confirmed that LBX2-AS1 was prominently enriched on RARα. The integrative results demonstrated that LBX2-AS1 activated FSTL3 by binding to TF RARα to hasten proliferation, migration and invasion of thyroid cancer.	Bioinformatics analysis indicated that lncRNA LBX2-AS1, RARα, FSTL3 were remarkably fostered in thyroid cancer tissue, and LBX2-AS1 was evidently correlated with clinical features. 	Yes	The integrative results demonstrated that LBX2-AS1 activated FSTL3 by binding to TF RARα to hasten proliferation, migration and invasion of thyroid cancer.	34858481
LBX2-AS1	LncRNA	Homo sapiens	Multiple Myeloma	MM patients	Regulation(LBX2 )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	Circulating LBX2-AS1 was up-regulated in MM patients and positively correlated to LBX2 expression. . Its up-regulation was also found in MM cells and primarily distributed in cytoplasm. Overexpressing LBX2-AS1 markedly strengthened LBX2 expression by increasing its mRNA stability. Rescue assays showed that silencing LBX2-AS1 distinctly weakened the pcDNA3.1-LBX2-induced increase in proliferation and decrease in apoptosis for MM cells. 		Yes	 LBX2-AS1 knockdown distinctly weakened proliferative ability and induced apoptosis in MM cells. Silencing LBX2-AS1 markedly weakened tumor growth.	34552959
LATS2-AS1-001	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	regulation[LATS2/YAP1 signaling pathway,EZH2]	qRT-PCR//RIP	 Decreased expression levels of LATS2-AS1-001 and LATS2 were confirmed in 357 GC tissues compared with the normal mucosa. Mechanistically, overexpressing LATS2-AS1-001 upregulated LATS2 and induced YAP1 phosphorylation via binding to EZH2. 		Yes	Moreover, ectopic expression of LATS2-AS1-001 decreased cell viability, induced G0/G1 phase arrest, and inhibited cell migration and invasion in GC cells. 	32514249
LASTR	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer cell lines 	Interaction(miR-137/TGFA/PI3K/AKT axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	qRT-PCR results showed that LASTR was highly expressed in lung cancer cell lines relative to the expression level in normal lung epithelial cell line.Analysis of the downstream mechanism of LASTR demonstrated that LASTR exerts the oncogene effect through the miR-137/TGFA axis. GSEA results indicated that LASTR exhibits its activity by activating the PI3K/AKT signaling pathway, which was validated by western blotting assay.		Yes	 Cell phenotype experiments indicated that knockdown of LASTR significantly inhibited proliferation and metastatic ability of lung cancer cells. 	35281858
LARRPM	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(TET1 /LINC00240 and CSF1)	In Vivo Experiment//qPCR//Invasion Assay//Migration Assay	 The lncRNA LARRPM was expressed at low levels in LUAD tissues and cells.  Mechanistically, LARRPM bound and recruited DNA demethylase TET1 to the promoter of its anti-sense strand gene LINC00240, leading to a decrease in DNA methylation level of the LINC00240 promoter and transcriptional activation of LINC00240. Functional rescue assays suggested that the lncRNA LINC00240 was responsible for the roles of LARRPM in the malignant behavior of LUAD cells. LARRPM decreased the binding of TET1 to the CSF1 promoter, resulting in increased DNA methylation of the CSF1 promoter and transcriptional repression of CSF1, which is responsible for the roles of LARRPM in macrophage M2 polarization and infiltration. 	The low expression of LARRPM was correlated with advanced stage and poor survival of patients with LUAD.	Yes	Functional experiments revealed that LARRPM suppressed LUAD cell proliferation, migration and invasion, and promoted apoptosis. LARRPM also repressed macrophage M2 polarization and infiltration. Taken together, LARRPM significantly restricted LUAD progression in vivo. 	36221069
LARP4	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC cell lines (including A549, NCI-H1650, NCI-H1299, and HCC827 cells)	Interaction( miR-367)	Transfection//qPCR//PCR//Invasion Assay//IF	CircRNA LARP4 was decreased in NSCLC cell lines (including A549, NCI-H1650, NCI-H1299, and HCC827 cells) compared to BEAS-2B cells. 		Yes	In NCI-H1650 cells, circRNA LARP4 overexpression inhibited cell proliferation, migration, and invasion, while promoting apoptosis. In A549 cells, circRNA LARP4 knockdown increased cell proliferation, migration, and invasion, while decreasing apoptosis. Moreover, miR-367 was decreased by the overexpression of circRNA LARP4, but increased by the knockdown of circRNA LARP4; and further luciferase reporter assay revealed that circRNA LARP4 could directly bind to miR-367.	34527128
LARP4	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[SMAD7]	qRT-PCR	Compared with adjacent tissues, circ LARP4 was lowly expressed in NSCLC tissues. Circ LARP4 could suppress the metastasis of NSCLC by up-regulating SMAD7.	 Meanwhile, expression of circ LARP4 was associated with the prognosis of NSCLC patients. 	Yes	Downregulated circ LARP4 was found in NSCLC cell lines as well. The migration and invasion abilities of NSCLC cells were significantly inhibited via overexpression of circ LARP4.	32141555
LCAT3	LncRNA	Homo sapiens	Lung Neoplasms	 lung adenocarcinomas 	Interaction(FUBP1 /c-MYC)	CCK8//qRT-PCR//RNA-seq	LCAT3 was found to be up-regulated in lung adenocarcinomas (LUAD), and its over-expression was associated with the poor prognosis of LUAD patients. LCAT3 upregulation is attributable to N6-methyladenosine (m6A) modification mediated by methyltransferase like 3 (METTL3), leading to LCAT3 stabilization. Mechanistically, LCAT3 recruited Far Upstream Element Binding Protein 1 (FUBP1) to the MYC far-upstream element (FUSE) sequence, thereby activating MYC transcription to promote proliferation, survival, invasion and metastasis of lung cancer cells.		Yes	Biologically, loss-of-function assays revealed that LCAT3 knockdown significantly suppressed lung cancer cell proliferation, migration and invasion in vitro, and inhibited tumor growth and metastasis in vivo.  LCAT3 knockdown induced cell cycle arrest at the G1 phase.	34274028
LDC1P	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,blood	Interaction[Wnt/β-catenin signalling pathway]	IHC//Western Blot//Wound Healing Assay//qRT-PCR//Colony Formation Assay//Transwell Assay	Here, we verified that LINC01225 was up-regulated in tumour tissues and plasma of GC.In conclusion, LINC01225 promotes the progression of GC through Wnt/β-catenin signalling pathway, and it may serve as a potential target or strategy for diagnosis or treatment of GC.	Analysis with clinicopathological information suggested that up-regulation of LINC01225 was associated with advanced disease and poorer overall survival. 	Yes	In addition, knockdown of LINC01225 led to retardation of cell proliferation, invasion and migration, and overexpression of LINC01225 showed the opposite effects. 	31460694
LAMC2-1:1	LncRNA	Homo sapiens	Colonic Neoplasms	COAD cell lines	Interaction(miR-216a-3p/HMGB3)	qRT-PCR//Transfection//Luciferase Report Assay	In this study, we found that the lnc-LAMC2-1:1 SNP rs2147578 was upregulated in COAD cell lines.Furthermore, lnc-LAMC2-1:1 SNP rs2147578 promoted colon cancer migration, invasion, and proliferation. Interestingly, lnc-LAMC2-1:1 SNP rs2147578 positively regulated HMGB3 expression via miR-216a-3p in colon cancer cells. 		Yes	Furthermore, lnc-LAMC2-1:1 SNP rs2147578 promoted colon cancer migration, invasion, and proliferation. Interestingly, lnc-LAMC2-1:1 SNP rs2147578 positively regulated HMGB3 expression via miR-216a-3p in colon cancer cells. 	36582685
LDLRAD4-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC specimens and cell lines	regulation[ LDLRAD4-AS1-LDLRAD4-Snail regulatory axis ]	Western Blot//Wound Healing Assay//qRT-PCR//FISH//Transwell Assay	In this study, we observed that lncRNA LDLRAD4-AS1 was located in the nucleus of CRC cells and that lncRNA LDLRAD4-AS1 was upregulated in most CRC specimens and cell lines.Our results demonstrated a previously unrecognized LDLRAD4-AS1-LDLRAD4-Snail regulatory axis involved in epigenetic and posttranscriptional regulation that contributes to CRC progression and metastasis.	Overexpression of lncRNA LDLRAD4-AS1 was correlated with poor prognosis in CRC patients. 	Yes	LncRNA LDLRAD4-AS1 upregulation enhanced the migration and invasion of CRC cells in vitro and facilitated CRC metastasis in vivo. 	32111819
LEMD1-AS1	LncRNA	Homo sapiens	Osteoarthritis	chondrocyte 	Interaction(miR-944/PGAP1)	RNA Pull-Down//Western Blot//CCK8//Flow Cytometry//qRT-PCR//Luciferase Report Assay//ELISA//EdU Staining	 LEMD1-AS1 bound to miR-944 and regulated its expression, and PGAP1 presented as a direct target gene of miR-944, which was confirmed by a dual-luciferase reporter assay. Inhibition of PGAP1 partially restored the effects of LEMD1-AS1/miR-944 on the proliferation, cell apoptosis, cell cycle distribution and inflammatory responses of LPS-treated chondrocytes. To conclude, the LEMD1-AS1/miR-944/PGAP1 axis may be a novel therapeutic candidate to target in OA treatment.		Yes	 Over-expression of LEMD1-AS1 or down-regulation of miR-944 significantly promoted viability, proliferation and inhibited cell apoptosis, cell cycle arrest and inflammatory responses of chondrocytes treated with LPS by CCK-8, EdU, flow cytometry and an ELISA assay.	35686740
LEMD1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(LEMD1/ PI3K-AKT signaling pathway)	CCK8//qRT-PCR//Wound Healing Assay//Western Blot	 In addition, both LEMD1-AS1 and its cognate LEMD1 were up-regulated in metastatic OSCC compared to nonmetastatic OSCC. Mechanistically, LEMD1-AS1 stabilized LEMD1 and increased its mRNA and protein levels, and consequently activated the PI3K-AKT signaling pathway to facilitate OSCC metastasis.		Yes	 Gain-of-function, loss-of-function, and rescue experiments indicated that LEMD1-AS1 upregulated LEMD1 to increase OSCC migration and invasion in vitro and in vivo. 	35983249
LEISA	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LAD tissues and cells	Interaction(STAT3 and IL-6 promoter)	In Vivo Experiment//RNA Pull-Down//Northern Blot//Western Blot//qRT-PCR//ChIP	Our data showed that LEISA was highly expressed in, and correlated with the clinical progression and prognosis of LAD.Mechanistically, we demonstrated that LEISA recruited STAT3 to bind the promoter of IL-6 and upregulated IL-6 expression. 		Yes	Ectopic expression of LEISA promoted the proliferation and suppressed apoptosis of LAD cells in vitro and in vivo. 	33859372
LEF-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[ LEF-AS1/miR-505/KIF3B axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	The expression of LEF-AS1 in CRC tissue specimens was found to be markedly higher than that in normal colon tissues. However, the down-regulation of LEF-AS1 reduces the proliferation rate and suppresses the invasiveness and metastasis of CRC cells through the LEF-AS1/miR-505/KIF3B axis.		Yes	After transfection with LEF-AS1 siRNA, the cell viability, as well as cell migration and invasion capacities, were both attenuated.	31773695
LEF1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 cell lines	Interaction(miR-5100/DEK/AMPK-mTOR Axis)	qRT-PCR//IHC//Luciferase Report Assay//Western Blot	 Studies have shown that miR-5100 acts by targeting the 3'UTR of DEK, and LEF1-AS1 regulates the expression of miR-5100 by sponging with mIR-5100. In conclusion, our results found that LEF1-AS1 and miR-5100 sponge function, and the miR-5100/DEK/AMPK/mTOR axis regulates autophagy and apoptosis in gastric cancer cells.		Yes	In addition, miR-5100 inhibits autophagy and promotes apoptosis in GC cells while LEF1-AS1 had the opposite effect. 	35563178
LEF1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-489/DIAPH1 axis]	qRT-PCR	We firstly showed that LEF1-AS1 expression was upregulated in human CRC tissues and cell lines.Mechanically, LEF1-AS1 functioned as competing endogenous RNA (ceRNA) for miR-489 to positively recover DIAPH1, thus playing an oncogenic role in CRC pathogenesis. 	Clinical study revealed that high LEF1-AS1 expression was positively associated with histological grade, lymph nodes metastasis, and decreased survivals of CRC patients.	Yes	Functionally, down-regulation of LEF1-AS1 using si-LEF1-AS1 decreased cell growth, migration and invasion, as well as increased apoptosis in CRC cells.	32248974
LEF1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation(Wnt/β-catenin/LEF1 pathway)	CCK8//qRT-PCR//Western Blot	Here, we identify that LEF1-AS1 and LEF1 are higher in CRC tissues than that in adjacent tissues, as well as upregulated in CRC cell lines than that in normal colorectal cells. Altered levels of LEF1-AS1 modulate LEF1 expression, while altered LEF1 could not regulate LEF1-AS1. LEF1-AS1 recruits MLL1 to the promoter region of LEF1, induces H3K4me3 methylation modification and mediates LEF1 transcription. FUT8 is a direct target of transcription factor LEF1, which regulates FUT8 level. Altered FUT8 also regulates the core fucosylation of CRC cells, and LEF1-AS1 mediates FUT8 level through activation of Wnt/β-catenin/LEF1 pathway, thereby resulting in β-catenin nuclear translocation. 		Yes	In addition, LEF1-AS1 mediates the proliferation, migration and invasion of CRC cells in vitro. LEF1-AS1 silence hinders the tumorigenesis, liver and lung metastasis of SW620 cells in vivo, while overexpressed FUT8 abolishes the suppressive impact of LEF1-AS1 repression on the biological behavior of SW620 cells.	34021424
LEF1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer patients	regulation[miR-30-5p/SOX9 Axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	 We found that LEF1-AS1 was upregulated in colon cancer patients and correlated with poor overall survival and recurrent-free survival. Our results indicated that LEF1-AS1 promoted migration, invasion and metastasis of colon cancer cells partially through miR-30-5p/SOX9 axis. 	 We found that LEF1-AS1 was upregulated in colon cancer patients and correlated with poor overall survival and recurrent-free survival. 	Yes	Besides, enforced expression of LEF1-AS1 in HT29 and T84 cells promoted migration, invasion, anchorage-independent growth, tumor xenograft formation and lung metastasis, while knockdown of LEF1-AS1 in COLO320 cells suppressed cell migration, invasion, anchorage-independent growth and tumor xenograft formation. 	32308428
LEF1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[microRNA-136-5p/WNK1]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Transwell Assay	 HCC tissues and cells contained high lncRNA LEF1-AS1 expression.Association of lncRNA LEF1-AS1 with WNK1 blocked the inhibitory effect of miR-136-5p on WNK1, which was confirmed by in vivo experiments.		Yes	LncRNA LEF1-AS1 upregulation triggered markedly increased HCC cell proliferation, migration, and invasion and human umbilical vein endothelial cell angiogenesis. In vivo silencing lncRNA LEF1-AS1 resulted in reduced tumor cell vitality and matrix metalloproteinase-9 and the vascular endothelial growth factor expression. 	32068261
LEF1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	interaction[miR-1285-3p]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We showed that LEF1-AS1 expression was upregulated in ovarian cancer tissues compared with normal tissues. Mechanistically, LEF1-AS1 exerted its oncogenic functions through interacting with miR-1285-3p to inhibit miRNA activity. 	 Besides, LEF1-AS1 level was positively correlated with lymph node metastasis and advanced stage.	Yes	 Moreover, LEF1-AS1 knockdown suppressed ovarian cancer cell proliferation, migration and invasion. 	32099465
LEF1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[Hippo signaling pathway]	IHC//Western Blot//Co-IP//qRT-PCR//RIP//MTT//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	 In this study, we unveiled that LEF1-AS1 markedly increased in oral squamous cell carcinoma (OSCC) tissues and cell lines.  In a word, we concluded that LEF1-AS1 served an oncogenic part in OSCC through suppressing Hippo signaling pathway by interacting with LATS1, suggesting the therapeutic and prognostic potential of LEF1-AS1 in OSCC.		Yes	 Functionally, LEF1-AS1 knockdown inhibited cell survival, proliferation and migration, whereas enhanced cell apoptosis and induced G0/G1 cell cycle arrest in vitro.	30983488
LEF1-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[LEF1-AS1/miR-489-3p/HIGD1A axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	Hence, in this study, we tested that LEF1-AS1 expression was significantly upregulated in glioma tissues and cell lines.In summary, our studies corroborated the regulatory mechanism of LEF1-AS1/miR-489-3p/HIGD1A axis in glioma, suggesting that targeting LEF1-AS1 might be a promising method for glioma therapy in the future.		Yes	Besides, knockdown of LEF1-AS1 repressed cell proliferation while activated apoptosis in glioma cells in vitro, and also suppressed tumor growth in vivo. 	32826866
LEF1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer tissues	Regulation[miR-489/SOX4 Axis ]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//RIP//Luciferase Report Assay//Transwell Assay	In the present study, we found that LEF1-AS1 was markedly upregulated in lung cancer tissues and could promote NSCLC cell proliferation and migration in vivo and in vitro. LEF1-AS1 could bind with miR-489 and further negatively regulate miR-489 to promote SRY-related HMG box transcription factor 4 (SOX4) expression. In conclusion, these data suggested that LEF1-AS1 promoted NSCLC tumorigenesis dependent on the miR-489-SOX4 axis and implicated the potential application of LEF1-AS1 for the prognosis and treatment of NSCLC.		Yes	In the present study, we found that LEF1-AS1 was markedly upregulated in lung cancer tissues and could promote NSCLC cell proliferation and migration in vivo and in vitro. 	31386568
LEF1-AS1	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tissues and cell lines	regulation[Wnt/β-catenin pathway]	qRT-PCR	 In our study, LEF1-AS1 expression was increased in retinoblastoma tissues and cell lines compared with paired adjacent normal tissues and the retinal pigment epithelial cell line, respectively.The in vitro assays suggested that silencing of LEF1-AS1 suppressed retinoblastoma cell proliferation, migration, and invasion through regulating the Wnt/β-catenin pathway. 	High LEF1-AS1 expression predicted poor disease-free survival in patients with retinoblastoma.	Yes	The in vitro assays suggested that silencing of LEF1-AS1 suppressed retinoblastoma cell proliferation, migration, and invasion through regulating the Wnt/β-catenin pathway. 	31990064
LEF1-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	cell lines	Expression[lower expressed]	qRT-PCR	We show that LEF1-AS1 is highly expressed in normal hematopoietic stem cells but barely detectable in myeloid malignant cell lines. 		Yes	Artificial LEF1-AS1 over-expression inhibited proliferation in HL60 and led to an upregulation of tumor suppressors p21 and p27, and reduced ERK1/2 activation.	30770626
LEF1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues and cells	Interaction(miR-221-5p/GJA1 Axis)	Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis	 In the current manuscript, we revealed the elevated expression of long noncoding RNA (lncRNA) LEF1-AS1 in HNSCC which was associated with the poor prognosis by bioinformatic analysis.Most importantly, we illustrated that LEF1-AS1 played as a competitive endogenous RNA (ceRNA) via sponging miR-221-5p and thereby positively regulated gap junction protein alpha 1 (GJA1) expression, thus aggravated tumor progression and EMT.	 In the current manuscript, we revealed the elevated expression of long noncoding RNA (lncRNA) LEF1-AS1 in HNSCC which was associated with the poor prognosis by bioinformatic analysis.	Yes	 Moreover, we noticed that LEF1-AS1 dramatically accelerated the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in HSCC cell line FaDu. 	35371339
LEF1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	AIPC tissues	regulation[Wnt/β-catenin pathway]	RIP//qRT-PCR//Transwell Assay//EdU Staining//ChIP	The next-generation sequencing results showed that LEF1-AS1 is significantly overexpressed in AIPC. Furthermore, our RT-qPCR assay data showed that LEF1-AS1 is overexpressed in AIPC tissues. 		Yes	Functional experiments showed that LEF1-AS1 promotes the proliferation, migration, invasion and angiogenic ability of AIPC cells in vitro and tumour growth in vivo by recruiting the transcription factor C-myb to the promoter of FZD2, inducing its transcription. 	33292271
LEF1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-221/PTEN Signaling]	Cell Proliferation Assay//qRT-PCR//Cell Apoptosis Assay	We found that LEF1-AS1 was upregulated in NSCLC patients.  LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling.		Yes	Overexpression of LEF1-AS1 and miR-221 promoted cancer cell proliferation and inhibited apoptosis. 	32547220
LEF1-AS1	LncRNA	Homo sapiens	Spinal Cord Injuries	 LPS-treated SCI and microglial cells	Interaction(miR-222-5p/RAMP3 )	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay	We revealed that LncRNA LEF1-AS1 was distinctly upregulated, whereas miR-222-5p was significantly downregulated in LPS-treated SCI and microglial cells.  Mechanistically, LEF1-AS1 served as a competitive endogenous RNA (ceRNA) by sponging miR-222-5p, targeting RAMP3. RAMP3 overexpression attenuated LEF1-AS1-mediated protective effects on LPS-mediated microglial cells from apoptosis and inflammation.		Yes	However, LEF1-AS1 knockdown enhanced cell viability, inhibited apoptosis, as well as inflammation of LPS-mediated microglial cells. On the contrary, miR-222-5p upregulation decreased cell viability, promoted apoptosis, and inflammation of microglial cells. 	33407665
LAMTOR5-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction(miR-210-3p)	Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	LAMTOR5-AS1 decreased in cervical cancer tissues, while miR-210-3p expression increased.	In the study of cervical cancer cells, it was found that the LAMTOR5-AS1 sponge miR-210-3p was associated with the malignant progression of cervical cancer. 	Yes	 Overexpression of LAMTOR5-AS1 could effectively inhibit the development of cervical cancer cells and might be chosen as a prognostic biomarker of cervical cancer.	36173004
LALTOP	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(Top2α)	Bioinformatics Analysis	LALTOP expression is increased in NSCLC tissues and cell lines.  RNA-RNA interaction assay showed that LALTOP bound and stabilized topoisomerase II alpha (Top2α) mRNA. Positive correlation can be found between LALTOP and Top2α mRNA expressions in clinical specimens. 		Yes	Moreover, LALTOP strongly promoted proliferation and migration of A549 and H1793 cells. 	34438347
KCNQ1OT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines	regulation[S1PR1,miR-149]	RNA Pull-Down//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 KCNQ1OT1 and S1PR1 were significantly increased, but miR-149 was decreased in HCC cells.Luciferase reporter assays and RNA pull-down assays revealed that KCNQ1OT1 directly targeted miR-149. In addition, miR-149 bound to the 3'-UTR of S1PR1. 		Yes	 Knockdown of KCNQ1OT1 or overexpression of miR-149 inhibited the invasion and migration of HCC cells.  In vivo assays showed that KCNQ1OT1 knockdown suppressed tumour growth. 	32753631
KILH	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(KRT19/β-catenin)	qRT-PCR	Here, we identify a novel lncRNA Linc-KILH (KRT19 interacting long noncoding RNA in hepatocellular carcinoma), which is significantly up-regulated in HCC tissues and positively correlated with larger tumor size, severer microvascular invasion, more intrahepatic metastasis and decreased survival of HCC patients.  Mechanistically, Linc-KILH interacts with KRT19 and then inhibits the phosphorylation of KRT19 on Ser35, thereby, enhancing the translocation of KRT19 from cytoplasm to membrane in KRT19 positive HCC cells. Additionally, we validated that KRT19 interacts with β-catenin but not RAC1 in HCC cells. Linc-KILH enhanced the interaction between β-catenin and KRT19 in cytoplasm and promoted the nuclear translocation of β-catenin in HCC cells. Furthermore, Linc-KILH could enhance the promoting function of KRT19 on Notch1 signaling with the existence of KRT19 in HCC cells. 	Here, we identify a novel lncRNA Linc-KILH (KRT19 interacting long noncoding RNA in hepatocellular carcinoma), which is significantly up-regulated in HCC tissues and positively correlated with larger tumor size, severer microvascular invasion, more intrahepatic metastasis and decreased survival of HCC patients. 	Yes	 Silence of Linc-KILH remarkably inhibited the proliferation and metastasis abilities of KRT19-positive HCC cells in vitro and in vivo. 	33767587
KIF4A	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(MicroRNA-144-3p/EZH2 Axis)	Western Blot//Transfection//qPCR//IF//MTT//PCR//Transwell Assay	Our findings demonstrated that circKIF4A was highly expressed in both GC tissues and cell lines, and high intratumoral circKIF4A expression predicted a poor prognosis in GC patients. Mechanistically, we found that circKIF4A was mainly located in the cytoplasm, could directly interact with microRNA- (miR-) 144-3p, and functions as a miRNA sponge to regulate EZH2 expression in GC cells. miR-144-3p inhibition or EZH2 restoration largely blocked the effects of circKIF4A knockdown on the malignant behaviors of GC cells.	Our findings demonstrated that circKIF4A was highly expressed in both GC tissues and cell lines, and high intratumoral circKIF4A expression predicted a poor prognosis in GC patients. 	Yes	In vitro gain- and loss-of-function assays indicated that circKIF4A knockdown suppressed the proliferation, migration, invasion, and EMT of GC cells, while these malignant behaviors were enhanced by circKIF4A overexpression. 	35466313
KDM7A-DT	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-450a-2-3p-PRAF2 axis]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	 The expression levels of JHDM1D-AS1 and miR-450a-2-3p in GC tissues and cell lines were higher and lower as compared to those in the corresponding normal controls, respectively. 	Moreover, high levels of JHDM1D-AS1 were closely related with metastasis and the GC TNM stage.	Yes	Functionally, JHDM1D-AS1 depletion caused an obvious reduction in cell proliferation and invasion both in vitro and in vivo, while the addition of miR-450a-2-3p inhibitor could nullify these effects. 	33245963
KDM7A-DT	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor samples and adjacent normal tissues,cell lines (A549, H1299, HCC827, H358, and H1975) 	Interaction[DHX15 ]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Cell Proliferation Assay//Invasion Assay//Transwell Assay	The expression level of JHDM1D-AS1 was significantly greater in NSCLC specimens than that in adjacent normal lung tissues.In addition, multiple NSCLC cell lines had an increased level of JHDM1D-AS1 compared to BEAS-2B bronchial epithelial cell lines.Collectively, the interaction between JHDM1D-AS1 and DHX15 accounts for NSCLC growth and metastasis. 	 High JHDM1D-AS1 expression is significantly correlated with advanced tumor, node, and metastasis (TNM) stage and lymph node metastasis. JHDM1D-AS1 expression serves as an independent prognostic factor for overall survival of patients with NSCLC. 	Yes	Functionally, JHDM1D-AS1 knockdown inhibits NSCLC cell aggressiveness both in vitro and in vivo, which is rescued by ectopic expression of JHDM1D-AS1. 	31739208
KDM4A-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-411-5p/KPNA2/AKT pathway)	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Transfection//qRT-PCR//FISH//IF//RIP//Luciferase Report Assay//Cell Proliferation Assay//IHC//Transwell Assay	Here we identified a novel lncRNA KDM4A-AS1, which was aberrantly overexpressed in HCC tissues, associated with unfavorable clinical features and poor prognosis of patients. Mechanistically, KDM4A-AS1 was inversely modulated by miR-411-5p at the post-transcriptional level and facilitated Karyopherin α2 (KPNA2) expression by competitively binding miR-411-5p, thereby activating the AKT pathway. 	Here we identified a novel lncRNA KDM4A-AS1, which was aberrantly overexpressed in HCC tissues, associated with unfavorable clinical features and poor prognosis of patients.	Yes	KDM4A-AS1 promoted HCC cell proliferation, migration, and invasion in vitro and contributed to HCC growth and lung metastasis in vivo. 	34903711
KDM1A	LncRNA	Homo sapiens	Glioblastoma	GBM cell lines	Regulation(upregulating H3K4me2 and downregulating H3K27me3)	In Vivo Experiment//Western Blot//H&E Staining//Flow Cytometry//qRT-PCR//IF//Microarray//Cell Proliferation Assay//IHC//ChIP	we found that the combination of AQB and GSK-LSD1 showed a powerful effect of inhibiting cell cycle processes by targeting CDKN1A, whereas apoptosis promoting effects of combination therapy were mediated by BBC3 in vitro. ChIP assays revealed that GSK-LSD1 and AQB regulate P21 and PUMA, respectively via upregulating H3K4me2 and downregulating H3K27me3.		Yes	Microarray analysis showed that AQB and GSK-LSD1 regulate cell cycle processes and induces apoptosis in GBM cell lines. 	34246782
KCNQ1OT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[microRNA-9-LMX1A]	Western Blot//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//EdU Staining//Transwell Assay	KCNQ1OT1 putatively targets miR-9. Its level is downregulated in human GC tissues.Taken together, KCNQ1OT1 inhibits GC cell progression via regulating miR-9 and LMX1A expression.		Yes	 Furthermore, KCNQ1OT1 overexpression inhibited GC cell survival, proliferation, migration and invasion, but inducing apoptosis activation. 	31915311
KCNQ1OT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells.	Interaction(miR-145-5p/ARF6 axis)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay	The expression levels of KCNQ1OT1 were markedly elevated in GC tissues and cells. The expression levels of miR-145-5p were significantly decreased in GC cells and correlated with the expression of KCNQ1OT1 in GC tumors. Moreover, KCNQ1OT1 directly binds with miR-145-5p, which is targeting ARF6. 		Yes	Knockdown of KCNQ1OT1 inhibited GC tumor growth, reduced GC cell viability and colony formation, and induced GC cell apoptosis. 	33682985
KCNQ1OT1	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer cell lines	regulation[hsa-miR-107]	CCK8//qRT-PCR//Luciferase Report Assay//Migration Assay	 We found that KCNQ1OT1 was significantly upregulated in breast cancer cell lines.Thus, loss of KCNQ1OT1 is associated with functional impairment in breast cancer cells, likely through inverse regulation of its sponging target, hsa-miR-107.		Yes	In lentiviral-transduced BT-549 and HCC1599 cells, KCNQ1OT1 knockdown impaired cancer cell functions, including in vitro proliferation and migration, and in vivo transplant growth. 	32379482
KCNQ1OT1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-34a / Notch3 axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 KCNQ1OT1 expression was up-regulated in BC tissues and high levels were associated with poorer prognosis. Up-regulation of KCNQ1OT1 was shown to inhibit miR-34a which was associated with blocking the inhibitory effect of miR-34a on BC cell proliferation, migration and invasion. Notch3 was found to be a downstream target of miR-34a with KCNQ1OT1 markedly inducing Notch3 expression in BC. Evidence for KCNQ1OT1/miR-34a/Notch3 axis was further established in clinical BC samples.	 KCNQ1OT1 expression was up-regulated in BC tissues and high levels were associated with poorer prognosis. 	Yes	ShRNA inhibition of KCNQ1OT1 expression in BC cell lines retarded proliferation, migration and invasion in vitro and tumor growth in vivo. 	34993814
KCNQ1OT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[ miR-129-5p/JAG1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 KCNQ1OT1 expression was significantly enhanced, while miR-129-5p expression was dramatically reduced in NSCLC tissues and cells.  KCNQ1OT1 induced proliferation, migration and invasion of NSCLC cells by sponging miR-129-5p and regulating JAG1 expression, indicating that KCNQ1OT1 was a therapeutic target for NSCLC.	Higher KCNQ1OT1 shortened overall survival and was positively associated with tumor stage and lymph node metastasis.	Yes	 KCNQ1OT1 knockdown inhibited proliferation, migration and invasion of NSCLC cells.	32377169
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms		Regulation[miR-217/ZEB1 axis]	RNA Pull-Down//ChIP//Western Blot//qRT-PCR//RIP//IF//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Based on the database analysis, KCNQ1OT1 was highly expressed in CRC samples and predicted the poor prognosis for CRC patients.  In brief, our research findings revealed that ZEB1-induced upregulation of KCNQ1OT1 improved the proliferation, migration and EMT formation of CRC cells via regulation of miR-217/ZEB1 axis.		Yes	 Functional experiments revealed that KCNQ1OT1 knockdown negatively affected the proliferation, migration and epithelial-mesenchymal transition (EMT) in CRC cells.	30794031
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	regulation[miR-329-3p/CTNND1 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The levels of KCNQ1OT1 and CTNND1 were significantly increased in CRC tissues and cells.Our results indicated that KCNQ1OT1 could positively regulate CTNND1 expression by sponging miR-329-3p, thereby boosting the progression of CRC. Our findings provided the underlying therapy targets for CRC.		Yes	Knockdown of KCNQ1OT1 suppressed proliferation, migration, invasion, and induced apoptosis in CRC cells.	32760218
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[ PI3K/AKT pathway]	qRT-PCR//Western Blot	KCNQ1OT1 was overexpressed in CRC tissues and cell lines via RT-qPCR analysis. These results suggest that KCNQ1OT1 may act as an oncogene through the PI3K/AKT signaling pathway in CRC.	GEPIA analysis demonstrated that high expression levels of KCNQ1OT1 in CRC tissues predicted a poor prognosis for patients with CRC.	Yes	Furthermore, the results from the cell viability assay, colony formation assay, wound healing assay, invasion assay and flow cytometric analysis demonstrated that KCNQ1OT1 knockdown significantly inhibited CRC cell proliferation, migration and invasiveness, and promoted CRC cell apoptosis, leading to cell cycle arrest.	32565985
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[HK2]	qRT-PCR//RNA Pull-Down//Colony Formation Assay//RIP	KCNQ1OT1 levels were significantly higher in CRC tissues than adjacent normal colorectal tissues (n=79). These findings show that KCNQ1OT1 promotes colorectal carcinogenesis by increasing aerobic glycolysis through HK2.		Yes	KCNQ1OT1-silenced CRC cells showed reduced proliferation, colony formation, extracellular acidification, and lactate and glucose secretion.	32564010
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms	tumor tissues and tumor cell-derived exosomes	Interaction(MiR-30a-5p/USP22 )	CCK8//RIP//Flow Cytometry//Luciferase Report Assay//Microarray//IF	The expression of lncRNA KCNQ1OT1 in tumor tissues and tumor cell-derived exosomes was significantly increased.		Yes	 The tumor-promoting effect of lncRNA KCNQ1OT1 was through the autocrine effect of tumor cell-derived exosomes, which mediates the miR-30a-5p/USP22 pathway to regulate the ubiquitination of PD-L1 and inhibits CD8+ T-cell response, thereby promoting colorectal cancer development. 	34350172
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms	Thirty matched CRC tissues and tumor-adjacent tissue 	Expression [highly expressed]	Flow Cytometry//qRT-PCR//Western Blot	Our results showed that the high expression of lncRNA KCNQ1OT1 was significantly related to poor overall survival across cancers, especially CRC. KCNQ1OT1 and CD155 showed significantly higher expression in CRC tissue than in normal tissue, and lncRNA KCNQ1OT1 expression was positively correlated with CD155 expression in CRC.	Our results showed that the high expression of lncRNA KCNQ1OT1 was significantly related to poor overall survival across cancers, especially CRC.  Interestingly, we found that COAD patients with high lncRNA KCNQ1OT1 expression and high CD8+ T cell infiltration levels had a worse prognosis than those with low lncRNA KCNQ1OT1 expression and high CD8+ T cell infiltration levels.	Yes	Finally, knockdown of lncRNA KCNQ1OT1 reduced CD155 expression in HCT116 and SW620 cells and enhanced the immune response in coculture with CD8+ T cells. 	33994860
KCNQ1OT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-216b-5p/ZNF146 axis )	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	KCNQ1OT1 expression was higher in CRC tissues and cell lines. KCNQ1OT1 accelerated the proliferation and motility of CRC cells through elevating ZNF146 expression via sponging miR-216b-5p. KCNQ1OT1/miR-216b-5p/ZNF146 axis might be underlying target for the diagnosis and treatment of CRC patients.		Yes	KCNQ1OT1 interference restrained the proliferation, migration and invasion of CRC cells. 	33394291
KCNQ1OT1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Expression[Expression[highly expressed]-expression]	qRT-PCR//Western Blot	 In this study, it is shown that the expression level of KCNQ1OT1 was increased in tumor, which indicated poor prognosis in colon cancer patients.		Yes	Using colon cancer cell lines HCT116 and SW480, it was demonstrated that knockdown of KCNQ1OT1 decreased the cell viability and increased the apoptosis rates Expression[up-expression]on L-OHP treatment.	31040703
KCNQ1OT1	LncRNA	Homo sapiens	Osteoarthritis	 cartilage tissues of post-traumatic OA patients	(miR-126-5p/TRPS1 axis)	qRT-PCR//RNA Pull-Down//Western Blot	Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA.miR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1.		Yes	Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. 	34108052
KIF9-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(RAI2/DNMT1)	qRT-PCR	We found that KIF9-AS1 expression was increased in HCC tissues. lncRNA KIF9-AS1-mediated RAI2 expression led to DNMT1 recruitment and regulated RAI2 DNA methylation. RAI2 overexpression inhibited the proliferation and migration and promoted the apoptosis of HCC cells.		Yes	 KIF9-AS1 knockdown inhibited the proliferation and migration, and facilitated the apoptosis of HCC cells. KIF9-AS1 knockdown inhibited subcutaneous tumor formation in vivo.	36276278
KIZ	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	regulation[miR-653/CXCR5 axis]	qRT-PCR	In the present study, PLK1S1 was upregulated in RCC tissues and cells, and PLK1S1 expression was also significantly elevated in stage IV RCC tissues.  In conclusion, the present study revealed that PLK1S1 promoted tumor progression and sorafenib resistance in RCC through regulation of the miR‑653/CXCR5 axis, which may offer a novel treatment strategy for patients with RCC.	Kaplan?Meier analysis showed that patients with high PLK1S1 expression had a shorter overall survival time compared with those with low PLK1S1 expression. 	Yes	Functional analyses demonstrated that a miR?653 inhibitor promoted short hairpin PLK1S1?attenuated cell proliferation, invasion and sorafenib resistance of RCC cells. 	33000253
LALR1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[SNORD72 ]	qRT-PCR//FISH	In this study, we demonstrated that lncRNA-LALR1 was significantly upregulated in HCC tissues compared with adjacent tissues and high expression of lncRNA-LALR1 was associated with advanced TNM stage, poor differentiation, and distant metastasis.  In conclusion, lncRNA-LALR1 is highly expressed in HCC and promotes tumor growth and invasion by upregulating SNORD72 to stabilize ID2 mRNA, implying that lncRNA-LALR1 might be a novel target for intervention of HCC.	In this study, we demonstrated that lncRNA-LALR1 was significantly upregulated in HCC tissues compared with adjacent tissues and high expression of lncRNA-LALR1 was associated with advanced TNM stage, poor differentiation, and distant metastasis. 	Yes	Knockdown of lncRNA-LALR1 obviously inhibited HCC cells growth and invasion in vivo and in vitro. 	32160589
KLF3-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell line	Interaction(miR-338-3p/MEF2C axis)	qRT-PCR//RIP	Elevated levels of KLF3-AS1 and MEF2C and reduced amounts of miR-338-3p were identified in OS. KLF3-AS1 targeted miR-338-3p, and miR-338-3p further targeted MEF2C. Inhibiting miR-338-3p inverted the cancer-suppressing effects of KLF3-AS1 silencing. Meanwhile, loss of MEF2C partially eliminated the effects brought about by miR-338-3p downregulation, namely the stimulation of cell growth and suppression of apoptosis.		Yes	 Silencing KLF3-AS1 induced apoptosis and attenuated proliferation in vitro and repressed the tumor growth in vivo.	36250223
LA16c?313D11.11	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	regulation[microRNA-205-5p-PTEN axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Transwell Assay	The expression levels of LA16c?313D11.11 and phosphatase and tensin homolog deleted on chromosome ten (PTEN) in human EAH and EC tissues were significantly decreased, whereas the expression levels of miR?205?5p in EAH and EC tissues were significantly increased, compared with the normal endometrium tissues. Therefore, LA16c‑313D11.11 acts as an effective ceRNA associated with a microRNA‑205‑5p‑PTEN axis.		Yes	Additionally, the overexpression of LA16c?313D11.11 significantly reduced the invasion, migration and viability of HEC?1A and Ishikawa cells in vitro. 	32319598
KTN1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	regulation[KTN1-AS1/miR-130a-5p/PDPK1 pathway ]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	We found that KTN1-AS1 expression was upregulated in NSCLC tissue and was positively associated with poor prognosis. Taken together, our results suggest that the KTN1-AS1/miR-130a-5p/PDPK1 pathway may be a potential therapeutic target for NSCLC.	We found that KTN1-AS1 expression was upregulated in NSCLC tissue and was positively associated with poor prognosis.	Yes	KTN1-AS1 knockdown inhibited cell growth and proliferation, increased apoptosis, and modulated the expression of cell cycle- and apoptosis-related proteins (cyclin A1, cyclin-dependent kinase 2, Bcl2, and Bax) in NSCLC cell lines and tumour xenografts in nude mice. 	32820252
KTN1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-23b/DEPDC1 axis]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	We identified a novel NSCLC-related lncRNA, KTN1 antisense RNA 1 (KTN1-AS1) which was demonstrated to be distinctly highly expressed in NSCLC.Overall, our findings imply that STAT1-induced upregulation of KTN1-AS1 display tumor-promotive roles in NSCLC progression via regulating miR-23b/DEPDC1 axis, suggesting that KTN1-AS1 may be a novel biomarker and therapeutic target for NSCLC patients.	 Clinical study also suggested that higher levels of KTN1-AS1 were associated with advanced clinical progression and a shorter five-year overall survival. 	Yes	Functionally, loss-of-function assays with in vitro and in vivo experiments revealed that KTN1-AS1 promoted the proliferation, migration, invasion and EMT progress of NSCLC cells, and suppressed apoptosis. 	32396871
KTN1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	esophageal cancer cells and ESCC tissues	Interaction(RBBP4/HDAC1)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay//ChIP	 Considerable upregulation of KTN1-AS1 was confirmed in esophageal cancer cells and ESCC tissues and its expression was associated with TNM stage, pathological differentiation, and lymph node metastasis.  SOX2 directly activated transcription of KTN1-AS1, and overexpression of KTN1-AS1 facilitated ESCC cells proliferation and invasion in vitro and in vivo.  Furthermore, KTN1-AS1 could bind to retinoblastoma binding protein 4 (RBBP4) in the nucleus and enhanced its binding with histone deacetylase 1 (HDAC1), thereby activating the epithelial-mesenchymal transition (EMT) process through downregulating E-cadherin expression at the epigenetic level. 	 Considerable upregulation of KTN1-AS1 was confirmed in esophageal cancer cells and ESCC tissues and its expression was associated with TNM stage, pathological differentiation, and lymph node metastasis. 	Yes	 SOX2 directly activated transcription of KTN1-AS1, and overexpression of KTN1-AS1 facilitated ESCC cells proliferation and invasion in vitro and in vivo. 	36418920
KTN1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[miR-23c/ERBB2IP axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Further analyses revealed that higher expression of KTN1-AS1 was observed in HCC tissues with large tumor size, high tumor grade and advanced TNM stage.Mechanistically, KTN1-AS1 inversely regulated miR-23c abundance in HCC cells. Further evidence supported that KTN1-AS1 acted as a competing endogenous RNA (ceRNA) by directly sponging miR-23c in HCC cells. Interestingly, erbb2 interacting protein (ERBB2IP), a known target of miR-23c, was positively regulated by KTN1-AS1 and its restoration reversed KTN1-AS1 knockdown attenuated HCC cell growth.	Further analyses revealed that higher expression of KTN1-AS1 was observed in HCC tissues with large tumor size, high tumor grade and advanced TNM stage.	Yes	Functionally, KTN1-AS1 knockdown suppressed cell proliferation and colony formation, and increased apoptosis of SMMC-7721 cells in vitro. Furthermore, silencing of KTN1-AS1 restrained tumor growth of HCC in vivo.	30551364
KTN1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR-505-3p/ZNF326 axis)	qRT-PCR//Wound Healing Assay//ChIP//Transwell Assay	The data showed that KTN1-AS1 and ZNF326 had a high expression in OC than in the normal tissue, and miR-505-3p exhibited a low expression in OC than in the normal tissue. In terms of mechanical exploration, KTN1-AS1 was transcriptionally activated by histone H3 on lysine 27 acetylation (H3K27ac) at the promoter region, and KTN1-AS1 increased ZNF326 expression by competitively adsorbing miR-505-3p.		Yes	The knockdown of KTN1-AS1 caused an inhibition in OC cell proliferation, migration, and invasion, and promoted cell apoptosis. 	35722429
KTN1-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer cells	Interaction(EP300/H3K27Ac)	qRT-PCR//Wound Healing Assay	 KTN1-AS1 silencing inhibited the proliferation, invasion, and migration of bladder cancer cells, while KTN1-AS1 overexpression had the obvious opposite effects. Mechanistically, KTN1-AS1 promoted the recruitment of EP300, a histone acetyltransferase that enriched acetylation of histone H3 at lysine 27 (H3K27Ac) in the KTN1 promoter region. This epigenetic modulation contributed to the up-regulation of KTN1, which affected bladder cancer growth and progression via the regulation of Rho GTPase (RAC1, RHOA, and CDC42)-mediated signaling.		Yes	 KTN1-AS1 silencing inhibited the proliferation, invasion, and migration of bladder cancer cells, while KTN1-AS1 overexpression had the obvious opposite effects. 	33480975
KTN1-AS1	LncRNA	Homo sapiens	Glioma	GBM tissues and cell lines	regulation[KTN1-AS1/miR-505-3p axis ]	Cell Proliferation Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1?AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Taken together, the results from the present provided novel insights into the roles of KTN1‑AS1 in GBM, and suggested that the KTN1‑AS1/miR‑505‑3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM.		Yes	 Furthermore, KTN1?AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo.	33125151
KTN1-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and PC cells	Interaction(microRNA-23b-3p)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//RNA-seq//Transwell Assay	We identified that KTN1-AS1 presented a most significant elevation in the PC tissues. KTN1-AS1 inhibited miR-23b-3p expression by binding to it.	We identified that high KTN1-AS1 expression was correlated with the poor survival rate of the PC patients.	Yes	Knockdown of KTN1-AS1 suppressed the proliferation and invasion of PC cells but accelerated their apoptosis, observably up-regulated pro-apoptotic Bax and Caspase-3 expression, and remarkably down-regulated the anti-apoptotic bcl-2 expression (P < 0.05). While on the contrary, KTN1-AS1 could further induce the proliferation/invasion and inhibit apoptosis of PC cells, and meanwhile, markedly declined Bax and Caspase-3 expression, and dramatically enhanced bcl-2 expression. 	34461605
KTN1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	Regulation(CDK1)	Cell Proliferation Assay//qRT-PCR//Cell Cycle Assay//Western Blot	 KTN1-AS1 was upregulated in NSCLC tissues and its expression level was positive correlated with CDK1 expression. KTN1-AS1 silencing induced G1 phase cell cycle arrest of NSCLC cells and downregulated CDK1. Moreover, KTN1-AS1 silencing suppressed NSCLC cell proliferation and CDK1 overexpression attenuated the effects of KTN1-AS1 silencing on cell proliferation. KTN1-AS1 may regulate cell cycle progression in NSCLC by regulating CDK1.	 KTN1-AS1 expression was not changed with clinical stages increasing, and higher KTN1-AS1 levels were associated with poor survival of NSCLC patients.	Yes	 KTN1-AS1 silencing induced G1 phase cell cycle arrest of NSCLC cells and downregulated CDK1. Moreover, KTN1-AS1 silencing suppressed NSCLC cell proliferation and CDK1 overexpression attenuated the effects of KTN1-AS1 silencing on cell proliferation. KTN1-AS1 may regulate cell cycle progression in NSCLC by regulating CDK1.	35381130
KTN1-AS1	LncRNA	Homo sapiens	Burkitt Lymphoma	different types of B cell lymphoma	Regulation( Myc-target genes)	Microarray//qRT-PCR//Western Blot	We show that the top Myc-induced lncRNA KTN1-AS1 is strongly upregulated in different types of B cell lymphoma compared with their normal counterparts. Global gene expression analysis upon KTN1-AS1 depletion shows a strong enrichment of key genes in the cholesterol biosynthesis pathway as well as co-regulation of many Myc-target genes, including a moderate negative effect on the levels of Myc itself. Our study suggests a critical role for KTN1-AS1 in supporting BL cell growth by mediating co-regulation of a variety of Myc-target genes and co-activating key genes involved in cholesterol biosynthesis. 		Yes	 Knockdown of KTN1-AS1 revealed a strong negative effect on the growth of three BL cell lines. 	35866590
KRT19P3	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[NF-κB pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	The present study confirmed the downregulation of KRT19P3 in GC tissues and cells.Enforced expression of KRT19P3 significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, KRT19P3 knockdown had opposite effects. 	Decreased expression of KRT19P3 was correlated with larger tumor size, advanced TNM stage, Lauren's classification, positive lymph node metastasis, and poor prognosis.	Yes	Enforced expression of KRT19P3 significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, KRT19P3 knockdown had opposite effects. 	31409899
KRT19P3	LncRNA	Homo sapiens	Breast Neoplasms	 BC tissues 	Expression [lower expressed]	qRT-PCR//Invasion Assay//EdU Staining//Migration Assay	 In the present study, we first discovered that KRT19P3 was downregulated in BC tissues compared with para cancer tissue. 	Then we showed that KRT19P3 could be used as a marker to differentiate BC from para cancer tissue. Comparison of clinical parameters showed an inverse relationship between the expression of KRT19P3 and pathological grade. 	Yes	 Increased expression of KRT19P3 markedly inhibited the proliferation, migration, and invasion rate of BC cells in vitro and tumor growth of BC in vivo. Conversely, KRT19P3 knockdown by siRNA markedly promoted the proliferation, migration, and invasion rate of BC cells after being transfected.	35059320
KRT16P3	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues	Regulation(JAK2/STAT3 signaling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//BrdU//Colony Formation Assay//Invasion Assay//Transwell Assay	We found KRT16P3 expression is significantly upregulated in TSCC tissues and positively associated with advanced clinicopathological features of TSCC patients, and it may serve as a poor prognostic factor. Furthermore, we also revealed that KRT16P3 knockdown suppresses EMT and JAK2/STAT3 signaling pathway.		Yes	 Functionally, KRT16P3 knockdown inhibits proliferation, migration, invasion and promotes apoptosis of TSCC cells. 	33220105
KRT16P2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues 	regulation[KRT16P2/miR-1294/EGFR axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 The present study analyzed online data and identified lncRNA KRT16P2 as a significantly upregulated long non-coding RNA (lncRNA) in LSCC.  In conclusion, we demonstrated a lncRNA KRT16P2/miR-1294/EGFR axis that regulates LSCC cell proliferation, invasion, and migration. 		Yes	 KRT16P2 knockdown in LSCC cells inhibited cancer cell proliferation, invasion, and migration. 	32655821
KLHDC7B-DT	LncRNA	Homo sapiens	Chlorophyll A		Regulation( IL-6 /STAT3 )	Western Blot//Migration Assay//qRT-PCR//FISH//Cell Proliferation Assay//ELISA//Invasion Assay//ChIP	In the present study, we identified a long noncoding RNA (lncRNA) KLHDC7B divergent transcript (KLHDC7B-DT), which was up-regulated in PDAC and correlated with poor survival of PDAC patients. Mechanistically, KLHDC7B-DT was found to directly bind IL-6 promoter, induce open chromatin structure at IL-6 promoter region, activate IL-6 transcription, and up-regulate IL-6 expression and secretion. Via inducing IL-6 secretion, KLHDC7B-DT activated STAT3 signaling in PDAC cells in an autocrine manner. 	In the present study, we identified a long noncoding RNA (lncRNA) KLHDC7B divergent transcript (KLHDC7B-DT), which was up-regulated in PDAC and correlated with poor survival of PDAC patients. 	Yes	Functional assays demonstrated that KLHDC7B-DT enhanced PDAC cell proliferation, migration, and invasion. 	33538300
KLF3-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells	Interaction(miR-223)	In Vivo Experiment//Wound Healing Assay//Invasion Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	" In this study, we found that KLF3-AS1 was down-regulated in gastric cancer cells. The mechanistic studies showed that KLF3-AS1 could act as the ""sponge"" for miR-223 and to repress miR-223 expression in gastric cancer cells. Overexpression of miR-223 reversed the inhibitory effects of KLF3-AS1 overexpression on gastric cancer cell proliferation, invasion, migration and EMT, and attenuated the enhanced effects of KLF3-AS1 overexpression on gastric cancer cell chemosensitivity to cisplatin. "		Yes	Overexpression of KLF3-AS1 repressed gastric cancer cell proliferation, growth. In addition, KLF3-AS1 overexpression also exerted inhibitory effects on the gastric cancer cell invasion, migration and EMT, but promoted chemosensitivity of gastric cancer cells to cisplatin. 	34745937
KLF3-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cell lines	regulation[Impairing miR-185-5p-Targeted KLF3 Inhibition]	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay//Transwell Assay	 LncRNA KLF3-AS1 was found to be poorly expressed in ESCC and could upregulate the expression of KLF3 by binding to miR-185-5p. Collectively, this study indicated that lncRNA KLF3-AS1 inhibited ESCC cell invasion and migration by impairing miR-185-5p-mediated inhibition of KLF3, highlighting a promising novel potential target for ESCC treatment.		Yes	 Furthermore, enhancement of lncRNA KLF3-AS1 resulted in reduced colony formation ability, cell invasion and migration, and tumor volume in vivo while promoting cell apoptosis in ESCC through downregulation of miR-185-5p. 	32193151
KLF3-AS1	LncRNA	Homo sapiens	Osteoarthritis	chondrocytes 	Interaction(YBX1/PI3K/Akt/mTOR signaling pathway)	RNA Pull-Down//Western Blot//qRT-PCR//Cell Apoptosis Assay//Cell Viability Assay	We found that MSC-Exo enhanced KLF3-AS1 expression in IL-1β-treated chondrocytes.  Moreover, KLF3-AS1 interacted with YBX1 in chondrocytes. MSC-Exo-mediated KLF3-AS1 activated PI3K/Akt/mTOR signaling pathway, which was abrogated by YBX1 silencing. MSC-Exo-mediated KLF3-AS1 repressed autophagy and apoptosis of chondrocytes by activating PI3K/Akt/mTOR signaling pathway.		Yes	 MSC-Exo-mediated KLF3-AS1 promoted cell viability and repressed apoptosis of IL-1β-treated chondrocytes. Rapamycin (autophagy activator) promoted cell viability and suppressed apoptosis of chondrocytes by activating autophagy. 	34964696
LENGA	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(BRD7/TP53 signaling)	RNA Pull-Down//Western Blot//Co-IP//Migration Assay//CCK8//FISH//RIP//qRT-PCR//Colony Formation Assay//Invasion Assay	 Next, we found that reduced expression of LENGA in GC was also associated with a shorter life expectancy. The proliferation, migration, and invasion of GC cells were increased after LENGA knockdown but restrained after LENGA overexpression in vitro and in vivo. 		Yes	The proliferation, migration, and invasion of GC cells were increased after LENGA knockdown but restrained after LENGA overexpression in vitro and in vivo. 	36477655
LENOX	LncRNA	Homo sapiens	Melanoma	 melanoma cells	Interaction(RAP2C)	In Vivo Experiment//qPCR//Flow Cytometry	Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer of oxidative phosphorylation) as a melanoma-specific lncRNA expressed in all known melanoma cell states and essential for melanoma survival in vitro and in vivo. Mechanistically, LENOX promoted association of the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637 phosphorylation, mitochondrial fusion, and oxidative phosphorylation. 	Aiming to overcome this, we identified LINC00518 (LENOX; lincRNA-enhancer of oxidative phosphorylation) as a melanoma-specific lncRNA expressed in all known melanoma cell states and essential for melanoma survival in vitro and in vivo. 	Yes	Mechanistically, LENOX promoted association of the RAP2C GTPase with mitochondrial fission regulator DRP1, increasing DRP1 S637 phosphorylation, mitochondrial fusion, and oxidative phosphorylation. LENOX expression was upregulated following treatment with MAPK inhibitors, facilitating a metabolic switch from glycolysis to oxidative phosphorylation and conferring resistance to MAPK inhibition.	36214632
LET	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	Interaction[regulating miR-373-3p]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	 LncRNA-LET expression was lower in ccRCC tissues than that in the matched adjacent non-tumor tissues (n = 16).  Moreover, we noted that lncRNA-LET may act as a target for oncomiR miR-373-3p. In contrast to lncRNA-LET, miR-373-3p expression was higher in ccRCC tissues. The binding between lncRNA-LET and miR-373-3p was validated. Two downstream targets of miR-373-3p, Dickkopf-1 (DKK1) and tissue inhibitor of metalloproteinase-2 (TIMP2), were positively regulated by lncRNA-LET in ccRCC cells. MiR-373-3p mimics reduced lncRNA-LET-induced up-regulation of DKK1 and TIMP2 levels, and attenuated lncRNA-LET-mediated anti-tumor effects in ccRCC cells. In vivo, lncRNA-LET suppressed the growth of ccRCC xenograft tumors.		Yes	In vitro, lncRNA-LET overexpression induced cell cycle arrest, promoted apoptosis and impaired mitochondrial membrane potential, whereas its knockdown exerted opposite effects.	31768131
LINC00261	LncRNA	Homo sapiens	Prostatic Neoplasms	 NEPC specimens	Interaction(CBX2-FOXA2 axes)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Colony Formation Assay//RIP//MTT//RNA-seq//ChIP-seq//IHC	Here, LINC00261 emerged as the top gene with over 3229-fold upregulation in NEPC. Consistently, LINC00261 expression was significantly upregulated in NEPC specimens in multiple patient cohorts.In the cell cytoplasm, LINC00261 binds to and sequesters miR-8485 from targeting the CBX2 mRNA, while inside the nucleus, LINC00261 functions as a transcriptional scaffold to induce SMAD-driven expression of the FOXA2 gene.		Yes	 Knockdown of LINC00261 in PC-3 cells dramatically attenuated its proliferative and metastatic abilities, which are explained by parallel downregulation of CBX2 and FOXA2 through distinct molecular mechanisms. 	33793068
LINC00243	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues	Interaction[sponging miR-507]	CCK8//qRT-PCR//RNA Pull-Down//Western Blot	LINC00243 expression increased in human NSCLC tissues and associated with poor prognosis of NSCLC patients.Mechanically, LINC00243 acted as a molecular sponge for miR-507, and miR-507 reversed the effect of LINC00243 on promoting proliferation and glycolysis of NSCLC cells. Moreover, LINC00243 modulated expression of endogenous miR-507-targeted PDK4. LINC00243 promotes proliferation and glycolysis in NSCLC cells by positively regulating PDK4 through sponging miR-507. LINC00243 could be the potential target for NSCLC treatment clinically.		Yes	 LINC00243 knockdown inhibited proliferation and glycolysis of NSCLC cells.	31595421
LINC00242	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells 	regulation[ LINC00242/miR-141/FOXC1 axis]	CCK8//qRT-PCR//RIP//Transwell Assay	 LINC00242 was highly expressed in GC tissues and cells and contributed to poor prognosis. Taken together, the present study demonstrates the oncogenic role of the LINC00242/miR-141/FOXC1 axis in GC, highlighting a theoretical basis for GC treatment.		Yes	 LINC00242 knockdown inhibited HGC27 cell viability, migration and invasion, and tube formation of HBMVECs.	32587479
LINC00240	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[ miR-124-3p / DNMT3B axis]	qRT-PCR//Luciferase Report Assay//RIP	Our findings suggested higher LINC00240 expression in GC tissues and cells.Then we reveal that LINC00240 acts as an oncogene in GC progression via the miR-99a-5p/IGF1R axis.		Yes	Through downregulating LINC00240, cell proliferation, invasion and migration were retarded in vitro, and tumorigenesis of GC cells was notably suppressed in vivo.	32526811
LINC00240	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and GC cell lines	Interaction(miR-338-5p/METTL3 axis)	Western Blot//Bioinformatics Analysis//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay	We first demonstrated that LINC00240 was upregulated in GC tissues and GC cell lines.  We further identified and validated the functional interaction between LINC00240 and miR-338-5p. miR-338-5p seemed to function as a downstream target negatively regulated by LINC00240, and miR-338-5p could target METTL3 at 3' UTR to downregulate its expression. In GC tissues, the expression of miR-338-5p was negatively correlated with LINC00240, and the expression of miR-338-5p was negatively correlated with METTL3. 	High expression of LINC00240 was associated with advanced TNM stage, a higher extent of distant metastasis and lymph nodes metastasis, and the poor overall and disease-free survival of the patients.	Yes	 In GC cell lines, the knockdown of LINC00240 inhibited GC cell proliferation and migration, but induced cell apoptosis. 	34842045
LINC00240	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer cell line	Interaction(miR-7-5p)	qRT-PCR//Luciferase Report Assay//Invasion Assay//Migration Assay	We found that LINC00240 was downregulated in lung cancer cell line after miR-7-5p transfection with an miR-7-5p mimic.  Further investigations revealed that the knockdown of LINC00240 induced the overexpression of miR-7-5p. 		Yes	The overexpression of miR-7-5p diminished cancer invasion and migration. The EGFR expression was down regulated after siRNA treatment for LINC00240.  Silencing LINC00240 suppressed the invasion and migration of lung cancer cells, whereas LINC00240 overexpression exerted the opposite effect. 	33422052
LINC00239	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	Interaction(MBP-1/c-Myc axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	LINC00239 was highly expressed in ESCC tissues and cells, and was related to poor prognosis of patients with ESCC. LINC00239 may function as an oncogenic lncRNA in ESCC through the LINC00239/MBP-1/c-Myc axis to activate EMT process.	LINC00239 was highly expressed in ESCC tissues and cells, and was related to poor prognosis of patients with ESCC. 	Yes	The proliferation, metastasis, and invasion ability as well as epithelial-mesenchymal transition (EMT) process were all enhanced in LINC00239-overexpressed ESCC cells. LINC00239 was upregulated in TGF-β1-treated ESCC cells.	34016746
LINC00210	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	interaction[sponging microRNA-328-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The results demonstrated that LINC00210 was upregulated in NSCLC tissues and cell lines compared with that in normal tissues and 16-HBE cells, and that LINC00210 expression was associated with a poor prognosis in patients with NSCLC (P<0.05).  These findings suggest that LINC00210 may serve as an oncogenic role in NSCLC by sponging miR-328-5p.	The results demonstrated that LINC00210 was upregulated in NSCLC tissues and cell lines compared with that in normal tissues and 16-HBE cells, and that LINC00210 expression was associated with a poor prognosis in patients with NSCLC (P<0.05). 	Yes	Furthermore, A549 cell transfection with small interfering (si)LINC00210#1 and siLINC00210#2 induced a significant decrease in cell proliferation, and migratory and invasive abilities compared with that in the control groups (P<0.05).	32266029
LINC00210	LncRNA	Homo sapiens	Glioma	glioma tissues	interaction[sponging miR-328]	qRT-PCR	The present study demonstrated that LINC00210 was significantly upregulated in glioma tissues, and high expression of LINC00210 was significantly associated with advanced clinical stage and poor prognosis in patients with glioma.Therefore, the present results suggested that LINC00210 may exert an oncogenic role in glioma via sponging miR-328.	The present study demonstrated that LINC00210 was significantly upregulated in glioma tissues, and high expression of LINC00210 was significantly associated with advanced clinical stage and poor prognosis in patients with glioma.	Yes	 It was found that LINC00210 knockdown significantly inhibited the proliferation and migration of U251 and T98G cells.	33110451
LINC00210	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC samples	Regulation[NOTCH3 pathway]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that LINC00210 expression was up-regulated in NPC samples.Through inhibiting miR-328-5p activity, LINC00210 promoted NOTCH3 expression in NPC, leading to activation of NOTCH3 signaling pathway. 	Besides, its overexpression was positively correlated with NPC metastasis while predicting poor prognosis.	Yes	Based on functional experiments, we revealed that LINC00210 contributed to NPC cell proliferation and invasion in vitro, and promotes tumor growth in vivo	30341249
LINC00210	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tissues 	Regulation[miR-195-5p/IGF1R/Akt axis ]	qRT-PCR	Here, we found that Linc00210 expression was upregulated in TC tissues compared to the matched noncancerous tissues. Mechanistically, Linc00210 served as a sponge for miR-195-5p, thereby counteracting its ability in downregulating the expression of IGF1R and the activation of PI3K/Akt signaling. 		Yes	Overexpression of Linc00210 augmented the proliferation, migration, and invasion of TC cells.	31240707
LINC00205	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and several cell lines	Regulation(miRNA-26a)	FISH//Luciferase Report Assay//RIP	Both public datasets and our data showed that the LINC00205 was highly expressed in GC tissues and several cell lines. Notably, GC patients with high level of LINC00205 had a poor prognosis in our cohort. Mechanistically, knockdown of LINC00205 by shRNAs suppressed GC cells proliferation, migration, invasion remarkably, and induced cell cycle arrest. Based on bioinformatics prediction, we found that LINC00205 might act as a competitive endogenous RNA (ceRNA) through targeting miR-26a. The level of miR-26a had negatively correlated with LINC00205 expression and was decreased among GC cell lines, tissues, and serum samples. Our results for the first time confirmed that miR-26a was a direct target of LINC00205 and might have the potential to become a plasma marker for clinical tumor diagnosis. Indeed, LINC00205 knockdown resulted in the dramatic promotion of miR-26a expression as well as inhibition of miR-26a potential downstream targets, such as HMGA2, EZH2, and USP15. These targets were essential for cell survival and epithelial-mesenchymal transition. Importantly, LINC00205 was able to remodel the miR-26a-mediated downstream silence, which identified a new mechanism of malignant transformation of GC cells. 	Our results for the first time confirmed that miR-26a was a direct target of LINC00205 and might have the potential to become a plasma marker for clinical tumor diagnosis.	Yes	Mechanistically, knockdown of LINC00205 by shRNAs suppressed GC cells proliferation, migration, invasion remarkably, and induced cell cycle arrest.	35013132
LINC00205	LncRNA	Homo sapiens	Lung Neoplasms	LC tissues and cells 	regulation[FUS ,CSDE1]	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP	In the present study, we observed the elevated expression of LINC00205 in LC tissues and cells through real-time quantitative PCR (RT-qPCR). These findings demonstrated that LINC00205 facilitates malignant phenotypes in LC by recruiting FUS to stabilize CSDE1, suggesting LINC00205 as a potential target for LC therapy.		Yes	Additionally, silencing LINC00205 inhibited LC cell growth and migration, but aggravated cell apoptosis.	32808651
LINC00205	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell line	Interaction(YY1/miR-26a-5p/CDK6 pathway)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	LINC00205 was strongly expressed in HCC tissues and cell lines. Mechanistically, we illustrated that LINC00205 could accelerate the proliferation of HCC cells by boosting CDK6 expression via sponging miR-26a-5p. Moreover, we unveiled that LINC00205 could be activated by transcription factor Yin Yang-1 (YY1) as its direct downstream target.	Elevated LINC00205 expression was positively associated with worse prognosis as well as pathological grade in HCC.	Yes	Suppression of LINC00205 could impede the proliferation of HCC cells by triggering the G0/G1-phase cell cycle arrest and apoptosis in vitro. 	34730201
LINC00205	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	Interaction(miR-185-5p)	In Vivo Experiment//Western Blot//qPCR//Migration Assay//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In this study, we discovered that LINC00205 was markedly upregulated in LUAD tissues and cell lines and correlated with poor prognosis of patients with LUAD. Notably, the tumor suppressor miR-185-5p was found to be a direct target of LINC00205. In addition, miR-185-5p diminished the promotion of cell proliferation and migration mediated by LINC00205, whereas miR-185-5p inhibition had the opposite effect. 	 In this study, we discovered that LINC00205 was markedly upregulated in LUAD tissues and cell lines and correlated with poor prognosis of patients with LUAD. 	Yes	 Our data showed that LINC00205 promoted the migration and proliferation of LUAD cells in vitro and tumor growth in vivo. 	34270733
LINC00205	LncRNA	Homo sapiens	Hepatoblastoma	HB tissues and cell lines	Regulation(microRNA-154-3p/Rho-associated coiled-coil Kinase 1 axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay			Yes	In addition, knockdown of Linc00205 led to suppression of HB development. Moreover, we identified that Linc00205 was able to directly bind to miR-154-3p, thus isolating miR-154-3p from its target Rho-associated coiled-coil Kinase 1 (ROCK1). 	35179516
LINC00200	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues,cell lines	regulation[miR-143-3p/SERPINE1 Axis]	qRT-PCR//Luciferase Report Assay	LINC00200 was found to be upregulated in GC tissues and cell lines. LINC00200 is significantly overexpressed in GC and accelerates GC progression through regulating miR-143-3p/SERPINE1 axis. 		Yes	 Moreover, knockdown of LINC00200 suppressed GC cell proliferation, invasion and migration in vitro and inhibited tumorigenesis in mouse xenografts. 	33141390
LINC00184	LncRNA	Homo sapiens	Cholangiocarcinoma	cholangiocarcinoma cells	Interaction(hsa-miR-23b-3p/ANXA2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	We discovered that LINC00184 expression was heightened in cholangiocarcinoma patients and cells. Knockdown of LINC00184 repressed cell proliferation, invasion, migration and adenine metabolism in cholangiocarcinoma cells. miR-23b-3p was regarded as a target of LINC00184 and its depletion perversed the inhibitive influence of LINC00184 silencing on cholangiocarcinoma cells. ANXA2 was a target of miR-23b-3p and was negatively modulated by miR-23b-3p. Moreover, ANXA2 was positively modulated by LINC00184 via sponging miR-23b-3p. In short, silencing of LINC00184 suppressed cell proliferation, invasion and migration through over-expression of miR-23b-3p and reducing of ANXA2 in cholangiocarcinoma cells. These findings contribute to understanding the influences of LINC00184, miR-23b-3p, and ANXA2 on cholangiocarcinoma and provide basis for cholangiocarcinoma treatment.		Yes	Knockdown of LINC00184 repressed cell proliferation, invasion, migration and adenine metabolism in cholangiocarcinoma cells. miR-23b-3p was regarded as a target of LINC00184 and its depletion perversed the inhibitive influence of LINC00184 silencing on cholangiocarcinoma cells. ANXA2 was a target of miR-23b-3p and was negatively modulated by miR-23b-3p.	33913242
LINC00174	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC clinical samples and cells 	Interaction(MiR-3127-5p/ E2F7 Axis)	qRT-PCR//Wound Healing Assay//Colony Formation Assay//Western Blot	LINC00174 was up-regulated in CRC clinical samples and cells and was related to the clinical characteristics of CRC patients.  Our research reveals that LINC00174 affected the biological characteristics of CRC cells through regulated miR-3127-5p/ E2F7 axis.	LINC00174 was up-regulated in CRC clinical samples and cells and was related to the clinical characteristics of CRC patients. 	Yes	High-expression of LINC00174, contrary to the effect of siLINC00174, promoted cell viability, proliferation, migration and invasion, up-regulated the expressions of N-Cadherin, Vimentin, E2F7, and inhibited the expression of E-Cadherin. 	34226413
LINC00244	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Regulation	qRT-PCR	To explore the epigenetic regulation of PD-L1, we identified an lncRNA, LINC00244, which reduced PD-L1 expression and predicted good clinical outcomes in hepatocellular carcinoma (HCC). LINC00244 inhibited the proliferation, invasion, and metastasis of HCC by downregulating PD-L1 expression. In addition, low LINC00244 expression activated epithelial-mesenchymal transition (EMT) pathways and facilitated the rapid growth and metastasis of HCC cells. Thus, LINC00244 is a potential therapeutic target for HCC.		Yes	LINC00244 inhibited the proliferation, invasion, and metastasis of HCC by downregulating PD-L1 expression. 	35266439
LINC00261	LncRNA	Homo sapiens	Acute Kidney Injury	serum of patients with sepsis 	Interaction(miR-654-5p/SOCS3 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA//Bioinformatics Analysis	In this study, we found the expression of LINC00261 was significantly decreased in the serum of patients with sepsis than healthy controls. A similar result was also observed in the mouse model of sepsis induced by lipopolysaccharide (LPS). Mechanistically, we confirmed that LINC00261 could function as a sponge to combine with microRNA-654-5p (miR-654-5p) which inhibits nuclear factor-κB (NF-κB) activity by targeting suppressor of cytokine signaling 3 (SOCS3). 		Yes	Further investigations revealed that overexpression of LINC00261 improved the viability, suppressed the apoptosis and reduced the generation of inflammatory cytokines in LPS-treated HK-2 cells. 	33481135
LET	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells 	Interaction(miR-548k )	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay	Mechanistically, we found that miR-548k directly targets and represses the expression of long noncoding RNA-LET (lncRNA-LET), and further down-regulates p53 and up-regulates NF90. In addition, we found that lncRNA-LET is down-regulated and inversely correlated with miR-548k in ESCC. 	Down-regulated lncRNA-LET also indicated poor overall survival of ESCC patients.	Yes	Functional assays demonstrated that lncRNA-LET inhibits the proliferation and migration of ESCC cells, and the effects of miR-548k on ESCC are dependent on the negative regulation of lncRNA-LET. 	29126868
LINC00261	LncRNA	Homo sapiens	Cardiomyocyte Hypoxia/Reoxygenation Injury	myocardial tissues and H9C2 cell	regulation[LINC00261/miR-23b-3p/NRF2 axis]	qRT-PCR//Luciferase Report Assay//RIP//ChIP	The expression of LINC00261 was significantly down-regulated in myocardial tissues and H9C2 cell. Our findings reveal a novel role for LINC00261 in regulating H/R cardiomyocyte apoptosis and the potency of the LINC00261/miR-23b-3p/NRF2 axis as a therapeutic target for the treatment of MIRI.		Yes	 Overexpression of LINC00261 improves cardiac function and reduces myocardium apoptosis. 	32558131
LINC00265	LncRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	ALL cell lines and blood of patients 	Interaction(miR-4500/STAT3 Axis)	In Vivo Experiment//RNA Pull-Down//Transfection//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//migration assay	 LINC00265 was highly expressed in ALL cell lines and blood of patients with ALL and facilitated the proliferation, migration, invasion, and growth of xenograft tumors of ALL cells. RNA pull-down and luciferase assays demonstrated that LINC00265 competitively targeted miR-4500 and enhanced STAT3 expression. Furthermore, miR-4500 inhibitors or overexpressed LINC00265 up-regulated STAT3 expression, and miR-4500 mimics or STAT3 shRNAs eliminated the LINC00265-induced malignancy of the ALL cells.		Yes	 LINC00265 was highly expressed in ALL cell lines and blood of patients with ALL and facilitated the proliferation, migration, invasion, and growth of xenograft tumors of ALL cells. silencing of LINC00265 expression with LINC00265 siRNA significantly inhibited the malignancy of the ALL cells.	34737643
LINC00261	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues of patients and cell lines	Interaction(microRNA-550a-3p/SDPR axis )	RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Reduced LINC00261, decreased SDPR and elevated miR-550a-3p exhibited in BC tissues of patients and cell lines.  LINC00261 up-regulated SDPR expression as a sponge of miR-550a-3p. Moreover, up-regulated miR-550a-3p reversed the inhibitive effect of elevated LINC00261 on BCSCs, and reduced SDPR reversed the promotive effect of decreased miR-550a-3p on BCSCs. 		Yes	Elevated LINC00261 suppressed BC cell viability, MS formation ability, migration and invasion of CD44+ /CD24-/low BCSCs. 	33274565
LINC00261	LncRNA	Homo sapiens	Lung Neoplasms	 LC tissues and cells	regulation[miR-1269a/FOXO1 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In LC, LINC00261 expression was down-regulated, and was associated with more advanced TNM stage, metastasis and a shorter survival time.Down-regulation of LINC00261 expression has a prognostic value in LC, and overexpression LINC00261 inhibits LC progression via targeting miR-1269a/FOXO1 axis.	In LC, LINC00261 expression was down-regulated, and was associated with more advanced TNM stage, metastasis and a shorter survival time.	Yes	 LINC00261 overexpression inhibited the growth and metastasis of LC cells in vitro and tumor growth in vivo.	32607060
LINC00261	LncRNA	Homo sapiens	Colonic Neoplasms	cell lines	Interaction[Wnt/β-catenin pathway]	RIP	Here, we found LINC00261 was reduced in colon cancer cells.In the current study, miR-324-3p was examined and miR-324-3p was greatly increased in colon cancer cells. Moreover, the association between miR-324-3p and LINC00261 was confirmed via performing RNA immunoprecipitation and RNA-pull-down experiments. In cancer biology, aberrant modulation of the Wnt signaling pathway remains a prevalent theme. Overexpression of LINC00261 obviously impaired colon cancer progression via inactivating the Wnt pathway. Furthermore, in the xenograft model assay, an increase of LINC00261 could suppress colon tumor growth via sponging miR-324-3p and inactivating the Wnt pathway. 		Yes	Meanwhile, overexpressed LINC00261 repressed colon cancer cell viability and proliferation capacity. In addition, colony cancer cell colony formation was inhibited and apoptosis was enhanced by upregulation of LINC00261.	31183860
LINC00261	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Regulation( TGF-β1/SMAD3 signaling)	qRT-PCR	Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinical pathological parameters and poor prognosis.Furthermore, we revealed that linc00261 suppressed the expression and phosphorylation of SMAD3 (p-SMAD3), which could be core transcriptional modulator in TGF-β1 signaling mediated EMT and the acquisition of stemness traits. A negative correlation between linc00261 and p-SMAD3 was determined in HCC samples.	Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinical pathological parameters and poor prognosis.	Yes	 Here, we show that linc00261 was down-regulated in TGF-β1 stimulated cells, and forced expression of linc00261 attenuated EMT and stem-like traits in HCC. Linc00261 also inhibited the tumor sphere forming in vitro and decreased the tumorigenicity in vivo.	35123494
LINC00261	LncRNA	Homo sapiens	Endometrial Neoplasms		Regulation[miRNA/FOXO1 expression]	qRT-PCR	We found that LINC00261 mRNA levels were downregulated in endometrial carcinoma, and LINC00261 overexpression inhibited endometrial carcinoma cell proliferation, migration, and invasion. LINC00261 elevates FOXO1 protein levels through reducing FOXO1-targeted miRNAs to suppress endometrial carcinoma cell proliferation, migration, and invasion.		Yes	LINC00261 overexpression inhibits cancer cell proliferation, migration, and invasion. 	30019459
LINC00261	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tumor tissues	Regulation(EBF1)	Western Blot//Transfection//qRT-PCR//migration assay//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	qRT-PCR analysis showed that LINC00261 level was markedly reduced in TC tumor tissues, as well as corresponding cell lines.  Bioinformatics analysis suggested that LINC00261 could target EBF1. Luciferase reporter gene experiment and qRT-PCR analysis suggested that LINC00261 could target EBF1 and that their expressions showed a negative correlation in TC tumor tissues and cells. 	Retrospective analysis showed that low expression of LINC00261 was in positive correlation with the pathological stage, lymphatic and distant metastasis in patients with TC, meanwhile, the expression of LINC00261 was also in positive correlation with overall survival rate of TC patients. 	Yes	Cell functional experiments confirmed that LINC00261 can inhibit the proliferative and migration ability of TC cells. Subsequently, the recovery experiment also suggested that silencing EBF1 could reverse the promotion effect of LINC00261 knockdown on the proliferative and migration ability of TC cells; while EBF1 overexpression could reverse the inhibition of LINC00261 on the proliferative and migration ability of TC cells.	34982424
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and serums	Expression[lower expressed]	qRT-PCR//MTT	The results showed that LINC00346, LINC00578, and LINC00673 were highly expressed, whereas LINC00671, LINC00261, and SNHG9 were lowly expressed in PC tissues and serums, and their expression levels were correlated with clinical stages. 	Survival analysis indicated that patients with high expression of LINC00346, LINC00578, or LINC00673 had significantly lower survival rate, while patients with high expression of LINC00671, LINC00261, and SNHG13 had significantly higher survival rate.	Yes	In addition, we also found that silence of LINC00346, LINC00578 and LINC00673 inhibited PC cell proliferation, and silence of LINC00671, LINC00261, and SNHG13 promoted PC cell proliferation.	30210701
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues and cell lines	regulation[miR-222-3p/HIPK2/ERK axis]	qRT-PCR//Luciferase Report Assay//RIP	LINC00261 was downregulated in pancreatic cancer tissues and cell lines. Moreover, LINC00261 exerted its biological function by binding to miR-222-3p to activate the HIPK2/ERK/c-myc pathway. 	Its reduced expression was correlated with advanced pathological stage and poor prognosis.	Yes	Forced expression of LINC00261 suppressed pancreatic cancer glycolysis and proliferation and induced cell cycle arrest and apoptosis.	33122827
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues	regulation[c-Myc expression]	ISH//qRT-PCR//RIP	 LINC00261 was significantly downregulated in PC tissues, and its expression was positively associated with the prognosis of PC patients. Our findings indicate that methylation-mediated LINC00261 suppresses PC progression by epigenetically repressing c-Myc expression.	 LINC00261 was significantly downregulated in PC tissues, and its expression was positively associated with the prognosis of PC patients.	Yes	Phenotypic studies indicated that LINC00261 overexpression significantly suppressed PC cell proliferation, migration and metastasis in vitro and in vivo.	32929371
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	cell lines	regulation[down-regulating miR-23a-3p]	Flow Cytometry//qRT-PCR//RIP//MTT//Invasion Assay//Transwell Assay	LINC00261 level was decreased in pancreatic cancer cells than that in normal pancreatic ductal epithelial cells.  In conclusion, LINC00261 overexpression repressed cell viability and invasion and enhanced apoptosis by decreasing miR-23a-3p expression in pancreatic cancer cells, indicating a new target for the treatment of pancreatic cancer.	Low level of LINC00261 indicated low survival probability of pancreatic cancer patients.	Yes	In conclusion, LINC00261 overexpression repressed cell viability and invasion and enhanced apoptosis by decreasing miR-23a-3p expression in pancreatic cancer cells, indicating a new target for the treatment of pancreatic cancer.	32590069
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	regulation[miR-552-5p/FOXO3 axis]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	Linc00261 expression was significantly decreased in PC tissues and cell lines, and reduced expression was associated with less favorable outcomes in patients with PC.Collectively, the present study demonstrated that Linc00261 inhibited metastasis and the Wnt signaling pathway of PC by regulating the miR‑552‑5p/FOXO3 axis. 		Yes	Linc00261 overexpression inhibited migration and invasion of PC cells in vitro, whereas knockdown of Linc00261 increased migration and invasion.	32020223
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	Pancreatic cancer tissues	Interaction(FOXP3/SCP2 axis)	In Vivo Experiment//IHC//Western Blot//Transwell Assay//Transfection//CCK8//qRT-PCR//FISH//RIP//Flow Cytometry//Luciferase Report Assay//ELISA//Colony Formation Assay//Bioinformatics Analysis//ChIP	LINC00261 was lowly expressed in PC tissues and cells. SCP2 was inhibited by LINC00261 through FOXP3. 		Yes	Functionally, upregulated LINC00261 or downregulated SCP2 led to reduced cell viability, migration, angiogenesis and tumourigenicity potentials. 	34541823
LINC00261	LncRNA	Homo sapiens	Pancreatic Neoplasms	Pc tissues and PC cells and PC stem cells	Regulation( ITIH5/GATA6 regulatory pathway)	In Vivo Experiment//Western Blot//Transwell Assay//Transfection//CCK8//qRT-PCR//FISH//RIP//Flow Cytometry//Luciferase Report Assay//Microarray//IHC//ChIP	Microarray analysis of differentially expressed genes and lncRNAs suggested that LINC00261 is downregulated in PC. Both LINC00261 and ITIH5 were confirmed to be downregulated in PC cells and PC stem cells.  The results of dual-luciferase reporter gene, ChIP, and RIP assays indicated that LINC00261 binds directly to GATA6, increasing its activity at the ITIH5 promoter. The presence of LINC00261 and GATA6 inhibited the self-renewal and tumorigenesis of PC stem cells, while silence of ITIH5 rescued those functions. 		Yes	These experiments revealed that the expression of stem cell markers was reduced, and cell proliferation, self-renewal ability, cell invasion, drug resistance, and tumorigenicity were all suppressed by upregulation of LINC00261 or ITIH5. 	34446696
LINC00261	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[interacting with miR-522-3p and suppressing Wnt signaling]	qRT-PCR	In this study, LINC00261 was delineated in NSCLC to be significantly downregulated in cancer tissues compared with corresponding adjacent normal tissues. Taken together, our study demonstrated that LINC00261 suppressed NSCLC cells progression via sponging miR-522-3p and inhibiting Wnt signaling. 	Low expression of LINC00261 predicted worse survival for patients with NSCLC. 	Yes	Overexpression of LINC00261 in NSCLC cell lines inhibited cell proliferation and invasion, meanwhile promoted apoptosis. 	31190356
LINC00261	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Expression[lower expressed]	qRT-PCR//Wound Healing Assay//MTT//Western Blot	We demonstrated that linc00261 was lowly expressed in NSCLC tissues and cells. 		Yes	Over-expression of linc00261 significantly inhibited proliferation, invasion and migration of NSCLC cells. On the contrast, knockdown of linc00261 promoted cell growth and metastasis of NSCLC cells.Linc00261 could slow down the growth of xenograft of NSCLC in vivo.	31115010
LINC00261	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues,cell lines 	Interaction[EMT process]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 LINC00261 was overexpressed in cancerous tissues and CCA cell lines compared with adjacent tissues and HIBEC, respectively.  Knockdown of LINC00261 expression in RBE and QBC939 cell lines inhibited cell proliferation, migration and invasion property and increased cell apoptosis and the EMT progression. Moreover, there was a strong correlation between LINC00261 and E-cadherin (CDH1) (p < 0.05), and low expression of E-cadherin (CDH1) has a poor overall survival and relapse-free survival in CCA patients (p < 0.05).	Up-regulation of LINC00261 was related to larger tumor size (p = 0.009), positive lymph node metastasis (p = 0.021), advanced TNM stages (p = 0.017) and higher postoperative recurrence (p = 0.009) for CCA patients. Additionally, univariate and multivariate analysis displayed that LINC00261 an independent prognostic factor in CCA patients.	Yes	Knockdown of LINC00261 expression in RBE and QBC939 cell lines inhibited cell proliferation, migration and invasion property and increased cell apoptosis and the EMT progression.	31812439
LINC00261	LncRNA	Homo sapiens	Myocardial Infarction	coronary heart disease tissues with MI	Interaction(miR-522-3p/TNRC6A )	Western Blot//Transfection//Flow Cytometry//FISH//qRT-PCR//MTT//Luciferase Report Assay	LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI.LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p.		Yes	 Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. 	34239606
LINC00261	LncRNA	Homo sapiens	Endometriosis	endometriosis tissues	Interaction[LINC00261/miR-132-3p/BCL2L11]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC00261 was significantly downregulated in endometriosis tissues and our study indicated that it suppresses proliferation and invasion of endometriosis cells functionally in vitro. These data defined LINC00261/miR-132-3p/BCL2L11 regulatory networks may be a novel therapeutic target for endometriosis.		Yes	LINC00261 was significantly downregulated in endometriosis tissues and our study indicated that it suppresses proliferation and invasion of endometriosis cells functionally in vitro. 	31105834
LINC00174	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-320/S100A10 axis]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//RIP//BrdU//Transwell Assay	We demonstrated that LINC00174 expression in HCC clinical samples was significantly increased and this was correlated with higher T stage. We demonstrate that LINC00174 functions as a sponge for miR-320, increases the expression level of oncogene S100A10 in HCC.	We demonstrated that LINC00174 expression in HCC clinical samples was significantly increased and this was correlated with higher T stage. 	Yes	Its overexpression remarkably accelerated proliferation and metastasis of HCC cells while reduced apoptosis. Accordingly, knockdown of it suppressed the malignant phenotypes of HCC cells.	32128852
LINC00174	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(miR-378a-3p/SSH2 axis and the TGF-β/SMAD pathway)	qRT-PCR//RNA Pull-Down//Western Blot	We found that LINC00174 was upregulated in OS tissues and cells. In conclusion, LINC00174 promotes OS cellular malignancy and tumorigenesis via the miR-378a-3p/SSH2 axis and the TGF-β/SMAD pathway, which might provide a novel insight for OS treatment.		Yes	LINC00174 knockdown repressed OS cell growth. 	34222341
LINC00174	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Regulation[miR-152-3p/SLC2A1 axis]	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ELISA//Transwell Assay	LINC00174 was overexpressed in glioma tissues and cell lines.LINC00174 could interact with miR-152-3p/SLC2A1 axes. The miR-152-3p inhibitor or the SLC2A1 overexpression could rescue the anti-tumor effect of LINC00174 knockdown on glioma cells.		Yes	LINC00174 knockdown inhibited cell proliferation, migration, invasion and glycolysis of glioma cells, and LINC00174 exerted a tumorigenesis role. Moreover, downregulation of LINC00174 also inhibited tumor volume and delayed the tumor growth in vivo.	31492194
LINC00174	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells 	Regulation[LINC00174/miR-1910-3p/TAZ pathway]	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	We observed that increased expression of LINC00174 in CRC tissues and cells in comparison to their corresponding controls.Taken together, our study discovered the oncogenic role of LINC00174 in clinical specimens and cellular experiments, showing the potential LINC00174/miR-1910-3p/TAZ pathway.	Moreover, the aberrant overexpression of LINC00174 indicated the poor prognosis of CRC patients.	Yes	Silence of LINC00174 was able to repress CRC cell growth in vitro and in vivo.	29729381
LIFR-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	regulation[miR-942-5p/ZNF471 axis]	qRT-PCR	Overexpression of miR-942-5p caused a reduction of LIFR-AS1 in NSCLC cells.we provide first evidence for the involvement of the LIFR-AS1/miR-942-5p/ZNF471 axis in NSCLC invasion and metastasis. LIFR-AS1 may represent a novel target for the treatment of NSCLC.		Yes	Functionally, LIFR-AS1 overexpression inhibited NSCLC cell migration and invasion, whereas LIFR-AS1 silencing yielded an opposite effect. In vivo studies confirmed that LIFR-AS1 overexpression suppressed lung metastasis of NSCLC cells. 	32489316
LIFR-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Epigenetics(hypermethylated)	qRT-PCR//Luciferase Report Assay	We identified a novel hypermethylated lncRNA, LIFR-AS1, that was downregulated and associated with tumorigenesis, metastasis, and poor prognosis in CRC.  Functional assays revealed that LIFR-AS1 could competitively bind to hsa-miR-29b-3p, and repressed colon cancer cell proliferation, colony formation and invasion. LIFR-AS1 also inhibited tumor growth in a mouse xenograft model of CRC.	We identified a novel hypermethylated lncRNA, LIFR-AS1, that was downregulated and associated with tumorigenesis, metastasis, and poor prognosis in CRC.  High methylation burden of LIFR-AS1 indicated a poor survival of CRC patients. 	Yes	 Functional assays revealed that LIFR-AS1 could competitively bind to hsa-miR-29b-3p, and repressed colon cancer cell proliferation, colony formation and invasion. LIFR-AS1 also inhibited tumor growth in a mouse xenograft model of CRC.	36316703
LIFR-AS1	LncRNA	Homo sapiens	Osteosarcoma	human mononuclear cells 	Interaction(miR-29a/NFIA axis)	CCK8//qRT-PCR	Then, the results of the high-throughput microarray assay showed that LIFR-AS1 was highly expressed and miR-29a was lowly expressed. Furthermore, LIFR-AS1 was identified as a miR-29a sponge, and NFIA was validated as a direct target of miR-29a. 		Yes	Functional assays demonstrated that knockdown of exosomal LIFR-AS1 could attenuate the promotion effects of macrophages-derived exosomes on osteosarcoma cell progression and miR-29a inhibition could reserve the effect of LIFR-AS1-knockdown exosomes. 	33794884
LIFR-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction(miR-31-5p/SIDT2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Tube Formation Assay//qRT-PCR//ELISA//Colony Formation Assay//Invasion Assay	The tumor size and lymphatic metastasis were correlated with LIFR-AS1 overexpression. LIFR-AS1 and SIDT2 expressions were suppressed in PTC tissues, while that of miR-31-5p was elevated in PTC tissues.This paper demonstrates that LIFR-AS1/miR-31-5p/SIDT2 axis modulated the development of PTC.	The tumor size and lymphatic metastasis were correlated with LIFR-AS1 overexpression.	Yes	Overexpressed LIFR-AS1 suppressed tumorigenesis in vivo.  LIFR-AS1 was negatively correlated with miR-31-5p. LIFR-AS1 sponged miR-31-5p to upregulate SIDT2, thereby inhibiting the viability, proliferation, migration, invasion, and the secretion of vascular endothelial growth factor (VEGF) of PTC cells and angiogenesis of human umbilical vein endothelial cells (HUVECs). 	34781815
LIFR-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cell lines and tumors	Interaction(miRNA-150-5p/ VEGFA/Akt signaling)	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	. In this study, we determined that PC cell lines and tumors exhibit increased LIFR-AS1 expression that correlates with larger tumor size, lymph node metastasis, and more advanced TNM stage. Mechanistically, we found that METTL3 induced m6A hyper-methylation on the 3' UTR of LIFR-AS1 to enhance its mRNA stability and LIFR-AS1 could directly interact with miR-150-5p, thereby indirectly up-regulating VEGFA expressions within cells. 	. In this study, we determined that PC cell lines and tumors exhibit increased LIFR-AS1 expression that correlates with larger tumor size, lymph node metastasis, and more advanced TNM stage. 	Yes	 Functionally, loss-of-function studies indicated that LIFR-AS1 knockdown decreased the proliferation, migration, and invasion of PC cells in vitro.	34658294
LIFR-AS1	LncRNA	Homo sapiens	stomach carcinoma	GC tissues and cells	interaction[sponging miR-4698,MEK/ERK pathway]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Decreased lncRNA LIFR?AS1 expression was observed in GC tissues and cells.The process was mediated via miR‑4698, MTUS1 and the MEK/ERK pathway.		Yes	Upregulated lncRNA LIFR?AS1 inhibited GC cell proliferation, migration and invasion.	33355363
LIFR-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	 thyroid cancer tissues and cells	Expression [highly expressed]	In Vivo Experiment//Western Blot//qRT-PCR//MTT//cell invasion assay//Cell Cycle Assay//EdU Staining	The results showed significant (p < 0.05) upregulation of LncRNA-LIFR-AS1 in thyroid cancer tissues and cells. However, silencing of LncRNA-LIFR-AS1 inhibited the viability and proliferation of human thyroid cancer cells inducing G2/M cell cycle arrest. 		Yes	The thyroid cancer cells exhibited remarkably lower invasion and migration under transcriptional knockdown of lncRNA-LIFR-AS1 which was also associated with downregulation of MMP-2 and MMP-9 expression.	33927978
LIFR-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	SOC patients	Expression(lower expressed)	Western Blot//ISH//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	LIFR-AS1 was lowly expressed in SOC, which was correlated with the poor prognosis of SOC patients.  LIFR-AS1 overexpression promoted the expressions of cleaved caspase-3 and E-cadherin while suppressing the malignant behaviors (proliferation, migration, and invasion) of SOC cells, the expressions of PCNA, N-cadherin, and Snail. Besides, silencing LIFR-AS1 exerted the effects opposite to overexpressed LIFR-AS1.	 Low expression of LIFR-AS1 in SOC was associated with the tumor size, clinical stage, lymph node metastasis, and distant metastasis.	Yes	 LIFR-AS1 overexpression promoted the expressions of cleaved caspase-3 and E-cadherin while suppressing the malignant behaviors (proliferation, migration, and invasion) of SOC cells, the expressions of PCNA, N-cadherin, and Snail. Besides, silencing LIFR-AS1 exerted the effects opposite to overexpressed LIFR-AS1.	35778954
LIF-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Expression[highly expressed]	FISH//Transwell Assay	 The expression level of Lnc-LIF-AS in cervical cancer tissues was higher than that in normal tissues and the expression level of Lnc-LIF-AS was positively correlated with the level of LIF. 		Yes	The overexpression of Lnc-LIF-AS can promote cell proliferation, migration and invasion in cervical cancer cells, and the core function domain of this lncRNA was located in the overlapping a 3'-UTR base sequence of LIF mRNA.	31085454
LICN00520	LncRNA	Homo sapiens	Melanoma	melanoma tissues	regulation[miR-125b-5p/EIF5A2 axis]	RNA Pull-Down//ChIP//Wound Healing Assay//CCK8//qRT-PCR//EdU Staining//Transwell Assay	We found that LICN00520 was found to be overexpressed in melanoma tissue.We also showed that LICN00520 promotes the growth and metastasis of melanoma in vivo through regulating miR-125b-5p/EIF5A2 axis.	High expression of LICN00520 is a risk factor for the prognosis of melanoma patients.	Yes	LINC00520 promotes the proliferation, invasion and migration of melanoma cells.	32466797
LICN00518	LncRNA	Homo sapiens	Melanoma	 melanoma tissue	Regulation[miR-204-5p/AP1S2 axis]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//ChIP	We found that LICN00518 was significantly upregulated in melanoma tissue, and high LICN00518 level was an independent risk factor for melanoma patients.LICN00518 exerted its role by decoying miR-204-5p to upregulate Adaptor Related Protein Complex 1 Sigma 2 Subunit (AP1S2) expression.		Yes	LICN00518 promoted the invasion and migration of melanoma cells.	31712557
LHFPL3-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(SFPQ /TXNIP)	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	 We showed that LHFPL3-AS2 is a novel lncRNA, significantly decreased in NSCLC tissues.  Moreover, downregulation of LHFPL3-AS2 reduced its specific interaction with SFPQ, resulting in more SFPQ binding to the promoter of TXNIP and causing the transcriptional repression of TXNIP, thus finally promoting the migration and invasion of NSCLC cells. Furthermore, LHFPL3-AS2 was shown to be regulated by EGR1 under hypoxia.	 LHFPL3-AS2 was further validated in an additional 93 paired samples of NSCLC. Low levels of LHFPL3-AS2 expression were highly correlated with poor overall survival, TNM stage, and metastasis of NSCLC patients. 	Yes	Enhanced expression of LHFPL3-AS2 inhibited NSCLC invasion and metastasis in vitro and in vivo.	35101541
LHFPL3-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-362-5p/CHSY1 Pathway)	qRT-PCR//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	 LHFPL3-AS1 was highly expressed in OSCC tissues and cell lines. LHFPL3-AS1 was the competing endogenous RNA (ceRNA) for miR-194-5p to enhance CHSY1 expression.	LHFPL3-AS1 level was correlated with survival rate.	Yes	LHFPL3-AS1 knockdown suppressed OSCC proliferation, migration and invasion. 	33833527
LHFPL3-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	regulation[LHFPL3-AS1/miR-580-3p/STAT3]	Northern Blot//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Invasion Assay	Data from our work suggested that LHFPL3-AS1 expression was markedly elevated in melanoma tissues and cells. Our study revealed a novel positive feedback loop LHFPL3-AS1/miR-580-3p/STAT3 in melanoma, which might contribute to finding potential therapeutic targets for melanoma.	Of note, patients with melanoma with high level of LHFPL3-AS1 were burdened with unfavorable prognosis.	Yes	 Functionally, it has been revealed that LHFPL3-AS1 exerted pro-growth, pro-invasion, and pro-EMT functions in melanoma.	32753471
LHFPL3	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cells and tissues	Interaction(microRNA-143-5p/homeobox A6 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	It was discovered that LHFPL3-AS1 and HOXA6 expression was elevated while the miR-143-5p level was depleted in radiation-resistant NPC cells and NPC tissues. The silenced LHFPL3-AS1 or augmented miR-143-5p repressed the proliferation, colony formation, migration and invasion of radiation-resistant NPC cells, while accelerated cell apoptosis in vitro. Silenced LHFPL3-AS1 hindered tumor growth in vivo. MiR-143-5p deletion reversed the effects of reduced LHFPL3-AS1; while HOXA6 upregulation reversed the effects of enriched miR-143-5p. LHFPL3-AS1 sponged miR-143-5p that targeted HOXA6. It is concluded that the down-regulated LHFPL3-AS1 retards the development of radiation-resistant NPC cells via sponging miR-143-5p to modulate HOXA6. This study reveals novel therapeutic targets for NPC treatment.		Yes	The silenced LHFPL3-AS1 or augmented miR-143-5p repressed the proliferation, colony formation, migration and invasion of radiation-resistant NPC cells, while accelerated cell apoptosis in vitro. Silenced LHFPL3-AS1 hindered tumor growth in vivo.	35176945
LGALS8-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction(miR-125b-5p/SOX12 Feedback)	Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Invasion Assay	The lncRNA LGALS8-AS1 was highly expressed in breast cancer and associated with poor survival. It upregulated SOX12 via competing as a competing endogenous RNA (ceRNA) for sponging miR-125b-5p and acted on the PI3K/AKT signaling pathway to promote the metastasis of breast cancer. Furthermore, SOX12, in turn, activated LGALS8-AS1 expression via direct recognition of its sequence binding enrichment motif on the LGALS8-AS1 promoter, thereby forming a positive feedback regulatory loop.	The lncRNA LGALS8-AS1 was highly expressed in breast cancer and associated with poor survival. 	Yes	 LGALS8-AS1 functioned as an oncogenic lncRNA that promoted the metastasis of breast cancer both in vitro and in vivo.	34745940
LETR1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	Regulation[Wnt/β-catenin signaling]	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//RIP//Colony Formation Assay	We found that a FOXO1-related lncRNA, LINC01197, was significantly decreased in PDAC malignant tissues and that its low expression predicted poor prognosis.Mechanistically, LINC01197 was found to bind to β-catenin and inhibit Wnt/β-catenin signaling activity by disrupting β-catenin binding to TCF4 in PDAC cells.		Yes	Moreover, LINC01197 was mainly localized in the nucleus and inhibited PDAC cell proliferation both in vitro and in vivo. 	31027497
LET	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues  and MDA-MB-231 cells	Expression[lower expressed]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 The expression of lncRNA LET was reduced in breast cancer tissues and MDA-MB-231 cells. 		Yes	Overexpression of lncRNA LET resulted in the inhibition of cell proliferation, invasion and migration ability, and promotion of cell apoptosis (p<0.05).	30280783
LIFR-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction[miR-197-3p]	IHC//Western Blot//ISH//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In the present study, we found that LIFR-AS1 was significantly down-regulated in both tissues and cell lines.Moreover, LIFR-AS1 was observed to up-regulate suppressor of fused gene (Sufu) expression by competitively binding to miR-197-3p in breast cancer cells.		Yes	Additionally, LIFR-AS1 knockdown promoted tumor growth in vivo 	31127025
LIFR-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric tumor tissues and cells	Interaction(miR-29a-3p/COL1A2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Colony Formation Assay//CCK8//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	The expression levels of LIFR-AS1 were significantly increased in gastric tumor tissues and cells, while the expression levels of miR-29a-3p were decreased.  The expression of miR-29a-3p was negatively correlated with the expression of LIFR-AS1 in gastric cancer tumor tissues. Bioinformatics analyses and integrated experiments revealed that LIFR-AS1 elevated the expression of COL1A2 through sponging miR-29a-3p, which further resulted in the progression of gastric tumor.		Yes	Knocking down of LIFR-AS1 inhibited proliferation, invasion and migration of gastric tumor cells, and induced apoptosis of gastric tumor cells. 	33407453
LIMD1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC samples and cells	regulation[LIMD1,hnRNP U]	RNA Pull-Down//CCK8//qRT-PCR//RIP//EdU Staining	Moreover, long noncoding RNA (lncRNA) LIMD1 antisense RNA 1 (LIMD1-AS1) was downregulated in NSCLC samples and cell lines. Mechanistically, LIMD1-AS1 stabilized LIMD1 mRNA through interacting with hnRNP U. Rescue experiments suggested that LIMD1-AS1 repressed NSCLC progression through LIMD1.		Yes	LIMD1-AS1 knockdown abrogated NSCLC cell growth in vitro and in vivo.	32239804
LINC00152	LncRNA	Mus musculus	acute myocardial infarction	serum	Regulation(Smad7)	CCK8//qRT-PCR//Transwell Assay	Serum level of LINC00152 was elevated in AMI patients. ROC curves demonstrated the diagnostic potential of LINC00152 in AMI (95% CI: 0.806-0.940, p = 0.034). In myocardial tissues collected from AMI mice, LINC00152 level was higher than those collected from mice of the sham group. LVEF and FS markedly decreased in AMI mice overexpressing LINC00152 on the 4th week of AMI modeling. After knockdown of LINC00152 in primary cardiac fibroblasts, proliferative and migratory abilities were declined, which were abolished by Smad7 intervention.	ROC curves demonstrated the diagnostic potential of LINC00152 in AMI (95% CI: 0.806-0.940, p = 0.034).	Yes	After knockdown of LINC00152 in primary cardiac fibroblasts, proliferative and migratory abilities were declined, which were abolished by Smad7 intervention.	34900025
LINC00173.v1	LncRNA	Homo sapiens	lung squamous cell carcinoma	SQC tissues	regulation[miR-511-5p,VEGFA ]	ISH//qRT-PCR//Luciferase Report Assay//RIP	 LINC00173.v1 was specifically upregulated in SQC tissues, which predicted poorer overall and progression-free survival in SQC patients.Our results further revealed that LINC00173.v1 promoted the proliferation and migration of vascular endothelial cells and the tumorigenesis of SQC cells by upregulating VEGFA expression by sponging miR-511-5p.	 LINC00173.v1 was specifically upregulated in SQC tissues, which predicted poorer overall and progression-free survival in SQC patients.	Yes	Overexpression of LINC00173.v1 promoted, while silencing LINC00173.v1 inhibited the proliferation and migration of vascular endothelial cells and the tumorigenesis of SQC cells in vitro and in vivo. 	32473645
LINC00173	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC and adjacent breast tissues	regulation[miR-490-3p]	qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	TNBCs expressed increased levels of LINC00173 relative to normal breast tissues.Altogether, LINC00173 functions as an oncogene in TNBC through antagonization of miR-490-3p. 	 TNBC patients with high tumoral LINC00173 levels had a lower recurrence-free survival and overall survival rate than those with low LINC00173 expression.	Yes	 Silencing of LINC00173 inhibited the proliferation, colony formation, and invasion of TNBC cells, whereas overexpression of LINC00173 exerted opposite effects.	32058222
LINC00173	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-765/NUTF2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	LINC00173 expression was elevated in glioma tissues and cells.Our research demonstrated that LINC00173 promotes glioma progression through targeting miR-765/NUTF2 axis.	 LINC00173 high expression predicted poor prognosis. 	Yes	 Loss of LINC00173 inhibited proliferation, migration and invasion.	32848473
LINC00173	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa specimens and cell lines	regulation[LINC00173/miR-338-3p/Rab25 pathways]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	We observed that the expression of LINC00173 and Rab25 was distinctly upregulated in both PCa specimens and cell lines, while miR-338-3p expression was significantly down-regulated. The discovery of the LINC00173/miR-338-3p/Rab25 pathways provided new thinking for the treatments of PCa.	 High LINC00173 expression was associated with Gleason score, preoperative PSA level and reduced patient survivals.	Yes	Functional assays revealed that knockdown of LINC00173 suppressed the proliferation, migration and invasion of PCa cells, and promoted apoptosis. 	33015770
LINC00165	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	interaction[STAT3 ]	qRT-PCR	In the present study, our results showed that LINC00165 was upregulated in GC tissues and cell lines and high expression of LINC00165 was correlated with tumor-node-metastasis stage, invasion depth, and overall survival of GC patients. Mechanistically, we revealed that LINC00165 functioned as a scaffold for interaction with Polycomb Repressive Complex 2 to promote the epithelial-mesenchymal transition in GC cells. 	In the present study, our results showed that LINC00165 was upregulated in GC tissues and cell lines and high expression of LINC00165 was correlated with tumor-node-metastasis stage, invasion depth, and overall survival of GC patients. 	Yes	Functional assays showed that LINC00165 knockdown inhibited the proliferation, migration and invasion of GC cells and LINC00165 overexpression stimulated their proliferation, migration and invasion. 	30448060
LINC00161	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	serum-derived exosomes from HCC patients and the supernatants of HCC cell lines 	Interaction(miR-590-3p/ROCK axis)	qRT-PCR//Western Blot	High levels of LINC00161 were detected in both serum-derived exosomes from HCC patients and the supernatants of HCC cell lines and were significantly associated with poor survival. Mechanistic study revealed that exosome-carried LINC00161 directly targeted miR-590-3p and induced its downstream target ROCK2, finally activating growth/metastasis-related signals in HCC. 	High levels of LINC00161 were detected in both serum-derived exosomes from HCC patients and the supernatants of HCC cell lines and were significantly associated with poor survival.	Yes	Functional study demonstrated that exosomal LINC00161 derived from HCC-cells were significantly associated with enhanced proliferation, migration, and angiogenesis in HUVECs in vitro, all of which were effectively inhibited when LINC00161 was sliced with shRNA in HCC-cells. In vivo experiment showed that LINC00161 loss inhibited tumorigenesis and metastasis of HCC. 	33414518
LINC00160	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer cells	Regulation(RCAN1)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	Silence of LINC00160 inhibited proliferation and promoted the apoptosis of prostate cancer cells, retarded the glycolysis of prostate cancer cells. By acting as a transcription activator, STAT3 induced LINC00160 expression, which regulated RCAN1 transcription epigenetically via binding to EZH2. Mechanically, LINC00160 mediated prostate cell proliferation and metabolism by repressing RCAN1 expression. In summary, LINC00160 may function as the novel marker for prostate cancer diagnosis and therapy.		Yes	 Silence of LINC00160 inhibited proliferation and promoted the apoptosis of prostate cancer cells, retarded the glycolysis of prostate cancer cells. 	35067783
LINC00158	LncRNA	Rattus norvegicus	Spinal Cord Injuries	SCI model rats	Regulation( LC3-II/LC3-I, Beclin-1, and p62 )	In Vivo Experiment	 The results showed that the expression of LINC00158 decreased and apoptotic cells increased in the SCI model rats. Meanwhile, we found the upregulated LC3-II/LC3-I, Beclin-1, and p62 in the SCI rats.  After OGD treatment, the expression of LINC00158 decreased significantly and the apoptosis of spinal cord neurons increased. OGD treatment resulted in upregulation of LC3-II/LC3-I and Beclin-1 and downregulation of p62 in primary spinal cord neurons, which could be eliminated by overexpression of LINC00158. 3-Methyladenine and chloroquine (autophagy inhibitor) reversed the inhibitory effect of LINC00158 overexpression on apoptosis of primary spinal cord neurons.		Yes	 The results showed that the expression of LINC00158 decreased and apoptotic cells increased in the SCI model rats. Meanwhile, we found the upregulated LC3-II/LC3-I, Beclin-1, and p62 in the SCI rats. 	36588354
LINC00115	LncRNA	Homo sapiens	Lung Neoplasms	 tumor tissues and cells	Interaction(miR-607/ITGB1 pathway)	CCK8//qRT-PCR//Transwell Assay	 LINC00115 was highly expressed in tumor tissues and cells.  Investigation to its molecular mechanism revealed that LINC00115 functioned as a competitive endogenous RNA (ceRNA), regulating the expression of ITGB1 by sponging miR-607 to affect tumor growth. The LINC00115/miR-607/ITGB1 signaling axis might be a novel therapeutic target in lung cancer.		Yes	LINC00115 promoted the malignant properties of tumor cells. 	34643030
LIN28B-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung		Interaction[IGF2BP1  ]	CCK8//RNA Pull-Down//RIP//Microarray	"In addition to the known let-7-LIN28B regulation loop, our results further revealed a let-7-independent Cis-regulator of LIN28B: LIN28B-AS1. LIN28B-AS1 is a CT long non-coding RNA (CT-lncRNA). It altered the messenger RNA stability of LIN28B by directly interacting with another CT protein IGF2BP1 but not with LIN28B and constituted a novel regulation network. In sum, we identify that LIN28B is an ""epi-driver"" of LUAD and clarify a new lncRNA-activated mechanism of LIN28B, which provide new candidate targets for precise anticancer therapy in the future."		Yes	In vitro and In vivo experiments confirmed that the activation of LIN28B could promote the proliferation and metastasis of LUAD cells and can influence cell cycle, DNA damage repair, and genome instability.	30353165
LINC00115	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue	regulation[LINC00115/miR-489-3p axis ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	In this study, we discovered that LINC00115 was significantly overexpressed in CRC, and its overexpression predicted poor patient outcomes. Deeper understanding of the LINC00115/miR-489-3p axis might provide potential therapeutic targets against CRC metastasis.	In this study, we discovered that LINC00115 was significantly overexpressed in CRC, and its overexpression predicted poor patient outcomes. 	Yes	Downregulation of LINC00115 markedly inhibited CRC cell proliferation, increased cell apoptosis, and suppressed cell migration and invasion. 	33193658
LINC00115	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Interaction(miR-212-5p/FZD5/Wnt/β-catenin axis)	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//cell invasion assay//Colony Formation Assay	 Our results showed that LINC00115 was significantly up-regulated in prostate cancer tissues, which was significantly associated with a poor prognosis for prostate cancer patients. In addition, LINC00115 served as a competing endogenous RNA (ceRNA) through sponging miR-212-5p to release Frizzled Family Receptor 5 (FZD5) expression. The expression of miR-212-5p was noticeably low in tumour tissues, and FZD5 expression level was down-regulated with the knockdown of LINC00115. Knockdown LINC00115 inhibited the Wnt/β-catenin signalling pathway by inhibiting the expression of FZD5.		Yes	Functional studies showed that knockdown LINC00115 inhibited cell proliferation and invasion. 	34697900
LINC00114	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction[suppressed miR-133b]	RNA Pull-Down//Co-IP//qRT-PCR//RIP//Luciferase Report Assay//ChIP	Data showed that LINC00114 was highly expressed, whereas miR-133b was downregulated in the CRC tissues and cells.These results demonstrated that LINC00114 suppressed miR-133b expression via EZH2/DNMT1-mediated methylation of its promoter region, indicating that LINC00114 might be a potential novel target for CRC diagnosis and treatment.		Yes	In vitro, silencing LINC00114 inhibited cell proliferation and impeded cell cycle at the G1/S phase by upregulating miR-133b. In vivo, LINC00114 knockdown reduced tumor growth.	31921641
LINC00052	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues	Interaction(miR-145-5p /TGFBR2 )	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Invasion Assay	 The expression levels of LINC00052 were found to be significantly higher in BC tissues compared with those in the adjacent normal tissues.LINC00052 was mainly expressed in the cytoplasm and was considered to bind with microRNA (miR)-145-5p based on various databases. Notably, the high expression levels of LINC00052 led to the low expression levels of miR-145-5p and high expression levels of TGF-β receptor II (TGFBR2). 		Yes	 Downregulation of LINC00052 expression in vitro significantly suppressed the proliferation, migration and invasion of BC cells. 	33777194
LINC00052	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-548p/Notch2/Pyk2 )	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	High LINC00052 expression was observed in breast cancer tissues and cells. MiR-548p, a target gene of LINC00052, partially rescued the effects of LINC00052 on proliferation, migration, and invasion of MCF7. Notch2 was the target of miR-548p and LINC00052 could promote Notch2 expression. Moreover, the phosphorylation of proline-rich tyrosine kinase 2 (Pyk2), a downstream factor of Notch2, was increased by LINC00052, and a Pyk2 mutant could inhibit the cell migration and invasion induced by LINC00052 overexpression in MDA-MB-468 cells, which was similar to the function of the miR-548p mimic. 		Yes	LINC00052 silencing inhibited the proliferation, migration, and invasion of MCF7 cells, and LINC00052 overexpression produced the opposite results.	35918619
LINC00052	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction[downregulating IGF2]	Western Blot//Wound Healing Assay//qRT-PCR//Cell Proliferation Assay//Transwell Assay	LINC00052 expression was remarkably downregulated in glioma samples compared with that in normal brain samples.These results above suggest that LINC00052 could repress cell migration, invasion and proliferation in glioma through downregulating IGF2, which may offer a new therapeutic intervention for glioma patients.		Yes	Moreover, cell proliferation, cell invasion and cell migration in glioma were inhibited after overexpression of LINC00052 in vitro.	35116894
LINC00052	LncRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Interaction[upregulating KLF6]	qRT-PCR//Wound Healing Assay//Transwell Assay//Western Blot	LINC00052 expression was remarkably downregulated in glioma samples compared with that in adjacent samples. These results suggested that LINC00052 could repress cell migration, invasion and proliferation in glioma through upregulating KLF6, which may offer a new therapeutic intervention for glioma patients.		Yes	Moreover, cell proliferation, invasion, and migration of glioma were inhibited after overexpression of LINC00052 in vitro.	31210314
LINC000466	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-539-5p)	Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC00466 was significantly upregulated in TNBC and showed close association with the clinical features of patients, which indicates the development, and severity of patients.	LINC00466 was significantly upregulated in TNBC and showed close association with the clinical features of patients, which indicates the development, and severity of patients.	Yes	LINC00466 functioned as a prognostic biomarker predicting the survival of patients and a tumor promoter improving the proliferation, migration, and invasion of TNBC cells through sponging miR-539-5p.	35216934
KCNQ1OT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-148a-3p/IGF1R Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In our study, we first observed the expression level of KCNQ1OT1 was distinctly up-regulated in HCC tissues and cell lines compared with adjacent non-cancer tissues and normal liver cell line. In conclusion, our results shown the oncogenic role of KCNQ1OT1 in HCC by regulating the miR-148a-3p/IGF1R axis and may provide a new insight and a potential therapeutic target for HCC.	 And clinical results indicated that higher expression of KCNQ1OT1 was correlated with poor prognosis of patients with HCC. 	Yes	Next, functional studies revealed that knockdown of KCNQ1OT1 induced apoptosis and repressed proliferation, migration and invasion of HCC cells. In addition, knockdown of KCNQ1OT1 suppressed xenograft tumor growth in vivo.	33349156
HSD11B1-AS1	LncRNA	Homo sapiens	skin melanoma	MM tissues	Expression(lower expressed)	Transfection//Wound Healing Assay//CCK8//qRT-PCR//RNA-seq//Colony Formation Assay//Invasion Assay//Transwell Assay	 Using data from The Cancer Genome Atlas database, novel lncRNA 11β-hydroxysteroid dehydrogenase type 1-antisense RNA 1 (HSD11B1-AS1) was identified, which was significantly downregulated in malignant melanoma and its downregulation was significantly associated with poor clinicopathological characteristics, including advanced T and pathological stage, Clark level, Breslow depth and ulceration and worse prognosis. Functional enrichment showed significantly enriched pathways in IFN-γ and -α response, TNF-α signaling via NF-κB and IL-2/STAT-5 and IL-6/JAK/STAT-3 signaling. 	 Using data from The Cancer Genome Atlas database, novel lncRNA 11β-hydroxysteroid dehydrogenase type 1-antisense RNA 1 (HSD11B1-AS1) was identified, which was significantly downregulated in malignant melanoma and its downregulation was significantly associated with poor clinicopathological characteristics, including advanced T and pathological stage, Clark level, Breslow depth and ulceration and worse prognosis. 	Yes	 Moreover, cell experiments in vitro, including Cell Counting Kit-8, colony formation, wound healing and Transwell assay, suggested that overexpression of HSD11B1-AS1 significantly inhibited melanoma cell proliferation, migration and invasion. 	34992686
ILF3-DT	LncRNA	Homo sapiens	Colonic Neoplasms	COAD tissue	Interaction(miR-619-5p/CAMK1D Axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//CCK8//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The results showed that the expression of ILF3-AS1 was significantly higher in COAD tissue than in normal adjacent samples, and this conclusion was confirmed in the available public datasets. After further exploring the mechanisms, we found that ILF3-AS1 serves as a competitive endogenous RNA of mir-619-5p. It can bind to mir-619-5p and reduce its expression, thus regulating the target gene CAMK1D. 		Yes	After ILF3-AS1 knockdown, the proliferation of COAD cell lines SW480 and HT29 was significantly inhibited. At the same time, the apoptosis was increased, and the invasion and migration abilities were decreased. 	33737811
IL21-AS1	LncRNA	Homo sapiens	Lupus Erythematosus, Systemic	 patients with SLE	Expression(lower expressed)	Flow Cytometry//qRT-PCR//Genotyping	 IL21-AS1 was expressed in the nucleus of CD4+ T and B cells, but its expression was decreased in patients with SLE. 	 Furthermore, we observed a significant negative correlation between IL21-AS1 expression and disease activity in patients with SLE (n = 53, p < 0.05).	Yes	 IL21-AS1 expression was positively correlated with mRNA levels of IL-2 but not IL-21, and it was associated with the proportion of activated T follicular regulatory (Tfr) cells. 	34895341
IL1R1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	We identified that AC007271.3 was up-regulated and positively correlated with advanced clinical stage, lymph node metastasis, poor histological differentiation and unfavorable prognosis.Our data indicated that AC007271.3 could promote cell proliferation, invasion and inhibit cell apoptosis of OSCC via the Wnt/β-catenin signaling pathway, which might provide a novel therapeutic approach for OSCC.	We identified that AC007271.3 was up-regulated and positively correlated with advanced clinical stage, lymph node metastasis, poor histological differentiation and unfavorable prognosis.	Yes	Overexpression of AC007271.3 remarkably promoted cell proliferation in vitro and in vivo, induced cell migration, invasion and inhibited apoptosis in vitro, while knockdown of AC007271.3 attenuated cell proliferation, migration, invasion and induced apoptosis. 	31759044
IL1R1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		regulation[miR-125b-2-3p/Slug]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC//ChIP	Taken together, these results suggested that the classical NF-κB pathway-activated AC007271.3 regulates EMT by miR-125b-2-3p/Slug/E-cadherin axis to promote the development of OSCC, implicating it as a novel potential target for therapeutic intervention in this disease.		Yes	Our previous studies confirmed that dysregulated function of long non-coding RNA (lncRNA) AC007271.3 was associated with a poor prognosis and overexpression of AC007271.3 promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. 	33311454
IL-17RA-1	LncRNA	Homo sapiens	Sepsis	THP-1 cells 	Interaction(miR-7847-3p/PRKCG-Mediated MAPK Signaling Pathway)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR	In addition, IL-17RA-1 could target binding to miR-7847-3p and inhibit its expression, and miR-7847-3p could also bind to PRKCG. Our experiments demonstrate that IL17-RA-1 attenuates the sepsis response through the miR-7847-3p/MAPK pathway, and this competing endogenous RNA (ceRNA) network may be a potential approach to predict and combat sepsis.		Yes	Compared with control, si-IL-17RA-1 significantly inhibited the cell viability and migration ability of THP-1, and levels of proinflammatory factors IL-6, IL-1β, and TNF-α secreted were markedly decreased, and the expression of IL-17RA-1, PRKCG, p-MEKK1, and p-JNK were markedly reduced. 	36274974
IKBKBAS	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	Interaction(miR-4741/IKKβ/NF-κB.)	Northern Blot//Western Blot//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	 The upregulated IKBKBAS functioned as a competing endogenous RNA (ceRNA) via competing with IKKβ mRNA for binding miR-4741, consequently leading to upregulation and activation of IKKβ, and ultimately activation of NF-κB. 		Yes	Herein, we reported a novel lncRNA IKBKBAS that activated NF-κB in lung adenocarcinoma (LUAD) by upregulating IKKβ, a key member of NF-κB signaling pathway, thereby promoting the metastasis of LUAD both in vitro and in vivo. 	34702815
IGKJ2-MALLP2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues	regulation[ miR-1911-3p/p21]	qRT-PCR//Luciferase Report Assay	The results of this study showed that the expression of IGKJ2-MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage.  As indicated from the mentioned findings, IGKJ2-MALLP2, which mediates p21 expression by targeting miR-1911-3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC.	The results of this study showed that the expression of IGKJ2-MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. 	Yes	As revealed by the results of in vitro experiments, IGKJ2-MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. 	32639636
IGHA1	LncRNA	Homo sapiens	Multiple Myeloma	MM patient samples and cell lines	Expression(highly expressed)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay	 LncRNA AL was highly expressed in MM patient samples and cell lines, and was significantly correlated with the disease stage of patients. Western blot analysis showed that knockdown of lncRNA AL significantly inhibited the expression of CDK2 and cyclin D1 and promoted the expression of cyclin suppressor p21.	 LncRNA AL was highly expressed in MM patient samples and cell lines, and was significantly correlated with the disease stage of patients. 	Yes	. Knockdown of lncRNA AL significantly inhibited the proliferation and colony formation of MM cells and induced cell cycle arrest in G0/G1 phase.  Knockdown of lncRNA AL significantly inhibited the proliferation of MM cells in nude mice.	35280429
IGFL2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[IGFL2-AS1/miR-802/ARPP19 axis]	qRT-PCR	We found that IGFL2-AS1 was highly expressed in GC tissues and cell lines.Therapies targeting the IGFL2-AS1/miR-802/ARPP19 axis can potentially improve GC treatment.		Yes	Knockdown of IGFL2-AS1 suppressed GC cell proliferation, migration, and invasion in vitro. 	31943339
IGFL2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tumor tissues and cells	Interaction(HIF-1α/CA9 )	qRT-PCR//Colony Formation Assay//Western Blot	 We discovered that IGFL2-AS1 was highly upregulated in CRC tumor tissues and cells. Mechanistic studies demonstrated that IGFL2-AS1 upregulated the CA9 level by affecting the degradation pathway of HIF-1α, which elucidates its pro-proliferative effect in CRC. The lncRNA IGFL2-AS1 mediated the inhibition of HIF-1α degradation in CRC and increased CA9 expression, thereby promoting CRC progression.		Yes	 IGFL2-AS1 can functionally promote CRC cell proliferation, migration, and invasion in vitro and accelerate CRC occurrence in vivo. 	36537608
IGFL2-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	colon adenocarcinoma (COAD) tissue and cell lines (HCT116, HCT8, HCT129, and SW480)	Expression(highly expressed)	qRT-PCR//Western Blot	The lncRNA IGFL2-AS1 was highly expressed in colon adenocarcinoma (COAD) tissue and cell lines (HCT116, HCT8, HCT129, and SW480). Western blot results showed that the inhibition of IGFL2-AS1 could significantly reduce the N-cadherin, HIF1A and KRAS protein expression, yet increase the E-cadherin protein level. IGFL2-AS1 was also positively correlated with M0 macrophages, M2 macrophages, and neutrophils but negatively correlated with CD4+ memory T cells and CD8+ T cells.	The COAD patients with high IGFL2-AS1 were associated with a worse prognosis. 	Yes	Meanwhile, the knockdown of IGFL2-AS1 could significantly suppress the proliferation and invasion of COAD cells. 	34377016
IGFL2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[ AC006262.5-miR-7855-5p-BPY2C axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Interestingly, we found that AC006262.5 is significantly upregulated in HCC tissues compared with adjacent normal tissues (Fig. 1B). In addition, our results revealed that AC006262.5 bound to and regulated miR-7855-5p, a tumor-suppressive miRNA, in HCC. Moreover, our data show that AC006262.5 regulates the expression of BPY2C via miR-7855-5p. Finally, we found that AC006262.5 and miR-7855-5p formed a regulatory loop. Upregulation of AC006262.5 resulted in decreased expression of miR-7855-5p, and downregulation of miR-7855-5p further facilitated the expression of AC006262.5.		Yes	 Here, we identified an enriched long non-coding RNA, AC006262.5, associated with HCC, that promoted the proliferation, migration, and invasiveness of HCC cells, both in vitro and in vivo.	32956593
IGFL2-AS1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC cells and tissues	Interaction(SATB1/Wnt/β-catenin signaling pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 IGFL2-AS1 was significantly up-regulated in TSCC cells and tissues, and IGFL2-AS1 knockdown inhibited cell proliferation, migration, invasion and EMT in TSCC. Moreover, IGFL2-AS1 functioned as a competing endogenous RNA (ceRNA) to sponge miR-1224-5p and thereby modulated SATB homeobox 1 (SATB1) expression. Additionally, SATB1 activated the Wnt/β-catenin signaling pathway in TSCC cells and IGFL2-AS1 regulated the Wnt/β-catenin signaling pathway and TSCC progression via elevating SATB1 expression.		Yes	 IGFL2-AS1 was significantly up-regulated in TSCC cells and tissues, and IGFL2-AS1 knockdown inhibited cell proliferation, migration, invasion and EMT in TSCC. 	34085359
IGFBP4-1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues 	regulation[JAK/STAT signaling pathway]	Western Blot//CCK8//qRT-PCR//Cell Apoptosis Assay//Cell Cycle Assay	The results showed that IGFBP4-1 was overexpressed in bladder cancer tissues compared with that in normal bladder tissues, and its expression level was positively correlated with poor prognosis in bladder cancer patients. In conclusion, IGFBP4-1 promoted bladder cancer progression by activating the JAK/STAT signaling pathway. 	The results showed that IGFBP4-1 was overexpressed in bladder cancer tissues compared with that in normal bladder tissues, and its expression level was positively correlated with poor prognosis in bladder cancer patients.	Yes	Overexpression of IGFBP4-1 markedly promoted cell proliferation and cell cycle progression, and inhibited cell apoptosis, while knockdown of IGFBP4-1 notably suppressed the proliferation, promoted cell apoptosis, and induced cell cycle arrest at the G0/G1 phase. 	32760196
IGF2BP2-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissuses	Regulation(Wnt/β-catenin pathway)	qRT-PCR//Transwell Assay	 In comparison with the normal tissue samples, OSCC showed higher expression of IGF2BP2-AS1 . Western blotting showed that expressions of β-catenin, Cyclin D1, Bcl-2, and MMP2 were downregulated, whereas Bax was upregulated following knockdown of IGF2BP2-AS1. The inhibitory effect of knockdown of IGF2BP2-AS1 on migration could be partially reversed by the Wnt/β-catenin pathway stimulator LiCl.	High expression of IGF2BP2-AS1 was associated with poor survival in OSCC patients. 	Yes	Further in vitro functional tests demonstrated that downregulation of IGF2BP2-AS1 in Cal27 and SCC9 cells significantly inhibited cell proliferation and migration, leading to cell-cycle arrest and cell apoptosis. 	34637162
IGF2-AS	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	interaction[ miR-195/CREB1 axis]	Flow Cytometry//qRT-PCR//RIP//Western Blot	Our data revealed that IGF2-AS was upregulated in GC tissues and predicted poor prognosis. In conclusion, our study suggested that IGF2-AS knockdown suppressed glycolysis and facilitated apoptosis in GC cells at least partly through sponging miR-195 and modulating CREB1 expression, highlighting a novel therapeutic strategy for GC treatment.		Yes	 IGF2-AS knockdown hampered glycolysis and accelerated apoptosis of GC cells.	34321174
IGF2-AS	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues, cell lines, and plasma	regulation[ PI3K/AKT/mTOR signaling pathway]	qRT-PCR//ChIP//RIP//Western Blot	 Here, we found that IGF2 antisense RNA (IGF2-AS) was significantly decreased in breast cancer tissues, cell lines, and plasma.Further investigation revealed that IGF2-AS inhibited the expression of its sense-cognate gene IGF2 in an epigenetic DNMT1-dependent manner, resulting in the inactivation of downstream oncogenic PI3K/AKT/mTOR signaling pathway. 	Patients with low IGF2-AS were more likely to develop larger tumor size and later clinical stage.	Yes	Overexpression of IGF2-AS evidently inhibited the proliferation and induced apoptosis of MCF-7 and T47D cells in vitro, as well as retarded tumor growth in vivo.	33175607
IGF2-AS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(microRNA-520h/cyclin-dependent kinase inhibitor 1A signaling pathway)	qRT-PCR//Western Blot	Our results showed that IGF2-AS expression was significantly down-regulated in HCC cells and tissues; lower IGF2-AS expression was significantly associated with poor prognosis of HCC patients; IGF2-AS sponged microRNA-520h (miR-520h) to up-regulate IGF2-AS expression, and miR-520h over-expression or cyclin-dependent kinase inhibitor 1A (CDKN1A) silencing reversed IGF2-AS reduced aggressive behaviors of HCC cells. 		Yes	IGF2-AS over-expression inhibited the viability, colony formation, invasion, and migration, while promoted apoptosis in vitro, and inhibited HCC xenograft growth in vivo; 	34516353
IL6-AS1	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive	patients	Interaction(miR-149-5p/ IL-6)	RNA Pull-Down//ISH//Transfection//qRT-PCR//FISH//RIP//Luciferase Report Assay	We identified a novel long noncoding RNA (lncRNA), interleukin 6 antisense RNA 1 (IL6-AS1), which is upregulated in this disease and is associated with airway inflammation. Mechanistically, cytoplasmic IL6-AS1 acts as an endogenous sponge by competitively binding to the microRNA miR-149-5p to stabilize IL-6 mRNA.		Yes	We found that IL6-AS1 promotes the expression of inflammatory factors, especially interleukin (IL) 6.	34323408
ILF3-DT	LncRNA	Homo sapiens	Retinoblastoma	RB tissues and cell lines	regulation[miR-132-3p/SMAD2 axis]	qRT-PCR	 In the present study, our work revealed that the lncRNA ILF3-AS1 was increased in both RB tissues and cell lines.Collectively, these data indicate that ILF3-AS1 is involved in RB progression through the miR-132-3p/SMAD2 axis, providing a novel and promising biomarker that can be used for the treatment of RB.		Yes	Repression of ILF3-AS1 suppressed both RB cell proliferation and invasion in vitro. ILF3-AS1 also promoted tumor growth in vivo.	32407730
IGF2-AS	LncRNA	Homo sapiens	gastric adenocarcinoma	GAC tissues	Interaction[sponging miR-503]	Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Colony Formation Assay//Transwell Assay	Our study found that lncRNA insulin growth factor 2 antisense (IGF2-AS) is up-regulated in gastric adenocarcinoma (GAC) tissues and correlated with poor prognosis in patients with GAC.Taken together, our results demonstrated that IGF2-AS takes important regulatory parts in GAC development by functioning as a ceRNA to regulate SHOX2 via sponging miR-503.		Yes	 In vivo tumorigenicity assay showed that knockdown of IGF2-AS significantly reduced tumor volume.	31183590
ILF3-DT	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal tissues	Expression[highly expressed]	qRT-PCR	lncRNA ILF3-AS1 expression was significantly up-regulated in the 68 nasopharyngeal carcinoma tissue samples compared to their adjacent normal tissue samples.	 Increased lncRNA ILF3-AS1 level was related to the advanced tumor node metastasis stage and the metastasis of nasopharyngeal carcinoma. Also, increased lncRNA ILF3-AS1 indicated poor prognosis of nasopharyngeal carcinoma patients.	Yes	Inhibition of lncRNA ILF3-AS1 reduced proliferation, invasion and migration of nasopharyngeal carcinoma cells.	32962500
IQANK1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cancer tissues and cell lines 	Expression[highly expressed]	qRT-PCR	In the present study, it was determined that, in comparison with paired para-tumorous tissues or normal esophageal epithelial cells, FAM83H-AS1 expression in cancer tissues and cell lines was markedly upregulated. 	Furthermore, FAM83H-AS1 expression was significantly elevated in patients with ESCC and lymph node metastasis or a late TNM stage, while no association with any other clinicopathological characteristics was detected.Furthermore, the overall and disease-free survival, as assessed by the Kaplan-Meier method, were significantly shortened in patients with high FAM83H-AS1 expression. 	Yes	A functional study then uncovered that knockdown of FAM83H-AS1 significantly suppressed the proliferation and migration of ESCC cells. 	33154766
IQANK1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Western Blot	In the present study, our results confirmed that lncRNA FAM83H-AS1 expression was overexpressed in HCC tissues relative to the adjacent normal tissues.Moreover, we found that the downregulating expression of lncRNA FAM83H-AS1 inhibited Wnt/β-catenin pathway by reducing β-catenin and WNT1 expression in HCC cells.	Furthermore, higher lncRNA FAM83H-AS1 expression significantly associated with tumor size and vascular invasion in patients with HCC. The Kaplan-Meier methods and log rank test demonstrated that increased lncRNA FAM83H-AS1 expression associated with shorter patient overall survival compared to lower lncRNA FAM83H-AS1 expression in patients with HCC.	Yes	Moreover, function assays by CCK-8 cell proliferation and transwell cell migration and invasion assays showed that the knockdown of lncRNA FAM83H-AS1 significantly inhibited cell proliferation, migration, and invasion ability in HCC. 	31599410
IQANK1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues,cell lines	Expression[Expression[highly expressed]-expression]	CCK8//qRT-PCR	 First, qRT-PCR was used to detect the expression of lncRNA FAM83H-AS1 in OC tissues and cell lines. The results showed that lncRNA FAM83H-AS1 was significantly Expression[Expression[up-expression]-expression]-regulated in both OC tissues and OC cells when compared with normal controls.		Yes	"The re_x0002_sults showed that Si-FAM83H-AS1 transfection 
significantly inhibited the expression of lncRNA 
FAM83H-AS1 in vitro. (Figure 3A)."	31210291
IQANK1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues,cell lines	Expression[highly expressed]	qRT-PCR//RNA Pull-Down//RIP	First of all, the obvious upregulation of FAM83H-AS1 was identified by qRT-PCR in OC tissues, especially in metastatic tissues, as well as in OC cell lines.		Yes	Through loss-of-function assays, we validated the inductive effect of FAM83H-AS1 in OC cell metastasis and radioresistance.	30831080
IQANK1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissue, cell lines	Expression[highly expressed]	qRT-PCR	In our results, the expression of FAM83H-AS1 was obviously elevated in bladder cancer tissue samples and bladder cancer cell lines compared with adjacent normal tissue samples and normal bladder epithelial cell lines, respectively. 	In addition, high expression of FAM83H-AS1 was associated with advanced clinical stage and the presence of muscularis invasion and served as an independent poor prognostic factor for overall survival in patients with bladder cancer. 	Yes	The loss-of-function study showed that silencing FAM83H-AS1 expression suppressed cell proliferation, migration, and invasion and induced cycle arrest at G0/G1 phase. 	30537032
IQANK1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues,cell lines	regulation[c-Myc-mediated ULK3]	Western Blot//Tunel//Colony Formation Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//IHC//Transwell Assay	High expression of FAM83H-AS1 was found in 82 BCa tissues and in BCa cell lines compared to the normal ones.This study evidenced that FAM83H-AS1 upregulates ULK3 expression through the transcription factor c-Myc and promotes the progression of BCa.		Yes	FAM83H-AS1 downregulation in T24 and BK10 cells inhibited viability, colony formation, migration, invasion, and angiogenesis of BCa cells and increased cell apoptosis. 	33289601
IQANK1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 tumor tissues and serum of patients with PDAC	Interaction(FAM83H/Wnt/β-catenin signaling)	CCK8//qRT-PCR//Wound Healing Assay	FAM83H-AS1 was highly expressed in the tumor tissues and serum of patients with PDAC, and was correlated with shorter survival.  Importantly, FAM83H protein manifested the similar malignant functions as that of FAM83H-AS1 in PDAC cells, and could bind to β-catenin. Specifically, FAM83H could decrease the ubiquitylation of β-catenin, and accordingly activated the effector genes of Wnt/β-catenin signaling.	FAM83H-AS1 was highly expressed in the tumor tissues and serum of patients with PDAC, and was correlated with shorter survival. 	Yes	 FAM83H-AS1 significantly promoted the proliferation, invasion and metastasis of PDAC cells, by protecting FAM83H mRNA from degradation. 	36171592
IQANK1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cell lines 	Interaction[E6-p300 pathway]	CCK8//RNA-seq	Interestingly, FAM83H-AS1 was found overexpressed in HPV-16 positive cervical cancer cell lines in an HPV-16 E6-dependent manner but independently of p53 regulation. Furthermore, FAM83H-AS1 was found to be regulated through the E6-p300 pathway. 		Yes	Knockdown of FAM83H-AS1 by siRNAs decreased cellular proliferation, migration and increased apoptosis. 	30842470
IQANK1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells and tissues	regulation[miR-136-5p/metadherin axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Our data show that the FAM83H-AS1 levels are increased in human TNBC cells and tissues. Together, our results demonstrate that FAM83H-AS1 functions as an oncogenic lncRNA that regulates miR-136-5p and MTDH expression during TNBC progression, and suggest that targeting the FAM83H-AS1/miR-136-5p/MTDH axis may serve as a novel therapeutic target in TNBC.		Yes	Importantly, our in vivo data show that FAM83H-AS1 also promotes tumor growth in TNBC mouse xenografts.	32074085
IQANK1	LncRNA	Homo sapiens	Prostatic Neoplasms	 cell lines	regulation[miR-15a/CCNE2 Axis]	ChIP//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, the results validate that AR signaling is involved in upregulating FAM83H-AS1 expression in PCa cells.Mechanically, we found that FAM83H-AS1 plays its roles through sponging miR-15a to promote CCNE2 expression. These findings indicate that FAM83H-AS1 is a novel diagnostic and therapeutic marker for PCa.		Yes	Loss-of-function assays demonstrate that FAM83H-AS1 acts as an oncogene in PCa by modulating cell proliferation, cell cycle, and migration. 	33614501
IPW	LncRNA	Homo sapiens	Carcinoma, Ductal	DCIS cells	Interaction( IPW-miR-29c-ID2 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Cell Proliferation Assay//Cell Cycle Assay//IHC//ChIP	We identified lncRNA IPW as a novel tumor suppressor critical for inhibiting DCIS growth.Ectopic expression of IPW in DCIS cells strongly inhibited cell proliferation, colony formation and cell cycle progression while silencing IPW in primary breast cells promoted their growth. Additionally, orthotropic implantation of cells with ectopic expression of IPW exhibited decreased tumor growth in vivo. Mechanistically, IPW epigenetically enhanced miR-29c expression by promoting H3K4me3 enrichment in its promoter region.		Yes	We identified lncRNA IPW as a novel tumor suppressor critical for inhibiting DCIS growth.Ectopic expression of IPW in DCIS cells strongly inhibited cell proliferation, colony formation and cell cycle progression while silencing IPW in primary breast cells promoted their growth. Additionally, orthotropic implantation of cells with ectopic expression of IPW exhibited decreased tumor growth in vivo. 	35078502
INHBA-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[AKT1 pathway]	qRT-PCR//RIP	The present study identified INHBA-AS1 as a kind of lncRNA with high expression in CRC tissues and cells.In summary, LncRNA INHBA-AS1 contributes to CRC progression through AKT1 pathway, and provides a new mechanism to regulate CRC development, as well as a potential target for treating CRC.		Yes	 Functionally, NHBA-AS1 downregulation in CRC cells suppressed CRC cell proliferation as well as colony formability. 	33090398
ILF3-DT	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-4429/RAB14 )	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. 		Yes	 ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. 	33525948
ILF3-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Expression [highly expressed]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	ILF3-AS1 and EZH2 increased, whereas CDKN2A reduced in CRC tissues and cells.	 ILF3-AS1 and EZH2 expression was linked to Dukes stage, distant metastasis, vascular invasion, and lymph node metastasis of CRC patients. 	Yes	Depleted ILF3-AS1 or reduced EZH2 suppressed proliferation, migration, colony-formation, and invasion ability, as well as facilitated apoptosis of CRC cells and attenuated the tumor growth in CRC mice.	34141456
ILF3-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Expression(highly expressed)	qRT-PCR//MeRIP//RNA Pull-Down//RIP	Here, we found that ILF3-AS1 expression was significantly elevated in HCC tissues and also associated with prognosis of patients with HCC.Mechanistically, ILF3-AS1 associated with ILF3 mRNA and inhibited its degradation. ILF3-AS1 increased ILF3 m6A level via recruiting N6-methyladenosine (m6A) RNA methyltransferase METTL3. Moreover, IFL3-AS1 enhanced the interaction between ILF3 mRNA and m6A reader IGF2BP1. 	Here, we found that ILF3-AS1 expression was significantly elevated in HCC tissues and also associated with prognosis of patients with HCC.	Yes	 Functional assays demonstrated that knockdown of ILF3-AS1 expression resulted in the suppression of proliferation, migration and invasion in HCC cells, whereas overexpression of ILF3-AS1 exerted opposite effects. Additionally, knockdown of IFL3-AS1 attenuated HCC tumorigenesis and metastasis in vivo. 	34491544
ILF3-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 hepatocellular carcinoma cells	Interaction(miR-628-5p/MEIS2 axis)	qRT-PCR	RT-qPCR analysis revealed that ILF3-AS1 was significantly upregulated in hepatocellular carcinoma cells.  Luciferase reporter, RNA pull down and RIP assays were used to investigate the relationship between ILF3-AS1 and downstream target genes. ILF3-AS1 competed with meis homeobox 2 (MEIS2) for miR-628-5p in hepatocellular carcinoma cells. ILF3-AS1 elevated the levels of key proteins on the Notch pathway.		Yes	 The hepatocellular carcinoma cell viability was suppressed by silenced ILF3-AS1. Transwell and wound healing assays showed that ILF3-AS1 downregulation inhibited cell invasion and migration. The levels of proteins associated with epithelial-mesenchymal transition (EMT) process and the Notch pathway were detected by western blot analysis. 	34053876
ILF3-DT	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Regulation[miR-212/SOX5 axis]	qRT-PCR	In this study, we showed that ILF3-AS1 expression was significantly up-regulated in both osteosarcoma tissues and cell lines.	 Clinical assays revealed that higher expression of ILF3-AS1 was associated with advanced clinical stage, distant metastasis and shorter overall survival. 	Yes	Functional investigations showed that knockdown of ILF3-AS1 suppressed the proliferation, migration and invasion of osteosarcoma cells, and promoted apoptosis. 	30819403
ILF3-DT	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	human CC tissues and cells	Interaction(miR‑454‑3p / PTEN)	Western Blot//Bioinformatics Analysis//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Survival Analysis//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The present study demonstrated that ILF3‑AS1 expression was significantly downregulated in human CC tissues and cells compared with adjacent tissues (ANTs) and normal cervical epithelial cells (NCEs), respectively. In conclusion, the present study indicated that ILF3‑AS1 inhibited CC cell proliferation and migration, and promoted CC cell apoptosis by inhibiting epithelial‑mesenchymal transition, and ILF3‑AS1 overexpression partially reversed the inhibitory effect of miR‑454‑3p on PTEN expression.	Patients with CC with high ILF3‑AS1 expression displayed higher survival rates compared with patients with low ILF3‑AS1 expression. 	Yes	Compared with the negative control (NC) group, ILF3‑AS1 overexpression significantly inhibited CC cell viability and migration, but significantly increased CC cell apoptosis. Moreover, ILF3‑AS1 overexpression significantly upregulated E‑Cadherin expression levels, but significantly downregulated N‑Cadherin and snail family transcriptional repressor 1 expression levels compared with the NC group. 	34080029
IGF2-AS	LncRNA	Homo sapiens	Prostatic Neoplasms	Pca tissues, cell lines	Regulation[ IGF2AS/IGF2 axis]	CCK8//qRT-PCR//Transwell Assay	IGF2AS was downregulated in both PCa cell lines and human PCa tumors. IGF2 was downregulated by IGF2AS overexpression. Conversely, IGF2 upregulation revered the suppressing function of IGF2AS on PCa proliferation and invasion.		Yes	 In VCaP and PC3 cells, lentivirus-induced IGF2AS overexpression suppressed cancer cell proliferation and invasion in vitro, and xenograft development in vivo.	30423304
IGF2-AS	LncRNA	Homo sapiens	Endometriosis	endometriotic cells	Interaction(miR-370-3p/IGF2 axis/PI3K/AKT/mTOR)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Invasion Assay//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Furthermore, insulin-like growth factor 2 antisense RNA (IGF2-AS) was uncovered to positively regulate IGF2 expression and enhanced proliferative, migratory, and invasive abilities of endometriotic cells. Mechanistically, miR-370-3p was found to bind with IGF2-AS and IGF2. IGF2-AS competitively bind with miR-370-3p to upregulate IGF2. Furthermore, IGF2-AS was revealed to activate the PI3K/AKT/mTOR signaling pathway through targeting miR-370-3p/IGF2 axis.		Yes	Furthermore, insulin-like growth factor 2 antisense RNA (IGF2-AS) was uncovered to positively regulate IGF2 expression and enhanced proliferative, migratory, and invasive abilities of endometriotic cells. 	36508036
KCNQ1OT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(microRNA‑504/CDK16)	qRT-PCR	In this study, we demonstrated that the expression of KCNQ1OT1 was abnormally increased in HCC tissues. Additionally, we found that KCNQ1OT1 exerted its effects partly by relying on the microRNA‑504 (miR‑504)‑mediated regulation of cyclin‑dependent kinase 16 (CDK16), in addition to the regulation of the glycogen synthase kinase 3β (GSK3β)/β‑catenin/Bcl‑2 signaling pathway. 	The ectopic high expression of KCNQ1OT1 was associated with liver cirrhosis, a larger tumor size, an advanced TNM stage, and a worse overall survival and tumor?free survival. 	Yes	 For the first time, to the best of our knowledge, we report that KCNQ1OT1 knockdown results in a decreased cell viability and colony formation ability, and an increased rate of apoptosis in vitro. The results from our in vivo results demonstrated that KCNQ1OT1 silencing attenuated tumor growth by impairing cell proliferation.	29532864
HULC	LncRNA	Homo sapiens	Colonic Neoplasms	CRC tissues and adjacent NCTs,cell lines(HCT116，SW480，HT30,LoVo)	Interaction[ miR-613 ]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	HULC was markedly up-regulated in 76.1% (51/67) of colon cancer tissues compared to the adjacent normal colon tissues. The findings in the study suggested that HULC might inhibit the tumor growth through miR-613 dependent RTKN modulation.	 	Yes	 HULC knockdown suppressed the proliferation, DNA synthesis and metastasis of human colon cancer cells in vitro. 	30551459
HULC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell line	regulation[miR-377-5p/HIF-1α pathway]	qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 The mRNA and protein expression levels of HULC were markedly increased, whereas the mRNA expression levels of miR-377-5p were decreased in HCC cell lines. In summary, our in vitro and in vivo findings confirmed HULC to play a role in the progression of HCC, with the underlying mechanism possibly involving the miR-377-5p/HIF-1α pathway.		Yes	HepG2 cell proliferation and invasion were suppressed in the Sh-HULC group, while miR-377-5p showed the opposite.Importantly, the in vivo experiments indicated that down-regulation of HULC could inhibit tumor growth.	33209874
HULC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	liver cancer cells	Interaction(miR-3200-5p/ATF4 Axis)	qRT-PCR	Here, we show that knockdown of HULC increases ferroptosis and oxidative stress in liver cancer cells. We also found changes in some related miRNAs in cells treated with HULC siRNA. Differential miRNA expression levels were determined with the use of high-throughput sequencing and prediction target genes identified using bioinformatics analysis. HULC was found to function as a ceRNA of miR-3200-5p, and miR-3200-5p regulates ferroptosis by targeting ATF4, resulting in the inhibition of proliferation and metastasis within HCC cells. In summary, these findings illuminate some of the molecular mechanisms through which downregulation of HULC induces liver cancer cell ferroptosis by targeting the miR-3200-5p/ATF4 axis to modulate the development of hepatocellular carcinoma.		Yes	Here, we show that knockdown of HULC increases ferroptosis and oxidative stress in liver cancer cells.	35615577
HULC	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	Oral cancer tissues and their adjacent normal tissues,cell lines (SCC9, SCC15, SCC25, CAL27) 	 Expression[highly expressed]	CCK8//qRT-PCR//Western Blot	Analysis of 30 pairs of clinical oral cancer tissues and their adjacent normal tissues revealed that HULC expression was higher in the cancer tissues than in the normal tissues.We also measured HULC levels in four OSCC cell lines (SCC15, SCC25, SCC9 and CAL27), which revealed that HULC expression was markedly up-regulated in the cancer cell lines relative to that in a normal oral keratinocyte cell line.	 	Yes	We report that HULC was abnormally up-regulated in oral cancer tissues and OSCC cell lines, and that suppression of HULC expression in OSCC cells not only inhibited the proliferation, drug tolerance, migration and invasion of the cancer cells, but also increased their apoptosis rate. Notably, in a mouse xenograft model, HULC depletion reduced tumorigenicity and inhibited the epithelial-to-mesenchymal transition process.	30677230
HULC	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	regulation[miR-372-3p/HMGB1 signalling axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our results revealed elevated HULC and decreased miR-372-3p expression in both osteosarcoma tissues and cell lines.Our study is the first to demonstrate that HULC may act as a ceRNA to modulate HMGB1 expression by competitively sponging miR-372-3p, leading to the regulation of osteosarcoma progression, which provides new insight into osteosarcoma diagnosis and treatment.		Yes	Overexpression of HULC or knockdown of miR-372-3p promoted osteosarcoma cell proliferation, migration and invasion and induced cell apoptosis.	32188407
HULC	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	Regulation(PTEN/AKT-PI3K-mTOR)	qRT-PCR//Western Blot	The expression of HULC was obviously higher in osteosarcoma tissues and cells compared with normal control. Furthermore, HULC increased the activity of AKT-PI3K-mTOR pathway by blocking PTEN in osteosarcoma cells. LY294002 inhibited the phosphorylation of AKT, mTOR, and PI3K. Overexpressing HULC enhanced cell migration and invasion of SAOS-2 cells and MG63 cells, while LY294002 reversed the effects.		Yes	 Moreover, cell proliferation, migration, and invasion were inhibited by HULC knockdown in osteosarcoma cells. HULC overexpression markedly increased osteosarcoma cell proliferation and tumor size in vivo.	36213832
HULC	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cell lines	regulation[miR-218/TPD52 Axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	HULC expression was upregulated in cervical cancer cell lines, and HULC promoted cervical cancer cell proliferation, migration and invasion.HULC promotes cervical cancer cell proliferation, migration and invasion via miR-218/TPD52 axis.		Yes	HULC expression was upregulated in cervical cancer cell lines, and HULC promoted cervical cancer cell proliferation, migration and invasion.	32103980
HULC	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(FOXM1/AGR2/HIF-1α axis)	RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Microarray// In Vivo Experiment//IHC//ChIP	HULC was upregulated in GBM tissues and GSCs, which may promote the progression of glioma.  In addition, HULC further stabilized FOXM1 expression in GSCs through ubiquitination, while FOXM1 activated AGR2 transcription to promote HIF-1α expression. Moreover, HULC promoted the glycolysis and stemness of GSCs through its regulation of the FOXM1/AGR2/HIF-1α axis, consequently exacerbating the occurrence and development of glioma.		Yes	On the other hand, silencing of HULC reduced the stemness, inhibited the proliferation, and promoted the apoptosis and differentiation of GSCs. 	35013529
HULC	LncRNA	Homo sapiens	Glioblastoma	U87 cells	regulation[RRAS expression]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	The results of present study suggest that lncRNA HULC promotes GBM cell proliferation, invasion, and migration by regulating RRAS expression, suggesting that RRAS may be a potential biomarker or therapeutic target for this cancer.		Yes	Overexpression of HULC led to increased cell proliferation, invasion, and migration. 	32606802
HULC	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	regulation[PI3K/AKT and Wnt/β-catenin pathways]	CCK8//qRT-PCR//Cell Apoptosis Assay//Western Blot	We discovered that HULC and miR-106a had relative high expression levels in PTC tissues and cells.Moreover, HULC overexpression boosted PI3K/AKT and Wnt/β-catenin pathways activities via raising miR-106a expression.		Yes	HULC overexpression enhanced TPC-1 cells viability and cell proliferative, migratory and invasive abilities. Silencing HULC induced TPC-1 cell apoptosis. 	31878795
HULC	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues,blood	Regulation[Wnt/β-catenin signaling pathway ]	CCK8//qRT-PCR//Transwell Assay//Western Blot	Highly expressed in the tissues and serum of pancreatic cancer patients, HULC showed good clinical value in distinguishing between patients with pancreatic cancer, patients with benign pancreatic diseases and healthy subjects.HULC is an effective marker for the diagnosis and prognosis of pancreatic cancer, which may affect the biological function of pancreatic cancer cells through the Wnt/β-catenin signaling pathway.	Patients with low expression of HULC had a significantly higher 3-year overall survival (OS) and 5-year OS than those with high expression. T staging, M staging, vascular invasion, and HULC were independent prognostic factors affecting the 3-year OS of patients with pancreatic cancer.	Yes	 Inhibition of HULC expression prevented the proliferation and invasion of pancreatic cancer cells, promoted apoptosis, and inhibited the expression of Wnt/β-catenin signaling pathway-related proteins, β-catenin, c-myc, and cyclin D1.	31857775
HULC	LncRNA	Homo sapiens	Pancreatic Neoplasms	PDAC cells	regulation[EMT signaling]	qRT-PCR//Luciferase Report Assay//Transwell Assay//Western Blot	 We previously verified that lncRNA HULC is up-regulated in PDAC cells and the intercellular transfer of HULC by EVs can promote PDAC cell invasion and migration through the induction of epithelial-mesenchymal transition (EMT). These results provide mechanistic insights into the development of PDAC by demonstrating that miR-622, as a miRNA downregulated by TGF-β, could target HULC and suppress invasion and migration by inhibiting EMT signaling via EV transfer. 		Yes	 We previously verified that lncRNA HULC is up-regulated in PDAC cells and the intercellular transfer of HULC by EVs can promote PDAC cell invasion and migration through the induction of epithelial-mesenchymal transition (EMT). 	32656089
HULC	LncRNA	Homo sapiens	Bone Neoplasms	neoplasm cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	 Compared to the human normal bone cell line, we found lncRNA HULC was over-expressed in all 6 bone neoplasm cell lines, and we finally chose HT1080 and Saos-2 cell lines, which possessed the highest lncRNA HULC expression level, for the subsequent studies.	We then observed that the expression level of lncRNA HULC was negatively correlated with overall survival rate of bone neoplasm patients, which means that lncRNA HULC has prognostic value in patients with bone neoplasms.	Yes	LncRNA HULC can promote the tumorigenesis of bone neoplasms through increasing the proliferation, invasion, and migration abilities and the expression level of EMT-related factors.	30120220
HULC	LncRNA	Homo sapiens	ovarian carcinoma	ovarian carcinoma tissue 	Expression[highly expressed]	CCK8//qRT-PCR	 In this study, we observed that circular RNA-ITCH was downregulated, while lncRNA HULC was upregulated in ovarian carcinoma. 		Yes	Overexpression of circular RNA-ITCH resulted in inhibited, while overexpression of HULC promoted the proliferation of cells of ovarian cancer cell lines.	32046413
HULC	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues and paired adjacent liver tissues,blood	Expression[highly expressed]	Western Blot//qPCR//CCK8//Luciferase Report Assay//Transwell Assay	HULC expression in serum exosomes of patients with HCC was higher than that in serum exosomes of healthy controls, and HULC levels were higher in liver cancer tissues than in tumor adjacent tissues. 	 The expression of HULC in serum exosomes and liver cancer tissues correlated with the tumor-node-metastasis (TNM) classification, and HULC expression in tissues correlated with that in serum exosomes.	Yes	Upregulation of HULC promoted HCC cell growth and invasion and repressed apoptosis. 	31558873
HULC	LncRNA	Homo sapiens	Liver Neoplasms	 human liver tumors	Interaction(p65/IkBkB/LC3II )	In Vivo Experiment//IHC//Western Blot//Migration Assay//qRT-PCR//Colony Formation Assay//Invasion Assay//IF	HULC was identified as a lncRNA that is highly upregulated in human liver tumors.  At a mechanistic level, HULC was able to promote the phosphorylation of p65 and IkBkB thus enhancing autophagy by increasing LC3II levels in a manner dependent upon the NF-κB pathway. HULC downregulation was also linked to impaired orthotopic HCC tumor growth in vivo. The link between HULC and autophagy may play a role in disease progression.		Yes	 In vitro, HULC was able to promote HCC malignancy, although its excess overexpression also led robust autophagic induction, promoting the increased expression of autophagy-associated genes including LC3 and Beclin-1. 	36213936
HULC	LncRNA	Homo sapiens	lung squamous cell carcinoma	LSCC tissues	Regulation[ PTPRO/NF-κB signaling pathway]	qRT-PCR	Significantly decreased level of lncRNA HULC was observed in LSCC samples compared with adjacent tissues.Moreover, lncRNA HULC could promote the proliferation of LSCC cells by downregulating the expression PTPRO dependent on the phosphorylation and activation of nuclear factor-κB (NF-κB). The present study firstly shows strong evidence supporting a critical role of lncRNA HULC in promoting LSCC by regulating PTPRO/NF-κB signaling pathway, which provides new promising biomarkers for LSCC.		Yes	Moreover, lncRNA HULC could promote the proliferation of LSCC cells by downregulating the expression PTPRO dependent on the phosphorylation and activation of nuclear factor-κB (NF-κB). 	31448453
HULC	LncRNA	Rattus norvegicus	Myocardial Reperfusion Injury	IR-injured myocardial tissue and the H/R-induced H9c2 cell	Interaction(miR-377-5p -NLRP3/Caspase-1/IL-1β axis )	Western Blot//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//ELISA	We found that HULC was downregulated and miR-377-5p was upregulated in IR-injured myocardial tissue and the H/R-induced H9c2 cell. Strikingly, dual luciferase reporter assay showed that HULC was a sponge of miR-377-5p. Subsequently, mechanism experiments revealed that NLRP3/Caspase‑1/IL‑1β was a target axis of miR-377-5p. Finally, rescue assay suggested that HULC-miR-377-5p -NLRP3/Caspase‑1/IL‑1β axis regulated the apoptosis and inflammation of H/R-induced H9c2 cells.		Yes	 In vitro, the protective effect of HULC overexpression on H9c2 cell viability and inflammation was offset by miR-377-5p silencing.	32674625
HSPA7	LncRNA	Homo sapiens	Glioblastoma	GBM TISSUES	Epigenetics(methylation)	Western Blot//Transfection//FISH//Transwell Assay//IF	We identified the m6A-modified pseudogene HSPA7 as a novel prognostic risk factor in GBM patients, with crucial roles in immunophenotype determination, stromal activation, and carcinogenic pathway activation. 		Yes	 We confirmed that HSPA7 promoted macrophage infiltration and SPP1 expression via upregulating the YAP1 and LOX expression of glioblastoma stem cells (GSCs) in vitro and in our clinical GBM tumor samples. We also confirmed that knockdown of HSPA7 might increase the efficiency of anti-PD1 therapy utilizing the GBO model, highlighting its potential as a novel target for immunotherapy.	34354698
HSPA7	LncRNA	Homo sapiens	Vascular Diseases	 Human aortic smooth muscle cells	Interaction(miR-223 )	Migration Assay//qRT-PCR//RIP//RNA-seq//ELISA	Among 380 RNAs differentially expressed between the plaque and control tissues, lncRNA HSPA7 was selected and confirmed to show upregulated expression upon oxLDL treatment. The effects of miR-223 inhibition and HSPA7 knockdown were also found in THP-1 cell-derived macrophages. The impact of HSPA7 on miR-223 was mediated in an AGO2-dependent manner. HSPA7 is differentially increased in human atheroma and promotes the inflammatory transition of vascular smooth muscle cells by sponging miR-223. 		Yes	 HSPA7 knockdown inhibited the migration of HASMCs and the secretion and expression of IL-1β and IL-6; however, HSPA7 knockdown recovered the oxLDL-induced reduction in the expression of contractile markers. Although miR-223 inhibition promoted the activity of Nf-κB and the secretion of inflammatory proteins such as IL-1β and IL-6, HSPA7 knockdown diminished these effects. 	34857901
HULC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[HULC/miR-2052/MET axis]	Western Blot//CCK8//RIP//qRT-PCR//Luciferase Report Assay	In the present study, we showed that HULC is overexpressed in HCC tissues, which correlates with an unfavorable prognosis in HCC patients.Our mechanistic studies showed that HULC works as a competing endogenous RNA for miR-2052, and that the MET receptor tyrosine kinase is a downstream target of miR-2052 in HCC. Furthermore, HULC inhibits miR-2052, thereby stimulating MET expression in HCC. Finally, MET overexpression reverses the effects of HULC depletion. In sum, our findings reveal a novel regulatory signaling cascade, the HULC/miR-2052/MET axis, which could potentially be exploited for therapeutic benefits in the treatment of HCC.		Yes	We also found that HULC promotes the proliferation, migration, and invasion of HCC cells in vitro, and xenograft tumor growth in vivo. 	31645479
HULC	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues	Regulation[PI3K/Akt pathway]	CCK8//qRT-PCR//MTT//Western Blot	 HULC expression level was increased in tumor tissues compared with adjacent healthy tissues in most patients.Serum level of HULC was higher in cancer patients than that in healthy control. LncRNA HULC overexpression can promote NSCLC cell proliferation and inhibit cell apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and further induce the activation of its downstream PI3K/Akt pathway.	 Serum level of HULC was increased with the increased stage of primary tumor (T stage). Serum HULC can be used to accurately predict NSCLC and its prognosis.	Yes	 HULC overexpression promoted tumor cell proliferation, but inhibited cell apoptosis. HULC overexpression also increased expression level of SPHK1 and phosphorylation level of Akt in NSCLC cell, but showed on significant effects on Akt expression. 	30575912
IGF1R	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissues and lung cancer cell lines	Expression[lower expressed]	qRT-PCR//RNA-seq	The expression level of circ-IGF1R was notably lower in lung cancer tissues and lung cancer cell lines than in the adjacent normal tissues and cells (P < 0.0001).	 In addition, the expression level of circ-IGF1R was associated with larger tumors (T2/T3/T4) and lymph node metastasis (N1/ N2/N3) (P < 0.05). 	Yes	 The overexpression of circ-IGF1R significantly inhibited the invasion and migration of the lung cancer cells. 	32107851
HULC	LncRNA	Homo sapiens	Breast Neoplasms	tumour tissues	Expression[highly expressed]	qRT-PCR	HULC was significantly upregulated in tumour tissues compared to non-tumoural margins (P <0.001).		Yes	The HULC knockdown induced apoptosis and suppressed cellular migration in breast cancer cell lines.	33107484
IGF1R	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[PI3K/AKT pathway ]	qRT-PCR//PCR//Western Blot	Circ-IGF1R levels were found to be significantly upregulated in HCC tissues compared with levels in paired peritumoural tissues.Further investigation revealed that PI3K/AKT signalling pathway activation was involved in the oncogenic functions of circ-IGF1R in HCC. Our study suggests that circ-IGF1R may be a potential target for the prevention and treatment of HCC.	The high expression levels of circ-IGF1R in HCC were associated with tumour size.	Yes	Moreover, knocking down circ-IGF1R with siRNA significantly attenuated cell proliferation and induced cell apoptosis and cell cycle arrest in vitro.	31377314
IGBP1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	cell lines and tissues of BC	regulation[IGBP1-AS1/miR-24-1/ZIC3 loop]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	 Significant down-regulation of IGBP1-AS1 was discovered in the cell lines and tissues of BC. LncRNA IGBP1-AS1/miR-24-1/ZIC3 axis as a loop can regulate the proliferation and invasion of BC cells.		Yes	With respect to its biological function, overexpression of IGBP1-AS1 had inhibitory effects on the invasion and proliferation of BC cells in vivo as well as in vitro.	32390766
IGBP1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC samples and cell lines	Interaction(miR-150-5p/ZEB1 )	qRT-PCR	 In the study, we found that IGBP1-AS1 was found to be significantly upregulated in the NPC samples and cell lines. Bioinformatics and reporter assays revealed an association between IGBP1-AS1 and miR-150-5p. The expression of ZEB1 was increased by the microRNA (miRNA) sequestering in human NPC.		Yes	 The knockdown of IGBP1-AS1 impeded in-vitro proliferation of the NPC cells.	35402187
IFNG-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	serum and tissue samples 	Interaction(miR-627-3p)	Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	IFNG-AS1 expression in both serum and tissue samples was elevated in patients. Serum IFNG-AS1 could diagnose colon adenoma and adenocarcinoma patients from the healthy control. Silence of IFNG-AS1 could be available for repressing cellular capacities via the sponge to miR-627-3p. Beyond that, downregulated expression of IFNG-AS1 may repress malignant progression of colon adenocarcinoma by regulating miR-627-3p.	IFNG-AS1 was rised in colon adenocarcinoma and it was relevant to tumor size, TNM stage, and poor prognosis of patients. High tissue IFNG-AS1 was correlated with several clinical characteristics and a shorter overall survival time. 	Yes	Silence of IFNG-AS1 could be available for repressing cellular capacities via the sponge to miR-627-3p. 	34872454
IDH1-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Expression[lower expressed]	Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry	The results from this work show that IDH1-AS1 is downregulated in the glioma tissues.		Yes	We found that when IDH1-AS1 is overexpressed cell proliferation is inhibited, cell cycle is arrested at the G1 phase, and the protein expression levels of cyclinD1, cyclinA, cyclinE, CDK2, and CDK4 are decreased. Moreover, we proved that overexpression of IDH1-AS1 inhibits the tumorigenesis of U251 cells, in vivo. 	32990028
IDH1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines	Interaction[regulating ATG5-mediated autophagy]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Microarray//Cell Proliferation Assay//Colony Formation Assay//ChIP	At first, the expression of IDH1-AS1 was identified to be upregulated in PCa samples and cell lines. Consequently, rescue assays demonstrated that IDH1-AS1 promoted proliferation and apoptosis in PCa via ATG5-induced autophagy.		Yes	 Functionally, loss-of function assays revealed that silencing of IDH1-AS1 inhibited cell proliferation and induced cell apoptosis both in vitro and in vivo.	31570703
IDH1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	 prostate cancer tissues and cell lines	regulation[Enhancing IDH1 Enzyme Activity]	Western Blot//CCK8//qRT-PCR//EdU Staining//Transwell Assay	IDH1-AS1 expression was found to be significantly increased in prostate cancer tissues and cell lines.Our experiments revealed that the carcinogenic effects of IDH1-AS1 in prostate cancer may depend on a new molecular mechanism, which directly alters IDH1 enzyme activity.		Yes	IDH1-AS1 knockdown significantly inhibited the proliferation and migration of prostate cancer cells.	32884284
ID2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines and HCC tissues	Regulation[HDAC8/ID2 pathway]	qRT-PCR	We found that ID2-AS1 expression decreased in metastatic HCC cell lines and HCC tissues, and lower ID2-AS1 expression predicted reduced overall survival in HCC patients. Taken together, our findings demonstrated that ID2-AS1 regulated adjacent ID2 transcription by manipulating chromatin modification and that the newly identified ID2-AS1/ID2 axis suppressed HCC metastasis by regulating EMT processes. 	We found that ID2-AS1 expression decreased in metastatic HCC cell lines and HCC tissues, and lower ID2-AS1 expression predicted reduced overall survival in HCC patients. 	Yes	ID2-AS1 significantly suppressed the migration, invasion and metastasis of HCC cells in vitro and in vivo. 	31730902
ICR	LncRNA	Mus musculus	Atherosclerosis	high fat diet-induced atherosclerosis model in mice	Regulation(NF-κB signaling )	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//IF//RNA-seq//Luciferase Report Assay//Transwell Assay//ChIP	In a high fat diet-induced atherosclerosis model in mice, ICR is upregulated in the development of atherosclerosis. Mechanistically, ICR stabilized the mRNA of ICAM1 in quiescent ECs; while under inflammatory stress, ICR upregulated ICAM1 in a nuclear factor kappa B (NF-κB) dependent manner. RNA-seq analysis showed pro-inflammatory targets of NF-κB were regulated by ICR. Furthermore, the chromatin immunoprecipitation assays showed that p65 binds to ICR promoter and facilitates its transcription. Interestingly, ICR, in turn, promotes p65 accumulation and activity, forming a positive feedback loop to amplify NF-κB signaling. Preventing the degradation of p65 using proteasome inhibitors rescued the expression of NF-κB targets suppressed by ICR. 		Yes	 After intravenous injection of adenovirus carrying shRNA for mouse ICR, the atherosclerotic plaque area was markedly reduced with the declined expression of ICR and ICAM1.	35714558
ICMT-DT	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Interaction[repressing p21 mediated by EZH2]	ChIP//Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	In this research, we found that LINC00337 was up-regulated in the gastric cancer cells and tissue specimens.The mechanical experiments showed that LINC00337 epigenetically repressed the p21 via EZH2-mediated inhibition. Overall, this finding suggests that LINC00337 acts as the oncogene to promote gastric cancer cells proliferation through epigenetically repressing p21 mediated by EZH2, providing a new insight for gastric cancer.		Yes	The functional experiments illustrated that LINC00337 silencing repressed the proliferation, invasion and tumor growth in vitro and in vivo.	31217892
ICMT-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	regulation[suppresses the expression of CNN1]	qRT-PCR//MTT//Transwell Assay	It was found that CNN1 downregulation and LINC00337 overexpression occurred in CRC tissues and cells.  Taken together, this study indicates that LINC00337 facilitates the tumorigenesis and angiogenesis in CRC via recruiting DNMT1 to inhibit the expression of CNN1.		Yes	CNN1 overexpression or LINC00337 knockdown restricted CRC cell proliferation, migration/invasion, and proangiogenetic potency in vitro, which was substantiated by the in vivo experiments evidenced by facilitated tumor growth and MVD as well as elevated Ki67 and VEGF.	33328585
ICMT-DT	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	interaction[binds to E2F1]	RNA Pull-Down//Western Blot//qRT-PCR//FISH//RIP	Here we identified Linc00337 is an oncogenic lncRNA during PDAC progression. We found that the expression of Linc00337 is elevated in PDAC tissues and the higher Linc00337 predicts dismal prognosis. Mechanistically, Linc00337 binds to E2F1 and functions as an E2F1 coactivator to trigger the targets expression during PDAC progression.	Here we identified Linc00337 is an oncogenic lncRNA during PDAC progression. We found that the expression of Linc00337 is elevated in PDAC tissues and the higher Linc00337 predicts dismal prognosis. 	Yes	Functionally, Linc00337 promotes PDAC cell proliferation and cell cycle transition both in vitro and in vivo. 	33054826
ICMT-DT	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung adenocarcinoma tissues	Interaction(miR-1285-3p/YTHDF1 )	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	 LINC00337 expression was remarkably upregulated in lung adenocarcinoma.With respect to the mechanism, LINC00337 knockdown boosted miR-1285-3p expression and then restrained YTHDF1 expression post-transcriptionally. Crucially, both miR-1285-3p decrement and YTHDF1 overexpression successfully reversed the influence on cell proliferation, migration, invasion, and apoptosis caused by LINC00337 shRNA.		Yes	 In addition, LINC00337 knockdown was shown to repress cell migration, invasion, and proliferation, as well as the cell cycle, and gear up apoptosis in lung adenocarcinoma in vitro and in vivo. 	34663343
ICMT-DT	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue and cell lines	Interaction[inhibiting TIMP2 by recruiting DNMT1]	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Invasion Assay//ChIP	In the NSCLC tissue and cell lines, LINC00337 was found to be remarkedly up-regulated.Mechanically, LINC00337 could recruit the epigenetic repressor DNMT1 to the promoter region of TIMP2 to silence its expression.	In the NSCLC tissue and cell lines, LINC00337 was found to be remarkedly up-regulated, and the ectopic LINC00337 overexpression indicated the poor survival of NSCLC patients.	Yes	In vitro, gain and loss of functional assays showed that LINC00337 promoted the progression of NSCLC cells, including proliferation and invasion. In vivo, LINC00337 knockdown inhibited the tumor growth of NSCLC cells.	31632575
IATPR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC cells and tissue	Regulation[downregulating Mcl-1]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	Linc-ITGB1 expression level in ccRCC samples was markedly higher than that of the adjacent ones. Our findings suggested that linc-ITGB1 could enhance ccRCC cell migration and invasion via downregulating Mcl-1.	The expression of linc-ITGB1 was closely related to the disease-free survival time of ccRCC patients. 	Yes	Moreover, the migration and invasion of ccRCC cells were remarkably enhanced after linc-ITGB1 upregulation in vitro. 	30915742
HYOU1-AS	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues and cells	Interaction(HYOU1)	In Vivo Experiment//RNA Pull-Down//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining	We identified an antisense lncRNA, HYOU1-AS, which is transcribed from the opposite strand of the hypoxia up-regulated 1 (HYOU1) gene, enriched in the nucleus and highly expressed in TNBC.  In mechanistic studies, we found that HYOU1-AS could promote the expression of HYOU1, a proliferative gene, through competitively binding to hnRNPA1, an RNA-binding protein, to relieve its post-transcriptional inhibition of the HYOU1 mRNA.		Yes	 HYOU1-AS knockdown could inhibit the proliferation and migration of the TNBC MDA-MB-231 cells, and reduce their xenograft tumor formation in nude mice. 	33422616
HUWE1	CircRNA	Homo sapiens	Neuronal Injury	SK-N-SH Cells	Interaction( miR-433-3p/FGF7 axis)	Western Blot//Transfection//Flow Cytometry//PCR//ELISA//IF	In conclusion, circ-HUWE1 knockdown alleviates Amyloid-β-induced neuronal injury in SK-N-SH cells via miR-433-3p release-mediated FGF7 depletion.		Yes	We discovered that circ-HUWE1 absence alleviated Amyloid-β-induced cell viability degradation, cell apoptosis, and inflammatory responses in SK-N-SH cells.	35670955
HULC	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation[miR-9-5p/MYH9 axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	Our results revealed that HULC was upregulated and miR-9-5p was downregulated in GC, and both were associated with clinicopathologic features of GC patients.A positive correlation was found between HULC expression and epithelial-to-mesenchymal transition (EMT) of GC tissues. Moreover, HULC repressed miR-9-5p expression by binding to miR-9-5p. The regulatory effects of HULC knockdown on GC cell proliferation, migration, invasion, EMT and apoptosis were reversed by introduction of anti-miR-9-5p. HULC regulated MYH9 expression by acting as a molecular sponge of miR-9-5p in GC cells. HULC knockdown inhibited tumor growth in vivo. 		Yes	The regulatory effects of HULC knockdown on GC cell proliferation, migration, invasion, EMT and apoptosis were reversed by introduction of anti-miR-9-5p.	31726371
Irag2-208	LncRNA	Rattus norvegicus	Spinal Cord Injuries	 SCI model rat and lipopolysaccharide (LPS)-stimulated PC12 cells	Interaction(miR-329-3p/IGF1R Axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA//EdU Staining	 TCTN2 expression was down-regulated in SCI model rat and lipopolysaccharide (LPS)-stimulated PC12 cells.TCTN2 targeted miR-329-3p and subsequently regulated the expression of its target IGF1R. Rescue assays suggested that miR-329-3p/IGF1R axis mediated the beneficial effects of TCTN2 exosomes on LPS-treated PC12 cells. 		Yes	 Tail vein injection of TCTN2 exosomes into rats significantly improved functional recovery of SCI. Meanwhile, TCTN2 exosomes treatment alleviated LPS-induced neuronal apoptosis, inflammation, and oxidative stress in vitro. 	34623606
IRAIN	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RC tissues and cells	regulation[VEGFA ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry	 LncRNA IRAIN was poorly expressed in RC tissues and cells with a primary localization in the nucleus, while VEGFA was highly expressed. LncRNA IRAIN was also able to suppress RC tumor growth via repression of VEGFA in an in vivo mouse xenograft model. 		Yes	Overexpression of lncRNA IRAIN or knockdown of VEGFA inhibited cell proliferation and migration and induced the apoptosis of RC cells. 	32983957
IRAIN	LncRNA	Homo sapiens	Multiple Myeloma	blood,cell lines	Interaction[miR-125b ]	CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	 The expression level of IRAIN in patients with MM was significantly lower compared to that in healthy individuals (Fig. 1A).Consistent with these data, the RPMI-8226 cell line expressed the highest level of miR-125b (Fig. 1F) and the lowest level of IRAIN (Fig. 1G).Furthermore, by using dual-luciferase reporter assays, IRAIN was identified as a target of miR-125b.		Yes	 Knockdown of IRAIN promoted MM cell proliferation in vitro.	31788123
KCNQ1OT1	LncRNA	Homo sapiens	Ischemic Stroke	blood	Interaction[miR‐200a/FOXO3/ATG7 pathway]	Western Blot//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	In this study, we revealed that potassium voltage‐gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1) was significantly upregulated in ischemic stroke. Mechanistically, KCNQ1OT1 acted as a competing endogenous RNA of miR‐200a to regulate downstream forkhead box O3 (FOXO3) expression, which is a transcriptional regulator of ATG7. Knockdown of KCNQ1OT1 might inhibit I/R‐induced autophagy and increase cell viability via the miR‐200a/FOXO3/ATG7 pathway. This finding offers a potential novel strategy for ischemic stroke therapy.		Yes	 Knockdown of KCNQ1OT1 remarkably reduced the infarct volume and neurological impairments in transient middle cerebral artery occlusion (tMCAO) mice. 	30945454
KCNQ1OT1	LncRNA	Homo sapiens	maxillary sinus squamous cell carcinoma	MSSCC tissues and MSSCC cell line (IMC-3)	Regulation[miR-204/EphA7 axis]	qPCR//Luciferase Report Assay	Herein, we found that KCNQ1OT1 expression was markedly upregulated in MSSCC tissues and MSSCC cell line (IMC-3) by using quantitative reverse transcription-polymerase chain reaction. Moreover, we confirmed KCNQ1OT1 could directly interact with miR-204 by bioinformatic prediction and dual luciferase assay, and miR-204 inhibitor markedly reversed MSSCC tumor phenotypes induced by shKCNQ1OT1. Finally, we demonstrated that KCNQ1OT1/miR-204 facilitated MSSCC progression by regulating Eph receptor A7 (EphA7).		Yes	 Loss-of-function experiments revealed that the deletion of KCNQ1OT1 inhibited cell proliferation, migration, and invasion. 	31709597
KCNQ1OT1	LncRNA	Homo sapiens	Fracture Healing	bone tissues	Interaction[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Western Blot	"Gene expression profiling and qRT-PCR revealed that lncRNA KCNQ1OT1 was significantly down-regulated in bone tissues of patients with delayed fracture healing.In HC-a cells, overexpression of lncRNA KCNQ1OT1 activated the Wnt/β-catenin signaling pathway, which could be suppressed by knocking down lncRNA KCNQ1OT1. Cell Counting Kit-8 (CCK-8) assay and 5(6)-carboxyfluorescein diacetate, succinimidyl ester (CFSE) results manifested that lncRNA KCNQ1OT1 remarkably promoted the proliferation and inhibited apoptosis of HC-a cells by activating the Wnt/β-catenin signaling pathway.
"		Yes	Compared with the control group, knocking down lncRNA KCNQ1OT1 remarkably reduced the serum levels of alkaline phosphatase (ALP) and osteoprotegerin (OPG) in rabbits, and markedly decreased bone trabecular growth index (p<0.05).	31210283
KCNQ1OT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cell lines	Regulation[ miRNA-27b-3p/HSP90AA1 axis]	qRT-PCR	We demonstrated that the KCNQ1OT1 level was upregulated in NSCLC tissues and cell lines.These data revealed a role for KCNQ1OT1 as an oncogene through miR-27b-3p/HSP90AA1 axis during NSCLC progression.	High KCNQ1OT1 level correlated with poor overall and progression-free survival in NSCLC patients.	Yes	 KCNQ1OT1 facilitated proliferation, migration, and invasion in H460 cells. Furthermore, knockdown of KCNQ1OT1 reduced the expression of HSP90AA1.	30471108
KCNQ1OT1	LncRNA	Homo sapiens	Osteoporosis	ADSCs-Exos	Interaction(miR-141-5p)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	TNF-α dose-dependently increased miR-141-5p expression, inhibited viability, and promoted apoptosis of osteoblasts. However, miR-141-5p silencing or cocultured with ADSCs-Exos attenuated these effects. In addition, KCNQ1OT1-Exos could more significantly attenuate the induced cytotoxicity and apoptosis compared to ADSCs-Exos. Moreover, miR-141-5p was confirmed as the target of KCNQ1OT1 by luciferase reporter assay.		Yes	TNF-α dose-dependently increased miR-141-5p expression, inhibited viability, and promoted apoptosis of osteoblasts. However, miR-141-5p silencing or cocultured with ADSCs-Exos attenuated these effects.	34712334
KCNQ1OT1	LncRNA	Homo sapiens	Osteoporosis	 osteoporotic patients	Interaction(miR-205-5p/RICTOR axis)	qRT-PCR//Transfection//Luciferase Report Assay//Western Blot	QPCR results indicated that KCNQ1OT1 and RICTOR were down-regulated, while miR-205-5p was up-regulated in the osteoporotic patients, as compared with non-osteoporotic controls. During the osteogenic differentiation of BMSCs, the expression of KCNQ1OT1 and RICTOR was upregulated, whereas miR-205-5p was downregulated. The interaction among KCNQ1OT1, miR-205-5p and RICTOR was validated by dual luciferase reporter system. KCNQ1OT1 promoted RICTOR expression via inhibiting miR-205-5p, therefore promoting osteogenesis as demonstrated by ALP assay, alizarin red staining and the increased expression of osteogenic markers (OPN, RUNX2 and OCN). Furthermore, KCNQ1OT1 overexpression or miR-205-5p inhibition could promote ALP activity and mineralization of BMSCs, while overexpressed miR-205-5p could reverse the effects of overexpressed KCNQ1OT1, and knockdown of RICTOR could reverse the effects of miR-205-5p inhibition.		Yes	 The interaction among KCNQ1OT1, miR-205-5p and RICTOR was validated by dual luciferase reporter system. KCNQ1OT1 promoted RICTOR expression via inhibiting miR-205-5p, therefore promoting osteogenesis as demonstrated by ALP assay, alizarin red staining and the increased expression of osteogenic markers (OPN, RUNX2 and OCN). Furthermore, KCNQ1OT1 overexpression or miR-205-5p inhibition could promote ALP activity and mineralization of BMSCs, while overexpressed miR-205-5p could reverse the effects of overexpressed KCNQ1OT1, and knockdown of RICTOR could reverse the effects of miR-205-5p inhibition.	35341776
KCNQ1OT1	LncRNA	Homo sapiens	Leukemia, Promyelocytic, Acute	clinical samples	Interaction(FUS/MAP3K1)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Bioinformatics Analysis//ChIP	The Cancer Genome Atlas database and our clinical samples, we found that KCNQ1OT1 was selectively highly expressed in APL. Further evidence showed that KCNQ1OT1 was mainly located in the cytoplasm of APL patient-derived NB4 cells and APL patient bone marrow samples. Mechanistically, KCNQ1OT1 bound to RNA binding protein FUS, and silencing either KCNQ1OT1 or FUS reduced the expression level and stability of MAP3K1 mRNA. Our results not only revealed that c-Myc transactivated KCNQ1OT1 and upregulated KCNQ1OT1 promoted APL cell proliferation, but also demonstrated that KCNQ1OT1 bound to FUS to synergistically stabilize MAP3K1 mRNA, thus facilitating APL cell proliferation. 		Yes	Functional assays demonstrated that knockdown of KCNQ1OT1 reduced APL cell proliferation and increased apoptosis. 	34404765
Kcnq1ot1	LncRNA	Mus musculus	Atherosclerosis	 atherosclerotic plaques of AS mice and  THP-1 cells	Interaction( miR-145-5p)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//ELISA	KCNQ1OT1 expression was upregulated and miR-145-5p was downregulated in atherosclerotic plaques of AS mice and ox-LDL-treated THP-1 cells. Additionally, KCNQ1OT1 acted as a molecular sponge of miR-145-5p and downregulated miR-145-5p expression. Furthermore, silencing miR-145-5p abolished the effect of KCNQ1OT1 knockdown.		Yes	Lipid metabolic disorders and inflammation in vivo and in vitro were attenuated by either KCNQ1OT1 knockdown or miR-145-5p overexpression. 	34464666
Kcnq1ot1	LncRNA	Mus musculus	Acute Kidney Injury	AKI model	Interaction(miR-204-5p/NLRP3 )	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//H&E Staining//ELISA	The results showed that Kcnq1ot1 was highly expressed in the AKI model in vivo and in vitro. Furthermore, Kcnq1ot1 inhibited miR-204-5p expression by competitively binding to miR-204-5p in HK-2 cells.  miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells in vitro. 		Yes	Kcnq1ot1 knockdown promoted cell proliferation and prevented apoptosis and inflammation.  Kcnq1ot1 knockdown in vivo promoted miR-204-5p expression, inhibited NLRP3 inflammasome activation, reduced levels of SCr, BUN, and KIM-1, and thus alleviated AKI and reduced apoptosis. 	34858199
Kcnq1ot1	LncRNA	Mus musculus	Hepatic Ischemia/Reperfusion Injury	hepatic tissue of HIRI mouse	Interaction(miR-142a-3p/HMGB1 axis)	qRT-PCR	Our data revealed that KCNQ1OT1 expression was ascending in hepatic tissue of HIRI mouse.Mechanistically, KCNQ1OT1 functioned as a competing endogenous RNA which sponged miR-142a-3p, therefore promoted HMGB1 expression to activate TLR4/NF-κB signaling pathway in HIRI.		Yes	Moreover, deprivation of KCNQ1OT1 mitigated I/R-induced hepatic injury and pyroptosis in vivo. Further experiments demonstrated that silencing KCNQ1OT1 promoted proliferation and inhibited pyroptosis in hypoxia/reoxygenation (H/R)-induced primary mouse hepatocytes. 	36308669
KCNQ1DN	LncRNA	Homo sapiens	Carcinoma, Renal Cell	renal cell carcinoma tissues	Interaction[downregulating c-Myc]	qRT-PCR//MTT//Tunel	 In the present study, we found that lncRNA KCNQ1DN was notably decreased in RCC tissues and cell lines. Mechanistically, KCNQ1DN inhibited the expression of c-Myc, which might further upregulate cyclin D1 and suppress p27 at mRNA and protein levels in RCC cells. Reporter gene assays revealed that the transcriptional activity of c-Myc promoter was inhibited by KCNQ1DN. The in vivo experiments in nude mice showed that KCNQ1DN overexpression dramatically repressed the growth of xenograft tumors and the expression of corresponding c-Myc. 		Yes	 Functional studies clarified that KCNQ1DN repressed the RCC cell growth and cell cycle progression. The in vivo experiments in nude mice showed that KCNQ1DN overexpression dramatically repressed the growth of xenograft tumors and the expression of corresponding c-Myc.	31528231
KCNMB2-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	Interaction(miR-374a-3p/ S100A10)	qRT-PCR//Colony Formation Assay	 We found that lncRNA KCNMB2-AS1 was significantly upregulated both in BC tissues and cell lines, the expression level was highly correlated with pathological TNM stage. Mechanistically, lncRNA KCNMB2-AS1 could function as a competitive endogenous RNA (ceRNA) through direct sponging miR-374a-3p, which regulated the expression of S100A10. 	 We found that lncRNA KCNMB2-AS1 was significantly upregulated both in BC tissues and cell lines, the expression level was highly correlated with pathological TNM stage.	Yes	Functionally, knockdown of lncRNA KCNMB2-AS1 dramatically inhibited the proliferation, migration, and invasion and of BC cells in vitro, and suppressed tumor growth in vivo. 	34367236
KCNMB2-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues	Interaction(miR-3194-3p/SAMD5 signal pathway)	Flow Cytometry//qRT-PCR	Here, we revealed the increased level of KCNMB2-AS1 in bladder cancer for the first time.Next, we revealed that KCNMB2-AS1 could interact with miR-3194-3p and uncovered that SAMD5 was a downstream target of miR-3194-3p.		Yes	Knockdown of KCNMB2-AS1 in vitro prevented the ability of proliferation, metastasis, and stemness of cancer cells. In vivo, the silencing of KCNMB2-AS1 also prevented tumor growth in vivo. 	34026626
KCNMB2-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCA tissues	Interaction(miR-3194-3p/PYGL axis)	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	We discovered that KCNMB2-AS1 was significantly upregulated in ESCA. KCNMB2-AS1 bound with miR-3194-3p, and glycogen phosphorylase L (PYGL) was a direct target of miR-3194-3p. KCNMB2-AS1 upregulated PYGL expression by directly binding with miR-3194-3p. 		Yes	 KCNMB2-AS1 downregulation suppressed the growth, invasion, migration and stemness of ESCA cells. 	34516362
KCNK15-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[ KCNK15-AS1-DNMT1-MAPK and KCNK15-AS1-HDAC1-AKT]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	 The expression of KCNK15-AS1 was lower in the tumor tissue compared to the normal tissue.In this study, we identified two regulatory axes, namely KCNK15-AS1-DNMT1-MAPK and KCNK15-AS1-HDAC1-AKT, which were associated with gastric cancer progression. Chidamide and 5-azacytidine might provide new modes for treating gastric cancer.		Yes	Both the overexpression of KCNK15-AS1 and the knockdown of the expression of miR-21 inhibited proliferation and promoted apoptosis and decreased the level of MMP-9, bcl-2, and MMP-2 but increased the level of Bax.	31572012
KCNK15-AS1	LncRNA	Homo sapiens	Osteoarthritis	ATDC5 cells	Interaction( RP11-445H22.4-miR-301a-CXCR4 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA	 In addition, miR-301a directly bound to RP11-445H22.4, and suppression of miR-301a inversed the effects of RP11-445H22.4 inhibition. Furthermore, CXCR4 was a direct target of miR-301a, and CXCR4 silencing increased cell viability, decreased apoptosis and inflammatory cytokines secretions in LPS-treated ATDC5 cells. Besides, we found that CXCR4 silencing blocked LPS-activated NF-κB and MAPK/ERK pathways.		Yes	 However, RP11-445H22.4 inhibition significantly rescued LPS-induced injuries by promoting cell viability, suppressing apoptosis and inflammatory cytokines secretions in ATDC5 cells. 	29414810
KCNA3	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[YAP1 ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Invasion Assay	We found that lncRNA kcna3 was lowly expressed in CRC tissues, and its low expression was closely associated with patients' higher TNM grade and the higher occurrence rate of lymphatic metastasis and distant metastasis, as well as shorter OS. In conclusion, this study revealed that lncRNA kcna3 exerts a tumor-inhibit role in CRC progression through down-regulating YAP1 expression, indicating that lncRNA kcna3/YAP1 might be served as a new prognostic biomarker and therapeutic target for CRC.	We found that lncRNA kcna3 was lowly expressed in CRC tissues, and its low expression was closely associated with patients' higher TNM grade and the higher occurrence rate of lymphatic metastasis and distant metastasis, as well as shorter OS.	Yes	 Enhanced expression of lncRNA kcna3 inhibited SW620 cells' proliferation, migration and invasion, and induced cell apoptosis in vitro, and repressed CRC tumor growth in vivo.	30099342
KB-1732A1.1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[miR-200 s ]	RNA Pull-Down//Northern Blot//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Microarray//BrdU//Colony Formation Assay	Further, LincK was frequently elevated in breast cancer compared with normal breast tissue in clinical samples.Mechanistically, LincK may share common miRNA response elements with PBK and ZEB1 and regulate the effects of miR-200 s.		Yes	Moreover, knockdown of LincK repressed tumorigenesis, and ectopic expression of LincK promoted tumor growth in MCF-7 xenograft model.	30795783
KB-1507C5.2	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
KCNQ1OT1	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	SCLC tissues	Expression [highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Microarray//Colony Formation Assay//Transwell Assay	The results showed that KCNQ1OT1 expression was upregulated in SCLC tissues and was a poor prognostic factor for patients with SCLC. Mechanistic investigation showed that KCNQ1OT1 can activate transforming growth factor-β1 mediated epithelial-to-mesenchymal transition in SCLC cells.		Yes	 Knockdown of KCNQ1OT1 inhibited cell proliferation, migration, chemoresistance and promoted apoptosis of SCLC cells.	33705625
KCNQ1OT1	LncRNA	Homo sapiens	Myocardial Infarction	MI patients, I/R mouse and H/R-induced cell model	Interaction(miR-26a-5p/ATG12 pathway.)	In Vivo Experiment//Western Blot//Transfection//Tunel//qRT-PCR//Luciferase Report Assay	KCNQ1OT1 was up-regulated while miR-26a-5p was decreased in MI patients, I/R mouse and H/R-induced cell model. Either KCNQ1OT1 knockdown or miR-26a-5p mimics caused inhibition of autophagy related 12 homolog (ATG12), which was the direct target of miR-26a-5p. In vivo, KCNQ1OT1 promoted cardiomyocytes apoptosis via miR-26a-5p/ATG12 pathway.		Yes	KCNQ1OT1 knockdown inhibited cell autophagy and protected cardiomyocytes from apoptosis by up-regulating miR-26a-5p. 	34089766
IRAIN	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation(IGF-1R-PI3K-NF-κB signaling pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 IRAIN was down-regulated in glioma tissues (compared with adjacent normal tissues), and the low IRAIN expression was significantly linked with the larger tumor volume and higher pathological stages.  The WB result showed that overexpressing IRAIN inactivated the IGF-1R-PI3K-NF-κB pathway. Additionally, the IGF-1R knockdown model was established in U251 cells. Si-IGF-1R induced cell proliferation inhibition, promoted cell death, and reduced cell migration and TMZ resistance, whereas Si-IGF-1R+IRAIN group showed no additional effects on glioma cells compared with the Si-IGF-1R group.		Yes	 Functionally, overexpressing IRAIN abated glioma cell proliferation, invasion, and migration, promoted apoptosis, and attenuated IGF-1R-PI3K-NF-κB expression and temozolomide (TMZ) resistance, which was also confirmed in the xenograft tumor experiment. 	35102541
KCNQ1OT1	LncRNA	Homo sapiens	Melanoma	 CD8+ T cells	Interaction(miR-34a/STAT3/PD-L1 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	KCNQ1OT1 regulated the progression of the melanoma via its action as a miR-34a sponge. STAT3 was found to be a downstream target of miR-34a, resulting in transcriptional regulation of Programmed cell death 1 ligand 1 (PD-L1). KCNQ1OT1 regulated STAT3 by targeting miR-34a. Knockdown of KCNQ1OT1 reduced PD-L1 level, enhanced CD8+ T cell cytotoxicity, and proliferation and inhibited apoptosis of CD8+ T cells.	KCNQ1OT1 was upregulated in melanoma tissues leading to a poor prognosis, and knocking down it inhibited melanoma cell proliferation, migration, and invasion. 	Yes	KCNQ1OT1 was upregulated in melanoma tissues leading to a poor prognosis, and knocking down it inhibited melanoma cell proliferation, migration, and invasion. 	36399467
KCNQ1OT1	LncRNA	Homo sapiens	Ovarian Neoplasms		Interaction[Wnt/β-catenin]	Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//Transwell Assay	 The proliferation rate of cells was overtly decreased in KCNQ1OT1 knockdown group but significantly increased in KCNQ1OT1 overexpression group. The results of both wound healing and transwell assays showed that the migration ability of cells was reduced in KCNQ1OT1 knockdown group but raised in KCNQ1OT1 overexpression group. According to flow cytometry, the cell cycle was clearly arrested in the G0/G1 phase in KCNQ1OT1 knockdown group. The results of Western blotting and fluorescence immunoassay revealed that compared with that in control group, the expression level of β-catenin protein evidently declined in KCNQ1OT1 knockdown group, but it was notably elevated in KCNQ1OT1 overexpression group.		Yes	"Results showed that compared with that in con_x0002_trol group, the proliferation rate of cells was sig_x0002_nificantly decreased in KCNQ1OT1 knockdown 
group but remarkably elevated in KCNQ1OT1 
overexpression group, showing statistically sig_x0002_nificant differences (p<0.05) (Figure 1)."	31696465
KCNQ1OT1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC cells 	regulation[MIR-142-5p/CAPN10 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We showed KCNQ1OT1 was elevated expression in OC cells and indicated poorer overall survival of OC patients. At length, we showed KCNQ1OT1 could regulate OC development via MIR-142-5p/CAPN10 axis.	We showed KCNQ1OT1 was elevated expression in OC cells and indicated poorer overall survival of OC patients. 	Yes	Besides, we found KCNQ1OT1 could promote OC cell proliferation and migration in vitro. 	31909901
KCNQ1OT1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Regulation(EIF2B5)	qRT-PCR//RIP//ChIP	Expression of lncRNA KCNQ1OT1 was increased in OC tissues and cells. EIF2B5 expression was downregulated in OC, which was inversely correlated with KCNQ1OT1. Knockdown of KCNQ1OT1 inhibited OC cell proliferation and metastasis. KCNQ1OT1 could downregulate EIF2B5 expression by recruiting DNA methyltransferases into EIF2B5 promoter. Furthermore, interference of EIF2B5 expression rescued KCNQ1OT1 depletion-induced inhibitory impact on OC cell proliferation and metastasis.		Yes	Knockdown of KCNQ1OT1 inhibited OC cell proliferation and metastasis.	36100884
KCNQ1OT1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR-125b-5p/CD147 axis)	CCK8//qRT-PCR	KCNQ1OT1 was high expression and miR-125b-5p was low expression in OC, and KCNQ1OT1 was negatively correlated with that of miR-125b-5p in OC specimens.  KCNQ1OT1 was positively correlated with that of CD147 in OC specimens, and KCNQ1OT1 accelerated OC progression via miR-125b-5p/CD147 axis.		Yes	 KCNQ1OT1 promoted OC cell proliferation and metastasis by binding to miR-125b-5p. miR-125b-5p targeted CD147, and which was negatively correlated with that of miR-125b-5p in OC specimens.	36191448
KCNQ1OT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissue and cell lines	Regulation[miR-145-5p/PCBP2 axis]	Western Blot//Wound Healing Assay//Tunel//CCK8//qRT-PCR//Flow Cytometry//IF//Colony Formation Assay//Transwell Assay	KCNQ1OT1 was significantly overexpressed in BC tissue and cell lines.KCNQ1OT1 serves as competing endogenous RNA (ceRNA) to up-regulate PCBP2 via sponging miR-145-5p in BC progression.		Yes	KCNQ1OT1 depletion repressed cell proliferation, migration and invasion, whereas encouraged cell apoptosis. 	31827399
KCNQ1OT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues	regulation[MiR-218-5p/HS3ST3B1]	qRT-PCR	In this study, we demonstrated that KCNQ1OT1 expression in bladder cancer tissues was notably up-regulated compared with in normal adjacent tissues, and KCNQ1OT1 modulated the malignant phenotypes of bladder cancer cells. In conclusion, KCNQ1OT1 can promote the progression of bladder cancer through regulation of miR-218-5p/HS3ST3B1, which is expected to serve as a new therapeutic target for bladder cancer.		Yes	Overexpressed miR-218-5p would inhibit the proliferation and metastasis of bladder cancer cells while facilitating apoptosis.	32820233
KCNQ1OT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[miR-185-5p/Rab14 axis]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 KCNQ1OT1 was upregulated in OSCC tissues and cells.KCNQ1OT1 silencing suppressed OSCC cell malignancy and downregulated miR-185-5p level, which showed upregulated expression in OSCC samples. Rab14 as a target gene of miR-185-5p was highly expressed in OSCC. KCNQ1OT1 knockdown impaired the invasion capability of OSCC cells, promoted apoptosis, and suppressed Rab14 expression. The inhibition of miR-185-5p in KCNQ1OT1 silencing cells reversed the suppression of Rab14 and restored the cancerous growth of OSCC cells. These results indicated that KCNQ1OT1 promoted OSCC tumorigenesis via the modulation of miR-185-5p/Rab14 axis, which may serve as a therapeutic target for the treatment of OSCC.		Yes	KCNQ1OT1 silencing suppressed OSCC cell malignancy and downregulated miR-185-5p level, which showed upregulated expression in OSCC samples.KCNQ1OT1 knockdown impaired the invasion capability of OSCC cells, promoted apoptosis, and suppressed Rab14 expression.	31755091
KCNQ1OT1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction[ sponging miR-4458 and upregulating CCND2]	CCK8//qRT-PCR	 Our work demonstrated the upregulation of KCNQ1OT1 in osteosarcoma through qRT-PCR. Collectively, the results of rescue experiments suggested that the oncogenic role of KCNQ1OT1 was performed through sponging miR-4458 and upregulating CCND2 during osteosarcoma development, providing a novel perspective of intervention in osteosarcoma management.		Yes	 loss of function assay (CCK-8, transwell migration) indicated KCNQ1OT1 promoted cell proliferation, migration in osteosarcoma.	31392505
KCNQ1OT1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[Wnt/β-catenin signaling,miR‑3666/KLF7 axis]	qRT-PCR	In the present study, a high KCNQ1OT1 expression was detected in human OS tissues and cell lines. Collectively, the present study demonstrates that KCNQ1OT1 facilitates OS progression and activates Wnt/β‑catenin signaling by targeting the miR‑3666/KLF7 axis.		Yes	 Loss?of?function assays demonstrated that KCNQ1OT1 silencing suppressed cell proliferative, migratory and invasive abilities in OS.	33416089
KCNQ1OT1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	interaction[ miR-129-5p]	qRT-PCR//MTT//Transwell Assay	The result revealed that KCNQ1OT1 was highly expressed in osteosarcoma tissues and cells.The luciferase reporter assay and pull-down assay demonstrated that KCNQ1OT1 directly interact with miR-129-5p. 		Yes	 KCNQ1OT1-siRNA inhibited the proliferation, invasion, and drug resistance of osteosarcoma cells. 	32953888
KCNQ1OT1	LncRNA	Homo sapiens	Osteosarcoma	cell lines	regulation[KCNQ1OT1/miR-34c-5p/ALDOA axis ]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Cycle Assay//IHC	Here, we report that lncRNA KCNQ1OT1 was upregulated in OS.Targeting the KCNQ1OT1/miR-34c-5p/ALDOA axis may be a potential therapeutic target in OS treatment.		Yes	Meanwhile, functional experiments demonstrated that the KCNQ1OT1 facilitated proliferation and suppressed apoptosis of OS cells. 	32332718
KCNQ1OT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	regulation[miR-491-5p/PKM2 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	In this study, KCNQ1OT1 was significantly up-regulated in CC patient cancerous tissues and cell lines, and its high expression was significantly related to tumor volume increase and poor differentiation. In conclusion, KCNQ1OT1 enhances CC cell progression through the miR-491-5p/PKM2 axis.	In this study, KCNQ1OT1 was significantly up-regulated in CC patient cancerous tissues and cell lines, and its high expression was significantly related to tumor volume increase and poor differentiation. 	Yes	KCNQ1OT1 overexpression significantly promoted CC cell proliferation, metastasis and radioresistance. On the contrary, KCNQ1OT1 knockdown compared to the control group inhibited the above biological behavior of CC cells.	33146005
KCNQ1OT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	clinical tumor tissue specimens and CC cell lines	 Interaction(miR-296-5p/HYOU1 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//Invasion Assay//Transwell Assay	Elevated KCNQ1OT1 and HYOU1 as well as reduced miR-296-5p were observed in clinical tumor tissue specimens and CC cell lines. Results revealed that upregulation of miR-296-5p counteracted the enhancing effects of overexpressed KCNQ1OT1 on the proliferative, migrative and invasive abilities of CC cells. Additionally, HYOU1 overexpression abolished the suppressing effects of silenced KCNQ1OT1 on the malignant behaviors of CC cells and tumor growth. 		Yes	Results revealed that upregulation of miR-296-5p counteracted the enhancing effects of overexpressed KCNQ1OT1 on the proliferative, migrative and invasive abilities of CC cells. Additionally, HYOU1 overexpression abolished the suppressing effects of silenced KCNQ1OT1 on the malignant behaviors of CC cells and tumor growth. 	34704918
KCNQ1OT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	HeLa cells	Interaction(KCNQ1OT1/miR-1270/LOXL2 axis )	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	KCNQ1OT1 expression was the highest in HeLa cells but lowest in SiHa cells whose upregulation improved the viability but inhibited the apoptosis in SiHa cells while knockdown of KCNQ1OT1 caused opposite results in HeLa cells. MiR-1270 was sponged and negatively modulated by KCNQ1OT1. MiR-1270 mimics caused low viability and high apoptosis of SiHa cells but miR-1270 inhibitor reverse its roles in HeLa cells. LOXL2, the target of miR-1270, positively interplayed with KCNQ1OT1 but had negative interaction with miR-1270. LOXL2 overexpression promoted viability and decreased apoptosis of SiHa cells but knockdown of LOXL2 restored its effects in HeLa cells. Moreover, LOXL2 and phosphorylated AKT (p-AKT) protein expressions were downregulated by suppressed KCNQ1OT1 and LOXL2 and miR-1270 mimics but promoted by overexpressed KCNQ1OT1 and LOXL2 and miR-1270 inhibitor. Additionally, LY294002 treatment caused low KCNQ1OT1 RNA expression and decreased LOXL2 and p-AKT protein expressions.		Yes	KCNQ1OT1 expression was the highest in HeLa cells but lowest in SiHa cells whose upregulation improved the viability but inhibited the apoptosis in SiHa cells while knockdown of KCNQ1OT1 caused opposite results in HeLa cells. 	35218109
KCNQ1OT1	LncRNA	Homo sapiens	Cholangiocarcinoma	tissues and cell lines	Regulation[miR-140-5p/SOX4 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	 As expected, KCNQ1OT1 was highly expressed in CCA tissues and cell lines.Mechanism investigation revealed that KCNQ1OT1 can act as a ceRNA to improve CCA progression by regulating miR-140-5p/SOX4 axis.		Yes	 Whereas, the negative effect of KCNQ1OT1 on the cell apoptosis was tested with flow cytometry analysis.	30243712
KCNQ1OT1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissues and cells	Interaction(miR-211-5p/CHI3L1 Pathway)	Western Blot//Migration Assay//RIP//Luciferase Report Assay//Transwell Assay	KCNQ1OT1 expression was upregulated in PCa tissues and cells. KCNQ1OT1 bound miR-211-5p competitively, and miR-211-5p targeted CHI3L1 3'-UTR. miR-211-5p expression was downregulated, whereas CHI3L1 (YKL-40) expression was upregulated. miR-211-5p levels were negatively correlated with KCNQ1OT1 expression and CHI3L1 mRNA. The decrease in YKL-40 expression in PCa cells induced by the downregulation of KCNQ1OT1 expression could be offset by miR-211-5p inhibitor transfection.		Yes	Downregulating this expression inhibited PCa cell invasion, proliferation, and metastasis. 	33688211
KCNQ1OT1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa cells	Interaction(miR-137-3p/PTP4A3 axis)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	These findings suggest that endosulfan can indeed promote cell migration and invasion via the KCNQ1OT1/miR-137-3p/PTP4A3 axis in PCa cells.		Yes	 Functionally, silencing of KCNQ1OT1 repressed cell migration and invasion, and caused alterations of EMT biomarkers and critical proteins in the TGF-β signaling pathway, which were all restored by co-transfection with anti-miR-137-3p or PTP4A3-WT plasmid.	35817112
KCNQ1OT1	LncRNA	Homo sapiens	Retinoblastoma	RB tissue	regulation[miR-153-3p/HIF-1α axis]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//RIP//Transwell Assay	The results of our study showed that KCNQ1OT1 expression was markedly enhanced in RB tissue samples, and KCNQ1OT1 knockdown had an inhibitory effect on the proliferation,In conclusion, our study indicates that KCNQ1OT1 can increase the malignancy of RB cells via regulating miR-153-3p/HIF-1α axis.		Yes	The results of our study showed that KCNQ1OT1 expression was markedly enhanced in RB tissue samples, and KCNQ1OT1 knockdown had an inhibitory effect on the proliferation,migration, invasion and viability of RB cells. 	33051357
KCNQ1OT1	LncRNA	Homo sapiens	Retinoblastoma	Fifty cases of Rbs and their adjacent normal tissues	Interaction(miR-134/TRIM44 pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 lncRNA KCNQ1OT1 was up-regulated in Rb tissues and Rb cell lines.  The analysis of the mechanism of KCNQ1OT1 showed that KCNQ1OT1 can sponge miR-134, and miR-134 may inhibit TRIM44 expression. 	In addition, the expression of KCNQ1OT1 was negatively correlated with the disease-free survival rate of RB patients.	Yes	Silencing KCNQ1OT1 could significantly inhibit the RB progression in vivo and in vitro.	33818859
KB-1460A1.5	LncRNA	Homo sapiens	Glioma	 clinical glioma tissues	Interaction(miR-130a-3p/TSC1/mTOR/YY1 feedback loop)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//IHC//Invasion Assay	In this study, using online data sets combined with collected clinical glioma tissues, we determined that the lncRNA KB-1460A1.5 is downregulated and positively correlated with prognosis in glioma. Mechanistically, tandem mass tag (TMT)-based quantitative proteomic analysis revealed that KB-1460A1.5 preferentially affects the Akt/TSC1/mTOR pathway.  KB-1460A1.5 was found to function as a competing endogenous RNA (ceRNA) to regulate the expression of TSC1, a key regulatory component of the mTOR pathway, by sponging miR-130a-3p in glioma cells. Furthermore, our data demonstrate that the mTOR pathway regulates the expression of the transcription factor Yin Yang 1 (YY1), which in turn binds directly to the KB-1460A1.5 promoter and affects the expression of KB-1460A1.5. 	In this study, using online data sets combined with collected clinical glioma tissues, we determined that the lncRNA KB-1460A1.5 is downregulated and positively correlated with prognosis in glioma. 	Yes	Functional experiments showed that overexpression of KB-1460A1.5 inhibits glioma cell proliferation, migration and invasion in vitro and in vivo, while downregulation of KB-1460A1.5 has the opposite effects. 	34728310
KAT7	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues 	Expression[lower expressed]	Western Blot//CCK8//Colony Formation Assay//EdU Staining//Transwell Assay	 The expression of lncRNA-KAT7 in CRC tissues was lower than that in matched normal tissues and normal intestinal epithelial cells (P < 0.05). Western blot analysis showed that the expression of lncRNA-KAT7 was up-regulated in HCT116 cells, the expression of E-cadherin increased, and the expression of Vimentin, MMP-2 and β-catenin protein was down-regulated so did the phosphorylation NF-κB P65. The results confirm that the expression of lncRAN-KAT7 can inhibit the malignant phenotype of CRC cells.	Decreased expression of lncRNA-KAT7 is associated with clinicopathological features of poor CRC patients.	Yes	 In vitro experiments showed that up-regulation of lncRNA-KAT7 expression in CRC cells inhibited cell proliferation and migration. In vivo animal experiments showed that the lncRNA-KAT7 also inhibited tumor growth. 	30858757
KASRT	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cell lines 	Regulation(P21/CCND1 pathway)	qRT-PCR//Western Blot	Lnc-KASRT expression was increased in most osteosarcoma cell lines compared to control cell line. Lnc-KASRT serves as a potential treatment target via regulating SRSF1-related KLF6 alternative splicing and following P21/CCND1 pathway in osteosarcoma.		Yes	Lnc-KASRT overexpression promoted cell viability, mobility, and anti-apoptotic marker expression, while reducing apoptosis rate and pro-apoptotic marker expression; meanwhile, it regulated SRSF1, KLF6 alternative splicing (increased KLF6-splice variant 1 (KLF6-SV1), decreased KLF6-wild type (KLF6-WT)), and followed P21/CCND1 pathway in U-2OS/Saos-2 cells. The lnc-KASRT knockdown exhibited opposite trends. 	34568030
JPX	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues, cells	regulation[inhibiting miR-197]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The Cancer Genome Atlas database and the RT?qPCR results indicated that JPX expression was upregulated and miR?197 expression was downregulated in patients with GC and in GC cells.Collectively, the results indicated that lncRNA JPX promoted GC progression by regulating CXCR6 and autophagy via inhibiting miR‑197. 	Moreover, high JPX expression and low miR?197 expression in patients with GC indicated poor prognosis.	Yes	Compared with the short hairpin RNA (sh) negative control (NC) group, NCI?N87 and MKN?45 cells in the shJPX group displayed decreased cell viability and invasion, as well as a wider scratch width. NCI?N87 and MKN?45 cells in the shJPX + miR?197 inhibitor group had increased viability and invasion, but a narrower scratch width compared with the shJPX group.	33215222
ITGB1-DT	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung cancer cells	Interaction(hsa-miR-30b-3p/ARNTL2 axis )	Transfection//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Our study identified the ITGB1-DT/ARNTL2 axis as a novel prognostic biomarker affects the prognosis of lung adenocarcinoma.		Yes	 The CCK-8, transwell, and colonu formation assays suggested that ITGB1-DT/ARNTL2 promotes the progression of lung adenocarcinoma. And hsa-miR-30b-3p reversed the ITGB1/ARNTL2-mediated oncogenic processes.	34906142
ITGB1-DT	LncRNA	Homo sapiens	lung non-small cell carcinoma	NSCLC patients and cells	Regulation( MAPK/ERK signaling)	Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	TGB1-DT was overexpressed in NSCLC.  In conclusion, inhibition of ITGB1-DT expression delayed the growth and metastasis of NSCLC using the MAPK/ERK signaling mechanism and enhanced the sensitivity of NSCLC to cisplatin drugs.	Elevated ITGB1-DT expression was related to the late T stage, N stage, M stage, short overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) of NSCLC patients.  ITGB1-DT was the independent risk factors for poor prognosis, and had diagnostic value for NSCLC patients.	Yes	Interfering with the ITGB1-DT expression can inhibit the proliferation, migration, and invasion of A549, H1299, and drug-resistant A549/DDP, possibly due to the inhibition of p38 MAPK and ERK phosphorylation levels.	35968342
ITGB1-DT	LncRNA	Homo sapiens	gastric adenocarcinoma	STAD tissues and cells	Expression(highly expressed)	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Invasion Assay	ITGB1-DT was expressed up-regulated in STAD tissues. GSEA results showed that ITGB1-DT may be involved in STAD progression through the insulin, p53, mechanistic target of rapamycin kinase (MTOR), and other signaling pathways. Overexpression of ITGB1-DT was significantly correlated with the levels of STAD B cells, T cells, T helper cells, CD8 T cells, cytotoxic cells, and other immune cells.	ITGB1-DT overexpression was associated with the T stage, therapeutic effect, overall survival, progression-free interval status, and poor prognosis in STAD patients. ITGB1-DT overexpression was valuable in diagnosing STAD and a negative factor affecting the prognosis of STAD patients.	Yes	Interference with ITGB1-DT expression inhibited STAD cell proliferation, invasion, and migration. 	35557569
ITGB1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell lines	Interaction[microRNA-10a]	CCK8//qRT-PCR//Colony Formation Assay	 LncRNA ITGB1 was found upregulated in BCa tissues and cell lines. The expression levels of ITGB1 and microRNA-10a in BCa tissues were negatively correlated. ITGB1 downregulation was found to be able to enhance microRNA-10a expression, suggesting that microRNA-10a may be a potential target for ITGB1 in BCa. In addition, cell reverse experiment also verified that ITGB1 could regulate the expression of microRNA-10a, and their interaction affected the malignant progression of BCa.		Yes	Knockdown of lncRNA ITGB1 remarkably inhibited cell proliferation. 	31486485
itchyE3ubiquitinproteinligase	CircRNA	Homo sapiens	Prostatic Neoplasms	cell lines(DU 145, 22RV1, VCaP, and PC-3)	Interaction[Targeting MiR-197]	CCK8//qRT-PCR	Circular RNA itchy E3 ubiquitin protein ligase expression was decreased in DU 145, 22RV1, VCaP, and PC-3 cells compared to RWPE cells. Cell apoptosis rate was elevated in circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids group compared to control overexpression plasmids group at 48 hours, and Western blot showed the similar results. Micro RNA-197 but not micro RNA-31 or micro RNA-432 was the target micro-RNA of circular RNA itchy E3 ubiquitin protein ligase. In rescue experiments, cell proliferation rate was elevated, but apoptosis rate was reduced in circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids/micro RNA (+) group compared to circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids group, indicating that circular RNA itchy E3 ubiquitin protein ligase upregulation inhibited cell proliferation but promoted apoptosis through downregulating micro RNA-197.		Yes	 In PC-3 cells, cell proliferation rate was reduced in circular RNA itchy E3 ubiquitin protein ligase overexpression plasmids group compared to control overexpression plasmids group at 48 hours and 72 hours.	31694481
ITCH	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cell lines and tissues	regulation[Wnt/β-catenin pathway]	qRT-PCR//RIP//PCR//IP//IF	Through RTq-PCR assays, we observed that cir-ITCH expression was attenuated in gastric cancer cell lines and tissues, with cir-ITCH expression in gastric cancer tissues with lymph node metastasis being considerably lower than that observed in gastric cancer tissues without lymph node metastasis. In summary, cir-ITCH was shown to prevent gastric cancer tumourgenesis through the Wnt/β-catenin signalling pathway by sequestering miR-17.	Through RTq-PCR assays, we observed that cir-ITCH expression was attenuated in gastric cancer cell lines and tissues, with cir-ITCH expression in gastric cancer tissues with lymph node metastasis being considerably lower than that observed in gastric cancer tissues without lymph node metastasis.	Yes	Moreover, in vivo and in vitro experimental results showed that cir-ITCH can act as a tumour suppressor to prevent gastric cancer tumourgenesis by sponging miR-17	33060778
ITCH	CircRNA	Homo sapiens	Stomach Neoplasms	 GC cell lines, GC tissues and their serum-derived exosomes	Interaction( miR-199a-5p/Klotho axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	In the present study, we found that circ-ITCH was down-regulated in GC cell lines, GC tissues and their serum-derived exosomes.Bioinformatic analysis and luciferase reporter assay confirmed that circ-ITCH acted as miR-199a-5p sponge and increased the level of Klotho. 		Yes	Functional assays showed that circ-ITCH overexpression inhibited the proliferation, migration, invasion and epithelial mesenchymal transition (EMT) of GC cells, whereas circ-ITCH knockdown appeared an opposite effect. 	33499704
ITCH	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	regulation[Wnt/β-catenin signaling pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	Compared with that in human normal liver L-02 cell line, the expression of circRNA-ITCH was significantly down-regulated in HCC Huh-7, U251, HB611 and SMMC-7721 cell lines (p<0.05).CircRNA-ITCH affects the proliferation and apoptosis of HCC cells through inhibiting the Wnt/β-catenin signal transduction pathway, thereby exerting a carcinogenic effect in the occurrence and development of HCC. 		Yes	According to the results of CCK-8 assay, colony formation assay and flow cytometry, the overexpression of circRNA-ITCH could obviously inhibit cell proliferation, suppress colony formation ability and induce apoptosis (p<0.05).	32862578
ITCH	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-106a/CDH1 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	Circ-ITCH was down-regulated in ovarian cancer and positively correlated with 5-year overall survival of patients with ovarian cancer. Circ-ITCH suppressed proliferation, invasion, glycolysis, and promoted apoptosis of ovarian cancer cells by modulating the miR-106a/CDH1 axis.	Circ-ITCH was down-regulated in ovarian cancer and positively correlated with 5-year overall survival of patients with ovarian cancer.	Yes	Functionally, circ-ITCH overexpression hindered proliferation, invasion, glycolysis and promoted apoptosis of ovarian cancer cells. 	32714095
ITCH	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	regulation[miR-421/PDCD4 Axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	ur results showed that circ-ITCH expression was remarkably decreased in OSCC tissues and cell lines.  In conclusion, our study reveals that circ-ITCH serves as a tumor suppressor in OSCC partly by regulating miR-421/PDCD4 axis.		Yes	Moreover, functional assays demonstrated that circ-ITCH overexpression significantly inhibited OSCC cell proliferation and induced cell apoptosis. 	32765068
ITCH	CircRNA	Homo sapiens	Osteosarcoma	cancer cell lines	regulation[cir-ITCH/miR-7/EGFR Pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 In this study, we performed experiments with the human osteoblast cell line hFOB1.19 and several osteosarcoma cancer cell lines and the results showed that the expression of cir-ITCH in osteosarcoma cancer cell lines was significantly upregulated compared to that in the human osteoblast cell line.In conclusion, our research uncovered an important role of the cir-ITCH/miR-7/EGFR pathway in the migration and invasion of osteosarcoma cells and suggested that cir-ITCH may be a prognostic marker and a promising therapeutic target for osteosarcoma.		Yes	In addition, the results showed that cir-ITCH could promote the migration, invasion, and growth of osteosarcoma cells. 	31960764
ITCH	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	regulation[microRNA-93-5p/FOXK2 Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our results showed that circ-ITCH was lowly expressed in both human cervical cancer tissues and cell lines.Mechanism investigations proved that circ-ITCH executed its tumor suppressive activity through sponging microRNA-93-5p (miR-93-5p) and regulating the expression of forkhead box K2 (FOXK2).		Yes	 Overexpression of circ-ITCH in HeLa cells significantly suppressed cell proliferation, migration, and invasion. A xenograft tumor model was established to evaluate the role of circ-ITCH in vivo.	31993998
ITCH	CircRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues & cell lines	Interaction(circ-ITCH/miR-214 axis)	In Vivo Experiment//IHC//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	a negative correlation between circ-ITCH and miR-214 expression and a positive correlation between circ-ITCH and PTEN expression were observed in NPC tissues. Downregulation of circ-ITCH expression was also observed in NPC cell lines. In addition, upregulation of circ-ITCH markedly inhibited NPC cell proliferation, migration and invasion. Furthermore, circ-ITCH was confirmed to exert its function by sponging miR-214. PTEN was found to be a direct target gene of miR-214 and its expression was negatively correlated with miR-214 expression in NPC tissues. Moreover, our results showed that the circ-ITCH/miR-214 axis regulated NPC proliferation, migration and invasion through regulating the expression of PTEN. Upregulation of circ-ITCH or PTEN blocked miR-214-mediated promotion of NPC tumorigenesis in vitro. Additionally, upregulation of circ-ITCH also suppressed NPC tumorigenesis in vivo.		Yes	 In addition, upregulation of circ-ITCH markedly inhibited NPC cell proliferation, migration and invasion. 	34612550
ITCH	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Regulation[miR-22-3p/CBL/β-catenin pathway]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	In this study, we reveal that lower levels of circRNA circ-ITCH are expressed in PTC tissues than in normal adjacent tissues.  In summary, our study reveals a novel signaling pathway of circ-ITCH/miR-22-3p/CBL/β-catenin involved in PTC development and progression.		Yes	Gain-of-functional assays show that circ-ITCH overexpression suppresses PTC cell proliferation and invasion and promotes apoptosis in vitro. Overexpression of circ-ITCH also leads to impaired tumor growth in vivo.	30190130
ITCH	CircRNA	Homo sapiens	Multiple Myeloma	Bone marrow	Expression[lower expressed]	qRT-PCR	Circ-ITCH expression was under-expressed in MM patients compared to healthy controls. 		Yes	In U226 cells, cell proliferation was decreased but apoptosis was elevated by circ-ITCH overexpression.	35117187
ITCH	CircRNA	Homo sapiens	Intervertebral Disc Degeneration	 IDD patients' nucleus pulposus (NP) tissues 	Interaction(miR-17-5p/SOX4 signaling/ Wnt/β-catenin)	Western Blot//qPCR//CCK8//Luciferase Report Assay//Cell Apoptosis Assay	Significantly, the expression levels of circITCH were elevated in the IDD patients' nucleus pulposus (NP) tissues relative to that of normal cases. Thus, we conclude that circITCH promotes ECM degradation in IDD by activating Wnt/β-catenin through miR-17-5p/SOX4 signaling.		Yes	CircITCH promoted apoptosis and decreased proliferation of NP cells. CircITCH contributed to ECM degradation, as demonstrated by increased ADAMTS4 and MMP13 expression and decreased aggrecan and collagen II expression. 	34015763
ITCH	CircRNA	Homo sapiens	ovarian carcinoma	ovarian carcinoma tissue 	Expression[lower expressed]	CCK8//qRT-PCR	 In this study, we observed that circular RNA-ITCH was downregulated, while lncRNA HULC was upregulated in ovarian carcinoma. 		Yes	Overexpression of circular RNA-ITCH resulted in inhibited, while overexpression of HULC promoted the proliferation of cells of ovarian cancer cell lines.	32046413
ITCH	CircRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction(miR-106b-5p/PDCD4 Axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	Results showed that circ-ITCH was low expressed in ccRCC tissues and cells. Mechanism investigations claimed that circ-ITCH exerted its metastasis-inhibitory activity via sponging miR-106b-5p and regulating the expression of PDCD4. Conclusively, circ-ITCH suppresses ccRCC metastasis by enforcing PDCD4 expression through binding miR-106b-5p. 		Yes	Downregulation circ-ITCH promoted cell migration, but overexpressing circ-ITCH inhibited cell migration and invasion in OSRC-2 and SW839 cells.	33969128
IRF1-AS	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction[IRF1 ]	RNA Pull-Down//Western Blot//ISH//CCK8//qRT-PCR//RIP//Luciferase Report Assay//RNA-seq//IHC	Furthermore, IRF1-AS was downregulated in ESCC tissues, and low expression correlated with poor prognosis.Mechanistically, IRF1-AS activates IRF1 (Interferon Regulatory Factor 1) transcription through interacting with ILF3 (Interleukin Enhancer Binding Factor 3) and DHX9 (DExH-Box Helicase 9). In turn, IRF1 binds to the IRF1-AS promoter directly and activates IRF1-AS transcription. Global analysis of IRF1-AS-regulated genes indicated that IRF1-AS activates the IFN response in vitro and in vivo. IRF1 knockdown in IRF1-AS-overexpressing cells abolished the antiproliferative effect and activation of the IFN response. 		Yes	Knockdown and overexpression of IRF1-AS revealed that IRF1-AS inhibits oesophageal squamous cell carcinoma (ESCC) proliferation and promotes apoptosis in vitro and in vivo.	31173852
ITGB1-DT	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	Interaction(microRNA‑7/HOXB13 )	qRT-PCR//Western Blot	The results revealed that LincIN expression was significantly increased in ESCC tissues and cell lines. On the whole, the findings of the present study suggest that LincIN is overexpressed and plays an oncogenic role in ESCC via the regulation of the NF90/miR‑7/HOXB13 axis. 	The increased expression of LincIN was positively associated with invasion depth, lymph node metastasis, TNM stage and a poor prognosis. 	Yes	 Functional assays revealed that the overexpression of LincIN promoted ESCC cell growth, migration and invasion.	33693959
ITGB2-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tumor and cell lines	Interaction(miR-328-5p/HMGA1 axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//Colony Formation Assay	We found that the expression level of ITGB2-AS1 was significantly higher in ccRCC tumor and cell lines, and highly expressed ITGB2-AS1 was also associated with a poorer prognosis.We further identified and confirmed the miRNA miR-328-5p as a target of ITGB2-AS1, and miR-328-5p negatively regulated the expression of HMGA1 protein. The anti-tumor effect of silencing ITGB2-AS1 could be partially rescued by inhibiting miR-328-5p activity or overexpressing HMGA1, indicating that ITGB2-AS1 promotes the survival and progression of ccRCC by modulating miR-328-5p/HMGA1 axis. 	We found that the expression level of ITGB2-AS1 was significantly higher in ccRCC tumor and cell lines, and highly expressed ITGB2-AS1 was also associated with a poorer prognosis.	Yes	Consistently, silencing ITGB2-AS1 inhibited proliferation, promoted apoptosis in ccRCC cell lines, and curbed the tumorigenesis in the Xenograft model, reduced tumorigenesis in a xenograft tumor growth model. 	34170494
ITGB2-AS1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tumor tissues and cell lines	regulation[miR-4319/RAF1 axis]	Western Blot//ISH//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The results showed that ITGB2-AS1 was elevated in both PDAC tumor tissues and cell lines, predicting a poor prognosis in PDAC patients.In conclusion, ITGB2-AS1 promoted PDAC progression via sponging miR-4319 to upregulate RAF1, suggesting the potential therapeutic target ability of ITGB2-AS1 in PDAC.	The results showed that ITGB2-AS1 was elevated in both PDAC tumor tissues and cell lines, predicting a poor prognosis in PDAC patients.	Yes	 Knocking down of ITGB2-AS1 suppressed PDAC cell proliferation, invasion, and migration but induced cell apoptosis in vitro. 	31957875
JPX	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[miR-25-3p/SOX4 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 We found that JPX was markedly upregulated, whereas miR-25-3p was markedly downregulated in CC tissues and cell lines, and the expression of JPX was negatively correlated with miR-25-3p in CC tissues.Our study demonstrates that JPX promotes cervical cancer progression through modulating the miR-25-3p/SOX4 axis, and may serve as a potential target for CC therapy.		Yes	Moreover, overexpression of JPX increased proliferation, migration and invasion of HeLa cells, whereas knockdown of JPX decreased proliferation, migration and invasion of HeLa cells. 	32943989
JPX	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Sample of the NSCLC tissues (n=45) and corresponding normal lung tissues (n=45)	Interaction(miR-5195-3p/VEGFA axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//cell invasion assay//IP//Colony Formation Assay	JPX and VEGFA were upregulated, and miR-5195-3p was downregulated in NSCLC. JPX is directly bound to miR-5195-3p. JPX regulated NSCLC cell proliferation, apoptosis and EMT by modulating miR-5195-3p.		Yes	JPX induced proliferation, colony number, invasion, migration, epithelial-mesenchymal transition (EMT), and inhibited apoptosis of NSCLC cells.	33613033
JPX	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	esophageal tissue and cells	Interaction(miR-516b-5p/VEGFA Axis)	CCK8//qRT-PCR//Western Blot	In the present study, we found JPX was highly expressed in esophageal tissue from ESCC patients. Mechanistically, the results showed that JPX functioned as a sponge of miR-516b-5p, which targeted vascular endothelial growth factor A (VEGFA) in ESCC cells. Interactions between miR-516b-5p and JPX or VEGFA were confirmed by luciferase reporter assays.		Yes	Functional assays demonstrated that JPX promoted ESCC cell proliferation, migration, and invasion in vitro, and accelerated tumor growth in vivo. Inhibition of JPX significantly attenuated the cell growth and mobility ability of ESCC cells in vitro.	35681693
JPX	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer metastatic tissues	regulation[JPX/miR-33a-5p/Twist1 axis,Wnt/β-catenin signaling]	Flow Cytometry//qRT-PCR//Colony Formation Assay//Western Blot	We observed that lncRNA JPX was upregulated in lung cancer metastatic tissues and was closely correlated with tumor size and an advanced stage. Mechanically, the JPX/miR-33a-5p/Twist1 axis participated in EMT progression by activating Wnt/β-catenin signaling.	We observed that lncRNA JPX was upregulated in lung cancer metastatic tissues and was closely correlated with tumor size and an advanced stage. 	Yes	Functionally, JPX promoted lung cancer cell proliferation in vitro and facilitated lung tumor growth in vivo. 	31941509
JPX	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	regulation[miR-944/CDH2 axis]	Tunel//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	LncRNA JPX was discovered as highly expressed in OSCC cells. In short, lncRNA JPX contributes to OSCC cell proliferation, migration, and invasion via miR-944/CDH2 axis, which offers a new direction for potential targeted treatment of OSCC.		Yes	Silencing lncRNA JPX restrained OSCC cell proliferation, migration, and invasion.	32881231
JPX	LncRNA	Homo sapiens	Osteosarcoma	 OS cells 	Regulation(Wnt/β-catenin pathway)	qRT-PCR//MTT	 Overexpression of lncRNA JPX into OS cell lines elevated the cell viability and proliferation, which was accompanied by the increased metastasis.  We also found that melatonin inhibited the OS progression by suppressing the expression of lncRNA JPX via regulating the Wnt/β-catenin pathway. 		Yes	 Overexpression of lncRNA JPX into OS cell lines elevated the cell viability and proliferation, which was accompanied by the increased metastasis. 	34547170
JPX	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(miR-33a-5p )	qRT-PCR//Wound Healing Assay//Western Blot	In this study, we found that lncRNA JPX was up-regulated in OS tissues and cells.Furthermore, it was verified that JPX acts as a sponge for miR-33a-5p, and that JPX regulated OS cell proliferation, migration and invasion through miR-33a-5p. Moreover, down-regulation of miR-33a-5p in OS contributed to PNMA1 upregulation, and PNMA1 depletion inhibited OS cell proliferation, migration and invasion in vitro. 		Yes	JPX down-regulation was observed to suppress OS cell proliferation, migration and invasion.	36067544
JHDM1D-AS1	LncRNA	Mus musculus	Brachial Plexus Neuropathies	 spinal cord tissues 	regulation[miR-101-3p/DUSP1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	We found significant downregulated expression of JHDM1D-AS1 and DUSP1 but upregulated expression of miR-101-3p in the spinal cord after tBPI. JHDM1D-AS1 exerted neuroprotective and anti-inflammatory effects in a rat model of tBPI by regulating miR-101-3p/DUSP1 axis.		Yes	Overexpression of JHDM1D-AS1 had a prominent neuroprotective effect by suppressing neuronal apoptosis and microglial inflammation through reactivation of DUSP1. 	33039970
ITGB2-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue samples and cell lines	Regulation[Wnt/β-catenin signalling]	Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	The expression levels of ITGB2-AS1 were up-regulated in osteosarcoma tissue samples and cell lines determined by qRT-PCR assay. Taken together, our study suggested that ITGB2-AS1 played critical roles in the development and progression of osteosarcoma via Wnt/β-catenin signalling, indicating that ITGB2-AS1 might be a valuable diagnostic biomarker and potential anticancer therapeutic target for osteosarcoma.	Osteosarcoma patients with high ITGB2-AS1 expression had a significantly poor prognosis.	Yes	In addition, knockdown of ITGB2-AS1 inhibited the proliferation and induced apoptosis of osteosarcoma cells using MTT assay and flow cytometry detection.	30260245
IUR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	interaction[miR-21 ]	CCK8//qRT-PCR//Western Blot	We found that IUR was down-regulated in ESCC, and low levels of IUR predicted poor survival of ESCC patients.Therefore, IUR may up-regulate PTEN by sponging miR-21 to regulate cancer cell proliferation and apoptosis in ESCC.	We found that IUR was down-regulated in ESCC, and low levels of IUR predicted poor survival of ESCC patients. 	Yes	Cell proliferation and apoptosis analysis showed that IUR and PTEN over-expression inhibited cancer cell proliferation and promoted apoptosis; while miR-21 over-expression played an opposite role. 	32124090
IUR	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	regulation[downregulates miR-144]	Cell Proliferation Assay//qRT-PCR//Western Blot	We aimed to explore the possible involvement of IUR in NPC. IUR and PTEN were downregulated, while miR-144 was upregulated in NPC.In conclusion, IUR can downregulate miR-144 to upregulate PTEN in NPC, therefore inhibiting NPC cell proliferation.		Yes	. Cell proliferation assay showed that overexpression of IUR and PTEN resulted in decreased NPC cell proliferation rate. 	32795216
IUR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues	interaction[Sponges miR-24 to Upregulate P53]	qRT-PCR//Wound Healing Assay//Transwell Assay	 We found that IUR was downregulated in LSCC.  In addition, subcutaneous tumor model in nude mice showed that overexpression of miR-24 attenuated the effects of overexpression of IUR on the expression of p53 and cancer cell proliferation.		Yes	Cell proliferation assay showed that overexpression of IUR and p53 led to decreased proliferation rate of LSCC cells, while overexpression of miR-24 led to increased proliferation rate of LSCC cells. We also illustrated that overexpression of IUR promoted cell migration and invasion while miR-24 had opposite effects.	33235495
IUR	LncRNA	Homo sapiens	prostate carcinoma	PC tissues	Interaction[upregulating miR-200]	qRT-PCR	We observed that IUR was downregulated in PC, and its expression levels decreased with the increase of clinical stages.Therefore, IUR can downregulate ZEB1 by upregulating miR-200 to inhibit PC cell invasion and migration.	We observed that IUR was downregulated in PC, and its expression levels decreased with the increase of clinical stages.	Yes	Cell invasion and migration analysis showed that IUR and miR-200 overexpression resulted in decreased invasion and migration rates. ZEB1 overexpression played an opposite role and attenuated the effects of IUR and miR-200 overexpression	31545930
IUR	LncRNA	Homo sapiens	stomach carcinoma	GC tissues 	regulation[downregulating ROCK1]	qRT-PCR//Transwell Assay	In this study, the authors showed that IUR was downregulated in GC. IUR is downregulated in GC and inhibits GC cell invasion and migration by downregulating ROCK1.	A follow-up study showed that low IUR expression levels predicted poor survival.	Yes	 ROCK1 overexpression resulted in increased GC cell invasion and migration, while IUR overexpression played an opposite role.	32783641
ITIH4-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Regulation[JAK/STAT3 Signaling]	ChIP//Western Blot//Co-IP//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//IF	Interestingly, a significant overexpression of ITIH4-AS1 was observed in CRC cell lines relative to normal NCM460 cells.  Additionally, we explained that ITIH4-AS1 upregulation in CRC was attributed to downregulation or even depletion of RE1 silencing transcription factor (REST), a presently identified transcriptional repressor for ITIH4-AS1. Meanwhile, the contribution of ITIH4-AS1 to CRC development was validated to rely on the activation of the JAK/STAT3 pathway. More importantly, we verified that FUS interacted with both ITIH4-AS1 and STAT3, and that ITIH4-AS1 evoked nuclear translocation of phosphorylated (p)-STAT3 in CRC through recruiting FUS. In summary, our findings unveiled for the first time that REST downregulation-enhanced ITIH4-AS1 exerts pro-tumor functions in CRC through FUS-dependent activation of the JAK/STAT3 pathway, implying that targeting ITIH4-AS1 may be a novel effective strategy for CRC therapy.		Yes	Also, we investigated the facilitating role of ITIH4-AS1 in CRC cell growth and metastasis both in vitro and in vivo. 	31557619
ITGB8-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction( miR-33b-5p and let-7c-5p/let-7d-5p/ITGA3 and ITGB3)	qRT-PCR//RNA-seq//Luciferase Report Assay//Western Blot	Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC.  Consistently, knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK, and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) markedly reduced cell proliferation and tumor growth in CRC, indicating the therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. 		Yes	Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation, and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1.	34371180
ITGB2-AS1	LncRNA	Homo sapiens	Breast Neoplasms		Regulation[ITGB2]	Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	In conclusion, LncRNA ITGB2-AS1 could promote the migration and invasion of breast cancer cells by up-regulating ITGB2.		Yes	The results of biological function experiments showed that ITGB2-AS1 could promote the migration and invasion of breast cancer.	29941860
HCG11	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Interaction(miRNA-490-3p/MAP3K9 Axis)	In Vivo Experiment//IHC//Western Blot//Transfection//qPCR//CCK8//FISH//Luciferase Report Assay//Cell Apoptosis Assay//H&E Staining//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	 HCG11 was highly expressed in NPC tissues and was positively associated with tumor stage, lymphatic metastasis, and poor prognosis. Mechanistically, miR-490-3p is a direct target of HCG11, oncogenic functions of HCG11 in NPC cell proliferation and migration can be partially reversed by the miR-490-3p inhibitor. HCG11 significantly increased mitogen-activated protein kinase MAPK kinase 9 (MAP3K9) levels by inhibiting miR-490-3p.		Yes	Functionally, HCG11 knockdown inhibited proliferation and migration and induced apoptosis of NPC cells. 	35463310
HCG11	LncRNA	Homo sapiens	Atherosclerosis	HUVECs	Interaction(miR-224-3p/JAK1 Axis)	Western Blot//Transfection//qPCR//Flow Cytometry//MTT//Luciferase Report Assay	And the levels of HCG11 and JAK1 was enhanced in ox-LDL-induced HUVECs, while miR-224-3p expression was reduced.Moreover, HCG11 could modulate the JAK1 expression via targeting miR-224-3p. The inhibitory effect of HCG11 silencing on cell pyroptosis and inflammation was reversed by miR-224-3p knockdown. Furthermore, overexpression of miR-224-3p could repress the ox-LDL-induced cell pyroptosis and inflammation via regulating JAK1 expression. Knockdown of HCG11 alleviated cell pyroptosis and inflammation induced by ox-LDL via targeting the miR-224-3p/JAK1 axis, indicating that HCG11 could be the latent target of diagnosis or treatment for AS.		Yes	Additionally, knockdown of HCG11 or miR-224-3p overexpression reversed the ox-LDL-induced cell viability decline and the increase of cell pyroptosis and inflammation-related proteins, including gasdermin D N-terminal (GSDMD-N), Caspase-1, NOD-like receptor family pyrin domain-containing 3 (NLRP3), interleukin 18 (IL-18), and interleukin 1beta (IL-1β). 	35931919
HCG11	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Interaction[AKT/mTOR pathway]	qRT-PCR//MTT//Transwell Assay//Western Blot	 More than that, lncRNA HCG11 inhibited phosphoinositide-3 kinase/protein kinaseB (PI3K/AKT) signaling pathway to suppress PCa progression. Our data showed the overexpression of HGC11-inhibited PI3K/AKT signaling pathway by downregulating miR-543 expression, resulting in the suppression of cell growth in PCa. This finding proved a new regulatory network in PCa and provided a novel therapeutic target of PCa.		Yes	Further investigation revealed that overexpression of HCG11 inhibited cell proliferation, invasion, and migration, whereas induced cell apoptosis by regulating miR-543 expression in vitro and in vivo.	31228307
FOXC2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(FOXC2)	RNA Pull-Down//Western Blot//MeRIP//CCK8//qRT-PCR//RIP//Transwell Assay	Here, we found that FOXC2-AS1 expression was significantly elevated in GC tissues and cells, and overexpression of FOXC2-AS1 indicated advanced TNM stage and shorter overall survival in GC patients.  Further investigation revealed that FOXC2-AS1 interacted with FOXC2 mRNA and repressed its degradation. FOXC2-AS1 recruited RNA methyltransferase NSUN2 to FOXC2 mRNA, increasing its m5C level and association with YBX1.	Here, we found that FOXC2-AS1 expression was significantly elevated in GC tissues and cells, and overexpression of FOXC2-AS1 indicated advanced TNM stage and shorter overall survival in GC patients. 	Yes	FOXC2-AS1 attenuated the proliferation, migration and invasion of GC cells, whereas overexpression of FOXC2-AS1 showed the opposite effects. 	34324140
FOXC2-AS1	LncRNA	Homo sapiens	Atherosclerosis	AS patients	regulation[miR-1253/FOXF1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	We found that FOXC2-AS1 was significantly upregulated in AS patients, which could be induced by ox-LDL and IL-6 in VSMCs. According to the results, we found that FOXC2-AS1 was upregulated in AS patients; furthermore, FOXC2-AS1 overexpression promoted cell proliferation and inhibited cell apoptosis via targeting miR-1253/FOXF1 signaling axis. 		Yes	 Furthermore, FOXC2-AS1 overexpression promoted proliferation and inhibited apoptosis in VSMCs. 	32271448
FOXC2-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissue and cells	Regulation[miR-1253/EZH2 axis]	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	Results stated that lncRNA FOXC2-AS1 was ectopically up-regulated in prostate cancer tissue and cells.  Mechanically, we found that miR-1253 targeted FOXC2-AS1 at the 3'‑untranslated regions (UTR), which in turn bind the EZH2 mRNA 3-UTR. Luciferase reporter assay and rescue experiment confirmed the FOXC2-AS1/miR-1253/EZH2 pathway. In conclusion, we confirmed that lncRNA FOXC2-AS1 accelerated the tumor progression of prostate cancer cells by regulating the proliferation and tumor growth through miR-1253/EZH2 axis.	 The over-expression of FOXC2-AS1 indicates the poor prognosis of prostate cancer patients. 	Yes	 Functionally, the gain- and loss-of-functional experiments revealed that FOXC2-AS1 promoted the proliferation and tumor growth of prostate cancer cells in vitro and in vivo. 	30389560
FOXC2-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tissues	regulation[silencing p15]	qRT-PCR//RIP//ChIP	 It was found that FOXC2-AS1 was upregulated in melanoma tissues, especially those with metastasis or stage II-IV. FOXC2-AS1 stimulates proliferative ability in melanoma via silencing p15.		Yes	 Knockdown of FOXC2-AS1 inhibited viability, and stimulated apoptosis in A375 and sk-mel-110 cells.	32964984
FOXC2-AS1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues and cells	Interaction(miR-6868-5p/E2F3 axis.)	ChIP//Western Blot//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	 FOXC2-AS1 expression was high in TSCC tissues and cells.  In the mechanism, it was verified that H3K27 acetylation (H3K27ac) triggered an increase in FOXC2-AS1 expression. Furthermore, FOXC2-AS1 was identified as a cytoplasmic lncRNA and served as a ceRNA to upregulate E2F3 expression via sponging miR-6868-5p.		Yes	Functional assays in vitro showed that silencing FOXC2-AS1 restrained cell proliferation, cell cycle, migration, invasion, and EMT.	34358374
FOXC2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissue	Interaction[silencing p15]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//ChIP	In this clinical NSCLC tissue samples, RT-PCR analysis revealed that lncRNA FOXC2-AS1 was up-regulated in the collected NSCLC tissue (Figure 1A, Table 1).  In conclusion, the results in this work confirmed that FOXC2-AS1 could aggravate NSCLC oncogenesis through repressing p15 expression via interacting EZH2, which provide new idea for the NSCLC therapeutic strategy.	 The ectopic high-expression level of FOXC2-AS1 is closely correlated with the limited NSCLC patients' survival. 	Yes	In the functional experiments, the knockdown of FOXC2-AS1 dramatically suppressed the NSCLC cells' (A549, H460) proliferation, accelerated the apoptosis and induced the cycle arrest at G0/G1 phase.	31396359
FOXC2-AC1	LncRNA	Homo sapiens	Lung Neoplasms	LCa tissues 	Interaction[regulating miR-107]	CCK8//qRT-PCR//Transwell Assay//Western Blot	 In this study, qRT-PCR results indicated that the expression level of FOXC2-AC1 in LCa was considerably higher than that in normal tissues, with statistically significant differences. In addition, miR-107 expression was found significantly reduced no matter in LCa cell lines or in tissues and showed a negative correlation with FOXC2-AC1. Subsequently, luciferase reporter gene assay demonstrated that overexpression of miR-107 significantly attenuated the luciferase activity of the wild-type FOXC2-AC1 vector without reducing the activity of the mutant vector or empty vector, further proving that FOXC2-AC1 could be targeted by miR-107 through this binding site. In addition, rescue experiment also found that FOXC2-AC1 and miR-107 have mutual regulation, which jointly affected the malignant progression of LCa.	Compared with patients with low expression of FOXC2-AC1, patients with high expression of FOXC2-AC1 had higher incidence of distant metastasis and lower overall survival rate.	Yes	Compared with the control group, the cell proliferation, invasion and metastasis capacities of FOXC2-AC1 overexpressing group were considerably enhanced, while opposite results were observed in the FOXC2-AC1 silencing group. 	30720176
FNDC3B	CircRNA	Homo sapiens	Stomach Neoplasms	 cell lines (AGS, SGC‐7901, MGC‐803, and BGC‐823)	Interaction[miR‑17‑5p]	Western Blot//qPCR//RIP//PCR//IP	We showed that circFNDC3B increased migration and invasion in gastric cancer (GC). Ectopic expression of circFNDC3B reduced the level of E‐cadherin protein to promote the epithelial–mesenchymal transition in GC. RNA immunoprecipitation assays and RNA pull‐Expression[down-expression] assays confirmed that circFNC3B increased CD44 expression, which was associated with cell adhesion, via the formation of a ternary complex of circFNDC3B‐IGF2BP3‐CD44 mRNA. These results indicated that circFNDC3B was associated with the degree of malignancy to highlight the specific characteristics of cell invasion.		Yes	However, Cell Counting Kit‐8 results showed that the overexpression of circFNDC3B inhibited cell proliferation, whereas silencing of circFNDC3B promoted cell proliferation (Figure S2).	30963578
FNDC3B	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC samples and cells	Interaction(miR-490-5p/TXNRD1)	RNA Pull-Down//Western Blot//ISH//Transfection//qPCR//Flow Cytometry//RIP//Proliferation Assay//PCR//Cell Proliferation Assay//IP//IHC//Invasion Assay//IF	We observed that circFNDC3B was upregulated in ESCC samples and cells, as well as ESCC-derived exosomes.  CircFNDC3B was a miR-490-5p sponge, and miR-490-5p inhibition reversed the role of exosomal circFNDC3B-downregulating in ESCC cells. TXNRD1 was a miR-490-5p target, and TXNRD1 elevation weakened the anti-cancer function of miR-490-5p upregulation in ESCC cells.		Yes	CircFNDC3B could be delivered via exosomes in tumor cells, and the colony formation, proliferation, migration, invasion, glycolysis, and in vivo growth ability of recipient cells were weakened after co-incubation with exosomal circFNDC3B-knockdown donor cells. 	35703190
FLVCR-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissue and cells	interaction[miR381-3p/CCND1]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	Prominently higher FLVCR-AS1 expression was found in OS tissue and cells, and was associated with poor prognosis (P<0.05, P<0.01, or P<0.001). FLVCR-AS1 promoted OS growth by upregulating CCND1 expression via downregulation of miR381-3p.		Yes	Compared with the siCtrl group, 143B and HOS cells of the siFLVCR-AS1 group had significantly lower OD450 values and clone numbers and obviously higher percentages of cells in the G1 phase and apoptosis (P<0.01 or P<0.001). 	32021264
FLVCR1-DT	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues ,cell lines	Interaction[targeting c-Myc]	qRT-PCR//Luciferase Report Assay//Western Blot	 High expression of FLVCR1-AS1 correlated with poor clinical outcomes and prognosis in patients with GC.The binding sites of micro RNA-155 (miR-155) on FLVCR1-AS1 were predicted using the miRDB program. Luciferase reporter assay was used to validate direct targeting of FLVCR1-AS1 by miR-155. The effects of FLVCR1-AS1 on expressions of c-Myc and p21 were assessed by western blotting. In vivo experiments were performed to analyze the effects of FLVCR1-AS1 on GC tumor growth.	High expression of FLVCR1-AS1 correlated with poor clinical outcomes and prognosis in patients with GC.	Yes	In vivo experiments were performed to analyze the effects of FLVCR1-AS1 on GC tumor growth.FLVCR1-AS1 promoted proliferation and invasion of GC cells by acting as a ceRNA to sponge miR-155.	30899380
FLVCR1-DT	LncRNA	Homo sapiens	Breast Neoplasms	BC cells	regulation[Wnt/β-catenin pathway,miR-381-3p/CTNNB1 axis]	RNA Pull-Down//Tunel//CCK8//qRT-PCR//RIP//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	 FLVCR1-AS1 was abnormally up-regulated in BC cells.FLVCR1-AS1 regulates BC malignant behavior via sequestering miR-381-3p and then freeing CTNNB1, implying a promising target for BC therapy.		Yes	Silencing FLVCR1-AS1 inhibited cell proliferation, migration, invasion, yet accelerating apoptosis.	32518523
FLVCR1-DT	LncRNA	Homo sapiens	Lung Neoplasms		Regulation[ Wnt/β-catenin signaling pathway]	qRT-PCR	 In this study, we found that the expression of FLVCR1-AS1 was increased in lung cancer tissues according to The Cancer Genome Atlas database. Similarly, FLVCR1-AS1 was significantly upregulated in lung cancer cell lines.In sum, FLVCR1-AS1 silencing inhibited the proliferation, migration, and invasion of lung cancer cells by inhibiting the activity of the Wnt/β-catenin signaling pathway.		Yes	Knockdown of FLVCR1-AS1 dramatically reduced the cell proliferation, migration, and invasion of SPCA1 and A549. 	30697812
FLVCR1-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-381/RAP2A axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results demonstrated that FLVCR1?AS1 was upregulated in CRC tissues and cells, and increased FLVCR1?AS1 expression levels in patients with CRC were associated with poor prognosis.Overall, the findings of the current study suggest that FLVCR1‑AS1 promotes CRC progression via the miR‑381/RAP2A pathway. These findings may provide a novel approach for CRC treatment.	The results demonstrated that FLVCR1?AS1 was upregulated in CRC tissues and cells, and increased FLVCR1?AS1 expression levels in patients with CRC were associated with poor prognosis.	Yes	FLVCR1?AS1 knockdown significantly attenuated the viability, migration and invasion ability of CRC cells.	33313944
FLVCR1-DT	LncRNA	Homo sapiens	Ovarian Neoplasms	OSC tissues,blood,cell line	Regulation[miR-513/YAP1 signaling]	Western Blot//Wound Healing Assay//CCK8//Colony Formation Assay//Transwell Assay	In this study, FLVCR1-AS1 expression was upregulated in OSC tissues, serums, and cells.Besides, FLVCR1-AS1 directly bound to miR-513 and downregulated its expression. Moreover, FLVCR1-AS1 reversed the effect of miR-513 on the OSC cell growth, which might be associated with the role of YAP1. Furthermore, in terms of mechanism, FLVCR1-AS1 promoted EMT in OSC cells. Finally, mice models further confirmed that knockdown FLVCR1-AS1 distinctly suppressed cell growth and EMT in vivo.		Yes	 Knockdown FLVCR1-AS1 decreased cell growth, migration, invasion, and EMT, as well as increased apoptosis in OSC cells, whereas, overexpression of FLVCR1-AS1 increased cell proliferation, migration, invasion, and EMT, and decreased apoptosis of OSC cells.	31412903
FLVCR1-DT	LncRNA	Homo sapiens	Osteosarcoma	Osteosarcoma tissues,cell lines	regulation[wnt/β-catenin pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	LncRNA FLVCR1-AS1 was upregulated in osteosarcoma, which was positively correlated to tumor size, WHO grade and distant metastasis, but negatively correlated to survival of osteosarcoma patients. FLVCR1-AS1 accelerates the progression of osteosarcoma via activating wnt/β-catenin pathway.	LncRNA FLVCR1-AS1 was upregulated in osteosarcoma, which was positively correlated to tumor size, WHO grade and distant metastasis, but negatively correlated to survival of osteosarcoma patients. 	Yes	 Overexpression of FLVCR1-AS1 markedly suppressed osteosarcoma cells to proliferate, migrate and invade.	33099956
FLVCR1-DT	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cells	Interaction(miR-381-3p/MAGT1 axis)	RNA Pull-Down//Western Blot//Transfection//Tunel//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In CC cells, FLVCR1-AS1 and MAGT1 were upregulated and miR-381-3p was downregulated. FLVCR1-AS1 sponged miR-381-3p, and MAGT1 was targeted by the FLVCR1-AS1/miR-381-3p axis.		Yes	FLVCR1-AS1 or MAGT1 knockdown or miR-381-3p augment restrained CC cell proliferation, migration and invasion, but facilitated cell apoptosis. 	35430713
FLVCR1-DT	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cell lines	Interaction(miR-23a-5p/SLC7A11)	qRT-PCT//Western Blot//Transfection//Migration Assay//CCK8//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The findings suggest that the expression of FLVCR1-AS1 was elevated in CC tissues and cell lines, and that high expression of FLVCR1-AS1 was associated with poor prognosis of CC patients.  In addition, via the dual-luciferase reporting assay and RIP assay were confirmed that FLVCR1-AS1 acted as a competitive endogenous RNA to inhibit the expression of microRNA (miR)-23a-5p, and miR-23a-5p targeted the 3'-untranslated region site of Solute carrier family 7 member 11 (SLC7A11) and negatively regulated the expression of SLC7A11. 	The findings suggest that the expression of FLVCR1-AS1 was elevated in CC tissues and cell lines, and that high expression of FLVCR1-AS1 was associated with poor prognosis of CC patients. 	Yes	 In addition, knockdown of FLVCR1-AS1 could inhibit the proliferation and migration, invasion and epithelial-mesenchymal transformation (EMT) of CC cells, as well as accelerating apoptosis, to inhibit the development of CC. 	35465835
FLVCR1-DT	LncRNA	Homo sapiens	Glioma	GBM tissues,cell lines	regulation[regulating miR-30b-3p]	CCK8//qRT-PCR//Transwell Assay	 FLVCR1?AS1 expression was significantly upregulated in GBM tissues compared with adjacent normal brain samples, and was higher in GBM cell lines compared with normal human astrocyte cells. The results from the present study demonstrated that FLVCR1‑AS1 may serve an oncogenic role in GBM and promote disease progression by interacting with miR‑30b‑3p. 		Yes	 The results from Cell Counting Kit?8 and Transwell assays confirmed that FLVCR1?AS1?knockdown inhibited GBM cell proliferation and invasion ability. 	32626942
FLVCR1-DT	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and PC cell lines	Interaction(KLF10 /PTEN/AKT pathway)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//migration assay//Cell Proliferation Assay//IHC//ChIP	FLVCR1-AS1 expression was low in both PC tissues and PC cell lines, and FLVCR1-AS1 downregulation was associated with a worse prognosis in patients with PC. Mechanistic investigations revealed that FLVCR1-AS1 acts as a ceRNA to sequester miR-513c-5p or miR-514b-5p from the sponging KLF10 mRNA, thereby relieving their suppressive effects on KLF10 expression. Additionally, FLVCR1-AS1 was shown to be a direct transcriptional target of KLF10.	FLVCR1-AS1 expression was low in both PC tissues and PC cell lines, and FLVCR1-AS1 downregulation was associated with a worse prognosis in patients with PC.	Yes	Functional experiments demonstrated that FLVCR1-AS1 overexpression significantly suppressed PC cell proliferation, cell cycle, and migration both in vitro and in vivo. 	34635142
FOXC2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[Ca2+-FAK signal pathway]	qRT-PCR	 In this study, we observed that lncRNA FOXC2-AS1 was upregulated in CRC tissues, and its high expression indicated the poor survival in CRC patients.  These results demonstrated that FOXC2-AS1 enhances FOXC2 mRNA stability to promote CRC proliferation, migration, and invasion by activation of Ca2+-FAK signaling, which implicates that FOXC2-AS1 may represent a latent effective therapeutic target for CRC progression.	 In this study, we observed that lncRNA FOXC2-AS1 was upregulated in CRC tissues, and its high expression indicated the poor survival in CRC patients. 	Yes	FOXC2-AS1 knockdown suppressed CRC cell growth, invasion, and metastasis in vitro and in vivo.	32513911
FOXCUT	LncRNA	Homo sapiens	gastric adenocarcinoma	gastric adenocarcinoma tissues	Expression[Expression[highly expressed]-expression]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	Expressions of lncRNA FOXCUT in cancer tissues of GA patients in TCGA database were significantly increased (p<0.001).	The survival rate of patients with low expressions of lncRNA FOXCUT was significantly increased (p=0.017, p=0.047). LncRNA FOXCUT is closely related to patients' tumor diameter, lymph node metastasis, TNM staging, and differentiation degree (p<0.05). 	Yes	We showed that the inhibition of the expressions of lncRNA FOXCUT can reduce the proliferation and invasion of GA cells and increase apoptosis, which can be used as a potential therapeutic target for GA.	31364114
FLNA	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer cells	Interaction( miR-486-3p/XRCC1 and CYP1A1)	colony Formation Assay//Western Blot//Transfection//qPCR//IF//PCR//Colony Formation Assay//Transwell Assay	MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells.Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. 		Yes	 Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic.	33500536
FOXCUT	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial cancer cells	Expression [highly expressed]	cell invasion assay//qRT-PCR//Transfection//Migration Assay	This study ascertained that lncRNA FOXCUT was highly expressed in endometrial cancer cells. 		Yes	Overexpression of lncRNA FOXCUT promoted EC cell proliferation, invasion, and migration, as well as epithelial-mesenchymal transition (EMT). In addition, overexpression of lncRNA FOXCUT could inhibit the apoptosis of cancer cells and block EC cells in S phase, whereas silencing lncRNA FOXCUT had the opposite effect.	34591391
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and GSCs	Interaction( TAF-1/NOTCH )	RNA Pull-Down//ChIP//Western Blot//Luciferase Report Assay//Microarray//IF	 LncRNA FOXD2-AS1, TAF-1 and NOTCH1 were found to be elevated in glioma tissues and GSCs, and silencing lncRNA FOXD2-AS1 inhibited stemness and proliferation, while promoting apoptosis and differentiation of GSCs. Mechanistically, lncRNA FOXD2-AS1 elevation promoted glioma in vivo by activating the NOTCH signalling pathway via TAF-1 upregulation. 		Yes	 LncRNA FOXD2-AS1, TAF-1 and NOTCH1 were found to be elevated in glioma tissues and GSCs, and silencing lncRNA FOXD2-AS1 inhibited stemness and proliferation, while promoting apoptosis and differentiation of GSCs.LncRNA FOXD2-AS1 overexpression also led to increased NOTCH1 by recruiting TAF-1 to the NOTCH1 promoter region, thereby promoting stemness and proliferation, while impairing cell apoptosis and differentiation. 	35419917
FOXD2-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms		Interaction[Sponging miR-7-5p]	IP//RIP//Western Blot	FOXD2-AS1 was upregulated in thyroid carcinoma tissues and cells.Silencing FOXD2-AS1 inhibited cancer stem cell-like phenotypes and attenuates the anoikis resistance in vitro. Downregulating FOXD2-AS1 represses the tumorigenesis of thyroid carcinoma cells in vivo. 	High expression of FOXD2-AS1 significantly correlated with clinical stage, recurrence of thyroid carcinoma. 	Yes	Silencing FOXD2-AS1 inhibited cancer stem cell-like phenotypes and attenuates the anoikis resistance in vitro. Downregulating FOXD2-AS1 represses the tumorigenesis of thyroid carcinoma cells in vivo. 	31024447
FOXD2-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction[miR-185-5p]	CCK8//qRT-PCR//Microarray//cell invasion assay//Colony Formation Assay//EdU Staining	 FOXD2-AS1 was significantly upregulated in PTC tissues, and high FOXD2-AS1 expression was positively associated with malignant potential factors in PTC patients. In addition, high level of FOXD2-AS1 expression was an unfavorable independent prognostic biomarker for patients with PTC.  Bioinformatics analysis indicated that activation of cell cycle and apoptosis pathways might be involved in the oncogenic function of FOXD2-AS1 in PTC. Moreover, we demonstrated that FOXD2-AS1 directly interacted with miR-185-5p as miRNA sponge and overexpression of FOXD2-AS1 partially reversed the suppressive effect of miR-185-5p in TPC cells.	 FOXD2-AS1 was significantly upregulated in PTC tissues, and high FOXD2-AS1 expression was positively associated with malignant potential factors in PTC patients. In addition, high level of FOXD2-AS1 expression was an unfavorable independent prognostic biomarker for patients with PTC. 	Yes	Moreover, we found that knockdown of FOXD2-AS1 could effectively inhibit PTC cell proliferation and invasion in vitro and suppress tumor growth of PTC in vivo.	31632522
FOXD2-AS1	LncRNA	Homo sapiens	Gallbladder Neoplasms	gallbladder cancer cells	regulation[MLH1 promoter methylation]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//FISH//RIP//EdU Staining//Transwell Assay	We found that lncRNA FOXD2-AS1 was highly expressed, while MLH1 was poorly expressed in gallbladder cancer cells.Thus, silencing of lncRNA FOXD2-AS1 suppressed the progression of gallbladder cancer via upregulation of MLH1 by inhibiting MLH1 promoter methylation.		Yes	Silencing of lncRNA FOXD2-AS1 or overexpression of MLH1 inhibited gallbladder cancer cell proliferation, invasion, and migration, while facilitating cell apoptosis in vitro as well as retarding tumor growth in vivo. 	32917950
FOXD2-AS1	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tissues and cells	Interaction(miRNA-31/PAX9)	Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	FOXD2-AS1 was upregulated, and miR-31 was lowly expressed in retinoblastoma.  lncRNA FOXD2-AS1 directly bound to miR-31 and regulated miR-31 expression in SO-RB50 cells. Cell proliferation and migration were inhibited by the miR-31 mimic. miR-31 mediated PAX9 expression via directly binding to PAX9 mRNA. A miR-31 inhibitor partially reversed the effect of FOXD2-AS1 knockdown on the proliferation and migration in SO-RB50 cells. FOXD2-AS1 knockdown reduced PAX9 expression in SO-RB50 cells. PAX9 had negative connection with miR-31, and it had positive relationship with FOXD2-AS1.		Yes	 Low expression of FOXD2-AS1 promoted cell proliferation and migration, and upregulation of FOXD2-AS1 inhibited proliferative and migratory abilities. 	35782084
FOXD2-AS1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues	regulation[NF-kB and ERK MAPK signaling pathways]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	 Compared to the normal tissues and samples, FOXD2-AS1 significantly highly expressed in TSCC tissues and in TSCC samples of TCGA data, and high expression of FOXD2-AS1 was associated with lymphatic metastasis and poor TNM stages. High expression of FOXD2-AS1 promotes TSCC progression through modulating NF-kB and ERK MAPK signaling pathways and is associated with TSCC poor prognosis, it could be a novel therapeutic target and prognostic biomarker for TSCC.	 Compared to the normal tissues and samples, FOXD2-AS1 significantly highly expressed in TSCC tissues and in TSCC samples of TCGA data, and high expression of FOXD2-AS1 was associated with lymphatic metastasis and poor TNM stages.	Yes	Downregulation of FOXD2-AS1 inhibited the migration and invasion of SCC-9 and CAL-27 cell lines.	32531865
FOXD2-AS1	LncRNA	Homo sapiens	laryngeal carcinoma	laryngeal cancer tissues	Interaction[targeting miR-206]	qRT-PCR//Luciferase Report Assay//MTT//Colony Formation Assay	: The expression of FOXD2-AS1 in laryngeal cancer tissues was significantly higher than that in normal tissues(t=10.012, P<0.05), and was associated with T staging of laryngeal cancer(χ=6.41, P=0.016). Double luciferase assay showed that FOXD2-AS1 could directly bind to miR-206, thus inhibiting the expression of miR-206. Further MTT assay indicated that inhibiting miR-206 attenuated the suppressing effect of si-FOXD2-AS1 on the proliferation of TU686 cells. 	The expression of FOXD2-AS1 in laryngeal cancer tissues was significantly higher than that in normal tissues(t=10.012, P<0.05), and was associated with T staging of laryngeal cancer(χ=6.41, P=0.016).	Yes	FOXD2-AS1 down regulated proliferation activity of TU686 cells(t=9.337, P<0.05).	31163553
FOXD2-AS1	LncRNA	Homo sapiens	skin melanoma	cutaneous melanoma tissues	Interaction[phospho-Akt ]	CCK8//qRT-PCR//Western Blot//Transwell Assay	In our study, FOXD2-AS1 expression has been found to be Expression[Expression[up-expression]-expression]regulated in cutaneous melanoma tissue specimens and cell lines compared with that in normal tissue specimens and normal human epidermal melanocyte, respectively. 	Furthermore, high expression of FOXD2-AS1 was obviously correlated with deep Breslow thickness, present ulceration, high Clark level and distant metastasis in cutaneous melanoma patients.	Yes	The results of loss-of-function study showed that inhibition of FOXD2-AS1 sExpression[Expression[up-expression]-expression]presses cutaneous melanoma cell proliferation, migration and invasion through regulating phospho-Akt expression. 	30426532
FOXD2-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Regulation[ miR-485-5p/KLK7 axis]	qRT-PCR	FOXD2-AS1 was found to observably upregulated in PTC tissues and cell lines. Rescue assays were conducted to verify the function of FOXD2-AS1/miR-485-5p/KLK7 axis in PTC progression.	Kaplan-Meier survival analysis revealed that high expression of FOXD2-AS1 was closely correlated with the unfavorable prognosis of patients with PTC.	Yes	Loss-of-function assays revealed that knockdown of FOXD2-AS1 or KLK7 greatly inhibited PTC cell proliferation and migration, while induced cell apoptosis.	30456805
FOXD2-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Expression[highly expressed]	Western Blot//Transwell Assay	The expression of FOXD2-AS1 was upregulated in HNSCC.	 The expression of FOXD2-AS1 was upregulated in HNSCC; it was positively related with the pathological stage as well as with poor prognosis in HNSCC patients.	Yes	FOXD2-AS1 silencing inhibited HNSCC cell migration and invasion, also influenced the expression of epithelial-mesenchymal transition-related molecules.	32762453
FOXD2-AS1	LncRNA	Homo sapiens	Pterygium	recurrent pterygium tissues	interaction[sponging miR-205-5p]	CCK8//qRT-PCR//Flow Cytometry//ChIP	 FOXD2-AS1 expression was up-regulated in recurrent pterygium tissues. In conclusion, FOXD2-AS1 is activated via its H3K27 acetylation and regulates VEGF-A expression by sponging miR-205-5p in recurrent pterygium.	Moreover, a high FOXD2-AS1 expression was associated with advanced stages, increased microvessel density and shorter recurrent-free survival. 	Yes	 Furthermore, we show that FOXD2-AS1 induced proliferation and inhibited apoptosis in a cell line derived from recurrent pterygia (HPF-R) at least partially through the regulation of the miR-205-VEGF pathway.	33098266
FOXD2-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC tissues	regulation[ miR-145-5p/CDK6 axis]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 We found FOXD2-AS1 was significantly upregulated in EC tissues compared with adjacent normal tissues, which was positively correlated with clinicopathological parameters of patients with EC. In conclusion, silening FOXD2-AS1 significantly inhibited the proliferation and invasion of EC cells by regulating the miR-145-5p/CDK6 axis. 		Yes	Downregulation of FOXD2-AS1 inhibited the proliferation and invasion by inducing apoptosis of EC cells. 	32524576
FOXD1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	stomach tissues,cell lines	regulation[ PI3K/AKT/mTOR pathway]	qRT-PCR	 Expression of FOXD1-AS1 was low in normal stomach tissues but was upregulated in GC cell lines.In conclusion, FOXD1-AS1 aggravates GC progression and chemoresistance by promoting FOXD1 translation via PIK3CA/PI3K/AKT/mTOR signaling.		Yes	Silencing of FOXD1-AS1 impaired GC cell proliferation and motility in vitro, and repressed tumor growth and metastasis in vivo.	32460412
FOXD1-AS1	LncRNA	Homo sapiens	Glioma	cell lines	Interaction[targeted both miR339-5p and miR342-3p]	Western Blot//Wound Healing Assay//qPCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	FOXD1-AS1 was upregulated and directly correlated with the glioma grade, and it was localized in both the nucleus and the cytoplasm of the glioma cell.These data indicated that FOXD1-AS1, a miR339/342 target, affected biological processes via protein eIF5a; thus, it might be considered as a new therapeutic target for glioblastoma.		Yes	FOXD1-AS1 silencing caused tumor suppressive effects via inhibiting cell proliferation, migration, and apoptosis, while FOXD1-AS1 overexpression resulted in opposite effects. Additionally, in vivo experiments showed that FOXD1-AS1 knockdown reduced tumor volume and weight. 	31102349
FOXD1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cells and tissues	regulation[sustaining FOXD1 expression]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//FISH//RIP//MTT//IHC//Transwell Assay	 We found that FOXD1-AS1 was over-expressed in NPC cells and tissues, and was significantly associated with poor survival rate in patients with NPC. 	 We found that FOXD1-AS1 was over-expressed in NPC cells and tissues, and was significantly associated with poor survival rate in patients with NPC. 	Yes	We also found that FOXD1-AS1 promotes cellular proliferation, migration, invasion, and glycolysis, and inhibits apoptosis by upregulating the expression of FOXD1. 	33294261
FOXCUT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[FOXC1/PI3K/AKT Pathway ]	qRT-PCR//MTT//Western Blot//Transwell Assay	 In this study, a novel long noncoding RNA (FOXCUT) was frequently overexpressed in CRC tissues and cell lines.Mechanistically, FOXCUT promotes the expression of FOXC1 to activate PI3K/AKT signaling pathway for its regulation of cell growth and proliferation.		Yes	Moreover, knockdown of FOXCUT significantly inhibited proliferation and invasion of CRC cell lines and resulted in downregulated expression of the matrix metalloproteinase 1 (MMP-1). 	32801872
FOXCUT	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	tumor tissues and adjacent tissues	Expression(highly expressed)	CCK8//qRT-PCR//Transfection	The expression level of FOXCUT was significantly increased in NPC tissues as compared with the adjacent tissues (P < 0.001). Compared with NP69 cells, CNE1, CNE2, SUNE2, HER2 and 5-8F cells all exhibited significantly increased expressions of FOXCUT (P < 0.001). In CNE1 cells, transfection with FOXCUT shRNA significantly inhibited cell proliferation and clone formation (P < 0.001), and caused obvious changes in cell morphology. FOXCUT knockdown significantly decreased the expressions of N-cad and vimentin, increased E- cad expression and the contents of MDA and LDH (P < 0.05), reduced vimentin- positive cells and the activity of SOD, and caused a shift of red fluorescent cells to green fluorescent cells and an increased percentage of green fluorescent cells. FOXCUT knockdown also resulted in significantly increased expressions of Bax/Bcl2 and cleaved Cas3/Cas3 and a lowered expression of c-Myc.		Yes	FOXCUT knockdown significantly decreased the expressions of N-cad and vimentin, increased E- cad expression and the contents of MDA and LDH (P < 0.05), reduced vimentin- positive cells and the activity of SOD, and caused a shift of red fluorescent cells to green fluorescent cells and an increased percentage of green fluorescent cells. FOXCUT knockdown also resulted in significantly increased expressions of Bax/Bcl2 and cleaved Cas3/Cas3 and a lowered expression of c-Myc.	34658347
FLVCR1-DT	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tumor tissues	Interaction[sponging miR-485-5p]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay	A significantly higher expression level of FLVCR1-AS1 was identified in CCA tumor tissues and the CCA cell lines HuCCT1 and CCLP1 compared with the normal controls. Mechanistically, FLVCR1-AS1 was demonstrated to sponge microRNA-485-5p (miR-485-5p) in human CCA. The expression of miR-458-5p was significantly decreased in CCA tissue compared with normal tissue, and Pearson's correlation analysis revealed that FLVCR1-AS1 expression was negatively correlated with miR-485-5p expression in CCA tissues.		Yes	Furthermore, FLVCR1-AS1 knockdown inhibited tumor growth in a xenograft model.	31404302
FLG-AS1	LncRNA	Homo sapiens	Diabetic Retinopathy	serum of DR patients	Interaction(miR-380-3p/SOCS6 Axis)	In Vivo Experiment//Western Blot//Transfection//Tunel//qRT-PCR//Luciferase Report Assay//ELISA	Compared to that in healthy controls, FLG-AS1 expression decreased 2.5-fold and miR-380-3p expression increased 2.6-fold in the serum of DR patients. The expression levels of FLG-AS1 and miR-380-3p were negatively correlated in DR patients (r = -0.3772, P = 0.003).  FLG-AS1 promoted the expression of SOCS6 by targeting miR-380-3p. Inhibition of miR-380-3p or overexpression of SOCS6 reduced inflammation, oxidative stress, and apoptosis of HG-treated ARPE-19 cells. FLG-AS1 mitigates DR by regulating retinal epithelial cell inflammation, oxidative stress, and apoptosis via the miR-380-3p/SOCS6 axis.		Yes	 Overexpression of FLG-AS1 reduced inflammation, oxidative stress, and apoptosis of HG-treated ARPE-19 cells and alleviated retinal injury in diabetic rats. 	35461393
FEZF1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Regulation[JAK-STAT3 Pathway]	CCK8//qRT-PCR//Western Blot	FEZF1-AS1 was overexpressed in ovarian cancer tissues compared to adjacent normal tissues.Our study demonstrated that FEZF1-AS1 exerted an oncogenic role in ovarian cancer via modulating JAK-STAT3 pathway.	Furthermore, higher expression of FEZF1-AS1 in ovarian cancer patients contributed to poorer prognosis.	Yes	FEZF1-AS1 knockdown significantly suppressed the proliferation and promoted apoptosis in ovarian cancer cells.	30416194
FGD5-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues and cell lines 	Interaction(miR-497-5p/PD-L1 Axis)	CCK8//qRT-PCR//Transwell Assay	Specifically, we found that lncRNA FGD5-AS1 and PD-L1 tended to be high-expressed, while miR-497-5p was low-expressed in CC tissues and cell lines compared to the normal adjacent tissues and cells. . Next, we found that lncRNA FGD5-AS1 positively regulated PD-L1 in CC cells by sponging miR-497-5p. 		Yes	Functionally, the data suggested that lncRNA FGD5-AS1 positively regulated while miR-497-5p negatively modulated malignant phenotypes, including cell proliferation, viability, invasion, migration, epithelial-mesenchymal transition (EMT), and tumorigenesis in CC cells. Interestingly, the inhibiting effects of lncRNA FGD5-AS1 ablation on CC development were abrogated by both silencing miR-497-5p and upregulating PD-L1. 	35845947
FGD5-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissues and cell lines	Regulation(miR-873-5p)	qRT-PCR	We found that the expression of FGD5-AS1 was upregulated in HCC tissues and cell lines. Moreover, the knockdown of FGD5-AS1 suppressed cell proliferation, migration and invasion, and induced apoptosis in HCC cells. Further studies demonstrated that FGD5-AS1 could function as a competitive RNA by sponging miR-873-5p in HCC cells. Moreover, GTPBP4 was identified as direct downstream target of miR-873-5p in HCC cells and FGD5-AS1mediated the effects of GTPBP4 by competitively binding with miR-873-5p. Taken together, this study demonstrated the regulatory role of FGD5-AS1 in the progression of HCC and identified the miR-873-5p/GTPBP4 axis as the direct downstream pathway. It represents a promising novel therapeutic strategy for HCC patients.		Yes	Moreover, the knockdown of FGD5-AS1 suppressed cell proliferation, migration and invasion, and induced apoptosis in HCC cells. Further studies demonstrated that FGD5-AS1 could function as a competitive RNA by sponging miR-873-5p in HCC cells.	34783233
FGD5-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	Tumor and normal adjacent tissues	Interaction(miR-223)	qRT-PCR	FGD5-AS1 was upregulated in HCC and its high expression indicated poor prognosis of patients. High expression of FGD5-AS1 enhanced HCC cell proliferation and stemness. Knockdown of FGD5-AS1 restrained tumor growth and stemness in mice. FGD5-AS1 directly sponged miR-223 and promoted the expression of ECT2 and FAT1 in HCC. Both knockdown of miR-223 and overexpression of ECT2 and FAT1 reversed FGD5-AS1 silencing-mediated suppression of HCC cell proliferation and stemness.	FGD5-AS1 was upregulated in HCC and its high expression indicated poor prognosis of patients	Yes	Knockdown of FGD5-AS1 restrained tumor growth and stemness in mice. 	35366388
FGD5-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	Interaction( miR-142-5p)	qRT-PCR//Luciferase Report Assay//RIP	First, we found that FGD5-AS1 was markedly up-regulated in OC. Mechanistically, it was revealed that FGD5-AS1 targeted miR-142-5p to repress its expression and function. Furthermore, miR-142-5p has a binding site for 3' UTR of PD-L1, and FGD5-AS1 could positively regulate PD-L1 expression via repressing miR-142-5p. 	 Moreover, its high expression level was associated with positive local lymph node metastasis and higher T stage in OC patients.	Yes	Gain-of-function and loss-of-function assays demonstrated that FGD5-AS1 facilitated the proliferation, migration, as well as invasion of OC cells.	33974163
FGD5-AS1	LncRNA	Homo sapiens	Osteosarcoma	 OSA tissues and cell lines,	Interaction(miR-506-3p/RAB3D axis)	qRT-PCR//RIP	It was demonstrated that the expression of FGD5-AS1 was up-regulated in OSA tissues and cell lines, and its high expression is associated with higher Enneking stage and poorer histological differentiation. The promoting effects of FGD5-AS1 overexpression on OSA cell proliferation and migration could be counteracted by miR-506-3p. Moreover, FGD5-AS1 competitively adsorbed miR-506-3p to repress its expression so as to up-regulate the expression of RAB3D. 		Yes	Gain-of-function and loss-of-function studies suggested that FGD5-AS1 facilitated OSA cells proliferation and migration. 	33891267
FGD5-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[wnt/β-Catenin Pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 FGD5-AS1 was significantly increased in glioma tissues and cells.Our research emphasized FGD5-AS1 acting as an oncogene by regulating wnt/β-catenin signaling pathway, thus providing some novel experimental basis for clinical treatment of glioma.		Yes	The in vivo tumor growth assay showed that FGD3-AS1 accelerated glioma tumorigenesis with activating wnt/β-catenin pathway.	32801867
FGD5-AS1	LncRNA	Homo sapiens	Glioblastoma	 GBM tumor tissues and cells	regulation[miR-129-5p/HNRNPK axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	FGD5-AS1 expression was increased in GBM tumor tissues and cells.FGD5-AS1 promoted GBM progression at least partly by regulating miR-129-5p/HNRNPK to activate Wnt/β-catenin signaling, suggesting the potential of FGD5-AS1 as a candidate target to improve GBM therapy.		Yes	Knockdown of FGD5-AS1 inhibited cell proliferation and invasion in vitro, and slowed tumor growth in vivo. 	32585241
FGD5-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	HUVEC, SW1736 and KAT18 TC cells 	Interaction(miR-6838-5p/VAV2 Axis)	Western Blot//In vivo experiment//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In this study, SW1736 and KAT18 TC cells with high expression of FGD5-AS1 were screened. This effect is achieved through activation of the miR-6838-5p/VAV2 axis. 		Yes	Overexpression of FGD5-AS1 enhanced proliferation, migration, angiogenesis, and permeability of HUVEC.	35528244
FGD5-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	 PC cells	Interaction(miR-520a-3p/KIAA1522 axis)	RNA Pull-Down//Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	As a result, the abnormal high expression of FGD5-AS1 was observed in PC cells.Moreover, FGD5-AS1 was proven to combine with miR-520a-3p directly. It was also confirmed that KIAA1522 could be targeted by miR-520a-3p. Rescue assay results indicated that overexpressed KIAA1522 could reverse the repressive function of silencing FGD5-AS1 on PC progression. 		Yes	And cell proliferative and migratory abilities could be restrained via FGD5-AS1 depletion. 	33794727
FGD5-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues and cell	Interaction(miR-497-5p/SEPT2 signaling)	qRT-PCR//Luciferase Report Assay//Western Blot	Specifically, LncRNA FGD5-AS1 sponged miR-497-5p to upregulate SEPT2 in LSCC cells in a competing endogenous RNA (ceRNA) mechanisms-dependent manner.  Interestingly, upregulated LncRNA FGD5-AS1 and downregulated miR-497-5p were observed in LSCC tissues and cells, and LncRNA FGD5-AS1 ablation inhibited cancer progression. Collectively, we conclude that targeting the LncRNA FGD5-AS1/miR-497-5p/SEPT2 signaling cascade may be an alternative strategy to treat LSCC in the clinic.		Yes	 Interestingly, upregulated LncRNA FGD5-AS1 and downregulated miR-497-5p were observed in LSCC tissues and cells, and LncRNA FGD5-AS1 ablation inhibited cancer progression. 	34003510
FGD5-AS1	LncRNA	Homo sapiens	Mouth Neoplasms	OC tissues and cells	regulation[ FGD5-AS1/ miR-153-3p/MCL1 axis ]	Wound Healing Assay//CCK8//qRT-PCR//EdU Staining//Transwell Assay	FGD5-AS1 was significantly increased in OC tissues and cells. CCK8 assay, Edu assay, wound healing assay and transwell assay were used to detect the FGD5-AS1/ miR-153-3p/MCL1 axis function on proliferation, migration and invasion in OC cells.		Yes	 Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of OC cells. 	32675387
FGD5-AS1	LncRNA	Homo sapiens	Mouth Neoplasms	OSCC tissue and cells	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 FGD5-AS1 expression was aberrantly up-regulated in OSCC tissue and cells.FGD5-AS1 regulates OSCC via competitively binding to miR-520b against USP21. I		Yes	Knockdown of FGD5-AS1 inhibited cell growth, migration, and invasion, yet promoted apoptosis.	31899825
FGD5-AS1	LncRNA	Homo sapiens	Osteonecrosis	hBMSCs	Interaction(miR-296-5p/STAT3 Axis)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	 In addition, lncRNA FGD5-AS1 acts as a sponge for miR-296-5p. Also, miR-296-5p directly targets STAT3. More importantly, miR-296-5p and STAT3 can affect the function of lncRNA FGD5-AS1 in Dex-treated hBMSCs.		Yes	Overexpression of lncRNA FGD5-AS1 promoted cell proliferation and restrained apoptosis in Dex-treated hBMSCs. 	35190765
FEZF1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-363-3p/HMGA2]	ISH//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//Transwell Assay	Here, we discovered that FEZF1-AS1 was upregulated in GC tissues and cell lines. In general, our findings clarified the critical regulatory role of FEZF1-AS1/miR-363-3p/HMGA2 axis in GCSC progression, providing a potential therapeutic target for GC.		Yes	Moreover, FEZF1-AS1 silence also suppressed cell proliferation, viability, invasion, and migration of GCSCs. 	32638620
FEZF1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	Interaction[Wnt/β-catenin pathway]	qRT-PCR//Wound Healing Assay//Cell Cycle Assay//Invasion Assay	FEZF1-AS1 was remarkably upregulated in ESCC tissues and cell lines.We also found that β-catenin was upregulated in ESCC tissues, and the level of it was positively correlated with the expression of FEZF1-AS1. Silencing of FEZF1-AS1 could decrease the mRNA and protein level of β-catenin, while overexpression FEZF1-AS1 could lead to the contrary.		Yes	Silencing of FEZF1-AS1 significantly inhibited the migration and invasion of ESCC cells, while overexpression of FEZF1-AS1 notably accelerated ESCC migration and invasion.	31191005
FEZF1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction[FEZF1-AS1/OTX1/EMT pathway]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	We verified that FEZF1-AS1 is highly expressed in CRC tissues and cell lines. Mechanistically, we discovered that reduced levels of the lncRNA FEZF1-AS1 inhibited the activation of epithelial-mesenchymal transition (EMT); the overexpression of orthodenticle homeobox 1 (OTX1) partially rescued the FEZF1-AS1-induced inhibition of protein expression. It indicated that FEZF1-AS1 may play a role in the occurrence and development of CRC by regulating the FEZF1-AS1/OTX1/EMT pathway. Furthermore, it was reported that FEZF1-AS1 is located in both the nucleus and cytoplasm of HCT116 cells. Dual-luciferase reporter assays verified that FEZF1-AS1 directly binds miR-30a-5p and negatively regulated each other. Further, we showed that 5'-nucleotidase ecto (NT5E) is a direct target of miR-30a-5p, and the inhibition of miR-30a-5p expression partially rescued the inhibitory effect of FEZF1-AS1 on NT5E. 		Yes	Through functional experiments, we found that reduced levels of FEZF1-AS1 significantly suppressed CRC cell migration, invasion, and proliferation and inhibited tumor growth in vivo. 	31270006
FEZF1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-363-3p/PRRX1 pathway)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We demonstrated that FEZF1-AS1 expression was upregulated in CRC, and its silencing reduced CRC cell proliferation, migration, invasion, and EMT.  MiR-363-3p could be inhibited by FEZF1-AS1, which inhibitor could reverse the suppressive effect of FEZF1-AS1 silencing on CRC progression. Paired-related homeobox 1 could be targeted by miR-363-3p, and the inhibitory effect of FEZF1-AS1 knockdown on CRC progression could also be eliminated by PRRX1 overexpression. Furthermore, interference of FEZF1-AS1 reduced the tumor growth of CRC in vivo.		Yes	We demonstrated that FEZF1-AS1 expression was upregulated in CRC, and its silencing reduced CRC cell proliferation, migration, invasion, and EMT. Furthermore, interference of FEZF1-AS1 reduced the tumor growth of CRC in vivo.	34286520
FEZF1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissues and cells	Interaction(FEZF1-AS1/miR-92b-3p/ZIC5 axis)	qRT-PCR//Wound Healing Assay	The expression of FEZF1-AS1 and ZIC5 was significantly higher and that of miR-92b-3p was lower in the colon cancer than in the normal colon tissues.  According to the prediction, FEZF1-AS1 and ZIC5 might competitively bind to miR-92b-3p, leading to the weakening of the inhibitory impact of miR-92b-3p on ZIC5 and increasing expression of ZIC5, thus further activating the PI3K/AKT signaling pathway, which led to the occurrence and development of colon cancer. 		Yes	 FEZF1-AS1 promoted the migration, proliferation, as well as invasion of RKO. 	36219353
FEZF1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines and tissues	interaction[miR-4443 ]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	In the present study, it was identified that FEZF1?AS1 was significantly upregulated in HCC cell lines and tissues, as determined by reverse transcription?quantitative polymerase chain reaction. Collectively, the present results demonstrated that FEZF1‑AS1 acts as an oncogene by acting as a sponge for miR‑4443.	Additionally, it was observed that higher expression of FEZF1?AS1 in patients with HCC indicated poorer prognosis.	Yes	Furthermore, it was identified that knockdown of FEZF1?AS1 markedly inhibited the proliferation, colony formation, migration and invasion of Hep3B and Huh7 cells, as determined by Cell Counting Kit?8, colony formation and Transwell assays. 	30365146
FEZF1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Regulated[up-regulated]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	lncRNA FEZF1-AS1 may strengthen the growth, migration and invasion of hepatocellular carcinoma cells.		Yes	In addition, knockdown or overexpression of lncRNA FEZF1-AS1 expression inhibited or enhanced the migration and invasion abilities as well as the levels of adhesion molecules in hepatocellular carcinoma cells.	31550856
FGD5-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	renal cancer tissues	regulation[ERK/AKT signalling]	Western Blot//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 LncRNA FGD5-AS1 was highly expressed in renal cancer tissues, especially in patients with metastasis.Mechanistically, lncRNA FGD5-AS1 can competitively interact with miR-5590-3p and regulate the downstream signalling of ErkAKT to enhance the malignancy of tumours. 		Yes	This effect facilitated the proliferation, migration, epithelial-mesenchymal transition and invasion of renal cancer cells. Silencing the expression of FGD5-AS1 with FGD5-AS1 siRNA significantly inhibited the malignancy of tumour cells.	32964964
FGD5-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Interaction[sponging miR-302e and upregulating CDCA7]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	FGD5-AS1 was increased in colorectal cancer cell lines compared to normal cell lines.LncRNA FGD5-AS1 could promote CRC progression through sponging miR-302e and upregulating CDCA7. 		Yes	Inhibition of FGD5-AS1 suppressed cell proliferation, migration, invasion, and accelerated cell apoptosis in CRC.	31332696
FKBP9P1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues	regulation[PI3K/AKT signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	FKBP9P1 expression was significantly up-regulated in HNSCC tissues (tumor vs. normal, 1.914 vs. 0.957, t = 7.746, P < 0.001) and cell lines (P < 0.01 in all HNSCC cell lines). Silencing lncRNA FKBP9P1 represses HNSCC progression and inhibits PI3K/AKT (phosphatidylinositol 3 kinase/AKT Serine/Threonine Kinase) signaling in vitro.	Besides, the median FKBP9P1 expression of HNSCC tissues (1.677) was considered as the threshold. High FKBP9P1 level was correlated with advanced T stage (P = 0.022), advanced N stage (P = 0.036), advanced clinical stage (P = 0.018), and poor prognosis of HNSCC patients (overall survival, P = 0.002 and disease-free survival, P < 0.001). 	Yes	Knockdown of FKBP9P1 led to marked repression in proliferation, migration, and invasion of HNSCC cells in vitro (P all < 0.01).	32769488
FGD5-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Interaction(miR-493-5p/DDX5 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	Expression of FGD5-AS1 in NSCLC tissues and cell lines was up-regulated.  FGD5-AS1 directly targeted miR-493-5p, while DDX5 was the target of miR-493-5p in NSCLC cells. 	Expression of FGD5-AS1 was in association with enlarged tumor size and lymph node metastasis of the patients.	Yes	Knockdown of FGD5-AS1 led to the inhibition of proliferation, migration, invasion and EMT of NSCLC cells.	33550957
FIRRE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation(CREB/PFKFB4 )	CCK8//qRT-PCR//Western Blot	 Here, we disclosed that the FIRRE level was frequently increased in HCC compared to nontumor tissues. Compared with normal liver cells, we also confirmed the upregulated level of FIRRE in HCC cells.Mechanistically, modulating FIRRE level did not affect the stability of PFKFB4 mRNA. FIRRE was mainly distributed in HCC cells' nucleus and promoted PFKFB4 transcription and expression via cAMP-responsive element-binding protein (CREB). PFKFB4 could abolish the effects of FIRRE knockdown on HCC cell proliferation and glycolysis. 	Notably, the FIRRE high expression was related to malignant clinical features, including advanced TNM stage and tumor size ≥5 cm, and conferred to worse survival of HCC. 	Yes	Functionally, FIRRE knockdown repressed the proliferation and glycolysis of HCCLM3 cells.Overexpression of FIRRE strengthened Huh7 cell proliferation and glycolysis. Notably, FIRRE positively regulated the glycolic enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) expression in HCC cells.	34093813
FIRRE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines and tissue samples	Interaction(MBNL3/PXN )	qRT-PCR	In this study, we found that FIRRE, a recently identified cancer-associated lncRNA located on chromosome X, is highly expressed in HCC cell lines and tissue samples, and its expression is positively correlated with poor HCC prognosis.  As for the potential mechanism, FIRRE specifically binds to the splicing factor MBNL3 to affect the expression of PXN to regulate the pathological characteristics of HCC cells.	In this study, we found that FIRRE, a recently identified cancer-associated lncRNA located on chromosome X, is highly expressed in HCC cell lines and tissue samples, and its expression is positively correlated with poor HCC prognosis. 	Yes	 In vitro and in vivo functional analyses showed that FIRRE could promote the proliferation, migration, and invasion of HCC. 	35988459
FIRRE	LncRNA	Homo sapiens	Gallbladder Neoplasms	60 GBC and 20 para-carcinoma tissue samples	Interaction(miR-520a-3p/YOD1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//RIP//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//IHC//Transwell Assay	FIRRE level was dramatically increased in GBC tissues compared to that in the adjacent non-tumor tissues. Mechanistically, FIRRE modulated YOD1 expression by sponging miR-520a-3p, thus contributing to the development of GBC.	High expression of FIRRE was closely related to clinical stage and poor prognosis in GBC patients. 	Yes	Moreover, FIRRE remarkably enhanced proliferation and migration, and inhibited apoptosis of GBC cells. 	34168678
FIRRE	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cells	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	qRT-PCR proved that lncRNA functional intergenic repeating RNA element (FIRRE) was up-regulated in DLBCL tissues and cells. Taken together, FIRRE activated Wnt/β-catenin signaling pathway to facilitate DLBCL cell growth via modulation of the nuclear translocation of β-catenin.	Based on Kaplan-Meier analysis, high FIRRE level was associated with the poor overall survival.	Yes	Subsequently, cell functional assays further revealed that FIRRE functioned as an oncogene by promoting cell proliferation and reducing cell apoptosis in DLBCL. 	30739786
FIRRE	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL cells	Interaction(PTBP1/Smurf2 )	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	FIRRE was specifically up-regulated in and essentially maintained multiple malignant behaviors of BCR-dependent DLBCL cells. Through the interaction with PTBP1, FIRRE promoted the mRNA decay of Smurf2, a ubiquitin ligase for the degradation BCR protein. Targeting FIRRE was sufficient to regulat Smurf2 and BCR expressions and inhibit DLBCL malignancy both in vivo and in vitro. FIRRE-PTBP1 interaction, by simulating Smurf2 mRNA decay and stabilizing BCR, promotes the development of DLBCL. 		Yes	Targeting FIRRE was sufficient to regulat Smurf2 and BCR expressions and inhibit DLBCL malignancy both in vivo and in vitro. 	35416325
Firre	LncRNA	Mus musculus	Neuralgia	spinal cord tissue 	regulation[suppressing HMGB1 expression]	qRT-PCR//RNA Pull-Down//RIP	FIRRE expression was upregulated in the spinal cord tissue of female CCI mice and LPS-induced microglial cells. Our findings indicated that lncRNA FIRRE downregulation inhibits the secretion of microglial cells-derived proinflammatory cytokines by decreasing HMGB1 expression, thereby relieving neuropathic pain of female mice.		Yes	The in vivo experiment showed that FIRRE knockdown alleviated neuropathic pain of CCI female mice. 	33151463
FGF7-5	LncRNA	Homo sapiens	Atherosclerosis	carotid plaque 	Regulation	RNA Pull-Down//Transfection//RIP//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	Next, lncRNA_FGF7-5 and lncRNA_GLRX3 targeted miR-2681-5p directly to upregulate ERCC4 expression.Taken together, these findings indicated that lncRNA_FGF7-5 and lncRNA_GLRX3 together reduced atherosclerosis-induced apoptosis of HUVECs via targeting miR-2681-5p to increase ERCC4 expression, thereby preventing the formation of carotid plaque and finally inhibiting atherosclerosis progression.		Yes	Silencing of lncRNA_FGF7-5 and lncRNA_GLRX3 promoted apoptosis and TP53 expression in HUVECs treated with ox-LDL; however, these effects were reversed by ERCC4-overexpression. 	36071684
FGF14-AS2	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction[sponging miR-205-5p]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	FGF14-AS2 was down-regulated while miR-205-5p was up-regulated in breast cancer tissues and cells and correlated with tumor stage and size.Moreover, FGF14-AS2 could directly bind to miR-205-5p, and the overexpression of FGF14-AS2 undermined the miR-205-5p induced effects on proliferation, migration, invasion, and apoptosis in breast cancer cells.	 FGF14-AS2 was down-regulated while miR-205-5p was up-regulated in breast cancer tissues and cells and correlated with tumor stage and size.	Yes	Functionally, the overexpression of FGF14-AS2 or miR-205-5p knockdown suppressed proliferation, migration, and invasion, and induced apoptosis of breast cancer cells.	31486497
FGF14-AS2	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[miR-370-3p/FGF14 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Transwell Assay	The lncRNA FGF14-AS2 was significantly downregulated in breast cancer tissues; patients with lower FGF14-AS2 expression had advanced clinical stage. Collectively, our findings support a model in which the FGF14-AS2/miR-370-3p/FGF14 axis is a critical regulator in breast cancer metastasis, suggesting a new therapeutic direction in breast cancer.	The lncRNA FGF14-AS2 was significantly downregulated in breast cancer tissues; patients with lower FGF14-AS2 expression had advanced clinical stage. 	Yes	 In vitro and in vivo assays of FGF14-AS2 alterations revealed a complex integrated phenotype affecting breast cancer cell migration, invasion, and tumor metastasis. 	33083023
FGF14-AS2	LncRNA	Homo sapiens	Colorectal Neoplasms	Colorectal Cancer tissues	regulation[RERG/Ras/ERK Signaling ]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	Via RT-qPCR, we confirmed the downregulation of FGF14-AS2 in collected colorectal carcinoma samples.  Taken together, the current study demonstrated FGF14-AS2 as a regulator of colorectal cancer development via downregulation of miR-1288-3p and inactivation of Ras/ERK signaling.		Yes	 Transfection of plasmid containing full length of FGF14-AS2 repressed cell proliferation and induced elevation of cell apoptosis in colorectal cancer cells.	32654025
FGF14-AS2	LncRNA	Homo sapiens	prostate carcinoma	prostate carcinoma tissue and cells	Interaction(miR-96-5p/AJAP1 axis)	In Vivo Experiment//Western Blot//qRT-PCR//FISH//RIP//MTT//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	FGF14-AS2 was a downregulated lncRNA in prostate carcinoma tissue and cells. FGF14-AS2 could restrain miR-96-5p expression while miR-96-5p hampered AJAP1.Moreover, miR-96-5p mimic presented a cancer promoter role in prostate carcinoma cells. AJAP1 expression level could affect levels of proteins related to epithelial-mesenchymal transition. 		Yes	 FGF14-AS2 could effectively decrease the biological behaviors of prostate carcinoma cells, while knock-down of FGF14-AS2 triggered opposite results. In vivo experiment suggested that overexpressing FGF14-AS2 could reverse the promotion of silenced AJAP1 on prostate carcinoma cell metastasis, thus to inhibit tumor growth.	34655124
FGF14-AS2	LncRNA	Mus musculus	Glioma	 glioma tissues 	Interaction(miR-320a/E2F1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 In the present study, we found that FGF14-AS2 expression was significantly elevated in glioma tissues and was associated with poor survival in glioma patients.In addition, FGF14-AS2 was observed to promote glioma progression via the miR-320a/E2F1 axis.	 In the present study, we found that FGF14-AS2 expression was significantly elevated in glioma tissues and was associated with poor survival in glioma patients.	Yes	Silencing FGF14-AS2 inhibited the proliferation, migration and invasion ability of glioma cells. In vivo assay showed that silencing FGF14-AS2 led to inhibition of tumour growth. 	34659533
FGD5‑AS1/microRNA‑133a‑3p	LncRNA	Rattus norvegicus	Sepsis	Mice HL-1 cardiac muscle cells	Interaction(FGD5‑AS1/miR‑133a‑3p/AQP1)	qRT-PCR//ELISA//RNA Pull-Down//Luciferase Report Assay	Compared with the control group, the expression of FGD5‑AS1 was decreased and the expression of miR‑133a‑3p was increased in the sepsis group. FGD5‑AS1 overexpression increased LPS‑induced expression of FGD5‑AS1 and AQP1, decreased the expression of miR‑133a‑3p, and inhibited the expression of the inflammatory cytokines, TNF‑α, IL‑6 and IL‑1β. Dual‑luciferase reporter and miRNA pull‑down assays confirmed the interaction of FGD5‑AS1, miR‑133a‑3p and AQP1. These results indicated that FGD5‑AS1 is the competitive endogenous RNA of miR‑133a‑3p on AQP1, and thus FGD5‑AS1 overexpression may be able to inhibit the inflammatory response in sepsis.		Yes	 FGD5‑AS1 overexpression increased LPS‑induced expression of FGD5‑AS1 and AQP1, decreased the expression of miR‑133a‑3p, and inhibited the expression of the inflammatory cytokines, TNF‑α, IL‑6 and IL‑1β. Dual‑luciferase reporter and miRNA pull‑down assays confirmed the interaction of FGD5‑AS1, miR‑133a‑3p and AQP1.	34498707
FGD5‑AS1	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissue samples and disease model cell lines	Interaction(hsa‑miR‑195‑5p/NUAK2 axis)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//Luciferase Report Assay//Invasion Assay//Transwell Assay	High expression of lncRNA FGD5-AS1 was detected in breast cancer tissue samples and disease model cell lines. It was identified that at a molecular level FGD5‑AS1 serves as a sponge of miR‑195‑5p and alters the expression of its downstream target gene NUAK2. In breast cancer lncRNA FGD5‑AS1 serve a key role in glycolysis and tumor progression via the miR‑195‑5p/NUAK2 axis. 		Yes	Silencing of FGD5‑AS1 led to decreased cell proliferation, migration and invasion. 	33880593
FGD5‑AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	 pancreatic cancer tissues and cell lines	Interaction( miR‑577/Wnt/β‑catenin signaling)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//MTT//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	The expression level of FGD5-AS1 was upregulated in pancreatic cancer tissues and cell lines. In conclusion, in pancreatic cancer, highly expressed FGD5‑AS1 activated the Wnt/β‑catenin signaling and promoted cancer cell proliferation, migration and invasion via suppression of miR‑577.		Yes	 FGD5‑AS1 knockdown inhibited pancreatic cancer cell proliferation, migration and invasion. 	34821374
FGD5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric cancer tisssues, cell lines	regulation[miR-153-3p/CITED2 Axis]	CCK8//qRT-PCR//Luciferase Report Assay	Both gastric cancer cell lines and human tumor samples showed aberrant FGD5-AS1 upregulation. We demonstrated that FGD5-AS1 can regulate human gastric cancer cell functions, possibly through its downstream epigenetic axis of hsa-miR-153-3p/CITED2.		Yes	 Lentiviral-induced FGD5-AS1 knockdown reduced cancer proliferation, 5-FU chemoresistance in vitro, and tumorigenicity in vivo. 	32849774
FGD5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(FZD3)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	FGD5-AS1 was upregulated in GC tissues compared to paracancerous ones.  FZD3 was the downstream target of FGD5-AS1. Protein levels of FZD3 and FZD5 were upregulated, while b-catenin, TGF-b and MMP9 were downregulated in GC cells with FGD5-AS1 knockdown. Knockdown of FZD3 abolished the regulatory effects of FGD5-AS1 on malignant phenotypes of GC cells. 	GC patients expressing a high level of FGD5-AS1 had higher risk of lymphatic metastasis or distant metastasis and worse prognosis than those with a low level. 	Yes	 Knockdown of FGD5-AS1 weakened proliferative and metastatic abilities in AGS and SGC-7901 cells. 	35848483
FGD5-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		interaction[hsa-miR-107,FGFRL1]	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	High-level expression of FGD5-AS1 was found in NSCLC. Thence, we concluded that lncRNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1.		Yes	FGD5-AS1 may promote the proliferation of NSCLC cells.	31919528
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[inhibiting P53]	qRT-PCR//RIP//ChIP	FOXD2-AS1 was significantly upregulated in glioma tissues and cells.  FOXD2-AS1 stimulated the proliferation of glioma by inhibiting P53, thus aggravating the progression of glioma.	The expression level of FOXD2-AS1 was positively correlated with tumor size and staging of glioma.	Yes	The silence of FOXD2-AS1 significantly decreased the viability and colony formation abilities of glioma cells. 	32373975
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	cell lines	interaction[binding to miR-506-5p]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. 		Yes	Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. 	33336050
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction[FOXD2-AS1/miR-31/CDK1 pathway]	qRT-PCR//Luciferase Report Assay	In this paper, FOXD2-AS1 was found to be upregulated in glioma tissues.Collectively, our results indicated that the FOXD2-AS1/miR-31/CDK1 axis influenced glioma progression, providing a potential new target for glioma patients.	In this paper, FOXD2-AS1 was found to be upregulated in glioma tissues. Its level was linked with glioma stage. Moreover, glioma patients expressing high level of FOXD2-AS1 suffered worse prognosis. 	Yes	 Further experiments demonstrated that silence of FOXD2-AS1 inhibited proliferation, arrested cell cycle and downregulated cyclin-dependent kinase 1 (CDK1) in human glioma cells. 	31347720
FTX	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues and cell lines	Expression(highly expressed)	In Vivo Experiment//Western Blot//Transfection//Tunel//Migration Assay//CCK8//qRT-PCR//Cell Cycle Assay//IHC//Invasion Assay	Reverse transcription-quantitative PCR analysis revealed that the expression levels of FTX were upregulated in thyroid cancer tissues and cell lines compared with those in normal tissues and cell lines, respectively. 	Survival analysis demonstrated that patients with upregulated FTX expression had a lower survival rate. 	Yes	Functional experiments revealed that the knockdown of FTX inhibited proliferation, cell cycle progression, migration and invasion, and induced apoptosis in thyroid cancer cells, while FTX overexpression accelerated proliferation, migration and invasion, and alleviated apoptosis in thyroid cancer cells. In addition, FTX knockdown significantly inhibited tumor growth in vivo. 	34345297
FTX	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC clinical tissue samples and cell lines	Expression[lower expressed]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay//IF	Here, we report that long non-coding RNA FTX expression level is down-regulated in NSCLC clinical tissue samples and cell lines. Furthermore, we find that FTX overexpression activates the expression of transcription factor FOXA2, an important regulator in lung cancer progression, and we reveal a novel FTX/miR-200a-3p/FOXA2 competing endogenous RNA regulatory axis in lung cancer cells. 		Yes	Ectopic expression of FTX inhibits proliferation and metastasis of lung cancer cells in vitro and in vivo.	32176463
FTX	LncRNA	Homo sapiens	Retinoblastoma	RB tissues and cancer cell lines	Interaction(miR-320a)	In Vivo Experiment//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	 In the present study, we found that the expression levels of FTX were notably elevated in RB tissues and cancer cell lines. 		Yes	Overexpression of FTX exacerbated the aggressive phenotypes (cell proliferation, migration and invasion) of RB cells. Downregulation of miR-320a obviously attenuated the inhibitory effects of knockdown of FTX in RB malignant phenotypes, and knockdown of WNK1 also reversed the impacts of miR-320a inhibitor on malignant phenotypes. In vivo experiments further confirmed that knockdown of FTX efficiently prevents tumor growth in vivo.	34720057
Ftx	LncRNA	Mus musculus	Epilepsy	hippocampus	Regulation[miR-21-5p/SOX7 axis]	Western Blot//Tunel//Flow Cytometry//qRT-PCR//Luciferase Report Assay	Our results showed that FTX is notably reduced in the hippocampus. Collectively, our study for the first time demonstrated the anti-apoptosis ability of FTX during epileptogenesis and uncovered a novel FTX-mediated mechanism in SE-induced neural apoptosis by targeting miR-21-5p/SOX7 axis, which provides a new target in developing lncRNA-based strategies to reduce SE-induced hippocampal neuron apoptosis.		Yes	 Moreover, the in vivo overexpression of FTX inhibited SE-induced hippocampus neuron apoptosis.	30871773
FTH1P3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Expression[highly expressed]	qRT-PCR//Wound Healing Assay//Transwell Assay//Western Blot	 The results showed that FTH1P3 was highly expressed in NSCLC tumor tissues and NSCLC-derived cell lines.Notably, FTH1P3 knockdown could decrease expression of N-cadherin, vimentin and Snail protein of NSCLC cells, but promote E-cadherin protein expression, which was in accordance with its effect on cell migration and invasion. To sum up, our data demonstrated that FTH1P3 predicts a poor prognosis and promotes metastasis and aggressiveness in NSCLC by inducing EMT, suggesting FTH1P3 may be a promising target for gene therapy of NSCLC.	The results showed that FTH1P3 was highly expressed in NSCLC tumor tissues and NSCLC-derived cell lines, and high expression of FTH1P3 was associated with advanced TNM stage and lymph node metastasis. NSCLC patients with high FTH1P3 expression had a poor overall survival relative to patients with low FTH1P3 expression. 	Yes	Through loss-of-function studies, FTH1P3 inhibition was demonstrated to suppress NSCLC cell migration and invasion in vitro.	31933766
FTH1P3	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Regulation[SP1/NF-kB pathway]	qRT-PCR//Wound Healing Assay//Colony Formation Assay	 FTH1P3 was significantly upregulated in ESCC tissues and cells (P < 0.001).  Silencing of FTH1P3 decreased the expression of specificity protein 1 (Sp1) and NF-kB (p65) in EC9706 and EC1.		Yes	 Knockdown of FTH1P3 notably decreased the proliferation, migration, and invasion capacity of ESCC cells. 	30119232
FTH1P3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[PI3K/Akt/GSK3b/ Wnt/β-catenin signaling]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	The expression level of FTH1P3 was significantly upregulated in OSCC tissues and cell lines. We demonstrated that FTH1P3 acted as a tumor promoter by regulating PI3K/Akt/GSK3β/Wnt/β-catenin signaling and could represent a novel prognostic marker in OSCC patients.	Higher expression of FTH1P3 in OSCC tissue was associated with T classification, N classification and TNM stage. Furthermore, Kaplan-Meier survival analysis showed that prognosis of patients with low FTH1P3 expression was much better than that of those with high expression. Cox regression analysis showed that FTH1P3 expression was an independent prognosis-predicting factor for OSCC patients. 	Yes	Loss-function assay showed that knockdown of FTH1P3 significantly suppressed the proliferation, migration and invasion of OSCC cells.	30556871
FTH1P3	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction[microRNA‑145]	qRT-PCR//Luciferase Report Assay	The results revealed that FTH1P3 was significantly upregulated in cervical cancer tissues compared with normal tissues.miR‑145 was predicted and validated as a direct target of FTH1P3. Moreover, FTH1P3 siRNA partially attenuated the effects of the miR‑145 inhibitor on cell viability and mobility in cervical cancer cells. 		Yes	vitro and in vivo, loss-of-function experiments showed that lncRNA SNHG20 knockdown inhibited proliferative ability, mammosphere-forming ability, ALDH1 expression, stem factors (LIN28, Nanog, Oct4, SOX2) and tumour growth. 	31789421
FTH1P3	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[miR-224-5p/TPD52 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//BrdU	The results revealed that FTH1P3 was up?regulated in glioma tissues, and FTH1P3 expression in high?grade glioma tissues was significantly higher compared with that in low?grade glioma tissues. Thus, the miR‑224‑5p/TPD52 axis may be a downstream mechanism of FTH1P3 in glioma progression. 	The results revealed that FTH1P3 was up?regulated in glioma tissues, and FTH1P3 expression in high?grade glioma tissues was significantly higher compared with that in low?grade glioma tissues. 	Yes	Upregulation of FTH1P3 promoted glioma cell proliferation and inhibited apoptosis. 	30221720
FTH1P3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues 	Expression[highly expressed]	qRT-PCR	 Quantitative real-time PCR (qRT-PCR) showed that FTH1P3 expression was significantly up-regulated in LSCC tissues than that in non-neoplastic tissues. In addition, overexpression of FTH1P3 resulted in an increase in cells in S phase and a decrease in cells in G0/G1 phase, whereas inhibition of FTH1P3 did the opposite effects. Taken together, these results suggested that increased expression of FTH1P3 predicts a poor prognosis and promotes aggressive phenotypes of LSCC by regulating cell proliferation, migration, invasion, apoptosis, and cell cycle, indicating FTH1P3 may serve as a promising therapeutic biomarker for the treatment of LSCC.	High FTH1P3 expression was positively correlated with the poor differentiation, high T classification, positive lymph node metastasis, and advanced clinical stage. Overall survival analysis showed that high levels of FTH1P3 predicted a poor prognosis in LSCC patients.	Yes	Moreover, elevated expression of FTH1P3 was found to increase LSCC cell proliferation, migration and invasion, and to inhibit cell apoptosis, Conversely, knockdown of FTH1P3 suppressed LSCC cell proliferation, migration and invasion, and induced cell apoptosis.	31142627
FTH1P3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LSCC patients and  LSCC cells	Interaction(miR-377-3p/LDHA Axis)	In Vivo Experiment//Western Blot//RIP//qRT-PCR//MTT//Luciferase Report Assay//IHC//ChIP	Upregulated FTH1P3 was associated with increased E2F1 expression in LSCC patients.  E2F1 was proved to induce FTH1P3 expression in LSCC cells.  FTH1P3 modulated miR-377-3p expression by targeting miR-377-3p. Interestingly, LDHA was identified to be a target of miR-377-3p, and FTH1P3 promoted LDHA expression by suppressing miR-377-3p. 		Yes	 The results showed that overexpression of FTH1P3 promoted cell viability and glycolysis in LSCC cells, but knockdown of FTH1P3 suppressed this behavior. 	33571038
Fscn1	CircRNA	Mus musculus	Alloimmune Rejection	mDCs	Expression [highly expressed]	Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//PCR//IP	Exonic circFSCN1 was highly expressed in the cytoplasm of mature DCs. 		Yes	Knockdown of circFSCN1 using siRNA arrested DCs at an immature state, impaired DC's ability to activate T cells and enhanced Treg generation. 	34052126
FRLnc1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells, tumor tissues, and serum of GC patients	Expression(highly expressed)	Western Blot//Migration Assay//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	The results of quantitative real-time PCR (qRT-PCR) revealed that the FRLnc1 expressions were up-regulated in GC cells, tumor tissues, and serum of GC patients. 	Up-regulation of FRLnc1 expression was closely correlated to lymph node metastasis (LNM) and TNM stage with the combination of relevant clinicopathological parameter analysis. 	Yes	 The in vitro functional analyses demonstrated that FRLnc1 knockdown by RNA interference suppressed cell proliferation and migration in HGC-27 cells, whereas FRLnc1 overexpression promoted cell proliferation and migration in MKN45 cells. After exosome treatment, the FRLnc1 expression was significantly increased in MKN45 cells, and the MKN45 cells showed increased ability of proliferation and migration.	33971889
FR215775	LncRNA	Homo sapiens	Rhinitis, Allergic	murine primary Th2 cells	Expression(highly expressed)	Flow Cytometry//qRT-PCR	We found that the expression of lncRNA FR215775 was specifically higher in the murine primary Th2 cells. 		Yes	After the knockdown of lncRNA FR215775, the proliferation of CD4+ T cells was inhibited, and the expressions of IL-4 and IL-5 in the cell culture supernatant were significantly decreased (P < 0.001), along with the percentage of Th2 cells (P < 0.05). 	35755169
FOXP4‑AS1	LncRNA	Homo sapiens	Lymphoma, Mantle-Cell	 MCL patients	Interaction(miR‑423‑5p/NACC1 )	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	Our results showed that FOXP4‑AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4‑AS1 was correlated with the unfavorable prognosis of patients. Mechanistically, FOXP4‑AS1 was found to act as a competing endogenous (ce)RNA for miR‑423‑5p to regulate the expression of nucleus accumbens‑associated 1 (NACC1). The negative regulation of FOXP4‑AS1 on miR‑423‑5p compared to that of miR‑423‑5p on NACC1 was determined at the mRNA or protein levels in MCL cells.	Our results showed that FOXP4‑AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4‑AS1 was correlated with the unfavorable prognosis of patients. 	Yes	Functionally, while FOXP4‑AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4‑AS1 overexpression had promotive effects on these cellular processes. 	33416160
FOXP4-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	Interaction(MLL2/H3K4me3/FOXP4)	CCK8//qRT-PCR//Western Blot	 Here, we demonstrated that FOXP4-AS1 was significantly increased in ESCC tissues and cell lines, associated with lymph node metastasis and TNM staging. The expression of FOXP4-AS1 and FOXP4 in ESCC tissues was positively correlated. Further research found that FOXP4-AS1, upregulated in ESCC, promotes FOXP4 expression by enriching MLL2 and H3K4me3 in the FOXP4 promoter through a “molecular scaffold”. Moreover, FOXP4, a transcription factor of β-catenin, promotes the transcription of β-catenin and ultimately leads to the malignant progression of ESCC. 	 Here, we demonstrated that FOXP4-AS1 was significantly increased in ESCC tissues and cell lines, associated with lymph node metastasis and TNM staging. 	Yes	Cell function experiments showed that FOXP4-AS1 promoted the proliferation, invasion and migration ability of ESCC cells. 	34970490
FOXP4-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cell lines and tissues	Interaction(miR-423-5p/NACC1 axis)	CCK8//qRT-PCR//ChIP	The results showed that FOXP4-AS1 was highly expressed in CRC cell lines and tissues. Furthermore, FOXP4-AS1 served as a molecular sponge for miR-423-5p, and NACC1 is a direct target of miR-423-5p. MiR-423-5p silencing or overexpression of NACC1 increased proliferation, migration, and invasion of HCT116 cells while suppressing apoptosis. We also found that the upregulation of FOXP4-AS1 was activated by ATF3 in CRC cells. Collectively, our results demonstrated that ATF3-activated FOXP4-AS1 aggravates CRC progression by regulating miR-423-5p/NACC1 axis, indicating a new target for CRC treatment.		Yes	 CRC progression was promoted by the overexpression of FOXP4-AS1 in HTC116 cells and animal models. 	35034547
FOXP4-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cells and tissues	Regulation( AKT signaling)	qRT-PCR//Western Blot	Patients in TCGA cohort with a higher FOXP4-AS1 expression showed a higher disease-free interval (DFI) rate, and the expression of FOXP4-AS1 is shown to be linked to the clinical stage, T stage, N stage, and extraglandular invasion condition of the TC patients. Mechanism analysis indicated that FOXP4-AS1 can play its functions by regulating the AKT signaling pathway, and AKT inhibitor treatment could attenuate the impact of FOXP4-AS1 on PTC progression. Furthermore, FOXP4-AS1 also negatively regulates the expression of its host gene FOXP4. Collectively, we showed that FOXP4-AS1 inhibited PTC progression although AKT signaling and FOXP4-AS1 plays a tumor-suppressor role in PTC tumorigenesis.	Patients in TCGA cohort with a higher FOXP4-AS1 expression showed a higher disease-free interval (DFI) rate, and the expression of FOXP4-AS1 is shown to be linked to the clinical stage, T stage, N stage, and extraglandular invasion condition of the TC patients. 	Yes	 Functionally, upregulated FOXP4-AS1 inhibited PTC cell proliferation, apoptosis, and migration, whereas it downregulated FOXP4-AS1-promoted progression of PTC. In vivo assay also confirmed the tumor inhibitory effect of FOXP4-AS1 in PTC growth.	35720005
FOXP4-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Regulation( ZC3H12D/H3K27me3/EZH2)	qRT-PCR//Colony Formation Assay//Western Blot	FOXP4-AS1 and EZH2 expression and H3K27me3 abundance were enhanced while ZC3H12D expression was depressed in HCC tissues and cells. 		Yes	Knockdown of FOXP4-AS1 suppressed biological functions of HCC cells as well as the weight and volume of HCC transplanted tumor. Depleting ZC3H12D reversed the effect of downregulated FOXP4-AS1 on HCC cells. FOXP4-AS1 suppressed ZC3H12D expression via mediating H3K27me3 by recruitment of EZH2.	34545456
FOXP4-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	Expression(highly expressed)	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The expression of FOXP4-AS1 was higher in HCC tissues than adjacent nontumourous tissues, whereas the low expression of FOXP4-AS1 was correlated with optimistic treatment outcomes, which suggested that FOXP4-AS1 may be an independent prognostic biomarker for HCC.	The expression of FOXP4-AS1 was higher in HCC tissues than adjacent nontumourous tissues, whereas the low expression of FOXP4-AS1 was correlated with optimistic treatment outcomes, which suggested that FOXP4-AS1 may be an independent prognostic biomarker for HCC.	Yes	Moreover, the downregulation of FOXP4-AS1 significantly reduced the cell proliferation and clonal abilities and inhibited the invasion, migration, and angiogenesis of hepatoma cells (P < 0.05).	33604387
FTX	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cell lines	regulation[miR-335-5p/NUCB2 axis]	Western Blot//Tunel//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	RT-qPCR showed that FTX expression was up-regulated in LUAD cell lines.FTX played an oncogenic role in LUAD and contributed to cancer development via targeting miR-335-5p/NUCB2 axis.		Yes	Loss-of-function assay indicated that FTX accelerated cell proliferation, migration and invasion, while inhibited cell apoptosis in LUAD. 	32226311
FTX	LncRNA	Homo sapiens	Osteosarcoma		regulation[miR-320a/TXNRD1]	qRT-PCR//Luciferase Report Assay	 QRT-PCR revealed that FTX and TXNRD1 were abnormally upregulated in OS, whereas miR-320a expression was significantly decreased. Taken all the experiment results together, this paper indicated that FTX impacted osteosarcoma cell proliferation and migration by modulating TXNRD1/miR-320a.		Yes	A series of functional experiments indicated that knockdown of FTX could suppress OS cell proliferation and migration, while facilitating apoptosis ability simultaneously. 	31920141
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	LncRNA FOXD2-AS1 was overexpressed in human glioma, and upregulated FOXD2-AS11 expression indicated higher WHO grade (p < 0.05).OXD2-AS1 could regulate the expression of HMGA2 via miR-185-5p.Knockdown of FOXD2-AS1 significantly inhibited proliferation and metastatic potential of glioma cells, whereas endogenous expression FOXD2-AS1 inhibited the glioma cell activity through targeting HMGA2.		Yes	Knockdown of FOXD2-AS1 significantly inhibited proliferation and metastatic potential of glioma cells, whereas endogenous expression FOXD2-AS1 inhibited the glioma cell activity through targeting HMGA2.	30860979
FTX	LncRNA	Homo sapiens	Osteosarcoma	 osteosarcoma tissues and cell lines	regulation[miR-214-5p/SOX4 axis ]	CCK8//qRT-PCR//Transwell Assay//Western Blot	The expression levels of FTX were increased in osteosarcoma tissues and cell lines and negatively correlated with the expression levels of miR-214-5p. FTX could promote proliferation, invasion and inhibited apoptosis by regulating miR-214-5p/SOX4 axis in osteosarcoma, suggesting that FTX might be a potential target for osteosarcoma treatment.		Yes	 sh-FTX inhibited the growth and metastasis of osteosarcoma.	32821116
GACAT3	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Expression [highly expressed]	qRT-PCR//ELISA	The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues. Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3. 		Yes	 Inhibition of cell proliferation, increased apoptosis, and decreased motility were observed in T24 and 5637 cell lines transfected by CRISPR-Cas13 targeting GACAT3.	33537343
GACAT3	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[GACAT3/miR-3127-5p/ELAVL1 signaling  ]	qRT-PCR	Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. 	Higher GACAT3 expression predicted lower survival rate.	Yes	Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells.	30317610
GACAT3	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues	Expression[highly expressed]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	It was demonstrated that GACAT3 was upregulated in liver cancer tissues. 		Yes	The inhibition of GACAT3 decreased the ability of hepatoma cells to proliferate and migrate, and increased apoptosis of the cells. 	32266036
GACAT1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	interaction[targeting microRNA-875-3p]	CCK8//qRT-PCR//Flow Cytometry	GACAT1 level was clearly enhanced in breast cancer tissues compared to that of the adjacent tissues.The mechanism may be through the regulation of the level of STON2 by adsorbing microRNA-875-3p.		Yes	Upregulation of GACAT1 promoted the proliferation and cycle of breast cancer cells including MCF-7 and BCap-37. 	32194758
GACAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cancer tissues and cell lines 	Interaction(miR-149)	qRT-PCR//Western Blot	GACAT1 was highly expressed in cancer tissues and cell lines of OSCC patients (P < 0.01), while miR-149 was low expressed (P < 0.01). LncRNA GACAT1 binds to miR-149 targeting. Knockdown of lncRNA GACAT1 and transfection with miR-149 inhibitor reversed the effect of GACAT1 silencing on OSCC cells. 		Yes	 The down-regulation of lncRNA GACAT1 inhibited the proliferation and migration of OSCC cells and promoted apoptosis and autophagy (P < 0.01). The transfection of miR-149 inhibitor had the opposite effect. 	34460438
GACAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[sponging microRNA-422a]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay	The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Taken together, these results revealed the novel role of the GACAT1/miR‑422a pathway in the progression of NSCLC cell lines, providing a possible therapeutic strategy for NSCLC treatment.	The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. 	Yes	Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. 	33416153
GACAT1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC samples and cell lines	Interaction(miR-149)	qRT-PCR//Migration Assay	 In this reference, we observed that GACAT1 was overexpressed in TSCC samples and cell lines. 25 TSCC specimens, GACAT1 expression was overexpressed in 18 patients (18/25, 72%) compared to non-tumour specimens. We observed that miR-149 expression was down-regulated in TSCC cell lines. Moreover, we observed that GACAT1 expression was negatively correlated with miR-149 expression. GACAT1 overexpression induced TSCC cell growth and migration via regulating miR-149 expression. 		Yes	Ectopic expression of GACAT1 induced cell growth and migration and promoted epithelial to mesenchymal transition in TSCC. In addition, ectopic expression of GACAT1 decreased miR-149 expression in SCC1 cell. 	34378327
GABPB1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[miR-519e-5p/Notch2 axis]	qRT-PCR	We found that an lncRNA, named GABPB1-AS1, was significantly upregulated in HPV16-positive CC tissues and cell lines. Mechanistically, GABPB1-AS1 acted as a competing endogenous RNA (ceRNA) by sponging miR-519e-5p, resulting in the de-repression of its target gene Notch2 which is well known as an oncogene. Therefore, GABPB1-AS1 functioned as a tumor activator in CC pathogenesis by binding to miR-519e-5p and destroying its tumor suppressive function. 	 GABPB1-AS1 expression in HPV16-positive CC tissues was positively associated with tumor size, lymph node metastasis, and FIGO stage.  High expression of GABPB1-AS1 was correlated with a poor prognosis for HPV16-positive CC patients.	Yes	 Functionally, E6-induced GABPB1-AS1 overexpression facilitated CC cells proliferation and invasion in vitro and in vivo. 	32844486
GABPB1-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues 	Interaction( MicroRNA-330/ZNF367/Cell Cycle Signaling Pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Invasion Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	 GABPB1-AS1 was highly expressed in the glioma tissues and associated with advanced WHO grades. miR-330 was a target transcript of GABPB1-AS1. miR-330 inhibition restored the malignancy of glioma cells. miR-330 directly bound to ZNF367. ZNF367 was highly expressed in glioma tissues and positively correlated with GABPB1-AS1 expression, and it was relevant to the cell cycle signaling pathway. 		Yes	GABPB1-AS1 knockdown reduced proliferation and invasiveness of glioma cells in vitro and in vivo. 	34276213
Gabarapl2	LncRNA	Mus musculus	Dry Eye Syndromes	DED mice	Regulation	In Vivo Experiment//qRT-PCR//RNA-seq//Bioinformatics Analysis	Chrnb2, Gabarapl2, and Usp31 were thereby confirmed as the most significantly altered lncRNAs. Pathway analysis revealed that the neuroactive ligand-receptor interaction signaling pathway was the most enriched, followed by the calcium signaling pathway and cytokine-cytokine receptor interaction. 		Yes	Following treatment of Gabarapl2 siRNA and Chrnb2 siRNA, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were significantly downregulated in the HCECs. 	34957168
FUT8-AS1	LncRNA	Homo sapiens	Melanoma	skin tissues	regulation[NRAS/MAPK Signaling]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//EdU Staining//Transwell Assay	We further confirmed that FUT8-AS1 is downregulated in melanoma. In conclusion, these findings demonstrate that FUT8-AS1 exerts tumor suppressive roles in melanoma via regulating NF90/miR-145-5p/NRAS/MAPK signaling axis. 		Yes	Furthermore, in vivo functional assays demonstrated that FUT8-AS1 represses melanoma growth and metastasis.	34094894
FTX	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation[miR-144/ZFX Axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	 Figure 1A shows that the expression of LncRNA-FTX in GC tissues was up-regulated compared with those in adjacent normal tissues (p < 0.05). We found that FTX promoted cell proliferation, migration, and invasion, as well as tumor growth, and this effect could latterly be attenuated by miR-144. ZFX attenuated the effects of FTX/miR-144 axis by sponging with miR-144.		Yes	 We found that FTX promoted cell proliferation, migration, and invasion, as well as tumor growth, and this effect could latterly be attenuated by miR-144. 	32021248
FTX	LncRNA	Homo sapiens	Stomach Neoplasms	tumor tissues	interaction[targeting miR-215]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	 We found that the expression of FTX in tumor tissues of 71 GC patients was higher than that in paracancerous tissues, and the prognosis of patients with high FTX was poor. According to these results, this study revealed that the previously neglected FTX-miR2153p-SIVA1 regulatory axis for the regulation of gastric cancer progression, which may be a potential target for the treatment of gastric cancer.	 We found that the expression of FTX in tumor tissues of 71 GC patients was higher than that in paracancerous tissues, and the prognosis of patients with high FTX was poor. 	Yes	Transferring overexpression plasmid of FTX into gastric cancer cells (MGC-803 and SGC-7901) promoted cell proliferation and the ratio of cells in G0-G1 phase was decreased. Transferring si-FTX to MGC-803 and SGC-7901 led to opposite results. 	32271421
FTX	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-192-5p/EIF5A2 Axis]	RNA Pull-Down//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 FTX was up-regulated in CRC tissues and cell lines, knockdown of FTX inhibited CRC cell proliferation, migration and invasion in vitro as well as suppressed CRC tumor growth in vivo.LncRNA FTX functioned as an oncogene to contribute to CRC progression by regulating miR-192-5p/EIF5A2 axis, providing a novel insight into the pathogenesis of CRC and a promising therapeutic target for CRC treatment.		Yes	 FTX was up-regulated in CRC tissues and cell lines, knockdown of FTX inhibited CRC cell proliferation, migration and invasion in vitro as well as suppressed CRC tumor growth in vivo.	32280242
FTX	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miRNA-590-5p/RBPJ Axis)	qRT-PCR//Western Blot	It was found that FTX was upregulated in CRC tissues and cells.  Meanwhile, miR-590-5p was the target of FTX, and RBPJ was the direct target of miR-590-5p. 		Yes	 Knockdown of FTX or overexpression of miR-590-5p can inhibit the proliferation, migration, and invasion of CRC cells. Besides, silencing of FTX could inhibit the expression of migration and invasion-related proteins in CRC cells. 	33389283
FTX	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues 	Interaction(miR-214-5p-JAG1 axis)	qRT-PCR//Western Blot//IHC//FISH	lncRNA FTX was found to be upregulated in CRC tissues by FISH. Mechanistically, lncRNA FTX sequestered miR-214-5p and thus released its repression on JAG1, driving the malignant progression of CRC.		Yes	The downregulation of endogenous lncRNA FTX expression inhibited CRC cell proliferation, migration, and invasion.	34733921
FTX	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC specimens and cell lines	Interaction(FTX/miR‑4429/UBE2C axis)	CCK8//qRT-PCR//RNA-seq	The results showed that lncRNA FTX and UBE2C were upregulated in RCC specimens and cell lines.The overexpression of lncRNA FTX in RCC cells upregulated UBE2C. Overall, the present study showed that lncRNA FTX was upregulated in RCC and could significantly promote the proliferative, migratory and invasive capacities, enhancing the viability and accelerating the cell cycle progression of RCC cells by exerting the miRNA sponge effect on miR‑4429 and thus upregulating UBE2C.		Yes	 In addition, the overexpression of lncRNA FTX promoted the cell viability and proliferative, migratory and invasive capacities of RCC cells and accelerated the cell cycle progression.	35866591
FOXP4-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cell lines	regulation[miR-136-5p/CBX4 Axis]	qRT-PCR//Luciferase Report Assay	We found FOXP4-AS1 expression was significantly higher in CC cell lines than in normal cell line. Mechanistically, we found FOXP4-AS1 acts as competing endogenous RNA (ceRNA) for microRNA-136-5p (miR-136-5p) to regulate chromobox 4 (CBX4) expression.		Yes	 Functionally, force FOXP4-AS1 expression increased CC cell proliferation, migration, and invasion, while FOXP4-AS1 knockdown caused opposite effects.	32256085
FOXP4-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues,cell lines	Regulation[FOXP4-AS1/FOXP4 axis]	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//ChIP	As expected, FOXP4-AS1 was expressed at a higher level in PCa samples compared to adjacent normal samples (Fig. ​(Fig.1c).1c). Consistently, the expression level of FOXP4-AS1 was found to be higher in PCa cell lines compared to human normal prostate epithelial cell RWPE-1 (Fig. ​(Fig.1f).1f). Collectively, we determined that PAX5-induced upregulation of FOXP4-AS1/FOXP4 axis promoted tumorigenesis of PCa.		Yes	Functionally, high FOXP4-AS1 level was associated with increased cell proliferation and decreased cell apoptosis, indicating that FOXP4-AS1 exerted oncogenic functions in the tumorigenesis of PCa. 	31209207
FOXP4-AS1	LncRNA	Homo sapiens	Lymphoma, Mantle-Cell	blood	regulation[miR-423-5p/NACC1 pathway]	CCK8//qRT-PCR//Transwell Assay	Our results showed that FOXP4?AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4?AS1 was correlated with the unfavorable prognosis of patients. In conclusion, FOXP4‑AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR‑423‑5p. 	Our results showed that FOXP4?AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4?AS1 was correlated with the unfavorable prognosis of patients. 	Yes	Functionally, while FOXP4?AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4?AS1 overexpression had promotive effects on these cellular processes. 	33416160
FOXP4-AS1	LncRNA	Homo sapiens	Sarcoma, Ewing	ES tissues	Expression(highly expressed)	Western Blot//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	Herein, we established that FOXP4-AS1 was up-regulated in ES and this correlated with poor prognosis.	Herein, we established that FOXP4-AS1 was up-regulated in ES and this correlated with poor prognosis.	Yes	On the contrary, up-regulation of FOXP4-AS1 promoted the growth, migration, as well as invasion of ES.	34765540
FOXD2‑AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Regulation[FOXD2‑AS1/miR‑150‑5p/PFN2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	 In the present study, it was identified that FOXD2‑AS1 expression was upregulated in BC tissue, cell lines and sphere subpopulation. Downregulation of FOXD2‑AS1 decreased the percentage of CD44 antigen+/signal transducer CD24- in breast cancer stem cell (BCSC) cells, and decreased the expression of numerous stem factors, including Nanog, octamer‑binding transcription factor 4 (Oct4), and sex determining region Y‑box 2 (SOX2), and inhibited the epithelial‑mesenchymal transition process. FOXD2‑AS1 was identified to be primarily located in the cytoplasm. Using bioinformatics analysis, a reporter gene assay and reverse transcription‑polymerase chain reaction assays, it was demonstrated that microRNA (miR)‑150‑5p was able to bind directly with the 3'‑untranslated region of FOXD2‑AS1 and PFN2 mRNA. miR‑150‑5p mimics decreased the cell proliferation, migration and invasion of BC cells. FOXD2‑AS1 knockdown significantly inhibited the miR‑150‑5p inhibitor‑induced increase in Nanog, Oct4 and SOX2 expression. The miR‑150‑5p inhibitor‑induced increase in N‑cadherin, and decrease in E‑cadherin and vimentin was inhibited by FOXD2‑AS1 knockdown. Profilin 2 (PFN2) expression was significantly upregulated in BC tissues. Additionally, the abnormal upregulation of PFN2 was associated with poor prognosis in patients with BC. FOXD2‑AS1 and PFN2 expression was positively correlated. Collectively, the present results demonstrated the role of the FOXD2‑AS1/miR‑150‑5p/PFN2 axis in the development of BC, and provides novel targets for the treatment of BC, and potential biomarkers for diagnosis and prognosis of BC.	 Additionally, the abnormal upregulation of FOXD2‑AS1 predicted poor prognosis in patients with BC.	Yes	Furthermore, downregulation of FOXD2‑AS1 decreased cell proliferation, and migratory and invasive abilities in BC cells, and decreased the growth of transplanted tumors in vivo.	30628646
FOXD2‑AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//FISH//EdU Staining//Transwell Assay	Firstly, it was revealed that the expression levels of FOXD2‑AS1 were significantly upregulated in OS tissues and cells, compared with in adjacent tissues and normal cells, as determined using reverse transcription‑quantitative polymerase chain reaction.	Notably, the overall survival of patients with relatively high FOXD2‑AS1 expression in OS tissues was significantly lower than that of patients with relatively low expression, as determined using Kaplan‑Meier analysis.	Yes	Knockdown of FOXD2‑AS1 inhibited the proliferation, migration and invasion of OS cells. 	31115575
FOXD2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 cell lines	regulation[FOXD2-AS1/S100A1/Hippo axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 The results indicated that FOXD2?AS1 expression was upregulated in breast cancer cell lines, and that FOXD2?AS1 downregulation significantly inhibited the proliferation, migration and invasiveness of MCF?7 and MDA?MB?468 cells. On the whole, the findings of the present study suggest that the FOXD2‑AS1/S100A1/Hippo axis is involved in the tumorigenesis and progression of breast cancer. 		Yes	 The results indicated that FOXD2?AS1 expression was upregulated in breast cancer cell lines, and that FOXD2?AS1 downregulation significantly inhibited the proliferation, migration and invasiveness of MCF?7 and MDA?MB?468 cells.	32945354
FOXD2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cells	Expression [highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Cell Apoptosis Assay//Transwell Assay	lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. 		Yes	Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells.	34873418
FOXD2-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC samples and cell lines	Interaction( miR-204-3p)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In our work, we found that lncRNA FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) was significantly increased in clinical ESCC samples and cell lines. Through bioinformatics analysis and luciferase reporter assays, microRNA (miR)-204-3p was proved to be a target of FOXD2-AS1. We further confirmed that FOXD2-AS1 was the upstream inhibitor of miR-204-3p and the down-regulation of miR-204-3p reversed the repressive effects of low expression of FOXD2-AS1 on ESCC progression. In addition, inhibition of FOXD2-AS1 effectively suppressed the tumor growth.		Yes	In addition, inhibition of FOXD2-AS1 effectively suppressed the tumor growth.	35778646
FOXD2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[miR-25-3p/Sema4C axis]	qRT-PCR//Transwell Assay	 In this study, we further confirmed the up-regulation of FOXD2-AS1 in CRC patients and showed that high FOXD2-AS1 level predicted poor survival.FOXD2-AS1 may regulate the miR-25-3p/Sema4C axis to promote the invasion and migration of CRC cells.	 In this study, we further confirmed the up-regulation of FOXD2-AS1 in CRC patients and showed that high FOXD2-AS1 level predicted poor survival.	Yes	Transwell assay showed that FOXD2-AS1 and Sema4C over-expression led to the increased invasion and migration rates of CRC cells. 	31908535
FOXD2-AS1	LncRNA	Homo sapiens	Osteoarthritis	cartilage tissues	Interaction[sponging miR-27a-3p]	qRT-PCR	 In the present study, we showed FOXD2-AS1 expression was upregulated and positively associated with the severity of OA patients.  Mechanistically, we found that FOXD2-AS1 upregulated the expression level of TLR4 by sponging miR-27a-3p. In addition, we revealed that miR-27a-3p mimics could abolish the effects of FOXD2-AS1 overexpression on cell proliferation, inflammation, and ECM degradation in chondrocytes. Therefore, we demonstrated that FOXD2-AS1 could play a crucial role in the progression of OA, at least partially, by regulating miR-27a-3p/TLR4 axis.		Yes	FOXD2-AS1 overexpression induced cell proliferation, inflammation and extracellular matrix (ECM) degradation in chondrocytes. 	30945573
FOXD2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	Mechanistically, FOXD2-AS1 was found to be activated by the transcription factor EGR1. Furthermore, FOXD2-AS1 could activate the Wnt/β-catenin signaling pathway. The mechanism contributed to the interaction between FOXD2-AS1 and Wnt/β-catenin signaling pathway was analyzed. It was uncovered that FOXD2-AS1 enhanced the activity of Wnt/β-catenin signaling pathway by epigenetically silencing the inhibitor of Wnt/β-catenin signaling pathway (DKK1). Rescue assays demonstrated that DKK1 and Wnt/β-catenin signaling pathway involved in FOXD2-AS1-mediated HCC progression.		Yes	Functionally, silenced FOXD2-AS1 efficiently suppressed HCC progression by regulating cell proliferation, apoptosis, migration and epithelial-mesenchymal transition (EMT). 	30929558
FOXD2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 hepatocellular carcinoma tissues	Regulation[MiR-185/AKT Axis]	Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//Luciferase Report Assay//Transwell Assay	FOXD2-AS1 was significantly upregulation in hepatocellular carcinoma tissues.FOXD2-AS1 knockdown suppressed Bel-7401 cell biological activities (proliferation, invasion, and migration) with miR-185 overexpression and AKT depressing in cell expression.		Yes	FOXD2-AS1 knockdown suppressed Bel-7401 cell biological activities (proliferation, invasion, and migration) with miR-185 overexpression and AKT depressing in cell expression.	31841454
FOXD2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[silencing CDKN1B(p27) via EZH2]	RNA Pull-Down//IHC//Western Blot//qRT-PCR//RIP//Cell Viability Assay//Cell Cycle Assay//Colony Formation Assay//ChIP	The data indicated that FOXD2-AS1 expression was increased in HCC specimens and cell lines.Our results revealed that FOXD2-AS1 could epigenetically silence CDKN1B by recruiting EZH2 to CDKN1B promoter region. Knocking down CDKN1B could restore the carcinogenic effect of FOXD2-AS1 on HCC. 	Furthermore, aberrant expression was correlated with tumor number and tumor size in HCC patients. 	Yes	 Silencing FOXD2-AS1 arrest cell cycle in the G0/G1 phase, inhibited colony formation, cell proliferation and suppressed the in vivo growth of subcutaneous tumors.	31004581
FOXD2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	regulation[miR-206/MAP3K1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	We found that FOXD2-AS1 was significantly upregulated in HCC cells in comparison to normal human liver cells, LO2.  In conclusion, this work implies FOXD2-AS1 accelerates HCC progression through sponging miR-206 and regulating MAP3K1 expression.		Yes	Furthermore, the inhibition of FOXD2-AS1 repressed HCC cell proliferation, enhanced cell apoptosis, and restrained cell invasion and migration. 	32558350
FOXD2-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Interaction(miR-4492)	CCK8//Luciferase Report Assay//Invasion Assay//Migration Assay	The results suggested that lncRNA FOXD2-AS1 was upregulated in ovarian cancer tissues and cell lines.  lncRNA FOXD2-AS1 was confirmed to directly target miR-4492. The expression of lncRNA FOXD2-AS1 and miR-4492 exhibited a negative correlation. 		Yes	si-FOXD2-AS1 was able to inhibit the proliferation, migration and invasion of ovarian cancer cells.	33717250
FOXD2-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Expression[highly expressed]	qRT-PCR//MTT//Colony Formation Assay//Western Blot	We found that FOXD2-AS1 was significantly highly expressed in OSCC tissues, and correlated with poor pathological grade and prognosis in patients with OSCC. 	We found that FOXD2-AS1 was significantly highly expressed in OSCC tissues, and correlated with poor pathological grade and prognosis in patients with OSCC. 	Yes	Cell viability and clone formation ability were significantly inhibited after the knockdown of FOXD2-AS1. 	33103475
FOXD2-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissue and cell lines 	Interaction[repressing p21]	ChIP//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In present research, the level of FOXD2-AS1 was significantly up-regulated in the OS tissue and cell lines compared to corresponding controls. Mechanistically, FOXD2-AS1 inhibited the expression of p21 via interacting with EZH2 to silence p21 gene expression. Overall, we conclude that FOXD2-AS1, induced by transcription factor HIF-1α, acts as an oncogene in the OS tumorigenesis and FOXD2-AS1 interacts with EZH2 to silence p21 protein. This finding could provide a novel insight and potential therapeutic target for the OS.	The aberrant high-expression of FOXD2-AS1 indicated the poor clinical prognosis of OS patients.	Yes	 Functionally, the knockdown of FOXD2-AS1 could repress the malignant biological properties of OS cells in vitro and vivo, including proliferation, invasion, apoptosis and tumor growth.	31228799
FOXD2-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma patients and cell line	Interaction( FOXD2-AS1/m6A/FOXM1 complex )	qRT-PCR//Western Blot	Clinical data unveiled that osteosarcoma patients with higher FOXD2-AS1 expression had a poorer overall survival rate compared to those with lower FOXD2-AS1 expression. Mechanistically, a remarkable m6A-modified site was found on the 3'-UTR of FOXD2-AS1, and m6A methyltransferase WTAP (Wilms' tumor 1 associated protein) promoted the methylation modification, thus enhancing the stability of FOXD2-AS1 transcripts. Furthermore, FOXD2-AS1 interacted with downstream target FOXM1 mRNA through m6A sites, forming a FOXD2-AS1/m6A/FOXM1 complex to heighten FOXM1 mRNA stability.	Clinical data unveiled that osteosarcoma patients with higher FOXD2-AS1 expression had a poorer overall survival rate compared to those with lower FOXD2-AS1 expression. 	Yes	Functional research illuminated that FOXD2-AS1 accelerated the migration, proliferation and tumor growth in vitro and in vivo.	35356854
FOXD2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction[downregulating CDX1]	CCK8//qRT-PCR//EdU Staining	FOXD2-AS1 was upregulated in CC tissues relative to those of para-tumor tissues, especially in those with larger tumor size and advanced tumor staging.FOXD2-AS1 is upregulated in CC and its high level predicts a poor prognosis of CC patients. It accelerates the malignant progression of CC via negatively regulating CDX1 level.	FOXD2-AS1 was upregulated in CC tissues relative to those of para-tumor tissues, especially in those with larger tumor size and advanced tumor staging.	Yes	The silence of FOXD2-AS1 attenuated SiHa and HeLa cells to proliferate.	31841177
FOXD2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer cells and tissue	Interaction(METTL3)	Western Blot//Transfection//MeRIP//Migration Assay//qRT-PCR//RIP//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//ChIP	Results illuminated that FOXD2-AS1 expression was significantly upregulated in cervical cancer cells and tissue, which was closely correlated to the unfavorable prognosis. Mechanistically, m6A methyltransferase methyltransferase-like 3 (METTL3) enhanced the stability of FOXD2-AS1 and maintained its expression. Moreover, FOXD2-AS1 recruited lysine-specific demethylase 1 (LSD1) to the promoter region of p21 to silence its transcription abundance. 	Results illuminated that FOXD2-AS1 expression was significantly upregulated in cervical cancer cells and tissue, which was closely correlated to the unfavorable prognosis.	Yes	Functionally, gain and loss-of-function assays showed that FOXD2-AS1 promoted the migration and proliferation of cervical cancer cells. Besides, FOXD2-AS1 silencing repressed the tumor growth in vivo.	34589576
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[miR-185-5p/CCND2 axis]	qRT-PCR	FOXD2-AS1 was upregulated in glioma tissue, cells, and sphere subpopulation.We also revealed that FOXD2-AS1 was mainly located in cytoplasm and microRNA (miR)-185-5p both targeted FOXD2-AS1 and CCND2 messenger RNA (mRNA) 3'-untranslated region (3'-UTR). miR-185-5p was downregulated in glioma tissue, cells, and sphere subpopulation. Downregulation of miR-185-5p was closely correlated with poor prognosis of glioma patients. In addition, miR-185-5p mimics decreased cell proliferation, migration, invasion, stemness, and EMT in glioma cells. CCND2 was upregulated in glioma tissue, cells, and sphere subpopulation. Upregulation of CCND2 was closely correlated with poor prognosis of glioma patients. CCND2 knockdown decreased cell proliferation, migration, invasion, and EMT in glioma cells. In glioma tissues, CCND2 expression was negatively associated with miR-185-5p, but positively correlated with FOXD2-AS1. FOXD2-AS1 knockdown and miR-185-5p mimics decreased CCND2 expression. Inhibition of miR-185-5p suppressed FOXD2-AS1 knockdown-induced decrease of CCND2 expression. Overexpression of CCND2 suppressed FOXD2-AS1 knockdown-induced inhibition of glioma malignancy.		Yes	Downregulation of FOXD2-AS1 decreased cell proliferation, migration, invasion, stemness, and epithelial-mesenchymal transition (EMT) in glioma cells and inhibited tumor growth in transplanted tumor.	30520141
FOXD2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[sponging miR-185 through targeting AKT1]	ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In this study, we found that FOXD2-AS1 expression was significantly up-regulated in both glioma tissues and cell lines. Mechanistically, our results showed that FOXD2-AS1 may act as an endogenous sponge by competing for miR-185, thereby regulating the targets of this miRNA. Taken together, our data firstly demonstrated that CREB1-induced FOXD2-AS1 contributed to glioma progression by upregulating AKT1 via competitively binding to miR-185, providing a novel strategy for targeting FOXD2-AS1 as a potential biomarker and a therapeutic target in glioma patients.	 High FOXD2-AS1 expression was significantly correlated with advanced WHO grade, KPS score and the shorter survival time of glioma patients.	Yes	Functional investigations revealed that knockdown of FOXD2-AS1 significantly suppressed glioma cells proliferation, migration, invasion and EMT, and promoted apoptosis.	30553445
FOXD3-AS1	LncRNA	Mus musculus	Reperfusion Injury	brain tissues	regulation[ miR-765/BCL2L13 axis]	Western Blot//Tunel//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	The up-regulation of FOXD3-AS1 and down-regulation of miR-765 were found in both mouse brains after cerebral ischemia/reperfusion (I/R) and neuroblastoma cells of neuro-2A (N2a) after oxygen-glucose deprivation/reoxygenation (OGD/R). We verified a critical signaling pathway of FOXD3-AS1/miR-765/BCL2L13 in regulating cerebral ischemia/reperfusion injury.		Yes	Furthermore, we found that neurological deficits and brain injury induced by I/R in vivo were attenuated by FOXD3-AS1 knockdown.	33068927
FOXD3-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CRC tissues and cells	Interaction[CRC tissues and cells]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	Quantitative real-time polymerase chain reaction showed the overexpression of FOXD3-AS1 in both CRC tissues and cells.In conclusion, FOXD3-AS1 promotes CRC progression by regulating miR-135a-5p/SIRT1 axis, shedding lights on the way to CRC treatments.	According to the survival analysis of The Cancer Genome Atlas database, FOXD3-AS1 upregulation implied lower survival rate of patients with CRC.  The Kaplan-Meier method demonstrated the prognostic value of FOXD3-AS1 for patients with CRC. 	Yes	To explore the effect of FOXD3-AS1 on CRC progression, loss-of-function experiments were carried out, whose results indicated that knockdown of FOXD3-AS1 suppressed cell proliferation, migration, and invasion, inhibited cell cycle and promoted cell apoptosis in vitro. In vivo experiments affirmed that FOXD3-AS1 affected tumor growth. 	31058315
FOXD3-AS1	LncRNA	Homo sapiens	skin melanoma	cutaneous melanoma cells and tissues	Interaction[miR-325/MAP3K2]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 LncRNA FOXD3-AS1 highly expressed in cutaneous melanoma cells and tissues.LncRNA FOXD3-AS1 could promote proliferation, invasion and migration of cutaneous malignant melanoma via regulating miR-325/MAP3K2 axis.		Yes	When LncRNA FOXD3-AS1 was knockdown, proliferation, invasion and migration of cutaneous malignant melanoma, and tumor weight was inhibited, and cell cycle was arrested. Tumor volume and weight were measured to confirm the effect of sh-FOXD3-AS1 in vivo.	31541886
FOXD3-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue samples and cell lines	Interaction(miR-135a-5p/CDK6 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	FOXD3-AS1 was significantly overexpressed in NSCLC tissue samples and cell lines compared with normal tissue samples and cells. The luciferase reporter assay demonstrated the direct binding interaction between FOXD3-AS1 and miR-135a-5p. It was also demonstrated that miR-135a-5p could bind to the 3' untranslated region of cyclin-dependent kinase 6 (CDK6) and negatively modulate its transcription. 		Yes	FOXD3-AS1 silencing expression significantly inhibited A549 and H1229 cell proliferation while inducing apoptosis compared with sh-NC group. Moreover, FOXD3-AS1 silencing led to the upregulation of miR-135a-5p in A549 and H1229 cells compared with sh-NC group	34733371
FOXP1-AS80	LncRNA	Homo sapiens	Nasopharyngeal carcinoma		interaction[miR-423-5p ]	qRT-PCR//Luciferase Report Assay//Western Blot	 The expression of FOXP4-AS1 was up-regulated in 80 cases with NPC, and these patients with a poor prognosis.  FOXP4-AS1upregulated STMN1 by interacting with miR-423-5p as a competing endogenous RNA (ceRNA) to promote NPC progression.	 The expression of FOXP4-AS1 was up-regulated in 80 cases with NPC, and these patients with a poor prognosis. 	Yes	 Functionally, high expression of FOXP4-AS1 in NPC was connected with promoted cell proliferation and inhibited apoptosis. Moreover, FOXP4-AS1 is located in the cytoplasm of CNE1 (NPC cell lines). 	32767327
Foxp1	LncRNA	Mus musculus	Carcinoma, Renal Cell	 RCC tissues and cells	Interaction(miR-423-5p/U2AF2 axis )	ISH//Migration Assay//CCK8//qRT-PCR//Invasion Assay//Transwell Assay	Firstly, we demonstrated the characterization and expression of circFOXP1 in RCC tissues and cells.To sum up, our study partially demonstrated that the novel ZNF263/circFOXP1/miR-423-5p/U2AF2 axis has a role in RCC progression. 		Yes	Next, by conducting a serial experiment, we found that downregulated circFOXP1 inhibited cell proliferation, migration, invasion, and the Warburg effect. 	34514002
FOXO3	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer (BC) tissues 	regulation[Regulating MiR-9-5p/TGFBR2]	qPCR//Western Blot//PCR//IF	We found that circ-FOXO3 was significantly down-regulated in bladder cancer (BC) tissues compared to normal bladder tissues. Furthermore, circ-FOXO3 regulates TGFBR2 expression through sponging miR-9-5p in BC cell lines.		Yes	We also found that circ-FOXO3 overexpression inhibited cell proliferation, migration and invasion in BC cell lines.	32612392
FOXO1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and corresponding adjacent tissues,cell lines(A549, H460, HCC827 and H129IMR-90)	Regulation[PI3K/AKT signaling pathway]	Western Blot//Migration Assay//qRT-PCR//MTT//cell invasion assay	LncFOXO1 was down-regulated in lung cancer tumor tissues and cells. LncFOXO1 inhibited lung cancer cell proliferation, metastasis, and induced apoptosis through down-regulating PI3K/AKT pathway.	 	Yes	Knockdown of lncFOXO1 significantly promoted A549 cells viability, colony formation and invasion.	31217928
FOXF1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines  	Expression[lower expressed]	Flow Cytometry//qRT-PCR//MTT	The expression of FENDRR was low in NSCLC tissues and cells in contrast to control tissues and cells		Yes	FENDRR enhancement could inhibit the proliferation ability and advance cell apoptosis of A549 cells.	31749883
FOXD3‑AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Interaction(miR‑128‑3p/LIMK1 axis )	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//IHC//Transwell Assay	OXD3‑AS1 expression was significantly increased in CC tissues and cell lines compared with adjacent healthy tissues and normal cervical epithelial cells, respectively. Moreover, the results demonstrated that FOXD3‑AS1 targeted and negatively regulated miR‑128‑3p, which indirectly upregulated LIMK1 expression. 	 High FOXD3‑AS1 expression was significantly associated with poor differentiation of tumor tissues, increased tumor size and positive lymph node metastasis.	Yes	FOXD3‑AS1 overexpression significantly increased CC cell proliferation, migration and invasion compared with the negative control (NC) group, whereas FOXD3‑AS1 knockdown resulted in the opposite effects compared with the small interfering RNA‑NC group.	33760158
FOXD3-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-127-3p/ARF6 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the present study, we found that the FOXD3-AS1 expression was significantly increased in breast cancer tissues compared with normal tissues and involved in the poor prognosis of patients.Mechanistically, FOXD3-AS1 functioned as a competing endogenous RNA (ceRNA) to upregulate ARF6 expression by targeting miR-127-3p. In addition, the roles of FOXD3-AS1 on cell proliferation and metastasis were achieved through miR-127-3p/ARF6 axis.	In the present study, we found that the FOXD3-AS1 expression was significantly increased in breast cancer tissues compared with normal tissues and involved in the poor prognosis of patients.	Yes	Functionally, knockdown of FOXD3-AS1 suppressed cell proliferation and metastasis abilities in vitro, and tumor growth in vivo. 	35678943
FOXD3-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-150/SRCIN1axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//Transwell Assay	 FOXD3-AS1 expression was significantly reduced in NSCLC tissues and cell lines, and low expression of FOXD3-AS1 was closely related to positive lymph node metastasis and relatively high tumor grade. FOXD3-AS1 indirectly enhances the expression of SRCIN1 by targeting miR-150, thereby inhibiting NSCLC progression.	 FOXD3-AS1 expression was significantly reduced in NSCLC tissues and cell lines, and low expression of FOXD3-AS1 was closely related to positive lymph node metastasis and relatively high tumor grade.	Yes	 FOXD3-AS1 over-expression inhibited the proliferation and invasion of H1299 cell lines, while its knockdown promoted the proliferation and invasion of A549 cells.	32924985
FOXD3-AS1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	regulation[miR-127-3p/MED28 axis]	qRT-PCR//Western Blot	Data mining and analysis of the clinical sample showed that FOXD3-AS1 expression was significantly up-regulated in lung cancer tissues.Our findings provided new evidence that the FOXD3-AS1 regulated NSCLC progression via targeting the miR-127-3p/MED28 axis.		Yes	In vitro functional assays demonstrated that FOXD3-AS1 overexpression promoted NSCLC cell proliferation and invasion, while FOXD3-AS1 knockdown exerted tumor-suppressive effects on NSCLC cells.	32196603
FOXD3-AS1	LncRNA	Homo sapiens	Melanoma	melanoma cells	regulation[miR-127-3p/FJX1 Axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	FOXD3-AS1 was markedly upregulated in melanoma cells.Overall, FOXD3-AS1 contributes to the progression of melanoma via miR-127-3p/FJX1 axis.		Yes	It was validated by loss-of-function assays that cell proliferation and migration were inhibited by FOXD3-AS1 deficiency, while cell apoptosis was facilitated by FOXD3-AS1 knockdown in melanoma. 	32354225
FOXD3-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[RICTOR]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Transwell Assay	FOXD3-AS1 was overexpressed in HCC, and HCC patients with the high level of FOXD3-AS1 had a poor prognosis.The interaction among FOXD3-AS1, miR-335, and RICTOR provides a novel insight for understanding the molecular mechanism of HCC, and FOXD3-AS1, miR-335, and RICTOR can be regarded as the potential targets for HCC treatment.	FOXD3-AS1 was overexpressed in HCC, and HCC patients with the high level of FOXD3-AS1 had a poor prognosis.	Yes	In addition, FOXD3-AS1 knockdown considerably inhibited the proliferation, migration, and invasion of Huh6 cells.	32191537
FOXD3-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC samples and cell lines	regulation[miR-296-5p/HMGA1 pathway]	qRT-PCR	 In this research, our group first reported that the levels of FOXD3-AS1 were distinctly elevated in CC samples and cell lines.  Moreover, mechanistic studies suggested that FOXD3-AS1 acted as an endogenous sponge by directly binding miR-296-5p, resulting in the suppression of miR-296-5p. 	 The distinct upregulation of FOXD3-AS1 was associated with lymphatic invasion, distant metastasis, and International Federation of Gynecology and Obstetrics stage, and also predicted poor clinical results of CC patients.	Yes	 Functional assays indicated that knockdown of FOXD3-AS1 distinctly suppressed CC progression via affecting cell proliferation, cell apoptosis, and metastasis. 	32959937
FOXD3-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	regulation[microRNA-185-3p upregulation]	RIP//RNA Pull-Down//Luciferase Report Assay	 Our findings revealed that lncRNA FOXD3-AS1 and FOXD3 exhibited increased expression levels, while miR-185-3p exhibited diminished levels in NPC.Our findings provide evidence indicating that lncRNA FOXD3-AS1 could bind to miR-185-3p to upregulate the FOXD3 expression, thereby promoting the development of NPC.	The levels of lncRNA FOXD3-AS1 and FOXD3 were further correlated with tumor node metastasis stage and pathological type of patients with NPC. 	Yes	In addition, lncRNA FOXD3-AS1 knockdown repressed cell stemness, colony formation, viability, invasion, migration, and in vivo tumor growth, and accelerated cell apoptosis.	33204001
FOXD3-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC tissues and cells	Interaction(YBX1/H3K27ac)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//ISH//Transfection//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//H&E Staining//Colony Formation Assay//Invasion Assay//ChIP	FOXD3-AS1 was highly expressed in NPC tissues and cells. FOXD3-AS1 could specifically bind to YBX1 and have a positive effect on the expression of YBX1. Bioinformatics analysis showed that the promoter of YBX1 had a high enrichment of H3K27ac, which promote mRNA transcription and protein translation of YBX1. 		Yes	Knockdown of FOXD3-AS1 significantly inhibited proliferation, migration, and invasion of NPC cells in vitro and vivo. 	34395290
FOXD3-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM cells and tissues	Interaction(miR-128-3p/WEE1 )	Western Blot//Transfection//Tunel//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	 This study found that FOXD3-AS1 was overexpressed in GBM cells and associated with dismal prognostic outcome in GBM patients. Given that both FOXD3-AS1 and WEE1 contain a binding site for miR-128-3p, FOXD3-AS1 could act as a competing endogenous RNA (ceRNA) to promote WEE1 expression by sponging miR-128-3p. 		Yes	Functional studies revealed that depletion of FOXD3-AS1 inhibited cell growth and induced apoptosis of GBM cells.	35191808
FOXD3-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues	Regulation[TGF-β1/Smads signaling pathway]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that the expression of lncRNA FOXD3-AS1was upregulated and it had negative correlation with the level of miR-296-5p in thyroid cancer tissues and cells. Further study revealed that miR-296-5p was a target of lncRNA FOXD3-AS1 and FOXD3-AS1 exerted anti-tumor effect through up-regulating miR-296-5p. Moreover, we found that FOXD3-AS1 knockdown suppressed the aggressive biological behaviors of thyroid cancer through inactivating the TGF-β1/Smads signaling pathway. Subsequently, the in vivo experiments further verified that the FOXD3-AS1/miR-296-5p axis exerted obvious anti-tumor effect through inhibiting tumor growth and metastasis and the TGF-β1/Smads signaling pathway was also inactivated in vivo by the inhibition of FOXD3-AS1.		Yes	LncRNA FOXD3-AS1 knockdown effectively suppressed cell proliferation and cell invasion in vitro. 	31678422
FEZF1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor specimens	Interaction(miR-107/Wnt/β-catenin axis )	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results showed that lncRNA FEZF1-AS1 level was prominently enhanced in HCC tumor specimens and overexpression of FEZF1-AS1 promoted the proliferation, migration and invasion of HCC cells. In mechanism, overexpression of FEZF1-AS1 reduced the expression of miR-107 which inhibited the activation of Wnt/β-catenin signaling. 	The results showed that lncRNA FEZF1-AS1 level was prominently enhanced in HCC tumor specimens and overexpression of FEZF1-AS1 promoted the proliferation, migration and invasion of HCC cells. 	Yes	Overexpression of β-catenin promoted cell proliferation, migration and invasion which were inhibited by FEZF1-AS1 downregulation. 	34023817
FEZF1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	cell lines and tissues	regulation[miR-130a-5p/SOX4 axis]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Colony Formation Assay	 Our data showed overexpression of FEZF1-AS1 in OC cell lines and tissues.In conclusion, our results revealed that FEZF1-AS1 promoted the metastasis and proliferation of OC cells by targeting miR-130a-5p and its downstream SOX4 expression.		Yes	Cell migration, proliferation, invasion, wound healing and colony formation were suppressed by silencing of FEZF1-AS1. In contrast, cell apoptosis was promoted by FEZF1-AS1 knock-down in vitro.	32135030
HCG11	LncRNA	Homo sapiens	Pancreatic Carcinoma	pancreatic carcinoma samples	Interaction(miR-579-3p/MDM2 axis/Notch/Hes1 signaling pathway)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	A significant increase of HCG11 was occurred in pancreatic carcinoma samples. Bioinformatics analysis revealed that HCG11 upregulated MDM2 expression by competitively targeting miR-579-3p. The rescue assays showed that miR-579-3p reversed cell behaviors caused by HCG11, and MDM2 reversed cell properties induced by miR-579-3p. The Notch1 intracellular domain (NICD) and Hes1 protein levels were increased by overexpression of HCG11/MDM2. Our observations highlighted that HCG11 contributed to the progression of pancreatic carcinoma by promoting growth and aggressiveness, and inhibiting apoptosis via miR-579-3p/MDM2/Notch/Hes1 axis.		Yes	Knockdown of HCG11 suppressed the progression of pancreatic carcinoma cells. 	34230221
FALEC	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial cancer tissues,cell lines	Expression[highly expressed]	qRT-PCR//MTT	In our research, FALEC expression was increased in endometrial cancer tissue samples and cell lines compared with corresponding paracancerous normal tissue samples and cell line, respectively.	Furthermore, we investigated the clinical significance of FALEC in endometrial cancer patients, and found endometrial cancer patients with advanced clinical stage or large tumor size had higher levels of FALEC expression than those with early clinical stage or small tumor size. 	Yes	The in vitro studies showed silencing of FALEC expression inhibited cell proliferation and arrested cell cycle at G0/G1. In conclusion, FALEC is overexpressed in endometrial cancer tissues and cells, and involved in regulating cell proliferation and cell-cycle.	31387003
F11-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[F11-AS1/miR-211-5p/NR1I3 axis ]	RNA Pull-Down//Western Blot//Wound Healing Assay//Tunel//Flow Cytometry//qRT-PCR//CCK8//RIP//FISH//Luciferase Report Assay//Transwell Assay	 Poor expression of lncRNA F11-AS1 was correlated with poor prognosis in patients with HBV-related HCC, and its down-regulation was caused by the HBx protein. lncRNA F11-AS1 was proved to up-regulate the NR1I3 expression by binding to miR-211-5p. Overexpression of lncRNA F11-AS1 reduced the proliferation, migration and invasion, yet induced apoptosis of HepG2.2.15 cells in vitro, which could be abolished by overexpression of miR-211-5p. Additionally, either lncRNA F11-AS1 overexpression or miR-211-5p inhibition attenuated the tumour growth and metastasis capacity of HepG2.2.15 cells in vivo. Collectively, lncRNA F11-AS1 acted as a modulator of miR-211-5p to positively regulate the expression of NR1I3, and the lncRNA F11-AS1/miR-211-5p/NR1I3 axis participated in HBV-related HCC progression via interference with the cellular physiology of HCC.		Yes	Overexpression of lncRNA F11-AS1 reduced the proliferation, migration and invasion, yet induced apoptosis of HepG2.2.15 cells in vitro, which could be abolished by overexpression of miR-211-5p. 	31880390
F11-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Regulation[F11-AS1/miR-3146/PTEN axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	To sum up, F11-AS1 suppresses LIHC progression by competitively binding with miR-3146 to regulate PTEN expression. The F11-AS1/miR-3146/PTEN axis is brand new.		Yes	Thereby, lncRNA F11‐AS1 suppresses LIHC cell proliferation and migration.	31168823
EZR‑AS1	LncRNA	Homo sapiens	Skin Neoplasms	 cSCC tissues and cells	Interaction(PI3K/AKT signaling pathway)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//Cell Viability Assay//Cell Apoptosis Assay//Invasion Assay//Transwell Assay	 EZR‑AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively. Moreover, EZR‑AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)‑PI3K/PI3K and p‑AKT/AKT in cSCC cells compared with the si‑NC group. The PI3K agonist 740Y‑P significantly reversed si‑EZR‑AS1‑mediated effects on SCC13 and SCL‑1 cell proliferation, migration, invasion and apoptosis.		Yes	Compared with the small interfering RNA (si)‑negative control (NC) group, si‑EZR‑AS1 significantly inhibited SCC13 and SCL‑1 cell proliferation, migration and invasion, but promoted cell apoptosis. By contrast, compared with the pc‑NC group, EZR‑AS1 overexpression significantly enhanced A431 cell proliferation, migration and invasion, but inhibited cell apoptosis.	33236153
EZR-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines (HCT8, HCT116, HT29, and SW620 cells)	Regulation[TGF-β signaling]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	The expression of lncRNA EZR-AS1 was significantly Expression[Expression[up-expression]-expression]-regulated in CRC cell lines (HCT8, HCT116, HT29, and SW620 cells), which was significantly different from that of normal human fetal colonic mucosa cells (FHC cells) (P<0.01). Silencing of lncRNA EZR-AS1 significantly Expression[down-expression]-regulated TGF-β, Smad2, and α-SMA expression in HCT116 and HT29 cells at the protein level (P<0.05). The intervention of SB431542 (a TGF-β receptor blocker) and silencing of Smad2 both significantly Expression[down-expression]-regulated lncRNA EZR-AS1 expression in HCT116 and HT29 cells (P<0.01). 		Yes	 HCT116 and HT29 cells were then transfected with EZR-AS1 shRNA (sh-EZR-AS1) to silence lncRNA EZR-AS1 (P<0.01). When compared with the Control, after transfection of SH-EZR-AS1, E-cadherin was Expression[Expression[up-expression]-expression]-regulated, Vimentin was Expression[down-expression]-regulated, the apoptosis rate was increased, the cell viability, wound healing rate, and the number of invasive cells were decreased in HCT116 and HT29 cells (P<0.05). Silencing of lncRNA EZR-AS also significantly reduced the tumor volume and weight in mice injected with sh-EZR-AS1-transfected HCT116 and HT29 cells (P<0.05). 	31693738
EZR-AS1	LncRNA	Homo sapiens	Skin Neoplasms	cSCC tissue and cells 	regulation[PI3K/AKT signaling pathway]	Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	EZR?AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively. In conclusion, the present study demonstrated that si‑EZR‑AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC.		Yes	Compared with the small interfering RNA (si)?negative control (NC) group, si?EZR?AS1 significantly inhibited SCC13 and SCL?1 cell proliferation, migration and invasion, but promoted cell apoptosis. By contrast, compared with the pc?NC group, EZR?AS1 overexpression significantly enhanced A431 cell proliferation, migration and invasion, but inhibited cell apoptosis.	33236153
EZR-AS1	LncRNA	Homo sapiens	Coronary Disease	blood	regulation[SMYD3]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The findings revealed that lncRNA EZR-AS1 was highly expressed in the peripheral blood of patients with CHD.Collectively, these results demonstrate that lncRNA EZR-AS1 plays an important role in HUVECs function via SMYD3 signaling.		Yes	In vitro experiments showed that the overexpression of EZR-AS1 could enhance proliferation, migration, and apoptosis by upregulating the expression of EZR in HUVECs; downregulation of lncRNA EZR-AS1 resulted in the opposite effect.	32596350
EXOSC2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cancer tissues and cells lines	Regulation[Erk1/2 signaling,STAT1 pathway]	CCK8//qRT-PCR//Colony Formation Assay	The expression level of lincRNA P7 was significantly aberrantly deceased in HCC cancer tissues and cells lines.Mechanistically, lincRNA P7 blocked Erk1/2 signaling and repressed activation of the STAT1 pathway.		Yes	Gain- and loss-of-function experiments revealed that overexpression of lincRNA P7 significantly inhibited the proliferation of HCC-derived cancer cells, whereas lincRNA P7 knockdown promoted cell growth.	30546827
EWSAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(miR-326/FBXL20 pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//IHC//Transwell Assay	We found that EWSAT1 was highly expressed in CRC tissues and cell lines and associated with poor overall survival. Moreover, miR-326 was found to be a target of EWSAT1, and miR-326 inhibitor could partially reverse the effects on CRC cell progression induced by si-EWSAT1. Subsequently, we validated FBXL20 as a vital downstream target for miR-326, and EWSAT1 positively regulated FBXL20 via miR-326 in vitro.	We found that EWSAT1 was highly expressed in CRC tissues and cell lines and associated with poor overall survival. 	Yes	 In vitro, knockdown of EWSAT1 suppressed the cell proliferation, migration and invasion. 	33469313
EWSAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Regulation( Hippo-YAP signaling)	qRT-PCR	 The results indicated that EWSAT1 was upregulated significantly in HCC relative to that in normal tissues and was correlated with an aggressive phenotype and low patient survival. Mechanistically, EWSAT1 binds directly to Yes-associated protein (YAP), promotes Sarcoma gene (Src)-induced phosphorylation of YAP, facilitates nuclear translocation of YAP, and consequently, activates the transcription of Hippo-YAP signaling target genes involved in cancer evolution. 		Yes	Functional experiments demonstrated that EWSAT1 could promote proliferation and HCC cell metastasis both in vitro and in vivo. 	36421017
EWSAT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	regulation[miR-330-5p]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In cervical cancer, the expression of EWSAT1 was enhanced and contributed to the poor prognosis.Our study revealed that EWSAT1 enhances CPEB4 expression through sponging miR-330-5p, thereby promoting cervical cancer development, which might provide potential therapeutic targets for clinically cervical cancer patients.	 In cervical cancer, the expression of EWSAT1 was enhanced and contributed to the poor prognosis.	Yes	Downregulated EWSAT1 expression inhibited Hela cell migration, proliferation, and invasion.	32556917
EWSAT1	LncRNA	Homo sapiens	Glioma		interaction[sponging miR-152-3p]	CCK8//Transwell Assay	Increased EWSAT1 was associated with the presence of necrosis on magnetic resonance imaging scans in patients with glioma.  The present study demonstrated that EWSAT1 interacted directly with miR-152-3p, and rescue experiments confirmed that EWSAT1 participated in glioma development by suppressing miR-152-3p. 		Yes	 Furthermore, knockdown of EWSAT1 was indicated to suppress the proliferative and invasive abilities of glioblastoma cell lines using Cell Counting Kit-8 and Transwell assays.	32724428
ET-20	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells	Regulation	Invasion Assay//Migration Assay//qRT-PCR//FISH//RNA-seq//IP//Transwell Assay//Bioinformatics Analysis//IF	 Both ET-20 and Tnc are regulated by the EMT master transcription factor Sox4.  Notably, ablation of ET-20 lncRNA effectively blocks Tnc expression and with it EMT. Mechanistically, ET-20 interacts with desmosomal proteins, thereby impairing epithelial desmosomes and promoting EMT. 		Yes	 Notably, ablation of ET-20 lncRNA effectively blocks Tnc expression and with it EMT.	34633031
ERLR	LncRNA	Homo sapiens	Vitreoretinopathy, Proliferative	 RPE cells 	Interaction(TCF4/MYH9 )	RNA Pull-Down//ChIP//Western Blot//Migration Assay//FISH//qRT-PCR//Microarray//Transwell Assay//IF	In this study, we found that ERLR is upregulated in RPE cells stimulated with transforming growth factor (TGF)-β1 as detected by lncRNA microarray and RT-PCR. Mechanistically, chromatin immunoprecipitation (ChIP) assays indicated that the transcription factor TCF4 directly binds to the promoter region of ERLR and promotes its transcription. ERLR mediates EMT by directly binding to MYH9 protein and increasing its stability. TCF4 and MYH9 also mediate TGF-β1-induced EMT in RPE cells. 		Yes	 In vitro, silencing ERLR in RPE cells attenuated TGF-β1-induced EMT, whereas overexpressing ERLR directly triggered EMT in RPE cells. In vivo, inhibiting ERLR in RPE cells reduced the ability of cells to induce experimental PVR.	33664479
ERLNC1	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues	Interaction[downregulating KiSS1]	qRT-PCR	 We found that TC0101441 levels were elevated in EOC tissues compared with those in normal controls and significantly correlated with an advanced clinical stage and lymph node metastasis.Furthermore, loss-of-function assays showed that TC0101441 promoted the invasive and metastatic capacities of EOC cells both in vitro and in vivo	TC0101441 was determined to be an independent prognostic predictor of overall survival (OS) and disease-free survival (DFS). 	Yes	Furthermore, loss-of-function assays showed that TC0101441 promoted the invasive and metastatic capacities of EOC cells both in vitro and in vivo	31577838
ERBIN	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cell lines and tissues	Interaction(miR-1263/CDK6 Axis)	colony Formation Assay//Western Blot//ISH//Transfection//Flow Cytometry//qRT-PCR//FISH//PCR//Colony Formation Assay//IF	The expression of circERBIN was upregulated in HCC cell lines and tissues, which was predictive of a poor prognosis in HCC patients.  Mechanistic investigations revealed that circERBIN regulated HCC proliferation by acting as a sponge of miR-1263, which subsequently targeted cyclin dependent kinase 6 and controlled G1/S transition.	The expression of circERBIN was upregulated in HCC cell lines and tissues, which was predictive of a poor prognosis in HCC patients. 	Yes	 Elevated circERBIN promoted G1/S transition of HCC cells, thus facilitating the proliferation and tumorigenesis of HCC cells. 	35530358
Erbb4-IR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	Interaction[downregulating miR-145]	qRT-PCR	It was observed that Erbb4-IR was upregulated in tumor tissues of patients with ESCC.In addition, miR-145 overexpression attenuated the effects of Erbb4-IR overexpression. Therefore, lncRNA Erbb4-IR may promote ESCC by downregulating miR-145.		Yes	Erbb4-IR overexpression led to downregulated miR-145, and increased rates of ECSS cell proliferation and decreased rates of ECSS cell apoptosis. 	31119810
Erbb4-IR	LncRNA	Homo sapiens	prostate carcinoma	prostate carcinoma tissues	regulation[ downregulating miR-21]	CCK8//qRT-PCR//Cell Apoptosis Assay	The results revealed that Erbb4-IR was downregulated in prostate carcinoma tissues compared with adjacent non-cancerous tissues, and that low expression of Erbb4-IR in tumor tissues was closely associated with poor survival.Therefore, the results of the present study suggested that lncRNA Erbb4-IR is downregulated in prostate carcinoma and may inhibit cancer development by downregulating miR-21.	The results revealed that Erbb4-IR was downregulated in prostate carcinoma tissues compared with adjacent non-cancerous tissues, and that low expression of Erbb4-IR in tumor tissues was closely associated with poor survival.	Yes	Moreover, Erbb4-IR overexpression increased apoptosis and inhibited the proliferation of prostate carcinoma cells. 	32269615
ERBB2	CircRNA	Homo sapiens	Asthma	ASMCs	Interaction(miR-98-5p/IGF1R)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//ELISA	CircERBB2 was identified to directly interact with miR-98-5p, and overexpression of miR-98-5p abolished the function of circERBB2 on PDGF-BB-stimulated ASMCs. IGF1R was identified as a target of miR-98-5p, and knockdown of IGF1R relieved the PDGF-BB-induced ASMCs proliferation and migration.		Yes	 The depletion of circERBB2 attenuated the proliferation, migration, and levels of inflammatory factors induced by PDGF-BB and cell apoptosis. 	34616159
EPS15-AS1	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer stem cells and tissues	Interaction(EPS15)	Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//cell invasion assay	 EPS15 was highly expressed in LCSCs, while lncRNA EPS15-AS1 was lowly expressed in LCSCs (P<0.05).  However, simultaneous overexpression of lncRNA EPS15-AS1 and EPS15 attenuated the effect of lncRNA EPS15-AS1 overexpression alone on proliferation and apoptosis of LCSCs.		Yes	 After silencing lncRNA EPS15-AS1, the proliferation, invasion, and EPS15 protein expression of LCSCs were promoted (P<0.05) while apoptosis was suppressed (P<0.05). After overexpression of lncRNA EPS15-AS1, the proliferation, invasion, and EPS15 protein expression of LCSCs were suppressed while the apoptosis ability was promoted. 	36398248
FALEC	LncRNA	Homo sapiens	tongue squamous cell carcinoma		Interaction[ECM1 ]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Microarray//Colony Formation Assay//EdU Staining//Transwell Assay	The focally amplified long non-coding RNA in epithelial cancer (FALEC) was found downregulated in the tissues of tongue squamous cell carcinoma (TSCC) and was predicted to present a good prognosis by bioinformatics analysis. RNA pull-down and RNA immunoprecipitation demonstrated that FALEC could recruit enhancer of zeste homolog 2 (EZH2) at the promoter regions of extracellular matrix protein 1 (ECM1), epigenetically repressing ECM1 expression. The data revealed that FALEC acted as a tumor suppressor in TSCC and may aid in developing a novel potential therapeutic strategy against TSCC.		Yes	 Experiments indicated that FALEC knockdown significantly increased the proliferation and migration of TSCC cells both in vitro and in vivo; however, FALEC overexpression repressed these malignant behaviors.	31335317
FALEC	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	blood	Expression[highly expressed]	qRT-PCR	FALEC was significantly up-regulated in the blood plasma from cervical cancer patients and had significant correlation with tumor size, the FIGO stage, and lymph node metastasis. 	FALEC was significantly up-regulated in the blood plasma from cervical cancer patients and had significant correlation with tumor size, the FIGO stage, and lymph node metastasis. 	Yes	 FALEC overexpression could stimulate proliferation and invasion of Hela cells.	31248657
EPIST	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	CSCs	Interaction(microRNA-127-3p/DUSP1/ERK axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	C5orf66-AS1 was found as the most upregulated long noncoding RNAs (lncRNAs) in CSCs after Exo treatment.  The integrated bioinformatic analyses and luciferase assays suggested that C5orf66-AS1 upregulated DUSP1 expression through sequestering microRNA-127-3p (miR-127-3p).DUSP1 inhibition increased the phosphorylation of ERK. To conclude, this research reported that MSC-derived Exo block malignant behaviors of HCC-sourced CSCs through a C5orf66-AS1/miR-127-3p/DUSP1/ERK axis.		Yes	Either artificial overexpression of miR-127-3p or silencing of DUSP1 blocked the inhibitory functions of Exo in the CSCs. Similar results were reproduced in vivo where Exo reduced the growth of xenograft formed by CSCs in nude mice, and this reduction was blocked upon miR-127-3p overexpression or DUSP1 silencing. 	34431063
FALEC	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction[microRNA-761/CRKL pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	 LncRNA FAL1 was highly expressed in OSCC tissues and cell lines.The mRNA expression of microRNA-761 was lowly expressed in OSCC tissues and cell lines. Dual-Luciferase reporter gene assay showed that lncRNA FAL1 directly bound to microRNA-761. Meanwhile, microRNA-761 expression was negatively regulated by FAL1. CRKL was verified as the target gene of microRNA-761. Both the mRNA and protein levels of CRKL were remarkably upregulated in OSCC tissues and cell lines. CRKL expression was found to be negatively regulated by microRNA-761 in OSCC cells. Lowly expressed microRNA-761 reversed the inhibitory effect of lncRNA FAL1 knockdown on the proliferative potential of OSCC cells. In addition, the overexpression of CRKL reversed the inhibitory effect of lncRNA FAL1 down-regulation on the proliferative potential of OSCC cells as well.		Yes	The proliferative capacity of OSCC cells was significantly inhibited by lncRNA FAL1 knockdown. 	31298329
FAM225A	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues	regulation[NETO2 and FOXP1 ]	Western Blot//Wound Healing Assay//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We discovered that FAM225A exhibited higher expression in ESCC. Our results suggested that FAM225A upregulated NETO2 and FOXP1 expression by sponging miR-206 to accelerate ESCC progression and angiogenesis.		Yes	The silence of FAM225A attenuated cell viability, migration, and invasion, but facilitated cell apoptosis in ESCC.	33006432
FAM225A	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Interaction(miR-197-5p/NONO )	In Vivo Experiment//Western Blot//ISH//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	We confirmed that upregulation of FAM225A in ESCC and overexpression of FAM225A was associated with poor outcome in ESCC patients using TCGA ESCC cohort.In summary, our findings suggest that lncRNA FAM225A promotes ESCC development and progression via sponging miR-197-5p and upregulating NONO expression. 	We confirmed that upregulation of FAM225A in ESCC and overexpression of FAM225A was associated with poor outcome in ESCC patients using TCGA ESCC cohort.	Yes	 Knockdown of FAM225A significantly inhibited cell growth, migration and invasion of ESCC cells in vitro and inhibited ESCC xenograft development in vivo.	33442405
FAM225A	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	Interaction[Sponge miR-590-3p/miR-1275 and Upregulate ITGB3]	Other	Here, based on a microarray analysis, we identified 384 dysregulated lncRNAs, of which, FAM225A was one of the most upregulated lncRNAs in NPC. Mechanistically, FAM225A functioned as a competing endogenous RNA (ceRNA) for sponging miR-590-3p and miR-1275, leading to the upregulation of their target integrin β3 (ITGB3), and the activation of FAK/PI3K/Akt signaling to promote NPC cell proliferation and invasion. In summary, our study reveals a potential ceRNA regulatory pathway in which FAM225A modulates ITGB3 expression by binding to miR-590-3p and miR-1275, ultimately promoting tumorigenesis and metastasis in NPC.		Yes	FAM225A functioned as an oncogenic lncRNA that promoted NPC cell proliferation, migration, invasion, tumor growth, and metastasis.	31331909
FAM225A	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cell lines	Interaction(FUS/CENP-N )	RNA Pull-Down//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//RIP//Invasion Assay	FAM225A and CENP-N expression levels were evaluated in NPC tissues and cell lines. FAM225A stabilized CENP-N mRNA by recruiting FUS. FAM225A activated cGAS-STING by regulating the expression of CENP-N to promote NPC cell proliferation, migration and EMT.		Yes	FAM225A knockdown inhibited NPC cell proliferation, migration and EMT. 	35809496
FAM222A-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor samples and cell lines	Interaction( miR-let-7f/MYH9 axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay	The expression of FAM222A-AS1 is significantly upregulated in CRC tumor samples and cell lines. Furthermore, FAM222A-AS1 was mainly distributed in the cytoplasm. It may directly bound to miR-let-7f and inhibit its expression and upregulate MYH9. In summary, FAM222A-AS1, as a novel oncogene in CRC, may promote the CRC progression by inhibiting miR-let-7f/MYH9 axis. The FAM222A-AS1/miR-let-7f/MYH9 signaling pathway may be a novel valuable target for inhibiting CRC.	 CRC patients with elevated FAM222A-AS1 expression in the tumor samples had unfavorable overall survival and disease-free survival.	Yes	 CRC patients with elevated FAM222A-AS1 expression in the tumor samples had unfavorable overall survival and disease-free survival.	35646686
FAM207BP	LncRNA	Homo sapiens	Adenocarcinoma of Lung	The tumor tissues and matched normal tissue specimens from 41 cases of LUAD patients	Expression [highly expressed]	Transfection//Wound Healing Assay//CCK8//qRT-PCR//Survival Analysis//RNA-seq//Transwell Assay	FAM207BP expression was distinctly higher in LUAD than normal tissues. RT-qPCR results confirmed that FAM207BP was significantly highly expressed in LUAD tissues and cells. 	Patients with its high expression indicated worse OS and DFS time. 	Yes	 Knockdown of FAM207BP distinctly suppressed cellular viability, migration and invasion for LUAD cells. Also, its expression was negatively related to B cell infiltration levels. 	33434533
FAM201A	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer tissues	Interaction[regulating ABCE1 expression ]	CCK8//qRT-PCR//Western Blot//Transwell Assay	High levels of FAM201A expression were more likely to present in patients with squamous type, M1 stage, and inferior overall survival.FAM201A may markedly induce migration and invasion of LSCC, resulting in the M1 stage and poor survival. These findings suggest the FAM201A-ABCE1 axis as a novel therapeutic target in LSCC.		Yes	 FAM201A knockdown inhibits cell proliferation, migration, and invasion of LSCC cells in vitro, and represses tumor growth in vivo.	31841188
FAM201A	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(miR-3163/MACC1 axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//IHC	FAM201A expression level was significantly enhanced in CRC cells compared with normal cells. By exploring molecular mechanism of FAM201A, we found that FAM201A acted as a sponge of miR-3163. More importantly, oncogene MACC1 was confirmed to be a direct target of miR-3163 and FAM201A modulated MACC1 expression level via competing for miR-3163. Subsequently, we testified that FAM201A exerted its role in the tumorigenesis and development of CRC through targeting miR-3163/MACC1. 		Yes	 Further, functional experiments illustrated that knockdown of FAM201A restrained cell growth, stemness and promoted chemoresistance of CRC cells. Animal assay certified that FAM201A expedited CRC cell growth in vivo. 	36067543
FAM201A	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	regulation[miR-186-5p/TNKS1BP1 axis]	ChIP//Wound Healing Assay//RIP//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	The results showed that FAM201A expression was significantly upregulated in TNBC tissues and cells.  Collectively, our study revealed that TCF3-activated FAM201A promoted aggressive phenotypes of TNBC cells by upregulating TNKS1BP1 expression.		Yes	Functionally, FAM201A knockdown inhibited TNBC cell proliferation, migration and invasion, and accelerated cell apoptosis.	33011533
FAM181A-AS1	LncRNA	Homo sapiens	Glioma	cell lines	regulation[sponging miR-129-5p and upregulating ZRANB2]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	 FAM181A-AS1 expression is higher in glioma cell lines compared to normal human astrocytes (NHA). These findings show that FAM181A-AS1 promotes gliomagenesis by enhancing ZRANB2 expression by sponging of miR-129-5p.		Yes	CCK-8, EdU, and colony formation assays show that FAM181A-AS1 knockdown decreases proliferation and colony formation in glioma cells, whereas, FAM181A-AS1 overexpression reverses these effects.	33080570
FAM13A-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cell lines	Interaction(miRNA-205-3p/DDI2 Axis)	In Vivo Experiment//Western Blot//ISH//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//IHC//Invasion Assay//Transwell Assay	. Low FAM13A-AS1 expression and high miRNA-205-3p expression were observed in cervical cancer tissues and cell lines (SiHa and HeLa).  In addition, FAM13A-AS1 negatively regulated the expression of miRNA-205-3p, while miRNA-205-3p reduced DDI2 expression, and miRNA-205-3p mimic reversed the effects of FAM13A-AS1 overexpression in vitro.		Yes	 Upregulating the expression of FAM13A-AS1 inhibited proliferation, migration, and invasion of SiHa and HeLa cells, while the apoptosis of SiHa and HeLa cells was increased. More importantly, LV-FAM13A-AS1 could improve tumor development in vivo. 	35783157
FAM13A-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	539 RCC patients 	Interaction(miR-141-3p)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//FISH//MTT//Luciferase Report Assay//Cell Cycle Assay//Invasion Assay	By analyzing the gene expression profiles of 539 RCC patients from the TCGA cohort and 40 RCC patients from an independent cohort, we identified FAM13A-AS1, a poorly studied lncRNA, upregulated in RCC patients. FAM13A-AS1 regulates the expression of NEK6 by decoying miR-141-3p. 		Yes	 Knockdown experiments revealed that FAM13A-AS1 promotes cell proliferation, migration, and invasion by interacting with miR-141-3p. 	35402517
FAM138B	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells and tissues	Interaction(miR-105-5p)	CCK8//qRT-PCR	The expression of FAM138B is down-regulated in NSCLC cells and tissues. FAM138B targets miR-105-5p, and there is a negative correlation between FAM138B and miR-105-5p. It is confirmed that FAM138B inhibits the progression of NSCLC by targeting miR-105-5p and can be a potential prognostic biomarker for NSCLC.		Yes	Overexpression of FAM138B can inhibit the expression level of miR-105-5p in NSCLC cells, and the ability of NSCLC cells to proliferate, migrate and invade is downregulated. 	36529892
FALEC	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues	Interaction[ECM1 ]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	Mechanistic investigations demonstrated that small interfering RNA-induced silencing of FALEC decreased expression of the nearby gene extracellular matrix protein 1 (ECM1) in cis. Additionally, ECM1 and FALEC expression were positively correlated, and high levels of ECM1 predicted shorter survival time in GC patients. Our results suggest that the downregulation of FALEC significantly inhibited the migration and invasion of GC cells through impairing ECM1 expression by exerting an enhancer-like function. Our work provides valuable information and a novel promising target for developing new therapeutic strategies in GC.		Yes	Further experiments revealed that FALEC knockdown significantly inhibited GC cells migration and invasion in vitro.	30984243
FALEC	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	Regulation(miR-203b/PIM3 axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Invasion Assay	The results showed that FALEC and PIM3 were highly expressed, while miR-203b was lowly expressed, in GC. FALEC knockdown repressed GC cell proliferation, migration, and invasion, and promoted apoptosis and autophagy in vitro. Meanwhile, FALEC knockdown prevented growth and induced GC autophagy in vivo. This shows that FALEC upregulated PIM3 by sponging miR-203b in GC cells. Besides, FALEC induced the malignant behaviors of GC cells by regulating the miR-203b/PIM3 axis.		Yes	 FALEC knockdown repressed GC cell proliferation, migration, and invasion, and promoted apoptosis and autophagy in vitro. 	35722357
FALEC	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction[miR-637/NUPR1 pathway]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Here our results demonstrate that lncRNA FAL1 is markedly upregulated in CRC tissues and cells Moreover, we demonstrate that lncRNA FAL1 promotes carcinogenesis of CRC cells via regulation of the miR-637/NUPR1 pathway. 		Yes	 Here our results demonstrate that lncRNA FAL1 is markedly upregulated in CRC tissues and cells, and lncRNA FAL1 promotes proliferation ability, migration and invasion in CRC cells.	30267804
FALEC	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	regulation[regulating miR-2116-3p-targeted PIWIL1]	Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	FALEC was aberrantly up-regulated in CRC.Our study revealed that FALEC promoted CRC progression via restoring the expression of miR-2116-3p-targeted PIWIL1, suggesting the potential application of targeting FALEC in the treatment of CRC.		Yes	FALEC knockdown could impair CRC cell proliferation, migration and invasion, whereas facilitate cell apoptosis.	33073675
FALEC	LncRNA	Homo sapiens	Colonic Neoplasms	colon tumor tissues	Expression[highly expressed]	qRT-PCR	Here, our results indicate that FAL1 expression was remarkably up-regulated in colon tumor tissues as compared to corresponding tumor-adjacent normal tissues.	Importantly, the cumulative survival rate of patients with high levels of FAL1 in tumor tissues was considerably lower than those with low FAL1 levels in tumor tissues. Cox regression analysis showed that lncRNA FAL1 could act as an independent prognostic factor in CRC. 	Yes	 Knockdown of FAL1 in HT29 cells attenuated cell proliferation and stimulated cell apoptosis. 	30290064
FALEC	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	regulation[Wnt/β-catenin signaling pathway]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The expression level of FALEC was significantly higher in PTC tissues than that of adjacent normal tissues.FALEC expression was up-regulated in PTC tissues and cell lines. Highly expressed FALEC facilitated the proliferation, migration, and invasion of PTC by regulating the Wnt/β-catenin signaling pathway.		Yes	CCK-8 assay revealed that the proliferation ability of PTC cells was remarkably weakened after down-regulation of FALEC in vitro. Wound healing and transwell assays demonstrated that, compared with si-normal control (NC) group, the migration and invasion capabilities declined significantly in si-FALEC group.	32373973
EPIST	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues, serum, and cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	C5orf66-AS1 expression was downregulated in GC cells compared to that in adjacent normal tissues.Serum C5orf66-AS1 levels were significantly lower in GC patients than in superficial gastritis (GS) and atrophic gastritis (GA) patients.		Yes	Additionally, in vitro overexpression of C5orf66-AS1 in AGS cells inhibited cell proliferation, migration, and invasion.	32308414
EPIST	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-149-5p)	CCK8//qRT-PCR	The results demonstrated that C5orf66-AS1 was significantly upregulated and miR-149-5p was significantly downregulated in OS tissues and cells (MG63 and U2OS). Bioinformatics analysis further confirmed that miR-149-5p could directly bind to C5orf66-AS1. 		Yes	In addition, C5orf66-AS1 silencing significantly inhibited the proliferation, invasion and migration of U2OS cells, and stimulated cell apoptosis. These findings were reversed using miR-149-5p inhibitor.Increased Bax expression and decreased Bcl-2 and MMP-9 expression were also observed in C5orf66-AS1-siRNA transfected U2OS cells, compared with the control group. 	34539861
FEZF1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction[targeting miR-196a]	CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	The results of qRT-PCR proved that the expression level of FEZF1-AS1 in OSCC tissues was significantly higher than that of para-carcinoma tissues, and the difference was statistically significant. Therefore, it was believed that FEZF1-AS1 might promote the malignant progression of OSCC by regulating miR-196a.	The pathological stage was significantly higher in patients with high-expression FEZF1-AS1 than those with low-expression FEZF1-AS1, while the overall survival rate was remarkably lower. 	Yes	The proliferation ability of cells in FEZF1-AS1 silencing group declined significantly when compared with the NC group.	31378890
EOLA1-DT	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissues 	Interaction(miR-146b-3p/PRSS8)	qRT-PCR//Wound Healing Assay//MTT//Western Blot	LINC00893 and PRSS8 were significantly downregulated, while miR-146b-3p was upregulated in colon cancer tissues compared to control group. Overexpressed LINC00893 or silenced miR-146b-3p suppressed the proliferation, migration, and invasion while promoting apoptosis in colon cancer cells (HCT116, SW620). Moreover, miR-146b-3p overexpression reversed the inhibitory effect of LINC00893, while PRSS8 knockdown rescued the suppressive effect of miR-146b-3p inhibitor on malignant cell behaviors in colon cancer. Furthermore, the tumor growth in mice was significantly reduced by LINC00893 overexpression.		Yes	Overexpressed LINC00893 or silenced miR-146b-3p suppressed the proliferation, migration, and invasion while promoting apoptosis in colon cancer cells (HCT116, SW620). Moreover, miR-146b-3p overexpression reversed the inhibitory effect of LINC00893, while PRSS8 knockdown rescued the suppressive effect of miR-146b-3p inhibitor on malignant cell behaviors in colon cancer. Furthermore, the tumor growth in mice was significantly reduced by LINC00893 overexpression.	35571488
ENTPD3-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues 	Interaction(miR-155/HIF-1α signaling)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//RIP//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	The results showed that the G > A mutation of rs67311347 created a binding motif of ZNF8 and subsequently upregulated ENTPD3-AS1 expression by acting as an enhancer.  Furthermore, ENTPD3-AS1 interacted with miR-155-5p and activated the expression of HIF-1α, which was an important tumor suppressor gene in the development of RCC. 	 The TCGA-KIRC and our cohorts both confirmed the downregulation of ENTPD3-AS1 in RCC tissues and demonstrated that increased ENTPD3-AS1 expression was associated with good OS and PFS. 	Yes	 The functional experiments revealed that overexpression of ENTPD3-AS1 inhibited cell proliferation in RCC cell lines and the effect could be rescued by knocking down HIF-1α.	34218253
ENST00000623984	LncRNA	Homo sapiens	Colonic Neoplasms	colorectal cancer tissues and cell lines	Expression(highly expressed)	qRT-PCR	The ENST000000623984 expression level was increased in colorectal cancer. 		Yes	 Knockdown of ENST000000623984 reduced cell viability, proliferation rate, cell migration and invasion.	34247468
ENST00000607393	LncRNA	Homo sapiens	Glaucoma, Open-Angle	Aqueous humor	Expression[highly expressed]	qPCR//Microarray	 ENST00000607393 was also significantly higher in the iris and plasma of POAG patients.		Yes	 Last, ENST00000607393 knockdown alleviated calcification of primary human trabecular meshwork cells in vitro.	30677397
ENST00000606790.1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	NPTC tissues or cell lines	regulation[ PI3K/AKT Pathway]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	ENST was significantly up-regulated in PTC tissues or PTC cell lines (PTC and IHH4 cell lines), compared to NPTC tissues or normal cell lines, respectively.Overall, our results demonstrated that ENST can promote PTC progression by activating the PI3K/AKT signaling pathway, suggesting that ENST can serve as a potential biomarker and new therapeutic target for patients with PTC.	 High expression of ENST was strongly correlated to lymph node metastasis and tumor size at diagnosis. 	Yes	 Silencing of ENST significantly inhibited cell growth and colony formation, arrested the cell cycle at G2/M phase, upregulated the expression of CHK1, downregulated the expression of CDC25C, and inhibited cell invasion.	32791924
ENST00000547547	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues 	Expression[lower expressed]	ISH//qRT-PCR//MTT//Transwell Assay	In the present study, we demonstrated that the ENST00000547547 level is significantly downregulated in CRC tissues compared to normal tissues.		Yes	. Furthermore, the overexpression of ENST00000547547 inhibited the cell proliferation, invasion and migration of CRC cells in vitro and decreased tumorigenesis ability in vivo. Furthermore, we provided the first evidence that ENST00000547547 inhibited the proliferation of CRC cells by affecting the cell cycle and apoptosis. 	30542703
ENST00000543604	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miRNA 564/AEG-1 or ZNF326/EMT )	CCK8//qRT-PCR//RNA Pull-Down//Western Blot	In this study, we found that the expression levels of lncRNA 604 were increased in CRC. LncRNA 604 could predict the prognosis of CRC and was an independent negative factor. LncRNA 604 exerted a synergistic effect with miRNA 564 or ZNF326 on the prognosis of CRC. LncRNA 604 could improve chemoresistance by increasing the expression of AEG-1, NF-κB, and ERCC1.		Yes	LncRNA 604 could promote CRC cell proliferation and metastasis through the miRNA 564/AEG-1 or ZNF326/EMT signaling axis in vivo and in vitro. 	36081570
ENST00000538705.1	LncRNA	Homo sapiens	Acute Coronary Syndrome	ACS patients, myocardial infarction rats	Interaction(ALOX15)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Microarray	Coexpression analysis indicated the interaction between ENST00000538705.1 and ALOX15. RT-qPCR confirmed the remarkable upregulation of circulating ENST00000538705.1 and ALOX15 in ACS patients. In HCAECs, ENST00000538705.1 knockdown lowered the expression of ALOX15 but ALOX15 did not alter the expression of ENST00000538705.1.		Yes	Silencing ENST00000538705.1 or ALOX15 weakened the proliferation and migration of HCAECs. Additionally, knockdown of ENST00000538705.1 or ALOX15 relieved myocardial damage, decreased serum TC and LDL levels, and elevated HDL levels in myocardial infarction rats.	35571613
ENST00000455974	LncRNA	Homo sapiens	Colonic Neoplasms	colon tissues	Regulated[up-regulated]	qRT-PCR	 Here, firstly, we observed that ENST00000455974 was gradual increased across colon normal-adenoma-carcinoma-metastasis sequence by quantitative real-time PCR.Mechanistically, ENST00000455974 was mainly located in the nucleus of colon cancer cells and it promoted the growth and metastasis of pMMR CC cells through up-regulating JAG2.	Thirdly, a higher level of ENST00000455974 was associated with a poorer patient survival. 	Yes	 Furthermore, Knockdown of ENST00000455974 led to reduced proliferation and migration of colon cancer cells.	30473216
ENST00000430471	LncRNA	Homo sapiens	Colorectal Neoplasms		regulation[Regulating the Expression of YBX-1]	qRT-PCR//Wound Healing Assay//RNA Pull-Down	Silencing of ENST00000430471 inhibits proliferation, migration, and invasion of CRC cells by regulating YBX-1 expression. 		Yes	Silencing of ENST00000430471 inhibits proliferation, migration, and invasion of CRC cells by regulating YBX-1 expression. 	32848471
ENST00000413528	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[miR-593-5p/PLK1 pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	 Expression of ENST00000413528 was significantly increased in glioma tissues and LN229 and U251 cells.lncRNA ENST00000413528 is closely related to the development of glioma via the miR-593-5p/PLK1 pathway.		Yes	Knockdown of ENST00000413528 in glioma cells inhibited cell proliferation and colony formation abilities, induced the G0/G1 arrest of the cell cycle, and promoted apoptosis.	30924320
ENSG00000231881	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Regulation[VEGFC signaling pathway]	Western Blot//Tube Formation Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 ENSG00000231881 expression level was substantially higher in colorectal cancer tissues than in paracancerous tissues and correlated with malignancy and prognosis.ENSG00000231881 could bind to miR-133b and consequently affect the cell functions through the regulation of VEGFC expression via miR-133b.		Yes	In colorectal cancer cells, ENSG00000231881 overexpression significantly promoted cell proliferation, metastasis, and tube formation in lymphatic epithelium, decreased miR-133b expression, and increased VEGFC expression. On the contrary, ENSG00000231881 interference expression showed exactly opposite results.	30581003
ENO1	CircRNA	Homo sapiens	Adenocarcinoma of Lung	 cell lines	Regulation[miR-22-3p/ENO1 axis]	TUNEL//Western Blot//ISH//Wound Healing Assay//Tunel//qRT-PCR//RIP//FISH//PCR//IP//IHC//IF	Circ-ENO1 and its host gene ENO1 were identified to be upregulated in LUAD cells.In summary, current study elucidated that circ-ENO1 promoted glycolysis and tumor progression in LUAD by miR-22-3p/ENO1 axis, indicating circ-ENO1 as a promising treatment target for LUAD patients.		Yes	Functionally, silencing circ-ENO1 retarded glycolysis, inhibited proliferation, migration and EMT, induced apoptosis. 	31767835
EMX2OS	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-654-3p/AKT3/PD-L1 Axis]	qRT-PCR//Luciferase Report Assay	EMX2OS is overexpressed in human ovarian cancer tissues. These results demonstrated that the EMX2OS/miR-654/AKT3/PD-L1 axis confers aggressiveness in ovarian cancer and may represent a therapeutic target for OC metastasis.		Yes	 Knockdown of EMX2OS reduced, while overexpression of EMX2OS enhanced the proliferation, invasion and sphere formation of OC cells. In addition, EMX2OS enhanced tumor growth in an in vivo xenograft model of human OC. 	32273754
EMX2OS	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues	regulation[cGMP-PKG pathway]	qRT-PCR//RNA Pull-Down//ChIP	 TCF12 and EMX2OS were both downregulated in PCa tissues and cells,EMX2OS, transcriptionally regulated by TCF12, played a synergy role with FUS protein in regulating the proliferation, migration and invasion of PCa cells by activating the cGMP-PKG pathway.		Yes	TCF12 and EMX2OS were both downregulated in PCa tissues and cells, and they negatively regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells.	32801740
EMX2OS	LncRNA	Homo sapiens	Wilms Tumor	Wilms' tumor patient samples	Interaction(miR-654-3p)	Other	EMX2OS expression was lower, while miR-654-3p level was higher in Wilms' tumor patient samples, and there was a negative correlation between EMX2OS and miR-654-3p. EMX2OS acted as a sponge of miR-654-3p. Overexpression of miR-654-3p abolished EMX2OS-mediated anti-cancer effects on Wilms' tumor cells. 		Yes	Overexpression of EMX2OS repressed growth, migration, invasion, and triggered apoptosis of Wilms' tumor cells.Finally, EMX2OS overexpression restrained Wilms' tumor growth in vivo.	35181613
EMC9	CircRNA	Homo sapiens	Retinoblastoma	RB tissues and cells	Interaction(miR-138-5p/SLC7A5 axis)	TUNEL//Western Blot//Transfection//Tunel//Flow Cytometry//qRT-PCR//Proliferation Assay//IF//PCR//Cell Proliferation Assay//IHC//Transwell Assay	Circ-FAM158A and SLC7A5 were overexpressed and miR-138-5p was downregulated in RB tissues and cells. MiR-138-5p was a direct target of circ-FAM158A, and miR-138-5p inhibition reversed the inhibitory effect of circ-FAM158A silence on the progression of RB cells. Additionally, SLC7A5 was identified as a target of miR-138-5p, and SLC7A5 overexpression abated the anti-tumor roles of miR-138-5p in RB cells. 		Yes	Circ-FAM158A knockdown inhibited RB cell proliferation, metastasis, and promoted apoptosis in vitro and in vivo. 	34102206
EMBP1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC cell lines and tumor tissue	regulation[EMBP1/miR-9-5p axis]	qRT-PCR	miR-9-5p was significantly down-regulated, and EMBP1 was significantly up-regulated, in RCC cell lines and tumor tissue. Our findings suggest an important role of the EMBP1/miR-9-5p axis dysregulation in RCC tumor progression.		Yes	 Overexpression of miR-9-5p or EMBP1 suppression in RCC cell lines significantly retarded their proliferative, migratory, and invasive behavior, in addition to promoting apoptosis and cell-cycle arrest. 	32482375
ELFN1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC cell lines	Regulation(ZBTB16/PI3K/AKT axis)	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	Bioinformatics analysis revealed increased expression of ELFN1-AS1 in GC, and abundant expression of ELFN1-AS1 was observed in the acquired GC cell lines. ELFN1-AS1 recruited DNA methyltransferases to the promoter region of ZBTB16 and induced transcriptional repression of ZBTB16 through methylation modification. Furthermore, downregulation of ZBTB16 activated the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and restored the proliferation and invasiveness of GC cells.		Yes	Knockdown of ELFN1-AS1 in GC cells weakened cell proliferation, invasion, migration, and resistance to apoptosis. In vivo, downregulation of ELFN1-AS1 reduced the growth rate of xenograft tumors in mice. 	35451560
ELFN1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction( miR-497/CCNE1 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The significant upregulation of ELFN1-AS1 was found in NSCLC tissues and cells, which was closely associated with the TNM stage, lymph node metastasis status, and overall survival of patients. Moreover, ELFN1-AS1 was found to serve as a sponge to binding with miR-497, and CCNE1 was demonstrated to be the downstream target of miR-497, which was speculated as the potential mechanism underlying the function of ELFN1-AS1.	The significant upregulation of ELFN1-AS1 was found in NSCLC tissues and cells, which was closely associated with the TNM stage, lymph node metastasis status, and overall survival of patients.	Yes	The knockdown of ELFN1-AS1 was found to inhibit the cellular processes and EMT of NSCLC.	35431233
EOLA1-DT	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissues and cell lines	Interaction( miR-3173-5p/SOCS3/JAK2/STAT3 pathway)	In Vivo Experiment//RNA Pull-Down//IHC//Migration Assay//qRT-PCR//RIP//Cell Proliferation Assay//Colony Formation Assay	 LINC00893 was downregulated in PCa tissues and cell lines, and patients with low expression of LINC00893 were associated with a poorer overall survival rate.We further demonstrated that LINC00893 acted as a sponge for miR-3173-5p and inhibited its activity, which in turn regulated the suppressor of cytokine signaling 3 (SOCS3)/Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling axis.	 LINC00893 was downregulated in PCa tissues and cell lines, and patients with low expression of LINC00893 were associated with a poorer overall survival rate.	Yes	 LINC00893 overexpression hindered the proliferation, epithelial-mesenchymal transition (EMT) as well as the migratory ability of PCa cells, and suppressed the tumorigenesis of PCa cells in nude mice. 	35818076
EOLA2-DT	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues and cells	Interaction(TIA-1/let-7e-5p )	Western Blot//Transfection//RIP//qRT-PCR//Luciferase Report Assay//Invasion Assay	We found that LINC00894 expression was markedly reduced in thyroid cancer tissues and cells, and low expression of LINC00894 was associated with poor prognosis in thyroid cancer. Additionally, let-7e-5p expression was substantially enhanced in CAL-62 and TPC-1 cells. LINC00894 overexpression promoted TIA-1 expression by acting as a sponge of let-7e-5p. Finally, let-7e-5p weakened the function of LINC00894 in thyroid cancer cells via reduction in TIA-1 levels. 	We found that LINC00894 expression was markedly reduced in thyroid cancer tissues and cells, and low expression of LINC00894 was associated with poor prognosis in thyroid cancer.	Yes	 LINC00894 overexpression inhibited the proliferation, migration, and invasion of CAL-62 and TPC-1 cells.	35776220
EPIST	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Regulation[ miR-637/RING1 axis]	qRT-PCR//Luciferase Report Assay//RIP	We found that lncRNAC5orf66-AS1 was significantly upregulated in cervical cancer tissues and cells. LncRNA C5orf66-AS1, as a competitive endogenous RNA (ceRNA), regulated the effect of RING1 on the proliferation, apoptosis and cell cycle of cervical cancer cells through adsorbing miR-637.		Yes	Over-expression of C5orf66-AS1 promoted the proliferation of cervical cancer cells, while downregulation of C5orf66-AS1 promoted the apoptosis of cervical cancer cells. 	30518760
EOLA2-DT	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells	Interaction(miR-429)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	High expression of LINC00894 was observed in breast cancer cells, and its overexpression significantly expedited cell proliferation and invasion. Moreover, LINC00894 positively regulated the expression of ZEB1 by competitively binding to miR-429.		Yes	High expression of LINC00894 was observed in breast cancer cells, and its overexpression significantly expedited cell proliferation and invasion. 	34079285
EPIST	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC cells 	Interaction(miR-149-5p/CTCF)	RNA Pull-Down//ChIP//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this study, we tested C5orf66-AS1 expression in TNBC cells using quantitative real-time PCR (qRT-PCR) and used functional assays to detect cell behaviors, which showed that C5orf66-AS1 was highly expressed in TNBC cells and that C5orf66-AS1 knockdown attenuated cell proliferation, migration, and invasion while promoting cell apoptosis. Through a luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and chromatin immunoprecipitation (ChIP) assay, we identified the binding capacity of C5orf66-AS1 to RNAs. Furthermore, miR-149-5p was proven to be sponged by C5orf66-AS1. CCCTC-binding factor (CTCF) was confirmed as the target of miR-149-5p and could transcriptionally activate C5orf66-AS1 expression in TNBC cells. We also discovered that C5orf66-AS1 activated the Wnt/β-catenin signaling pathway by upregulating catenin beta 1 (CTNNB1). Importantly, CTNNB1 could be targeted by miR-149-5p. 		Yes	In this study, we tested C5orf66-AS1 expression in TNBC cells using quantitative real-time PCR (qRT-PCR) and used functional assays to detect cell behaviors, which showed that C5orf66-AS1 was highly expressed in TNBC cells and that C5orf66-AS1 knockdown attenuated cell proliferation, migration, and invasion while promoting cell apoptosis. 	35499320
EPIC1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation(Ang2/Tie2 axis)	qRT-PCR	EPIC1 expression was significantly upregulated in NSCLC tissues and cell lines. We postulate that EPIC1 promotes tumor angiogenesis by activating the Ang2/Tie2 axis in NSCLC.		Yes	Furthermore, the overexpression of EPIC1 in NSCLC cells stimulated HUVEC channel formation and proliferation by activating Ang2/Tie2 signaling, and the opposite results were obtained when EPIC1 was silenced in NSCLC cells.  The density of new blood vessels was simultaneously increased by EPIC1 overexpression in vivo, using CAM angiogenesis model and a nude mouse tumor model. 	33359744
EPIC1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues,epithelial cells	interaction[MYC]	qRT-PCR	We show that Lnc-EPIC1 expression is significantly higher in established/primary human lung cancer cells than that in human lung epithelial cells. Lnc-EPIC1 is also elevated in human lung cancer tissues. Together, our results show that Lnc-EPIC1 promotes human lung cancer cell growth possibly by targeting MYC.		Yes	Silencing of Lnc-EPIC1 by targeted siRNA significantly inhibited human lung cancer cell growth, survival and proliferation, whiling inducing G1-S cell cycle arrest and cell apoptosis.	30029875
EPIC1	LncRNA	Homo sapiens	Colonic Neoplasms	colon tissues and colon epithelial cells	Expression[highly expressed]	qRT-PCR//IP//RNA Pull-Down	We show that Lnc-EPIC1 expression is elevated in human colon cancer tissues and primary human colon cancer cells.		Yes	In the primary human colon cancer cells, Lnc-EPIC1 siRNA largely inhibited cancer cell growth, proliferation, migration and invasion. Further, Lnc-EPIC1 silencing induced significant apoptosis activation in colon cancer cells.	33170148
EPIC1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cell lines	Interaction[MEF2D ]	qRT-PCR//MTT//Transwell Assay//Western Blot	 EPIC1 was down-regulated, but MEF2D was up-regulated in OS tissues and OS cell lines.Targeting relationship between EPIC1 and MEF2D was confirmed by RNA pull-down and RNA immunoprecipitation (RIP). The MEF2D protein binding to ubiquitin was significantly increased in OS cells overexpressing EPIC1. The co-transfection with pcDNA-EPIC1 and pcDNA-MEF2D rescued the inhibition of cell viability and invasion caused by the overexpression of EPIC1. 		Yes	Overexpression of EPIC1 inhibited cell viability and invasion of OS cells.Overexpression of EPIC1 suppressed tumor growth in the OS xenograft model.	30703420
EPIC1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissue	Interaction[YAP1 ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay	In this study, we found that the expression of the lncRNA EPIC1 (Lnc-EPIC1) is high in PC and closely related to tumor size, TNM staging and lymph node metastasis status.The results show that Lnc-EPIC1 interacts with YAP1 to promote the progression of PC.	In this study, we found that the expression of the lncRNA EPIC1 (Lnc-EPIC1) is high in PC and closely related to tumor size, TNM staging and lymph node metastasis status.	Yes	Silencing Lnc-EPIC1 by siRNA targeting could significantly inhibit the cell growth and colony formation ability of PC cells and induced G1/S cell cycle arrest and apoptosis in PC cells. An Lnc-EPIC1-overexpressing lentiviral vector promoted the growth of PC cells. 	31810603
EPIC1	LncRNA	Homo sapiens	Gallbladder Neoplasms	plasma  and paracancerous tissues of GBC patients	Interaction(LncRNA LET)	CCK8//qPCR//Cell Apoptosis Assay	The present study found that EPIC1 was upregulated in tumor tissues than in paracancerous tissues of GBC patients, and plasma levels of EPIC1 were significantly correlated with levels of EPIC1 in tumor tissues. LncRNA LET was downregulated in tumor tissues than in paracancerous tissues and was inversely correlated with EPIC1 in both tumor tissues and paracancerous tissues. 		Yes	Overexpression of EPIC1 led to downregulated LET, and LET overexpression also mediated the downregulation of EPIC1. EPIC1 led to accelerated GBC cell proliferation and inhibited apoptosis. Overexpression of LET played opposites roles. 	34653690
EPIC1	LncRNA	Homo sapiens	Cholangiocarcinoma	cholangiocarcinoma tissues	Expression[highly expressed]	Flow Cytometry//qRT-PCR//RIP//MTT//Colony Formation Assay	In this study, our results indicate that the LncRNA-EPIC1 expression were significantly increased in cholangiocarcinoma tissues, compared to adjacent normal tissues. 		Yes	Loss-and-gain of Lnc-EPIC1 contributes to the CCA cell growth, colony formation, cell apoptosis and also cell cycle. 	30205958
EPHB4	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[circEPHB4/miR-637/SOX10/Nestin axis]	colony Formation Assay//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//PCR//IP//Colony Formation Assay//IF	Here, we found that circEPHB4 (hsa_circ_0081519) and SOX10 were up-regulated and microRNA (miR)-637 was down-regulated in glioma tissues and cell lines. In conclusion, the circEPHB4/miR-637/SOX10/Nestin axis plays a central role in controlling stem properties, self-renewal and glycolysis of glioma cells and predicts the overall survival of glioma patients.		Yes	Functionally, silencing circEPHB4 or increasing miR-637 levels in glioma cells was sufficient to inhibit xenograft growth in vivo.	33085838
EPEL	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tumors	Interaction[ROCK1 ]	qRT-PCR//Western Blot//Transwell Assay	The results revealed that EPEL was Expression[Expression[up-expression]-expression]regulated in tumor tissues compared with adjacent tissues. Furthermore, EPEL overexpression promoted the migration and invasion of osteosarcoma cells and induced overexpression of ROCK1.		Yes	 Furthermore, EPEL overexpression promoted the migration and invasion of osteosarcoma cells and induced overexpression of ROCK1.	30867743
EPB41L5	CircRNA	Homo sapiens	Glioblastoma	glioblastoma tissues and cell lines	interaction[EPB41L5,miR-19a]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	Circ-EPB41L5 was downregulated in glioblastoma tissues and cell lines compared to the normal brain tissues and cell lines. The current study highlights a novel suppressive function of circ-EPB41L5 and reveals that circ-EPB41L5/miR-19a/EPB41L5/p-AKT regulatory axis plays a striking role in the progression of glioblastoma, which provides a novel insight into the mechanisms underlying glioblastoma.	 Low circ-EPB41L5 expression was correlated to the poor prognosis of glioblastoma patients, while the overexpression inhibited proliferation, clone formation, migration, and invasion abilities of glioma cells, and the suppression had counter effects.	Yes	 Low circ-EPB41L5 expression was correlated to the poor prognosis of glioblastoma patients, while the overexpression inhibited proliferation, clone formation, migration, and invasion abilities of glioma cells, and the suppression had counter effects.	31905344
EPB41L4A-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Regulation[miR-301a-5p-FOXL1 axis]	FISH//Luciferase Report Assay//Western Blot//qRT-PCR	 Here, we have identified a novel lncRNA EPB41L4A-AS2, which is significantly downregulated both in HCC cells and tissues, and plays a negative regulatory role in HCC proliferation and invasion. 		Yes	Also, in vivo experiments proved that EPB41L4A-AS2 suppress tumor growth and extrahepatic metastasis (lung) via the miR-301a-5p-FOXL1 axis.	30971290
EPB41L4A-DT	LncRNA	Homo sapiens	Ovarian Neoplasms	cell lines	Interaction[microRNA-103a]	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//Transwell Assay	RT-qPCR was conducted to detect the expression of EPB41L4A-AS2 in 126 OC tissues and paracancerous tissues, the results of which documented that EPB41L4A-AS2 was poorly expressed in OC tissues compared with in paracancerous tissues (P < 0.05; Figure 1b).  RUNX1T1 was a target gene of miR-103a and EPB41L4A-AS2 bound to miR-103a. Moreover, EPB41L4A-AS2 increased RUNX1T1 expression by decreasing miR-103a expression. EPB41L4A-AS2-overexpressing SK-OV-3 cells exhibited inhibited proliferation, migration, colony formation and invasion, which was rescued by overexpression of miR-103a or silencing of RUNX1T1. Besides, overexpressed EPB41L4A-AS2 repressed tumour formation in vivo. Altogether, the current study demonstrates that overexpressed EPB41L4A-AS2 can potentially bind to miR-103a to promote the expression of RUNX1T1, thereby inhibiting OC, highlighting the potential of EPB41L4A-AS2 as a target for OC.		Yes	EPB41L4A-AS2 increased RUNX1T1 expression by decreasing miR-103a expression. EPB41L4A-AS2-overexpressing SK-OV-3 cells exhibited inhibited proliferation, migration, colony formation and invasion, which was rescued by overexpression of miR-103a or silencing of RUNX1T1. Besides, overexpressed EPB41L4A-AS2 repressed tumour formation in vivo.	31645082
EPB41L4A-DT	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells 	Interaction(MiR-107/LATS2 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Cycle Assay//EdU Staining//Transwell Assay	Mechanistically, in the nucleus we identified that EPB41L4A-AS2 relies on binding to YBX1 to reduce the stability of Snail mRNA to enhance the expression of E-cadherin and reverse the progression of epithelial-to-mesenchymal transition (EMT). In the cytoplasm, we found that EPB41L4A-AS2 blocked the invasion and migration of NPC cells by promoting LATS2 expression via sponging miR-107. 		Yes	Biological analyses showed that overexpression of EPB41L4A-AS2 reduced the metastasis and invasion of NPC in vitro and in vivo, but had no significant effect on cell proliferation. 	34131399
EPB41L4A-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[Rho/ROCK pathway]	qRT-PCR	 In this study, we found that lncRNA EPB41L4A-AS1 was highly expressed in CRC tissues and was associated with poor prognosis and tumor metastasis in patients with CRC. Mechanically, we found that EPB41L4A-AS1 may participate in the development of CRC by activating the Rho/Rho-associated protein kinase signaling pathway. 		Yes	In vitro studies showed that the knockdown of EPB41L4A-AS1 inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition of CRC cells.	32557646
EPB41L4A-AS1	LncRNA	Homo sapiens	Aging	neurons and glial-derived cells.	Regulation(damaging synthesis of NAD+ and ATP)	Western Blot//Transfection//qRT-PCR//Bioinformatics Analysis//ChIP	EPB41L4A-AS1 was downregulated in aging and Alzheimer's disease. EPB41L4A-AS1 related genes were found to be enriched in the electron transport chain and NAD synthesis pathway. Furthermore, these genes were highly associated with neurodegenerative diseases and positively correlated with EPB41L4A-AS1. In addition, biological experiments proved that the downregulation of EPB41L4A-AS1 could reduce the expression of these genes via histone H3 lysine 27 acetylation, resulting in decreased NAD and ATP levels, while EPB41L4A-AS1 overexpression and nicotinamide riboside treatment could restore the NAD and ATP levels.		Yes	biological experiments proved that the downregulation of EPB41L4A-AS1 could reduce the expression of these genes via histone H3 lysine 27 acetylation, resulting in decreased NAD and ATP levels, while EPB41L4A-AS1 overexpression and nicotinamide riboside treatment could restore the NAD and ATP levels.	34758883
EPB41	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-486-3p/eIF5A axis)	Western Blot//ISH//Transfection//qPCR//Proliferation Assay//FISH//RIP//IF//RNA-seq//PCR//Cell Proliferation Assay//IP//Transwell Assay	 The results show that the circ-EPB41 was upregulated in NSCLC tissues and cell lines. Luciferase reporter experiments confirmed that miR-486-3p/eIF5A were downstream targets of circ-EPB41.	 Increased circ-EPB41 expression in NSCLC was significantly correlated with malignant characteristics, and positive to post-surgical overall survival of NSCLC patients.	Yes	 Reduced circ-EPB41 expression in NSCLC decreased cell proliferation and invasion in both in vitro and in vivo experiments.	35725615
FAM225A	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction( MiR-206/ADAM12 )	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay//Transwell Assay	 In gastric cancer, FAM225A and ADAM12 expressions were up-regulated, while miR-206 expression was down-regulated.  MiR-206 inhibitor partially offset the effects of siFAM225A. Moreover, FAM225A competitively bound to miR-206 to up-regulate ADAM12 expression. Overexpressed ADAM12 partially reversed the effect of miR-206 mimic on the biological characteristics of gastric cancer cells and EMT-related proteins.		Yes	 Opposite to the regulatory effects of overexpressed FAM225A, blocking FAM225A expression reduced cell viability, migration, invasion and number of cell clones, increased E-Cadherin expression, inhibited N-Cadherin and Vimentin expressions, and ultimately promoted tumor growth. 	34539984
FAM225B	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cell lines 	Interaction(miR-613/CCND2 axis)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	 We observed a remarkable increase of FAM225B in NPC tissues and cell lines compared with controls.  Mechanically, FAM225B functioned as an endogenous sponge by competing for miR-613 binding to up-regulate CCND2 expression. More importantly, rescue experiments further demonstrated that the suppressive impacts of FAM225B knockdown on cell proliferation, migration and invasion were significantly reversed after CCND2 overexpression. 	Also, highly expressed FAM225B was closely correlated with advanced TNM stage, distant metastasis, and poor overall survival. 	Yes	Interestingly, loss-of-function analysis revealed that FAM225B knockdown significantly inhibited tumor growth in vitro and in vivo, and decreased the migratory and invasive capacity of NPC cells. 	34255617
FAM230B	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction(miR-378a-3p/WNT5A axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Invasion Assay//Migration Assay//qRT-PCR//RNA-seq//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis	 In this study, we found consistently elevated expression levels of the lncRNA FAM230B in PTC tissues, both in newly generated RNA-seq data and in datasets from the GEO and TCGA databases. Mechanistically, FAM230B sponged miR-378a-3p and showed competitive binding to the 3'-UTR of WNT5A. FAM230B overexpression resulted in elevated WNT5A expression and thereby regulated the epithelial-mesenchymal transition in PTC cells. Finally, we verified that both miR-378a-3p overexpression and WNT5A silencing effectively offset the impacts of FAM230B on PTC cell migration and invasion. 	We demonstrated that the expression of FAM230B can be used for the diagnosis of PTC and is also strongly associated with lymph node metastasis. 	Yes	Functionally, FAM230B promoted the migration and invasion of PTC cells in vitro and in vivo. 	33578293
FER1L4	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues and cancer cell lines	Interaction(miR-133a-5p/Prx1 Axis)	CCK8//qRT-PCR	FERIL4 was significantly upregulated in OSCC tissues and cancer cell lines. Knockdown of FER1L4 significantly enhanced the expression of miR-133a-5p by sponging it, and then downregulated Prx1 expression.	Moreover, high level of FER1L4 predicted a poor prognosis of OSCC patients. 	Yes	Silencing of FER1L4 not only significantly inhibited cell growth, invasion, migration and induced apoptosis in SCC-9 and HN4 cells in vitro, but also effectively suppressed the tumorigenesis of OSCC cells in vivo.	33568918
FER1L4	LncRNA	Homo sapiens	Osteosarcoma	cell lines	Regulation[PI3K/AKT signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay	Results showed that FER1L4 was observed to be lowly expressed in osteosarcoma cell lines (US-O2, MG-63 and SaOS-2 cells), especially MG63 cells.In conclusion, the study indicated that FER1L4 acted as a tumor suppressor in osteosarcoma via activating PI3K/AKT pathway may be a new prognostic biomarker and potential therapeutic target for osteosarcoma intervention.		Yes	Besides, overexpression of FER1L4 remarkably repressed the proliferation, migration and invasion of MG63 cells.	31000382
FER1L4	LncRNA	Homo sapiens	Parkinson Disease	Neural stem cells 	Interaction( miR-874-3p/Ascl2)	qRT-PCR//Western Blot	In the present research, we noted that FER1L4 is upregulated in NSCs induced with TNFα. Using Starbase online software, we identified that FER1L4 is one potential target gene of miR-874-3p. Ectopic expression of FER1L4 decreases miR-874-3p expression in NSCs. We identified Ascl2 is one target gene for miR-874-3p. Overexpression of FER1L4 enhances Ascl2 expression in NSCs. Furthermore, we proved that FER1L4 modulates the proliferation and differentiation of NSCs via regulating Ascl2.		Yes	Ectopic expression of FER1L4 suppresses NSCs proliferation and induces NSCs differentiated into neurons and astrocytes. 	35559379
FER1L4	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction[FER1L4/miR-372/E2F1]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	In this study, it was found that the expression of LncRNA FER1L4 is upregulated in high-grade gliomas than in low-grade cases and that a high expression of LncRNA FER1L4 predicts poor prognosis of gliomas.Besides, it is found in our study that LncRNA FER1L4 expression is positively correlated with E2F1 mRNA expression. After knockdown of FER1L4 expression, E2F1 expression is significantly down-regulated, whereas the expression of miR-372 is significantly up-regulated; the up-regulation of miR-372 leads to significant down-regulation of FER1L4 and E2F1 expression. In addition, it is also found that FER1L4 can be used as competitive endogenous RNA to interact or bind with miR-371 and thereby up-regulate E2F1, thus promoting the cycle and proliferation of glioma cells. It may be one of the molecular mechanisms in which FER1L4 plays its oncogene-like role in gliomas.		Yes	Meanwhile, in vitro study suggests that expression of FER1L4 with SiRNA knockdown obviously suppresses cell cycle and proliferation. It is further demonstrated by experiments that the FER1L4 knockdown suppresses growth of in vivo glioma.	30887657
FER1L4	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction( miR-612/ Cadherin 4 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//IHC//Invasion Assay	Upregulated expression of FER1L4 in PTC tissues was positively correlated with lymph node metastasis (P = 0.020), extrathyroidal extension (P = 0.013) and advanced TNM stages (P = 0.013). Mechanistically, FER1L4 could competitively bind with miR-612 to prevent the degradation of its target gene CDH4. This condition was further confirmed in the rescue assays.	Upregulated expression of FER1L4 in PTC tissues was positively correlated with lymph node metastasis (P = 0.020), extrathyroidal extension (P = 0.013) and advanced TNM stages (P = 0.013). 	Yes	In addition, knockdown of FER1L4 suppressed PTC cell proliferation, migration, and invasion, whereas ectopic expression of FER1L4 inversely promoted these processes. 	34289835
FER1L4	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 cell lines	regulation[AKT/ERK signaling pathway]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 The results of the present study revealed that FER1L4 expression levels were downregulated in AMC?HN?8 and Tu 686 cells.Further studies indicated that the aforementioned changes could be reversed by IGF‑1, indicating FER1L4 may regulate the progression of LSCC cells by inhibiting the AKT/ERK signaling pathway.		Yes	Notably, FER1L overexpression significantly reduced the cell viability, proliferation, migration and invasion of LSCC cells, while promoting apoptosis. 	33174027
FER1L4	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	interaction[miR-92a-3p,FBXW7]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Western Blot	It was found that FER1L4 was lower in prostate cancer tissues than normal tissues.  Bioinformatic analysis, RT-qPCR, RNA pull down assay and dual luciferase assay showed that FER1L4 upregulated F-box/WD repeat-containing protein 7 (FBXW7) tumor suppressor via sponging miR-92a-3p.		Yes	Overexpression of FER1L4 inhibited cell proliferation and promoted cell apoptosis in prostate cancer cells. 	32140077
FENDRR-205	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues,cell lines	Expression[lower expressed]	qRT-PCR//RNA-seq	Subsequently, four lncRNAs (upregulated ENST00000433108; downregulated ENST00000598996, ENST00000524265 and ENST00000398461) and two mRNAs (upregulated CCNB1 and CDK1) in 64 pairs of BC and adjacent normal tissues and four BC cell lines were detected using reverse transcription?quantitative PCR and these results were consistent with the sequencing data. 	The low expression level of ENST00000598996 and ENST00000524265 was correlated with unfavorable clinicopathological parameters, and shorter progression?free and overall survival time, whereas, ENST00000433108 was not associated with either.	Yes	 The in vitro functional experiments also revealed that the overexpression of ENST00000598996 and ENST00000524265 decreased the proliferation, migration, and invasion abilities of BC cells. 	33000254
FENDRR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-421/SIRT3/Notch-1 Axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Invasion Assay//Transwell Assay	FENDRR expression was downregulated in GC tissues and cell lines. MiR-421 mimic reversed the inhibitory effect of FENDRR on the growth of AGS and SGC-7901 cells. 		Yes	Overexpression of FENDRR or SIRT3 inhibited tumor proliferation and invasion, and promoted apoptosis.The overexpression of Notch-1 reversed the inhibitory effect of SIRT3 on AGS cell. MiR-421 mimic reversed the inhibitory effect of FENDRR on the growth of AGS and SGC-7901 cells.  Nude mice injected with FENDRR overexpressing AGS cells had smaller tumor volume and weight and weaker tumor cell proliferation ability.	34938121
FENDRR	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer cell lines and tissues	Expression [lower expressed]	Wound Healing Assay//Colony Formation Assay//Migration Assay//qRT-PCR//MTT//IHC//Transwell Assay	We found that FENDRR expression was lower in breast cancer cell lines and cancerous tissues than in the adjacent normal tissues. 	Low expression of FENDRR was associated with a shorter overall survival and a shorter progression-free survival in breast cancer patients (p<0.001, p<0.001, respectively). 	Yes	We found that FENDRR inhibits breast cancer cell proliferation and migration and promotes cell apoptosis, while FENDRR knockdown promotes breast cancer cell proliferation and migration and suppresses cell apoptosis. Finally, we also detected that FENDRR overexpression could inhibit tumor growth in a xenograft model.	29559798
FENDRR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[miR-761]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//IHC//Transwell Assay	We found a marked down-regulation of FENDRR in NSCLC tissues compared to tumor-adjacent tissues. We found that FENDRR was down-expressed in NSCLC and the over-expression of FENDRR inhibited the malignant phenotypes of NSCLC cell by binding to miR-761 competitively.	 Low expression of FENDRR was identified as a predictive factor for poor prognosis of patients with NSCLC.	Yes	The over-regulation of FENDRR inhibited the proliferation, migration and invasion capacities of NSCLC cell and promoted the apoptosis of NSCLC cell in vitro whereas the down-regulation of FENDRR caused the opposite results. Moreover, the over-expression of FENDRR restrained the growth of NSCLC cell in vivo. 	30556873
FENDRR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer tissues,cell line	Expression[lower expressed]	qRT-PCR	 We found that lncRNA FENDRR expression was significantly decreased in lung cancer tissues and cells, especially in NSCLC cells.		Yes	Then we constructed NSCLC cells with FENDRR stable overexpression and revealed that FENDRR overexpression attenuated the stemness of NSCLC cells, evident by decreased stemness markers expression and capacity of cell spheroid formation.	30981768
FENDRR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Regulation[miR-761/TIMP2 axis]	Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	we found that FENDRR was downregulated in lung adenocarcinoma (LUAD) or lung squamous cell carcinoma (LUSC) tissue compared to that in normal tissue (Fig. 1B).	Further prognostic analysis using Kaplan-Meier Plotter (http://kmplot.com/analysis/index.php?p = service&cancer = lung) revealed that the overall survival of patients with low level of FENDRR was worse when compared to that patient had high level of FENDEE (Fig. 1C). 	Yes	As shown in Fig. 2C, D, up-regulation of FENDRR reduced the proliferation of H1975 and A549 cells, while si-FENDRR promoted the growth of H1975 and A549 cells. We also observed that down-regulation of FENDRR enhanced the colony formation of NSCLC cells whereas over-expression of FENDRR reduced the colony formation of NSCLC cells (Fig. 2E-2 F).	31545237
FENDRR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[ miR-18a-5p/ING4 axis]	qRT-PCR	In this study, we reveal that lncRNA FENDRR is downregulated in CRC and negatively correlated with advanced stage and poor clinical outcomes of patient with CRC.Mechanistically, FENDRR interacts with miRNA-18a-5p (miR-18a-5p) and subsequently regulates the expression of inhibitor of growth 4 (ING4) in CRC cell. Interestingly, ING4 repression or miR-18a-5p rescues FENDRR induced proliferation and aggressive phenotypes inhibition of CRC cell. 		Yes	Overexpression of FENDRR represses the proliferation, migrate and invasive capacities of CRC cell in vitro, and upregulation of FENDRR inhibits the growth and distant metastatic capacity of CRC cell in vivo.	31724220
FENDRR	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer cells	Interaction(Sox2 mRNA 3'UTR)	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	Here, we identified that lncRNA FENDRR level was remarkably lower in spheres formed by colorectal cancer cells compared to that in parental cancer cells. 		Yes	Overexpression of lncRNA FEDNRR attenuates the CSC-like traits of colorectal cancer spheres.Overexpression of lncRNA FEDNRR attenuates the CSC-like traits of colorectal cancer spheres. 	34697986
FENDRR	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues,cell lines	Interaction[repressing SOX4]	CCK8//qRT-PCR//Transwell Assay//Western Blot	We determined that attenuation of FENDRR was a frequent event in colon cancer tissues and colon cancer cell lines, in contrast to their normal counterparts. Furthermore, through a series of in vitro and in vivo assays, we reported the discovery of FENDRR modulating the expression of SOX4 protein, and hence in the progression of colon cancer. 		Yes	Moreover, ectopic expression of FENDRR repressed colon cancer cell viability, invasion and epithelial-mesenchymal transition. 	31213846
FENDRR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Interaction[sponging miR-423-5p]	RNA Pull-Down//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//ELISA//EdU Staining	Therefore, this study's main purpose was to explore the mechanism of tumor suppressor lncRNA FENDRR in regulating the immune escape of HCC cells. Notably, it was further validated through this study that lncRNA FENDRR competitively bound to microRNA-423-5p (miR-423-5p), and miR-423-5p specifically targeted growth arrest and DNA-damage-inducible beta protein (GADD45B). The effects that lncRNA FENDRR and miR-423-5p have on the cell proliferation and apoptosis, the immune capacity of regulatory T cells (Tregs), and the tumorigenicity of HCC cells were examined through overexpressing or the knocking down of lncRNA FENDRR and miR-423-5p both in vitro and in vivo. Subsequently, lncRNA FENDRR and GADD45B were revealed to have poor expressions in HCC. Meanwhile, miR-423-5p was highly expressed in HCC. 		Yes	 Importantly, overexpressed lncRNA FENDRR and downregulated miR-423-5p diminished cell proliferation and tumorigenicity, and promoted apoptosis in HCC cells, thus regulating the immune escape of HCC mediated by Tregs.	31351327
FENDRR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[ down-regulating glypican-3]	CCK8//qRT-PCR//Western Blot	We found that the expression levels of FENDRR were significantly down-regulated in HCC tissues and cells.Taken together, we provided the first evidence for the inhibitory activity of FENDRR in HCC, which is causally linked to targeting GPC3 at the epigenetic level. Restoration of FENDRR may be a potential approach to prevent HCC progression and metastasis.		Yes	FENDRR overexpression could inhibit the growth of HCC cells in vitro and in vivo.Moreover, up-regulation of FENDRR suppressed the migration and invasion of HCC cells.	30573358
FENDRR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	CAFs	Regulation(PI3K/AKT Pathway)	qRT-PCR//Western Blot	Quantitative polymerase chain reaction (qPCR) results demonstrated that FENDRR expression is lower in CAFs compared to normal fibroblasts (NFs) of OSCC patients.  Further experiments confirmed that the downregulation of FENDRR can activate the PI3K/AKT pathway in NFs and enhances the expression of matrix metalloproteinase 9 (MMP9). 		Yes	Besides, we co-cultured human umbilical vein endothelial cells (HUVECs) with CAFs, and the tube-forming ability of HUVECs co-cultured with CAFs overexpressing FENDRR decreased significantly. However, activation of the AKT pathway of CAFs overexpressing FENDRR can weaken the inhibitory effect of FENDRR on angiogenesis.	34327132
FENDRR	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	interaction[EZH2]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Transwell Assay	 The results revealed that lincFOXF1 expression is significantly decreased and strongly related to Enneking stage as well as metastasis in osteosarcoma patients.The present findings indicate that lincFOXF1 is involved in the progression of osteosarcoma through binding with EZH2, further regulating GIT1 expression. 	The results revealed that lincFOXF1 expression is significantly decreased and strongly related to Enneking stage as well as metastasis in osteosarcoma patients.	Yes	Further experiments showed that lincFOXF1 inhibits the migration, invasion and metastasis of cells in vitro and vivo.	32945076
FER1L4	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction[PI3K/AKT pathway]	qRT-PCR//Western Blot	In the present study, the levels of FER1L4 were decreased significantly in OS tissues and cell lines compared with non-tumorous tissues or hFOB1.19. In addition, the expression of PI3K, p-AKT (Ser470) and p-AKT (Thr308) was upregulated by siFER1L4, while decreased upon overexpression of FER1L4. MicroRNA (miRNA) -18a-5p, an osteosarcoma-promoting miRNA which was suggested a target of FER1L4 in osteosarcoma, was identified to be a functional target of FER1L4 on the regulating of cell apoptosis and EMT, presently. The effects of FER1L4 overexpression on the markers of cell apoptosis, proliferation, EMT, and stemness and PI3K/AKT signaling were all reversed by miR-18a-5p upregulation. Furthermore, the suppressor of cytokine signaling 5 (SOCS5) was confirmed a target gene of miR-18a-5p by luciferase gene reporter assay and SOCS5 suppression by miR-18a-5p attenuated the effects of FER1L4 overexpression on the OS cells apoptosis and the expressed levels of PI3K, AKT, Twist1, N-cadherin and Vimentin. In conclusion, our data indicated thatthe overexpression of FER1L4 promoted apoptosis and inhibited the EMT markers expression and PI3K/AKT signaling pathway activation in OS cells via downregulating miR-18a-5p to promote SOCS5.		Yes	Knockdown of FER1L4 in OS cells decreased the apoptosis rate, but increased the OS cell proliferation, upregulated the expression levels of CD133 and Nanog, as well as promoted Twist1 expression, increased the N-cadherin and Vimentin expression. 	31473323
FER1L4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction[ PI3K/AKT signal pathway]	qRT-PCR//Wound Healing Assay//Western Blot	Downregulation of FER1L4 in hepatocellular carcinoma tissues and cells was demonstrated by qRT-PCR analysis. Importantly, Western blot assays revealed that PII3K/AKT signal pathway were involved in mediating the progression regulation role of FER1L4 in HCC cells.		Yes	Besides, FER1L4 overexpression evidently attenuated the cell proliferation, migration and invasion, but prompted cell apoptosis.	30382631
FAM230B	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	 bone marrow mononuclear cells	Interaction(MiR-140)	BrdU//qRT-PCR//RNA Pull-Down	High FAM230B expression level and low miR-140 expression level were observed in AML.FAM230B and miR-140 were inversely correlated and directly interacted with each other. FAM230B could be detected in both cytoplasm and nuclear samples. MiR-140 overexpression downregulated FAM230B expression and suppressed the enhancing effects of FAM230B overexpression on cell proliferation.		Yes	MiR-140 overexpression downregulated FAM230B expression and suppressed the enhancing effects of FAM230B overexpression on cell proliferation.	35666685
FER1L4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[PTEN ]	qRT-PCR//MTT//Colony Formation Assay//Western Blot	 The results indicated that FER1L4 was expressed at a low level in human HCC tissues compared with adjacent normal tissues.In addition, PTEN was highly expressed in HCC tissues compared with normal adjacent tissues and was positively associated with FER1L4.		Yes	 Functional studies indicated that FER1L4 may inhibit the proliferative ability of HCC cells. In addition, it was demonstrated that FER1L4 inhibited the proliferative ability of HCC cells in vitro, and silencing FER1L4 expression by small interfering RNAs promoted the growth of HCC tumors in vivo. 	30431133
FEZF1-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-144/CXCR4 axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	The levels of FEZF1-AS1 and CXCR4 were strikingly up-regulated, and miR-144 was notably down-regulated in OS tissues and cells. Furthermore, FEZF1-AS1 promoted cell proliferation, Warburg effect and suppressed cell apoptosis in osteosarcoma via miR-144/CXCR4 axis, this novel pathway may provide a basis for the further study of osteosarcoma.		Yes	Functionally, FEZF1-AS1 silencing or miR-144 overexpression inhibited cell viability, the glucose and lactate productions and promoted cell apoptosis in Saos-2 and HOS cells.	32308422
FEZF1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction(miRNA-1254)	Western Blot//ISH//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	By clinical analysis, lncRNA FEZF1-AS1 was high expression in cervical cancer tissues and high expression was closely correlated with poor prognosis in cervical cancer patients. However, with miR-1254 expression inhibiting, the cell biological activities were significantly increased in si-FEZF1-AS1+miRNA inhibitor groups (p < .001, respectively).	By clinical analysis, lncRNA FEZF1-AS1 was high expression in cervical cancer tissues and high expression was closely correlated with poor prognosis in cervical cancer patients.	Yes	 In vitro study, the SiHa and HeLa cell biologically including cell proliferation, migration, and invasion of si-FEZF1-AS1 group which knockdown lncRNA FEZF1-AS1 were significantly depressed (p < .001, respectively).	34531986
FEZF1-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM cells	Interaction(miR-363-3p/ NOB1)	RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 FEZF1-AS1 possessed high expression in GBM cells. With the help of bioinformatics prediction and mechanism assays, FEZF1-AS1 was found to bind to miR-363-3p and NOB1 was determined to be the downstream gene. Finally, results of rescue assays verified that the suppressive function of FEZF1-AS1 inhibition on GBM development were restored by miR-363-3p depletion or overexpression of NOB1.		Yes	Down-regulation of FEZF1-AS1 suppressed GBM cell proliferation, migration and invasion while inducing cell apoptosis. 	34530115
FEZF1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	regulation[ITGA11/miR-516b-5p axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Microarray	In the present study, FEZF1?AS1 was selected using Arraystar Human lncRNA microarray and was identified to be upregulated in NSCLC tissues and negatively associated with the overall survival of patients with NSCLC. Overall, the present findings demonstrated that FEZF1‑AS1 was upregulated and acted as an oncogene in NSCLC by regulating the ITGA11/miR‑516b‑5p axis, suggesting that FEZF1‑AS1 may be a potential prognostic biomarker and therapeutic target for NSCLC.	In the present study, FEZF1?AS1 was selected using Arraystar Human lncRNA microarray and was identified to be upregulated in NSCLC tissues and negatively associated with the overall survival of patients with NSCLC. 	Yes	Loss?of?function assays revealed that FEZF1?AS1 inhibition decreased cell proliferation and migration, and arrested cells at the G2/M cell cycle phase.	33174014
FEZF1-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 (LAD) tissues and cell lines	Interaction(FEZF1 )	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, we demonstrated that lncRNA forebrain embryonic zinc finger protein 1 (FEZF1) antisense RNA1 (FEZF1-AS1) is markedly upregulated in human lung adenocarcinoma (LAD) tissues and cell lines and is associated with poor prognosis.Further studies revealed that downregulation of FEZF1-AS1 reduced mRNA and protein expression of its sense-cognate gene FEZF1 in LAD cells, and vice versa. Correlation analysis indicated that there was a positive correlation between FEZF1-AS1 and FEZF1 expression in LAD tissues. Additionally, rescue assay confirmed that the function of FEZF1-AS1 in LAD was mediated by FEZF1. 	In the present study, we demonstrated that lncRNA forebrain embryonic zinc finger protein 1 (FEZF1) antisense RNA1 (FEZF1-AS1) is markedly upregulated in human lung adenocarcinoma (LAD) tissues and cell lines and is associated with poor prognosis.	Yes	 Loss of function revealed that deletion of FEZF1-AS1 expression significantly inhibited the LAD cell proliferation, invasion, and migration. 	29510777
FEZF1-AS1	LncRNA	Homo sapiens	Rectal Neoplasms	rectal cancer tissues and cells.	Interaction(miR-632/FAM83A axis)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	In the present study, we discover that FEZF1-AS1 is significantly upregulated in rectal cancer tissues and cells.Furthermore, FEZF1-AS1 functions as a competing endogenous RNA (ceRNA) for miR-632, resulting in the suppression of family with sequence similarity 83, member A (FAM83A).		Yes	Knocking down of FEZF1-AS1 suppresses cell proliferation, migration, and invasion , and tumorigenesis . 	35607960
FEZF1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines	Regulation[Notch signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	We found that FEZF1-AS1 expressions were distinctly reduced in human PCa tissues and cell lines compared with their non-tumor counterparts, and its higher levels were strongly associated with lymph node metastasis (p=0.012) and Angiolymphatic invasion (p=0.022). Mechanistic assays demonstrated that FEZF1-AS1 exhibited its tumor-promotive roles by activating the Notch signaling pathway.	We found that FEZF1-AS1 expressions were distinctly reduced in human PCa tissues and cell lines compared with their non-tumor counterparts, and its higher levels were strongly associated with lymph node metastasis (p=0.012) and Angiolymphatic invasion (p=0.022). Then, Kaplan-Meier assays showed that patients with higher expressions of FEZF1-AS1 were shown to predict unfavorable overall survival. 	Yes	Functional investigations suggested that knockdown of FEZF1-AS1 could suppress cells proliferation, trigger late apoptosis, and inhibit cells invasion and migration. 	31298365
FEZF1-AS1	LncRNA	Homo sapiens	Retinoblastoma	retina tissue,cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay	In our results, levels of FEZF1-AS1 expression were elevated in retinoblastoma tissue specimens and cell lines compared with adjacent normal retina tissue specimens and human retinal pigment epithelial cell line, respectively. he correlation analysis indicated that high FEZF1-AS1 expression was significantly correlated with present choroidal invasion and optic nerve invasion. Survival analysis suggested that retinoblastoma patients in high FEZF1-AS1 expression group had obviously short disease-free survival (DFS) compared with retinoblastoma patients in low FEZF1-AS1 expression group, and high FEZF1-AS1 expression was an independent unfavorable prognostic factor for DFS in retinoblastoma patients. 		Yes	Loss-of-function study indicated silencing FEZF1-AS1 expression inhibited retinoblastoma cell proliferation, invasion and migration. 	31076545
FEZF1-AS1	LncRNA	Homo sapiens	Retinoblastoma	cells 	regulation[miR-1236-3p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results of the present study revealed that the levels of FEZF1?AS1 were significantly upregulated in different Rb cell lines, with the most prominent upregulation observed in Y79 cells.In conclusion, the findings of the present study suggested that lncRNA‑FEZF1‑AS1 may promote the viability, migration, invasion and EMT of Rb cells by modulating miR‑1236‑3p.		Yes	In addition, the cell viability, invasive and migratory abilities, and the ability to undergo epithelial?mesenchymal transition (EMT), were significantly inhibited following the transfection of short hairpin RNA (shRNA)?FEZF1?AS1 into Y79 cells. 	32901841
FEZF1-AS1	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tissues and cells	Interaction(miR-363-3p/PAX6)	In Vivo Experiment//Western Blot//qPCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//IHC	 In current study, FEZF1-AS1 was up-regulated in retinoblastoma tissues and cells.  The interaction between FEZF1-AS1 and microRNA-363-3p (miR-363-3p) was confirmed. FEZF1-AS1 down-regulated miR-363-3p and up-regulated PAX6. PAX6 was a target gene of miR-363-3p. EZF1-AS1 promoted retinoblastoma cell viability and suppressed apoptosis via PAX6. 		Yes	FEZF1-AS1 overexpression enhanced retinoblastoma cell viability, promoted cell cycle, and inhibited apoptosis. Conversely, FEZF1-AS1 knockdown reduced cell viability, cycle, and elevated apoptosis. Further, we demonstrated that FEZF1-AS1 contribute to tumor formation in vivo. 	33432525
FEZF1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	Interaction(MiR-367-3p/SLC12A5 Signal Axis)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	FEZF1-AS1 was highly expressed in CC cells. Importantly, mechanism experiments confirmed that miR-367-3p could bissnd to FEZF1-AS1 and SLC12A5. The rescue assays determined that FEZF1-AS1 could up-regulate SLC12A5 through binding to miR-367-3p.		Yes	. Moreover, FEZF1-AS1 depletion suppressed proliferation, migration, invasion, and induced cell apoptosis. 	34362591
FEZF1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC patients	interaction[NOTCH1,miR-34a]	qPCR//Western Blot//Transwell Assay	 FEZF1-AS1 was up-regulated in NSCLC patients. FEZF1-AS1 promoted NSCLC cell migration and invasion through the up-regulation of NOTCH1 by serving as a sponge of miR-34a.	Increased expression levels of FEZF1-AS1 were observed with the increase in clinical stages.	Yes	Analysis of cell migration and invasion showed increased cell invasion and migration rates after FEZF1-AS1 and NOTCH-1 over-expression.	32349744
FEZF1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues and cells	Interaction(miR-4497 targeting GBX2)	Western Blot//Transfection//Wound Healing Assay//qPCR//CCK8//Luciferase Report Assay//Transwell Assay	 FEZF1-AS1 was highly expressed in LSCC tissues and cells.  FEZF1-AS1 targeted and negatively modulated miR-4497. Inhibition of miR-4497 markedly restored the FEZF1-AS1 silence-repressed cell viability of TU686 and UM-SCC-17A cells. Further, FEZF1-AS1 could positively regulate GBX2 via negative regulation of miR-4497. 		Yes	Silence or elevation of FEZF1-AS1 inhibited or promoted the migration and invasion of TU686 and UM-SCC-17A cells. 	33550476
FERRE	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	regulation[miR-19a-5p/EZH2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Results showed that expression of FERRE and EZH2 were upregulated in human breast cancer tissues and cells. We found that lncRNA-FERRE was upregulated in human breast cancer patients, which could accelerate tumor proliferation, migration and invasion as a molecular sponge by modulating the inhibitory effect of miR-19a-5p on oncogene EZH2.		Yes	qRT-PCR and CCK-8 assay showed that FERRE expression is associated with the proliferation of breast cancer cells, upregulated FERRE contributed to cell proliferation of MCF-7. Transwell assay showed that FERRE was associated with the migration ability of tumor cells, increased expression of FERRE promoted the migration and invasion of breast cancer cells. 	33215433
FER1L4	LncRNA	Homo sapiens	Stomach Neoplasms	cell line	regulation[ Hippo-YAP signaling pathway]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	 Results indicated that the expression level of FER1L4 was distinctly decreased in GC cells, as evidenced by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis.Taken together, these results demonstrated that lncRNA FER1L4 suppressed cell proliferation, invasion, migration and lymphatic metastasis of GC cells by inactivation of the Hippo-YAP pathway, providing novel insights into regulatory mechanism under GC and new strategies for clinical practice.		Yes	By using cell proliferation assay, Transwell assay, wound healing assay and western blotting, we found out that overexpression of FER1L4 in SGC-7901 cells hindered the capacities of cell proliferation, invasion, migration and lymphatic metastasis. 	33042432
FER1L4	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	Regulation[PI3K/AKT signaling pathway]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	In the present study, it was demonstrated that the expression level of FER1L4 was significantly decreased in clinical lung cancer tissues and in cultured lung cancer cells, as evidenced by reverse transcription‑quantitative polymerase chain reaction analysis.  Overexpression of FER1L4 led to a reduction in the expression levels of phosphoinositide 3‑kinase (PI3K)/protein kinase B (Akt) in A549 and 95D cells, whereas, activation of PI3K/Akt signaling using a small molecular inhibitor of phosphatase and tensin homolog, reversed the inhibitory effects of FER1L4 on cell proliferation and metastasis. 		Yes	Overexpression of FER1L4 in lung cancer cell lines A549 and 95D inhibited colony formation, cell proliferation and cell migration capacity, measured by colony formation assays, cell proliferation assays and Transwell assays, respectively. 	31115514
FER1L4	LncRNA	Homo sapiens	Lung Neoplasms	NSCLC tissues and cell lines,blood	regulation[PTEN/AKT/p53 signaling pathway ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 The results revealed that FER1L4 was significantly downregulated in NSCLC plasma and tissues and lung cancer cell lines compared to corresponding controls.The present study indicated that FER1L4 may inhibit cell proliferation and promote apoptosis of NSCLC cells via the PTEN/AKT/p53 pathway, which provides a better understanding of the pathogenesis of NSCLC and may provide a novel potential therapeutic target for clinical treatment.		Yes	Moreover, a significant decrease of cell proliferation, migration and invasion were observed in FER1L4?overexpressed cells.	33416121
FER1L4	LncRNA	Homo sapiens	Colorectal Neoplasms	cancer cells	Interaction(miR-1273g-3p/PTEN )	ISH//Tunel//CCK8//qRT-PCR//ChIP	FER1L4 sponged the expression of miR-1273g-3p, which, in turn, increased PTEN expression, leading to cell-cycle arrest.		Yes	 Both FER1L4 and p73 knockdown enhanced the migration and invasion rate of colorectal cancer cells. FER1L4 also plays a critical role in p73-mediated cell-cycle arrest and apoptosis.	35198876
FER1L4	LncRNA	Homo sapiens	Osteoarthritis	 plasma and synovial fluid	Regulation(IL-6 )	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	Our data showed that whereas lncRNA FER1L4 is downregulated in OA patients, IL-6 is upregulated. The plasma FER1L4 levels among the OA cases were suppressed with disease progression and old age, and the down-regulation could efficiently discriminate OA patients from normal subjects. Taken together, our data demonstrates that FER1L4 could efficiently identify OA cases from normal subjects, and can also modulate the expression of IL-6 in human chondrocytes.	The plasma FER1L4 levels among the OA cases were suppressed with disease progression and old age, and the down-regulation could efficiently discriminate OA patients from normal subjects. 	Yes	In addition, upregulation of FER1L4 inhibited IL-6 expression in human chondrocyte cells, and treatment with different concentrations of exogenous IL-6 did not affect the expression of FER1L4. 	34158566
FENDRR	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	Expression[lower expressed]	RNA Pull-Down//ChIP//Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression.		Yes	 Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. 	30983519
FENDRR	LncRNA	Homo sapiens	Melanoma	MM tissues and cell lines	regulation[ JNK/c-Jun pathway]	qRT-PCR//MTT//Western Blot//Transwell Assay	FENDRR was down-regulated in MM tissues and cell lines.Our results demonstrated that FENDRR mediated the metastasis phenotype of MM cells by inhibiting the expressions of MMP2 and MMP9 and antagonizing the JNK/c-Jun pathway.		Yes	 Knockdown of FENDRR facilitated MM cells proliferation, migration and invasion in A375 cells, while overexpressing FENDRR had reverse results.	32134466
FENDRR	LncRNA	Homo sapiens	endometrial endometrioid adenocarcinoma, secretory variant	cancerous tissues	Regulation(SOX4 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//MeRIP//qRT-PCR//RIP//Cell Apoptosis Assay//Cell Proliferation Assay	The expression level of LncRNA FENDRR was decreased and the N-methyladenosine (m6A) methylation levels of LncRNA FENDRR was elevated in cancerous tissues of EEC patients. LncRNA FENDRR overexpression suppressed cell proliferation and facilitated cell apoptosis in the EEC cell line HEC-1B by reducing the protein level of SRY-related HMG box transcription factor 4 (SOX4).Interference of LncRNA FENDRR reversed the inhibitory effect of sh-YTHDF2 on cell proliferation and the promoting effect of sh-YTHDF2 on cell apoptosis in HEC-1B cells by silencing FENDRR.		Yes	 In vitro experiments demonstrated that YTH domain-containing 2 (YTHDF2), an m6A reader, recognized the abundance of m6A-modified LncRNA FENDRR in EEC cells and promoted its degradation.Finally, in vivo experiments confirmed that overexpression of LncRNA FENDRR retarded the growth of EEC cells. 	33692441
Fendrr	LncRNA	Rattus norvegicus	Pancreatitis	pancreatic tissues	Interaction(PRC2/ATG7)	In Vivo Experiment//ChIP//Western Blot//Transfection//Tunel//qRT-PCR//RIP//Cell Apoptosis Assay//H&E Staining//ELISA//IHC//IF	Higher FENDRR and impaired autophagy were displayed in both AP mouse models and cell models. FENDRR knockdown dramatically attenuated caerulein- or TLC-S-induced AR42J cells apoptosis and autophagy suppression. Further mechanistic experiments implied that the action of FENDRR is moderately attributable to its repression of ATG7 via direct interaction with the epigenetic repressor PRC2. Moreover, the silencing of FENDRR significantly induced the promotion of ATG7, thus alleviating the development of AP in vivo.		Yes	FENDRR knockdown dramatically attenuated caerulein- or TLC-S-induced AR42J cells apoptosis and autophagy suppression.Moreover, the silencing of FENDRR significantly induced the promotion of ATG7, thus alleviating the development of AP in vivo. 	33417179
FAM83A-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	 esophageal cancer tissues and cell lines	interaction[binding to miR-495-3p]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	 It was found that FAM83A-AS1 was upregulated in esophageal cancer tissues and cell lines. FAM83A-AS1 is upregulated in esophageal cancer, and it stimulates migratory potential in esophageal cancer by negatively regulating miR-495-3p.	Higher rates of lymphatic and distant metastasis and worse survival were observed in esophageal cancer patients expressing higher level of FAM83A-AS1.	Yes	 Besides, the knockdown of FAM83A-AS1 suppressed migratory potential in OE19 cells, while the overexpression of FAM83A-AS1 yielded the opposite trend in OE33 cells. 	33015782
FAM83A-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Regulation[FAM83A-AS1/miR-150-5p/MMP14 axis]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//FISH//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In this study, we found FAM83A-AS1 to be upregulated in LUAD tissues and closely associated with tumor size, lymph node metastasis, and TNM stage.Collectively, we conclude that the novel FAM83A-AS1/miR-150-5p/MMP14 axis regulates LUAD progression, suggesting an innovative therapeutic strategy for this cancer.	 In this study, we found FAM83A-AS1 to be upregulated in LUAD tissues and closely associated with tumor size, lymph node metastasis, and TNM stage. In addition, high FAM83A-AS1 expression correlated positively with a poor prognosis.	Yes	Functional investigation revealed that FAM83A-AS1 promotes LUAD cell proliferation, migration, invasion and the epithelial-mesenchymal transition (EMT) in vitro and tumor growth in vivo.	31522616
FAM83A-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung adenocarcinoma tissues	Regulation(FAM83A )	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Invasion Assay//Transwell Assay	High expression of FAM83A-AS1 in lung adenocarcinoma (LUAD) was closely associated with low overall survival (OS) and progression-free survival (PFS).Furthermore, FAM83A-AS1 promoted NSCLC progression via ERK signaling pathways. Mechanistically, FAM83A-AS1 post-transcriptionally increased FAM83A expression by enhancing pre-mRNA stability.	High expression of FAM83A-AS1 in lung adenocarcinoma (LUAD) was closely associated with low overall survival (OS) and progression-free survival (PFS).	Yes	Functionally, high FAM83A-AS1 expression increased LUAD cell proliferation and metastasis, indicating that FAM83A-AS1 exerted its oncogenic functions.	33687144
FAM83A-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues	Interaction(miR-495-3p/FAM83A )	Western Blot//Bioinformatics Analysis//Transfection//Invasion Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	 FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. 	High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. 	Yes	Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells.	33732373
FAM83A-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung cancer cells and tissue samples	Interaction(miR-141-3p)	Western Blot//Bioinformatics Analysis//Invasion Assay//Migration Assay//CCK8//qRT-PCR//IF//Luciferase Report Assay//Cell Proliferation Assay//EdU Staining//Transwell Assay	FAM83A-AS1 expression was remarkably raised in lung cancer cells and tissue samples; however, miR-141-3p level markedly reduced relative to healthy samples.  According to our results, FAM83A-AS1/miR-141-3p axis plays an important role in LUAD occurrence and development.		Yes	 FAM83A-AS1 silencing suppressed EMT, growth, invasion and migration of LUAD cells. 	35164653
FAM83A-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cells	Interaction(HIF-1α/ glycolysis axis)	Western Blot//Co-IP//Migration Assay//CCK8//qRT-PCR//Invasion Assay	Besides, we revealed that FAM83A-AS1 could affect glycolysis by regulating HIF-1α degradation. Finally, we found that FAM83A-AS1 knockdown could inhibit tumor growth and suppress the expression of HIF-1α and glycolysis-related genes in vivo. 		Yes	 In addition, we uncovered that FAM83A-AS1 could promote the migration and invasion of LUAD cells, as well as influence the stemness of LUAD cells in vivo and vitro. Moreover, FAM83A-AS1 was shown to promote glycolysis in LUAD cell lines in vitro and in vivo, and was found to influence the expression of genes related to glucose metabolism. 	35002507
FAM83A-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung cancer tissues	Regulation(AMPKα and ULK1 )	Western Blot//Flow Cytometry//qRT-PCR//RNA-seq//Cell Proliferation Assay//Colony Formation Assay	We found that FAM83A-AS1 was up-regulated in lung cancer and elevated expression was associated with poor patient survival.  Mechanistically, serval oncogenic proteins such as EGFR, MET, PI3K, and K-RAS were decreased upon FAM83A-AS1 silencing, while phosphor AMPKα and ULK1 were increased. 	We found that FAM83A-AS1 was up-regulated in lung cancer and elevated expression was associated with poor patient survival. 	Yes	Functional study indicated that FAM83A-AS1 knockdown reduced cell proliferation, migration, invasion, and colony formation in cancer cells. FAM83A-AS1 silencing induced autophagy and cell cycle arrest at G2. 	35635086
FAM83A-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction(miR-214/CDC25B axis)	Transfection//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//Transwell Assay	Here, we discovered that FAM83A-AS1 was strongly expressed in ESCC tissues.  Mechanistically, we found that FAM83A-AS1 regulated miR-214 expression, and there was a negative correlation between miR-214 and FAM83A-AS1 in ESCC. Rescue assay indicated that miR-214 could impair the suppressing effect of cell migration induced by FAM83A-AS1 depletion.Furthermore, CDC25B was a direct target of miR-214, and FAM83A-AS1 enhanced CDC25B expression while miR-214 positively CDC25B expression in ESCC.	FAM83A-AS1 abundance was associated with TNM stages and the differentiation grade of ESCC patients. 	Yes	 Functionally, inhibiting FAM83A-AS1 repressed cell proliferation, migration, and invasion in ESCC. In addition, we found that FAM83A-AS1 accelerated the cell cycle while inhibited cell apoptosis. 	33442418
FAM66C	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer cells	Expression[highly expressed]	qRT-PCR	Real-time PCR showed that FAM66C highly expressed in prostate cancer cells, and knockdown FAM66C by siRNAs resulted in significant inhibition of cell growth. 		Yes	Real-time PCR showed that FAM66C highly expressed in prostate cancer cells, and knockdown FAM66C by siRNAs resulted in significant inhibition of cell growth. 	32430927
FAM66C	LncRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues and cells	Interaction(hsa-miR-23b-3p/KCND2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	 FAM66C was increased in ICC tissues and cells, increased cell viability, glycolysis, migration and invasion, and decreased apoptosis were shown in FAM66C overexpressing cells.Mechanistic analyses revealed that FAM66C regulated the downstream target gene KCND2 by sponging miR-23b-3p. These data revealed that FAM66C was able to drive ICC tumor progression and glycolytic activity via the miR-23b-3p/KCND2 axis, indicating FAM66C may be a viable target for treating ICC.		Yes	 FAM66C was increased in ICC tissues and cells, increased cell viability, glycolysis, migration and invasion, and decreased apoptosis were shown in FAM66C overexpressing cells. FAM66C effect on ICC was further validated in murine xenograft assays. 	34418280
FAM3D-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Regulation[NF-κB signaling pathway]	CCK8//qRT-PCR//Transwell Assay//Western Blot	The expression of FAM3D-AS1 was significantly decreased in colorectal cells (Figure 1B). Moreover, we proved that FAM3D-AS1 inhibits CRC development through NF-κB signaling pathway. 		Yes	Overexpression of FAM3D-AS1 significantly inhibited the cell proliferation, cell survival rates, and invaded cells. 	31147452
FAM30A	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal tissues and cells	Interaction[Wnt/β-catenin pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 In this study, we found that lncRNA KIAA0125 was downregulated in colorectal tissues and cells. Besides, KIAA0125 inhibited epithelial-mesenchymal transition through Wnt/β-catenin signaling in CRC. Our findings suggested that KIAA0125 may act as an oncosupressor gene and could be considered as a potential diagnosis biomarker in CRC.		Yes	The functional study demonstrated that overexpression of KIAA0125 suppressed cell proliferation, migration, and invasion whereas the reversal effects were seen in silencing experiment.	31228314
FAM238C	LncRNA	Homo sapiens	Retinoblastoma	RB tissues	Interaction[Sponging miR-3619-5p ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC00202 expression in RB tissues is higher than that in the paired adjacent normal tissues, which has correlation with poor prognosis in RB. In summary, high LINC00202 levels are correlated with poor prognosis in RB, and it promotes RB progression by sponging miR-3619-5p and therefore up-regulating RIN1 expression.Key words: LINC00202, miR-3619-5p, retinoblastoma, progression, RIN1.		Yes	RB cell proliferation, migration and invasion were weakened by LINC00202 depletion, but enhanced by LINC00202 overexpression.	30905893
FAM238C	LncRNA	Homo sapiens	Retinoblastoma	 RB tumor tissues 	regulation[miR-204-5p/HMGCR axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 LINC00202 expression was upregulated in RB tumor tissues and LINC00202 knockdown inhibited RB cell proliferation, glycolysis, and stimulated apoptosis in vitro as well as impeded tumor growth in vivo. In all, LINC00202 promoted RB cell proliferation, glycolysis, and suppressed apoptosis by regulating the miR-204-5p/HMGCR axis, suggesting a novel therapeutic target for patients with RB.		Yes	 LINC00202 expression was upregulated in RB tumor tissues and LINC00202 knockdown inhibited RB cell proliferation, glycolysis, and stimulated apoptosis in vitro as well as impeded tumor growth in vivo. 	33817232
FAM230B	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cell lines	regulation[miR-27a-5p/TOP2A Axis]	qRT-PCR//Luciferase Report Assay	We found that FAM230B was highly expressed in gastric cancer cell lines and mainly located in the cytoplasm. Our study showed that lncRNA FAM230B might function to promote GC. FAM230B functioned as a ceRNA by sponging miR-27a-5p and enhancing TOP2A expression.		Yes	FAM230B overexpression promoted the proliferation, migration, and invasion of AGS cells and repressed their apoptosis; it also facilitated tumor growth in vivo.In contrast, FAM230B knockdown suppressed the proliferation, migration, and invasion of MGC0803 cells, but enhanced their apoptosis and inhibited tumor growth in vivo.	32910366
FAM230B	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-1182)	qRT-PCR//MTT//Colony Formation Assay//Western Blot	We found that FAM230B and premature miR-1182 were highly upregulated in CRC, while mature miR-1182 was downregulated in CRC.FAM230B was detected in both nucleus and cytoplasm, and it directly interacted with miR-1182. 		Yes	 FAM230B overexpression increased the expression levels of premature miR-1182 but decreased the expression levels of mature miR-1182 in CRC cells. FAM230B promoted CRC cell proliferation, increased cell viability, accelerated colony formation, and suppressed the role of miR-1182 in inhibiting CRC cell proliferation.	36262247
FAM230B	LncRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(miR-203)	qRT-PCR	FAM230B and premature miR-203 were upregulated in OS, whereas mature miR-203 was downregulated in OS cells. FAM230B was detected in the cytoplasm and directly interacted with premature miR-203. FAM230B overexpression in OS cells increased premature miR-203 level and decreased mature miR-203 level. 		Yes	FAM230B increased cell proliferation and suppressed the role of miR-203 in inhibiting cell proliferation. FAM230B in the cytoplasm may sponge premature miR-203, thereby inhibiting miR-203 maturation to increase OS cell proliferation.	35377981
FAM230B	LncRNA	Homo sapiens	Osteosarcoma	 OS cells and tissues	Interaction(miR-302b )	qRT-PCR//RNA Pull-Down	 Increased FAM230B and premature miR-302b and decreased mature miR-302b were observed in OS. FAM230B was detected in both nuclear and cytoplasm samples and directly interacted with premature miR-302b.FAM230B overexpression in OS cells 143B and HOS decreased miR-302b maturation and increased cell invasion and migration, while miR-302b overexpression suppressed cell invasion and migration. FAM230B silencing restrained cell invasion and migration, and miR-302b inhibitor accelerated cell invasion and migration. MiR-302b knockdown significantly reversed the suppressive effects of shFAM230B on migration and invasion of 143B and HOS cells.		Yes	FAM230B overexpression in OS cells 143B and HOS decreased miR-302b maturation and increased cell invasion and migration, while miR-302b overexpression suppressed cell invasion and migration. FAM230B silencing restrained cell invasion and migration, and miR-302b inhibitor accelerated cell invasion and migration. MiR-302b knockdown significantly reversed the suppressive effects of shFAM230B on migration and invasion of 143B and HOS cells.	35639175
FAM83A-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction[binding with NOP58 ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//FISH//Colony Formation Assay//Transwell Assay	In the present study, we found the abundantly increased expression level of FAM83A-AS1 in HCC tissues and cells. In conclusion, FAM83A-AS1 facilitated HCC progression by binding with NOP58 to enhance the stability of FAM83A. These findings offer a novel biological insight into HCC treatment.		Yes	FAM83A-AS1 inhibition hampered cell proliferation, migration and elevated cell apoptosis in HCC.	31696213
FAM83A-AS1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissue 	Interaction[increasing FAM83A ]	CCK8//qRT-PCR//Migration Assay//Western Blot	We then proceeded to validate the expression levels of these 10 NATs in 10 paired normal tissues and cancer tissues from patients with NSCLC by qRT‐PCR analyses. The results showed that seven NATs were significantly upregulated in these patients, particularly FAM83A‐AS1 (Figure ​(Figure2B).2B). Because FAM83A‐AS1 was the most overexpressed AS in cancer tissues (Figure ​(Figure2B),2B), we chose FAM83A‐AS1 for further studies.In summary, lncRNA FAM83A-AS1 promotes LUAD by increasing FAM83A expression.		Yes	Finally, overexpression of FAM83A-AS1 promoted LUAD cell proliferation and invasion.	30659636
FAM83A-AS2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Expression(highly expressed)	qRT-PCR	AC068228.1 expression was significantly elevated in LUAD tissues compared with normal tissues. GSEA and infiltration analysis confirmed that AC068228.1 expression was significantly correlated with immune cells infiltrating in LUAD. 	Higher expression of AC068228.1 was strongly correlated with adverse clinical outcomes and was identified as an independent prognostic marker for LUAD patients. 	Yes	Knockdown of AC068228.1 inhibited the cell proliferation and cell migration of LUAD.	35280807
FAUP4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-6760-5p, miR-6512-3p, miR-1298-5p, miR-6720-5p, miR-4516, and miR-6782-5p/HOTTIP )	qRT-PCR	PAARH functioned as a competing endogenous RNA to upregulate HOTTIP via sponging miR-6760-5p, miR-6512-3p, miR-1298-5p, miR-6720-5p, miR-4516, and miR-6782-5p. The expression of PAARH was significantly positively associated with HOTTIP in HCC tissues.		Yes	 Gain- and loss-of function assays revealed that PAARH facilitated HCC cellular growth, migration, and invasion, repressed HCC cellular apoptosis, and promoted HCC tumor growth and angiogenesis in vivo.	35110549
FBXL19‑AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC tissues and cells	Interaction( miR-431/PBOV1 axis)	Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 It was demonstrated that the expression levels of FBXL19‑AS1 and PBOV1 were upregulated in NPC tissues and cells, whereas miR‑431 expression was downregulated. FBXL19‑AS1 directly interacted with miR‑431. miR‑431 could target the 3'‑untranslated region of PBOV1. Overexpression of PBOV1 neutralized the miR‑431‑mediated suppression of NPC progression. Moreover, FBXL19‑AS1 could regulate PBOV1 by sponging miR‑431 in NPC cells. I		Yes	 FBXL19‑AS1 silencing inhibited the viability, migration and invasion of C666‑1 and SUNE1 cells, whereas these effects could be alleviated by suppressing miR‑431. 	34278444
FBXL19-AS1	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Regulation[miR-876-5p/FOXM1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//RIP	FBXL19-AS1 was expressed at a high level in breast cancer cells.  In addition, the location of FBXL19-AS1 in the cytoplasm was detected by fluorescent in situ hybridization assay, while FBXL19-AS1 regulated the expression of Forkhead box M1 (FOXM1) by directly absorbing miR-876-5p. Through rescue assays, it was observed that FOXM1 overexpression recovered the inhibited tumor growth caused by FBXL19-AS1 downregulation. We affirmed the function of FBXL19-AS1 in breast cancer and described the mechanism of the FBXL19-AS1/miR-876-5p/FOXM1 axis. The current work presents the molecular mechanism which underlies FBXL19-AS1 in breast cancer and suggests a comprehensive, feasible FBXL19-AS1-mediated therapeutic approach for treating breast cancer.		Yes	Loss-of-function experiments revealed that silencing FBXL19-AS1 could impair cell proliferation and induce cell apoptosis in breast cancer.	31696201
FBXL19-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Expression[highly expressed]	Western Blot//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	The results of qRT-PCR showed that the expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells was up-regulated.		Yes	According to the results of the colony formation assay, the proliferative capacity of NSCLC cells was decreased after the interference with lncRNA FBXL19-AS1 expression. In flow cytometry, it was indicated that the cell cycle was arrested at the G0/G1 phase in the experimental group compared with that in the control group. The transwell assay results showed that the migratory and invasive abilities of NSCLC cells were weakened after the interference with lncRNA FBXL19-AS1 expression. 	31210311
FBXL19-AS1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	Regulation[miR-431-5p/RAF1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, we found that FBXL19-AS1 expression was up-regulated in lung cancer tissues and cell lines.Together, these results indicated that FBXL19-AS1 was involved in progression and angiogenesis in lung cancer by targeting miR-431-5p/RAF1 axis, which provided a new insight into the therapeutic strategies of lung cancer.		Yes	FBXL19-AS1 knockdown inhibited cell proliferation, migration, invasion, and angiogenesis in lung cancer cells. 	30610161
FBXL19-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	interaction[miR-346]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We first showed that lncRNA FBXL19-AS1 was upregulated in OS tissues and cell lines. Furthermore, we proved that miR-346 could directly target FBXL19-AS1 through luciferase assays, suggesting FBXL19-AS1 could sponge miR-346.		Yes	 In vitro experiments showed that FBXL19-AS1 promoted OS cell proliferation, migration, and invasion.	30555237
FBXL19-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction( miR-193a-5p/COL1A1.)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	FBXL19-AS1 and COL1A1 were significantly up-regulated in CC tissues, while miR-193a-5p was significantly down-regulated.  Mechanistically, FBXL19-AS1 functioned as a competitive endogenous RNA (ceRNA) and inhibited the expression of miR-193a-5p, which targeted at the 3'-UTR site of COL1A1 and negatively regulated COL1A1 expression.		Yes	Overexpression of FBXL19-AS1 significantly promoted the proliferation, migration, invasion, EMT and growth of CC cells and inhibited apoptosis, while knockdown of FBXL19-AS1 had the opposite effects.  On the other hand, miR-193a-5p inhibited the proliferation and metastasis of CC cells. 	34399848
FBXL19-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Interaction[sponging miR-203a-3p]	qRT-PCR	In this study, we observed that FBXL19-AS1 was significantly upregulated in LUAD tissues and high FBXL19-AS1 expression in LUAD was associated with a poor prognosis. Mechanistically, we identified FBXL19-AS1 could act as a miR-203a-3p sponge using dual-luciferase reporter assay. 		Yes	Moreover, cell viability and apoptosis analysis revealed that FBXL19-AS1 knockdown could arrest LUAD cells in G0/G1 phase and inhibit cell proliferation, migration and invasion in vitro and inhibited LUAD tumor progress in vivo.	31566718
FBXL19-AS1	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues	Interaction(KLF2)	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Cell Cycle Assay//EdU Staining//ChIP	FBXL19-AS1 was highly expressed in HCC tissues, especially in those larger than 5 cm in tumor size and worse tumor stage. FBXL19-AS1 was mainly distributed in nucleus and interacted with EZH2 and SUZ12. 	FBXL19-AS1 was highly expressed in HCC tissues, especially in those larger than 5 cm in tumor size and worse tumor stage. 	Yes	Knockdown of FBXL19-AS1 suppressed proliferation, cell cycle progression and induced apoptosis of HCC cells. Moreover, silence of FBXL19-AS1 attenuated the recruitment ability of EZH2 on KLF2. 	34564989
FAT1	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	tumor tissue	Interaction(miR-548g)	qRT-PCR//RIP//PCR//IP//Invasion Assay	 CircFAT1 expression levels were significantly lower in tumor tissue than in adjacent non-tumorous mucosal tissue (p = 0.01). The expression of miR-548g was upregulated by the downregulation of circFAT1. The overexpression of miR-548g also promoted ESCC cell migration and invasion. Recurrence-free survival (p = 0.02) and cancer-specific survival (p = 0.04) rates were significantly higher in patients with elevated circFAT1 expression levels.		Yes	The downregulation of circFAT1 expression promoted ESCC cell migration and invasive ability, but not proliferation. 	34185205
FAM83C-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	tumor tissues 	regulation[SEMA3F ,EZH2]	qRT-PCR	FAM83C-AS1 is upregulated in tumor tissues and cells of CRC, which is negatively correlated with SEMA3F expression.Our data thus demonstrate that the epigenetic role of FAM83C-AS1 in suppression of SEMA3F expression through stabilization of EZH2 to drive CRC progression, which may be conducive to discovering novel therapeutic targets for the treatment of CRC.		Yes	Reciprocally, knockdown of FAM83C-AS1 exhibits inhibitory effects on the malignant transformation of CRC.	33109776
FAS-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	regulation[regulating miR-19a-5p]	qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	FAS-AS1 was remarkably down-regulated in NSCLC cells.FAS-AS1 suppressed cell proliferation, migration, and invasion by sponging miR-19a-5p in NSCLC, indicating that FAS-AS1 might be a potential biomarker and therapeutic target for NSCLC.		Yes	 FAS-AS1 inhibited cell proliferation, migration, and invasion in NSCLC cells.	32329854
FARSA	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-330-5p/LASP1 axis]	colony Formation Assay//Western Blot//qPCR//PCR//Colony Formation Assay//IF	circ-FARSA was upregulated in CRC tissues and cell lines, and its expression had a significant association with the overall survival of CRC patients.Silencing of circ-FARSA restricted the growth of CRC through regulating the miR-330-5p/LASP1 axis, providing a novel regulatory mechanism for CRC tumorigenesis.	circ-FARSA was upregulated in CRC tissues and cell lines, and its expression had a significant association with the overall survival of CRC patients.	Yes	 Knockdown of circ-FARSA inhibited the proliferation, migration, and invasion of CRC cells in vitro.	32473899
FAM99B	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression[lower expressed]	qRT-PCR	FAM99B was found to be downregulated in HCC tissues compared with adjacent normal tissues based on TCGA, GEO, and qRT-PCR data.	Our results revealed that downregulated FAM99B was significantly associated with vascular invasion, advanced histologic grade, and T stage. Kaplan-Meier analysis using TCGA data indicated that decreased FAM99B levels were significantly associated with poor overall survival in patients with HCC.	Yes	HCC. Moreover, overexpression of FAM99B significantly inhibited cell proliferation, migration, and invasion in vitro.	31243545
FAM99A	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Expression(lower expressed)	qRT-PCR	The three public online databases and qRT-PCR data showed that FAM99A was frequently downregulated in HCC tissues and inversely correlated with microvascular invasion and advanced histological grade of HCC patients. A subcutaneous xenograft tumor model demonstrated that overexpression of FAM99A significantly inhibited the tumor growth of HCC cells in vivo. Seven tumor-related proteins (PCBP1, SRSF5, SRSF6, YBX1, IGF2BP2, HNRNPK, and HNRNPL) were recognized as possible FAM99A-binding proteins by the RNA pull-down and mass spectrometry assays.	Kaplan-Meier survival analysis indicated that decreased FAM99A was significantly associated with poor overall survival of HCC patients based on TCGA database (P = 0.040), ICGC data portal (P < 0.001), and our HCC cohort (P = 0.010). 	Yes	Upregulation of FAM99A suppressed the proliferation, colony formation, migration, and invasion capacities of HCC cells in vitro, and knockdown of FAM99A had the opposite effects.	36289466
FAM88C	LncRNA	Homo sapiens	Pterygium	pterygium tissues	Interaction( PI3K/PDK1 pathway and Akt/mTOR signaling pathway )	Western Blot//IF//migration assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Notably, we identified a novel lncRNA, LOC102724238, which we named pterygium positively-related lncRNA (lnc-PPRL), was up-regulated in pterygium.  Further study of underlying mechanisms demonstrated that lnc-PPRL may exert its biological effect by activating canonical PI3K/PDK1 pathway, and subsequently promoting the activation of Akt/mTOR signaling pathway and its downstream effectors.Interestingly, lnc-PPRL was also proved to influence YAP nuclear localization. 		Yes	 Lnc-PPRL showed to be preferentially accumulated in cytoplasm, and it can promote cell proliferation, migration and invasion of human pterygium epithelium cells (hPECs). 	35304111
FAM87A	LncRNA	Homo sapiens	Glioma	glioma tissue and cells	Interaction( miR-424-5p/PPM1H )	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//FISH//MTT//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	qRT-PCR result indicated that FAM87A was abnormally downregulated in glioma tissue and cells. Results of bioinformatics, dual luciferase, and RIP assays unveiled that FAM87A and miR-424-5p act upon each other. In addition, miR-424-5p targeted 3'-UTR of PPM1H. Also, effects of miR-424-5p/FAM87A on glioma cells were identified via the cell function experiments. FAM87A suppressed PPM1H by binding to miR-424-5p.	Survival analysis suggested that the FAM87A expression was negatively correlated with the survival rate.	Yes	Effects of FAM87A on human glioma cell lines were also analyzed by MTT, Edu, and transwell assays. FAM87A hastened proliferation and migration of glioma cells. 	34712356
FAM84B-AS	LncRNA	Homo sapiens	Stomach Neoplasms	 cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot//Microarray	Next, FAM84B-AS expression was detected in gastric cancer cell lines. FAM84B-AS exhibited high expression in AGS and MKN45(Fig. 2A). 	Expression[up-expression]	Yes	FAM84B-AS interference significantly inhibited the proliferation and invasion abilities of gastric cancer cells and significantly increased the percentage of apoptosis.	30638658
FAM83H	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell line 	Interaction(miR-545-3p/HS6ST2 axis)	CCK8//qRT-PCR	The results revealed that FAM83H-AS1 is highly expressed in lung cancer tissues, and its knockdown inhibits lung cancer cell invasion and proliferation reducing tumor growth in vivo. Besides, we found that FAM83H-AS1 targets miR-545-3p, and a negative correlation exists between their expression in lung cancer tissues. Simultaneously, miR-545-3p negatively regulates heparan sulfate 6-O-sulfotransferase (HS6ST2). Moreover, inhibition of miR-545-3p promoted HS6ST2 protein expression and lung cancer cell invasion. FAM83H-AS1 favors non-small cell lung cancer by targeting the miR-545-3p/HS6ST2 axis, supporting the possibility of developing FAM83H-AS1 as a target for NSCLC intervention.		Yes	The results revealed that FAM83H-AS1 is highly expressed in lung cancer tissues, and its knockdown inhibits lung cancer cell invasion and proliferation reducing tumor growth in vivo. 	35260044
GACAT3	LncRNA	Homo sapiens	Osteoarthritis	osteoarthritis synoviocytes	Expression[IL-6/STAT3 signaling pathway]	qRT-PCR	We found that GACAT3 expression was significantly increased in OAS compared with NS.Moreover, GACAT3 could impact the proliferation of OAS by interleukin-6/signal transducer and activator of transcription-3 (IL-6/STAT3) signaling pathway.		Yes	GACAT3 expression was decreased in OAS after transfection with siRNA and the cell proliferation in OAS after transfection with siRNA was significantly inhibited. The cell cycle was arrested in G0/G1 phase and the apoptosis rate was increased in OAS after transfection with siRNA. 	30178830
GACAT3	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissue and cell specimens	Interaction(miR-149/FOXM1)	CCK8//qRT-PCR	GACAT3 amounts were elevated in ESCC tissue and cell specimens. Furthermore, GACAT could directly interact with miR-149. In addition, colony formation and invasion assays verified that GACAT3 promotes ESCC tumor progression through miR-149. Moreover, GACAT3 acted as a competing endogenous RNA (ceRNA) to modulate FOXM1 expression.		Yes	Functional studies showed that GACAT3 silencing reduced the proliferation, migration and invasion of cultured ESCC cells, and decreased tumor growth in mice. 	34496842
H19	LncRNA	Homo sapiens	Adenocarcinoma of Lung	Lung adenocarcinoma tissues and adjacent tissues 	Interaction[CDH1]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//ChIP	The results exhibited that compared with the adjacent tissues, the expression of lncRNA H19 was significantly elevated and the mRNA expression of CDH1 was notably decreased in the lung adenocarcinoma tissues 		Yes	 A549 cells with silencing of lncRNA H19, overexpression of CDH1 or reduced CDH1 methylation by demethylating agent 5-Az had sExpression[Expression[up-expression]-expression]pressed cell proliferation, sphere-forming ability, apoptosis, migration and invasion, in addition to inhibited EMT process. Silencing lncRNA H19 could reduce methylation level of CDH1. In vivo, A549 cells with silencing lncRNA H19, overexpression of CDH1 or reduced CDH1 methylation exhibited low tumorigenicity, reflected by the smaller tumour size and lighter tumour weight. Taken together, this study demonstrates that silencing of lncRNA H19 inhibits EMT and proliferation while promoting apoptosis of lung adenocarcinoma cells by inhibiting methylation of CDH1 promoter.	31317666
H19	LncRNA	Homo sapiens	Endometriosis	endometriosis	Interaction[targeting ITGB3 via modulating miR-124-3p]	cell invasion assay//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	We found that ectopic endometrial cells taken from women with endometriosis showed elevated levels of lncRNA-H19, with expression levels correlating to disease progression.Coinciding with this change was an increase in microRNA-124-3p (miR-124-3p) and a decrease in integrin beta-3 (ITGB3) levels. The addition of a miR-124-3p inhibitor mitigated this decrease in ITGB3. Up-regulation of miR-124-3p markedly suppressed ITGB3 expression by binding to the 3' untranslated region (3' UTR), while inhibition of miR-124-3p had the opposite effect. ITGB3 overexpression potently counteracted the effects of miR-124-3p mimics on ectopic endometrial cells.		Yes	Knockdown of H19 in ectopic endometrial cells inhibited cell proliferation and invasion.	31085188
H19	LncRNA	Homo sapiens	Stroke	blood	Regulation[H19-miR-19a-Id2 axis]	RNA Pull-Down//Western Blot//Transfection//Tunel//Flow Cytometry//RIP//qRT-PCR//Luciferase Report Assay	This study found that H19 levels were elevated in the serum of stroke patients, as well as in the ischemic penumbra of rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury and neuronal cells with oxygen glucose deprivation (OGD). Lastly, with gain and loss of function studies, dual luciferase reported assay, RNA immunoprecipitation (RIP) and pull-down experiments, we demonstrated the dual competitive interaction of miR-19a with H19 and the 3'-UTR of Id2 mRNA, resulting in the identification of the H19-miR-19a-Id2 axis. With biological studies, we also revealed that H19-miR-19a-Id2 axis modulated hypoxia induced neuronal apoptosis. This study demonstrates that the identified H19-miR-19a-Id2 axis plays a critical role in hypoxia induced neuronal apoptosis, and blocking this axis may serve as a novel therapeutic strategy for ischemic brain injury.		Yes	Further, knockdown of H19 with siRNA alleviated cell apoptosis in OGD neuronal cells, and inhibition of H19 in MCAO/R rats significantly decreased neurological deficit, brain infarct volume and neuronal apoptosis. 	31170091
H19	LncRNA	Homo sapiens	Hodgkin Disease	HL tissues and cell lines	Interaction[AKT pathway]	CCK8//qRT-PCR//Western Blot	H19 was overexpressed in HL tissues and cell lines compared with those of controls. AKT expression was upregulated in HL tissues compared with RH tissues, and was positively regulated by H19. Western blot results also indicated that H19 overexpression upregulated protein expression of AKT in HL cells.	HL patients with huge lump and in Ann Arbor stage III-IV presented higher expression of H19. Besides, H19 expression was negatively correlated to overall survival (OS) of HL patients.	Yes	In vitro experiments suggested that H19 downregulation decreased proliferation and viability of HL cells.	31128034
H19	LncRNA	Homo sapiens	Aortic Aneurysm, Abdominal	AAA tissues	Interaction[H19/let-7a/IL-6]	Western Blot//qRT-PCR//Luciferase Report Assay//ELISA//IHC	 qRT-PCR detected the upregulation of H19 in human and mouse AAA tissue samples.In vivo overexpression of H19 increased vascular inflammation and induced AAA formation, which was supported by exacerbated aortic morphology, maximum aortic diameter values, elastin degradation, expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1), and macrophage infiltration. H19 suppression resulted in the opposite effects. A rescue experiment indicated that IL-6 neutralization significantly mitigated the aortic inflammation and AAA formation evoked by H19 overexpression. Luciferase reporter assays and ex vivo experiments using VSMCs and macrophages confirmed that H19 induced aneurysm formation in part via endogenous competition with the let-7a microRNA to induce the transcription of its target gene, IL-6. This mechanism was further validated by in vivo experiments using a mutant H19 that could not effectively bind let-7a. Collectively, our study revealed a pathogenic H19/let-7a/IL-6 inflammatory pathway in AAA formation, which offers a new potential therapeutic strategy for AAA.		Yes	In vivo overexpression of H19 increased vascular inflammation and induced AAA formation, which was supported by exacerbated aortic morphology, maximum aortic diameter values, elastin degradation, expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1), and macrophage infiltration.	30991034
H19	LncRNA	Homo sapiens	Adrenocortical Carcinoma		Expression(lower expressed)	qRT-PCR//IF//Western Blot	he administration of higher concentration of DACi was able to down-regulate the protein level of Beclin1 and p62 and to induce the conversion of LC3B-I into the active LC3B-II form, thus confirming an active autophagic process. Neither the active protein level nor the activity of caspases 8 and 3 was prompted by the DACi, thus excluding the involvement of the executioners of apoptosis in H295R decay. The DACi restore H19, the autophagy markers and trigger cell death in ACC cells. The re-activation of autophagy would represent a novel strategy for the treatment of patients affected by this severe malignancy.		Yes	H19 knock down in H295R cells was not able to modulate the expression level of autophagy transcripts. Instead, H19 knock down was able to impede the ability of DACi to modulate the protein level of the autophagy markers.	34726962
H19	LncRNA	Homo sapiens	Mouth Neoplasms	cell lines	Regulation[miR-107/CDK6 signaling axis]	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	Compared with that in HIOEC cells, the expression of H19 was significantly increased in CAL27 cells (P<0.05).H19 could bind specifically to the 3'-UTR of miR-107 to modulate the expression of miR-107. Compared with that in HIOEC cells, the expression of miR-107 significantly decreased in CAL27 cells (P<0.05). The expression of miR-107 increased after transfection with siRNA H19, and anti-mir-107 co-transfection could promote the invasion and migration ability of siRNA H19 in CAL27 cells (P<0.05). Compared with that in HIOEC cells, CDK6 expression significantly increased in CAL27 cells (P<0.05), and the expression level of the gene was coregulated by H19 and miR-107 (P<0.05).		Yes	After transfection with siRNA H19, the expression of H19 decreased, and the invasion and migration ability of CAL27 cells were inhibited (P<0.05).	31512829
H19	LncRNA	Homo sapiens	Mouth Neoplasms	 oral cancer cell lines and CAFs	Interaction(miR-675-5p/PFKFB3 signaling pathway)	Western Blot//Transfection//qRT-PCR//FISH//RNA-seq//Luciferase Report Assay//IHC//Bioinformatics Analysis//IF	 In the present study, by using RNA sequencing and bioinformatics analysis, we analyzed the lncRNA/mRNA profiles of normal fibroblasts (NFs) derived from normal tissues and CAFs derived from patients with oral squamous cell carcinoma (OSCC). LncRNA H19 was identified as a key lncRNA in oral CAFs and was synchronously upregulated in both oral cancer cell lines and CAFs  . We found that knockdown of lncRNA H19 by siRNA suppressed the MAPK signaling pathway, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) and miR-675-5p. Furthermore, the lncRNA H19/miR-675-5p/PFKFB3 axis was involved in promoting the glycolysis pathway in oral CAFs, as demonstrated by a luciferase reporter system assay and treatment with a miRNA-specific inhibitor. 		Yes	Using small interfering RNA (siRNA) strategies, we determined that lncRNA H19 knockdown affected proliferation, migration, and glycolysis in oral CAFs. 	33762576
H19	LncRNA	Homo sapiens	Mouth Neoplasms	 iCell-h120 cells	Regulation(ZEB1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Colony Formation Assay	Here, we identify an H19 transcript variant that lacks exon 4 in oral cancer specimens and carcinoma-derived cells. Through binding the ZEB1 mRNA, the variant H19 transcript without exon 4 promotes the expression of ZEB1 protein during epithelial-mesenchymal transition (EMT). 		Yes	 Depletion of H19 by short hairpin RNAs (shRNAs) targeting exon 1 but not exon 4 significantly inhibited oral cancer iCell-h120 cells growth and invasion in vitro and tumorigenesis of these cells in vivo. 	33270342
H19	LncRNA	Homo sapiens	Wilms Tumor	 HFWT cells, nephroblastoma tissues 	Interaction(miR-675/TGFBI axis)	CCK8//qRT-PCR//Tunel//Western Blot	The gene expression levels of lncRNA H19 and miR-675 were markedly downregulated in nephroblastoma tissues (p<0.05), while that of TGFBI was notably upregulated (p<0.05). It upregulated the expressions of miR-675 and Caspase-8 (p<0.05), and downregulated TGFBI (p<0.05). Besides, miR-675 was able to upregulate Caspase-8 (p<0.05) and downregulate TGFBI (p<0.05). In addition, the protein expression of Caspase-8 was downregulated (p<0.05), while that of TGFBI was upregulated (p<0.05) after the knockdown of miR-675 in HFWT cells.		Yes	 LncRNA H19 could reduce the proliferative ability of HFWT cells (p<0.05) and stimulates apoptosis rate (p<0.05). 	35731049
H19	LncRNA	Homo sapiens	Thyroid Carcinoma, Anaplastic	 thyroid tissues	Expression[highly expressed]	CCK8//qRT-PCR//migration assay//cell invasion assay//Colony Formation Assay	 Expression of H19 was detected in 19 ATC and 19 normal thyroid tissues by real-time quantitative polymerase chain reaction. 		Yes	H19 inhibited proliferation, migration, and invasion and induced apoptosis in 8505C cells in vitro and inhibited tumorigenesis and metastasis in vivo. 	31299871
H19	LncRNA	Homo sapiens	Osteoporosis	OP samples 	regulation[LncRNA H19/miR-29a-3p axis]	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay	The expression of lncRNA H19 was significantly upregulated in OP samples compared with the health control. Thus, we concluded that lncRNA H19/miR-29a-3p axis was involved in the development of OP.		Yes	Furthermore, the knockdown of lncRNA H19 was validated to promote the expression of pro-inflammatory mediators, repress cell proliferation and inhibit cell apoptosis in vitro.	33207859
H19	LncRNA	Homo sapiens	Respiratory Distress Syndrome	MH-S & MLE-12	Interaction(microRNA-423-5p/FOXA1 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC	The expression of H19 and FOXA1 was significantly up-regulated, while the expression of miR-423-5p was down-regulated in LPS-induced ARDS rats. Silencing of H19 decreased the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1, and VEGF, the contents of TNF-α, IL-1β, IL-6, and VEGF in BALF, and histology score in LPS-induced ARDS rats. H19 knockdown also reduced the fibrosis scores and the protein expression of vimentin and α-SMA, and elevated the protein expression of E-cadherin in LPS-induced ARDS rats. Furthermore, silencing of miR-423-5p and overexpression of FOXA1 reversed the inhibitory effects of si-H19 on the inflammation and fibrosis of LPS-induced MH-S cells.		Yes	Silencing of H19 decreased the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1, and VEGF, the contents of TNF-α, IL-1β, IL-6, and VEGF in BALF, and histology score in LPS-induced ARDS rats. H19 knockdown also reduced the fibrosis scores and the protein expression of vimentin and α-SMA, and elevated the protein expression of E-cadherin in LPS-induced ARDS rats. Furthermore, silencing of miR-423-5p and overexpression of FOXA1 reversed the inhibitory effects of si-H19 on the inflammation and fibrosis of LPS-induced MH-S cells.	33629893
H19	LncRNA	Homo sapiens	Keloid	 keloid tissues and fibroblasts	Interaction(miR-769-5p/EIF3A pathway)	Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	Our study found that lncRNA H19 expression was increased in keloid tissues and fibroblasts.  Further experiments showed that microRNA (miR)-769-5p could be sponged by H19, and its knockdown reversed the suppression effect of H19 knockdown on keloid formation. Eukaryotic initiation factor 3A (EIF3A) was found to be a target of miR-769-5p, and its overexpression inverted the inhibition effect of miR-769-5p overexpression on keloid formation.		Yes	Besides, H19 knockdown hindered the proliferation, migration, invasion, extracellular matrix (ECM) deposition, and enhanced the apoptosis of keloid fibroblasts. 	33389493
H19	LncRNA	Homo sapiens	Keloid	 keloid tissue and fibroblasts	Interaction(miR-196b-5p/SMAD5)	qRT-PCR	H19 and SMAD5 expression was upregulated in keloid tissue and fibroblasts, whereas miR-196b-5p expression was downregulated.  miR-196b-5p was identified as a H19 sponge, and SMAD5 was identified as a miR-196b-5p target. 		Yes	 Knockdown of H19, overexpression of miR-196b-5p, or knockdown of SMAD5 inhibited the viability and proliferation of keloid fibroblasts and promoted apoptosis. Overexpression of H19 or SMAD5 and knockdown of miR-196b-5p promoted viability and proliferation and inhibited apoptosis. 	34974806
H19	LncRNA	Homo sapiens	Pituitary Neoplasms	ulcerative edge tissues of DFU	interaction[binding to miR-29b]	qRT-PCR	In the ulcerative edge tissues of DFU, high expression of lncRNA H19 and FBN1 and low expression of miR-29b were observed. Altogether, upregulation of lncRNA H19 can elevate the expression of FBN1 through competitively binding to miR-29b, which enhances the proliferation, migration, and inhibits apoptosis of fibroblasts, thus facilitating the wound healing of DFU.		Yes	Silencing of lncRNA H19 led to inhibited proliferation, migration, and enhanced apoptosis of fibroblasts, accompanied by downregulated FBN1 but upregulated miR-29b, which diminished the expression of TGF-β1, Smad3, FN, and Col-1 and reduced extracellular matrix accumulation.	33174326
H19	LncRNA	Homo sapiens	Aortic Aneurysm, Thoracic	TAA aorta tissues and serum and vascular smooth muscle cell (VSMC)	Interaction(miR-1-3p/ADAM10 Axis )	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay	H19 was increased in TAA aorta tissues and serum and vascular smooth muscle cell (VSMC), and hindered proliferation as well as promoted apoptosis and extracellular matrix (ECM) degradation of VSMC.  Moreover, miR-1-3p was decreased, and ADAM10 was upregulated in TAA aorta tissues and VSMC. The mechanical analysis confirmed that H19 affected ADAM10 expression by targeting miR-1-3p. 		Yes	H19 was increased in TAA aorta tissues and serum and vascular smooth muscle cell (VSMC), and hindered proliferation as well as promoted apoptosis and extracellular matrix (ECM) degradation of VSMC. 	34478010
H19	LncRNA	Homo sapiens	Diffuse Intrinsic Pontine Glioma	DIPG Tissue	Interaction( let-7 microRNAs)	Transfection//Wound Healing Assay//RNA-seq//Cell Proliferation Assay//Bioinformatics Analysis	We found that H19 expression was higher in DIPG vs. normal brain tissue and other pedHGGs. Mechanistically, H19 buffers let-7 microRNAs, resulting in the up-regulation of oncogenic let-7 target (e.g., SULF2 and OSMR)		Yes	H19 knockdown resulted in decreased cell proliferation and survival in DIPG cells. 	34502082
H19	LncRNA	Homo sapiens	Acute Lung Injury	sepsis patient	Expression(lower expressed)	qRT-PCR//ELISA//Luciferase Report Assay//Western Blot	 lncRNA H19 was downregulated in sepsis. lncRNA H19 alleviated sepsis-induced ALI by inhibiting pulmonary apoptosis and inflammation, serving as a biochemical marker and therapeutic target for sepsis.	The AUC of lncRNA H19 for early diagnosis of sepsis was 0.8197 (95% CI, 0.77 to 0.91).	Yes	Upregulation of lncRNA H19 inhibited TNF-α, IL-6, IL-17, caspase-3, caspase-9 and Bax and increased Bcl-2. 	35317444
H19	LncRNA	Homo sapiens	neuroendocrine carcinoma	pNEN tissues	Regulation[PI3K/AKT/CREB signaling]	RNA Pull-Down//qPCR//RNA-seq	H19 was significantly upregulated in pNEN tissues with malignant behaviors, and the upregulation predicted poor prognosis in pNENs.Furthermore, VGF was downregulated when H19 was knocked down, and VGF promoted cell proliferation, migration and invasion. Mechanistic investigations revealed that H19 activated PI3K/AKT/CREB signaling and promoted pNEN progression by interacting with VGF. These findings indicate that H19 is a promising prognostic factor in pNENs with malignant behaviors and functions as an oncogene via the VGF-mediated PI3K/AKT/CREB pathway. 		Yes	In vitro and in vivo data showed that H19 overexpression promoted tumor growth and metastasis, whereas H19 knockdown led to the opposite phenotypes.c	31117050
H19	LncRNA	Homo sapiens	Myocardial Infarction	MI patients	Interaction(PBX3/CYP1B1-dependent manner)	Western Blot//Transfection//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//ELISA	Downregulated H19 and upregulated CYP1B1 were observed in MI patients. Overexpression of CYP1B1 could abrogate the suppressive effect of H19 on pyroptosis of cardiomyocytes. H19 could inhibit activity of CYP1B1 promoters by regulating PBX3.		Yes	Transfection of H19 overexpression or CYP1B1 knockdown could attenuate the MI progression in MI rats. In hypoxic cardiomyocytes, H19 overexpression or CYP1B1 knockdown could also inhibit NLRP3, ASC, caspase-1, IL-1β, and IL-18 in addition to suppressing cell apoptosis rate and promoting cell proliferation rate. 	33389498
H19	LncRNA	Homo sapiens	Lung Injury	 CLP mice models and LPS-induced cell injury models	Interaction(miR-301a-3p/Adcy1)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA//EdU Staining	 LncH19 was lowly expressed in CLP mice models and LPS-induced cell injury models. MiR-301a-3p could be sponged by lncH19, and its overexpression could reverse the inhibition of lncH19 on LPS-induced cell injury. Adcy1 was a target of miR-301a-3p, and its expression was upregulated by lncH19. Silencing of Adcy1 could abolish the suppressive effect of the miR-301a-3p inhibitor on LPS-induced cell injury.		Yes	Overexpressed lncH19 could alleviate CLP-induced lung injury in mice, as well as LPS-induced cell apoptosis, inflammation, and oxidative stress.	35438054
H19	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues 	regulation[miR-675-5p/GPR55]	qRT-PCR//Luciferase Report Assay	LncRNA H19 was expressed at lower levels in TSCC tissues than in normal tissues.  The lncRNA H19/miR-675-5p/GPR55 axis might inhibit cell proliferation, invasion and migration in TSCC.		Yes	 When lncRNA H19 was overexpressed, miR-675-5p expression levels were also upregulated, leading to reduced proliferation, invasion and migration of CAL27 and SCC9 cells. 	35117434
H19	LncRNA	Homo sapiens	Glioma	cell lines	Regulation[miR-138/HIF-1α/VEGF axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay			Yes	 We investigated the regulatory roles and downstream molecular mechanisms of lncRNA H19 in glioma by knockdown H19, which inhibited the proliferation, migration and angiogenesis of glioma cells. Moreover, miR-138 acted as a target of H19 as detected by luciferase reporter assays.	31777264
H19	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[Wnt/β-catenin signaling pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 H19 expression in glioma tissues was higher than that in para-carcinoma tissues and associated with poor prognosis in glioma patients. Downregulation of H19 decreased DVL2, cyclin D1, and β-catenin expression and increased GSK-3β expression. The inhibitory effects of downregulation of H19 on glioma cell proliferation, invasion, and migration were reversed by SKL2001 via the activation of the Wnt/β-catenin signal pathway, which was further enhanced by inhibition of the Wnt/β-catenin signal pathway by XAV939.		Yes	Cell proliferation, invasion, and migration significantly decreased, the percentage of glioma cells in G0/G1 significantly increased, the percentage of glioma cells in the S phase significantly decreased, and apoptosis significantly increased in U251 and U87MG cells transfected with siRNA-H19 compared to those in the siRNA-NC group. 	31173296
H19	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	regulation[Wnt5a/β-Catenin Pathway ]	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	H19 and Wnt5a expression were remarkably upregulated in glioma tissues and cells, whereas miR-342 expression was downregulated. H19 regulates glioma cell growth and metastasis through miR-342 to mediate Wnt5a/β-catenin signaling pathway, which provides new therapeutic targets for glioma treatment.		Yes	Moreover, functional analysis confirmed that knockdown of H19 or overexpression of miR-342 suppressed glioma cell proliferation, migration, and angiogenesis in vitro. 	33161527
H19	LncRNA	Homo sapiens	Glioma	glioma cells 	Interaction(miR-200a/CDK6/ZEB1 axis)	In Vivo Experiment//Western Blot//Transfection//qPCR//CCK8//Luciferase Report Assay//Microarray//Transwell Assay	As a novel oncogenic factor, up-regulation of H19 was able to promote the proliferation of glioma cells by targeting miR-200a.In summary, our findings suggested that the expression of H19 was elevated in glioma, which could promote the growth, invasion and migration of tumor cells via H19/miR-200a/CDK6/ZEB1 axis. 		Yes	As a novel oncogenic factor, up-regulation of H19 was able to promote the proliferation of glioma cells by targeting miR-200a.Furthermore, elevated miR-200a levels could reverse H19-induced cell growth and metastasis.	34796112
H19	LncRNA	Homo sapiens	Glioma	glioma cells 	Regulation(mTOR/ULK1 pathway.)	Western Blot//Transfection//CCK8//qRT-PCR//EdU Staining//Transwell Assay	We observed that overexpressed H19 promoted the proliferation and migration in glioma cells.  In conclusion, we validate that H19 contributes to the proliferation and autophagy of glioma cells through the mTOR/ULK1 pathway.		Yes	We observed that overexpressed H19 promoted the proliferation and migration in glioma cells. The autophagy of U87 cells was suppressed when H19 was overexpressed and enhanced when H19 was silenced.	33661803
H19	LncRNA	Homo sapiens	Glioma	human glioma cell lines	Interaction(miR-152 )	In Vivo Experiment//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	The results showed that H19 expression was upregulated and miR-152 expression was downregulated in human glioma cell lines.  Taken together, H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression, providing evidence for the potential application of H19 as a biomarker and therapy target for glioma.		Yes	 H19 downregulation or miR-152 upregulation suppressed glioma cell proliferation and invasion in vitro.	29422115
H19	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal tissues	Interaction[ let-7]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	H19 was aberrantly over-expression in nasopharyngeal carcinoma, which intimately associated with poorer prognosis.Mechanistically, H19 competitively sponged let-7 genes and therefore Expression[up-expression]-regulated HRAS, which consequently contributed to its oncogenic activity in nasopharyngeal carcinomas. 		Yes	 H19-deficency significantly inhibited cell viability and sExpression[up-expression]pressed cell proliferation. Furthermore, both migrative and invasive capacity were compromised by H19 knockdown. H19-silencing remarkably delayed xenograft tumour progression and lung metastasis. 	31556327
H19	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	 In NPC cells, lncRNA H19 was up-regulated.		Yes	Silencing lncRNA H19 inhibited the proliferation of NPC C666-1 cells and promoted apoptosis, while overexpression of lncRNA H19 promoted the proliferation of NPC C666-1 cells and inhibited apoptosis. 	32736275
H19	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cells	Interaction(miR-491-5p)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//CCK8//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	The expression H19 was increased in GBM and was positively correlated with LC3 or Beclin-1.  H19 regulated the autophagy signaling pathway at least partly via miR-491-5p. Increased H19 expression in GBM exerts oncogenic effects by sponging miR-491-5p and enhancing autophagy. Therefore, H19 may be explored as a target for GBM therapy.		Yes	Silencing H19 inhibited growth and promoted apoptosis in GBM cells both in vitro and in vivo, and miR-491-5p was identified as one of the important mediators. 	35506168
H19	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tissues	Interaction[PI3K/AKT pathway]	Flow Cytometry//qRT-PCR//MTT//Western Blot	The results indicated that H19 was upregulated in TC tissues.Silencing of H19 inhibited the cell viability and promoted apoptosis of FTC-133 and TPC-1 TC cells, accompanied by an increased expression of B-cell lymphoma 2 (Bcl-2)-associated X protein and caspase 3, and repressed expression of Bcl-2. The results of western blot analysis suggested that the levels of phosphorylated phosphoinositide-3 kinase (PI3K) and phosphorylated AKT were attenuated by H19 silencing. These results suggest that lncRNA H19 exerts an oncogenic function in TC, in part through the PI3K/AKT pathway.		Yes	Silencing of H19 inhibited the cell viability and promoted apoptosis of FTC-133 and TPC-1 TC cells, accompanied by an increased expression of B-cell lymphoma 2 (Bcl-2)-associated X protein and caspase 3, and repressed expression of Bcl-2. 	31410148
H19	LncRNA	Homo sapiens	Multiple Myeloma	MM patients	interaction[miR-152-3p]	qRT-PCR//Luciferase Report Assay//IHC	We found that levels of H19 and BRD4 were upregulated and the expression of miR-152-3p was downregulated in MM patients. Taking these results together, H19 knockdown suppresses MM tumorigenesis via inhibiting BRD4-mediated cell proliferation through targeting miR-152-3p, implying that H19 is a promising biomarker and drug target for MM.		Yes	 Knockdown of H19 repressed proliferation and enhanced apoptosis and cell cycle G1 arrest by upregulating miR-152-3p in MM cells. Furthermore, H19 knockdown suppressed the growth of xenograft tumor, reduced Ki-67 and BRD4 levels, and increased cell apoptosis in xenograft tumor tissues. 	31712391
H19	LncRNA	Homo sapiens	Pancreatic Neoplasms	PDAC tissues	Regulation[H19/miR-194/PFTK1 axis]	qRT-PCR	In PDAC tissues, the expression of H19 and PFTK1 were upregulated. As analyzed by TCGA and predicted by online tools, miR-194 was negatively correlated with PFTK1 and might bind to both H19 and PFTK1, which was further confirmed by luciferase reporter and RNA immunoprecipitation assays. Moreover, the effect of H19 knockdown on PFTK1 protein and the cell proliferation and migration could be partially reversed by miR-194 inhibition; H19/miR-194 axis modulated PDAC cell proliferation and migration through PFTK1 downstream Wnt signaling. Results suggested that rescuing miR-194 expression in PDAC can inhibit lncRNA H19 and PFTK1 expression, subsequently suppressing PDAC cell proliferation and migration. Due to the complexity of the lncRNA-miRNA-mRNA network, further in vivo experiments examining potential side effects are needed in future study to explore the clinical application of these findings.		Yes	H19 knockdown suppressed the cell proliferation and migration of PDAC, while PFTK1 overexpression partially attenuated the suppressive effect of H19 knockdown.	30474270
H19	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung adenocarcinoma tissues	Interaction[ targeting miR-29b-3p and modifying STAT3]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 Simultaneously, expression of epithelial‑mesenchymal transition (EMT)‑specific proteins was significantly altered, i.e. increased epithelial cadherin expression, as well as decreased vimentin, Snail and Slug expression. Furthermore, miR‑29b‑3p was verified to be targeted and regulated by H19, and STAT3 was targeted and modified by miR‑29b‑3p. Ultimately, STAT3 was identified to decrease lung adenocarcinoma cell viability, survival, apoptosis and EMT imposed by miR‑29b‑3p. In conclusion, the results of the present study indicated that lncRNA H19/miR‑29b‑3p/STAT3 signaling was involved in the development of lung adenocarcinoma, which may be critical for developing effective diagnostic and treatment strategies for lung adenocarcinoma.		Yes	 The results indicated that highly expressed H19 and poorly expressed miR‑29b‑3p could serve as predictors for the poor prognosis of lung adenocarcinoma patients. Additionally, si‑H19 and miR‑29b‑3p mimic significantly increased the apoptosis of lung adenocarcinoma cells, and decreased the survival rate and viability of cells.	30747209
H19	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LAC tissues and cells	Interaction(Mutant p53 R175H)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay	Mtp53 R175H and H19 were over-expressed in LAC tissues and cells, while H19 over-expression extended the p53 half-life and enhanced transcriptional activity. Combined with anti-p53, ShH19 can significantly inhibit tumor growth in vivo.		Yes	Mtp53 R175H and H19 were over-expressed in LAC tissues and cells, while H19 over-expression extended the p53 half-life and enhanced transcriptional activity. Combined with anti-p53, ShH19 can significantly inhibit tumor growth in vivo.	36139647
H19	LncRNA	Homo sapiens	Alzheimer Disease	 Aβ25-35-treated PC12 cells as well as in brain tissues of AD mice	Interaction(MiR-129/HMGB1  axis)	RNA Pull-Down//Western Blot//Flow Cytometry//FISH//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	Elevated H19, HMGB1 and decreased miR-129 were found in Aβ25-35-treated PC12 cells as well as in brain tissues of AD mice. H19 could specifically bind to miR-129. MiR-129 specifically suppressed HMGB1 expression. 		Yes	Silenced H19 or elevated miR-129 promoted viability, inhibited apoptosis, prevented mitochondrial membrane potential dysfunction and decreased oxidative stress in Aβ25-35-treated PC12 cells. 	33410377
H19	LncRNA	Homo sapiens	Diabetes Mellitus, Type 2	tissues 	Regulation(p53 )	Wound Healing Assay	Mechanistically, lncH19 relieves the cell cycle arrest of fibroblasts and increases macrophage infiltration in injured tissues via inhibiting p53 activity and GDF15 releasement. Furthermore, exosomes derived from adipocyte progenitor cells efficiently restore the impaired diabetic wound healing via delivering lncH19 to injured tissue. 		Yes	Mechanistically, lncH19 relieves the cell cycle arrest of fibroblasts and increases macrophage infiltration in injured tissues via inhibiting p53 activity and GDF15 releasement. Furthermore, exosomes derived from adipocyte progenitor cells efficiently restore the impaired diabetic wound healing via delivering lncH19 to injured tissue. 	35472819
H19	LncRNA	Homo sapiens	Melanoma	melanoma tissues	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry	H19 was highly expressed in melanoma tissues compared to normal adjacent skin tissues, and the tissue expression level of H19 from melanoma patients with metastasis was significantly higher than that from patients without distant metastasis.	In addition, the high expression of H19 in melanoma tissues was associated with advanced tumor invasion and TNM stage, distal metastasis, lymph node metastasis and shorter overall survival in patients with melanoma. 	Yes	The in vitro functional assays showed that knockdown of H19 inhibited cell growth, invasion and migration and also induced cell apoptosis as well as G0/G1 arrest in melanoma cells.	29950863
H19	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues ,cell lines	Interaction[Sponging miR-let-7]	Transwell Assay//qRT-PCR//Luciferase Report Assay//Western Blot	Here we found that the expression of H19 was elevated in TSCC tissues compared with adjacent normal tissues.  Moreover, we demonstrated that the expression of H19 was higher in metastasized tumors compared with unmetastasized tumors.	 Moreover, we demonstrated that the expression of H19 was higher in metastasized tumors compared with unmetastasized tumors.	Yes	 Moreover, we demonstrated that the expression of H19 was higher in metastasized tumors compared with unmetastasized tumors.	29523225
H19	LncRNA	Homo sapiens	Skin Neoplasms	 cSCC tissues and cSCC cell lines	Interaction(microRNA‑675/p53axis)	Western Blot//Transfection//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The results of the present study revealed that the expression levels of H19 and miR‑675 were upregulated in cSCC tissues and cSCC cell lines. The overexpression of H19 upregulated the expression levels of its predicted target, miR‑675, which subsequently promoted the EMT process and downregulated the expression levels of p53.		Yes	The knockdown of H19 or miR‑675 expression inhibited cell proliferation, migration and invasion, but induced cell apoptosis.  In addition, the expression levels of EMT‑related markers were also downregulated. 	33649811
H19	LncRNA	Homo sapiens	Heart Injuries	 H9C2 cells	Interaction(miR-93-5p/SORBS2 Axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//ELISA	H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury via regulation of the miR-93-5p/SORBS2 axis. 		Yes	Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. 	32996061
GACAT3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tissues and A549cell	Interaction(TIMP2/MMP10)	qRT-PCR//MTT//Luciferase Report Assay	Using lncRNA array analysis, we found that GACAT3 expression increased significantly. TIMP2, confirmed a direct target of GACAT3 by bioinformatics analysis and our experiments, may be involved in the GACAT3-induced upregulation of MMP10.		Yes	Further studies showed that overexpression of ectopic GACAT3 in A549 cells promoted cell proliferation and migration, and enhanced the sensitivity of lung cancer cells to radiotherapy.	29565489
H1-10-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	regulation[H1FX-AS1/miR-324-3p/DACT1 axis ]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	Lower H1FX-AS1 expression in CC tissues was found to be associated with the poor prognosis of CC patients. Therefore, H1FX-AS1 is a new prognostic predictor and targeting the factors in the H1FX-AS1/miR-324-3p/DACT1 axis is the novel potential therapeutic strategy for CC.	Lower H1FX-AS1 expression in CC tissues was found to be associated with the poor prognosis of CC patients. 	Yes	 Over-expression of H1FX-AS1 inhibited CC cell proliferation, migration and invasion, while induced apoptosis by sponging miR-324-3p to up-regulate the DACT1 expression level.	32760225
GSTP1P1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[ miR-142-3p/Bach-1 Axis]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients.Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis.	The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients.	Yes	In addition, Lnc712 promoted HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by miR-142-3p mimic.  Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice.	33177878
GSTP1P1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(MiR-129-5p)	Cell Proliferation Assay//qRT-PCR//Transfection	Lnc712 was upregulated in OS and was inversely correlated with miR-129-5p.  In OS cells, Lnc712 overexpression failed to significantly affect miR-129-5p, while miR-129-5p overexpression led to downregulated Lnc712. Cell proliferation showed that Lnc712 overexpression resulted in increased cell proliferation rate. MiR-129-5p overexpression played an opposite role and reversed the effect of Lnc712 overexpression.		Yes	 In OS cells, Lnc712 overexpression failed to significantly affect miR-129-5p, while miR-129-5p overexpression led to downregulated Lnc712. Cell proliferation showed that Lnc712 overexpression resulted in increased cell proliferation rate. MiR-129-5p overexpression played an opposite role and reversed the effect of Lnc712 overexpression.	33732018
GSTM3TV2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-597/FOSL2 Axis)	qRT-PCR	We observed that the expression of lncRNA GSTM3TV2 and FOSL2 were upregulated in HCC. The luciferase reporter assays showed that lncRNA GSTM3TV2 could be directly bound to miR-597, and the level of miR-597 was also decreased in the tumor tissues. lncRNA GSTM3TV2 could stabilize FOSL2 expression, resulting in the oncogenic properties of lncRNA GSTM3TV2 in HCC.		Yes	Knockdown of lncRNA GSTM3TV2 significantly inhibited cell proliferation. Meanwhile, the migration and invasion of HCC cells were greatly decreased by the downregulated lncRNA GSTM3TV2. 	34458365
GSEC	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cell lines	regulation[miR-588/ EIF5A2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that the expression of LncRNA GSEC was up-regulated in osteosarcoma cell lines.In summary, this study shows that LncRNA GSEC promotes the proliferation and invasion of OS through the regulation of miR-588/EIF5A2 pathway, which might provide a new strategy for the treatment of osteosarcoma in the future.		Yes	 Overexpression of LncRNA GSEC promoted the proliferating and migratory capacity, and inhibited the apoptosis of osteosarcoma cells. Conversely, knockdown of LncRNA GSEC resulted in the opposite effect.	32868080
GSEC	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cancer cell line	Interaction(miR-202-5p/AXL Axis.)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	GSEC was significantly upregulated in TNBC tissues and cancer cell lines, and high level of GSEC was associated with advanced tumor stage, positive lymph-node metastasis and the poor prognosis of TNBC patients. GSEC regulated the expression of AXL by directly sponging miR-202-5p. Downregulation of miR-202-5p attenuated GSEC knockdown-induced inhibition on TNBC cell proliferation, invasion and migration in vitro. Meanwhile, overexpression of AXL obviously reversed the inhibitory effects of miR-202-5p mimics in TNBC progression in vitro.	GSEC was significantly upregulated in TNBC tissues and cancer cell lines, and high level of GSEC was associated with advanced tumor stage, positive lymph-node metastasis and the poor prognosis of TNBC patients.	Yes	Knockdown of GSEC effectively inhibited TNBC cell proliferation, invasion and migration in vitro. 	33907418
GSEC	LncRNA	Homo sapiens	Sepsis	cell line	Expression(highly expressed)	qRT-PCR//Luciferase Report Assay//Western Blot	 Performing in vitro experiments, we found that the expression of GSEC lncRNA and PFKFB3 was increased when neutrophils were treated with inflammatory stimuli. In addition, we found that GSEC lncRNA-induced PFKFB3 expression was essential for mediating dHL-60 cell inflammatory cytokine expression. Performing mechanistic experiments, we found that glycolytic metabolism with PFKFB3 involvement supported inflammatory cytokine expression.		Yes	Knockdown and overexpression experiments showed that GSEC lncRNA was essential for mediating PFKFB3 mRNA expression and stability in neutrophil-like dHL-60 cells.	34907156
GRIK1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell line(GES-1)	Interaction(miR-375/IFIT2 Axis)	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our results show a decreased expression of GRIK1-AS1 in gastric cancer tissues compared to adjacent normal gastric tissues. Gastric cell lines also have reduced levels of GRIK1-AS1 compared to gastric epithelial cell line GES-1. Our results revealed a novel mechanism of GRIK1-AS1 as a sponge to miR-375 that impacts gastric cancer progression via modulating target mRNA IFIT2 translation		Yes	Ectopic expression of GRIK1-AS1 in gastric cancer cell lines significantly inhibits cellular viability, migration, and invasion.	34660323
GREP1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC cells and clinical samples	Regulation( Wnt/β-catenin pathway)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 We found that LINC00514 expression was elevated in NSCLC cells and clinical samples and that increased LINC00514 expression predicted poorer patient prognosis. Altogether, this study provides the latest convincing evidence that LINC00514 facilitates the malignant biological behavior of NSCLC cells through activation of the Wnt/β-catenin pathway, which might offer a beneficial approach for the treatment of NSCLC.	 We found that LINC00514 expression was elevated in NSCLC cells and clinical samples and that increased LINC00514 expression predicted poorer patient prognosis.	Yes	Silencing LINC00514 suppresses proliferation, migration, and invasion of NSCLC cells. Downregulation of LINC00514 inhibited Wnt/β-catenin signaling and epithelial-mesenchymal transition (EMT).Moreover, suppression of the biological phenotypes of NSCLC cells induced by LINC00514 gene silencing was restored after LiCl treatment. Finally, we found that silencing LINC00514 attenuated the growth of xenograft tumors in vivo.	35653786
GREP1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	Interaction(miR‑378a‑5p/SPHK1 signaling axis)	CCK8//qRT-PCR//Western Blot	The present study found that LINC00514 and sphingosine kinase 1 (SPHK1) were both upregulated in ESCC tissues and cells, and their high expression levels were closely associated with Tumor?Node?Metastasis stage, lymph node metastasis and poor prognosis of patients with ESCC.Mechanistically, LINC00514 functioned as a competing endogenous RNA by sponging microRNA (miR)‑378a‑5p, resulting in the upregulation of SPHK1, which was accompanied by the activation of lipogenesis‑related pathways, to promote ESCC cell proliferation and invasion. 	The present study found that LINC00514 and sphingosine kinase 1 (SPHK1) were both upregulated in ESCC tissues and cells, and their high expression levels were closely associated with Tumor-Node-Metastasis stage, lymph node metastasis and poor prognosis of patients with ESCC.	Yes	Functionally, knockdown of LINC00514 inhibited cell proliferation and invasion, and led to the downregulation of lipogenesis?related proteins, including SPHK1, fatty acid synthase, acetyl?coenzyme (Co)A carboxylase α and stearoyl?CoA desaturase 1, whereas LINC00514 overexpression promoted cell proliferation and invasion in ESCC KYSE150 and KYSE30 cells, and upregulated expression of lipogenesis?related proteins.	34533201
GREP1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[Regulating miR-708]	qRT-PCR//ChIP	We showed that LINC00514 expressions were distinctly upregulated in both OS tissues and cell lines, especially in advanced cases.Our findings revealed SP1-induced upregulation of LINC00514 as an oncogene in OS through competitively binding to miR-708, suggesting that there are potential diagnostic and treatment values of LINC00514 in OS.	 High levels of LINC0051 were positively correlated with advanced tumor stages, distant metastasis, and reduced survival of patients with OS. 	Yes	Functional experiments indicated that silencing of LINC00514 suppressed the ability of cell growth, colony formation and metastasis, whereas promoted cell apoptosis in vitro. 	32523373
GREP1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Regulation[miR-204-3p/CDC23 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC00514 expression was significantly upregulated in papillary thyroid cancer (PTC) tissues by bioinformatics analysis. RNA-FISH showed that LINC00514 mainly locates in the nucleus of PTC cells. Through bioinformatics prediction, we identified that LINC00514 served as the sponge for miR-204-3p, and miR-204-3p directly targeted CDC23. Thus, LINC00514 promoted CDC23 expression via restraining miR-204-3p activity, leading to PTC progression. In sum, our findings demonstrated that LINC00514 contributes to PTC progression and might be a potential target for PTC therapy.		Yes	 Loss-of-function studies revealed that LINC00514 silencing inhibited the proliferation, migration and invasion of PTC cells while promoting apoptosis in vitro. Moreover, LINC00514 knockdown suppressed PTC growth in vivo.	30553447
GREP1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	regulation[miR-28-5p]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay	 In this study, LINC00514 was shown to be upregulated in PC tissues and cell lines.his study is the first to characterize the oncogenic function of the long noncoding RNA LINC00514 in pancreatic cancer progression by acting as a competing endogenous RNA (ceRNA) of miR-28-5p to upregulate Rap1b expression. 	Increased LINC00514 expression was significantly associated with the clinical progression and prognosis of PC patients.	Yes	In addition, silencing LINC00514 inhibited PC cell proliferation, migration and invasion, while LINC00514 overexpression promoted these processes. 	32771045
GREP1	LncRNA	Homo sapiens	cervical squamous cell carcinoma		 Interaction(miR-708-5p/HOXB3 axis)	Invasion assay//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our results showed that the expression of LINC00514 was up-regulated in human CSCC tissues and cell lines. 		Yes	Knockdown of LINC00514 significantly inhibited the proliferation and invasion of CSCC cells, as well as suppressed tumorigenesis of CSCC in vivo. In addition, LINC00514 was found to work as a miRNA sponge for miR-708-5p and suppressed the expression of miR-708-5p in CSCC cells. 	34652879
GRASLND	LncRNA	Homo sapiens	Glioma	gliomas	Interaction(miR-665/HMGA1 axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	RNF144A-AS1 and HMGA1 were high-expressed in gliomas, and miR-665 was low-expressed in gliomas, which led to the increase of glioma cell viability, proliferation, migration and invasion ability and insufficient apoptosis ability. Overexpression of RNF144A-AS1 suppressed the expressions of Bax and cleaved caspase-3, and promoted Bcl-2 expression. RNF144A-AS1 up-regulated the expression of HMGA1 by targeting miR-665, thereby promoting the development of glioma cells.		Yes	RNF144A-AS1 and HMGA1 were high-expressed in gliomas, and miR-665 was low-expressed in gliomas, which led to the increase of glioma cell viability, proliferation, migration and invasion ability and insufficient apoptosis ability. 	34560189
GPC5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	Interaction(miR-93/106a )	Western Blot//qRT-PCR//Cell Viability Assay//Cell Apoptosis Assay//Cell Cycle Assay//IHC//ChIP	 In the present study, we demonstrate that GPC5-AS1 is downregulated in GC cells and tissues, and this aberrant expression is regulated by MeCP2 through CpG site binding in the promoter region.Mechanistically, we demonstrated that GPC5-AS1 stabilizes GPC5 mRNA by acting as a molecular sponge for miR-93 and miR-106a, thereby reducing GC tumor progression.		Yes	Importantly, we also demonstrate that GPC5-AS1 overexpression suppresses cell proliferation, colony formation, and cell cycle transition; induces apoptosis in vitro; and inhibits tumorigenicity in vivo. 	35183057
GPC3-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Regulation[GPC3-AS1/GPC3 axis]	qRT-PCR	A quantitative reverse transcriptase-polymerase chain reaction confirmed that GPC3-AS1 was up-regulated in CC cells compared to normal CRL-2614 cells.  GPC3-AS1 positively regulated its nearby gene glypican 3 (GPC3). Significant up-regulation of GPC3 was also observed in CC cells, consistently with GPC3-AS1. In addition, GPC3-AS1 and GPC3 synergistically promoted the proliferative and migratory abilities of CC cells. Mechanistic investigation showed that ELK1 acted as the transcription activator of GPC3-AS1 and GPC3, thus contributing to their up-regulation in CC cells. Rescue assays indicated that the ELK1-induced GPC3-AS1/GPC3 axis promoted cell proliferation and migration in CC.		Yes	 Loss-of-function assays demonstrated the negative effect of GPC3-AS1 depletion on CC cell proliferation and migration. 	31168873
GOLPH3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells	Interaction(miRNA-1299/LIF axis)	RNA Pull-Down//Western Blot//Transfection//Proliferation Assay//qRT-PCR//PCR//Invasion Assay//IF	The expression of circGOLPH3 was upregulated in OSCC cells. Mechanistically, circGOLPH3 functioned as a microRNA sponge and downregulated miR-1299 expression. miR-1299 downregulated the expression of LIF by targeting its 3'-untranslated region. Inhibition of the circGOLPH3/miR-1299/LIF axis suppressed the growth, migration, and invasion of OSCC cells. These findings indicate that the circGOLPH3/miR-1299/LIF axis promotes OSCC cell growth, migration, and invasion and that this axis is a potential therapeutic target for OSCC.		Yes	circGOLPH3 promoted the growth of OSCC in vitro and in vivo. Additionally, circGOLPH3 upregulated OSCC cell migration and invasion. 	35481460
GNAS-AS1	LncRNA	Homo sapiens	Osteoarthritis	cartilage tissues	Interaction[ACSL6  ]	qRT-PCR//Western Blot	Highly elevated levels of Nespas and Acyl-CoA synthetase 6 (ACSL6) were observed in OA patients.Overall, we suggest that elevated Nespas level in OA are associated with OA pathogenesis by suppressing miRs targeting ACSL6 and subsequent ACSL6 upregulation.		Yes	Both Nespas overexpression and ACSL6 upregulation into human chondrocytes induced typical OA characteristics, such as downregulation of type II collagen; upregulation of type I collagen, metalloproteinase 13, and caspase-1 and -3; and dysfunction of mitochondria and peroxisome.	28805067
GNAS-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS cells and tissues	Expression(highly expressed)	CCK8//qRT-PCR	The expression of lncRNA GNAS-AS1 was significantly increased in OS cells and tissues, and related to Enneking staging and distant metastasis. 	The expression of lncRNA GNAS-AS1 was significantly increased in OS cells and tissues, and related to Enneking staging and distant metastasis. Patients with high lncRNA GNAS-AS1 expression represented shorter overall survival and was an independent prognostic predictor of OS. 	Yes	 LncRNA GNAS-AS1 knockdown inhibited cell proliferation, migration, and invasion by regulated miR-490-3p partly at least.	34321018
GTF2IRD2P1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 human bladder cancer tissues and cell lines	Regulation(Wnt/β‑catenin signaling pathway)	qRT-PCR//Western Blot	GTF2IRD2P1 expression was found to be lower in both human bladder cancer tissues and cell lines (UM-UC-3, RT4, and 5637), and elevated in T24 compared to the corresponding normal controls. Meanwhile, overexpression of GTF2IRD2P1 inhibited the proliferation of UM-UC-3 and prolonged the cell cycle. The silencing of GTF2IRD2P1 significantly increased the proliferation and shortened the cell cycle of T24 cells and induced Wnt signaling activity to promote the progression of bladder cancer. 		Yes	 Meanwhile, overexpression of GTF2IRD2P1 inhibited the proliferation of UM-UC-3 and prolonged the cell cycle. The silencing of GTF2IRD2P1 significantly increased the proliferation and shortened the cell cycle of T24 cells and induced Wnt signaling activity to promote the progression of bladder cancer. 	35433119
H19	LncRNA	Rattus norvegicus	Renal Insufficiency, Chronic	model rats and VSMCs	Interaction(microRNA-138/TLR3)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Microarray//IF	 Long non-coding RNA (lncRNA) H19 was upregulated in the aortic tissues after HPD treatment. H19 bound to microRNA (miR)-138 to block its inhibitory effect on TLR3 mRNA and activated the NF-κB signaling pathway. Downregulation of H19 or TLR3 alleviated, whereas downregulation of miR-138 aggravated the calcification and vascular damage in model rats and VSMCs. 		Yes	Downregulation of H19 or TLR3 alleviated, whereas downregulation of miR-138 aggravated the calcification and vascular damage in model rats and VSMCs. 	35435133
H19	LncRNA	Homo sapiens	Prostatic Neoplasms	Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. 	Regulation	Western Blot//Transwell Assay//qRT-PCR//RIP//Luciferase Report Assay//RNA-seq//IHC//Invasion Assay//ChIP	Extensive computational analysis has identified a high degree of association between the long noncoding RNA (lncRNA) H19 and NEPC, with the longest isoform highly expressed in NEPC. H19 facilitates the PRC2 complex in regulating methylation changes at H3K27me3/H3K4me3 histone sites of AR-driven and NEPC-related genes. 		Yes	. H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. It is also essential for the proliferation and invasion of NEPC. 	34934057
H19	LncRNA	Rattus norvegicus	Chronic Constriction Injury	rats	Interaction(miR-141/GLI2 axis)	In Vivo Experiment//RNA Pull-Down//qRT-PCR//Luciferase Report Assay//ELISA//Bioinformatics Analysis	LncRNA H19 was upregulated in the tissues of rats. Furthermore, miR-141 was reduced in CCI rats and restored by the lncRNA H19 knockdown, suggesting the potential negative associations of miR-141 with lncRNA H19. GLI2 targeted miR-141 and GLI2 was increased in CCI rats. Additionally, the neuropathic pain was inhibited by the inhibition of GLI2 in rats, which was reversed by the miR-141 inhibitors.		Yes	 Also, thermal hyperalgesia and mechanical allodynia were inhibited by lncRNA H19 suppression in rats.Moreover, IL-1β, IL-6 and TNF-α protein concentrations were suppressed by the downregulation of lncRNA H19 in rats.	34999183
H19	LncRNA	Homo sapiens	Aortic Dissection	thoracic aorta tissues of AD patients	Interaction(miR-193b-3p)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	LncRNA H19 was abnormally high-expressed in thoracic aorta tissues of AD patients, and it could competitively bind to and inhibit miR-193b-3p. 		Yes	In the PDGF-BB group, the expressions of H19, matrix metallopeptidase (MMP) 2 (MMP-2) and MMP-9 were up-regulated and the expressions of miR-193b-3p, α-SMA, and SM22α were down-regulated; moreover, the proliferation and migration rate of HASMCs were increased.  However, H19 silencing reversed the regulation of PDGF-BB on HASMCs. More interestingly, miR-193b-3p inhibitor could partially reverse the effect of H19 silencing. In addition, the above results were verified by animal experiments, showing that shH19 and up-regulated miR-193b-3p could significantly reduce the thoracic aorta pathological damage in AD mice.	33403385
H19	LncRNA	Homo sapiens	Acute Kidney Injury	murine ischemic kidney tissue, Ecs, TECs	Interaction(miR-30a-5p)	In Vivo Experiment//Western Blot//Transfection//qPCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//IHC//EdU Staining//ChIP	H19 is upregulated in kidney biopsies of patients with AKI, in murine ischemic kidney tissue, and in cultured and ex vivo sorted hypoxic endothelial cells (ECs) and tubular epithelial cells (TECs). Sponging of miR-30a-5p mediated the effects, which, in turn, led to target regulation of Dll4, ATG5, and Snai1.		Yes	 H19 overexpression promotes angiogenesis in vitro and in vivo. In vivo, transient AAV2-mediated H19 overexpression significantly improved kidney function, reduced apoptosis, and reduced inflammation, as well as preserving capillary density and tubular epithelial integrity. 	33478972
H19	LncRNA	Homo sapiens	Pneumonia	WL-38 cell 	Interaction(miR-22-3p/NLRP3 axis)	Western Blot//Transfection//Tunel//qRT-PCR//MTT//Luciferase Report Assay//ELISA//Bioinformatics Analysis//IF	In the LPS induced pneumonia model, LncRNA H19 silences inhibited LPS-induced WL-38 cell pyroptosis, and LncRNA H19 overexpression promotes LPS-induced WL-38 cell pyroptosis. Also, LncRNA H19 acts as a sponge of miR-22-3p, which targets NLRP3, and NLRP3 attenuates the effect of LncRNA H19 silencing on LPS-induced WL-38 cell pyroptosis.		Yes	In the LPS induced pneumonia model, LncRNA H19 silences inhibited LPS-induced WL-38 cell pyroptosis, and LncRNA H19 overexpression promotes LPS-induced WL-38 cell pyroptosis. Also, LncRNA H19 acts as a sponge of miR-22-3p, which targets NLRP3, and NLRP3 attenuates the effect of LncRNA H19 silencing on LPS-induced WL-38 cell pyroptosis.	34786066
H19	LncRNA	Homo sapiens	Pneumonia	peripheral blood of patients with pneumonia, WI-38 cells	Interaction(miR-140-5p/TLR4 Axis)	qRT-PCR//ELISA//MTT	LncRNA H19 and TLR4 were up-regulated, while miR-140-5p was downregulated in peripheral blood of patients with pneumonia and LPS-treated WI-38 cells compared with their controls. H19 targeted miR-140-5p and it inversely regulated miR-140- 5p expression. MiR-140-5p targeted TLR4 and it inversely regulated TLR4 expression. H19 positively regulated TLR4 expression. Moreover, inhibition of miR-140-5p or overexpression of TLR4 reversed the effects of H19 silencing on cell viability, inflammation, and apoptosis in LPS-induced WI-38 cells.		Yes	Silencing of H19 or miR-140-5p mimics facilitated cell viability, whereas repressed apoptosis and reduced content of TNF-α, IL-6, and IL-1β in LPS-induced WI-38 cells. 	35392782
H19	LncRNA	Homo sapiens	Liver Cancer Bone Metastasis	cells with distinct bone metastasis ability	Regulation(PPP1CA-induced inactivation of the p38MAPK pathway)	In Vivo Experiment	H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up-regulating zinc finger E-box binding homeobox 1 through the sequestration of microRNA (miR) 200b-3p.		Yes	Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo.	33615520
H19	LncRNA	Homo sapiens	Lung Neoplasms	 lung bronchial epithelial cell (16HBE) and COE induced malignant transformed cell 	Interaction(H19/miR-29a-3p/COL1A1 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//RNA-seq	 H19 and COL1A1 were significantly higher in Rf than in 16HBE and miR-29a-3p was reverse.  Regulatory investigation revealed H19 increased COL1A1 expression by sponging miR-29a-3p.  In conclusion, all these indicated H19 functioned as a ceRNA to increase COL1A1 by sponging miR-29a-3p and promoted COE-induced cell malignant transformation.		Yes	Knockdown of H19, COL1A1 or overexpression of miR-29a-3p in Rf cells could inhibit cell proliferation, increased cell adhesion and p53 level. However, knockdown of H19 while suppressing the miR-29a-3p partially rescue the malignant phenotype of Rf caused by H19. 	36150622
H19	LncRNA	Mus musculus	Osteoarthritis	OA mice	Interaction(TP53, IL-38, IL-36R)	IF//Luciferase Report Assay//ChIP//Western Blot	 TP53 was responsible for lncRNA H19-mediated upregulation of IL-38. Furthermore, it was found that the anti-inflammatory effects of IL-38 were achieved by its binding with the IL-36 receptor (IL-36R). Overexpression of H19 reduced the expression of inflammatory factors and chondrocyte apoptosis, which was abrogated by knockdown of IL-38 or TP53.		Yes	 TP53 was responsible for lncRNA H19-mediated upregulation of IL-38. Furthermore, it was found that the anti-inflammatory effects of IL-38 were achieved by its binding with the IL-36 receptor (IL-36R). Overexpression of H19 reduced the expression of inflammatory factors and chondrocyte apoptosis, which was abrogated by knockdown of IL-38 or TP53.	35942891
H19	LncRNA	Mus musculus	Atherosclerosis	aortic tissues	Interaction[upregulating PKD1 ]	Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//H&E Staining//ChIP	H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1. The present study provides evidence that H19 recruits CTCF to downregulate the expression of PKD1, thereby promoting vulnerable plaque formation and intraplaque angiogenesis in mice with atherosclerosis.		Yes	 Moreover, opposite results were found in the aortic tissues of atherosclerosis mice treated with H19 or CTCF overexpression.	31757932
H19	LncRNA	Mus musculus	Atherosclerosis	thoracic aortas	regulation[p53]	CCK8//qRT-PCR//Western Blot	Compared with the control group, mouse weight and plaque area were all increased in the AS model group, as was the expression of H19.Results from the present study indicated that knockdown of H19 may prevent AS deterioration through increased p53‑mediated VSMC apoptosis.		Yes	 Knockdown of H19 reduced the proliferation and induced apoptosis of VSMCs, and increased the expression of p53, cleaved caspase3 (c?caspase3) and p53 upregulated modulator of apoptosis, as well as enhancing the interaction between Bax and p53 proteins. 	32945413
H19	LncRNA	Mus musculus	Atherosclerosis	 mouse blood and aorta 	Interaction(miR-146a-5p/ANGPTL4 Pathway)	Western Blot//Transfection//FISH//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	The outcomes from this research illustrated that the expression of lncRNA H19 was elevated in mouse blood and aorta with lipid-loaded macrophages and atherosclerosis. The upregulation of lncRNA H19 decreased the miR-146a-5p expression but increased the levels of ANGPTL4 in mouse blood and aorta and THP-1 cells. 		Yes	Adeno-associated virus (AAV)-mediated lncRNA H19 overexpression significantly increased the atherosclerotic plaque area in apoE-/- mice supplied with a Western diet. 	34820432
H19	LncRNA	Mus musculus	Myocardial Infarction	myocardial tissue	Interaction[ regulating KDM3A]	RNA Pull-Down//Western Blot//RIP//qRT-PCR//Luciferase Report Assay	We found that H19 was significantly down-regulated after MI. Bioinformatics analysis and dual-luciferase assays revealed that, mechanistically, miR-22-3p was a direct target of H19, which was also confirmed by RIP and RNA pull-down assays in primary cardiomyocytes. In addition, bioinformatics analysis and dual-luciferase reporter assays also demonstrated that miRNA-22-3p directly targeted the KDM3A gene. Moreover, subsequent rescue experiments further verified that H19 regulated the expression of KDM3A to ameliorate MI-induced myocardial injury in a miR-22-3p-dependent manner. The present study revealed the critical role of the lncRNAH19/miR-22-3p/KDM3A pathway in MI. These findings suggest that H19 may act as a potential biomarker and therapeutic target for MI.		Yes	Functionally, enforced H19 expression dramatically reduced infarct size, improved cardiac performance and alleviated cardiac fibrosis by mitigating myocardial apoptosis and decreasing inflammation. However, H19 knockdown resulted in the opposite effects.	31755219
H19	LncRNA	Mus musculus	Colitis, Ulcerative	 colon tissues	Interaction(miR-331-3p/TRAF4 )	RNA Pull-Down//qPCR//Luciferase Report Assay//ELISA//Bioinformatics Analysis	 H19 was highly expressed in colon tissues.Mechanically, lncRNA-H19 is bound to miR-331-3p to inhibit its expression. TRAF4 is a target of miR-331-3p. Inhibition of miR-331-3p or overexpression of TRAF4 could reverse the alleviating role of lncRNA-H19 in intestinal injury of UC mice.		Yes	Silencing H19 attenuated intestinal injury of UC mice, manifested by reductions in weight loss, DAI, histopathological scores, IL-1β and TNF-α, and increases in colon length and IL-10. 	35483327
H19	LncRNA	Mus musculus	Diabetic Cardiomyopathies	C57/BL-6j mice	Regulation(PI3K/AKT/mTOR axis)	In Vivo Experiment//qPCR//Bioinformatics Analysis//Western Blot	 H19 could reduce the expression of p-PERK, p-IRE1α, ATF6, CHOP, cleaved caspase-3, cleaved caspase-9, cleaved caspase-12, and BAX proteins in cardiac tissues. Furthermore, H19 repressed oxidative stress, ERS and apoptosis in vitro. Moreover, the effect of H19 on ERS-associated apoptosis might be rescued by LY294002 (the specific inhibitor for PI3K and AKT).		Yes	 H19 improved left ventricular dysfunction in DM. H19 could reduce cardiomyocytes apoptosis and improve fibrosis in vivo. 	36044268
H19	LncRNA	Mus musculus	Brain Injuries	HIBD cell model	Interaction(miR-107 and Up-Regulating Vascular Endothelial Growth Factor)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//FISH//RIP//Luciferase Report Assay//IF			Yes	H19 overexpression reduced neuronal apoptosis and alleviated cognitive dysfunction in HIBD rats.	33608066
H19	LncRNA	Mus musculus	Pulmonary Fibrosis	pulmonary fibrotic tissues	Regulation[H19-miR-140-TGF-β/Smad3 signaling]	qRT-PCR//ELISA//Luciferase Report Assay//Western Blot	 Here, our observations showed that H19 expression was significantly upregulated and that of microRNA 140 (miR-140) was markedly reduced in pulmonary fibrotic tissues from idiopathic pulmonary fibrosis (IPF) patients and transforming growth factor β1 (TGF-β1)-induced HBE and A549 cells. The study of molecular mechanisms showed that H19 functioned via reduction of miR-140 expression by binding to miR-140. The increase of miR-140 inhibited TGF-β1-induced pulmonary fibrosis, and H19 upregulation diminished the inhibitory effects of miR-140 on TGF-β1-induced pulmonary fibrosis, which was involved in the TGF-β/Smad3 pathway. Taken together, our findings showed that H19 knockdown attenuated pulmonary fibrosis via the regulatory network of lncRNA H19-miR-140-TGF-β/Smad3 signaling, and H19 and miR-140 might represent therapeutic targets and early diagnostic and prognostic biomarkers for patients with pulmonary fibrosis.		Yes	 Furthermore, animal experiments showed that H19 knockdown attenuated BLM-induced pulmonary fibrosis in mice.	30988156
H19	LncRNA	Mus musculus	Sepsis	 kidney tissues of IRI mice	Interaction(miR-196a/Wnt/β-Catenin Signaling)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//IHC//IF	lncRNA-H19 is upregulated, and miR-196a-5p is downregulated in kidney tissues of IRI mice.Moreover, miR-196a-5p is a direct target of lncRNA-H19. lncRNA-H19 overexpression promotes kidney fibrosis and activates fibroblasts during AKI-CKD development, while miR-196a-5p overexpression reversed these effects in vitro. Furthermore, lncRNA-H19 overexpression significantly upregulates Wnt1 and β-catenin expression in kidney tissues and fibroblasts of IRI mice, while miR-196a-5p overexpression downregulates Wnt1 and β-catenin expression in kidney tissues and fibroblasts of IRI mice.		Yes	Moreover, miR-196a-5p is a direct target of lncRNA-H19. lncRNA-H19 overexpression promotes kidney fibrosis and activates fibroblasts during AKI-CKD development, while miR-196a-5p overexpression reversed these effects in vitro. 	34818249
H19	LncRNA	Mus musculus	Bronchopulmonary Dysplasia	 Hyp-induced mice	Interaction(miR-17/STAT3)	Other	Hyp-induced mice showed increased alveolar diameter, septum, and hyperemia and inflammatory cell infiltration, upregulated H19, decreased overall number and significantly reduced RAC on the 7th and 14th days after birth, which were reversed in the si-H19-treated mice. Moreover, H19 competitively bound to miR-17 to upregulate STAT3. IL-6 and IL-1β expressions and p-STAT3 and STAT3 levels were downregulated after inhibition of H19.		Yes	VEGF was upregulated and TGF-β1 and SPC was decreased in si-H19-treated mice. 	33285606
H19	LncRNA	Rattus norvegicus	Polycystic Ovary Syndrome	ovarian tissues & serum samples and cumulus cells	Regulation(Cyp17)	In Vivo Experiment//qRT-PCR//Western Blot	tudies have suggested that the increased testosterone synthesis seen in PCOS is driven in part by increased activity of CYP17A1, the rate-limiting enzyme for the formation of androgens in the gonads and adrenal cortex, which represents a critical factor driving enhanced testosterone secretion in PCOS. In this work, we evaluated the hypothesis that dysregulation of the noncoding RNA H19 results in aberrant CYP17 and testosterone production. To achieve this, we measured Cyp17 in ovarian tissues of H19 knockout mice, and quantified serum testosterone levels, in comparison with wild-type controls. We also evaluated circulating and ovarian H19 expression and correlated results with the presence or absence of PCOS in a group of women undergoing evaluation and treatment for infertility. We found that the loss of H19 in a mouse model results in decreased ovarian Cyp17, along with decreased serum testosterone in female mice. Moreover, utilizing serum samples and cumulus cells from women with PCOS, we showed that circulating and ovarian levels of H19 are increased in women with PCOS compared to controls. Findings from our multimodal experimental strategy, involving both a mouse model of dysregulated H19 expression and clinical serum and ovarian cellular samples from women with PCOS, suggest that the loss of H19 may disrupt androgen production via a Cyp17-mediated mechanism. Conversely, excess H19 may play a role in the pathogenesis of PCOS-associated hyperandrogenemia.		Yes	We found that the loss of H19 in a mouse model results in decreased ovarian Cyp17, along with decreased serum testosterone in female mice. 	34655046
H19	LncRNA	Rattus norvegicus	Cerebral Hemorrhage	rats with ICH	Regulation( NF-κBp65 and IKKβ expression)	qRT-PCR//ELISA//Western Blot	 In addition, the expression of lncRNA H19 in the brain tissue in the ICH group was significantly higher than that in the sham group. Western blot results showed that the expression of NF-κBp65 and IKKβ was significantly higher, and IκBα expression was lower in the perivascular hematoma tissue in the ICH group compared with the sham group. Compared with the sh-NC group, NF-κBp65 and IKKβ expression were significantly lower and IκBα was significantly higher in the sh-H19 group.		Yes	 After further interference with lncRNA H19 expression (sh-H19 group), the levels of all the above indicators were reversed and the neurological damage was improved.	35075368
H19	LncRNA	Homo sapiens	Glioma	glioma tissues	interaction[miR-130a-3p ]	qRT-PCR//Luciferase Report Assay//RIP	H19 was overexpressed in glioma tissues.H19 and SOX4 are both direct target of miR-130a-3p. H19 could compete with SOX4 via sponging miR-130a-3p.		Yes	Down-regulation of H19 led to the inhibition of migration, invasion and EMT process with a reduction in N-cadherin and Vimentin.	30282068
H19	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer tissues and cell lines	regulation[p53/TNFAIP8 pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of lncRNA H19 and TNFAIP8 was up-regulated in breast cancer tissues and cell lines, especially in triple-negative breast cancer (TNBC). Our findings provide insight into a novel mechanism of lncRNA H19 in tumorigenesis and metastases of breast cancer and demonstrate H19/p53/TNFAIP8 axis as a promising therapeutic target for breast cancer, especially for TNBC.		Yes	 Functionally, knockdown of lncRNA H19 or TNFAIP8 coused the capacities of cell proliferation, migration, and invasion were suppressed, and cell cycle arrest was induced, as well as that the EMT markers were expressed abnormal.	32514245
H19	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues,cell lines (Eca109, kyse410, kyse510, TE-1, TE-5)	Regulation[STAT3/EZH2 axis]	Western Blot//qRT-PCR//RIP//MTT//Transwell Assay	Our results showed that the mRNA level of H19 was significantly increased in EC versus normal tissue(P < 0.01, Fig.1A). This result was validated in five EC cell lines (Eca109, kyse410, kyse510, TE-1, TE-5) and HEEC. Compared to HEEC, the level of H19 was elevated in all five PC cell lines, of which Eca109 and TE-5 had exhibited the most significant increase in H19 expression (Fig. 1B).Our results showed that the mRNA level of H19 was significantly increased in EC versus normal tissue(P < 0.01, Fig.1A).		Yes	KnockExpression[down-expression] of lncRNA H19 repressed cell proliferation, migration and invasion as well as EMT and metastasis via STAT3-EZH2-β-catenin pathway, while lncRNA H19 regulated STAT3 negatively regulated let-7c in EC cell lines.	31102664
HAND2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues 	Interaction(microRNA-21-5p/TIMP3/VEGFA axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//Flow Cytometry//RIP//FISH//Luciferase Report Assay//Transwell Assay	HAND2-AS1 and TIMP3 were downregulated in cervical cancer, which were identified to be associated with a poor prognosis of patients with cervical cancer.  Moreover, HAND2-AS1 was upregulated the expression of TIMP3 through competitively binding to miR-21-5p.  In summary, HAND2-AS1 may exert inhibitory effects on cervical cancer cell growth and cervical cancer development through its regulation on the miR-21-5p/TIMP3/VEGFA axis. 	HAND2-AS1 and TIMP3 were downregulated in cervical cancer, which were identified to be associated with a poor prognosis of patients with cervical cancer. 	Yes	Overexpressed HAND2-AS1 or downregulated miR-21-5p inhibited cell proliferation, migration, and invasion while promoting cell apoptosis, in association with increased expression of proteins in VEGFA signaling pathway.  These changes were reversed by silencing of TIMP3.Overexpressed HAND2-AS1 reduced the tumor formation ability in nude mice. 	33139818
HAND2-AS1	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines.	Interaction(CDK6 )	Western Blot//Transfection//CCK8//qRT-PCR//Transwell Assay	Our results revealed that HAND2-AS1 expression was significantly downregulated in the glioma tissues and cell lines.However, overexpression of CDK6 could partially block the inhibitory role of HAND2-AS1 on cell proliferation as well as cell invasion and migration in glioma cell lines.		Yes	 Moreover, overexpression of HAND2-AS1 attenuated the proliferation, invasion, and migration in glioma cell lines. 	35548927
HAND2-AS1	LncRNA	Homo sapiens	Atherosclerosis	 plasma from patients with atherosclerotic plaques and macrophages 	Interaction(miR-1208/SIRT1 axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	 As a result, SIRT1 and HAND2-AS1 expression significantly decreased in plasma from patients with atherosclerotic plaques and macrophages originating from THP-1 induced by ox-LDL.  Altogether, HAND2-AS1 targeting miR-1208/SIRT1 axis alleviates the formation of foam cells within AS. 		Yes	Lentivirus mediated HAND2-AS1 overexpression markedly inhibited lipid absorption and deposition within foam cells originating from THP-1 macrophages. 	34780888
HAND2-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tumor tissues	Interaction[ROCK1 ]	CCK8//qRT-PCR//Western Blot	 In the present study, it was revealed that lncRNA HAND2-AS1 was Expression[down-expression]regulated, whereas Rho-associated protein kinase 1 (ROCK1) mRNA was Expression[Expression[up-expression]-expression]regulated in tumor tissues when compared with the healthy tissues of patients with melanoma. Expression levels of lncRNA HAND2-AS1 and ROCK1 were inversely correlated in tumor tissues, but not in healthy tissues. 		Yes	 LncRNA HAND2-AS1 overexpression led to inhibited melanoma cancer cell proliferation and an increased expression level of ROCK1. 	31423160
HAND2-AS1	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer cells	regulation[SOCS5,JAK-STAT Pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The authors discovered the downregulated HAND2-AS1 in liver cancer cells. HAND2-AS1 enhanced inactivation of the JAK-STAT pathway through sponging miR-3118 and facilitating SOCS5 to retard cell proliferation and migration in liver cancer.		Yes	HAND2-AS1 augmentation apparently impaired the capacity of liver cancer viability, proliferation, and migration. 	32155348
HAND2-AS1	LncRNA	Homo sapiens	gastric adenocarcinoma	GA tissues and cells	regulation[miR-184/HIF3A signaling]	qRT-PCR//Luciferase Report Assay//Transwell Assay//Western Blot	The HAND2-AS1 and HIF3A expressions were down-regulated and miR-184 expression was up-regulated in GA tissues and cells. LncRNA HAND2-AS1 could inhibit GA cell proliferation, migration and invasion abilities and glycolytic process induced by hypoxia through miR-184/HIF3A signaling.		Yes	 In addition, HAND2-AS1 rescued enhanced AGS cell proliferation, cell migration, cell invasion abilities and glycolytic process caused by hypoxia via miR-184/HIF3A.	32431548
HAND2-AS1	LncRNA	Homo sapiens	esophagus squamous cell carcinoma	ESCC tissue	Interaction[regulating microRNA-21]	CCK8//qRT-PCR//Transwell Assay	In this study, we found that lncRNA HAND2-AS1 was Expression[down-expression]regulated, while microRNA-21 ( miRNA-21) was Expression[Expression[up-expression]-expression]regulated in tumor tissues than in adjacent healthy tissues of ESCC patients.Expression levels of lncRNA HAND2-AS1 and miRNA-21 were significantly and inversely correlated in tumor tissues but not in healthy tissues.miRNA-21 overexpression failed to affect lncRNA HAND2-AS1 expression but significantly attenuated the inhibitory effect of lncRNA HAND2-AS1 overexpression on cancer cell proliferation, migration, and invasion.		Yes	lncRNA HAND2-AS1 overexpression resulted in Expression[down-expression]regulation of miRNA-21 in cells of ESCC cell lines and inhibited cell proliferation, migration, and invasion. 	30520131
HAND2-AS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	blood	Interaction[downregulating ROCK1]	Western Blot//qPCR//CCK8//ELISA//Transwell Assay	The current study revealed that lncRNA HAND2-AS1 was downregulated, while Rho-associated protein kinase 1 (ROCK1) was upregulated in serum of human papillomavirus (HPV)-positive and -negative patients with CSCC compared with healthy controls.Additionally, lncRNA HAND2-AS1 overexpression led to reduced expression levels of ROCK1 in HPV-positive and -negative human CSCC cell lines but not in normal cervical cell lines. ROCK1 overexpression did not significantly affect the expression of lncRNA HAND2-AS1 in all the cell lines investigated. lncRNA HAND2-AS1 overexpression inhibited, while ROCK1 overexpression promoted the proliferation, migration and invasion of HPV-positive and -negative human CSCC cell lines but not normal cervical cell lines. ROCK1 overexpression attenuated the effects of lncRNA HAND2-AS1 overexpression on cancer cell proliferation, migration and invasion. lncRNA HAND2-AS1 may inhibit cancer cell proliferation, migration and invasion by downregulating ROCK1 in HPV-positive and -negative CSCC.		Yes	 lncRNA HAND2-AS1 overexpression inhibited, while ROCK1 overexpression promoted the proliferation, migration and invasion of HPV-positive and -negative human CSCC cell lines but not normal cervical cell lines.	31555362
HAND2-AS1	LncRNA	Homo sapiens	Arthritis, Rheumatoid	RA synovial tissues	Interaction(miR-143-3p/TNFAIP3/NF-κB pathway)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA//Transwell Assay	HAND2-AS1 was lowly expressed in RA synovial tissues, and HAND2-AS1 re-expression suppressed the proliferation, motility, and inflammation and triggered the apoptosis in RA-FLSs via the inactivation of NF-κB pathway. Mechanistically, HAND2-AS1 directly sponged miR-143-3p and positively regulated TNFAIP3 expression, the target of miR-143-3p. 		Yes	HAND2-AS1 was lowly expressed in RA synovial tissues, and HAND2-AS1 re-expression suppressed the proliferation, motility, and inflammation and triggered the apoptosis in RA-FLSs via the inactivation of NF-κB pathway. 	33549125
HAND2-AS1	LncRNA	Homo sapiens	Diabetes Mellitus	plasma 	Expression[lower expressed]	qRT-PCR//Cell Apoptosis Assay	LncRNA HAND2-AS1 was downregulated in diabetic patients with chronic renal failure but not in diabetic patients without obvious complications.		Yes	Overexpression of lncRNA HAND2-AS1 inhibited the apoptosis of mouse podocyte cells under high glucose treatment.	32411303
HAGLROS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[repressing miR-100 and up-regulating SMARCA5]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Up-regulated HAGLROS expression was observed in NSCLC tissues and cell lines.These results conclude that HAGLROS is a tumor promoter in NSCLC, and it regulates the malignant phenotypes of NSCLC cells via miR-100/SMARCA5 axis.		Yes	Over-expressed HAGLROS promoted the malignant phenotypes of NSCLC cells; conversely, HAGLROS knockdown repressed the malignant phenotypes of NSCLC cells.	35307327
HAGLROS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	non-small cell lung cancer tissues	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay	We identified HAGLROS was significantly overexpressed in non-small cell lung cancer samples compared to normal tissues. 	Higher expression of HAGLROS was significantly associated with shorter overall survival time in patients with non-small cell lung cancer. 	Yes	Moreover, we found knockdown of HAGLROS in non-small cell lung cancer cells remarkably suppressed tumour proliferation, migration and invasion.	32484214
HAGLROS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[miR-5095/ATG12 axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	The level of HAGLROS was higher in HCC tissues and correlated with clinical performances including tumor stages or tumor differentiation.Our results revealed that HAGLROS is highly expressed in HCC, and its high level may correlate with the progression and development of HCC involving the processes of cell viability, apoptosis, and autophagy through the miR-5095/ATG12 axis and PI3K/AKT/mTOR signals.	The level of HAGLROS was higher in HCC tissues and correlated with clinical performances including tumor stages or tumor differentiation. In contrast to the lower level, a higher level of HAGLROS correlated with a shorter survival time of patients with HCC.	Yes	The suppression of HAGLROS decreased cell viability, promoted apoptosis, and inhibited autophagy. 	31082725
HAGLROS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-26b-5p/KPNA2)	CCK8//qRT-PCR	In the current study, HAGLROS exhibited a higher level in HCC tissues and cells.vMechanistically, HAGLROS could competitively bind to miR-26b-5p to prevent the suppression of miR-26b-5p on its downstream target gene Karyopherin α2 (KPNA2). Moreover, the inhibitory effects of HAGLROS knockdown on cell malignant behaviors were reversed due to the miR-26b-5p down-regulation or KPNA2 overexpression. It was interesting to note that HAGLROS inactivated p53 signaling through targeting miR-26b-5p/KPNA2. 	HAGLROS expression was positively correlated with tumor size, TNM stage and poor clinical prognosis.	Yes	Loss-of-function experiments showed that knockdown of HAGLROS significantly lowered cell proliferation, cell cycle progression, migration, invasion and epithelial to mesenchymal transition (EMT) but induced apoptosis in vitro. Consistently, tumor growth in the nude mice was effectively slowed by the depletion of HAGLROS.	35291921
HAGLROS	LncRNA	Homo sapiens	Ovarian Neoplasms	 OV cells	Interaction(miR-26b-5p)	qRT-PCR//Tunel//Western Blot	The results indicated that HAGLROS was highly expressed in OV cells. Further study revealed that HAGLROS acted as a sponge for miR-26b-5p and positively regulated its expression. 		Yes	Interference of HAGLROS led to a decrease in the proliferation, but an increase in the apoptosis of OV cells, accompanied by downregulated expression levels of Ki67 and Bcl-2, and upregulated expression levels of Bax and cleaved caspase-3. 	34194557
HAGLROS	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma samples and cell lines 	regulation[HAGLROS/miR-152/ROCK1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In our study, we found that the expression of HAGLROS increased osteosarcoma samples and cell lines compared with normal tissues and cells. The results showed HAGLROS/miR-152/ROCK1 axis might act as a novel therapeutic strategy for osteosarcoma.		Yes	 HAGLROS knockdown inhibited certain functions of U2OS and SW1353 cells in vitro. Moreover, HAGLROS depletion inhibited tumor growth and metastasis in vivo. 	32963586
HAGLROS	LncRNA	Homo sapiens	Esophageal Neoplasms	EC cell lines and tissues	Interaction(miR-206- NOTCH3 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	HAGLROS is upregulated in esophageal squamous cell carcinoma (ESCC) tissues and predicts poor prognosis. HAGLROS promotes EC cell tumorigenesis in vivo. HAGLROS participates in the HAGLROS/miR-206/NOTCH3 regulatory axis in EC cells.		Yes	Silent HAGLROS is negatively associated with malignant behavior in EC cells. Low expression of HAGLROS can induce decreased invasive and migratory abilities in EC cells. Downregulated HAGLROS significantly inhibits the proliferation of EC cells and accelerates apoptosis. 	34790377
HAGLROS	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	 DLBCL tissues and cells	Interaction(miR-100)	In Vivo Experiment//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	HAGLROS was upregulated in DLBCL tissues and cells, and closely associated with advanced clinicopathological features.  Further experiments revealed that HAGLROS negatively regulated the expression of miR-100 in DLBCL, and the expression of miR-100 and HAGLROS showed an inverse correlation in DLBCL tissues. 	HAGLROS was upregulated in DLBCL tissues and cells, and closely associated with advanced clinicopathological features. Upregulation of HAGLROS resulted in poor survival outcomes in DLBCL patients.	Yes	. In addition, HAGLROS knockdown inhibited the proliferation, migration, and invasion of DLBCL cells in vitro. 	34888946
HAGLROS	LncRNA	Homo sapiens	lung carcinoma	LCa tissues	Interaction[sponging microRNA-152]	qRT-PCR	 HAGLROS was highly expressed in LCa tissues compared with adjacent normal tissues. MicroRNA-152 was negatively correlated with HAGLROS in LCa. Rescue experiments showed that the knockdown of microRNA-152 reversed the regulatory effects of HAGLROS on proliferative and migratory abilities of LCa cells.	 LCa patients with a higher expression of HAGLROS presented significantly worse tumor stage, a higher rate of lymphatic metastasis, and a lower survival. 	Yes	The knockdown of HAGLROS significantly attenuated the proliferative and migratory abilities of LCa cells.Meanwhile, HAGLROS over-expression obtained the opposite results.	31378893
HAGLROS	LncRNA	Homo sapiens	Wilms Tumor	nephroblastoma cell lines	Expression(highly expressed)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//IF//Cell Apoptosis Assay//Cell Proliferation Assay//Transwell Assay	Experiment results showed that HAGLROS expressed highly in nephroblastoma cell lines.		Yes	 HAGLROS knockdown prevented cells from proliferating, and also showed suppressive impact on migration and invasion in HFWT cells.  In addition, knockdown of HAGLROS showed a facilitative effect on apoptosis and an inhibitory effect on autophagy.  Stimulation of autophagy alleviated HAGLROS silencing-induced apoptosis, while inhibition of autophagy reversed the effect in nephroblastoma cells. 	35358010
HAND2-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	tumor tissues and adjacent healthy tissues, 	Interaction[KLHDC7B]	CCK8//qRT-PCR//Western Blot	In patients with early-stage TNBC, the expression level of lncRNA HAND2-AS1 was Expression[down-expression]regulated, whilst runt-related transcription factor 2 (RUNX2) mRNA was Expression[Expression[up-expression]-expression]regulated in tumor tissues, compared with paired healthy tissues. Expression levels of lncRNA HAND2-AS1 and RUNX2 mRNA were inversely correlated in tumor tissues, but not in paired healthy tissues. Decreased plasma expression levels of lncRNA HAND2-AS1 were observed in TNBC patients compared with those in healthy controls, and the Expression[down-expression]regulation of lncRNA HAND2-AS1 distinguished patients with TNBC from healthy controls.		Yes	lncRNA HAND2-AS1 overexpression inhibited RUNX2 expression, whilst RUNX2 overexpression did not significantly affect lncRNA HAND2-AS1 expression in the MDA-MB-231 and BT-20 cell lines. lncRNA HAND2-AS1 overexpression resulted in the inhibition of cell proliferation, while RUNX2 overexpression promoted the proliferation of TNBC cells. RUNX2 overexpression partially reversed the effects of lncRNA HAND2-AS1 overexpression on cancer cells. 	31788122
HAND2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells	regulation[C16orf74,E2F4]	Western Blot//Transwell Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//ChIP	HAND2-AS1 exhibited poor expression in cervical cancer, and HAND2-AS1 overexpression suppressed the proliferation, colony formation, migration and invasion of cervical cancer cells.In conclusion, this study provided evidence on the inhibitory effect of HAND2-AS1 on the development of cervical cancer through the suppression of C16orf74 expression by recruiting transcription factor E2F4. 		Yes	HAND2-AS1 exhibited poor expression in cervical cancer, and HAND2-AS1 overexpression suppressed the proliferation, colony formation, migration and invasion of cervical cancer cells.	32314545
H19	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	blood	Interaction[targeting miR-29a-3p]	CCK8//Luciferase Report Assay//Flow Cytometry//Western Blot	The expression of lncRNA-H19 in AML patients was markedly higher than that in normal controls and compared with human embryonic kidney (HEK)-293T cells, AML cell Kasumi-1 exhibited an increased lncRNA-H19 expression. It is bound to micro RNA (miR)-29a-3p in a targeted manner. and the expression level of miR-29a-3p in AML patients was prominently lower than that in normal controls. After miR-29a-3p was inhibited, the expression of intranuclear β-catenin was significantly increased and the Wnt/β-catenin pathway critical molecules T-cell factor (TCF) and lymphoid enhancer factor 1 (LEF1) were evidently up-regulated after the down-regulation of miR-29a-3p.		Yes	LncRNA-H19 could promote cell proliferation, but suppress cell apoptosis.	31389605
HAS2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Regulation(HAS2 )	qRT-PCR//Wound Healing Assay//Cell Viability Assay	Moreover, the survival of patients with ER-negative tumors was higher when the expression of HAS2-AS1 was elevated.Unexpectedly, in these ER-negative cell lines, HAS2-AS1 is involved neither in the regulation of HAS2 nor in HA deposition. 	Moreover, the survival of patients with ER-negative tumors was higher when the expression of HAS2-AS1 was elevated.	Yes	 Experiments with ER-negative cell lines as MDA-MB-231 and Hs 578T revealed that the overexpression of either the full-length HAS2-AS1 or its exon 2 long or short isoforms alone, strongly reduced cell viability, migration, and invasion, whereas HAS2-AS1 silencing increased cell aggressiveness. 	35395387
HAS2-AS1	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissue,cell lines	Regulation[ miR-466/RUNX2 axis]	ChIP//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the cells and tissue of EOC, HAS2-AS1 expression was markedly up-regulated.Mechanical investigation found that HAS2-AS1 could relive the RUNX2 protein expression via sponging the miR-466, acting as miRNA sponge. In conclusion, this finding suggests the CREB1/HAS2-AS1/miR-466/RUNX2 axis in the in the EOC tumorigenesis, providing the novel insight for the molecular mechanism of EOC.	Besides, the overexpression of HAS2-AS1 indicated the poor clinical outcome of EOC patients. 	Yes	Functionally, HAS2-AS1 knockdown suppressed the proliferation, invasion and tumor growth of EOC cells in vitro and in vivo. 	31082772
HAS2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[PI3K/AKT signaling pathway ]	qRT-PCR	 In our research, HAS2-AS1 expression was elevated in glioma tissues compared with normal brain tissues. In vitro studies suggested that knocking down HAS2-AS1 expression inhibited glioma cell viability, migration, and invasion through phosphoinositide 3-kinase/protein kinase B signaling pathway. 	. Moreover, high levels of HAS2-AS1 expression was observed in patients with glioma with high WHO grade (III-IV) or large tumor size ( > 4 cm). The survival analysis from The Cancer Genome Atlas showed glioma cases with high HAS2-AS1 expression that had shorter disease-free survival time and overall survival time than those with low HAS2-AS1 expression. 	Yes	In vitro studies suggested that knocking down HAS2-AS1 expression inhibited glioma cell viability, migration, and invasion through phosphoinositide 3-kinase/protein kinase B signaling pathway. 	30790335
HAS2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[USF1 ]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay//ChIP	HAS2-AS1 was highly expressed in glioma tissues and cells, and was significantly associated with poor prognosis.These results suggested that the transcription factor USF1 induced up-regulation of lncRNA HAS2-AS1 and promoted glioma cell invasion and migration.	HAS2-AS1 was highly expressed in glioma tissues and cells, and was significantly associated with poor prognosis.	Yes	Silencing HAS2-AS1 expression inhibited glioma cell migration, invasion and EMT.	32776110
HAS2-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM cell lines	Interaction(miR-137/LSD1)	In Vivo Experiment//IHC//Western Blot//Transfection//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay	 HAS2-AS1 expression was upregulated in GBM cell lines, and HAS2-AS1 was localized mainly in the cytoplasm.  Furthermore, HAS2-AS1 functioned as a ceRNA (competing endogenous RNA) of miR-137, leading to the disinhibition of its downstream target LSD1. The miR-137 level was downregulated by HAS2-AS1 overexpression and upregulated by HAS2-AS1 knockdown. In a subsequent study, LSD1 expression was negatively regulated by miR-137, while miR-137 reversed the LSD1 expression levels caused by HAS2-AS1. 		Yes	 In vitro, high HAS2-AS1 expression promoted proliferation, and knockdown of HAS2-AS1 significantly inhibited proliferation. Furthermore, HAS2-AS1 functioned as a ceRNA (competing endogenous RNA) of miR-137, leading to the disinhibition of its downstream target LSD1. 	34094916
HAR1A	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung adenocarcinoma tissues	Regulation(STAT3)	qRT-PCR//Western Blot	We found that lncRNA Highly Accelerated Region 1A (HAR1A) is significantly downregulated in lung adenocarcinoma (LUAD) and negatively associated with prognosis.  Additionally, the knockdown of HAR1A accelerated NSCLC cell proliferation but inhibited apoptosis and vice versa. HAR1A regulated cellular activities through the STAT3 signaling pathway. The tumor-suppressing role of HAR1A was verified in the mouse model.	We found that lncRNA Highly Accelerated Region 1A (HAR1A) is significantly downregulated in lung adenocarcinoma (LUAD) and negatively associated with prognosis. 	Yes	 Additionally, the knockdown of HAR1A accelerated NSCLC cell proliferation but inhibited apoptosis and vice versa. HAR1A regulated cellular activities through the STAT3 signaling pathway. The tumor-suppressing role of HAR1A was verified in the mouse model.	35740511
HAND2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	regulation[miR-769-5p/TCEAL7]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Downregulation of HAND2-AS1 was found in GC tissues and cell lines.Taken together, our study showed that HAND2-AS1 exerts its tumor suppressive role in GC via regulating miR-769-5p/TCEAL7.		Yes	HAND2-AS1 overexpression inhibited GC cell proliferation, invasion, and arrested cell cycle at G0/G1 phase, whereas HADN2-AS1 knockdown significantly promoted cell proliferation and invasion.	32952069
HAND2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	regulation[miR-3118/PHLPP2 axis]	RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the current study, HAND2-AS1 was discovered to be low expressed in BC cell lines, and overexpression of HAND2-AS1 could repress proliferation, migration, and invasion but facilitate apoptosis in BC cells.In summary, our study testified that HAND2-AS1 suppressed BC growth by targeting the miR-3118/PHLPP2 axis, indicating that HAND2-AS1 could be regarded as a potential target for BC treatment.		Yes	In the current study, HAND2-AS1 was discovered to be low expressed in BC cell lines, and overexpression of HAND2-AS1 could repress proliferation, migration, and invasion but facilitate apoptosis in BC cells.	33015182
HAND2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	interaction[miR-1275,SOX7]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Downregulation of HAND2-AS1 was detected in breast cancer and was associated with adverse clinical features and prognosis. LncRNA HAND2-AS1 sponging miR-1275 restrains proliferation and metastasis of breast cancer cells by regulating SOX7 expression.	Downregulation of HAND2-AS1 was detected in breast cancer and was associated with adverse clinical features and prognosis. 	Yes	 Furthermore, overexpression of HAND2-AS1 restrained cell viability, migration and invasion in breast cancer.	31683462
HAND2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,blood	Interaction[TGF-β1]	Flow Cytometry//qRT-PCR//Western Blot//Transwell Assay	In our study, we observed that levels of HAND2-AS1 were lower in tumor tissues than that in adjacent healthy tissues. Compared with healthy controls, plasma levels of HAND2-AS1 were lower, while levels of transforming growth factor β (TGF-β) were higher in NSCLC patients. Cancer cells with lncRNA HAND2-AS1 overexpression showed down-regulated TGF-β1, while TGF-β1 treatment showed no significant effects on lncRNA HAND2-AS1 expression. TGF-β1 attenuated the inhibitory effects of lncRNA HAND2-AS1 overexpression on cell migration, invasion and stemness. We concluded that lncRNA HAND2-AS1 may regulate the migration, invasion and stemness of NSCLC cells through interactions with TGF-β1.		Yes	LncRNA HAND2-AS1 overexpression inhibits, while exogenous TGF-β1 treatment promotes cell migration and invasion ability and cancer cell stemness.	30509963
HAND2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung tissues and serum 	regulation[ PI3K/Akt pathway]	CCK8//qRT-PCR//Cell Apoptosis Assay//Western Blot	HAND2-AS1 expression was significantly down-regulated in NSCLC. We conclude that HAND2-AS1 may suppress the proliferation of NSCLC cells by targeting PI3K/Akt pathway.	 HAND2-AS1 and tumor size of NSCLC patients were closely associated. Serum HAND2-AS1 can be used to effectively distinguish osteosarcoma patients from healthy controls, and it can also be used to predict prognosis of osteosarcoma patients. 	Yes	HAND2-AS1 overexpression inhibited osteosarcoma cell proliferation, promoted cell apoptosis, and down-regulated phosphorylation of PI3K/Akt pathway-related proteins. 	32975291
HAND2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	interaction[ miR-1275,KLF14 ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In our study, we found that lncRNA HAND2-AS1 was markedly downregulated in CRC tissues. In conclusion, our study demonstrated that HAND2-AS1 exerts a suppressive role in CRC by sponging miR-1275 and modulating KLF14 expression.	And its expression level was negatively correlated with metastasis and advanced stage in CRC patients. Furthermore, we showed that HAND2-AS1 low expression predicted poor prognosis.	Yes	Functionally, we found that overexpression of HAND2-AS1 obviously attenuated the proliferation and invasion of CRC cells. Ectopic expression of HAND2-AS1 also inhibited tumor propagation in vivo. 	30078677
HAND2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[microRNA-300/SOCS5 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS5 axis.	HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival.	Yes	HAND2-AS1 over-expression reduced viability and proliferation in HCC cells. 	32224127
HAND2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	serum 	regulation[ROCK2 ]	qRT-PCR	It was found that levels of HAND2?AS1 in serum were significantly lower, while serum levels of Rho?associated protein kinase 2 (ROCK2) in HCC patients were significantly increased compared with hepatitis B (HB) patients and healthy controls.It was therefore concluded that HAND2‑AS1 might mediate the downregulation of ROCK2 in HCC to inhibit cancer cell migration, proliferation and invasion.		Yes	 HAND2?AS1 overexpression inhibited, while ROCK2 overexpression promoted HCC cell migration, proliferation and invasion. 	31922232
HAND2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 plasma of  patients with early-stage HCC 	Expression [lower expressed]	qRT-PCR//Western Blot	The plasma level of HAND2-AS1 was downregulated and that of RUNX2 was upregulated in patients with early-stage HCC compared with those in healthy controls.		Yes	HAND2-AS1 overexpression led to the downregulation of RUNX2 expression in human HCC cells, whereas RUNX2 failed to significantly affect HAND2-AS1 expression. HAND2-AS1 overexpression inhibited and RUNX2 overexpression promoted the proliferation of HCC cells. RUNX2 overexpression attenuated the inhibitory effects of HAND2-AS1 overexpression on cancer cell proliferation.	33566427
HAND2-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction(miR-146/RARB)	qRT-PCR//Luciferase Report Assay	Based on the RT2 lncRNA PCR Arrays analysis, we validated HAND2-AS1 declined in bladder cancer and negatively correlated with the depth of invasion and grades.  Besides, one of the HAND2-AS1 sponges, miR-146, elevated in bladder cancer and targeted the tumor suppressor, retinoic acid receptor beta (RARB). We further demonstrated that the HAND2-AS1: miR-146: RARB complex promoted Caspase 3-mediated apoptosis by suppressing COX-2 expression. 	Based on the RT2 lncRNA PCR Arrays analysis, we validated HAND2-AS1 declined in bladder cancer and negatively correlated with the depth of invasion and grades. 	Yes	 The overexpression of HAND2-AS1 in human bladder cancer cells 5637 and RT4 hampered cell proliferation by provoking Caspase 3-triggered cell apoptosis. 	34238300
HAND2-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	Interaction(miR-17-5p/ KLF9 Axis)	qRT-PCR//Wound Healing Assay//Luciferase Report Assay	 Results showed that HAND2-AS1 was downregulated in BC tissues, and its overexpression significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo. Furthermore, miR-17-5p was shown to be a direct target of HAND2-AS1, and it reversed the inhibitory effect of HAND2-AS1 on BC malignancies. Also, as a downstream factor of miR-17-5p, KLF9 silencing was demonstrated to mediate the role of miR-17-5p inhibitor in BC cell proliferation and invasion. 		Yes	 Results showed that HAND2-AS1 was downregulated in BC tissues, and its overexpression significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo.Knockdown of HAND2-AS1 caused an opposite effect on BC cell malignancies. 	35007433
HAND2-AS1	LncRNA	Homo sapiens	Osteosarcoma	Tumor tissues and adjacent healthy tissues	Expression[lower expressed]	CCK8//qRT-PCR//Western Blot	The results revealed that the expression levels of HAND2-AS1 were reduced in cancer tissues compared with those in healthy tissues.	 	Yes	HAND2-AS1-knockdown promoted osteosarcoma cell proliferation, increased glucose uptake and upregulated GLUT1 expression. 	31423193
HAGLROS	LncRNA	Homo sapiens	lung non-small cell carcinoma	NSCLC tissues and cell lines	Interaction(miR-100)	Northern Blot//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Up-regulated HAGLROS expression was observed in NSCLC tissues and cell lines. HAGLROS repressed miR-100 expression to promote SMARCA5 expression in NSCLC cells, and miR-100 overexpression or SMARCA5 knockdown counteracted the oncogenic functions of HAGLROS.		Yes	Over-expressed HAGLROS promoted the malignant phenotypes of NSCLC cells; conversely, HAGLROS knockdown repressed the malignant phenotypes of NSCLC cells. 	35307327
HAGLR	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Regulation[HOXD-AS1/miR-421/SOX4 axis ]	qRT-PCR	 Our results revealed that HOXD-AS1 was upregulated in BCa tissues and cell lines, and high HOXD-AS1 expression was correlated with aggressive clinicopathological characteristics of BCa patients. Therefore, we shed light on that HOXD-AS1/miR-421/SOX4 axis may be considered as a novel therapeutic target for the treatment of BCa patients.		Yes	Further gain-of-function and loss-of-function analysis showed that HOXD-AS1 overexpression promoted, whereas HOXD-AS1 knockdown inhibited BCa cell proliferation, cell cycle progression, migration, and invasion, indicating that HOXD-AS1 may function as a novel oncogene in BCa. 	30730081
HAGLR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	interaction[miR-217]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The results demonstrated that HOXD?AS1 was upregulated in CRC tissues and cell lines, and that overexpression of HOXD?AS1 was associated with poor prognosis in patients with CRC.Mechanistically, HOXD‑AS1 functioned as a competing endogenous RNA for miR‑217. 	The results demonstrated that HOXD?AS1 was upregulated in CRC tissues and cell lines, and that overexpression of HOXD?AS1 was associated with poor prognosis in patients with CRC.	Yes	Furthermore, knockdown of HOXD?AS1 inhibited cell proliferation, cell invasion, epithelial?mesenchymal transition and stem cell formation in vitro, as well as tumor growth and metastasis in vivo.	29749477
HAGLR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-526b-3p/CCND1 Axis]	CCK8//qRT-PCR//Western Blot//Transwell Assay	HOXD-AS1 was highly expressed in CRC, and high expression of HOXD-AS1 was related to the poor prognosis of patients with CRC.HOXD-AS1 upregulated the expression of CCND1 to promote the proliferation, migration, and invasion of CRC through targeting miR-526b-3p.	HOXD-AS1 was highly expressed in CRC, and high expression of HOXD-AS1 was related to the poor prognosis of patients with CRC.	Yes	Function experiment results revealed that miR-526b-3p inhibitor could reverse the suppressive effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of CRC cells. 	32640404
H19	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[H19/miR-152-3p/TCF4 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	In vitro, we observed that H19 was overexpressed in GC tissues and cell lines.The H19/miR-152/TCF4 axis may provide a new perspective for treating GC.		Yes	After knockdown of H19, the IC50 of ADM was decreased and cell apoptosis rates increased in both BGC-823ADM and MGC-803ADM cells. 	35117758
H19	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Regulation(Wnt/β-catenin signaling)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//IF//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	 H19 was overexpressed in GC tissues and cell lines and related to poor prognosis for GC patients. Mechanistically, H19 could induce β-catenin to transfer into nucleus and activate Wnt/β-catenin signaling, thus promoting EMT and metastasis of GC cells.		Yes	In vitro and in vivo assays verified the promotion of H19 on GC cell epithelial to mesenchymal transition (EMT) and metastasis.	34348271
H19	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Interaction[miR-138]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 We found that H19 was upregulated in breast cancer tissues and cells and associated with poor prognosis.  Additionally, miR-138 was identified as a direct target of H19 and SOX4; overexpression of miR-138 inhibited the proliferation, invasion and migration of MDA-MB-231 and MCF-7 cells, but promoted apoptosis, which were abrogated by SOX4 overexpression. Downregulated miR-138 induced cell proliferation, invasion and migration, but inhibited apoptosis of MDA-MB-231 and MCF-7 cells, which were promoted by SOX4 overexpression. In addition, miR-138 overexpression reversed the effects of H19 in breast cancer cells; silencing of H19 inhibited tumor growth and downregulate EMT markers in vivo.		Yes	 Downregulated H19 suppressed the proliferation, invasion and migration of breast cancer cells, but promoted cell cycle arrest and apoptosis.	31217890
H19	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction[binds miR-93-5p to regulate STAT3]	Western Blot//CCK8//RIP//qRT-PCR//Luciferase Report Assay	"The results showed that the expression level of
STAT3 in MDA‐MB‐231 cells was higher than that in
MCF‐7 cells (Figure 1).Our study revealed a new network in the expression of STAT3 involving H19 and miR-93-5p, which may contribute to a better understanding of breast cancer pathogenesis and provide new insights into the treatment of this disease."		Yes	overexpression of H19 promoted proliferation, migration, and invasion, whereas knockdown of H19 reduced proliferation, migration, and invasion in vitro. 	30256448
H19	LncRNA	Homo sapiens	Breast Neoplasms	cancer tissues and cancer cell lines	regulation[H19-miR-130a-3p-SATB1 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We demonstrated that H19 expression was higher in cancer tissues and cancer cell lines than in adjacent non-tumor tissues and normal cell lines, respectively. Our data uncovered a novel mechanism of BC progression based on the H19-miR-130a-3p-SATB1 axis.		Yes	H19 silencing inhibited the proliferation, migration and invasion of BC cells, and induced apoptosis. 	33324070
H19	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[miR-203]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	It was found that compared with normal adjacent tissues, H19 expression was elevated in NSCLC tissues along with a decreased miR-203 expression level. 	It was also found that patients who were in advanced clinical stages had a higher H19 and a lower miR-203 expression compared to normal tissues. The overall survival time of patients with higher H19 expression was shorter compared with the lower H19 expression group.	Yes	Upregulation of A549 enhanced cell proliferation and promoted invasion. 	30214583
H19	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	Interaction[inhibiting miR-200a]	RNA Pull-Down//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 H19 expression was elevated in the lung cancer tissues and cell lines.Meantime, RNA pull-down assay showed that H19 interacted with miR-200a, and miR-200a inhibited the activity of H19-fused luciferase. Furthermore, H19 overexpression inhibited miR-200a function and thereby upregulated miR-200a target genes, ZEB1 and ZEB2.H19 sponged and inhibited miR-200a to de-repress expression of ZEB1 and ZEB2, and thereby enhanced lung cancer proliferation and metastasis.		Yes	 H19 overexpression promoted the lung cancer cell growth, cell migration and invasion, as well as the epithelial mesenchymal transition (EMT).	31187349
H19	LncRNA	Homo sapiens	Colorectal Neoplasms		interaction[binding to hnRNPA2B1]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Transwell Assay	We found the expression of lncRNA H19 was significantly upregulated in primary tumor and metastatic tissues, correlated with poor prognosis in CRC.Our findings demonstrate the role of H19/hnRNPA2B1/EMT axis in regulation CRC metastasis, suggested H19 could be a potential biomarker to predict prognosis as well as a therapeutic strategy for CRC.		Yes	Ectopic H19 expression promoted the metastasis of colorectal cancer cells in vitro and in vivo, and induced epithelial-to-mesenchymal transition (EMT).	32698890
H19	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	Interaction[regulating microRNA-22 via EMT pathway]	CCK8//qRT-PCR//Western Blot	LncRNA H19 was highly expressed in HBV-related HCC tissues.Western blot results demonstrated that lncRNA H19 remarkably decreased the protein expressions of EMT pathway-related genes, including N-cadherin, Vimentin, β-catenin and MMP-9. In addition, rescue experiments demonstrated that lncRNA H19 remarkably promoted malignant development of HBV-related HCC via regulating microRNA-22.	The expression of lncRNA H19 was positively correlated with lymph node metastasis and distant metastasis, whereas negatively correlated with the overall survival of HBV-related HCC patients. 	Yes	Results of in vitro experiments showed that lncRNA H19 knockdown significantly downregulated cell proliferation and invasion.	31298392
H19	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Regulation[H19/miR-326 axis]	qRT-PCR	 We found that H19 was significantly elevated and miR-326 was decreased in HCC cells including Hep3B, HepG2, MHCC-97L, SK-hep1, Hun7, SMCC-7721 compared with LO2 cells, respectively. H19 downregulation can increase miR-326 expression in HCC cells. Meanwhile, miR-326 mimics can also inhibit HCC progression, whereas miR-326 inhibitors exhibited a reverse phenomenon by modulating H19 expression. In addition, a negative association between H19 and miR-326 was predicted and confirmed. Furthermore, the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression. Here, by performing bioinformatics analysis, TWIST1 was identified as a downstream target of miR-326. The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR-326 and modulate TWIST1 levels in HCC pathogenesis. Taken these together, these findings indicated that H19/miR-326/TWIST1 axis was involved in HCC development and can indicate a novel HCC target.		Yes	 In the subsequent experiments, we observed that inhibition of H19 can repress HCC cell growth, migration, and invasion in vitro.	30362512
H19	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Regulation[miR-15b/CDC42/PAK1 axis]	IHC//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	H19 and CDC42 were up-regulated while miR-15b was down-regulated in HCC cells and tissues.miR-15b interacted with H19 and CDC42 3'-UTR.  H19 knockdown suppressed CDC42/PAK1 pathway and EMT progress.		Yes	H19 knockdown inhibited proliferation, migration and invasion, and increased apoptosis, which was rescued by miR-15b inhibitor. 	30543848
H19	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 human hepatoma cells	Expression(highly expressed)	CCK8//qRT-PCR//Western Blot	 The NR2F1-AS1 and H19 levels were high in human hepatoma cells, and AUCs of lncRNA NR2F1-AS1 and lncRNA H19 were both >0.8. 	The lncRNA NR2F1-AS1 and lncRNA H19 were associated with HCC staging. 	Yes	After transfection of pcDNA3.1-NR2F1-AS1, si-NR2F1-AS1, NC, pcDNA3.1-H19, si-H19 BEL-7402 and Huh-7 cells, silencing NR2F1-AS1 and H19 expression can promote apoptosis and inhibit cell growth, while silencing their over-expression can inhibit the EMT process of Huh-7 cells.	33568940
H19	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients 	Expression(highly expressed)	qRT-PCR	Circulating lncRNA-H19 levels were significantly increased in HCC patients in both cohorts (p = .013; p < .0001). EpCAM+ CD133+ cells showed a stem cell-like phenotype, self-renewal capacity, upregulation of pluripotent gene expression and overexpressed lncRNA-H19 (p < .001).	In addition, lncRNA-H19 levels increased accordingly with BCLC staging (p < .0001) and decreased after a partial and complete therapeutic response (p < .05). 	Yes	Suppression of lncRNA-H19 by antisense oligonucleotide treatment significantly reduced the self-renewal capacity (p < .001). EpCAM, CD133 and lncRNA-h19 expression increased accordingly with disease progression in HFHCC-fed mice (p < .05) and also in liver tissue from HCC patients (p = .0082).	35243752
H19	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cells	Interaction(microRNA-140/Wnt1 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	H19 expression was upregulated in OC tissues and cells, and its overexpression was associated with a poor prognosis of OC.  H19 upregulated Wnt1 expression through targeting miR-140 in OC cells.	H19 expression was upregulated in OC tissues and cells, and its overexpression was associated with a poor prognosis of OC. 	Yes	si-H19 remarkably reduced OC cell proliferation and migration. H19 upregulated Wnt1 expression through targeting miR-140 in OC cells.	34002485
H19	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC patients and cell lines	Interaction(miR-140-5p/PI3K/AKT signaling pathway)	Western Blot//Wound Healing Assay//Flow Cytometry//MTT//Transwell Assay	H19 was highly expressed while miR-140-5p was lowly expressed in OC patients and cell lines (P < 0.050). Online prediction and dual-luciferase reporter (DLR) confirmed that H19 directly binds miR-140-5p. Western blot assay indicated overexpression activated the PI3K/AKT signaling pathway in OC cells. 		Yes	The proliferation, invasion, migration ability, and epithelial-mesenchymal transition (EMT) of OC cells were reduced after inhibiting H19 expression, and the apoptosis rate was increased. Transfection of cells with miR-140-5p mimics brought opposite effects. 	34250088
H19	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and human OC cell lines	Expression(highly expressed)	qRT-PCR//Wound Healing Assay//Invasion Assay//Transwell Assay	H19 is upregulated remarkably in primary OC tissues and human OC cell lines (OVCAR3, SKOV3, A2780, and Caov-3). 	We found that the median PFS was longer in patients with lower levels of H19 than in those with high levels, suggesting that overexpression of H19 was linked to poor prognosis in OC patients. 	Yes	Intriguingly, the depletion of H19 expression induced by small interfering RNA inhibited the capability of migration and invasion of OC cell lines. Restoration of H19 in OC cell lines significantly increased cell migration and invasion. 	35072217
H19	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissue 	Expression [highly expressed]	qRT-PCR	H19 expression level was significantly higher in bladder cancer tissue compared to adjacent tissues (p< 0.05), and is correlated with advanced clinical stage (p< 0.05). In those metastatic patients, H19 expression level is significantly higher than those without metastasis (p< 0.05). 	H19 expression level was significantly higher in bladder cancer tissue compared to adjacent tissues (p< 0.05), and is correlated with advanced clinical stage (p< 0.05). In those metastatic patients, H19 expression level is significantly higher than those without metastasis (p< 0.05). H19 expression is up-regulated in bladder cancer, and is probably related with cancer clinical stage and metastasis. 	Yes	RNA interference is applied to knockdown H19 expression in bladder cancer cell, and found potentiated E-cadherin expression (p< 0.05), accompanied with weakened metastatic potency (p< 0.05). Cell transfection reveals up-regulation of E-cadherin expression in bladder cancer cells when H19 expression is suppressed, accompanied with weakened metastasis potency.	29614625
H19	LncRNA	Homo sapiens	Osteosarcoma	OS and corresponding normal adjacent tissue	Interaction(miR‑29a‑3p/LASP1  )	qRT-PCR//Wound Healing Assay//Transwell Assay	 H19 was found to be overexpressed in OS compared with corresponding normal adjacent tissue.  In addition, H19 served as a competing endogenous ncRNA targeting microRNA‑29a‑3p and activating LIM and SH3 domain protein 1 and modulating the OS cell phenotype. 		Yes	 In addition, H19 served as a competing endogenous ncRNA targeting microRNA‑29a‑3p and activating LIM and SH3 domain protein 1 and modulating the OS cell phenotype. 	34328197
H19	LncRNA	Homo sapiens	Osteosarcoma	 tumor tissue 	Regulation [ p‑PI3K and p‑AKT]	qRT-PCR//Western Blot	Expression level of H19 was significantly elevated in tumor tissue compared with adjacent healthy tissue. Significantly decreased levels of p‑PI3K and p‑AKT, and elevated level of IκBα were observed in H19 knockdown osteosarcoma cells compared with control osteosarcoma cells, while no significant differences in levels of PI3K and AKT were observed. Therefore, the present study demonstrated that knockdown of lncRNA H19 can inhibit migration and invasion of human osteosarcoma cells by inhibiting the nuclear factor-κB pathway.	Expression level of H19 was positively associated with distant metastasis of osteosarcoma (P<0.01), but not with gender and age. Overall survival of patients with osteosarcoma with high H19 level was significantly shorter compared with patients with low H19 expression (P<0.05). 	Yes	H19 knockdown significantly reduced migration and invasion ability of osteosarcoma cells. 	29568924
H19	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[NF-κB]	Western Blot//CCK8//qRT-PCR//ELISA//Transwell Assay	 H19 expression was upregulated in H. pylori-infected GC tissues and cells.Moreover, H19 overexpression promoted the proliferation, migration and invasion of H. pylori-infected GC cells via enhancing NF-κB-induced inflammation.		Yes	Moreover, H19 overexpression promoted the proliferation, migration and invasion of H. pylori-infected GC cells via enhancing NF-κB-induced inflammation.	31787851
H19	LncRNA	Homo sapiens	Stomach Neoplasms	GC primary tumor and para-cancerous tissues,cell lines(AGS,GES-1)	Regulation[H19/miR‑22‑3p/Snail1 axis  ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results revealed that H19 expression was significantly upregulated, whereas the expression level of miR-22-3p was decreased in the GC tissues compared with the para-cancerous tissues .In summary, these findings provide novel insight into the potential regulatory roles of H19 in GC, and suggest that the H19/miR‑22‑3p/Snail1 axis may prove to be a promising therapeutic target for the treatment of patients with GC.	 	Yes	Furthermore, the downregulation of H19 suppressed the proliferation, invasion, migration and epithelial‑mesenchymal transition of GC cells in vitro and suppressed tumor growth in vivo. 	31081061
H20	LncRNA	Mus musculus	Aortic Aneurysm, Abdominal	AAA tissues	Interaction[H19/let-7a/IL-7]	Western Blot//qRT-PCR//Luciferase Report Assay//ELISA//IHC	 qRT-PCR detected the upregulation of H19 in human and mouse AAA tissue samples.In vivo overexpression of H19 increased vascular inflammation and induced AAA formation, which was supported by exacerbated aortic morphology, maximum aortic diameter values, elastin degradation, expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1), and macrophage infiltration. H19 suppression resulted in the opposite effects. A rescue experiment indicated that IL-6 neutralization significantly mitigated the aortic inflammation and AAA formation evoked by H19 overexpression. Luciferase reporter assays and ex vivo experiments using VSMCs and macrophages confirmed that H19 induced aneurysm formation in part via endogenous competition with the let-7a microRNA to induce the transcription of its target gene, IL-6. This mechanism was further validated by in vivo experiments using a mutant H19 that could not effectively bind let-7a. Collectively, our study revealed a pathogenic H19/let-7a/IL-6 inflammatory pathway in AAA formation, which offers a new potential therapeutic strategy for AAA.		Yes	In vivo overexpression of H19 increased vascular inflammation and induced AAA formation, which was supported by exacerbated aortic morphology, maximum aortic diameter values, elastin degradation, expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1), and macrophage infiltration.	30991034
HAGLR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CESC cells and tissues	Interaction(ELF1/FRRS1)	In Vivo Experiment//Western Blot//Transfection//CCK8//Flow Cytometry//RIP//qRT-PCR//IHC//EdU Staining	HOXD-AS1 and FRRS1 were overexpressed in CESC.  HOXD-AS1 elevated the level of FRRS1 by binding ELF1. Furthermore, HOXD-AS1 contributed to the CESC growth in mouse models. HOXD-AS1 promotes CESC by up-regulating FRRS1 via ELF1.		Yes	After transfection of sh-HOXD-AS1, sh-ELF1 or sh-FRRS1, the proliferation of SiHa and Hela cells was inhibited and their apoptosis was promoted; while HOXD-AS1 overexpression had opposite effects on CESC development.Co-transfection of sh-FRRS1 and pCDNA3.1-HOXD-AS1 could abolish the tumor suppressive effect of FRRS1 knockdown. 	34985386
HAGLR	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cells	regulation[miR-185-5p/CDK4/CDK6 axis]	Western Blot//CCK8//qRT-PCR//EdU Staining//Transwell Assay	Compared with normal colon cancer tissues and cells, the expression of HAGLR was increased in colon cancer tissues and cells. Lnc HAGLR promoted the development of colon cancer by miR-185-5p/CDK4/CDK6 axis, and lnc HAGLR might be potential target for colon cancer.		Yes	 In addition, the expression of HAGLR down-regulation inhibited the growth, migration, and invasion of colon cancer cells.	32606801
HAGLR	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC cells and tissues	Interaction[HOXD-AS1/miR-186-5p/PIK3R3 pathway]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Microarray//Transwell Assay	HOXD-AS1 was found to be significantly over-expressed in EOC tumors. The novel HOXD-AS1/miR-186-5p/PIK3R3 pathway was clinically relevant as we observed a significantly inverse correlation between HOXD-AS1/miR-186-5p and between miR-186-5p/PIK3R3 in an independent cohort of 200 EOC tissues.		Yes	SiRNA inhibition of HOXD-AS1 reduced cell migration, invasion, and epithelial-mesenchymal transition (EMT) in EOC cells in vitro by preventing HOXD-AS1 directly binding to miR-186-5p, and resulting in down-regulating of PIK3R3.	30823895
HAGLR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues,cell lines	Interaction[MEK/ERK pathway]	qRT-PCR//Western Blot	The Cancer Genome Atlas data analysis and experimental validation showed that HOXD-AS1 was increased in HCC tissues/cell lines and positively relevant to histologic grade.  In vitro loss-of-function experiments revealed that silencing of HOXD-AS1 could dramatically suppress the proliferation, migration, and invasion, and induce S or/and G2/M phase cell cycle arrest as well as apoptosis of Bel-7402 and MHCC97H cells accompanying the changes in expression levels of cyclin B1, cyclin D1, BCL-2, BAX, and MMP2. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis indicated that HOXD-AS1 has the potential to affect p53, tumor necrosis factor (TNF), mitogen-activated protein kinase (MAPK) pathway, and Western blot results further validated that HOXD-AS1 silencing could inhibit the MEK/ERK pathway in Bel-7402 cells. Collectively, HOXD-AS1, as an oncogenic lncRNA, might exert crucial functions in HCC progression and serve as a potential diagnostic biomarker and therapeutic target for HCC.		Yes	In vivo assay also showed that HOXD-AS1 silencing could markedly reduce xenograft tumor volume and weight of HCC cells.	31231887
HAGLR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-6785-5p]	qRT-PCR	 It was found that HAGLR level was higher in HCC tissues than paracancerous ones and correlated with rates of lymphatic metastasis and distant metastasis but not with age, gender, and tumor staging in HCC patients.  LncRNA HAGLR stimulates proliferative and metastatic potentials in HCC via negatively regulating miR-6785-5p level, thus exacerbating the development of HCC.	Survival analysis uncovered that HAGLR level was negatively linked to overall survival in HCC.	Yes	After knockdown of HAGLR, proliferative, and metastatic potentials in Bel-7402 and Hub7 cells were attenuated. 	33015776
HAGLR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-326/SLC27A4]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Here, we elaborated that HOXD-AS1 was overexpressed in HCC tissues than that in the adjacent normal tissues and the level of HOXD-AS1 was related with the aggressive phenotypes of HCC. All these findings indicated that HOXD-AS1-miR-326-SLC27A4 axis participated into the progression of HCC.		Yes	 Functionally, downregulation of HOXD-AS1 repressed the proliferation, invasion abilities of HCC cell in vitro and the distant metastasis of HCC cell in vivo.	32425696
HAGLR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells and tissues	Interaction(miR-203a-5p)	ISH//qRT-PCR//Transwell Assay//Western Blot	 HOXD-AS1 overexpression in OSCC predicted poor survival.  HOXD-AS1 was predicted to interact with miR-203a-5p, but its expression was not significantly correlated with miR-203a-5p. HOXD-AS1 overexpression increased Annexin A4 expression, while miR-203a-5p overexpression decreased Annexin A4 expression in OSCC cells. Transwell assays showed that invasion and migration of OSCC cells were enhanced by HOXD-AS1 and Annexin A4 overexpression but were reduced by miR-203a-5p overexpression. In addition, miR-203a-5p overexpression suppressed the role of HOXD-AS1 in cell movement and Annexin A4 expression.	 HOXD-AS1 overexpression in OSCC predicted poor survival. 	Yes	HOXD-AS1 overexpression increased Annexin A4 expression, while miR-203a-5p overexpression decreased Annexin A4 expression in OSCC cells. Transwell assays showed that invasion and migration of OSCC cells were enhanced by HOXD-AS1 and Annexin A4 overexpression but were reduced by miR-203a-5p overexpression. In addition, miR-203a-5p overexpression suppressed the role of HOXD-AS1 in cell movement and Annexin A4 expression.	35152529
HAGLR	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue and cells	interaction[p57,EZH2]	Western Blot//CCK8//qRT-PCR//RIP//Cell Cycle Assay//ChIP	Results revealed that HOXD-AS1 expression level was significantly up-regulated in osteosarcoma tissue and cells, moreover, the aberrant overexpression predicted the poor prognosis of osteosarcoma patients. In conclusion, our study confirmed that HOXD-AS1 could interact with EZH2, and then repress p57 expression, to aggravate osteosarcoma oncogenesis. which provide new idea for the osteosarcoma tumorigenesis.	Results revealed that HOXD-AS1 expression level was significantly up-regulated in osteosarcoma tissue and cells, moreover, the aberrant overexpression predicted the poor prognosis of osteosarcoma patients. 	Yes	 Loss-of-functional experiments indicated that HOXD-AS1 silencing inhibited the osteosarcoma cells proliferation and induced G1/G0 phase arrest in vitro, and repressed tumor cell growth in vivo.	30119259
HAGLR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[miR-877-3p/FGF2 axis]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 HOXD-AS1 was overexpressed in CC tissues and cell lines.HOXD-AS1 functions as a tumor-promoting lncRNA via the miR-877-3p/FGF2 axis in CC.	Its higher level predicted worse prognosis of CC patients.	Yes	SiRNA mediated knockdown of HOXD-AS1 repressed CC cell migration and invasion, and its overexpression did the opposite.	32977766
HAGLR	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells	Interaction(miR-93-5p/SRSF1 axis)	RNA Pull-Down//Western Blot//Tunel//qRT-PCR//FISH//IF//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	HAGLR was found to be highly expressed in TNBC tissues and cells, and inhibiting HAGLR suppressed cell proliferation, migration, and invasion and promoted cell apoptosis in TNBC. Meanwhile, miR-93-5p was shown to bind to HAGLR and SRSF1. In addition, SRSF1 plays an oncogenic role in TNBC. Importantly, HAGLR could activate the Wnt signaling pathway by sponging miR-93-5p to upregulate SRSF1; thus, accelerating TNBC progression.		Yes	HAGLR was found to be highly expressed in TNBC tissues and cells, and inhibiting HAGLR suppressed cell proliferation, migration, and invasion and promoted cell apoptosis in TNBC. 	34128362
HAGLR	LncRNA	Rattus norvegicus	Neuralgia	CCI rats and SH-SY5Y cells 	Interaction(miR-182-5p/ATAT1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//FISH//qRT-PCR//Luciferase Report Assay//ELISA	HAGLR displayed high levels in spinal cords of CCI rats and in LPS treated SH-SY5Y cells.Mechanistically, HAGLR bound with miR-182-5p in SH-SY5Y cells. ATAT1 served as a target of miR-182-5p. HAGLR activated the NLRP3 inflammasome by ATAT1. 		Yes	Knockdown of HAGLR inhibited inflammation and neuron apoptosis of LPS treated SH-SY5Y cells.	33626373
HAGLR	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tumor tissues	Expression [highly expressed]	RNA Pull-Down//Western Blot//Transfection//MeRIP//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Invasion Assay	IGF2BP2 was highly expressed in TC tumor tissues. IGF2BP2 knockdown weakened cell proliferative, migratory, and invasive abilities, and induced cell cycle arrest and cell apoptosis in TC cells. LncRNA HAGLR expression was markedly upregulated and positively associated with IGF2BP2 expression in TC tissues. IGF2BP2 knockdown reduced HAGLR expression and transcript stability in TC cells. 		Yes	HAGLR overexpression weakened the effects of IGF2BP2 loss on cell proliferation, migration, invasion, apoptosis, and cell cycle progression in TC cells. HAGLR overexpression weakened the effects of IGF2BP2 loss on cell proliferation, migration, invasion, apoptosis, and cell cycle progression in TC cells.	34340128
HAGLR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	papillary thyroid cancer tissues and cell lines 	Expression[highly expressed]	qRT-PCR	The results showed HOXD-AS1 is overexpressed in papillary thyroid cancer tissues and cell lines compared with matching nontumor tissue specimens and normal thyroid cell line, respectively.	 High expression of HOXD-AS1 was associated with elderly people, advanced clinical stage, large tumor size, present lymph node metastasis, and distant metastasis.	Yes	The study in vitro suggested reduced HOXD-AS1 expression inhibited papillary thyroid cancer cell proliferation, migration, and invasion, and promoted cell-cycle arrest. 	30317670
HAGLR	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cells	Interaction(miR-664b-3p/PLAC8 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	HOXD-AS1 was significantly upregulated in PC tissues than in paired adjacent tissues.  Mechanically, HOXD-AS1 upregulated PLAC8 by targeting miR-664b-3p. In conclusion, HOXD-AS1 was upregulated in PC tissues, promoting the proliferation, invasion, and migration of PC cells via the miR-664b-3p/PLAC8 axis.	Moreover, HOXD-AS1 was related to the advanced TNM stage.	Yes	 Meanwhile, HOXD-AS1 promoted the proliferation, invasion, and migration of PC cells. 	35279480
HAGLR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Expression[lower expressed]	Western Blot//CCK8//qRT-PCR//FISH//RIP//Microarray	 Here, we reported that HAGLR (also called HOXD-AS1) was frequently down-regulated in lung adenocarcinoma (LUAD) tissues.Mechanistically, HAGLR could physically interact with DNMT1, and recruit DNMT1 on E2F1 promoter to increase local DNA methylation.	 Here, we reported that HAGLR (also called HOXD-AS1) was frequently down-regulated in lung adenocarcinoma (LUAD) tissues, and decreased HAGLR expression was clinically associated with shorter survival of LUAD patients.	Yes	Preclinical studies using multiple LUAD cells and in vivo mouse model indicated that HAGLR could attenuate LUAD cell growth in vitro and in vivo. 	31194977
HAGLR	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	regulation[regulating miR-520c-3p/MYCN]	qRT-PCR//Luciferase Report Assay//RIP//ChIP	In this study, HOXD-AS1 expression was significantly upregulated in CCA tissues and cells compared with control groups, respectively.SP1/HOXD-AS1/miR-520c-3p/MYCN plays a vital role in initiation and progression of CCA, and HOXD-AS1 is expected to be an efficient biomarker and therapeutic target.	 Increased HOXD-AS1 was markedly correlated with lymph node invasion, advanced TNM stage and poor survival of CCA patients.	Yes	 Functionally, gain- and loss-of-function experiments demonstrated that HOXD-AS1 facilitated tumor proliferation, migration, invasion, EMT, stemness and drug resistance in vitro and in vivo. 	32857725
HAGLR	LncRNA	Homo sapiens	Prostatic Neoplasms	 serum exosomes	Interaction(miR-361-5p/FOXM1 axis)	In Vivo Experiment//qRT-PCR	Here, we discovered an exosomal lncRNA HOXD-AS1 is upregulated in castration resistant prostate cancer (CRPC) cell line derived exosomes and serum exosomes from metastatic PCa patients, which correlated with its tissue expression. This sheds a new insight into the regulation of PCa distant metastasis by exosomal HOXD-AS1 mediated miR-361-5p/FOXM1 axis, and provided a promising liquid biopsy biomarker to guide the detection and treatment of metastatic PCa.		Yes	Further investigation confirmed exosomal HOXD-AS1 promotes prostate cancer cell metastasis in vitro and in vivo by inducing metastasis associated phenotype. 	34864822
HAGLR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines 	Regulation[HOXD-AS1-HOXD3-Integrin β3 regulatory axis ]	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//Colony Formation Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//Invasion Assay//ChIP	We observed that HOXD-AS1 was located in the nucleus of CRC cells and that nuclear HOXD-AS1 was downregulated in most CRC specimens and cell lines.Mechanistic investigations revealed that HOXD-AS1 could suppress HOXD3 transcription by recruiting PRC2 to induce the accumulation of the repressive marker H3K27me3 at the HOXD3 promoter. Subsequently, HOXD3, as a transcriptional activator, promoted Integrin β3 transcription, thereby activating the MAPK/AKT signalling pathways.		Yes	HOXD-AS1 downregulation enhanced proliferation and migration of CRC cells in vitro and facilitated CRC tumourigenesis and metastasis in vivo.	30823921
HAGLR	LncRNA	Homo sapiens	Dermatomyositis	DM patients	Interaction(RUNX3/Foxp3)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//H&E Staining	 HAGLR was up-regulated and Foxp3 was down-regulated in DM patients. Besides, RUNX3 protein levels were decreased in DM patients, while its mRNA levels did not change significantly. The proportion of Treg cells was down-regulated in DM patients. In addition, interference with HAGLR could increase the levels of Foxp3, RUNX3 protein level, and the proportion of Treg cells. Besides, there was an interaction between HAGLR and RUNX3. We also found that knockdown of HAGLR and RUNX3 restored the increased Treg cells induced by HAGLR knockdown alone. Interference with HAGLR could increase the protein levels of RUNX3, high levels of RUNX3 further promoted the expression of the Foxp3, thus restoring the number of Treg cells and easing the development of DM.		Yes	In vivo experiments indicated that injection with adv-HAGLR increased Treg cell proportion and attenuated DM development. 	35064420
GNAS-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal carcinoma cells	regulation[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	GNAS-AS1 was upregulated in NPC. GNAS-AS1 exerted its function by regulating Wnt/β-catenin pathway. GNAS-AS1 functioned as an oncogenic role via mediating β-catenin expression.		Yes	GNAS-AS1 promoted cell proliferation, cell migration, and cell invasion in vitro. 	32271425
GNAS-AS1	LncRNA	Homo sapiens	Keloid	keloid clinical tissues and HKF cells	Interaction( miR-188-5p/RUNX2 axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 GNAS-AS1 and RUNX2 expressions were remarkably enhanced, and miR-188-5p expression was decreased in keloid clinical tissues and HKF cells. GNAS-AS1 targeted miR-188-5p to regulate RUNX2 expression. In addition, the inhibition effects of GNAS-AS1 knockdown on HKF cells could be reversed by inhibition of miR-188-5p or overexpression of RUNX2, while RUNX2 overexpression eliminated the suppressive efficaciousness of miR-188-5p mimics on HKF cells growth. GNAS-AS1 knockdown could regulate the miR-188-5p/RUNX2 signaling axis to inhibit the growth and migration in keloid cells. 		Yes	GNAS-AS1 overexpression promoted cells proliferation, migration, and invasion, while GNAS-AS1 knockdown had the opposite trend. Furthermore, overexpression of GNAS-AS1 reversed the inhibitory effect of 5-FU on cell proliferation, migration, and invasion. MiR-188-5p inhibition or RUNX2 overexpression could enhance the proliferation, migration, and invasion of HKF cells. 	36036334
GNAS-AS1	LncRNA	Homo sapiens	Breast Neoplasms	ER+ breast cancer tissues and cell lines	regulation[miR-433-3p/GATA3 axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Transwell Assay	 The expression of GNAS-AS1 was obviously increased in ER+ breast cancer tissues and cell lines, as well as M2 macrophages. GNAS-AS1/miR-433-3p/GATA3 axis promoted proliferation, metastasis of ER+ breast cancer cells by accelerating M2 macrophage polarization. 		Yes	 GNAS-AS1 facilitated the capabilities of proliferation, migration and invasion of ER+ breast cancer cells by accelerating M2 macrophage polarization via directly sponging miR-433-3p.	32538432
GAS5	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial carcinoma tissue	Regulation[GAS5/miR-222-3p/p27 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	In this work, we found that lncRNA GAS5 was under-expressed in the endometrial carcinoma tissue specimens, especially these samples with type 2 diabetes mellitus. In conclusion, these results confirmed the vital regulation of GAS5/miR-222-3p/p27 axis in the endometrial carcinoma tumorigenesis.	Besides, the aberrant under-expression of GAS5 was correlated with the advanced tumor stage as well as poor prognosis outcome.	Yes	Enforced GAS5 expression repressed the tumor phenotype of endometrial carcinoma cells, including proliferation and invasion.	31105847
GAS5	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	regulation[ miR-23a-3p/PTEN/PI3K/AKT Pathway]	qRT-PCR//RNA Pull-Down//RIP	In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells.In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.		Yes	Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. 	33121268
GAS5	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-663a/RHOB axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The GAS5 expression level was significantly decreased in OS tissues and cells compared with normal tissues and cells, and could negatively regulate miR-663a expression.To sum up, we showed lncRNA GAS5 regulates OS progression via regulating the miR-663a/RHOB axis.		Yes	Overexpression of GAS5 and RHOB suppresses, while overexpression of miR-663a stimulates, OS cell proliferation, migration, and invasion in vitro. 	32982421
GAS5	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Expression[highly expressed]	CCK8//qRT-PCR//EdU Staining//Western Blot	The expression of GAS5 was decreased and methylation state of GAS5 was elevated in cervical cancer.		Yes	Overexpression of GAS5 inhibited proliferation, cell cycle progression, invasion, migration while inducing apoptosis of cervical cancer cells as well as suppressed tumor growth and metastasis in nude mice. 	31206689
GAS5	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Expression[lower expressed]	qRT-PCR//Transwell Assay	The results showed that GAS5 was significantly (p < 0.05) downregulated in human cervical cancer tissues.		Yes	The transwell assays showed that GAS5 overexpression significantly (p < 0.05) inhibited the migration and invasion of the C33A and HeLa cervical cancer cells. 	32105659
GAS5	LncRNA	Homo sapiens	Glioma		Regulation[miR-18a-5p]	ISH//qRT-PCR	Taken together, our findings suggest that GAS5 is a tumor suppressor in human gliomas that acts in part by repressing miR-18a-5p.		Yes	In this study, we demonstrated that overexpression of GAS5 inhibits malignant phenotypes in glioma cells, including proliferation, migration, and invasion, whereas GAS5 knockdown enhances these phenotypes.	30078184
GAS5	LncRNA	Homo sapiens	Glioma	glioma tissues	interaction[targeting microRNA-106b ]	Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Significant higher expression of miR-106b, and lower expression of GAS5 and PTEN in the glioma tissues were observed. GAS5 could regulate the EMT process, and the migration of gliomas cells through miR-106b targeting PTEN. 		Yes	 GAS5 could regulate the expression of PTEN through targeting miR-106b, and further influence EMT process, and the proliferation, migration, and invasion of gliomas cells. 	32991951
GAS5	LncRNA	Homo sapiens	Glioma	glioma cells	regulation[GAS5/miR-424 signaling]	Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	GAS5 and miR-424 were significantly down-regulated in glioma cells.GAS5, by inhibiting methylation and boosting expression of miR-424, inhibits AKT3 signaling and suppresses multiple malignant phenotypes.		Yes	Functionally, GAS5, by up-regulating miR-424, inhibited cell proliferation, migration, and invasion, while increased apoptosis of glioma cells in vitro, and suppressed xenograft growth in vivo.	32472311
GAS5	LncRNA	Homo sapiens	Glioma	GSCs, glioma tissues	Interaction(miR-23a/E-cadherin axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In these, it was found that the lncRNA growth arrest-specific 5 (GAS5) expression was downregulated in GSCs and high-grade glioma tissues, compared with normal human astrocyte cells (NHAs) and normal brain tissues, respectively, which also showed a positive correlation with patient survival. Mechanistically, GAS5 directly sponged miR-23a, which in turn functioned as an oncogene by inhibiting E-cadherin, through the assays of reverse transcription-quantitative PCR (RT-qPCR) and luciferase reports. In addition, rescue experiments demonstrated that GAS5 could promote the expression and function of E-cadherin in a miR-23a-dependent manner.	In these, it was found that the lncRNA growth arrest-specific 5 (GAS5) expression was downregulated in GSCs and high-grade glioma tissues, compared with normal human astrocyte cells (NHAs) and normal brain tissues, respectively, which also showed a positive correlation with patient survival. 	Yes	 Functional assays revealed that knocking down GAS5 expression promoted the proliferation, invasion, migration, stemness, and tumorigenicity of GSGs, while suppressing their apoptosis. 	36460802
GAS5	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC  tissue	Interaction[silencing PTEN via EZH2]	RNA Pull-Down//ChIP//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	 Our results indicated that GAS5 expression was elevated in NPC tissues and cells. Moreover, GAS5 could epigenetically suppress PTEN expression via recruiting enhancer of zeste homolog 2 (EZH2). PTEN knockdown could reverse the inhibitory effect of GAS5 inhibition on NPC progression. Furthermore, GAS5 knockdown suppressed the tumor growth in vivo. In summary, knockdown of GAS5 repressed proliferation, migration and invasion, and promoted apoptosis in NPC through epigenetically silencing PTEN via recruiting EZH2.		Yes	GAS5 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NPC cells. 	35527982
GAS5	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal carcinoma tissues and cells	regulation[GAS5/miR-4465 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	We observed that the expression of lncRNA GAS5 was upregulated in nasopharyngeal carcinoma tissues and cells.The GAS5/miR-4465/COX2 axis in nasopharyngeal carcinoma pathogenesis was confirmed, which would provide a new therapeutic target for nasopharyngeal carcinoma.		Yes	Down-regulation of lncRNA GAS5 inhibited the proliferation and promoted apoptosis of nasopharyngeal carcinoma cells.	33092435
GAS5	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues	Regulation(hsa-miR-1297)	CCK8//qRT-PCR//Luciferase Report Assay//cell invasion assay//Bioinformatics Analysis	"Compared to the adjacent nontumor tissues and the normal human intrahepatic biliary epithelial cell, the expression of GAS5 was markedly increased in CCA tissues (p<0.001) and cell lines (p<0.01), respectively. CCA patients with high GAS5 expression tended to present lymph node metastasis (p<0.001) and had advanced clinical stage (p=0.006). The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. In addition, the function study showed that GAS5 acted as a ""sponge"" to downregulate hsa-miR-1297, thus modulating CCA cell proliferation and invasion."	Compared to the adjacent nontumor tissues and the normal human intrahepatic biliary epithelial cell, the expression of GAS5 was markedly increased in CCA tissues (p<0.001) and cell lines (p<0.01), respectively. CCA patients with high GAS5 expression tended to present lymph node metastasis (p<0.001) and had advanced clinical stage (p=0.006). The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. 	Yes	 The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. 	33790648
GAS5	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissue,cell lines	Interaction[miR-21 ]	CCK8//qRT-PCR//Western Blot	This study demonstrated that GAS5 was significantly downregulated in LSCC tissue and human LSCC cell lines.GAS5 suppresses LSCC progression through the negative regulation of miR-21 and its targets involved in cell proliferation and apoptosis, indicating that GAS5 may serve as a biomarker and potential target for LSCC therapy.		Yes	 In addition, the ectopic expression of GAS5 significantly inhibited cell proliferation and promoted apoptosis. 	31572003
GAS5	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LSCC cell lines	Interaction(miR-26a-5p/ULK2)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	The expression level of GAS5 was frequently decreased in LSCC cell lines, and up-regulated GAS5 inhibited AMC-HN-8 cells viability and induced apoptosis. While down-regulated GAS5 had opposite results in Tu 177 cells, GAS5 was found to act as a microRNA sponge in a pathway to regulate miR-26a-5p and its target gene ULK2. 		Yes	 The expression level of GAS5 was frequently decreased in LSCC cell lines, and up-regulated GAS5 inhibited AMC-HN-8 cells viability and induced apoptosis. More importantly, we found that GAS5 activated autophagy, with enhanced autophagy-related proteins after GAS5 overexpression.	33551645
GAS5	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cells	Expression[lower expressed]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	GAS5 was down-regulated in PCa tissues and cells. 		Yes	GAS5 overexpression suppressed cell viability and migration while facilitated radiosensitivity of PCa cells.	33061579
GAS5	LncRNA	Homo sapiens	Melanoma	melanoma tissues	regulation[EZH2,CDKN1C]	qRT-PCR//RNA Pull-Down//RIP	High expression of EZH2 and poor expression of lncRNA GAS5 and CDKN1C was observed in melanoma tissues and found to be correlated with the reduction in survival expectancy of melanoma patients.The evidence provided by our study highlighted the involvement of lncRNA GAS5 in the translational suppression of EZH2 as well as the upregulation of CDKN1C, resulting in the promotion of melanoma cell apoptosis and oxidative stress.		Yes	Overexpression of lncRNA GAS5 or CDKN1C or EZH2 knockdown could inhibit cell viability but enhance melanoma cell apoptosis and oxidative stress. 	32308561
GAS5	LncRNA	Homo sapiens	Endometrial Neoplasms	 EC tissues and TAM	Interaction( miR-21-PTEN-AKT AND YAP1)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//IHC	Quantitative PCR results showed that GAS5 expression decreased in EC tissues and primary TAMs from EC tumors. These antitumor effects of GAS5 on TAMs were mediated by the activation of the miR-21-PTEN-AKT pathway and inhibition of YAP1.		Yes	"Direct coculture of GAS5-overexpressing TAMs and EC cells showed that GAS5 enhanced phagocytosis, antigen presentation, and activation of cytotoxic T cells, and repressed ""Don't eat me"" signals between TAMs and EC cells.  Tumor formation in immunodeficient mice showed that GAS5-overexpressing macrophages could repress EC formation in vivo."	35534987
GAS5	LncRNA	Homo sapiens	Liver Neoplasms	cell lines	Interaction[ miR-544/RUNX3]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//ELISA	Compared with a control group, lncRNA GAS5, RUNX3, and NCR1 were down-regulated in NK cells of patients with liver cancer, whereas miR-544 expression was up-regulated in NK cells of patients with liver cancer.Activated NK cells had higher IFN-γ level. Knockdown of GAS5 in activated NK cells decreased IFN-γ secretion, NK cell cytotoxicity, the percentage of CD107a+ NK cells, and the apoptosis rate of HepG2 and Huh7 cells. We also proved the interaction of GAS5 and miR-544, and the negative regulation role of GAS5 on miR-544. GAS5 overexpression in activated NK cells increased RUNX3 expression, IFN-γ secretion, the NK cell cytotoxicity, the percentage of CD107a+ NK cells, and the apoptosis rate of HepG2 cells, while miR-544 mimic abolished the promotion effect of GAS5 overexpression.		Yes	Finally, in vivo experiments indicated an inhibition effect of GAS5 in tumor growth. 	30774011
GAS5	LncRNA	Homo sapiens	Laryngeal Neoplasms	40 paired laryngeal cancer tissues and adjacent normal tissues	Interaction(PI3K/AKT/mTOR Signaling Pathway)	Western Blot//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Transwell Assay	In the current study, lncRNA GAS5 was downregulated in laryngeal cancer tissues and its low expression was closely associated with poor tumor differentiation, advanced TNM stage, lymph node metastasis, and shorter overall survival time. Mechanistically, our data showed that the overexpression of lncRNA GAS5 significantly regulated the PI3K/AKT/mTOR signaling pathway.	In the current study, lncRNA GAS5 was downregulated in laryngeal cancer tissues and its low expression was closely associated with poor tumor differentiation, advanced TNM stage, lymph node metastasis, and shorter overall survival time. 	Yes	 In addition, lncRNA GAS5 upregulation significantly inhibited laryngeal cancer cell proliferation both in vitro and in vivo. Moreover, in response to lncRNA GAS5 overexpression, more laryngeal cancer cells were arrested at the G2/M stage, accompanied by increased cell apoptosis rates and suppressed migration and invasion capacities.	33641529
GAS5	LncRNA	Homo sapiens	Osteosarcoma	Osteosarcoma tissue,cell lines	Interaction[CtBP1-HDAC1/2-IRF1 ]	Western Blot//Co-IP//qRT-PCR//MTT//Microarray//ChIP	Here, we discovered that GAS5 was downregulated in cancerous osteosarcoma tissues and cells. 		Yes	Specifically, GAS5 overexpression in the U2OS osteosarcoma cell line induced TP53, Bax and Bim levels but inhibited DDB2, TGFB and ROS1 expression, resulting in the inhibition of cell proliferation, invasion, colony formation and in vivo tumor formation. 	31337976
GAS5	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cell lines(HSC3, HSC6, SCC15, SCC25, UM1, and Cal-27)	Regulation[miR-21/PTEN axis]	qRT-PCR//Wound Healing Assay//Transwell Assay	Among the tested OSCC cells, GAS5 were relatively highly expressed in HSC6 and SCC25 cells, while low expressed in SCC15 and UM1 cells (Fig. 1A). Furthermore, miR-21 overexpression reversed the effect of GAS5. Western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki-67 were up-regulated, indicating enhanced proliferation. E-cadherin was down-regulated, while N-cadherin, vimentin, and snail1 were increased, indicating augmented epithelial-mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR-21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition in OSCC through the miR-21/PTEN axis and might be a novel therapeutic target for OSCC.		Yes	qRT-PCR, cell viability, wound-healing, and transwell assays showed that knockdown of GAS5 increased miR-21 expression and promoted proliferation, migration, invasion, and epithelial-mesenchymal transition of OSCC cells.In contrast, overexpression of GAS5 showed the opposite effects.	30576678
GAS5-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-106b-5p/TUSC2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	GAS5-AS1 expression was downregulated in glioma tissues and cells, and upregulation of GAS5-AS1 expression inhibited glioma cell proliferation, migration, and invasion. GAS5-AS1 expression was correlated with the glioma tumor grade.In summary, lncRNA GAS5-AS1 inhibited glioma proliferation, migration, and invasion by sponging miR-106b-5p and regulating the expression of TUSC2. 		Yes	GAS5-AS1 expression was downregulated in glioma tissues and cells, and upregulation of GAS5-AS1 expression inhibited glioma cell proliferation, migration, and invasion. GAS5-AS1 expression was correlated with the glioma tumor grade. In nude mice, upregulation of GAS5-AS1 markedly suppressed glioma tumor growth.	32072565
GAS5	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	50 pairs of BC tissues 	Interaction(miR-18a-5p/AXIN2/GSK3β axis)	qRT-PCR//FISH	We analyzed the expression of GAS5 in 50 pairs of BC tissues and found that GAS5 was low expressed in BC tissues compared with normal mucosal tissues. Chromatin isolation by RNA purification (ChIRP), RNA immunoprecipitation (RIP) and luciferase assay demonstrated the target binding relationship of GAS5 with miR-18a-5p. Rescue experiments demonstrated that GAS5 promoted the proliferation and migration of BC cells through target binding of miR-18a-5p. Moreover, miR-18a-5p bound to its targets AXIN2 and GSK3β, which in turn affected the expression of Wnt/β-catenin pathway-related proteins. 		Yes	In vitro and in vivo experiments showed that GAS5 could affect the proliferation and migration of BC cells.	36331809
GAS5	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines	Interaction[Akt/mTOR pathway]	qRT-PCR//Luciferase Report Assay	Herein, the decreased GAS5 and increased miRNA-106a-5p levels were observed in GC and cell lines. Taken together, our findings conclude the GAS5 overexpression suppresses tumorigenesis and development of gastric cancer by sponging miR-106a-5p through the Akt/mTOR pathway.		Yes	Functional experiments showed that GAS5 overexpression suppressed GC cell proliferation, migration and invasion capabilities, and promoted apoptosis, while miRNA-106a-5p overexpression inverted the functional effects induced by GAS5 overexpression. In vivo, GAS5 overexpression inhibited tumor growth by negatively regulating miRNA-106a-5p expression.	31182630
GAS5	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric cancer tisssues, cell lines	interaction[p53 ]	ISH//qRT-PCR//RNA Pull-Down//RIP	GAS5 expression was markedly decreased in GC tissues and cell lines, and its low expression was strongly related to GC metastasis and unsatisfactory prognosis.	GAS5 expression was markedly decreased in GC tissues and cell lines, and its low expression was strongly related to GC metastasis and unsatisfactory prognosis.	Yes	GAS5 overexpression repressed GC cell migration and invasion by targeting p53.	31530437
GAS5	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	regulation[ miR-21]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 GAS5 was low expression and miR-21 was high expression in gastric cancer tissues and cells.miR-21 is a GAS5 target and GAS5 inhibits the proliferation of gastric cancer cells by targeting miR-21.		Yes	GAS5 overexpression reduced the proliferation, migration, and invasion of gastric cancer cells and increased the apoptosis of gastric cancer cells. 	31910411
GAS5	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines	Interaction(miR-34c )	Bioinformatics Analysis	 We revealed that lncRNA GAS5 regulates miR-34c by targeting E2F1. Additionally, we found that lncRNA GAS5, independently of p53, inhibits GC proliferation through the ATM/p38 MAPK signaling pathway. Accordingly, our results support that E2F1 is an engaging target of drug development in tumor growth and aggressive proliferation of GC, and favorable results can be achieved through tumor suppressor lncRNA GAS5/miR-34c axis in GC.		Yes	 We revealed that lncRNA GAS5 regulates miR-34c by targeting E2F1. Additionally, we found that lncRNA GAS5, independently of p53, inhibits GC proliferation through the ATM/p38 MAPK signaling pathway. Accordingly, our results support that E2F1 is an engaging target of drug development in tumor growth and aggressive proliferation of GC, and favorable results can be achieved through tumor suppressor lncRNA GAS5/miR-34c axis in GC.	36316351
GAS5	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[regulating miR-216b]	qRT-PCR//Luciferase Report Assay//Transwell Assay	 Compared with paracancerous tissues, in breast cancer tissues, the expression of GAS5 was increased and the expression of miR-216b was decreased. GAS5 can target on miR-216b to regulate the biological behavior and epithelial-mesenchymal transition of breast cancer cells.	 The expression of GAS5 in the tissues with lymph node metastasis of breast cancer was markedly increased. 	Yes	The inhibition of GAS5 can promote the apoptosis of breast cancer cells; GAS5 can specifically bind to the 3' UTR of miR-216b.	32432750
GAS5	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-221-3p/IRF2 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	GAS5 expression was down-modulated in NSCLC tissues and cell lines. GAS5 overexpression restrained the proliferation, migration and invasion of NSCLC cells, while miR-221-3p, which was targeted and negatively modulated by GAS5, worked oppositely. Restoration of miR-221-3p markedly reversed the effects of GAS5 on NSCLC cells. Additionally, GAS5 increased IRF2 expression in NSCLC cells by repressing miR-221-3p.		Yes	GAS5 overexpression restrained the proliferation, migration and invasion of NSCLC cells, while miR-221-3p, which was targeted and negatively modulated by GAS5, worked oppositely. Restoration of miR-221-3p markedly reversed the effects of GAS5 on NSCLC cells. 	34022918
GAS5	LncRNA	Homo sapiens	Lung Neoplasms	cell lines	Regulation[miR-205/PTEN Axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	The results indicated that GAS5 was drastically downregulated in lung cancer cell lines.The luciferase reporter assays determined that miR-205 was a direct target of GAS5 in lung cancer. Moreover, the Phosphatase and tensin homologue (PTEN) was known as a direct target of miR-205 and miR-205/PTEN rescued the effects of GAS5 in NSCLC cells. CONCLUSIONS To sum up, our results illustrate that upregulation of GAS5 in NSCLC suppresses its growth, migration, and invasion via the miR-205/PTEN axis.		Yes	Further functional analysis showed that down-expression of GAS5 remarkably induced NSCLC growth, migration, and invasion. 	30926767
GAS5	LncRNA	Homo sapiens	Lung Neoplasms	cell line	Regulation	qRT-PCR//IHC//Western Blot//Transwell Assay	Cell invasion and migration were inhibited markedly in GAS5 overexpressed cell line. Cell cycle results indicated that the percentage of S-phase cells was increased,and G2-phase was reduced in the GAS5 overexpression cell line. Tumor size was suppressed obviously after GAS5 overexpression treatment. GAS5 markedly inhibited the expression of E-cadherin and induced the expression of N-cadherin. GAS5 overexpression significantly inhibited lung cancer cell proliferation by increasing the E-cadherin and decreasing N-cadherin. 		Yes	Cell invasion and migration were inhibited markedly in GAS5 overexpressed cell line. Cell cycle results indicated that the percentage of S-phase cells was increased,and G2-phase was reduced in the GAS5 overexpression cell line. Tumor size was suppressed obviously after GAS5 overexpression treatment. GAS5 markedly inhibited the expression of E-cadherin and induced the expression of N-cadherin. GAS5 overexpression significantly inhibited lung cancer cell proliferation by increasing the E-cadherin and decreasing N-cadherin. 	33976738
GAS5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//Western Blot	Initially, poor expression of GAS5 was observed in CRC tissues and cells.Taken together, the results of the study conclude that lncRNA GAS5 inhibited the activation of the Wnt/β-catenin signaling pathway, thereby suppressing the angiogenesis, invasion, and metastasis of CRC.		Yes	Upregulated GAS5 repressed CRC cell invasion and migration in vitro, as well as subcutaneous tumor growth, angiogenesis, and liver metastases in vivo.	30672001
GAS5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC patients and cell lines	Interaction(miR‑34a/mTOR/SIRT1 pathway )	qRT-PCR//Western Blot	Our results suggested that GAS5 was downregulated and acted as a molecular sponge of miR‑34a during CRC progression. miR‑34a participated in regulating GAS5‑suppressed CRC cell macroautophagy and induced apoptosis through the mTOR/SIRT1 pathway. Our results suggested that the GAS5/miR‑34a/SIRT1/mTOR negative regulatory feedback loop mediated CRC cell macroautophagy, and maintained the cells in an autonomous equilibrium state, but not excessive activation state, which functions as a strong antiapoptotic phenotype during human CRC progression.		Yes	 GAS5‑mediated macroautophagy was maintained in an equilibrium state that might have a protective effect on CRC cell apoptosis. The mTOR signaling pathway suppressed GAS5 expression and formed a negative regulation feedback loop with miR‑34a in CRC cells. 	33416133
GAS5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-10b)	CCK8//qRT-PCR	The expression of GAS5 was downregulated in CRC tissues and cell lines. The overexpression of GAS5 can inhibit cell proliferation and progression, induce apoptosis in vitro, and inhibit the growth of CRC tumor in vivo. 		Yes	The overexpression of GAS5 can inhibit cell proliferation and progression, induce apoptosis in vitro, and inhibit the growth of CRC tumor in vivo. 	35103069
GAS5	LncRNA	Homo sapiens	Colorectal Neoplasms	tumor tissues and CRC cells	Interaction(miR-21/LIFR Axis)	Transwell Assay//qRT-PCR//Luciferase Report Assay//Western Blot	 GAS5 was significantly decreased in tumor tissues and CRC cells, and the low expression of CAS5 in CRC promoted tumor metastasis and decreased the survival of patients.Furthermore, GAS5 increases the expression level of target gene LIFR to promote the apoptosis of CRC cells by binding to miR-21. 		Yes	 GAS5 knockdown increases the cell viability, inhibits apoptosis, and promotes migration. Xenografted tumors in nude mice studies showed that GAS5 knockdown promoted tumor growth and caused worse lesions in colorectal.	36062165
GAS5	LncRNA	Homo sapiens	Colorectal Neoplasms	HCT116 cells	Interaction(miR-21/PTEN/Akt axis)	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	These results indicated that inhibition of GAS5 up regulated the expression level of miR-21, promoted cell proliferation, invasion and migration, decreased G(1)-phase cells and increased S-phase cells, and suppressed cell apoptosis (P<0.05). Moreover, inhibition of GAS5 up regulated the expressions of Snail, N-cadherin, vimentin, Sox2, CD44, Oct2 and p-Akt in HCT-116 cells (P<0.05), while down regulated the expressions of E-cadherin and PTEN (P<0.05). Inhibition of miR-21 reversed the impact of GAS5 knockdown on PTEN/Akt signaling pathway (P<0.05). 		Yes	These results indicated that inhibition of GAS5 up regulated the expression level of miR-21, promoted cell proliferation, invasion and migration, decreased G(1)-phase cells and increased S-phase cells, and suppressed cell apoptosis (P<0.05). Moreover, inhibition of GAS5 up regulated the expressions of Snail, N-cadherin, vimentin, Sox2, CD44, Oct2 and p-Akt in HCT-116 cells (P<0.05), while down regulated the expressions of E-cadherin and PTEN (P<0.05). Inhibition of miR-21 reversed the impact of GAS5 knockdown on PTEN/Akt signaling pathway (P<0.05). 	36380665
GAS5	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cells	Regulation(IFN/STAT1)	CCK8//qRT-PCR//Colony Formation Assay	 The results showed that upregulation of GAS5 significantly inhibited papillary thyroid cancer cell growth, migration and invasion in vitro. RNA transcriptome sequencing was performed to explore the underlying targets of GAS5. 	In this study, we confirmed a negative correlation between the GAS5 expression level and papillary thyroid carcinoma clinicopathologic characteristics, such as the tumor size, lymph node metastasis, the TNM stage and BRAFV600E mutation. 	Yes	 The results showed that upregulation of GAS5 significantly inhibited papillary thyroid cancer cell growth, migration and invasion in vitro. RNA transcriptome sequencing was performed to explore the underlying targets of GAS5. 	35366462
GAS5	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue	Interaction[Sponging miR-135b]	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	 Decreased GAS5 and increased miR-135b in HCC inversely correlate with each other and both correlate with poor prognosis of HCC patients.Mechanistically, GAS5 is a target of miR-135b. Furthermore, GAS5 positively regulates expression of RECK, also a target of miR-135b, which further inhibits MMP-2 expression and contributes to invasion repression.		Yes	Functionally, GAS5 suppresses while miR-135b promotes HCC cell invasion capacities in vitro.	30733959
GAS5	LncRNA	Homo sapiens	Ovarian Neoplasms	OA tissues 	interaction[miR-196a-5p,HOXA5 ]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	LncRNA GAS5 depressed OA development by targeting miR-196a-5p and thereby down-regulating HOXA5 expression, providing substance for developing lncRNA-based strategies to treat OA.	Lower GAS5 expression and higher miR-196a-5p expression were associated with larger tumor size (≥5 cm) and more advanced FIGO stage (III-IV) of OA patients (P < 0.05).	Yes	Transfection of si-GAS5, miR-196a-5p mimic or si-HOXA5 conferred OA cells with stronger viability, faster proliferation and smaller percentage of apoptosis (P < 0.05). After injecting mice models with si-GAS5, miR-196a-5p mimic or si-HOXA5, a larger tumor size was also observed within the rats (P < 0.05). 	30201235
GAS5	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Regulation[GAS5/miR-21/SPRY2 signaling pathway]	qRT-PCR//MTT//Western Blot	It was identified that the expression levels of GAS5 and Sprouty homolog 2 (SPRY2) were significantly downregulated, while the expression level of microRNA (miR)-21 was significantly upregulated in ovarian cancer tissues and cell lines compared with adjacent non-tumor tissues and normal ovarian epithelial cells, respectively.Luciferase assay data indicated that miR-21 was a direct target of GAS5 and that SPRY2 was a target gene of miR-21 in ovarian cancer-derived A2780 cells. 		Yes	 GAS5 overexpression significantly inhibited the proliferation of ovarian cancer cells, which was accompanied by the downregulation of miR-21 and the upregulation of SPRY2.	29896229
GAS5	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC samples and cell lines	Interaction(miR-96-5p/PTEN axis)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	Our results demonstrated decreased expression levels of GAS5 and PTEN in OC samples and cell lines, while miR-96-5p was up-regulated when compared with the controls. GAS5 overexpression could significantly reduce OC cell proliferation and invasion ability via suppression of miR-96-5p expression. Moreover, GAS5 could influence the PTEN/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway.		Yes	GAS5 overexpression could significantly reduce OC cell proliferation and invasion ability via suppression of miR-96-5p expression. 	35071464
GAS5	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder tissues	regulation[ miR-21 and PTEN]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	The expression level of GAS5 was decreased and that of miR-21 was increased, indicating a negative correlation between the two.  GAS5 could exert antiproliferative and proapoptotic effects on bladder cancer cells through miR-21 and PTEN.	Patients with high GAS5 level and low miR-21 level had relatively longer survival rates.	Yes	GAS5 inhibited bladder cancer cells proliferation and promoted apoptosis, and miR-21 had the opposite effects. 	32069387
GAS5	LncRNA	Homo sapiens	prostate carcinoma	Tumor tissue and adjacent healthy tissue	Interaction[Interact with MicroRNA-145]	CCK8//qRT-PCR	In the present study, miR-145 and lncRNA GAS5 expression levels were demonstrated to be Expression[down-expression]regulated in tumor tissues compared with adjacent healthy tissues of patients with prostate carcinoma. miR-145 and lncRNA GAS5 expression levels were found to be positively and significantly correlated in tumor tissues, but not in adjacent healthy tissues.		Yes	Overexpression of miR-145 and lncRNA GAS5 promoted apoptosis and inhibited cell proliferation in prostate carcinoma cell lines, whereas lncRNA GAS5 knockExpression[down-expression] had an opposite effect. In addition, lncRNA GAS5 knockExpression[down-expression] partially attenuated the effect of miR-145 overexpression of cancer cell proliferation and apoptosis. Therefore, miR-145 may inhibit cell proliferation and induce apoptosis in human prostate carcinoma by Expression[Expression[up-expression]-expression]regulating lncRNA GAS5.	31423164
GAS5	LncRNA	Homo sapiens	Myocardial Infarction	post-MI myocardial cells	Regulation[miR-525-5p/CALM2 axis]	Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	 Our data showed that the expression of GAS5 and CALM2 in PMMC was significantly upregulated, while the expression of miR-525-5p was downregulated.These data suggested that lncRNA GAS5 promoted the development and progression of MI via targeting of the miR-525-5p/CALM2 axis and it has the potential to be explored as a therapeutic target for the treatment of MI in the future.		Yes	Overexpression of GAS5 and CALM2 profoundly promoted the apoptosis of myocardial cell. However, the proliferation of myocardial cell was inhibited by the upregulation of GAS5 and CALM2. 	31429119
GAS5	LncRNA	Homo sapiens	Sepsis	THP-1 cells	Interaction(miR‑23a‑3p/TLR4 )	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//ELISA//Bioinformatics Analysis	The results revealed that LPS increased the expression of GAS5 in THP-1 cells, and GAS5 knockdown effectively inhibited inflammation and cell apoptosis in the LPS?induced sepsis model. In addition, the results of the luciferase reporter assays indicated that both GAS5 and TLR4 directly target miR‑23a‑3p. 		Yes	The results revealed that LPS increased the expression of GAS5 in THP?1 cells, and GAS5 knockdown effectively inhibited inflammation and cell apoptosis in the LPS?induced sepsis model. 	33982771
GAS5	LncRNA	Homo sapiens	Hepatoblastoma	HCC tissues and cells	Interaction( CHOP signal pathway)	In Vivo Experiment//IHC//Western Blot//RIP//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay	Lower expression levels of Gas5 were determined in HCC tissues and cells by quantitative reverse transcription-polymerase chain reaction.78 kDa glucose-regulated protein (GRP78) was identified as a direct target of Gas5 by Rip-qPCR and Western blot analysis assay. Further studies indicated that the knockdown of CHOP by shRNA partially reversed Gas5-mediated apoptosis in HepG2 cells.		Yes	Overexpressed Gas 5 lentiviral vectors were constructed to analyze their influence on cell viability, migration, invasion, and apoptosis. Gas5 inhibited HepG2 cell growth and induced cell apoptosis via upregulating CHOP to activate the ER stress signaling pathway. Magnetic resonance imaging showed that the ectopic expression of Gas5 inhibited the growth of HCC in nude mice. 	34636091
Gas5	LncRNA	Mus musculus	Diabetic Cardiomyopathies	 heart tissues	interaction[miR-34b-3p/AHR]	qRT-PCR//ELISA//Luciferase Report Assay//Western Blot	Compared with normal mice, GAS5 was severely down-regulated in heart tissues of DCM mice.In summary, our study demonstrates that GAS5 acts as a competing endogenous RNA to enhance AHR expression by sponging miR-34b-3p, which consequently represses NLRP3 inflammasome activation-mediated pyroptosis to improve DCM. 		Yes	GAS5 overexpression improved cardiac function and myocardial hypertrophy in DCM mice. 	33092444
Gas5	LncRNA	Mus musculus	renal fibrosis	renal tissues	Interaction[miR-96-5p]	qRT-PCR	In this study, the lncRNA GAS5 was upregulated in both TGF-β1-treated HK-2 cells and the kidneys of HDF/STZ mice.Knockdown of GAS5 relieved renal tubular epithelial fibrosis. This effect was mediated by the downregulation and functional inactivation of miR-96-5p. Furthermore, miR-96-5p was downregulated in DKD mice, and this downregulation attenuated the repression of FN1(fibronectin, FN) and led to its upregulation. The decrease in miR-96-5p was partially attributed to the miRNA-sponge action of GAS5.Our research demonstrates that knockdown of lncRNA GAS5 leads to antifibrosis by competitively binding miR-96-5p, which inhibits the expression of FN1. These results indicate that targeting lncRNA GAS5 may be a promising therapeutic strategy for preventing DKD.		Yes	Knockdown of GAS5 relieved renal tubular epithelial fibrosis. 	31810140
Gas5	LncRNA	Mus musculus	Non-alcoholic Fatty Liver Disease	HFD mice	Interaction(microRNA-29a-3p/NOTCH2 axis)	In Vivo Experiment//Western Blot//Transfection//RIP//qRT-PCR//Luciferase Report Assay//RNA-seq//H&E Staining//Oil Red O Staining//ELISA//IHC	We showed that NAFLD activity score was elevated in the HFD mice. Moreover, GAS5 overexpression enhanced NOTCH2 levels in liver cells and promoted NAFLD progression by sponging miR-29a-3p in vivo. Furthermore, miR-29a-3p inhibited NAFLD progression by targeting NOTCH2 in vivo. 		Yes	GAS5 knockdown attenuated HFD-induced hepatic steatosis and lipid accumulation and reduced NAFLD activity score in HFD mice. In addition, GAS5 knockdown reduced serum triglyceride cholesterol levels and inhibited alanine aminotransferase and aspartate aminotransferase activities in HFD mice.	35322757
Gas5	LncRNA	Mus musculus	Cerebral Infarction	brain tissues	Regulation[notch1 signaling pathway]	qRT-PCR//Western Blot	 Reverse transcription-polymerase chain reaction (RT-PCR) showed that the lncRNA GAS5 expression in brain tissues of rats in CI group was significantly higher than that of rats in Sham group (p<0.05).The inhibitory effect of lncRNA GAS5 knockdown on the apoptosis of neurons in CI rats may be related to the activation of the Notch1 signaling pathway.		Yes	TTC staining results revealed that lncRNA GAS5 knockdown could remarkably reduce the CI area of rats in CI group (p<0.05).	31799679
Gas5	LncRNA	Mus musculus	Non-alcoholic Fatty Liver Disease	high fat diet-fed mice and free fatty acid-stimulated cells	Regulation(miR-26a-5p/PDE4B & cAMP/CREB pathway)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Oil Red O Staining//IF	GAS5 was activated in vitro and in vivo fatty liver models. Knockdown of GAS5 reduced lipid droplet accumulation, DNL associated enzymes and preserved mitochondrial function, while GAS5 overexpression exacerbated hepatic lipid accumulation. Mechanistically, GAS5 sponged miR-26a-5p to increase PDE4B expression and subsequently modulated DNL and mitochondrial function via the cAMP/CREB pathway.		Yes	Knockdown of GAS5 reduced lipid droplet accumulation, DNL associated enzymes and preserved mitochondrial function, while GAS5 overexpression exacerbated hepatic lipid accumulation.	35957809
Gas5	LncRNA	Rattus norvegicus	Aortic Aneurysm, Abdominal	SMCs	Regulation(EZH2-mediated RIG-I signaling pathway)	Western Blot//Co-IP//Tunel//Flow Cytometry//RIP	Increased GAS5 and RIG-I but decreased EZH2 were found in aortic tissues of AAA mice. EZH2 overexpression inhibited AAA formation and suppressed SMC apoptosis. Functionally, EZH2 blocked the RIG-I signaling pathway and consequently inhibited SMC apoptosis. GAS5 regulated EZH2 transcription in a negative manner in SMCs. Knockdown of GAS5 attenuated SMC apoptosis, which was reversed by EZH2 inhibition or RIG-I overexpression.		Yes	Knockdown of GAS5 attenuated SMC apoptosis, which was reversed by EZH2 inhibition or RIG-I overexpression.	34781960
Gas5	LncRNA	Rattus norvegicus	Brain Injuries	HIBD neonatal rats	Interaction(microRNA-128-3p/Bax/Akt/GSK-3β axis)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//H&E Staining//ELISA	Downregulated miR-128-3p and upregulated GAS5 and Bax mRNA were found in HIBD neonatal rats.Downregulation of lncRNA GAS5 prevents mitochondrial apoptosis in neonatal HIBD rats by regulating the miR-128-3p/Bax/Akt/GSK-3β axis.		Yes	Inhibition of lncRNA GAS5 in HIBD neonatal rats suppressed mitochondrial apoptosis. miR-128-3p knockdown annulled the inhibitory effect of inhibiting lncRNA GAS5 on mitochondrial apoptosis.	34718247
Gas5	LncRNA	Rattus norvegicus	Cerebral Ischaemia/Reperfusion Injury	model rats	Interaction(miR-1192/STAT5A/AQP4 )	In Vivo Experiment//Western Blot//Transfection//Tunel//CCK8//FISH//Flow Cytometry//qRT-PCR//Luciferase Report Assay//ChIP	GAS5 and STAT5A were strongly expressed in stroke patients, and inhibition of GAS5 or STAT5A in model rats improved neurological function, reduced infarction and neuronal apoptosis, and diminished cerebral water content and astrocyte activation. Mechanistically, GAS5 targeted miR-1192, which negatively regulated STAT5A.  Silencing of GAS5 and overexpresion of AQP4 led to lower cell viability and higher apoptosis and inflammation than GAS5 silencing alone. 		Yes	GAS5 and STAT5A were strongly expressed in stroke patients, and inhibition of GAS5 or STAT5A in model rats improved neurological function, reduced infarction and neuronal apoptosis, and diminished cerebral water content and astrocyte activation. Furthermore, GAS5 or STAT5A downregulation restored proliferation and restrained apoptosis and inflammation in OGD/R-induced astrocytes.	36195691
GAPLINC	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	interaction[miR-378,MAPK1 ]	CCK8//qRT-PCR//Luciferase Report Assay	The lncRNA GAPLINC expression was upregulated and positively correlated with MAPK1 expression in gastric cancer tissues and cells.Taken together, lncRNA GAPLINC promotes gastric cancer cell proliferation by acting as a molecular sponge of miR-378 to modulate MAPK1 expression.		Yes	Additionally, lncRNA GAPLINC promoted the expression of MAPK1 and the enhancement of GC cell proliferation and cell cycle progression by LncRNA GAPLINC was dependent on MAPK1 in vitro and in vivo.	29785127
GAPLINC	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[miR-661/eEF2K Signaling Pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//FISH//Luciferase Report Assay//Colony Formation Assay	We found that GAPLINC expression was up-regulated in NSCLC tissues and cell lines.Our findings indicate that GAPLINC promotes NSCLC tumorigenesis by regulating miR-661/eEF2K cascade and provide new insights for the pathogenesis underlying NSCLC and potential targets for therapeutic strategy.	Overexpression of GAPLINC was associated with poor prognosis in patients with NSCLC. 	Yes	Silencing of GAPLINC significantly inhibited cell proliferation, promoted apoptosis, and induced cell cycle arrest in the G0/G1 phase. Results from xenograft transplantation showed that GAPLINC silencing inhibited the tumor growth in vivo.	30522114
GAPLINC	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	Surgical tissue samples of 40 patients undergoing ESCC radical surgery	Expression [highly expressed]	CCK8//qRT-PCR//Transwell Assay	The expression of lncRNA GAPLINC in ESCC tissues was significantly higher than that in corresponding adjacent normal tissues (P<0.05) and correlated with the degree of tumor differentiation (P<0.05). Compared with human esophageal normal epithelial cell lines, the expression of LncRNA GAPLINC was significantly higher in the human ESCC cell line (P<0.05). 		Yes	CCK-8 assays showed that LncRNA GAPLINC overexpression increased the growth rate of cells (P<0.05). Transwell experiments showed that LncRNA GAPLINC overexpression increased the ability of cell migration and invasion compared to control cells (P<0.05). Annexin V assay revealed that LncRNA GAPLINC silencing increased early stage apoptosis (P<0. 05).	34262290
GAPLINC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	The upregulated expression of GAPLINC was found both in HCC tissues and cells. 	The expression of GAPLINC was correlated with tumor stage, distant metastasis and pathological grade of HCC. Moreover, GAPLINC was confirmed as an independent risk factor for prognosis of patients with HCC. 	Yes	In HCC-LM3 and MHCC-97H cells, cells transfected with GAPLINC siRNA inhibited cell migration, invasion, proliferation and EMT in HCC cells. 	31415284
GAPLINC	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot//Transwell Assay	In our results, GAPLINC expression is elevated in osteosarcoma tissues and cell lines, and correlated with advanced Enneking stage, present distant metastasis, and poor histological grade.	Survival analyses indicated that GAPLINC expression was negatively associated with overall survival, and GAPLINC high-expression was an independent risk factor in osteosarcoma patients. 	Yes	 The in vitro studies showed knockdown of GAPLINC depressed osteosarcoma cell migration and invasion via inhibiting CD44 expression, but no effect on cell proliferation.	30177521
GAPLINC	LncRNA	Homo sapiens	Glioblastoma	GBM  tissues and cell lines	Interaction[sponging miR-331-3p]	Wound Healing Assay//Invasion Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	We found that GAPLINC expression was significantly up-regulated in both GBM tissues and cell lines. Our findings suggested that GAPLINC served as an oncogenic lncRNA in GBM through negative modulation of miR-331-3p, providing a novel treatment targeting for GBM.	The overexpression of GAPLINC was associated with shorter overall survival and disease-free survival. 	Yes	Functional assays indicated that GAPLINC silencing suppressed GBM cells proliferation, migration, and invasion, and promoted apoptosis. 	30657584
GAPLINC	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[TGF-β1 ]	qRT-PCR//Western Blot	We showed that GAPLINC was up-regulated in NSCLC tissues and positively correlated with TGF-β1. TGF-β1 may mediate lncRNA GAPLINC expression to promote NSCLC cell invasion and migration.	Follow-up study showed that high GAPLINC level in NSCLC tissue was closely correlated with poor survival rate of NSCLC patients. 	Yes	 Over-expressions of TGF-β1 and GAPLINC resulted to accelerated migration and invasion of NSCLC cells.	31447565
GAPLINC	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction(miR-135b-5p/CSF1 Axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//IHC//Transwell Assay	GAPLINC was significantly upregulated in RCC tissues and cell lines and was associated with a poor prognosis in RCC patients. Mechanistically, we found that GAPLINC upregulates oncogene CSF1 expression by acting as a sponge of miR-135b-5p.		Yes	Knockdown of GAPLINC repressed RCC growth in vitro and in vivo, while overexpression of GAPLINC exhibited the opposite effect. 	34722262
GALNT5	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	interaction[HSP90]	qRT-PCR	This lncRNA was transcribed independently of the coding region of GALNT5 and was determined to be markedly upregulated in human gastric carcinoma relative to their corresponding normal gastric tissues by quantitative RT-PCR (qRT-PCR) analysis of tissues from 122 gastric carcinoma patients. Our results also indicated that GALNT5 uaRNA might function in gastric cancer by binding with HSP90.	 The expression of GALNT5 uaRNA was significantly correlated with the TNM stage and with lymph node metastasis. 	Yes	Further results demonstrated that GALNT5 uaRNA facilitated the proliferation and migration of gastric cancer cells in vitro and promoted tumor growth in a mouse model of human gastric cancer.	29743591
GAL	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRLM tissues and cells	Interaction(GLUT1)	qRT-PCR//RNA Pull-Down//Western Blot	 Here, we report an lncRNA, GAL (glucose transporter 1 (GLUT1) associated lncRNA), that was upregulated in CRLM tissues compared with primary colorectal cancer (CRC) tissues or matched normal tissues and was associated with the overall survival rates of CRLM patients. Mechanistically, GAL interacted with the GLUT1 protein to increase GLUT1 SUMOylation, inhibiting the effect of the ubiquitin-proteasome system on the GLUT1 protein. 	 Here, we report an lncRNA, GAL (glucose transporter 1 (GLUT1) associated lncRNA), that was upregulated in CRLM tissues compared with primary colorectal cancer (CRC) tissues or matched normal tissues and was associated with the overall survival rates of CRLM patients. F	Yes	Functionally, GAL served as an oncogene because it promoted CRC cell migration and invasion in vitro and enhanced the ability of CRC cells to metastasize from the intestine to the liver in vivo.	35149838
GACAT3	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction( miR-497)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Here, we found that GACAT3 showed a higher expression in GC tissues and cell lines.Mechanistically, we proved that GACAT3 directly binds to microRNA-497 (miR-497), and GACAT3 expression was inversely correlated with miR-497 expression. 	Increased GACAT3 level was significantly associated with a shorter overall survival of patients with GC.	Yes	Functionally, we demonstrated that knockdown of GACAT3 significantly inhibited proliferation, colony formation, migration, and invasion of GC cells in vitro. Moreover, underexpression of GACAT3 decreased tumorigenesis in vivo.	29091858
Gas5	LncRNA	Mus musculus	Myocardial Infarction	the hearts of MI-modeled rat	regulation[PDCD4,miR-21]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	Decreased expressions of GAS5 and PDCD4 as well as increased miR-21 level were observed in the hearts of MI-modeled rat, accompanying with morphologically myocardial cell injury, as well as collagen deposition and fibrosis, and elevated levels of cTnl, CK, CK-MB and LDH. LncRNA-GAS5 regulates PDCD4 expression to mediate MI-induced cardiomyocyte apoptosis via targeting miR-21, suggesting that GAS5 could be a therapeutic target for MI.		Yes	 In the cell model, the knockdown of GAS5 promoted cell survival, prevented cell cycle arrest and inhibited cell apoptosis while the overexpression of GAS5 showed the opposite effects.	32308118
Gas5	LncRNA	Mus musculus	Coronary Artery Disease	CAD tissues	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	 Overexpression of GAS5 in CAD rats determines improvement of hyperlipidemia, attenuation of myocardial injury, inhibition of cardiomyocyte apoptosis, oxidative stress, inflammatory injury, and abnormal activation of the Wnt/β-catenin signaling pathway in myocardial tissues.		Yes	 Overexpression of GAS5 in CAD rats determines improvement of hyperlipidemia, attenuation of myocardial injury, inhibition of cardiomyocyte apoptosis, oxidative stress, inflammatory injury, and abnormal activation of the Wnt/β-catenin signaling pathway in myocardial tissues.	30511472
Gas5	LncRNA	Mus musculus	Atherosclerosis	arteries 	Interaction[upregulation of miR-135a]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Our data revealed that GAS5 was upregulated in AS mice model and ox-LDL-treated macrophages.In conclusion, our study suggested that GAS5 silencing repressed the malignant progression of AS at least partly through upregulation of miR-135a. 		Yes	GAS5 silencing alleviated lipid metabolic disorders and inflammation in AS mice and ox-LDL-treated macrophages.	31545249
GAS5	LncRNA	Homo sapiens	ovarian clear cell carcinoma	OCCC tissues and cell lines	Interaction(miR-31-5p/ARID1A axis)	RNA Pull-Down//Western Blot//Transfection//RIP//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	GAS5 and ARID1A levels were significantly decreased, while miR-31-5p levels were strongly elevated in the OCCC tissues and cell lines. LncRNA GAS5 inhibited cell viability and invasion of OCCC through activation of ARID1A by sponging miR-31-5p.	Patients with lower GAS5/ARID1A levels had shorter overall survival times. 	Yes	Overexpression of GAS5 or inhibition of miR-31-5p suppressed cell viability and invasion of OCCC cells and upregulated the protein levels of ARID1A.  Moreover, overexpression of miR-31-5p reversed the effects of overexpression of GAS5. 	34414664
GAS5	LncRNA	Homo sapiens	Leukemia, B-Cell		Interaction[sponging miR-222]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results showed that the expression of lncRNA GAS5 was decreased in B lymphocytic leukaemia patients compared with the healthy group, and the levels of lncRNA GAS5 in B lymphocytic leukaemia cell lines were significantly higher than those in the normal B cell line, whereas the levels of miR-222 were increased in B lymphocytic leukaemia patients compared with the healthy group. Finally, the luciferase reporter assay showed a direct target interaction between lncRNA GAS5 and miR-222. The regression analysis showed a negative correlation between the levels of lncRNA GAS5 and miR-222. Thus, our data suggested that lncRNA GAS5 could effectively sponge miR-222 to modulate human B lymphocytic leukaemia cell tumourigenesis and metastasis. 		Yes	Moreover, cell culture experiments indicated that lncRNA GAS5 overexpression decreased B lymphocytic leukaemia cell proliferation, promoted B lymphocytic leukaemia cell apoptosis, arrested B lymphocytic leukaemia cells in the G1 phase of the cell cycle, and inhibited B lymphocytic leukaemia cell invasion.	31594210
GAS5	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	blood 	regulation[IL-6]	qRT-PCR//ELISA//Cell Apoptosis Assay	 GAS5 was upregulated in plasma of PCOS patients. GAS5 is upregulated in PCOS and regulates cell apoptosis and the expression of IL-6.		Yes	 Cell apoptosis analysis showed that overexpression of GAS5 significantly decreased apoptosis rate of KGN cells. Silencing of GAS5 increased the rate of KGN cell apoptosis.	33308258
GAS5	LncRNA	Homo sapiens	Uveal melanoma	UM cells and clinical specimens	regulation[GAS5/miR-21 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our experiments demonstrated that GAS5 was markedly downregulated in UM cells and clinical specimens. Taken together, our findings suggest that GAS5/miR-21 axis is implicated in the pathogenesis of UM and might serve as a potential therapeutic target.		Yes	Overexpression of GAS5 inhibited, whereas knockdown of GAS5 promoted the viability, migration, and invasion of UM cells.	33273862
GAS5	LncRNA	Homo sapiens	Arthritis, Rheumatoid	RA synovial tissues and RAFLSs	Interaction(miR-128-3p/HDAC4 axis)	RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//IHC//Invasion Assay	 GAS5 and HDAC4 were downregulated, and miR-128-3p was upregulated in RA synovial tissues and RAFLSs. GAS5 acted as a miR-128-3p sponge to upregulate HDAC4 expression. Besides, GAS5/miR-128-3p/HDAC4 axis regulated RA progression partially through the AKT/mTOR pathway. 		Yes	Function analysis indicated that GAS5 curbed proliferation, migration, invasion, inflammation, and facilitated apoptosis of RAFLSs. Rescue assay confirmed that miR-128-3p overexpression or HDAC4 knockdown weakened the inhibitory effect of GAS5 or anti-miR-128-3p on RA development. 	33611674
GAS5	LncRNA	Homo sapiens	Arthritis, Rheumatoid	serum samples of RA patients and in RA-FLSs	Interaction( miR-222-3p/Sirt1 signalling axis)	Western Blot//Transfection//qPCR//CCK8//Flow Cytometry//RIP//Luciferase Report Assay//BrdU//ELISA	GAS5 expression was found to be downregulated in the serum samples of RA patients and in RA-FLSs. Mechanistically, GAS5 indirectly regulates Sirt1 expression by binding miR-222-3p. Further experiments confirmed that Sirt1 overexpression restored the anti-RA activity of GAS5 under miR-222-3p mimic.		Yes	GAS5 overexpression or the inhibition of miR-222-3p impeded the activity of RA-FLSs by repressing their proliferation and inflammation and by promoting apoptosis. 	33215529
GAS5	LncRNA	Homo sapiens	Arthritis, Rheumatoid	synovial tissue	Interaction(miR-361-5p/PDK4 )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining	By qRT-PCR, GAS5 and PDK4 were found to be overexpressed in synovial tissue, fibroblast-like synoviocytes of RA patients and LPS-induced chondrocytes, while the miR-361-5p expression was significantly reduced. PDK4 targeted by miR-361-5p could inhibit RA, and partially eliminated the effect of miR-361-5p on RA. Our study suggested that GAS5 suppressed RA by competitively adsorbing miR-361-5p to modulate PDK4 expression.		Yes	GAS5 overexpression resulted in a decrease in the proliferation and Bcl-2 protein expression, and an increase in the Bax protein level. On the contrary, miR-361-5p sponged by GAS5 could accelerate chondrocyte proliferation, inhibit apoptosis. 	34715498
GAS5	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive	MRC-5 cell line	Interaction(miR‑223‑3p/NLRP3 axis)	Western Blot//qPCR//CCK8//RIP//Luciferase Report Assay//ELISA//Bioinformatics Analysis//IF	Additionally, LPS induced the increase in GAS5 mRNA expression levels and the release of inflammatory factors (IL‑2, IL‑6, IL‑10 and TNF‑α), suggesting that GAS5 is implicated in pyroptosis in COPD.  A dual‑luciferase assay demonstrated that GAS5 could directly bind to microRNA‑223‑3p (miR‑223‑3p), and NLRP3 is a direct target of miR‑223‑3p. Furthermore, GAS5 reduced the expression levels of miR‑223‑3p, while it increased the expression levels of NLRP3. 		Yes	 Furthermore, upregulation of GAS5 promoted cell death and inhibited proliferation in the MRC‑5 cell line.  Additionally, increased GAS5 expression significantly promoted the production of caspase‑1, IL‑1β, IL‑18, cleaved GSDMD and NLR pyrin domain containing protein 3 (NLRP3). 	35583006
GAS5	LncRNA	Homo sapiens	Diabetic Foot	skin tissues	Interaction(TAF15/HIF1A/VEGF pathway)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Tube Formation Assay//CCK8//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining//ChIP	GAS5 and HIF1A were downregulated in the skin tissues of DFU patients, and GAS5 overexpression promoted cell proliferation, wound healing and tubule formation in HG-treated HUVECs.In addition, GAS5 facilitated HIF1A expression by interacting with TAF15. Rescue assays demonstrated that the suppression of HIF1A/VEGF pathway activation partially reversed the functional roles of GAS5 in HUVECs.  Furthermore, GAS5 accelerated wound healing by activating the HIF1A/VEGF pathway in mice with DFUs. GAS5 activates the HIF1A/VEGF pathway by binding to TAF15, resulting in accelerated wound healing in DFUs.		Yes	GAS5 and HIF1A were downregulated in the skin tissues of DFU patients, and GAS5 overexpression promoted cell proliferation, wound healing and tubule formation in HG-treated HUVECs.	33875793
GAS5	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction( SPACA6-miR-125a/let-7e Axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We showed that lncRNA-GAS5 expression decreased in high-grade glioma tissues and cells, which might be associated with poor prognosis. We further discovered that GAS5 inhibited the viability of glioma cells through miR-let-7e and miR-125a by protecting SPACA6 from degradation. Moreover, GAS5 played an anti-oncogenic role in GBM through the combined involvement of let-7e and miR-125a in vivo and in vitro. 	We showed that lncRNA-GAS5 expression decreased in high-grade glioma tissues and cells, which might be associated with poor prognosis. 	Yes	GAS5 overexpression lowered cell viability, suppressed GBM cell migration and invasion, and impaired the stemness and proliferation of glioma stem cells (GSCs).	36106122
GAS5	LncRNA	Homo sapiens	Neuroendocrine Tumors	PitNET tissues and cells	Interaction(miR-27a-5p/cylindromatosis axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	 These results suggest that lncRNA GAS5 acts as an endogenous sponge by binding miR-27a-5p to increase the expression of its target gene CYLD, thereby inhibits PitNETs cell proliferation and tumor growth.		Yes	 In vivo lncRNA GAS5 overexpression inhibited GH3 cell tumor growth, while miR-27a-5p mimic or silenced CYLD attenuated the effect of lncRNA GAS5 on GH3 cell tumor growth. 	35435104
GAS5	LncRNA	Homo sapiens	Osteosarcoma	hFOB 1.19 and U2OS osteosarcoma cells	Interaction(miR-21)	qRT-PCR//Transfection//Invasion Assay//Migration Assay	In this study, we report the status of growth arrest specific 5 (GAS5) in lung metastatic osteosarcomas. GAS5 was generally downregulated in osteosarcoma patients (n = 24) compared to healthy controls (n = 10) and even more so in patients with lung metastatic disease(n = 11) compared to the patients without metastasis (n = 13). We also report a role of miR-21 in GAS5-mediated effects. Downregulation of GAS5 in hFOB 1.19 and U2OS osteosarcoma cells enhanced their migration and invasion, along with an upregulated epithelial-mesenchymal transition (EMT), as evidenced by downregulated E-cadherin and upregulated vimentin, ZEB1, and ZEB2. Downregulation of GAS5 also resulted in a significantly increased expression of miR-21. Moreover, downregulation of such elevated miR-21 was found to reverse the effects of GAS5 silencing. miR-21 was also found to be elevated in osteosarcoma patients with its levels particularly high in patients with lung metastasis. Our observations reveal a possible role of GAS5 and miR-21 in lung metastasis of osteosarcoma, presenting them as novel targets for therapy.		Yes	Moreover, downregulation of such elevated miR-21 was found to reverse the effects of GAS5 silencing. 	34386496
GAS5	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL cell lines	Interaction(miR‑18a‑5p/RUNX1 axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//FISH//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Bioinformatics Analysis//ChIP	The expression levels of GAS5 and RUNX1 were downregulated; however, miR‑18a‑5p expression was upregulated in the DLBCL cell lines compared with the normal controls.GAS5 directly interacted with miR‑18a‑5p by acting as a competing endogenous RNA (ceRNA) and reversed the low expression of RUNX1 induced by miR‑18a‑5p.  Moreover, RUNX1 enhanced BAX expression by directly binding to the BAX promoter. 		Yes	 Additionally, the knockdown of RUNX1 reversed the inhibitory effects of GAS5 on the proliferation and cell cycle G1 arrest, and its promoting effects on the apoptosis of OCI‑Ly3 and TMD8 cells.	34698360
GAS5	LncRNA	Homo sapiens	Adenocarcinoma, Follicular	 FTC tissues and cells	Interaction(miR-221-3p/CDKN2B axis )	In Vivo Experiment//Western Blot//Transfection//FISH//qRT-PCR//RIP//Luciferase Report Assay//IHC	Our results displayed that GAS5 was downregulated, while miR-221-3p was upregulated in FTC tissues and cells. GAS5 acted as a sponge of miR-221-3p, and CDKN2B was a target gene of miR-221-3p. Additionally, GAS5 inhibited cell cycle and proliferation of FTC cells via reducing miR-221-3p expression to enhance CDKN2B expression.		Yes	 What's more, overexpression of GAS5 or miR-221-3p inhibition induced G0/G1 phase arrest and inhibited cell proliferation of FTC cells. 	34130294
GAS5	LncRNA	Homo sapiens	HIV	CD4 T cells	Interaction(miR-21)	Flow Cytometry//qRT-PCR//Western Blot	 We found that GAS5 negatively regulates miR-21 expression, which in turn controls critical signaling pathways involved in DNA damage and cellular response. These results indicate that targeting the GAS5-miR-21 axis may improve activity and longevity of CD4 T cells in ART-treated PLHIV. 		Yes	 We found that GAS5 negatively regulates miR-21 expression, which in turn controls critical signaling pathways involved in DNA damage and cellular response. 	33776993
GAS5	LncRNA	Homo sapiens	Asthma		Interaction(miR-217/HDAC4 axis)	qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Western Blot	TGF-β1, GAS5, HDAC4 were up-regulated, while miR-217 was down-regulated in bronchial mucosal tissues of asthmatic children and TGF-β1-treated BEAS-2B cells. Mechanically, GAS5 acted as a sponge for miR-217 to regulate the expression of HDAC4.		Yes	Furthermore, overexpression of HDAC4 rescued the effects of GAS5 knockdown on viability and apoptosis of TGF-β1-induced BEAS-2B cells. GAS5 knockdown induced cell viability and hampered cell apoptosis in TGF-β1-stimulated BEAS-2B cells by regulating the miR-217/HDAC4 axis.	33864612
GAS5	LncRNA	Homo sapiens	Mycoplasma pneumoniae pneumonia	Serum	Expression(highly expressed)	qRT-PCR//Transfection//ELISA	 lncRNA GAS5 is highly expressed in the serum of children with MPP and inhibits LAMPs-induced apoptosis and alveolar macrophage inflammation.		Yes	 lncRNA GAS5 is highly expressed in the serum of children with MPP and inhibits LAMPs-induced apoptosis and alveolar macrophage inflammation.	36034211
GAS5	LncRNA	Homo sapiens	Coronary Artery Disease	AS	Interaction(MicroRNA-194-3p/TXNIP Axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//H&E Staining//IHC	aised GAS5 and TXNIP and degraded miR-194-3p expression levels exhibited in AS. GAS5 bound to miR-194-3p while miR-194-3p targeted TXNIP. 		Yes	Depleting GAS5 or restoring miR-194-3p enhanced proliferation and depressed apoptosis of ECs in AS. 	33638792
GAS5	LncRNA	Homo sapiens	Sepsis-Associated Renal Injury	sepsis-induced renal injury models	Interaction(miR-579-3p/SIRT1/PGC-1α/Nrf2 signaling pathway)	Western Blot//Transfection//Tunel//Flow Cytometry//RIP//qRT-PCR//Luciferase Report Assay//H&E Staining//ELISA	GAS5 and SIRT1 were downregulated, whereas miR-579-3p was upregulated in in vitro and in vivo sepsis-induced renal injury models.GAS5 negatively and directly regulated miR-579-3p to reduce cell pyroptosis via the activation of SIRT1/PGC-1a/Nrf2 pathway. In addition, miR-579-3p suppressed PGC-1a/Nrf2 pathway to induce cell pyroptosis by directly targeting SIRT1. 		Yes	GAS5 negatively and directly regulated miR-579-3p to reduce cell pyroptosis via the activation of SIRT1/PGC-1a/Nrf2 pathway. In addition, miR-579-3p suppressed PGC-1a/Nrf2 pathway to induce cell pyroptosis by directly targeting SIRT1. What's more, overexpression of GAS5, or knockdown of miR-579-3p, enhanced SIRT1 expression that led to the improved survival rate, reduced the weight loss, and relieved renal injuries in septic mice. 	34010066
GAS5-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction[increasing GAS5 stability ]	qRT-PCR	The GAS5-AS1 expression in CC tissues was markedly decreased when compared with that in the adjacent normal tissues.Mechanistically, it was found that GAS5-AS1 interacted with the tumor suppressor GAS5, and increased its stability by interacting with RNA demethylase ALKBH5 and decreasing GAS5 N6-methyladenosine (m6A) modification. Moreover, it was shown that m6A-mediated GAS5 RNA degradation relied on the m6A reader protein YTHDF2-dependent pathway.	The downregulation of GAS5-AS1 was significantly correlated with the advanced FIGO stage, distant metastasis, lymphatic metastasis and poor prognosis in patients with CC.	Yes	Functionally, GAS5-AS1 drastically reduced CC cell proliferation, migration and invasion in vitro, and remarkably suppressed CC tumorigenicity and metastasis in vivo.	31497208
GMDS-DT	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Regulation[ miR-96-5p/CYLD signaling]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	In this study, we found that the expression of lncRNA GMDS-AS1 was significantly reduced in lung adenocarcinoma (LUAD) tissues and cells.Further studies revealed that GMDS-AS1 is a target gene of miR-96-5p, and GMDS-AS1 regulates proliferation and apoptosis of LUAD cells in association with miR-96-5p. In addition, we also confirmed that CYLD lysine 63 deubiquitinase (CYLD) is also a target gene of miR-96-5p. Through various validations, we confirmed that GMDS-AS1 can act as a ceRNA to upregulate the expression of CYLD by sponging miR-96-5p. Moreover, the intervention of GMDS-AS1/miR-96-5p/CYLD network can regulate the proliferation and apoptosis of LUAD cells. In this study, we revealed that the GMDS-AS1/miR-96-5p/CYLD network based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for targeted therapy of LUAD.		Yes	Upregulated GMDS-AS1 can significantly inhibit the proliferation of LUAD cells and promote cell apoptosis in vitro and in vivo. 	31860169
GIHCG	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	Interaction[repressing miR-200b]	qRT-PCR	Our results revealed that GIHCG is up-regulated in cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cell line, respectively.  In summary, this study demonstrated that GIHCG functions as an oncogene in cervical cancer via repressing miR-200b. 		Yes	Functionally, we found that overexpression of GIHCG promotes cell proliferation, inhibits cell apoptosis, and promotes cell migration of cervical cancer cells.	30719165
GIHCG	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cell lines	Regulation[ miR-429]	qRT-PCR	In our study, we showed that that the expression level of GIHCG was upregulated in TSCC tissues and cell lines.Our results suggested that GIHCG/miR-429 might play a vital role in TSCC progression.	In addition, we indicated that high GIHCG expression was positively associated with poor overall survival. 	Yes	Moreover, ectopic expression of GIHCG enhanced TSCC cell cycle, proliferation, and migration. Elevated expression of GIHCG inhibited the miR-429 expression in TSCC cells.	29953645
GIAT4RA	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues,cell lines	Interaction[ binding to 227-589 AA of LSH]	RNA Pull-Down//Western Blot//ISH//Co-IP//Migration Assay//CCK8//qRT-PCR//RIP//IHC//Invasion Assay	 Here, we showed that GIAT4RA, a poorly characterized lncRNA LOC102723729, was significantly decreased in lung cancer cells and tissues.Mechanistically, GIAT4RA was essential for the degradation of chromatin modifier lymphoid-specific helicase (LSH) by counteracting the deubiquintination in proteasome pathway by binding to 227-589 AA of LSH. GIAT4RA interfered with ubiquitin hydrolase Uchl3-mediated interaction and stabilization of LSH. LSH knockdown rescued GIAT4RA-promoted features, and LSH overexpression prevented GIAT4RA-induced phenotypes. 	Here, we showed that GIAT4RA, a poorly characterized lncRNA LOC102723729, was significantly decreased in lung cancer cells and tissues; while no association was observed with clinical risk factors, expression was linked with clinical stage and lymphatic metastasis. Higher expression of GIAT4RA was linked with overall survival in NSCLC.	Yes	GIAT4RA inhibited many characteristics of tumorigenesis including cell growth, clonal formation, migration and invasion, epithelial-mesenchymal transition, tumor sphere and tumor growth in vivo. 	31417184
GHSROS	LncRNA	Homo sapiens	Breast Neoplasms	breast tissue	Expression[highly expressed]	qRT-PCR	 Reverse transcription‑quantitative polymerase chain reaction revealed that GHSROS expression was significantly upregulated in breast tumour tissues compared with normal breast tissue. 		Yes	Induced overexpression of GHSROS in the MDA‑MB‑231 breast cancer cell line significantly increased cell migration in vitro, without affecting cell proliferation, a finding similar to our previous study on lung cancer cell lines.	31638176
GHSROS	LncRNA	Homo sapiens	Prostatic Neoplasms	tissues and cell lines( PC3, DU145, and LNCaP cells)	Expression [highly expressed]	In Vivo Experiment//Migration Assay//qRT-PCR//RNA-seq//Cell Proliferation Assay//IHC//Transwell Assay			Yes	Increased cellular proliferation of GHSROS-overexpressing PC3, DU145, and LNCaP prostate cancer cell lines in vitro was recapitulated in a subcutaneous xenograft model	33585078
GHRLOS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines and tissues 	Interaction(miR-346/APC Axis)	Western Blot//CCK8//qRT-PCR//RIP//Colony Formation Assay//ChIP	We found lncRNA GHRLOS was decreased in NSCLC cell lines and tissues which correlated with poor prognosis of NSCLC patients. Our data demonstrated that overexpression of lncRNA GHRLOS suppressed cancer cell proliferation and invasion as well as promoted cell apoptosis by regulating the expression of CDK2, PCNA, E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Moreover, lncRNA GHRLOS was upregulated by the binding of TP53 to the GHRLOS promoter. The binding target of lncRNA GHRLOS was identified to be miR-346. 	We found lncRNA GHRLOS was decreased in NSCLC cell lines and tissues which correlated with poor prognosis of NSCLC patients	Yes	Our data demonstrated that overexpression of lncRNA GHRLOS suppressed cancer cell proliferation and invasion as well as promoted cell apoptosis by regulating the expression of CDK2, PCNA, E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Moreover, lncRNA GHRLOS was upregulated by the binding of TP53 to the GHRLOS promoter. The binding target of lncRNA GHRLOS was identified to be miR-346. 	33968785
GHET1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	GHET1 was up-regulated in breast cancer tissues and cell lines, and the up-regulation of GHET1 was positively correlated with larger tumor size, advanced clinical stage, lymph node metastasis and shorter overall survival. 	GHET1 was up-regulated in breast cancer tissues and cell lines, and the up-regulation of GHET1 was positively correlated with larger tumor size, advanced clinical stage, lymph node metastasis and shorter overall survival. 	Yes	Knockdown of GHET1 suppressed cell proliferation, invasion and migration, and induced apoptosis and G0/G1 cell cycle arrest in MCF-cells. 	29843220
GHET1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[PI3K/AKT/Cyclin D1/MMP2/9]	Western Blot//ISH//Wound Healing Assay//qRT-PCR//MTT//IHC//Transwell Assay	RT-PCR showed that lncRNA GHET1 and c-Myc expression in cancer tissue were significantly Expression[Expression[up-expression]-expression]regulated compared with those in adjacent samples (both P < 0.05, Figure 2A and ​and2B).2B). The results indicate that lncRNA GHET1 inhibition directly sExpression[Expression[up-expression]-expression]presses EGFR expression, significantly inhibiting the Expression[down-expression]stream PI3K/AKT/Cyclin D1/MMP2/9 pathway. 		Yes	In vitro, lncRNA GHET1 knockExpression[down-expression] sExpression[Expression[up-expression]-expression]pressed cell proliferation, migration, and invasion and enhanced cell apoptosis by maintaining MCF-7 cells in the G1 phase of the cell cycle. Furthermore, lncRNA GHET1 knockExpression[down-expression] reduced the expression of EGFR and related proteins.	30787968
GHET1	LncRNA	Homo sapiens	Breast Neoplasms	TNBC patients' tissues and the TNBC cell lines	Interaction(miR-377-3p/GRSF1 Signaling Axis)	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay	lncRNA GHET1 was significantly upregulated in the TNBC patients' tissues and the TNBC cell lines. Additionally, overexpression of lncRNA GHET1 upregulated both MMP-9 and MMP-2 protein expression levels. Correlation analysis found that miR-377-3p had a positive relationship with GRSF1, but had a negative relationship with lncRNA GHET1. miR-377-3p mimic attenuated the effects of lncRNA GHET1 on cellular proliferation, apoptosis, and migration of the TNBC cells.		Yes	Overexpression of lncRNA GHET1 significantly increased the proliferation and migration ability, but decreased apoptosis in the TNBC cells. 	35509860
GHET1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues,cell lines	Expression[highly expressed]	qRT-PCR//Microarray	In the present study, the expression of GHET1 in RCC tissues and the 786-O, A498 and 293 cell lines was assessed by reverse transcription-quantitative polymerase chain reaction. 	 High expression levels of GHET1 were associated with distant metastasis and clinical stage severity, thus, high GHET1 expression may serve as a predictor for a poor prognosis. 	Yes	Furthermore, silencing GHET1 suppressed cell growth, weakened cell migration and inhibited EMT of RCC cells in vitro.	30867747
GHET1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Interaction[HIF1α ]	qRT-PCR//MTT//Colony Formation Assay//Western Blot	 In the present study, we found that the long non-coding RNA gastric carcinoma high expressed transcript 1 (GHET1) was overexpressed in ovarian cancer tissues and cell lines.  Mechanistically, the candidate binding partners of GHET1 were explored by pull-down and mass spectrum. Of note, GHET1 was found to interact with the E3 ubiquitin ligase von Hippel-Lindau (VHL), which consequently blocked VHL-mediated degradation of hypoxia-inducible factor-1α (HIF1α) and enhanced the protein level of HIF1α in ovarian cancer cells. The up-regulated HIF1α promoted the glucose uptake and lactate generation of ovarian cancer cells. Collectively, our results suggested the oncogenic function of GHET1 via up-regulating the glycolysis in ovarian cancer and can be considered as a promising anti-cancer target.	Up-regulation of GHET1 was positively correlated with the tumor size and metastasis of the ovarian cancer patients.	Yes	Overexpression of GEHT1 significantly promoted the proliferation and colony formation of ovarian cancer cells.	30988076
GHET1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	 cell lines	regulation[GHET1/miR-105/RAP2B axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	GHET1 expression was elevated in AML cell lines compared with normal bone marrow mononuclear cells.This study demonstrated that the GHET1/miR-105/Rap2B axis may be a critical signaling pathway involved in AML progression.		Yes	GHET1 knockdown led to inhibition of proliferation and promoted the differentiation and apoptosis of AML cell lines. 	33123297
GHET1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues,cell lines	Expression[highly expressed]	qRT-PCR	In our study, we found GHET1 expression was markedly elevated in cervical cancer tissue specimens and cell lines compared with adjacent normal cervical tissue specimens and human normal cervical cell line, respectively. 	Then, we found high expression of GHET1 is a useful biomarker to discriminate cervical cancer tissues from non-tumorous tissues, and associated with advanced clinical stage, lymph node metastasis, distant metastasis and poor histological grade in cervical cancer patients.	Yes	Knockdown of GHET1 expression markedly inhibits cervical cancer cell proliferation, migration, and invasion. The loss-of-function study indicated knockdown of GHET1 expression markedly inhibits cervical cancer cell proliferation, migration, and invasion.	30948501
GHET1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	regulation[AKT/mTOR and Wnt/β-catenin signaling pathways]	Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay//IF	We proposed to examine the biological role of GHET1 in CC and the underlying mechanism and validated the up-regulated expression of GHET1 in CC cell lines. In conclusion, we revealed that down-regulation of GHET1 suppresses cervical cancer progression through regulating AKT/mTOR and Wnt/β-catenin signaling pathways, indicating GHET1 as a promising molecular biomarker for CC treatment improvement.		Yes	Loss-of-function assays demonstrated that down-regulation of GHET1 inhibited cell growth, migration and epithelial-to-mesenchymal transition (EMT) in CC. 	31682716
GHET1	LncRNA	Homo sapiens	Thyroid Neoplasms	 TC tissues	Expression [highly expressed]	Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Transwell Assay	Our results showed that LncRNA GHET1 was significantly more upregulated in TC tissues than in adjacent normal tissues. LncRNA GHET1 was also increased in thyroid cancer cell lines compared to normal thyroid cell lines. The upregulation of LncRNA GHET1 was significantly associated with tumor invasion, gender, and lymph node metastasis in patients with thyroid cancer. The in vitro studies showed that silencing LncRNA GHET1 in BCPAP cells inhibited cell proliferation, cell invasion, and migration. Silencing of LncRNA GHETI also promoted the cell apoptotic rate, caused an increase in the cell population at the G0/G1 phase, and decreased the cell population at the S phase. 	A recent study indicated that an increased LncRNA GHET1 expression level is associated with poor OS, tumor progression, and TNM stage in patients with multiple tumors and may serve as a useful prognostic biomarker in Chinese cancer patients	Yes	The in vitro studies showed that silencing LncRNA GHET1 in BCPAP cells inhibited cell proliferation, cell invasion, and migration. Silencing of LncRNA GHETI also promoted the cell apoptotic rate, caused an increase in the cell population at the G0/G1 phase, and decreased the cell population at the S phase. 	35116711
GHET1	LncRNA	Homo sapiens	Prostatic Neoplasms	PC tissues	Regulation[HIF-1α/Notch-1 signaling pathway ]	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	We found that GHET1 showed higher expression in PC tissues and had a negative correlation with KLF2 expression. Additionally, si-GHET1 transfection induced KLF2 upregulation and HIF-1α/Notch-1 signal pathway suppression, which could be rescued by si-KLF2 transfection. These results suggest the key role of GHET1 in PC progression. Moreover, GHET1 might be explored to be a potential target for clinical treatment of PC.		Yes	Knockdown of GHET1 significantly suppressed the cell proliferation, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis. 	30609158
GHET1	LncRNA	Homo sapiens	Head and Neck Neoplasms	HNC tissues	Expression[highly expressed]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The expression level of GHET1 was significantly increased in HNC tissues, compared with paired adjacent normal tissues.	High GHET1 expression was significantly associated with advanced Tumor-Node-Metastasis stages and poor prognosis.	Yes	Furthermore, inhibition of GHET1 suppressed cell proliferation, induced cell apoptosis and caused cell cycle arrest in vitro. In addition, GHET1 silencing inhibited cell migration and invasion. 	29725422
GHET1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cancer tissues	regulation[PTEN/PI3 K/AKT signalling pathway]	Western Blot//Wound Healing Assay//Tunel//Flow Cytometry//qRT-PCR//MTT//IHC//Transwell Assay	The expression levels of lncRNA GHET1 and PTEN protein differed significantly between cancer and adjacent normal tissues (P< 0.05) and were negatively correlated in the clinical data. GHET1 knockdown suppressed cervical carcinoma development via the PTEN/PI3 K/AKT signalling pathway.		Yes	 In vitro, proliferation rateswere significantly down-regulated in SiHa and HeLa cells. The GHET1 knockdown (si-GHET1) groups showed significantly higher G1 phase and apoptosis rates and significantly suppressed invasion and migration abilities compared with the normal control (NC) group (P< 0.05 for all). 	32176622
GFRA1	CircRNA	Homo sapiens	Prostatic Neoplasms	 PCa tumor tissues	Interaction(miR-3064-5p/HECTD1 axis)	RNA Pull-Down//Western Blot//qPCR//RIP//PCR//IP//ELISA//Bioinformatics Analysis//IF	In this study, circRNA microarrays using four pairs of PCa tissues were utilized to show that circGFRA1 was upregulated in PCa tumor tissues, our results showed that LMX1B could bind to the GFRA1 promoter and regulate circGFRA1 expression in PCa cells and circGFRA1 upregulated HECTD1 expression through sponging miR-3064-5p. 		Yes	CircGFRA1 is suggested to play an oncogene role in PCa progression as the silencing of circGFRA1 inhibited the proliferation, migration, and immune escape activity of PCa cells.	35832649
GDNFOS1	LncRNA	Homo sapiens	Glioblastoma		Regulated[up-regulated]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 Overall, GDNF expression, cell viability and invasion ability of glioblastoma cells significantly increased with GDNFOS1 overexpression and decreased with GDNFOS1 interference.		Yes	The invasive ability was significantly decreased in the GDNFOS1 interference group when compared with the negative control group. 	31316623
GIHCG	LncRNA	Homo sapiens	Cholangiocarcinoma	 cholangiocarcinoma tissue	Expression(highly expressed)	qRT-PCR//FISH	The expression of lncRNA GIHCG in cholangiocarcinoma tissue is significantly increased, closely related to tumor size and lymph node metastasis.	The results of the comprehensive analysis of survival, ROC, and correlation analysis with clinical data showed that lncRNA GIHCG has a significant correlation with lymph node metastasis in patients with cholangiocarcinoma. 	Yes	 Transwell results showed that lncRNA GIHCG could promote the migration of cholangiocarcinoma cells. 	35196779
GIHCG	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues and cancer cell lines	regulation[miR-29b-3p/ANO1 Axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	GIHCG was significantly upregulated in esophageal cancer tissues and relevant cancer cell lines.Our study revealed that lncRNA GIHCG promoted the progression of esophageal cancer by targeting the miR-29b-3p/ANO1 axis, suggesting that GIHCG might be a novel therapeutic target for esophageal cancer.		Yes	Downregulation of GIHCG significantly inhibited the growth, colony formation, invasion, migration and induced apoptosis of esophageal cancer cells in vitro.	33408485
GAS6	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cell lines	Regulation(AMP-activated protein kinase/mTOR signaling pathway)	In Vivo Experiment//IHC//Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	GAS6-AS1 was found to be upregulated in ccRCC tissues and cell lines, and patients with high GAS6-AS1 expression levels exhibited a poor prognosis. Small interfering (si)RNA GAS6-AS1 inhibited the activity, colony formation, invasiveness and glycolysis of OSRC-2 and SW839 cells, while GAS6-AS1 overexpression promoted these functions. Moreover, si-GAS6-AS1 increased the phosphorylation level of AMP-activated protein kinase (AMPK) and decreased that of mTOR, as well as decreasing proliferating cell nuclear antigen (PCNA), MMP-2 and hexokinase-2 (HK2) expression, which were reversed by inhibiting AMPK or mTOR. In addition, the silencing of GAS6-AS1 suppressed the growth of xenografted tumors and attenuated the expression of PCNA, MMP-2 and HK2 in tumor tissues. These findings conclude that GAS6-AS1 regulated the proliferation, invasiveness and glycolysis of ccRCC cells by regulating the AMPK/mTOR signaling pathway, and suggest that GAS6-AS1 may be a potential therapeutic target for ccRCC.	GAS6-AS1 was found to be upregulated in ccRCC tissues and cell lines, and patients with high GAS6-AS1 expression levels exhibited a poor prognosis. 	Yes	Small interfering (si)RNA GAS6-AS1 inhibited the activity, colony formation, invasiveness and glycolysis of OSRC-2 and SW839 cells, while GAS6-AS1 overexpression promoted these functions. 	34429767
GIHCG	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	Regulation[microRNA-429]	CCK8//qRT-PCR//Colony Formation Assay	GIHCG was highly expressed, whereas microRNA-429 was lowly expressed in OC tissues than that of paracancerous tissues.GIHCG is highly expressed in OC, which promotes OC development by stimulating cell cycle progression and cell proliferation by regulating microRNA-429.	OC patients with higher expression of GIHCG showed shorter OS than those with lower expression.	Yes	 GIHCG overexpression in HEY cells promoted cell cycle and colony formation abilities, which were reversed by microRNA-429 overexpression.	30556850
Gm9795	LncRNA	Rattus norvegicus	non-alcoholic steatohepatitis	 liver tissues 	Interaction(NF-kB/JNK pathway )	In Vivo Experiment//qRT-PCR//Western Blot//Microarray	A total of 381 lncRNAs were found to be not only highly expressed in NAFLD, but also is going to go even higher in NASH. A novel LncRNA-gm9795 was significantly highly expressed in liver tissues of NASH animal models and NASH cell models. By staining with Nile red, we found that gm9795 did not affect the fat accumulation of NASH. However, gm9795 in NASH cell models significantly promoted the expression of TNF [Formula: see text], IL-6, IL-1[Formula: see text], the important inflammatory mediators in NASH. At the same time, we found that gm9795 upregulated the key molecules in endoplasmic reticulum stress (ERS), while NF-[Formula: see text]B/JNK pathways were also activated. When ERS activator Thapsigargin (TG) was introduced in cells with Ggm9757 si-RNA, NF-[Formula: see text]B and JNK pathways were activated.		Yes	The role and mechanism of LncRNA-gm9795 in NASH were explored by knocking down or over-expressing its expression.	33750416
Gm47283	LncRNA	Homo sapiens	Myocardial Infarction	cardiomyocyte 	Interaction(miR-706/ Ptgs2/ferroptosis axis)	In Vivo Experiment//qRT-PCR//Western Blot	First, we identified 10 dysregualted lncRNAs and found that lncRNA Gm47283 was the top risk factor in MI. Bioinformatics analysis predicted that lncRNA Gm47283 exerted function via targeting miR-706 and Ptgs2. Ptgs2 was also the known regulator of ferroptosis. 		Yes	Inhibition or overexpression of lncRNA Gm47283 could regulate Ptgs2 expression and downstream ferroptosis activity. Overexpression of miR-706 could inhibit the expression of Ptgs2 and the activity of ferroptosis, thereby attenuated cellular injury. 	35485136
Gm44593	LncRNA	Homo sapiens	Hearing Loss	HEI-OC1 cells	Interaction(miR-29b/WNK1)	Transfection//Tunel//RIP//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	The expression of lncRNA Gm44593 was significantly upregulated upon H2O2 and starvation treatment.  We also proved that miR-29b is the direct target of lncRNA Gm44593. Overexpression of miR-29b completely restored the effect induced by lncRNA Gm44593. In addition, we provided evidences that WNK1 is the direct target of miR-29b. 		Yes	Overexpression of lncRNA Gm44593 manifestly reduced the cell death rates. The ATP content, mtDNA content and mitochondrial membrane potential were alleviated upon overexpression of lncRNA Gm44593.	34967279
GM18840	LncRNA	Homo sapiens	Myocardial Infarction	cardiac muscle tissues and myocardial cells	Interaction(cis-regulatory regions of genes involved in developmental processes, such as Junb, Rras2, and Bcl3)	In Vivo Experiment//RNA Pull-Down//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Bioinformatics Analysis	Gm18840 was upregulated after myocardial infarction in both in vivo and in vitro MIRI models. Gm18840 was 1,471 nt in length and localized in both the cytoplasm and the nucleus of HL-1 cells. Functional studies showed that the knockdown of Gm18840 promoted the apoptosis of HL-1 cells. Gm18840 directly interacts with histones, including H2B, highlighting a potential function in transcriptional regulation. Further ChIRP-seq and RNA-seq analyses showed that Gm18840 is directly bound to the cis-regulatory regions of genes involved in developmental processes, such as Junb, Rras2, and Bcl3.		Yes	 Functional studies showed that the knockdown of Gm18840 promoted the apoptosis of HL-1 cells. 	34322480
Gm16638-201	LncRNA	Mus musculus	Nervous System Diseases	hippocampus (HIP) of CUMS	Regulation(14-3-3Ɛ Pathway)	Bioinformatics Analysis	In conclusion, we found that overexpression of Gm16638-201 negatively regulated several target genes and inhibited the 14-3-3Ɛ pathway in the PFC of CUMS induced depressive mice. This promising result suggests that Gm16638-201 may be a potential novel therapeutic target for depression.		Yes	We further confirmed the down-regulation of 14-3-3Ɛ and the nine predicted target genes in the PFC of CUMS mice except for Sgip1 and IL-16. In addition, they were also down-regulated in the primary cortical cell cultures with overexpression of Gm16638-201 constructed using an adenoviral-medicated gene expression system.	36328497
Gm15290	LncRNA	Homo sapiens	Lung Neoplasms	tumor tissues,cell lines 	Regulation[miR-615-5p]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Transwell Assay	First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively.The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2, and SHMT2		Yes	Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis.	30287504
Gm14320	LncRNA	Mus musculus	Melanoma	 mouse melanoma B16 cells	Interaction(miR-344d-3-5p/Prc1 (and Nuf2) axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	In this study, integrative analysis of whole transcriptome sequencing data demonstrated that lncRNA-Gm31932 is significantly decreased in all-trans retinoic acid (ATRA)-induced and sodium 4-phenylbutanoate (PB-4)-induced mouse melanoma B16 cells. Furthermore, a series of experiments (luciferase reporter assay, RNA pull-down assay, and western blotting) showed that lncRNA-Gm3932 down-regulated Prc1 and Nuf2 by competitively sponging miR-344d-3-5p, which subsequently reduced the expression of cell cycle-related proteins CDK2, CDC2, and Cyclin B1, and increased the expression of P21 and P27.		Yes	 Silencing lncRNA-Gm31932 could inhibit B16 cell proliferation, with cell cycle arrest at the G0/G1 phase and obvious differentiation characteristics, e.g., increased cell volume, melanin content and tyrosinase (Tyr) activity.	35393397
Gm12610	LncRNA	Mus musculus	acute myocardial infarction	heart tissues	Interaction[ IL-33/ST2 pathway]	RNA Pull-Down//Western Blot//Co-IP//Tunel//RIP//qRT-PCR	Compared with sham group, lncRNA ANRIL and ST2 expression levels were up-regulated, and the apoptosis of myocardial cells was increased in heart tissues of AMI group. LncRNA ANRIL regulated myocardial cell apoptosis through IL-33/ST2 pathway.		Yes	In vivo experiments found that interfering lncRNA ANRIL relieved myocardial cell apoptosis and improved heart function in AMI mice.	31674275
Gm12610	LncRNA	Mus musculus	Diabetic Nephropathies	renal cortical tissues from ANRIL knockout (KO) mice and wild type (WT) mice	Regulation	In Vivo Experiment//RNA-seq	These findings suggest that as ANRIL regulates a large number of molecules of pathogenetic significance, it may potentially be a drug target for DN and other chronic diabetic complications.		Yes	ANRIL knockout (KO) prevented a large number of such alterations. The altered transcripts include metabolic pathways, apoptosis, extracellular matrix protein synthesis and degradation, NFKB related pathways, AGE-RAGE interaction pathways etc. ANRIL KO prevented majority of these pathways.	35984863
Gm12610	LncRNA	Mus musculus	Cerebral Infarction	brain tissue	Regulation[NF-κB signaling pathway]	qRT-PCR//Tunel//Western Blot	 Polymerase Chain Reaction (PCR) results revealed that the expression level of lncRNA ANRIL in the CI group was significantly increased when compared with that of the sham group (p<0.05).At the same time, knockdown of lncRNA ANRIL markedly decreased the level of Bax, whereas increased the expression of Bcl-2 (p<0.05). Besides, the number of apoptotic cells in the CI + lncRNA ANRIL siRNA group was remarkably decreased (p<0.05). In addition, lncRNA ANRIL down-regulation remarkably inhibited the phosphorylation of p65 (p<0.05).		Yes	The results of mNSS and TTC staining manifested that knockdown of lncRNA ANRIL could significantly reduce CI-induced neurological deficits and CI area (p<0.05). 	31799680
Gm12610	LncRNA	Mus musculus	Uremic Cardiomyopathy	 UC mice	Interaction(miR-181b-5p/S1PR1 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//IF	ANRIL/S1PR1 were up-regulated and miR-181b-5p was down-regulated in UC mice. ANRIL silencing up-regulated miR-181b-5p and down-regulated S1PR1 (a target of miR-181b-5p).		Yes	ANRIL silencing increased the body weight, recovered renal function [decreased blood urea nitrogen (BUN) and serum creatinine (Scr)] and cardiac function [decreased left ventricular end-diastolic diameter (LVEDD), LV end-systolic diameter (LVESD), LV systolic anterior wall thickness (LVAWS), LV end-diastolic anterior wall thickness (LVAWD), myocardial performance index (MPI), and isovolumic relaxation time (IVRT); increased LV ejection fraction (LVEF), LVEF/MPI, fractional shortening (FS), and E- and A-waves (E/A)], inhibited the inflammation [decreased interferon (IFN)-γ, interleukin (IL)-2, IL-10, and tumor necrosis factor (TNF)-α], and relieved pathological injuries and fibrosis. ANRIL silencing also recovered the viability and inhibited the inflammation of activated T cells in vitro, and inhibited T cell activation in UC mice in vivo. In addition, miR-181b-5p overexpression exhibited same effects with ANRIL silencing in UC. ANRIL silencing inhibited T cell activation through regulating miR-181b-5p/S1PR1, contributing to the remission of UC.	36302829
Gm12610	LncRNA	Mus musculus	Ischemic Stroke	MCAO/R mice	Interaction(miR-671-5p/NF-κB Pathway)	Western Blot//Transfection//FISH//qRT-PCR//Luciferase Report Assay//RNA-seq//H&E Staining//Cell Proliferation Assay//ELISA	 The results showed that ANRIL levels increased in IS model, downregulation of ANRIL reduced infract area, neurological deficit scores and injured cells, and prolong fall latency time in MCAO/R mice, improved cell viability and reduced cell cytotoxicity in OGD/R cells.  This work clarified that downregulation of ANRIL reduced neuroinflammation by negatively regulating miR-671-5p to inhibit NF-κB in IS models, which provided a theoretical foundation for the protective effect of downregulating ANRIL for IS patients.		Yes	 The results showed that ANRIL levels increased in IS model, downregulation of ANRIL reduced infract area, neurological deficit scores and injured cells, and prolong fall latency time in MCAO/R mice, improved cell viability and reduced cell cytotoxicity in OGD/R cells. 	35359242
GLS-AS	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	Interaction[Myc/GLS pathway]	RNA Pull-Down//Northern Blot//Co-IP//FISH//RIP//Luciferase Report Assay//ChIP	GLS-AS was downregulated in pancreatic cancer tissues compared with noncancerous peritumor tissues. Collectively, our study implicates a novel lncRNA-mediated Myc/GLS pathway, which may serve as a metabolic target for pancreatic cancer therapy, and advances our understanding of the coupling role of lncRNA in nutrition stress and tumorigenesis.		Yes	 Ectopic overexpression of GLS-AS inhibited proliferation and invasion of pancreatic cancer cells by repressing the Myc/GLS pathway.	30563888
GLIS2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue and cell lines	regulation[NF-κB pathway]	Western Blot//ISH//qPCR//FISH//PCR//Microarray//IF	We revealed that circGLIS2 expression was higher in CRC tissue and cell lines. Overall, our study reveals that circGLIS2, acting as a potential oncogene, maintains the abnormal activation state of the NF-κB signaling pathway via the miR-671 sponge mechanism in CRC cells.		Yes	Gain-and-loss function assays showed that circGLIS2 was involved in the regulation of cell migration.	32968054
GLIDR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cells	Interaction(miR-1270/TCF12 axis)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	On the basis of the outcomes of RT-qPCR experiments, the relative expression of GLIDR was evidently up-regulated in LUAD cells, while that of miR-1270 was down-regulated. Luciferase reporter, RNA pull down and RIP assays indicated that GLIDR could sponge miR-1270 in LUAD. Additionally, TCF12 was proved as the target gene of miR-1270. 		Yes	The down-regulation of GLIDR inhibits cell proliferation in accordance with the results of CCK-8, EdU and colony formation assays, and accelerates cell apoptosis according to the results of flow cytometry and JC-1 analyses. 	34369267
GK-IT1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	Interaction(DUSP6/ERK/MAPK pathway)	Migration Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//Invasion Assay	In this study we identified an unreported lncRNA, termed GK-IT1 that was aberrantly overexpressed in ESCC tissues and cells. Mechanistically, GK-IT1 competitively bound to mitogen-activated protein kinase 1 (MAPK1) to prevent the interaction between dual specificity phosphatase 6 (DUSP6) and MAPK1, thereby controlling the phosphorylation of MAPK1 and promoting ESCC progression.	 GK-IT1 was closely associated with advanced clinical stage, and it was an independent prognostic indicator of ESCC.	Yes	 Functional assays verified that GK-IT1 significantly promoted ESCC proliferation, invasion, and migration, and suppressed ESCC apoptosis and autophagy. Furthermore, tumorigenesis experiments in nude mice indicated that GK-IT1 promoted ESCC tumor growth and metastasis. 	35608100
GIHCG	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[miR- 1281]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In GC, GIHCG was significantly overexpressed and significantly increased cell proliferation and migration, with the possible mechanism of upregulatingTLE1 expression through adsorption of miR-1281.		Yes	In GC, GIHCG was significantly overexpressed and significantly increased cell proliferation and migration, with the possible mechanism of upregulatingTLE1 expression through adsorption of miR-1281.	31050210
GIHCG	LncRNA	Homo sapiens	Breast Neoplasms	BCa tumor tissue	Interaction[microRNA-1281]	CCK8//qRT-PCR//EdU Staining	RT-PCR results showed that the GIHCG level was remarkably higher in the BCa tumor tissue than in adjacent ones. QRT-PCR results indicated that silencing GIHCG increased the expression of miR-1281, thereby promoting the malignant progression of BCa. Also, the silence of miR-1281 reversed the effect of GIHCG on the proliferative capacity of BCa, thus increasing the cell anti-apoptotic ability.	 Compared with patients with low expression of GIHCG, patients with high expression of GIHCG had higher pathological grades and a lower overall survival.	Yes	Besides, the proliferation ability of BCa cells in GIHCG knockdown groExpression[up-expression] was significantly decreased compared with NC groExpression[up-expression].	31858553
GIHCG	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues 	Expression(highly expressed)	CCK8//Flow Cytometry//RIP//EdU Staining	GIHCG is upregulated in RCC tissues compared with adjacent normal renal tissues. Serum GIHCG level is significantly reduced after radical resection of RCC. 	Increased expression of GIHCG is positively correlated with advanced TNM stages, Fuhrman grades, and poor prognosis. Serum GIHCG level is also significantly upregulated in RCC patients and correlated with advanced TNM stages. 	Yes	Functional assays showed that knockdown of GIHCG significantly represses proliferation and migration of RCC cells.	29364470
GCC2-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung adenocarcinoma tissue	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay//FISH	GCC2-AS1 expression was significantly upregulated in lung adenocarcinoma tissues as compared with normal tissues.	An elevated level of GCC2-AS1 was strongly correlated with shorter overall survival time and was identified as an independent prognostic marker for LUAD patients.	Yes	Depletion of GCC2-AS1 inhibited the proliferation and invasion of LUAD cells in vitro.	33575222
GAU1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer sample	Interaction(GALNT8)	qRT-PCR//Survival Analysis	 In the human cancer transcriptome library MiTranscriptome, we identified GAU1 as the top upregulated lncRNA in colorectal cancer (CRC) by sample set enrichment analysis (overexpression ranking percentile = 99.75%, P < 10-50), which is coexpressed with the potential oncogene GALNT8 (Spearman rho = 0.67, P = 2.44 × 10-23, TCGA dataset n = 184).  Experimental data revealed that GAU1 regulates the expression of GALNT8.		Yes	overexpression of either GAU1 or GALNT8 significantly promotes the cell cycle and proliferation of CRC cell lines and correlates with poor prognosis in patients with CRC (P = 3.04 × 10-2), while silencing of GAU1 or GALNT8 suppressed the cancer cell proliferation and induced the CRC cell line resistance to oxaliplatin in vitro treatment. 	34239555
GATD3	LncRNA	Homo sapiens	Breast Neoplasms	tumor and adjacent non-tumor breast tissues	Regulation[Oct4/Sox2/miR-302/miR-106b axis]	qRT-PCR//Western Blot	The ES1 expression level was detected as significantly higher in cancerous tissues compared to the adjacent non-cancerous samples.Altogether, for the first time, our findings reveal that ES1 controls the proliferation and death of breast cancer cells by regulating the Oct4/Sox2/miR-302/miR-106b axis.	 	Yes	Knockdown experiments show that ES1 suppression in breast cancer cells restricts cancer cell proliferation and cell cycle progression. Moreover, ES1 inhibition can also induce apoptosis and cellular senescence. 	30927330
GASAL1	LncRNA	Homo sapiens	Heart Failure	blood	Interaction[TGF-β1]	qRT-PCR//ELISA//Western Blot	We found that plasma levels of TGF-β1 were significantly higher, while levels of GASL1 in plasma were significantly lower in chronic heart failure (CHF) patients compared to the control group. GASL1 expression was not significantly affected by TGF-β1 overexpression in cardiomyocytes, while cardiomyocytes with GASL1 overexpression showed downregulated TGF-β1. Overexpression of GASL1 led to a decreased, while TGF-β1 overexpression led to an increased apoptotic rate of cardiomyocytes under H2O2 treatment. In addition, TGF-β1 overexpression attenuated the effect of GASL1 overexpression.	Low pretreatment plasma levels of GASL1 were closely associated with poor survival of CHF patients.	Yes	Overexpression of GASL1 led to a decreased, while TGF-β1 overexpression led to an increased apoptotic rate of cardiomyocytes under H2O2 treatment	31223316
GASAL1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cell lines	regulation[Wnt3a/β-catenin signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	LncRNA GASL1 was down-regulated in ESCC cell lines, and GASL1 inhibited ESCC cell progression and regulated cell cycle arrest in ESCC cells.In conclusion, lncRNA GASL1 regulates cell migration, invasion and cell cycle stagnation by inactivating the wnt/β-catenin signaling.		Yes	LncRNA GASL1 was down-regulated in ESCC cell lines, and GASL1 inhibited ESCC cell progression and regulated cell cycle arrest in ESCC cells. In vivo, GASL1 inhibited tumor growth. 	33248356
GAS8-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues 	Interaction(miR-21-3p)	CCK8//qRT-PCR//RNA Pull-Down//Transwell Assay	Results of the present study demonstrated that the expression levels of GAS8-AS1 in gastric cancer tissues were significantly decreased, whereas its expression did not differ among cancer tissues at different clinical stages. In addition, the expression levels of miR-21-3p were markedly increased in cancer tissues, and miR-21-3p expression was negatively associated with the expression of GAS8-AS1. The direct interaction between GAS8-AS1 and miR-21-3p was predicted using the starBase database and was confirmed by using an RNA pull-down assay.	 Low expression levels of GAS8-AS1 predicted poor 5-year survival rates for 70 patients with gastric adenocarcinoma from the Affiliated Hospital of Xuzhou Medical University (Xuzhou, China) during patient follow-up. 	Yes	 In addition, the overexpression of GAS8-AS1 inhibited cancer cell proliferation, while the overexpression of miR-21-3p promoted cancer cell proliferation and attenuated the effects of GAS8-AS1. Overexpression of miR-21-3p promoted cancer cell migration and invasion, whereas overexpression of GAS8-AS1 did not affect cell migration or invasion. 	34992681
GAS8-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	cell lines	Regulation[ miR-135b-5p/CCND2 axis]	qRT-PCR	We found that GAS8-AS1 was down-regulated in PTC cell lines and inhibited proliferation and cycle of PTC cell.In addition, we also proved that overexpressed GAS8-AS1 inhibited tumor formation in vivo GAS8-AS1 suppresses PTC cell growth through the miR-135b-5p/CCND2 axis.		Yes	 We found that GAS8-AS1 was down-regulated in PTC cell lines and inhibited proliferation and cycle of PTC cell. 	30429236
GAS8-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	interaction[binding with Beclin1]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Colony Formation Assay//EdU Staining//Transwell Assay	 LncRNA GAS8-AS1 was decreased in OC tissues and cell lines, and high expression of GAS8-AS1 indicated a higher 5-year survival rate of OC patients.Our study suggested GAS8-AS1 inhibited OC progression by activating autophagy via binding with Beclin1, and GAS8-AS1 might be a potential therapeutic target for OC clinical treatment.	 LncRNA GAS8-AS1 was decreased in OC tissues and cell lines, and high expression of GAS8-AS1 indicated a higher 5-year survival rate of OC patients.	Yes	Overexpression of GAS8-AS1 suppressed growth of OC cells, while deletion of GAS8-AS1 promoted the progression of OC cells. 	33116622
GAS8-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM patients and the healthy controls	Regulation(lncRNA NEAT1)	Western Blot//Transfection//qRT-PCR//Cell Proliferation Assay//Invasion Assay//Transwell Assay	GAS8-AS1 was downregulated, while lncRNA NEAT1 was upregulated in the plasma of GBM patients. 		Yes	 Overexpression of GAS8-AS1 reduced the expression levels of NEAT1 in GBM cells, while knock-down of GAS8-AS1 increased the expression levels of NEAT1. However, overexpression of NEAT1 showed no significant effects on the expression of GAS8-AS1. Knock-down of GAS8-AS1 promoted GBM cell proliferation and invasion and enhanced the activation of the Wnt/β-catenin pathway. However, the effects of knock-down of GAS8-AS1 were alleviated by the knock-down of NEAT1.	33942556
GAS8-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	PTC tissues and cell lines	regulation[miR-187-3p/ATG5 and miR-1343-3p/ATG7 Axes]	CCK8//qRT-PCR//IHC//Luciferase Report Assay	We found that GAS8-AS1 was downregulated in PTC tissues and cell lines. In conclusion, upregulation of ATF2 activated GAS8-AS1-promoted autophagy of PTC cells by sponging oncogenic miR-187-3p and miR-1343-3p and upregulating the expression of ATG5 and ATG7, respectively, making GAS8-AS1 a potential prognostic biomarker and therapeutic target for PTC.	In patients with PTC, low GAS8-AS1 expression was associated with higher tumor-node-metastasis (TNM) stage and lymph node metastasis (LNM).	Yes	Functionally, GAS8-AS1 significantly promoted autophagy and inhibited PTC cell proliferation in vitro and promoted tumorigenesis in vivo.	33230459
GAS8-AS	LncRNA	Homo sapiens	Colorectal Neoplasms	blood	Interaction[lncRNA AFAP1-AS1]	CCK8//qRT-PCR	In the present study we found that plasma GAS8-AS1 was upregulated in early stage CRC patients, and downregulation of GAS8-AS1 effectively distinguished CRC patients from healthy controls.GAS8-AS1 overexpression mediated the downregulation of AFAP1-AS1 in colon cancer cells, while AFAP1-AS1 overexpression did not significantly affect GAS8-AS1 expression. Expression level of GAS8-AS1 decreased, while expression level of AFAP1-AS1 increased with the increase of primary tumor diameters.		Yes	 GAS8-AS1 overexpression led to inhibited, while AFAP1-AS1 overexpression led to promoted proliferation of CRC cells, and AFAP1-AS1 overexpression reduced the inhibitory effects of GAS8-AS1 overexpression on cancer cell proliferation. 	31132513
GAS6-DT	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction[upregulation of FUT4]	Migration Assay//CCK8//qRT-PCR//Invasion Assay//Transwell Assay	GAS6-AS2 expression was high in BC tumors.With regard to its mechanism, GAS6-AS2 acted as a competing endogenous RNA that sponged microRNA-493 (miR-493), thereby increasing the expression of fucosyltransferase IV (FUT4). Either miR-493 inhibition or FUT4 upregulation abrogated the consequences of GAS6-AS2 knockdown in BC cells. These results revealed that GAS6-AS2 sponges miR-493 to enhance the malignant characteristics of BC in vitro and in vivo by increasing FUT4 expression. Thus, this lncRNA is an effective therapeutic target in BC and a promising diagnostic biomarker of this cancer.	 GAS6-AS2 expression was high in BC tumors, manifesting a strong correlation with tumor size, lymph node metastasis, TNM stage, and shorter overall survival in patients with BC.	Yes	 A knockdown of GAS6-AS2 restricted BC cell proliferation, migration, and invasion in vitro and retarded tumor growth in vivo.	31839366
GAS6-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[PI3K/AKT/FoxO3a signaling pathway ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	GAS6-AS2 was up-regulated in HCC tissues and cells. In conclusion, GAS6-AS2 knockdown suppressed proliferation, migration, and invasion but promoted apoptosis of HCC cells by impeding PI3K/AKT/FoxO3a signaling pathway through regulating the GAS6-AS2/miR-493-5p/OTUB1 axis.		Yes	knockdown inhibited proliferation, migration, and invasion but promoted apoptosis. MiR-493-5p, a target of GAS6-AS2, was down-regulated in HCC tissues and cells.	31933797
GAS6-DT	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	cell lines	Regulation[GAS6-AS2/miR-298/CDK9 axis]	Western Blot//Wound Healing Assay//RIP//qRT-PCR//MTT//Luciferase Report Assay//Cell Cycle Assay//Transwell Assay	Moreover, expression of GAS6-AS2 was also increased in bladder cancer cells compared with normal bladder cells. In mechanism, GAS6-AS2 could function as a competitive endogenous RNA (ceRNA) via direct sponging miR-298, which further regulating the expression of CDK9.		Yes	Finally, we also proved that GAS6-AS2 knockdown suppressed tumour growth and metastasis in vivo.	30394665
GAS6-DT	LncRNA	Homo sapiens	Osteosarcoma	OS specimens and cell lines	regulation[miR-934/BCAT1 axis]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	We found that GAS6-AS2 was distinctly upregulated in both OS specimens and cell lines. Mechanistically, GAS6-AS2 positively regulated the expression of BCAT1 through sponging miR-934.	 Distinct up-regulation of GAS6-AS2 in OS was correlated with advanced clinical stages and shorter survivals. 	Yes	Furthermore, GAS6-AS2 knockdown caused tumor suppressive effects via reducing cellular proliferation, migration and invasion, and promoting OS cell apoptosis. 	32269179
GAS6-DT	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells 	Interaction(miR-144-3p/ MAPK6 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//EdU Staining	GAS6-AS2 was up-regulated, while miR-144-3p was suppressed in NSCLC cells compared with normal lung cells.GAS6-AS2 suppression could inhibit the progression of NSCLC cells, and miR-144-3p could attenuate the effect. GAS6-AS2 could function as a competitive endogenous RNA (ceRNA) via direct sponging miR-144-3p-3p, which further regulating the expression of MAPK6. 		Yes	The knockdown of GAS6-AS2 could greatly suppress the tumor growth of NSCLC in vivo.	33459113
GAS6-DT	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction[GAS6/AXL/AKT/ERK signals]	CCK8//ELISA//qPCR//Western Blot	 In this study, we found that lncRNA GAS6-AS2 is significantly elevated in melanoma tissues and cells. Collectively, our data identified GAS6-AS2 as an oncogenic lncRNA in melanoma via activation of GAS6/AXL/AKT/ERK signals.	 Elevated expression of GAS6-AS2 is positively correlated with advanced stages and poor prognosis in melanoma. 	Yes	Functional assays demonstrated that ectopic expression of GAS6-AS2 promotes proliferation and inhibits apoptosis of melanoma cells. In contrast, knockdown of GAS6-AS2 inhibits proliferation and promotes apoptosis of melanoma cells. Furthermore, in vivo functional assays showed that GAS6-AS2 promotes melanoma xenograft growth.	31162889
GAS6-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 BCa cell	Interaction(miR-215-5p/SOX9 axis)	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	A decline in GAS6-AS1 level led to a significant decrease in BCa cell proliferation, and the ability for colony formation. Here, GAS6-AS1 competed as endogenous RNA by sequestering microRNA-215-5p (miR-215-5p) causing an enhanced expression of SRY-box transcription factor 9 (SOX9). 		Yes	A decline in GAS6-AS1 level led to a significant decrease in BCa cell proliferation, and the ability for colony formation. Here, GAS6-AS1 competed as endogenous RNA by sequestering microRNA-215-5p (miR-215-5p) causing an enhanced expression of SRY-box transcription factor 9 (SOX9). 	34976151
GAS6-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-370-3p/miR-1296-5p and FUS/TRIM14 )	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	GAS6-AS1 was greatly elevated in CRC and positively associated with unfavorable prognosis of CRC patients.Moreover, GAS6-AS1 exerted oncogenic function by competitively binding to miR-370-3p and miR-1296-5p, thereby upregulating TRIM14. Furthermore, we verified that GAS6-AS1 and TRIM14 both interact with FUS and that GAS6-AS1 stabilized TRIM14 mRNA by recruiting FUS. 	GAS6-AS1 was greatly elevated in CRC and positively associated with unfavorable prognosis of CRC patients.	Yes	Functionally, GAS6-AS1 positively regulates CRC proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and induces CRC growth and metastasis in vivo.	35962353
GAS6-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML tissues	Interaction(YBX1/MYC axis)	qRT-PCR//RIP//ChIP	We identified GAS6-AS1 was overexpressed in AML, and its aberrant function lead to more aggressive leukemia phenotypes and poorer survival outcomes.  We revealed that GAS6-AS1 directly binds Y-box binding protein 1 (YBX1) to facilitate its interaction with MYC, leading to MYC transactivation and upregulation of IL1R1, RAB27B and other MYC target genes associated with leukemia progression. 	We identified GAS6-AS1 was overexpressed in AML, and its aberrant function lead to more aggressive leukemia phenotypes and poorer survival outcomes. 	Yes	 Further, lentiviral-based GAS6-AS1 silencing inhibited leukemia progression in vivo.	34753494
GAS6-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	tumor tissues	Interaction(E2F1/GLUT1)	In Vivo Experiment//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	We discovered that overexpression of GAS6-AS1 suppressed tumor progression of LUAD both in vitro and in vivo. Mechanically, GAS6-AS1 was found to repress the expression of glucose transporter GLUT1, a key regulator of glucose metabolism.  Further investigation identified that GAS6-AS1 directly interacted with transcription factor E2F1 and suppressed E2F1-mediated transcription of GLUT1, and GAS6-AS1 was downregulated in LUAD tissues and correlated with clinicopathological characteristics and survival of patients. 	GAS6-AS1 was downregulated in LUAD tissues and correlated with clinicopathological characteristics and survival of patients. 	Yes	We discovered that overexpression of GAS6-AS1 suppressed tumor progression of LUAD both in vitro and in vivo. 	34141461
GAS6-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD samples and cell lines	Interaction(miR-24-3p/GTPase IMAP Family Member 6)	In Vivo Experiment//Transfection//Wound Healing Assay//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 The expression of GAS6-AS1 was notably downregulated in LUAD samples and cell lines and associated with a poor prognosis. Down-expressed GAS6-AS1 acted as a sponge for miR-24-3p and down-regulated the expression of its target, GTPase IMAP Family Member 6. 	The expression of GAS6-AS1 was notably downregulated in LUAD samples and cell lines and associated with a poor prognosis. 	Yes	 GAS6-AS1 overexpression inhibited the migration and invasion of A549 and H1650 cells. 	34513660
GASAL1	LncRNA	Homo sapiens	stomach carcinoma		regulation[PI3K/AKT and ras/raf/MEK/ERK pathways]	CCK8//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	GASL1 restrained GC cell proliferation and metastasis and blocked PI3K/AKT and ras/raf/MEK/ERK pathways by sponging miR-106a.		Yes	On cell metastasis, up-regulation of GASL1 decreased cell migration, invasion and related proteins matrix metalloproteinase (MMP)-9 and Vimentin levels. Meanwhile, silencing GASL1 exerted opposite effects on GC cells.	32897806
GASAL1	LncRNA	Homo sapiens	stomach carcinoma	gastric cancer tissues	Regulation[Wnt/β-catenin signaling pathway]	CCK8//qRT-PCR//Western Blot	The expression level of lncRNA GASL1 was significantly downregulated in gastric cancer tissues compared with adjacent normal tissues from patients with gastric carcinoma.  GASL1 overexpression downregulated, while GASL1 knockdown Expression[up-expression]regulated β-catenin expression.	 Serum GASL1 levels distinguished patients with gastric carcinoma from healthy controls, and low expression levels of GASL1 were associated with decreased postoperative survival time. 	Yes	 GASL1 overexpression downregulated, while GASL1 knockdown Expression[up-expression]regulated β-catenin expression. GASL1 overexpression inhibited, and GASL1 knockdown promoted gastric cancer cell proliferation. 	30988785
GASAL1	LncRNA	Homo sapiens	prostate carcinoma	PC tissues	Interaction[GLUT-1]	CCK8//qRT-PCR	The results demonstrated that GASL1 was significantly downregulated in the tissue and serum of patients with PC compared to those of healthy subjects.A GASL1 expression vector was transfected into PC cells prior to assessment of cell proliferation and expression of B cell lymphoma 2 (Bcl-2) and glucose transporter 1 (GLUT-1) by Cell Counting Kit-8 and western blotting, respectively. Overexpression of GASL1 Expression[up-expression]regulated Bcl-2 expression and downregulated GLUT-1 expression.	In addition, GASL1 was used to distinguish patients with PC from healthy controls, and low expression levels of GASL1 were associated with short survival time. Expression levels of GASL1 were significantly associated with tumor size. 	Yes	GASL1 overexpression inhibited PC cell growth. Overexpression of GASL1 Expression[up-expression]regulated Bcl-2 expression and downregulated GLUT-1 expression. 	31186749
GATA6-AS	LncRNA	Homo sapiens	cervical squamous cell carcinoma	cervical squamous cell carcinoma tissues,blood	Interaction[downregulating MTK-1]	qRT-PCR//Western Blot//Transwell Assay	It was identified that the expression levels of GATA6-AS were lower in tumor tissues compared with healthy tissues.In addition, serum levels of GATA6-AS were higher in patients compared with healthy controls. The expression levels of MTK-1 were also reduced following GATA6-AS overexpression. Therefore, the present study proposed that downregulated GATA6-AS expression was associated with tumor metastasis in cervical squamous cell carcinoma, and that GATA6-AS expression may inhibit cancer cell migration and invasion by downregulating MTK-1.	 The serum levels of GATA6-AS were associated with tumor metastasis, and may serve as a potential diagnostic and prognostic marker for cervical squamous cell carcinoma. 	Yes	 Furthermore, GATA6-AS overexpression inhibited cancer cell migration and invasion. 	31404324
GATA6-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-543/RKIP axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	GATA6-AS1 was significantly lowly expressed in NSCLC tissues and cell lines, and its low expression level was significantly correlated with larger tumor size and positive lymph node metastasis. 	GATA6-AS1 was significantly lowly expressed in NSCLC tissues and cell lines, and its low expression level was significantly correlated with larger tumor size and positive lymph node metastasis. 	Yes	GATA6-AS1 overexpression inhibited the proliferation, migration, invasion and epithelial-mesenchymal transition of NSCLC cells, while GATA6-AS1 knockdown caused the opposite effects. 	33061622
GATA6-AS1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissue 	interaction[Sponges miR-324-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Expression of GATA6-AS1 was decreased in lung cancer based on the analysis of RNA sequencing dataset, TCGA data and RT-qPCR of clinical tissue samples.Oncogene miR-324-5p was predicted to interact with GATA6-AS1.		Yes	Via overexpression of GATA6-AS1, it was revealed that GATA6-AS1 inhibited lung cancer cell proliferation and invasion.	33061453
GATA6-AS	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[downregulating microRNA-25-3p]	CCK8//qRT-PCR	In the present study it was found that GATA6-AS was downregulated in tumor tissues compared with adjacent normal tissues. MicroRNA (miR)-25-3p was upregulated in tumor tissues compared with adjacent normal tissues and was inversely associated with GATA6-AS in tumor tissues only. The overexpression of miR-25-3p in gastric cancer cells resulted in no significant changes in the expression levels of GATA6-AS, whereas overexpression of GATA6-AS led to significantly downregulated miR-25-3p levels. Furthermore, overexpression of GATA6-AS inhibited cancer cell proliferation, with no effect on migration and invasion. The overexpression of miR-25-3p resulted in increased proliferation of cancer cells and attenuated the effects of GATA6-AS overexpression. Thus, it is postulated that GATA6-AS inhibits proliferation of gastric cancer cells by downregulating miR-25-3p.		Yes	Furthermore, overexpression of GATA6-AS inhibited cancer cell proliferation, with no effect on migration and invasion. 	31611972
GATA6-AS	LncRNA	Homo sapiens	Endometrial Neoplasms	17 pairs of EC tissues and adjacent ones	Interaction(MMP)	qRT-PCR//Luciferase Report Assay//Western Blot	Our data showed that GATA6-AS expression in EC tissue specimens was remarkably lower than that in adjacent ones. Meanwhile, luciferase assay confirmed the binding relationship between GATA6-AS and MMP9.		Yes	 In vitro cell experiments revealed that overexpression of GATA6-AS markedly attenuated the proliferation ability of EC cells while elevated their apoptosis. 	34761584
GATA6-AS	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	blood	regulation[down-regulating miR-205]	qRT-PCR	We found that plasma GATA6-AS expression was down-regulated in CSCC patients than that in healthy females, and HPV infection did not significantly affect the plasma expression of GATA6-AS. Taken together, these results suggest that GATA6-AS may inhibit cell proliferation and promote cell apoptosis in CSCC by down-regulating miR-205.		Yes	 In addition, GATA6-AS over-expression inhibited CSCC cell proliferation and promoted CSCC cell apoptosis, while miR-205 over-expression played opposite roles and attenuated the effects of GATA6-AS over-expression on CSCC cells.	33167959
GATA6-AS	LncRNA	Homo sapiens	Glioma	Glioma tissue	Interaction[Downregulating lncRNA TUG1]	CCK8//qRT-PCR	GATA6-AS was significantly upregulated in glioma. TUG1 was significantly downregulated in glioma and was inversely correlated with GATA6-AS. GATA6-AS overexpression led to TUG1 downregulation, whereas TUG1 overexpression failed to significantly affect GATA6-AS. 		Yes	GATA6-AS overexpression promoted glioma cell proliferation and inhibited apoptosis	31809214
GATA6-AS	LncRNA	Homo sapiens	Gallbladder Neoplasms	GBC tissues  	Interaction[downregulating miR-421]	Invasion Assay//PCR//Transwell Assay	We found that GATA6-AS was downregulated in tumor tissues than in adjacent healthy tissues of GBC patients, and GATA6-AS expression levels in tumor tissues decreased with the increase of clinical stages. MiR-421 overexpression failed to significantly affect GATA6-AS in GBC cells, while GATA6-AS overexpression resulted in inhibited miR-421 expression.MiR-421 overexpression led to increased migration and invasion rates of GBC. Rescue experiments (co-transfection) showed that miR-421 overexpression led to attenuated effects of GATA6-AS overexpression.	We found that GATA6-AS was downregulated in tumor tissues than in adjacent healthy tissues of GBC patients, and GATA6-AS expression levels in tumor tissues decreased with the increase of clinical stages. 	Yes	 GATA6-AS overexpression led to decreased migration and invasion rates of GBC cells. 	31632058
GATA6-AS	LncRNA	Homo sapiens	Lymphoma, Mantle-Cell	blood	Interaction[downregulating GLUT1]	CCK8//qRT-PCR//Western Blot	It was found that plasma lncRNA GATA6-AS expression level was downregulated in patients with MCL, compared with that in healthy controls.	Downregulation of lncRNA GATA6-AS has potential diagnostic value in early stage MCL.	Yes	Additionally, lncRNA GATA6-AS overexpression inhibited, whilst GLUT1 overexpression promoted the proliferation of JVM-2 and Z-138 MCL cells; GLUT1 overexpression partially reversed the inhibitory effects of lncRNA GATA6-AS overexpression.	31402946
GATA3‑AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Interaction(miR‑30b‑5p‑Tex10 axis )	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	Upregulation of GATA3‑AS1 was revealed in PC tissues and cell lines. Collectively, these data indicated that the GATA3‑AS1‑miR‑30b‑5p‑Tex10 axis modulates tumorigenesis in PC, which may be associated with the Wnt/β‑catenin signaling pathway.		Yes	Knockdown of GATA3‑AS1 in PANC‑1 or AsPC‑1 cells markedly reduced cell viability, cell proliferation, and cell invasion abilities, while cell apoptosis was increased. In addition, GATA3‑AS1 knockdown suppressed the stemness of PANC‑1 and AsPC‑1 cells by decreasing the spheroid formation ability. A tumor xenograft in vivo assay demonstrated that GATA3‑AS1 knockdown inhibited tumorigenicity of AsPC‑1 cells. 	33760161
GASAL1	LncRNA	Homo sapiens	Glioma	 tumor tissues, paired adjacent healthy tissues and serum	Interaction[TGF-β1]	CCK8//qRT-PCR//Western Blot	The results demonstrated that a majority of patients with glioma (56/62, 90.3%) had significantly decreased expression of GASL1 in tumor tissues compared with expression in paired adjacent healthy tissues (P<0.05; Fig. 1), indicating that Expression[down-expression]regulation of GASL1 may be involved in the pathogenesis of glioma.In glioma cell lines with GASL1 overexpression, TGF-β1 expression was decreased and proliferation was inhibited. GASL1 knockExpression[down-expression] in glioma cell lines led to increased TGF-β1 expression and proliferation. TGF-β1 treatment had no effect on GASL1 expression, but TGF-β1 treatment partially rescued the inhibition of proliferation in cells overexpressing GASL1. Therefore, GASL1 may inhibit tumor growth of glioma by inactivating the TGF-β signaling pathway.	All patients were followed Expression[Expression[up-expression]-expression] for 5 years or until their mortality to determine the survival rate. The Kaplan-Meier method was used to plot survival curves and the two groExpression[Expression[up-expression]-expression]s were compared using a log-rank test. As presented in Fig. 3, the overall survival rate of patients with a low serum level of GASL1 was significantly worse compared with that of patients with a high serum level of GASL1.	Yes	GASL1 overexpression inhibited glioma cell proliferation and Expression[down-expression]regulated TGF-β1 expression, but TGF-β1 treatment decreased the effect of GASL1 overexpression on proliferation.	31186801
GATA3-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[decreased PTEN, CDKN1A, and TP53]	CCK8//qRT-PCR	GATA3-AS1 was significantly upregulated in HCC tissues compared with matched normal tissues. Our data suggested that GATA3-AS1 promotes cell proliferation and metastasis of HCC by suppression of PTEN, CDKN1A, and TP53.	The high expression of GATA3-AS1 was significantly correlated with larger tumor size, advanced TNM stage, and more lymph node metastasis. High GATA3-AS1 expression was markedly correlated with shorter overall survival times of HCC patients. 	Yes	 Furthermore, knockdown of GATA3-AS1 obviously inhibited Hep3B and HCCLM3 cell growth and migration, whereas overexpression of GATA3-AS1 had the opposite effects.	31871924
GATA3-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues and EC cells	Interaction(miR-361/ARRB2 axis)	qRT-PCR//Western Blot	GATA3-AS1 and ARRB2 were upregulated while miR-361 was downregulated in human EC tissues and EC cells. GATA3-AS1 negatively regulated miR-361 expression. ARRB2 was the direct target of miR-361 and could activate the Src/Akt pathway. In vivo, GATA3-AS1 knockdown suppressed tumor progression by upregulating the miR-361 expression. lncRNA GATA3-AS1 promoted EC invasion and migration by the miR-361/ARRB2 axis, which indicated that GATA3-AS1 might be a promising therapeutic option for advanced EC progression. 		Yes	GATA3-AS1 knockdown constrained cell proliferation, invasion, migration, and EMT while promoting the apoptosis of EC cells by upregulating miR-361. 	35788718
GATA3-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	regulation[stabilizing PD-L1 protein and degrading GATA3 protein]	qRT-PCR	GATA3-AS1 was markedly overexpressed in TNBC tissues and cells. GATA3-AS1 contributed to TNBC progression and immune evasion through stabilizing PD-L1 protein and degrading GATA3 protein, offering a new target for the treatment of TNBC.		Yes	Knockdown of GATA3-AS1 suppressed TNBC cell growth and enhanced the resistance of TNBC cells to immune response. 	32687248
GATA3-AS1	LncRNA	Homo sapiens	Pre-Eclampsia	placental samples with PE	Interaction(miR-488-3p/ROCK1 Axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	Our results showed that GATA3-AS1 and ROCK1 were overexpressed while miR-488-3p was downregulated in placental samples with PE. Mechanically, GATA3-AS1 acted as a molecular sponge of miR-488-3p and miR-488-3p targeted ROCK1 in trophoblast cells.  In rescue assays, ROCK1 overexpression or miR-488-3p downregulation reversed the effects of GATA3-AS1 silencing on trophoblast cell phenotypes. GATA3-AS1 is overexpressed in PE and promotes PE progression by the miR-488-3p/ROCK1 axis.		Yes	Functionally, GATA3-AS1 overexpression promoted trophoblast cell apoptosis and inhibited cell proliferation, migration, and invasion.	35993943
GATA2-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	Interaction(mir-940/PTPN12 axis)	RNA Pull-Down//Western Blot//Colony Formation Assay//Flow Cytometry//RIP//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	The expression of GATA2-AS1 and PTPN12 was reduced, while miR-940 expression was enhanced in ESCC tissues and cell lines. Bioinformatics analysis, dual luciferase and RIP assays revealed that GATA2-AS1 upregulated PTPN12 expression by competitively targeting miR-940. miR-940 reversed the inhibitory effect of GATA2-AS1 on the biological behavior of ESCC cells.		Yes	 In vivo experiments showed that GATA2-AS1 inhibited the progression of ESCC cells toward malignancy.	35364057
GATA2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(GATA2)	Tunel//RIP//qRT-PCR//FISH//ChIP	GATA2-AS1 and GATA2 were highly expressed in CRC cells.GATA2-AS1 expression was positively correlated with GATA2. GATA2-AS1 recruited DEAD-box helicase 3 X-linked (DDX3X) to stabilize GATA2 mRNA. GATA2 combined with GATA2-AS1 promoter to enhance GATA2-AS1 expression.		Yes	Knockdown of GATA2-AS1 and GATA2 impeded CRC cell proliferation, invasion, EMT and cancer stemness, and induced cell apoptosis. 	35752837
GASAL1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells	Interaction(miR-193b-5p/USP10  axis)	qRT-PCR//Wound Healing Assay//FISH//Transwell Assay	GASAL1 displayed a high expression in HCC cells and GASAL1 knockdown led to impeded cell proliferation and migration, as well as tumor progression. A series of mechanism analysis demonstrated GASAL1 could sponge miR-193b-5p to raise the expression of USP10. Moreover, USP10 could induce PCNA deubiquitination to promote HCC cell growth. 		Yes	GASAL1 displayed a high expression in HCC cells and GASAL1 knockdown led to impeded cell proliferation and migration, as well as tumor progression. 	34914965
LINC00265	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow and serum	Regulation[PI3K-AKT pathway]	qRT-PCR//Western Blot	LINC00265 was significantly highly expressed in the bone marrow and serum of AML patients.Our findings not only demonstrated that LINC00265 contributes to AML proliferation, migration and invasion via modulation of PI3K/AKT signaling, but also suggested the potential value of LINC00265 as a clinical prognostic and a diagnostic marker for AML.	 Clinical assay indicated that AML patients with higher serum LINC00265 expression suffered poorer overall survival. 	Yes	Functionally, overexpression of LINC00265 suppressed the capability of proliferation, migration and invasion in AML cell lines.	30536332
LINC00265	LncRNA	Homo sapiens	Colorectal Neoplasms		Interaction[targeting EGFR]	Western Blot//CCK8//qRT-PCR//Invasion Assay//Transwell Assay	The expression level of LINC00265 is increased in CRC tissues.Our results indicate that LINC00265 induces cell proliferation, migration and inhibits CRC cells apoptosis by targeting EGFR. LINC00265 could be served as a diagnostic factor and therapeutic target for CRC patients.		Yes	 In addition, further experiments indicated that LINC00265 knockdown impaired cell proliferation and invasion, promoted cell cycle distribution and apoptosis in HT29 cells.	31824175
LINC00273	LncRNA	Homo sapiens	Ovarian Neoplasms	cells and tissues	Expression(highly expressed)	CCK8//qRT-PCR//Western Blot//Transwell Assay	 LINC00273 expression was significantly more increased in the cancerous ovarian tissues than the adjacent tissues. The LINC00273 expression of the ovarian cancer cell lines was higher than that of the normal ovarian epithelial cells. LINC00273 knockdown also promoted E-cadherin expression in the ovarian cancer cells, and inhibited vimentin, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and N-cadherin, expression to inhibit the invasion and migration ability of the ovarian cancer cells. The in vivo experiments indicated that LINC00273 knockdown suppressed in vivo cancer cell proliferation in the ovaries.		Yes	LINC00273 knockdown greatly suppressed the proliferative and clonogenic function of these cancerous cells. The flow cytometry results revealed that LINC00273 knockdown notably induced G0/G1 phase arrest in the ovarian cancer cells. 	36388777
hsa_circ_0084927	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	regulation[circ_0084927/miR-1179/CDK2 regulatory network]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU	 Our results indicated that circ_0084927 was up-regulated in CC tissues and cells. Our results also provided novel candidate targets for CC treatment in that it revealed the circ_0084927/miR-1179/CDK2 regulatory network that strengthened CC aggressiveness.		Yes	Findings also revealed that circ_0084927 silence inhibited CC cell proliferation and adhesion while facilitating apoptosis and triggering cell cycle arrest. 	32699532
circOSBPL10	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	regulation[miR-1179/UBE2Q1 axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay	CircOSBPL10 characterized with cyclic structure was revealed to possess elevated expression in CC cells.FOXA1-induced circOSBPL10 facilitates CC progression through miR-1179/UBE2Q1 axis, highlighting a strong potential for circOSBPL10 to serve as a promising therapeutic target in CC.		Yes	CircOSBPL10 downregulation elicited suppressive impacts on CC cell proliferation and migration. 	32831649
circNFATC3	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues, cell lines	regulation[SDC2]	qRT-PCR//Luciferase Report Assay//Western Blot	 We found that circNFATC3 expression was upregulated in primary CC tissues and positively correlated with CC tumor size and stromal invasion.Our data indicate that circNFATC3 sponges miR-9-5p to regulate SDC2 expression and, thereby, to promote CC tumor development.	 We found that circNFATC3 expression was upregulated in primary CC tissues and positively correlated with CC tumor size and stromal invasion.	Yes	 In addition, we found that exogenous circNFATC3 overexpression enhanced the proliferation, migration and invasion of HeLa cells, while its knockdown reduced the malignancy of SiHa cells.	32902825
hsa_circ_0000285	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissue and cells	regulation[miR197-3p-ELK1 Axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	 circ_0000285 abundance was enhanced in CC tissue and cells and mainly located in cytoplasm. Knockdown of circ_0000285 repressed CC development by increasing miR197-3p and decreasing ELK1.		Yes	Silence of circ_0000285 suppressed cell viability and colony formation, arrested the cell cycle at the G0/G1 phase, and induced apoptosis and autophagy in CC cells. 	32982457
LOC146880	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC cell lines	Interaction(miR-328-5p/FSCN1/MAPK axis)	In Vivo Experiment//Western Blot//Transwell Assay//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//IF	Moreover, CREB-binding protein (CBP) and H3K27 acetylation levels were significantly higher in the LOC146880 promoter in ESCC cell lines than in the controls. Bioinformatics analysis, dual luciferase reporter assays, and RNA immunoprecipitation assays showed that LOC146880 regulates FSCN1 expression in ESCC cells by sponging miR-328-5p. Moreover, FSCN1 expression correlated with activation of the MAPK signaling pathway in ESCC cells and tissues.		Yes	 LOC146880 silencing inhibited in vitro proliferation, invasion, migration, and epithelial-mesenchymal transition of ESCC cells. LOC146880 silencing also induced G1-phase cell cycle arrest and apoptosis in ESCC cells.  In vivo xenograft tumor volume and liver metastasis were significantly reduced in nude mice injected with LOC146880-silenced ESCC cells as compared to those injected with control shRNA-transfected ESCC cells. 	34016787
hsa_circ_0003204	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines 	regulation[MAPK pathway]	qRT-PCR//Western Blot	We found that circRNA hsa_circ_0003204 was significantly upregulated in CC tissues.  The MAPK pathway was different in hsa_circ_0003204 over-expression or down-expression cells, compared to parental cells.		Yes	The function and potential molecular mechanisms of hsa_circ_0003204 were also investigated in vitro and in vivo. Hsa_circ_0003204 knockdown reduced cell growth, migration, and invasion but promoted cells apoptosis.	33047994
hsa_circ_0084927	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	regulation[miR-142-3p/ARL2 axis]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	The expression of circ_0084927 and ARL2 was enhanced in cervical cancer tissues and cells, while the expression of miR-142-3p was opposite to them.Circ_0084927 accelerated the progression of cervical cancer partly by mediating the miR-142-3p/ARL2 axis.		Yes	Circ_0084927 knockdown significantly blocked cervical cancer cell proliferation, migration and invasion and induced cell cycle arrest.	33061617
hsa_circ_0084927	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells 	regulation[miR-634/TPD52 Axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	Hsa_circ_0084927 and TPD52 were upregulated while miR-634 was downregulated in CC tissues and cells. Hsa_circ_0084927 accelerated CC advancement via upregulating TPD52 via sponging miR-634, offering a new evidence to support hsa_circ_0084927 as a promising target for CC treatment.		Yes	Hsa_circ_0084927 silencing reduced tumor growth in vivo and induced cell cycle arrest, apoptosis, and curbed proliferation, colony formation, migration, and invasion of CC cells in vitro. 	33061631
LOC107985656	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-106b-5p/LATS1 axis)	qRT-PCR//MTT//RNA Pull-Down	Results showed that LncRNA LOC107985656 was downregulated in HCC tissues and cells. LOC107985656 could activate the tumor-suppressive Hippo pathway by repressing yes association protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1, also known as TAZ) (two homologs of Yki) protein expression in HCC. Further investigation suggested that LOC107985656 regulated the expression of LATS1 by acting as a sponge for absorbing miR-106b-5p in HCC cells.		Yes	Upregulation of LOC107985656 inhibited the proliferation of HCC cells, whereas its knockdown promoted this phenomenon. 	34565286
circPVT1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms		Expression[highly expressed]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//FISH//Luciferase Report Assay	In this research, bioinformatics analysis and RT-PCR analysis showed that hsa_circ_0009143 (circRNA_PVT1) was up-regulated in cervical cancer. 		Yes	 Knockdown of circRNA_PVT1 inhibits the migration and invasion of cervical cancer cells and would prevent pulmonary metastasis. Overexpression of circRNA_PVT1 induced migration and invasion of cervical cancer cells, which would result in the promotion of pulmonary metastasis.	33109773
hsa_circ_0007364	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	regulation[miR-101-5p/MAT2A axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 hsa_circ_0007364 was upregulated in CC,hsa_circ_0007364 promoted CC cell progression hsa_circ_0007364/miR-101-5p/MAT2A axis in CC.	In the present study, we used bioinformatics analysis and a series of experimental analysis to characterize a novel circRNA, hsa_circ_0007364 was up-regulated and associated with advanced clinical features in CC patients.	Yes	Hsa_circ_0007364 inhibition notably suppressed the proliferation and invasion abilities of CC cells in vitro and reduced tumor growth in vivo.	33138667
hsa_circ_0102171	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cells	interaction[targeting  miR-4465/CREBRF axis]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Interestingly, we discovered that circ_0102171 expressed at a high level in CC tissues and cells. Finally, in vivo data supported that silencing circ_0102171 hindered CC cell growth. In conclusion, circ_0102171 aggravates CC progression via targeting miR-4465/CREBRF axis.		Yes	Functionally, silencing circ_0102171 prohibited cell proliferation, migration and invasion, and strengthened cell apoptosis in CC in vitro.	33615474
circAGFG7	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Regulation[miR-370-3p/RAF1 signaling]	qRT-PCR	The levels of circAGFG1 was abundant in CC cells in comparison with normal cervical cell End1/E6E7. circAGFG1 promoted proliferation and migration of CC cells via enhancing the activity of RAF/MEK/ERK pathway by sponging miR-370-3p and further regulating RAF1.		Yes	 The inhibitory effect of decreased circAGFG1 level on the proliferative and migratory abilities of CC cells was assessed. 	31703640
hsa_circ_0075341	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Regulation[miR-149-5p/AURKA axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our data showed that the expression of hsa_circ_0075341 was significantly upregulated and associated with larger tumor size, advanced FIGO stage, and lymph-node metastasis in cervical cancer patients.Collectively, our data suggested that hsa_circ_0075341 promoted cervical cancer cell proliferation and invasion through regulating the miR-149-5p/AURKA axis, which provided a novel therapeutic target for cervical cancer treatment.	Our data showed that the expression of hsa_circ_0075341 was significantly upregulated and associated with larger tumor size, advanced FIGO stage, and lymph-node metastasis in cervical cancer patients.	Yes	Hsa_circ_0075341 inhibition reduced cervical cancer cell proliferation and invasion in vitro. 	31706100
hsa_circ_0005576	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cell lines	Regulation[miR-153/KIF20A axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	 In the present study, we analyzed two GSE microarrays to screen for CC-specific circRNAs and found two circRNAs both expressed in CC cells and tissues. Among them, circ_0005576 was significantly overexpressed in both CC tissues and cell lines.Mechanistically, circ 0005576 was mainly located in the cytoplasm and served as a sponge of miR-153-3p to increase kinesin family member 20A (KIF20A) expression. Rescue assays further validated the effects of circ_0005576/miR-153-3p/KIF20A axis on CC proliferation, migration and invasion. In conclusion, our research reveals a novel circ_0005576/miR-153-3p/KIF20A axis promoting CC progression, which may suggest a new insight into the pathogenesis of CC.	 Furthermore, upregulated circ_0005576 was positively associated with advanced FIGO stage, lymph node metastasis, but was negatively related with overall survival of CC patients.	Yes	Additionally, circ_0005576 knockdown induced a suppressed cell growth, colony formation and metastasis of HeLa and SiHa cells.	31545253
circCLK3	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Regulation[circCLK3/miR-320a/FoxM1 axis]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We found that the level of circCLK3 was remarkably higher in cervical cancer tissues than in adjacent normal tissues, and closely associated with tumor differentiation, FIGO stage and depth of stromal invasion.The pull-down, luciferase reporter and RIP assays demonstrated that circCLK3 directly bound to and sponge miR-320a. MiR-320a suppressed the expression of FoxM1 through directly binding to 3'UTR of FoxM1 mRNA. In addition, FoxM1 promoted cell proliferation, migration, and invasion of cervical cancer, while miR-320a suppressed cell proliferation, migration, and invasion through suppressing FoxM1, and circCLK3 enhanced cell proliferation, migration and invasion through sponging miR-320a and promoting FoxM1 expression. In summary, circCLK3 may serve as a novel diagnostic biomarker for disease progression and a promising molecular target for early diagnoses and treatments of cervical cancer.	We found that the level of circCLK3 was remarkably higher in cervical cancer tissues than in adjacent normal tissues, and closely associated with tumor differentiation, FIGO stage and depth of stromal invasion.	Yes	Down-regulated circCLK3 evidently inhibited cell growth and metastasis of cervical cancer in vitro and in vivo, while up-regulated circCLK3 significantly promoted cell growth and metastasis in vitro and in vivo. 	31831728
circATP8A2	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues,cell lines	Regulation[miR-433/EGFR axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Circ-ATP8A2 was significantly enhanced in CC specimens and cells. For the mechanism exploration, circ-ATP8A2 sponges miR-433 to release its suppression on epidermal growth factor receptor (EGFR) expression at post-transcriptional level. What's more, circ-ATP8A2 could promote cell progression by miR-433/EGFR axis in CC cells. Collectively, this work might offer a potential treatment target for CC. ABBREVIATIONS.		Yes	Knockdown of circ-ATP8A2 inhibited cell proliferation, migratory and invasive capacities and increased apoptotic cells.	31029604
circEIF4G2	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Interaction[miR‑218/HOXA1 pathway]	CCK8//qRT-PCR//Wound Healing Assay//Colony Formation Assay	 In the present study, circRNA isoform of eukaryotic translation initiation factor 4γ2 (circEIF4G2) was revealed to be significantly upregulated in CC tissues and cell lines.  Additionally, circEIF4G2 was identified to serve as a sponge for microRNA‑218 (miR‑218), which targeted homeobox A1 (HOXA1). Furthermore, circEIF4G2 may increase the expression levels of HOXA1 by sponging miR‑218. Rescue experiments suggested that transfection with a miR‑218 inhibitor attenuated the inhibitory effects of circEIF4G2 knockdown on cell proliferation, migration and invasion. Furthermore, silencing HOXA1 reversed the effects of the miR‑218 inhibitor on CC cells. Collectively, the present findings suggested that circEIF4G2 promoted cell proliferation and migration via the miR‑218/HOXA1 pathway.		Yes	circEIF4G2 knockdown suppressed the malignant features of CC cells, including cell proliferation, colony formation, migration and invasion. 	30896864
hsa_circ_0007534	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	Regulation[miR-498/BMI-1 signaling]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The expression of hsa_circ_0007534 was upregulated in cervical cancer tissues and cell lines. MicroRNA-498 (miR-498) was identified as a target of the miRNA encoded by hsa_circ_0007534. Levels of miR-498 were decreased in cervical cancer tissues, a finding that was inversely correlated with hsa_circ_0007534 expression. miR-498 overexpression repressed the proliferation and invasion of cervical cancer cells. B-cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) was verified as a target gene of miR-498. BMI-1 overexpression reversed the effects of hsa_circ_0007534 depletion or miR-498 overexpression on cervical cancer cell proliferation and invasion.		Yes	Depletion of hsa_circ_0007534 decreased both the proliferation and invasion of cervical cancer cells. 	31445025
circSLC26A4	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues,cell lines	Regulation[miR-1287-5p/HOXA7 Axis]	Western Blot//CCK8//qRT-PCR//FISH//RIP//RNA-seq//Luciferase Report Assay//Transwell Assay	Here, a novel identified circRNA, circSLC26A4, was found to be upregulated in cervical cancer tissue and cells.  Furthermore, circSLC26A4 acted as the sponge of miR-1287-5p; moreover, miR-1287-5p targeted the 3' UTR of HOXA7 mRNA. Mechanistically, RNA binding protein (RBP) quaking (QKI) was identified to interact with the QKI response elements (QREs) in SLC26A4 gene introns, thereby promoting circSLC26A4 biogenesis.	Clinically, the high expression of circSLC26A4 was related to the poor survival of cervical cancer patients. 	Yes	Functionally, cellular experiments indicated that circSLC26A4 knockdown repressed the proliferation, invasion, and tumor growth in vitro and in vivo. 	31896069
circUBAP2	CircRNA	Homo sapiens	Uterine Cervical Neoplasms		regulation[miR-361-3p/SOX4 axis]	RNA Pull-Down//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	CircUBAP2 was up-regulated in CC tissues and cell lines and high circUBAP2 expression predicated poor outcome.CircUBAP2 represents a prognostic marker and contributes to tumor growth and metastasis via modulating miR-361-3p/SOX4 axis in CC, which indicates a potential therapeutic target for CC treatment.	CircUBAP2 was up-regulated in CC tissues and cell lines and high circUBAP2 expression predicated poor outcome.	Yes	Knockdown of circUBAP2 suppressed cell proliferation, migration, invasion and EMT, while induced apoptosis in CC in vitro, and inhibited tumor growth and metastasis in vivo.	32760224
hsa_circ_0000069	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues ,cell lines 	regulation[miR-873-5p/TUSC3 axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We firstly demonstrated that hsa_circ_0000069 was significantly upregulated and closely related to the lymph node metastasis, and poor prognosis of CC patients.We demonstrated a critical hsa_circ_0000069-miR-873-5p-TUSC3 function network involved in the CC progression, which provides mechanistic insights into the roles of CircRNAs in CC progression and a promising therapeutic target for CC treatment.	We firstly demonstrated that hsa_circ_0000069 was significantly upregulated and closely related to the lymph node metastasis, and poor prognosis of CC patients.	Yes	Besides, hsa_circ_0000069 promoted CC cell proliferation, migration, and invasion. The knockdown of hsa_circ_0000069 also inhibited CC tumor growth in vivo. 	32655319
hsa_circ_0067934	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues,cell lines	Regulation[miR-545/EIF3C axis ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circ_0067934 was overexpressed in CC tissues and cell lines.Mechanistically, silencing circ_0067934 increased miR-545 expression. MiR-545 repressed EIF3C expression through targeting its 3'-untranslated region. MiR-545 sExpression[Expression[up-expression]-expression]pressed the proliferation, migration, and invasion of CC cells, whereas restoration of EIF3C could rescue the effects of circ_0067934 knockExpression[down-expression].	Circ_0067934 Expression[Expression[up-expression]-expression]regulation was associated with advanced stage, lymph node metastasis, and poor prognosis in CC patients.	Yes	KnockExpression[down-expression] of circ_0067934 sExpression[Expression[up-expression]-expression]pressed the proliferation, colony formation, migration, invasion, and epithelial-mesenchymal transition of CC cells in vitro. Circ_0067934 loss also inhibited CC tumor growth in vivo. 	30362562
hsa_circ_0000745	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	regulation[miR-409-3p/ATF1 Axis]	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0000745 and ATF1 were upregulated, whereas miR-409-3p was downregulated in CC tissues and cells. Circ_0000745 promoted the progression of CC through modulating miR-409-3p/ATF1 axis, indicating a promising biomarker for CC therapy.		Yes	Knockdown of circ_0000745 repressed proliferation, migration, invasion, and glycolysis of CC cells. 	32644859
hsa_circ_0023404	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction(miR-636)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//EdU Staining//Transwell Assay	circ_0023404 and CYP2S1 expression were increased, and miR-636 was decreased in cervical cancer tissues and cells. 		Yes	Moreover, circ_0023404 knockdown could repress proliferation, migration, invasion, and promote apoptosis of cervical cancer cells in vitro. Mechanically, circ_0023404 could regulate CYP2S1 expression by sponging miR-636. 	34825467
circYPEL2	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissue and CC cell lines	Expression [highly expressed]	qPCR//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	CircYPEL2 exhibited significantly high expression in CC tissue and strong stability in CC cell lines. 		Yes	Furthermore, knockdown and overexpression of circYPEL2 indicated the potential involvement in CC proliferation, migration and invasion. Finally, the downstream regulatory genes of circYPEL2 were investigated by knockdown experiment in CC cell lines with high-throughput sequencing. 	35052380
LOC389332	LncRNA	Homo sapiens	microinvasive gastric cancer	EGC tissues	Expression[highly expressed]	CCK8//qRT-PCR//Wound Healing Assay	The results in the validation phase revealed that LOC389332 was remarkably overexpressed in gastric carcinoma tissues, precancerous lesions, and gastric cancer cells		Yes	Functional study showed that knockdown of LOC389332 expression could inhibit cell proliferation and migration. LncRNA expression microarray on the LOC389332 knockdown cell line model revealed that 393 mRNAs were differentially expressed.	31884510
circPGAP3	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction(miR-769-5p/p53 axis)	In Vivo Experiment//RNA Pull-Down//Transfection//Immunoblotting//CCK8//qRT-PCR//FISH//Luciferase Report Assay//ChIP	we found a circRNA derived from PGAP3, referred as circ-PGAP3 (hsa_circ_0106800, chr17:37843549-37844086), which was significantly downregulated in CC tissues. 	Low circ-PGAP3 was closely linked to poor prognosis. 	Yes	And overexpression of circ-PGAP3 significantly reduced CC cell proliferation in vitro and tumor growth in vivo. In terms of mechanism, circ-PGAP3 was transcriptionally elevated by p53, a well-recognized tumor suppressor, and circ-PGAP3 was located in the cytoplasm where sponged miR-769-5p to increase the levels of p53 and its downstream targets.	33591461
circARHGAP12	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissue and cells	Interaction(m6A/FOXM1 manner)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//MeRIP//CCK8//qRT-PCR//FISH//RIP	 In the present study, our sequencing data revealed that a novel m6A-modified circRNA (circARHGAP12, hsa_circ_0000231) upregulated in the cervical cancer tissue and cells. Interestingly, the m6A modification of circARHGAP12 could amplify its enrichment. 		Yes	Functional experiments illustrated that circARHGAP12 promoted the tumor progression of cervical cancer in vivo and vitro. 	34392306
hsa_circ_101996	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction(miR-1236-3p/TRIM37 axis)	Western Blot//ISH//Wound Healing Assay//CCK8//RIP//Survival Analysis//Luciferase Report Assay//Cell Cycle Assay	Our results in this study suggested that circRNA_101996 was over-expressed in cervical cancer patients. The molecular investigations indicated that circRNA_101996 could increase the expression level of miR-1236-3p, tripartite motif-containing 37 (TRIM37), through binding to miR-1236-3p and reducing its expression. 		Yes	circRNA_101996 up-regulation remarkably assisted cell proliferation, cell cycle progression, and cell migration in cervical cancer, while circRNA_101996 knockdown exerted the inverse effects. 	33728810
circZFR	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 Cervical cancer tissues	Expression [highly expressed]	circRIP//Western Blot//Co-IP//qRT-PCR//Cell Proliferation Assay//Cell Cycle Assay//IHC	We identified the circRNA signature of upregulated circRNAs between cervical cancer and paired adjacent normal tissues. Functionally, circZFR knockdown represses the proliferation, invasion, and tumor growth. Furthermore, circRNA pull-down experiments combined with mass spectrometry unveil the interactions of circZFR with Single-Stranded DNA Binding Protein 1 (SSBP1). Mechanistically, circZFR bound with SSBP1, thereby promoting the assembly of CDK2/cyclin E1 complexes. The activation of CDK2/cyclin E1 complexes induced p-Rb phosphorylation, thus releasing activated E2F1 leading to cell cycle progression and cell proliferation.	Clinicopathological features of 40 cervical cancer patients (30 with and ten without paired normal tissues) showed that increased expression of circZFR was positively associated with lymphatic metastasis (Table ​(Table1,1, P =0.049), squamous cell carcinoma antigen (SCC Ag) value (Table ​(Table1,1, P =0.049), and Ki67 value (Table ​(Table1,1, P =0.003). However, circZFR was not associated with age, tumor stage, invasion depth, or vascular invasion	Yes	Functionally, circZFR knockdown represses the proliferation, invasion, and tumor growth. 	33516252
hsa_circ_CSPP1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	regulation[PI3K-Akt Signaling Pathway]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Hsa_circ_CSPP1 and ITGB1 were high-expressed in cervical cancer, while miR-361-5p was low-expressed. Circular RNA hsa_circ_CSPP1 regulates cell migration and proliferation in cervical cancer through miR-361-5p/ITGB1 in PI3K-Akt signaling pathway.		Yes	Hsa_circ_CSPP1 knockdown or miR-361-5p overexpression could suppress cervical cancer cell proliferation and migration, whereas promoted cell apoptosis.	32046405
hsa_circ_0000388	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC clinical samples 	regulation[miR-337-3p/ TCF12 Axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	Circ_0000388 expression in CC clinical samples was upregulated and this was correlated with unfavorable pathological indexes.Circ_0000388 was a novel oncogenic circRNA in CC, and promoted cancer progression via regulating miR-337-3p and TCF12, and could be potentially used as a diagnostic biomarker and therapy target.		Yes	Circ_0000388 remarkably enhanced the proliferation and metastasis of CC cells.	32119786
loc339803	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-30a-5p/ SNAIL1 axis)	CCK8//qRT-PCR//EdU Staining	The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients. Further studies demonstrated that loc339803 functioned as a competing endogenous RNA (ceRNA) by directly binding to miR-30a-5p, thus up-regulating the expression of SNAIL1, a target gene of miR-30a-5p.	The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients.	Yes	Loc339803 can promote the migration and invasion of HCC cells in vivo and in vitro.	33442404
LOC339524	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cells (J82, T24, UM-UC-3 and 5637)	Interaction(miR-875-5p/COPS7A signaling axis)	qRT-PCR//Luciferase report assay//Western Blot	 It was found that LOC339524 expression levels were markedly downregulated in BCa tissues and cells (J82, T24, UM-UC-3 and 5637).In conclusion, the findings of the present study suggested that LOC339524 may inhibit cell proliferation in BCa by targeting the miR-875-5p/COPS7A signaling axis.		Yes	LOC339524 overexpression was revealed to suppress the proliferation of BCa cells. 	34584547
circAGFG1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[downregulating p53]	CCK8//qRT-PCR//RIP//EdU Staining//ChIP	CircAGFG1 was upregulated in CC tissues and cell lines.  CircAGFG1 is upregulated in CC. By recruiting EZH2, circAGFG1 downregulates p53 and thus exerts a carcinogenic role to accelerate the malignant progression of cervical cancer.	 Besides, the circAGFG1 level was closely related to worse tumor staging, a higher rate of metastasis, and larger tumor size in CC patients.	Yes	The knockdown of circAGFG1 attenuated the proliferative ability of SiHa and HeLa cells.	32141537
hsa_circ_103973	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissue samples and cell lines	interaction[miR-335]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	Circ_103973 was found to be highly expressed in both GSE102686 and GSE113696 datasets as well as in CC tissue samples and cell lines.	Higher levels of circ_103973 were correlated to a worse outcome of CC patients. 	Yes	Knockdown of circ_103973 significantly promoted CC cell apoptosis and inhibited CC cell proliferation in vitro.	32184614
hsa_circ_0031288	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells and tissue	regulation[Hsa_circ_0031288/hsa-miR-139-3p/Bcl-6 regulatory feedback]	qRT-PCR//Wound Healing Assay//RNA Pull-Down//Transwell Assay	hsa_circ_0031288 and B-cell CLL/lymphoma 6 (Bcl-6) exhibited high expression in cervical cancer cells and tissue, while hsa-miR-139-3p exhibited low expression.In the cervical cancer HeLa cell line, the hsa_circ_0031288/hsa-miR-139-3p/Bcl-6 regulatory axis affects cell migration and proliferation, and its mechanism may involve hsa_circ_0031288 acting as a sponge for hsa-miR-139-3p, thereby relieving the transcriptional inhibition of Bcl-6. 		Yes	Reducing hsa_circ_0031288 and Bcl-6 expression or increasing hsa-miR-139-3p expression significantly inhibited the migration, invasion, proliferation, and growth of xenograft and HeLa cells.	32277518
hsa_circ_9119	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells and tissues	interaction[miR-126/MDM4]	qRT-PCR	circ9119 and MDM4 were initially overexpressed, and miR-126 expression was found to be reduced in CC cells and tissues.The dual-luciferase reporter assay highlighted that circ9119 functioned as an miR-126 ceRNA to increase MDM4 expression.		Yes	 A series of mimics, inhibitors, overexpressing plasmids or siRNAs were introduced into CC cells to alter the circ9119, miR-126, and MDM4 expressions. Cell-based experiments showed that silencing of circ9119 or the upregulation of miR-126 resulted in suppressed proliferation, accompanied by the induced apoptosis of CC cells. 	32385717
circNRIP1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	regulation[PTP4A1/ERK1/2 pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	QRT-PCR confirmed that circNRIP1 was upregulated in CC tissues, where its expression was correlated with lymphovascular space invasion. Finally, we confirmed that circNRIP1 exerts its effect, at least partially, by sponging miR-629-3p and thereby regulating the PTP4A1/ERK1/2 pathway.		Yes	Besides, both in vitro and in vivo experiments demonstrated that circNRIP1 promotes cell proliferation, migration, and invasion.	32457332
hsa_circ_0008285	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[miR-211-5p/SOX4 Axis]	qRT-PCR//Luciferase Report Assay//RIP	 In the present study, we identified a new circRNA hsa_circ_0008285, which was significantly up-regulated in CC tissues and cell lines.  Therefore, our research highlighted that hsa_circ_0008285 promoted CC progression via serving as a ceRNA of miR-211-5p to release SOX4, which might provide a potential therapeutic target for tumor treatment.		Yes	Loss-of-function assays showed that hsa_circ_0008285 suppression reduced the proliferation and invasion of CC cells in vitro and reduced tumor growth in vivo. 	32547228
hsa_circ_0000520	CircRNA	Homo sapiens	Uterine Cervical Neoplasms		interaction[binding with miR-146b-3p]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that hsa_circ_0000520(circ_0000520) was decreased in CC tissues and cell lines.Mechanismly, circ_0000520 and PAX5 were revealed to directly bind to miR-146b-3p, and circ_0000520 could indirectly regulate PAX5 by sponging miR-146b-3p.		Yes	Functional studies indicated circ_0000520 overexpression in vitro repressed CC cell proliferation, invasion and migration, while promoted CC cell apoptosis. 	32592222
hsa_circ_101308	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Expression[lower expressed]	qRT-PCR//RNA Pull-Down//Transwell Assay	CircRNA_101308 was significantly downregulated in CC tissues.	 The level of circRNA_101308 was much lower in CC patients with lymph node metastasis or deep myometrial invasion compared to those patients without lymph node metastasis and superficial myometrial invasion.	Yes	CircRNA_101308 overexpression inhibited CC cell proliferation, invasion and migration. 	32606970
hsa_circ_0000745	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cc tissues	Interaction[E-cad]	qRT-PCR//Western Blot//Transwell Assay//Microarray	hsa_circ_0000745 was Expression[up-expression]regulated in CC, and its level positively correlated with the level of its linear messenger RNA isoform.		Yes	 The role of hsa_circ_0000745 was illuminated by knocking down hsa_circ_0000745 in CC cells, and the results revealed that reducing hsa_circ_0000745 inhibited cell proliferation, migration, and invasion in CC by Expression[up-expression]regulating E-cadherin (E-cad) expression. 	31256433
hsa_circ_0000263	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 cell lines( HeLa, CaSki, SiHa, C‐33A, and SW756)	Interaction[TGF-β1]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	By using western blot and immunohistochemistry, we confirmed that hsa_circ_0000263 can regulate the expression of murine double minute 4 (MDM4) by affecting miR-150-5p, and finally affect the expression of p53 gene. We found that hsa_circ_0000263 was significantly Expression[Expression[up-expression]-expression]regulated in cervical cancer cells. In addition, the knockExpression[down-expression] of hsa_circ_0000263, would inhibit cell proliferation and migration ability.		Yes	In addition, the knockExpression[down-expression] of hsa_circ_0000263, would inhibit cell proliferation and migration ability.	30569515
lncRP5	LncRNA	Homo sapiens	ovarian carcinoma	OC patients and cell lines	Interaction(lncRP5/miR-545-5p/PTP4A1 axis )	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	RT-qPCR shows lncRP5 is significantly upregulated in OC patients and cell lines, and it is mainly located in the cytoplasm of OC cells.Moreover, the binding relationship between lncRP5 and miR-545-5p is predicted by bioinformatics and is further verified by luciferase assay. Functionally, the regulatory effects of lncRP5 and miR-545-3p are negatively related; miR-545-5p serves as a tumor suppressor in OC. Further studies demonstrate that PTP4A1 is the target gene of miR-545-5p. Overexpression of PTP4A1 abrogates the inhibitory function of miR-545-5p on OC cell growth and metastasis. 		Yes	The results of CCK-8, colony formation, and transwell assays demonstrate that overexpression of lncRP5 greatly contributes to malignant behaviors of OC cells, while inhibition of lncRP5 shows the opposite effects. 	35538027
LOC100127888	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cancer tissues 	Expression(highly expressed)	CCK8//Transwell Assay//IHC//Microarray	 The expression of LncA was significantly upregulated in CRC cancer tissues compared with the corresponding noncancer tissues.	High LncA expression in cancer tissues was associated with pathological classification, depth of invasion, lymph node metastasis, TNM stage and distant metastasis. LncA expression was an unfavorable prognostic factor for CRC patients. Furthermore, LncA combined with clinical variables exhibited synergistic potential for the prediction of CRC prognosis.	Yes	Low expression of LncA in HT 29 and HCT116 cells could decrease cell proliferation, and the migration and invasion of these cells was inhibited by knockdown of LncA.	34991861
LNMAS	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells	Interaction(HMGB1/TWIST1 and STC1)	In Vivo Experiment//Western Blot//ISH//Transfection//Wound Healing Assay//qRT-PCR//RNA-seq	In this study, we identified a lncRNA termed lymph node metastasis associated suppressor (LNMAS), which was downregulated in LN-positive cervical cancer patients and correlated with LN metastasis and prognosis. Mechanistically, LNMAS exerts its metastasis suppressive activity by competitively interacting with HMGB1 and abrogating the chromatin accessibility of TWIST1 and STC1, inhibiting TWIST1-mediated partial EMT and STC1-dependent immune escape from macrophage phagocytosis. We further demonstrated that the CpG sites in the promoter region of LNMAS was hypermethylated and contributed to the downregulation of LNMAS. 		Yes	Functionally, LNMAS suppressed cervical cancer cells metastasis in vitro and in vivo. 	35152264
lnc-XR_003496198	LncRNA	Homo sapiens	Duck Hepatitis A Virus Type 1 (Dhav-1)	DHAV-1-infected duck embryo fibroblasts	Regulation	qRT-PCR//Western Blot	Functional annotation analyses indicated that the putative target genes of DELs participated in diverse vital biological processed, including immune responses, cellular metabolism, and autophagy. For example, we confirmed the dysregulation of pattern recognition receptors (TLR3, RIG-I, MDA5, LGP2, cGAS), signal transducers (STAT1), transcription factors (IRF7), immune response mediators (IL6, IL10, TRIM25, TRIM35, TRIM60, IFITM1, IFITM3, IFITM5), and autophagy-related genes (ULK1, ULK2, EIF4EBP2) using RT-qPCR. Finally, we confirmed that one DHAV-1 induced lncRNA-XR_003496198 is likely to inhibit DHAV-1 replication in DEFs. Our study comprehensively analyzed the lncRNA profiles upon DHAV-1 infection and screened the target genes involved in the innate immune response and autophagy signaling pathway, thereby revealing the essential roles of duck lncRNAs and broadening our understanding of host-virus interactions.		Yes	inally, we confirmed that one DHAV-1 induced lncRNA-XR_003496198 is likely to inhibit DHAV-1 replication in DEFs. 	35531338
lncWDR26	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[SIX3]	RNA Pull-Down//Western Blot//qRT-PCR//Cell Cycle Assay//ChIP	Here, we reported that lncWDR26 was significantly downregulated in HCC tissues and cells.Mechanistically, lncWDR26 suppressed HCC growth and metastasis by inhibiting WDR26 transcription. Notably, lncWDR26 was associated with SIX homeobox 3 (SIX3), and this association was required for the repression of WDR26 transcription.	Moreover, decreased lncWDR26 expression correlates with larger tumor size, higher clinical stage, and tumor metastasis, and also predicts poor prognosis in patients with HCC. 	Yes	In HCC cells, overexpression of lncWDR26 inhibited growth and metastasis, both in vitro and in vivo.	29736313
lnc-W5	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines and tissues	Expression [lower expressed]	In Vivo Experiment//Migration Assay//CCK8//Colony Formation Assay//Invasion Assay	The results showed that lncRNA W5 expression was significantly downregulated in HCC cell lines and tissues.  In vitro experiments showed that ectopic overexpression of lncRNA W5 suppressed HCC cell proliferation, migration and invasion; conversely, silencing of lncRNA W5 promoted cell proliferation,   In addition, acting as a tumor suppressor gene in HCC, lncRNA W5 inhibited the growth of HCC xenograft tumors in vivo.		Yes	In vitro experiments showed that ectopic overexpression of lncRNA W5 suppressed HCC cell proliferation, migration and invasion; conversely, silencing of lncRNA W5 promoted cell proliferation,   In addition, acting as a tumor suppressor gene in HCC, lncRNA W5 inhibited the growth of HCC xenograft tumors in vivo.	33505150
lnc-UCID	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cell lines	Regulation(Stabilization of Snail)	qRT-PCR//Western Blot	"Lnc-UCID was upregulated in human HCC tissues and HCC cell lines. The expression of Snail positively correlated with lnc-UCID abundance, and the interaction between lnc-UCID and Snail mRNA prevented miR-122, miR-203, miR-30b, miR-34a or miR-153 binding to the 3'-UTR of Snail. Transfection of Snail greatly rescued the migration and invasion of HCC cells.
"		Yes	Lnc-UCID promoted the cells' mobility and invasiveness by enhancing the EMT process of HCC cells.	33536764
lncTSI	LncRNA	Homo sapiens	Aortic Valve, Calcification of	valve interstitial cells	Regulation(TGF-β/Smad3 pathway)	In Vivo Experiment//Western Blot//FISH//Luciferase Report Assay//IHC//ChIP	lncTSI was highly expressed in VICs treated with TGF-β1.lncTSI was transcriptionally regulated by Smad3 and reversely inhibited TGF-β1-induced Smad3 phosphorylation and downregulated profibrotic gene expression. Silencing lncTSI increased TGF-β1-induced Smad3 phosphorylation, and subsequently, upregulated RUNX2 and collagen I expressions in VICs.  While overexpression of lncTSI reversed the production of RUNX2 and collagen I in VICs. In a mouse CAVD model of 24 week 0.25 % high-cholesterol diet feeding, overexpression of lncTSI significantly reduced calcium deposition, RUNX2, pSmad3, and collagen I expression in aortic valve leaflets, with less aortic valve stenosis.		Yes	Silencing lncTSI increased TGF-β1-induced Smad3 phosphorylation, and subsequently, upregulated RUNX2 and collagen I expressions in VICs.  While overexpression of lncTSI reversed the production of RUNX2 and collagen I in VICs. In a mouse CAVD model of 24 week 0.25 % high-cholesterol diet feeding, overexpression of lncTSI significantly reduced calcium deposition, RUNX2, pSmad3, and collagen I expression in aortic valve leaflets, with less aortic valve stenosis.	36273649
lnc-TRAF1-4:1	LncRNA	Homo sapiens	Arthritis, Rheumatoid	chondrocyte 	Interaction(miR-27a-3p/CXCL1 )	Western Blot//qRT-PCR//RNA-seq//Cell Cycle Assay//Transwell Assay	 Mechanistically, lnc-TRAF1-4:1 upregulated CXCL1 expression through sponging miR-27a-3p as a competing endogenous RNA (ceRNA) in chondrocytes identifying by Dual-luciferase reporter gene assay. Summarily, exosomal lncRNA TRAFD1-4:1 derived from RA-FLSs suppressed chondrocyte proliferation and migration through degrading CECM by upregulating CXCL1 as a sponge of miR-27a-3p. 		Yes	Besides, RNA sequencing and verification by qRT-PCR revealed that exosomal long non-coding RNA (lncRNA) tumor necrosis factor-associated factor 1 (TRAF1)-4:1 derived from RA-FLSs treated with TNFα was a candidate lncRNA, which also inhibited chondrocyte proliferation and migration through degrading CECM. 	36481205
lnc-TDRG1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-214-5p/SEMA4C axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Invasion Assay	 We found Lnc-TDRG1 was highly expressed in CC tissues and cells and it was upregulated in response to hypoxia. 		Yes	Loss-of-functional experiment suggested that knockdown of lnc-TDRG1 impede invasion, hypoxia-induced glycolysis in vitro and tumor growth in vivo, which was abolished by knockdown of miR-214-5p or overexpression of SEMA4C. 	33394293
lnc-TCF7	LncRNA	Homo sapiens	Multiple Myeloma	MM  tissues and cell lines	Interaction( miR-203/Jagged1-Notch1 signaling pathway)	qRT-PCR//Western Blot	 lnc-TCF7 expression was increased in patients with MM compared with the healthy controls and was positively related to β-2-microglobulin expression and International Staging System stage, while negatively associated with complete response, EFS and OS. In vitro, lnc-TCF7 was upregulated in MM cells compared with normal bone marrow plasma cells, and its knockdown suppressed MM cell proliferation while promoting apoptosis. Compensation experiments showed that miR-203 inhibition promoted MM progression by regulating the Jagged1-Notch1 signaling pathway in lnc-TCF7-knockdown cells. 	 lnc-TCF7 expression was increased in patients with MM compared with the healthy controls and was positively related to β-2-microglobulin expression and International Staging System stage, while negatively associated with complete response, EFS and OS. 	Yes	In vitro, lnc-TCF7 was upregulated in MM cells compared with normal bone marrow plasma cells, and its knockdown suppressed MM cell proliferation while promoting apoptosis. Compensation experiments showed that miR-203 inhibition promoted MM progression by regulating the Jagged1-Notch1 signaling pathway in lnc-TCF7-knockdown cells. 	33841573
lnc-STYK1-2	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction(miR-146b-5p /ITGA2 / AKT/STAT3/NF-kB signaling)	qRT-PCR//Bioinformatics Analysis	Alterations in lncRNA profiles, including decreased lnc-STYK1-2 expression, were detected in bladder cancer tissues compared with adjacent noncancerous tissues.  lnc-STYK1-2 siRNA promoted miR-146b-5p and reduced ITGA2 expression in bladder cancer cells. Moreover, miR-146b-5p suppressed ITGA2 expression in bladder cancer cells through direct association. Also, lnc-STYK1-2 directly associated with miR-146b-5p. Finally, miR-146b-5p inhibitors abrogated the alterations in bladder cell functions, ITGA2 expression, and phosphorylation of AKT, STAT3, and P65 proteins in 5637 and T24 cells induced by lnc-STYK1-2 silencing.		Yes	 lnc-STYK1-2 silencing effectively promoted proliferation, migration, and invasion in two bladder cancer cell lines, 5637 and T24, and their tumorigenesis in nude mice. 	34332611
lnc-Sox2ot	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC cells	Interaction(miR-200/Sox2)	qRT-PCR//RIP	We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. 	We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. 	Yes	We also confirmed the transmission of the exosomes from producer cells to recipient PDAC cells, exosomal Sox2ot can promote tumor invasion and metastasis in vitro and in vivo. We further confirmed tumor generated exosomes could excrete to tumor cell or blood circulation in vivo condition. 	29643475
LncSNHG16	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction[targeting microRNA-146a-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 LncSNHG16 was highly expressed in OS tissues and cell lines. LncSNHG16 is highly expressed in OS tissues and cell lines, participating in the development of OS by downregulating microRNA-146a-5p to upregulate NOVA1 expression.	Its expression was positively correlated with the tumor stage of OS patients.Receiver operating characteristic (ROC) curves suggested that lncSNHG16 can be used as a clinical indicator to distinguish OS patients from healthy controls. Survival analysis indicated a negative correlation between lncSNHG16 expression and survival of OS patients.	Yes	Overexpression of lncSNHG16 enhanced the proliferative and migratory potentials of OS cell lines 143B and MNNG/HOS. 	30657551
lncSNHG15	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[absorbing miR-211-3p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 The expression of lncSNHG15 in NSCLC tissues was significantly higher than that of para-cancerous tissues.High expression of lncSNHG15 promoted the proliferation and migration of NSCLC cells by upregulating ZNF217 by adsorbing miR-211-3p.	 In particular, the expression of lncSNHG15 in NSCLC patients with stage III-IV was higher than those with stage I-II.	Yes	lncSNHG15 over-expression remarkably promoted the proliferation and migration of NSCLC cells (A549 and H358). 	30840276
LncSNHG1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(miR-181b-5p/SMAD2 axis)	qRT-PCR//Western Blot//Luciferase Report Assay//Colony Formation Assay	LncSNHG1 was overexpressed both in CRC tissues and cell lines, while the miR-181b-5p expression was decreased in CRC cell lines. Meanwhile, LncSNHG1 enhanced EMT progress through regulation of the miR-181b-5p/SMAD2 axis.		Yes	After knock-down of LncSNHG1, the proliferation, invasion, and migration of HT29 and SW620 cells were all decreased. 	35310912
lncSLCO1C1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissue and cells	Interaction(miR-211-5p and miR-204-5p/SSRP1 )	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 LncSLCO1C1 was highly upregulated in GC tissue samples and associated with GC patients' poor overall survival. . Mechanistically, lncSLCO1C1 serves as a scaffold for the structure-specific recognition protein 1 (SSRP1)/H2A/H2B complex and regulates the function of SSRP1 in reducing DNA damage. Meanwhile, lncSLCO1C1 functions as a sponge to adsorb miR-204-5p and miR-211-5p that target SSRP1 mRNA, and thus increases SSRP1 expression.  Meanwhile, lncSLCO1C1 functions as a sponge to adsorb miR-204-5p and miR-211-5p that target SSRP1 mRNA, and thus increases SSRP1 expression. 	 LncSLCO1C1 was highly upregulated in GC tissue samples and associated with GC patients' poor overall survival. Patients with high expressions of both lncSLCO1C1 and SSRP1 have poor overall survival, highlighting the role of lncSLCO1C1 in GC progression.	Yes	 LncSLCO1C1 was highly upregulated in GC tissue samples and associated with GC patients' poor overall survival. 	35474446
Lnc-SLC4A1-1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines,blood	Interaction[NF-κB/CXCL8]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Transwell Assay	Lnc-SLC4A1-1 was significantly up-regulated in BC tissue, serum samples and cell lines.  Lnc-SLC4A1-1 interacted with NF-κB to promote CXCL8 expression. Lnc-SLC4A1-1 could promote the development of BC.		Yes	 In BC cells, lnc-SLC4A1-1 knockdown promoted cell apoptosis and suppressed cell proliferation, migration and invasion.	31556319
Lnc-SELPLG-2:1	LncRNA	Homo sapiens	Osteosarcoma	 osteosarcoma cells and samples	Interaction(hsa-miR-10a-5p/BTRC )	qRT-PCR//RNA-seq	Lnc-SELPLG-2:1 was highly expressed in osteosarcoma compared to normal cells and bone and marrow samples. The prediction, dual luciferase assay, and response test results indicated that hsa-miR-10-5p and BTRC were involved in the lnc-SELPLG-2:1 cascade. Unlike lnc-SELPLG-2:1, hsa-hsa-miR-10a-5p had opposite expression and function. Competitive binding of lnc-SELPLG-2:1 to hsa-hsa-miR-10a-5p prevented BTRC from miRNA-mediated degradation, thereby activating the expression of VIM, MMP9, and MMP2, promoting osteosarcoma cell proliferation, migration, and invasion, and inhibiting apoptosis.		Yes	 Inhibition of lnc-SELPLG-2:1 accelerated cell apoptosis and suppressed cell proliferation, migration, and invasion, whereas lnc-SELPLG-2:1 overexpression had the opposite effect.Moreover, inhibiting lnc-SELPLG-2:1 in an in vivo model decreased tumor size and suppressed the expression of cell migration-related proteins. 	36199080
Lnc-S100B-2	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells	Regulation(MLLT10)	Western Blot//qRT-PCR//Luciferase Report Assay//IHC//IF	Lnc-S100B-2 was obtained, and high expression of Lnc-S100B-2 was predicted to be associated with a lower survival rate. At the gene and protein levels, the expressions of PCNA, Ki67, and Bcl-2 were decreased in the sh-Lnc-S100B-2 group, sh-MLLT10 group, and sh-Lnc-S100B-2 + sh-MLLT10 group, while the expressions of cleaved caspase 3, caspase 9, and Bax were increased. In vivo, the volume and mass of the tumor decreased in the sh-Lnc-S100B-2 + sh-MLLT10 group. 	Lnc-S100B-2 was obtained, and high expression of Lnc-S100B-2 was predicted to be associated with a lower survival rate. 	Yes	After silencing Lnc-S100B-2 and MLLT10, the proliferative activity of CRC cells decreased, and the apoptosis rate increased. 	35126515
lncRsp1	LncRNA	Homo sapiens	Fusarium graminearum	putative sugar transporter gene	Regulation(Fgsp1)	qRT-PCR	In our previous RNA sequencing (RNA-Seq) study, we discovered that lncRsp1 is an lncRNA that is located +99 bp upstream of a putative sugar transporter gene, Fgsp1, with the same transcription direction. Functional studies revealed that ΔlncRsp1 and ΔFgsp1 were normal in growth and conidiation but had defects in ascospore discharge and virulence on wheat coleoptiles. Moreover, lncRsp1 and Fgsp1 were shown to negatively regulate the expression of several deoxynivalenol (DON) biosynthesis genes, TRI4, TRI5, TRI6, and TRI13, as well as DON production. Further analysis showed that the overexpression of lncRsp1 enhanced the ability of ascospore release and increased the mRNA expression level of the Fgsp1 gene, while lncRsp1-silenced strains reduced ascospore discharge and inhibited Fgsp1 expression during the sexual reproduction stage. In addition, the lncRsp1 complementary strains lncRsp1-LC-1 and lncRsp1-LC-2 restored ascospore discharge to the level of the wild-type strain PH-1. 		Yes	Further analysis showed that the overexpression of lncRsp1 enhanced the ability of ascospore release and increased the mRNA expression level of the Fgsp1 gene, while lncRsp1-silenced strains reduced ascospore discharge and inhibited Fgsp1 expression during the sexual reproduction stage. I	34841640
LNRRIL6	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction[ IL-6/STAT3 pathway]	CCK8//qRT-PCR//Western Blot	 In this study, we report the identification of a novel lncRNA, named long noncoding RNA regulating IL-6 transcription (LNRRIL6), which is upregulated in CRC tissues and cell lines.  Taken together, these findings identify a novel lncRNA, LNRRIL6, that promotes CRC cell survival through activation of the IL-6/STAT3 pathway and suggest that LNRRIL6 may be a potential prognostic biomarker and therapeutic target for CRC.		Yes	Functional experiments showed that enhanced expression of LNRRIL6 promotes CRC cell proliferation and survival in vitro and CRC tumor growth in vivo. Conversely, depletion of LNRRIL6 inhibits CRC cell proliferation and survival in vitro and CRC tumor growth in vivo.	31246342
LOC100129620	LncRNA	Homo sapiens	Osteosarcoma	hBMSCs	Interaction(miR-335-3p)	qRT-PCR//Western Blot	The results show that LOC100129620 can promote the proliferation and migration of osteosarcoma cells. LOC100129620 can promote the proliferation of osteosarcoma in vivo. LOC100129620 can bind to miR-335-3p and regulate its function. MiR-335-3p mediates the regulatory effects of LOC100129620 on CDK6. 		Yes	The results show that LOC100129620 can promote the proliferation and migration of osteosarcoma cells. LOC100129620 can promote the proliferation of osteosarcoma in vivo. 	34015762
hsa_circ_101996	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues,cell lines( SiHa, C33A, CaSki, and Hela)	Interaction[HOTAIR,TPX2 ]	CCK8//qRT-PCR//Luciferase Report Assay	". Besides, hsa_circR_x0002_NA_101996 expression in cervical cancer tissues was much higher
compared with adjacent normal tissues (Figure 1b), and much higher in
cervical cancer cell lines compared with human cervical epithelial cells.Mechanistically, we demonstrated that hsa_circRNA_101996 served as a sponge of miR-8075, which targeted TPX2 in cervical cancer cells."		Yes	 We found that knockExpression[down-expression] of hsa_circRNA_101996 significantly inhibited the proliferation, cell cycle, migration, and invasion of cervical cancer cells. 	30633364
LOC100130075	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cells	Interaction(E2F1/MDM2 )	RNA Pull-Down//Western Blot//Transfection//Tunel//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//ChIP	The high expression pattern of LOC100130075 and MDM2 and a positive correlation between them were firstly verified in CC cells. Furthermore, we verified through mechanism assays including ChIP, RNA pull-down, as well as luciferase reporter assays that LOC100130075 bound to E2F transcription factor 1 (E2F1) to activate MDM2 transcription. Furthermore, the result of rescue assays manifested that MDM2 overexpression reversed the inhibitory function of LOC100130075 deficiency on CC development. 		Yes	 Then, it was verified that LOC100130075 interference suppressed the proliferation and enhanced the apoptosis of CC cells.	35201567
LOC105374902	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell line	Interaction[as a sponge of miR-1285-3p]	Northern Blot//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay	We characterized a significantly upregulated lncRNA LOC105374902 induced by TNF-α. Then, we found that TNF-α accelerated the binding of STAT3 to the promoter region of lncRNA LOC105374902 and promoted its expression. Mechanistically, lncRNA LOC105374902 directly bond to miR-1285-3p as a competing endogenous RNA (ceRNA) to derepress RPL14		Yes	functional analysis indicated that both lncRNA LOC105374902 and RPL14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) of CC cells.	30935691
LOC105372579	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[miR-4316/FOXP4 signaling ]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	LOC105372579 was highly expressed in HCC tissues and cell lines.Thus, our findings supported that LOC105372579 contributes to HCC cell proliferation, migration, invasion, and EMT by activating miR-4316/FOXP4 signaling.		Yes	LOC105372579 silencing suppressed the proliferation of HCC cells in vitro. We also validated that LOC105372579 knockdown inhibited the migration, invasion, and epithelial-mesenchymal transition of HCC cells. Xenograft assay demonstrated that LOC105372579 promotes tumor growth in vivo.	31114338
LOC102724163	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction((miR)-508-5p/MUC19 )	CCK8//qRT-PCR//Wound Healing Assay//Invasion Assay	In the present study, analysis of The Cancer Genome Atlas database and reverse transcription-quantitative PCR demonstrated that LOC102724163 expression levels were significantly upregulated in BC tissues compared to matched adjacent normal tissues and were associated with an unfavorable prognosis in patients with BC.  In the mechanistical aspect, LOC102724163 sponged microRNA (miR)-508-5p to elevate MUC19 expression. Additionally, rescue assays ascertained the function of the LOC102724163/miR-508-5p/MUC19 axis in the proliferation and invasion of BC cells. 	In the present study, analysis of The Cancer Genome Atlas database and reverse transcription-quantitative PCR demonstrated that LOC102724163 expression levels were significantly upregulated in BC tissues compared to matched adjacent normal tissues and were associated with an unfavorable prognosis in patients with BC. 	Yes	Gain or loss of function assays indicated that overexpression of LOC102724163 significantly increased tumorgenicity in vivo and cell migration, proliferation and invasion in vitro.	35154431
LOC101929552	LncRNA	Homo sapiens	Osteosarcoma	OS cells	regulation[NR_136400/miR-8081/TUSC5 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, we demonstrated that NR_136400 was downregulated in OS cells and that its downregulation promoted OS cell proliferation, apoptosis, and invasion.  Taken together, a newly identified regulatory mechanism of the lncRNA NR_136400/miR-8081/TUSC5 axis was systematically studied in OS, providing a promising target for therapeutic treatment.		Yes	In the present study, we demonstrated that NR_136400 was downregulated in OS cells and that its downregulation promoted OS cell proliferation, apoptosis, and invasion. 	32499696
LOC101928963	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction[ Binding to PMAIP1 ]	Flow Cytometry//qRT-PCR//MTT//Western Blot	Decreased cell apoptosis and PMAIP1 expression, as well as overexpressed LOC101928963, were exhibited among spinal cord glioma tissues. The data obtained during the study highlighted the inhibitory role of LOC101928963 silencing in spinal cord glioma through the increase in PMAIP1, which suggests a potential target in the treatment of spinal cord glioma.		Yes	LOC101928963 overexpression was observed to promote cell proliferation and cell-cycle entry and inhibit the process of apoptosis. 	31670198
LOC101928834	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	 bone marrow 	regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	We identified a novel lncRNA, LOC101928834, which was significantly up-regulated in the bone marrow of patients with MDS and acute myeloid leukemia (AML). Moreover, functional analysis showed that LOC101928834 promoted cell proliferation and cell cycle progression, and activated Wnt/β-catenin signaling pathway in vitro. 		Yes	Moreover, functional analysis showed that LOC101928834 promoted cell proliferation and cell cycle progression, and activated Wnt/β-catenin signaling pathway in vitro. 	32463458
LOC101928477	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissue and ESCC cell lines	Expression [lower expressed]	Wound Healing Assay//Colony Formation Assay//qRT-PCR//FISH//Cell Viability Assay//IHC//IF	We determined that LOC101928477 expression was inhibited in ESCC tissue and ESCC cell lines when compared with controls. 		Yes	Moreover, forced expression of LOC101928477 effectively inhibited ESCC cell proliferation, colony formation, migration, and invasion via suppression of epithelial-mesenchymal transition (EMT).  Furthermore, LOC101928477 overexpression inhibited in situ tumor growth and lung metastasis in a mouse model.	33713583
LOC101928316	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues ,cell lines	Regulation[PI3K-Akt-mTOR signaling pathway]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	In the present study, we have found that LOC101928316 was significantly downregulated in gastric cancer (GC) tissues specimen, GC cell lines. LOC101928316 molecular mechanism investigates suggested that LOC101928316 can regulate PI3K-Akt-mTOR signaling pathway and change the GC development progression in vivo and in vitro. In vivo experiment also revealed that LOC101928316-Overexpression can inhibit the tumorigenicity of GC cells in tumor-burdened experimental nude mice (P ＜ 0.05). LOC101928316 may function as anti-oncogene and also plays an important role in GC tumorigenesis. Collectively, our data provided the key role of LOC101928316 in the tumorigenesis of GC. In addition, the present study elucidates LOC101928316 potential regulatory network, which may help us to lead a better knowing of the pathogenesis of GC and probe the lncRNA as a novel biomarker to diagnosis and therapy for this malignant tumor.	In the present study, we have found that LOC101928316 was significantly downregulated in gastric cancer (GC) tissues specimen, GC cell lines, and associated with the GC patients tumor, node, and metastasis (TNM) stage and degree of differentiation (P ＜ 0.05).	Yes	LOC101928316 overexpression can significantly inhibit SGC-7901 cell migration, invasion, and proliferation (P＜0.05).	31207155
LOC101928134	LncRNA	Mus musculus	Osteoarthritis	knee joint synovial tissues	Regulation[JAK/STAT signaling pathway]	qRT-PCR	LOC101928134, which was found to be highly expressed in knee joint synovial tissues of OA rats, regulated the expression of IFNA1 gene and inhibited JAK/STAT signaling pathway.These results demonstrate that downregulation of LOC101928134 suppresses the synovial hyperplasia and cartilage destruction of OA rats via activation of JAK/STAT signaling pathway by upregulating IFNA1, providing a new candidate for the treatment of OA.		Yes	Downregulation of LOC101928134 resulted in reduced knee joint synovitis, relived inflammatory damage, and knee joint cartilage damage of OA rats. 	30456844
LOC101927746	LncRNA	Homo sapiens	Colorectal Neoplasms		Interaction[ inhibiting miR-584-3p and activating SSRP1]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that LOC101927746 expression was significantly increased in CRC tissues according to the GEO dataset. In terms of its mechanism, LOC101927746 could serve as a competing endogenous RNA to inhibit miR-584-3p and activate its target gene SSRP1. The expression of miR-584-3p was inversely correlated with either LOC101927746 or SSRP1 in CRC tissues. The overexpression of SSRP1 or inhibition of miR-584-3p could reverse the effects of LOC101927746 knockdown in CRC cells. Taken together, our results suggest that the LOC101927746/miR-584-3p/SSRP1 axis modulates CRC progression.		Yes	Functionally, we demonstrated that LOC101927746 silencing significantly suppressed the proliferation, migration, and invasion of CRC cells. 	30616889
LOC101927476	LncRNA	Homo sapiens	Ovarian Neoplasms	metastatic tumors	Regulation(GATA4)	qRT-PCR//Wound Healing Assay	RT-PCR assay showed that 20 out of 22 patients had significantly lower expression of LOC101927476 in their metastatic tumors compared with primary tumors. The relative expression of GATA4 in OE-LOC101927476 group was (1.86±0.25), significantly higher than 1.00 of OE-EV group (P=0.001). In patients with high expression of LncRNA LOC101927476, the expression level of GATA4 was (2.93±0.35), which was higher than (0.29±0.06) of LOC101927476 low expression group (P=0.001).		Yes	 Transwell assay showed that overexpression of LOC101927476 significantly inhibited the invasion and migration capacities of 3AO cells. The numbers of invading and migrating 3AO cells infected with OE-LOC101927476 lentivirus were (357±63) and (699±65), respectively, lower than (661±95) and (1 024±76) in OE-EV group (P<0.050). In contrast, the numbers of invading and migrating OVCA429 cells with LOC101927476 knockdown were (512±72) and (472±40), respectively, higher than (309±13) and (363±27) in sg-Control group (P<0.050). Wound healing assay results showed that after 48 hours, the percentage of scratch healing of 3AO cells in OE-LOC101927476 group was (10.86±0.63)%, significantly lower than (57.38±4.42)% of OE-EV group (P=0.009). After 24 hours, the percentage of scratch healing of OCVA429 cells in sg-LOC101927476 group was (59.98±1.34)%, significantly higher than (23.15±2.03)% of sg-Control group (P=0.004). CCK-8 assays showed that the OD value of 3AO cells in OE-LOC101927476 group was (2.07±0.08), significantly lower than (2.29±0.04) of OE-EV group (P=0.009). The OD value of OVCA429 cells in sg-LOC101927476 group was (2.13±0.03), significantly higher than (1.93±0.03) of sg-Control group (P=0.001). 	35073656
LOC100996425	LncRNA	Homo sapiens	Prostate	 110 PCa tissue samples 	Interaction(HNF4A-mediated AMPK/mTOR pathway)	Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//H&E Staining//IHC	LOC100996425 was up-regulated, while HNF4A was down-regulated in the PCa tissues. HNF4A was a target gene of LOC100996425. The activation of AMPK pathway involved in the cancer progression mediated by LOC100996425. Down-regulation of LOC100996425 retards progression of PCa through HNF4A-mediated AMPK/mTOR pathway.		Yes	PCa cells transfected with either siLOC100996425 or HNF4A displayed reduced rates of PCa cell proliferation and migration while elevating cell apoptosis. 	34309216
LOC100912373	LncRNA	Mus musculus	Arthritis, Rheumatoid	synovial tissues,fibroblast-like synoviocytes	regulation[PDK1,miR-17-5p]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	The results showed that lncRNA LOC100912373 localized in the cytoplasm and was highly expressed in the synovial tissues and FLSs of AA rats.In conclusion, lncRNA LOC100912373 may upregulate the expression of PDK1 by sponging miR-17-5p, accelerating the phosphorylation of AKT and inducing the proliferation of FLSs, thus promoting the occurrence and development of RA.		Yes	 LncRNA LOC100912373 overexpression promoted the proliferation of FLSs.	33437356
LOC100911498	LncRNA	Rattus norvegicus	Neuralgia	SNI rats	Expression(highly expressed)	In Vivo Experiment//qRT-PCR//IHC//Western Blot	Our results suggested that the level of LOC100911498 in SNI rats was markedly higher than that in the sham group		Yes	the MWT values in rats were treated with LOC100911498siRNA were increased, and the expression levels of P2X4R, Iba-1, p-p38 and BDNF in SNI+ LOC100911498siRNA group were reduced compared with those in the SNI group.	33949153
LOC100507144	LncRNA	Homo sapiens	Colorectal Neoplasms	tumors	Interaction(CD44/Nanog/Sox2/miR-302/miR-21 axis)	qRT-PCR//Transwell Assay//Western Blot	Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. Our findings revealed that the knocking-down of LOC100507144 inhibited the expression of crucial stemness factors, including CD44, Nanog, and Sox2, and accordingly resulted in suppressing their targets, miR-302 and miR-21. 	Our expression data represented that the expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. 	Yes	 Loss-of-function examinations demonstrated that LOC100507144 contributed to CRC cell proliferation by restricting apoptosis, cellular senescence, and promoting cell cycle. Gain-of-function experiments also confirmed these results. Our data illustrated that LOC100507144 enhanced the migration and the epithelial to mesenchymal transition (EMT) of CRC cells, accompanied by the generation of cells with stemness characteristics. 	34882869
LOC100506114	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	Cancer-associated fibroblasts	Interaction(GDF10)	Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//FISH//qRT-PCR//IHC//IF	 Here, we first identify an uncharacterized lncRNA, LOC100506114, which is significantly upregulated in CAF and is involved in the functional transformation of normal fibroblasts (NF) and CAF. The profile of gene co-expression analysis shows that growth differentiation factor 10 (GDF10) is positively correlated with the expression of LOC100506114. CAF promote stromal fibroblast activation and the proliferation and migration of tumor cells by secreting GDF10. 		Yes	Expression of LOC100506114 enhances the expression of fibroblast activation protein alpha and α-smooth muscle actin in NF and promotes malignant characteristics of NF and CAF in vivo and in vitro. 	33657265
LOC100505851	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer and adjacent tissues	Expression(lower expressed)	PCR	LncRNA LOC100505851 was significantly expressed at lower levels in cancer tissues than in adjacent tissues (P<0.001). Its expression was related to human epidermal growth factor receptor 2 (HER2) expression (P=0.003) and molecular subtype based on immunohistochemistry (P=0.001).	LncRNA LOC100505851 was located mainly in the nucleus and was significantly downregulated in breast cancers. Its expression was related to a higher pCR rate and better RFS and OS, indicating its potential value as a novel predictive and prognostic biomarker in breast cancer.	Yes	LncRNA LOC100505851 was significantly expressed at lower levels in cancer tissues than in adjacent tissues (P<0.001). Its expression was related to human epidermal growth factor receptor 2 (HER2) expression (P=0.003) and molecular subtype based on immunohistochemistry (P=0.001).	34268074
LOC100505817	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	Interaction(miR-20a-reduced WT1)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Microarray//Transwell Assay	 The results found poor expression LOC100505817 was poorly expressed in GC cells and tissues.  Wnt/β-catenin pathway and EMT in GC cells were suppressed by LOC100505817 through miR-20a-inhibted WT1. 		Yes	Overexpressed LOC100505817 resulted in the significant reduction of cell proliferation, migration and invasion as well as the expression of Wnt2b, β-catenin, CyclinD1, N-cadherin, Vimentin and snail, while increased cell apoptosis along with the expression of E-cadherin.	34385891
LOC100132707	LncRNA	Homo sapiens	Uveal melanoma	cell lines	regulation[ LOC100132707/JAK2 axis]	qRT-PCR//Transwell Assay	 LOC100132707 expression in metastatic UM cell line MM28 was significantly higher than that of the non-metastatic UM cell lines, MP38, MP46 and MP65, as well as the expressions of LOC100132707-related genes, including XRN1, PARP14, JAK2, DDX60, BUB1 and SAMD9L. The LOC100132707/JAK2 axis might serve as a potent target for the prevention and treatment of UM metastasis.		Yes	LOC100132707 downregulation significantly repressed cell migration and invasion abilities, whereas overexpressing JAK2 rescued these effects.	33364785
hsa_circ_0000228	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cell lines	Interaction(microRNA-195-5p/ lysyl oxidase-like protein 2 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	In this study, we demonstrated that circ_0000228 showed a remarkable up-modulation in CC tissues and cell lines.		Yes	 Circ_0000228 knockdown repressed the growth and metastatic potential of CC cells. Mechanistically, circ_0000228 facilitated CC progression through sponging miR-195-5p and up-modulating LOXL2 expression. 	34308761
hsa_circ_0001247	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines 	Interaction( miR-1270)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//BrdU//Transwell Assay	Compared with that in adjacent tissues and normal cervical epithelial cells, circ_0001247 expression in CC tissues and cell lines was significantly increased; circ_0001247 sponged miR-1270 in CC cells; miR-1270 diminished the promoting effect of circ_0001247 by inactivating the ZEB2.		Yes	 knocking down circ_0001247 expression could inhibit the proliferation and metastasis of CC cells, and promote apoptosis, while circ_0001247 overexpression worked oppositely	33386495
LOXL1-AS1	LncRNA	Homo sapiens	Medulloblastoma	 medulloblastoma tissues	Regulation[PI3K/AKT Pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	It was initially found that LOXL1-AS1 was significantly overexpressed in clinical medulloblastoma tissues compared with the adjacent noncancerous tissues. These results suggest that LncRNA LOXL1-AS1 promoted the proliferation and metastasis of medulloblastoma by activating the PI3K-AKT pathway, providing evidence that knockdown of LncRNA LOXL1-AS1 might be a potential therapeutic strategy against medulloblastoma.	 LOXL1-AS1 was also highly expressed in medulloblastoma at advanced stages and differentially expressed in a series of medulloblastoma cell lines.	Yes	Knockdown of LOXL1-AS1 using shRNAs significantly inhibited cell viability and colony formation capacities in D283 and D341 cells. 	30050750
LOXL1-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction[LOXL1-AS1/miR-423-5p/MYBL2]	RNA Pull-Down//ChIP//Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our present study suggested that LOXL1-AS1 expression was considerably increased in LUAD tissues and cells.hese findings manifested the carcinogenic role of LOXL1-AS1 and LOXL1-AS1/miR-423-5p/MYBL2 feedback loop in LUAD, which could be helpful to explore effective therapeutic strategy for LUAD patients.		Yes	Moreover, LOXL1-AS1 deficiency notably hampered cell proliferation and migration as well as dramatically facilitated cell apoptosis.	31758653
LOXL1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[targeting miR-324-3p]	CCK8//qRT-PCR	The expression of LOXL1-AS1 was overexpressed in NSCLC specimens than adjacent control specimens.These results indicated that LOXL1-AS1 enhanced NSCLC cell proliferation and invasion via sponging miR-324-3p in NSCLC cell.		Yes	Ectopic expression of LOXL1-AS1 promoted H1299 cell and H23 cell proliferation.	31737192
LOXL1-AS1	LncRNA	Homo sapiens	Cholangiocarcinoma	 CCA tissues	Interaction[miR-324-3p ]	qRT-PCR	LOXL1-AS1 was found overexpressed in CCA tissues screened by high-throughput sequencing technology. Moreover, luciferase reporter and rescue assays indicated that LOXL1-AS1 functioned as a ceRNA to elevate ATP-binding cassette transporter A1 (ABCA1) level by sponging miR-324-3p and exhibited the malignant phenotypes of CCA cells, thereby playing an oncogenic role in CCA. Taken together, this study reveals that LOXL1-AS1 might act as a potential biomarker and therapeutic target for CCA clinical application.	 Additionally, upregulation of LOXL1-AS1 was associated with lymph node invasion, advanced TNM stages and unfavorable prognosis.	Yes	Loss-of-function and gain-of-function experiments were conducted and validated that LOXL1-AS1 could facilitate cell proliferation, migration and invasion and attenuate cell apoptosis. 	31003776
LOXL1-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues and cell lines	interaction[miR-28-5p,RAP1B ]	colony Formation Assay//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	LOXL1-AS1 was found markedly up-regulated in EC tissues and cell lines. In summary, LOXL1-AS1 exerted oncogenic roles in EC progression by sponging miR-28-5p and thereby upregulating RAP1B. This finding might provide potential targets for EC therapy.		Yes	LOXL1-AS1 knockdown displayed evident suppression in cell proliferation, migration and invasion, as well as promotion in cell apoptosis. 	32006897
LOXL1-AS1	LncRNA	Homo sapiens	Liver Neoplasms	 liver cancer tissues and cells 	Interaction(miR-377-3p/NFIB axis)	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Colony Formation Assay//Bioinformatics Analysis	In the present study, LOXL1-AS1 expression was significantly upregulated in liver cancer tissues and cells compared with in normal liver tissues and cells, respectively.Subsequently, LOXL1-AS1 acted as a microRNA (miR)-377-3p sponge, and nuclear factor I B (NFIB) was confirmed as the downstream target of miR-377-3p in liver cancer cells. Additionally, rescue assays suggested that NFIB overexpression countervailed the inhibitory influence of LOXL1-AS1 silencing on liver cancer cellular processes. 	High LOXL1-AS1 expression was associated with poor clinical outcomes in patients with liver cancer.	Yes	 Furthermore, LOXL1-AS1-knockdown suppressed glucose metabolism, proliferation, migration and epithelial-mesenchymal transition (EMT) of liver cancer cells.	34267816
LOXL1-AS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC tissues  	interaction[miR-21]	Transwell Assay//qRT-PCR//Luciferase Report Assay//Western Blot	We observed that LOXL1-AS1 was downregulated in CSCC.Therefore, LOXL1-AS1 may promote CSCC cell invasion and migration by sponging miR-21 to upregulate RHOB.		Yes	Cell invasion and migration analysis showed decreased invasion and migration rates of CSCC cells after LOXL1-AS1 and RHOB overexpression.	32881598
LOXL1-AS1	LncRNA	Homo sapiens	Laryngeal Neoplasms	cells	regulation[miR-589-5p/TRAF6 axis]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LOXL1-AS1 was overexpressed in laryngocarcinoma cells. LOXL1-AS1 promotes the proliferation and migration of laryngocarcinoma cells through absorbing miR-589-5p to upregulate TRAF6 expression.		Yes	Silencing of LOXL1-AS1 suppressed cell proliferation, migration and EMT in laryngocarcinoma. 	33061856
LOXL1-AS1	LncRNA	Homo sapiens	Coronary Disease	HCAEC	Interaction(miR-16-5p)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ELISA//Bioinformatics Analysis//IF	LOXL1-AS1 was highly expressed in CHD patients. LOXL1-AS1 had diagnostic value for CHD and predictive value for MACE occurrence. ox-LDL-treated HCAECs showed reduced viability, increased IL-1β and IL-18 concentrations, and elevated NLPR3, cleaved-caspase-1, and GSDMD-N levels. LOXL1-AS1 silencing promoted cell viability and reduced pyroptosis. LOXL1-AS1 bound to miR-16-5p and miR-16-5p targeted SNX16. Inhibition of miR-16-5p reversed the inhibitory effect of LOXL1-AS1 silencing on HCAEC pyroptosis.	LOXL1-AS1 had diagnostic value for CHD and predictive value for MACE occurrence. 	Yes	LOXL1-AS1 silencing promoted cell viability and reduced pyroptosis. LOXL1-AS1 bound to miR-16-5p and miR-16-5p targeted SNX16.	34633594
circTICRR	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cells	Interaction(HuR/GLUD1 )	In Vivo Experiment//RNA Pull-Down//Northern Blot//Western Blot//CCK8//qRT-PCR//FISH//RIP//RNA-seq//Cell Apoptosis Assay	Here, we identified the overexpression of circTICRR, a circular RNA, in cervical cancer. CircTICRR interacted with HuR protein via binding to F287/F289 in the RRM3 domain of HuR, stabilizing GLUD1 mRNA and elevating the level of GLUD1 protein. 		Yes	In vitro experiments showed that knockdown of circTICRR activated autophagy, and consequently promoted apoptosis and inhibited proliferation in cervical cancer cells, and vice versa.  In vivo experiments revealed that knockdown of circTICRR suppressed the growth of transplanted tumors. 	35595754
hsa_circ_0011385	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC samples and cell lines	Interaction(miR-149-5p/PRDX6 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Tube Formation Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//IHC//Transwell Assay	We observed that hsa_circ_0011385 and PRDX6 were up-regulated while miR-149-5p was down-regulated in CC samples and cell lines. Hsa_circ_0011385 could mediate PRDX6 expression through binding to miR-149-5p. MiR-149-5p silencing reversed hsa_circ_0011385 knockdown-mediated effects on CC cell angiogenesis and malignancy. PRDX6 overexpression overturned the inhibitory effects of miR-149-5p overexpression on angiogenesis and malignant behaviors of CC cells. In conclusion, hsa_circ_0011385 accelerated angiogenesis and malignant behaviors of CC cells by regulating the miR-149-5p/PRDX6 axis, manifesting that hsa_circ_0011385 might be a therapeutic target for CC.	CC patients with high hsa_circ_0011385 expression possessed a shorter overall survival. 	Yes	Hsa_circ_0011385 knockdown reduced tumor growth in vivo and facilitated apoptosis, cell cycle arrest, impeded proliferation, metastasis, invasion, and angiogenesis of CC cells in vitro.	35240453
LONP2	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and BC cells	Interaction(microRNA-584-5p)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	CircLONP2 was significantly upregulated in precancerous BC tissues and BC cells. CircLONP2 depletion inhibited cell viability, proliferation, and invasion of BC cell lines, which could be partially rescued by miR-584-5p inhibitor. Further experiments indicated that miR-584-5p regulates cell viability, proliferation, and invasion via directly targeting YAP1. 		Yes	CircLONP2 depletion inhibited cell viability, proliferation, and invasion of BC cell lines, which could be partially rescued by miR-584-5p inhibitor. Further experiments indicated that miR-584-5p regulates cell viability, proliferation, and invasion via directly targeting YAP1. 	35358000
LOLA1	LncRNA	Homo sapiens	Leukoplakia, Oral		(AKT/GSK-3β pathway)	Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//Cell Apoptosis Assay//Microarray//Cell Proliferation Assay//Cell Cycle Assay//Invasion Assay//Transwell Assay	 The results of qRT-PCR revealed that LOLA1 aberrant expression was validated in tissue samples and cell lines from the normal oral mucosa, OL to OSCC.		Yes	Cell function assays showed that LOLA1 significantly influenced cell migration, invasion, and epithelial-mesenchymal transition (EMT) protein expression.	33969929
hsa_circ_0087429	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells 	Interaction(miR-5003-3p/OGN axis)	In Vivo Experiment//IHC//Western Blot//Transfection//Wound Healing Assay//Invasion Assay//Tube Formation Assay//CCK8//qRT-PCR//RIP//IF//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	circ_0087429 is significantly downregulated in cervical cancer tissues and cells and negatively correlated with International Federation of Gynecology and Obstetrics (FIGO) staging and lymphatic metastasis in cervical cancer patients.OGN is significantly downregulated in cervical cancer tissues and cells. circ_0087429 can upregulate the expression of OGN by competitively binding with miR-5003-3p, thereby reversing EMT and inhibiting the progression of cervical cancer. EIF4A3 can inhibit circ_0087429 expression by binding to its flanking regions.		Yes	circ_0087429 can significantly inhibit the proliferation, migration, invasion and angiogenesis of cervical cancer in vitro and tumour growth and metastasis in vivo.	35513835
hsa_circ_0005576	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction( miR-1305/PAIP1 axis)	In Vivo Experiment//IHC//Western Blot//Transfection//Invasion Assay//Migration Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Circ_0005576 and PAIP1 were upregulated, while miR-1305 was downregulated in CC tissues and cells. Meanwhile, circ_0005576 could sponge miR-1305 to promote PAIP1 expression. Furthermore, PAIP1 overexpression relieved the influence of circ_0005576 silence on the growth of CC cells. 		Yes	Knockdown of circ_0005576 suppressed the proliferation, migration, and invasion of CC cells, while the silence of miR-1305 facilitated the development of CC cells. Additionally, circ_0005576 silence hindered CC tumor growth in vivo. 	35378711
hsa_circ_0036602	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-34-5p,miR-431-5p/HMGB1)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	 Circ0036602 was upregulated in HPV-16 positive CC and correlated with a poor prognosis.  Further studies showed that circ0036602 could bind to miR-34-5p and miR-431-5p to regulate the expression of the target gene HMGB1.	 Circ0036602 was upregulated in HPV-16 positive CC and correlated with a poor prognosis.  Moreover, circ0036602 expression significantly correlated with the clinicopathologic characteristics.	Yes	 Knockdown of circ0036602 inhibited CC cell proliferation, migration, and invasion. 	35145563
hsa_circ_400029	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cells and tissue	Interaction(miR-1285-3p/TLN1 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//FISH//Flow Cytometry//Luciferase Report Assay//Cell Cycle Assay//Transwell Assay//EdU Staining//IF	 To begin with, circRNA_400029 was upregulated in CC cells and tissue. Interestingly, miR-1285-3p targeted circRNA_400029 and down-regulated of miR-1285-3p could reverse the effects of circRNA_400029 weak-expression on progression and apoptosis of CC cells. Moreover, TLN1 was up-regulated in CC cells and identified as a direct target of miR-1285-3p. Meanwhile, we found that miR-1285-3p negatively regulated the function of TLN1. Finally, the circRNA_400029/miR-1285-3p/TLN1 axis could affect tumor growth in vivo.		Yes	 Knockdown circRNA_400029 inhibited cell proliferation, migration and invasion while induced cell apoptosis.	35069901
hsa_circ_0018289	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cells	Interaction(miR-1294/ICMT axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//IF//Colony Formation Assay//EdU Staining//Transwell Assay	 Hsa_circ_0018289 was elevated in CC tissues and cells, its deficiency could repress growth, metastasis, and glycolysis of CC cells in vitro, as well as hamper tumor growth in vivo.Hsa_circ_0018289 sponged miR-1294 while miR-1294 bound with ICMT, and the inhibition of miR-1294 or addition of ICMT could partially relieve the effect caused by hsa_circ_0018289 depletion.		Yes	 Hsa_circ_0018289 was elevated in CC tissues and cells, its deficiency could repress growth, metastasis, and glycolysis of CC cells in vitro, as well as hamper tumor growth in vivo.	35312113
circCCDC134	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction( miR-503-5p/MYB)	In Vivo Experiment//RNA Pull-Down//Transfection//qRT-PCR//FISH//RIP//ChIP-seq//IHC	The results revealed that circCCDC134 recruited p65 in the nucleus and acted as a miR-503-5p sponge to regulate the expression of MYB in the cytoplasm, ultimately stimulating HIF1A transcription and facilitating CC growth and metastasis.		Yes	The results revealed that circCCDC134 recruited p65 in the nucleus and acted as a miR-503-5p sponge to regulate the expression of MYB in the cytoplasm, ultimately stimulating HIF1A transcription and facilitating CC growth and metastasis.	36028854
LOC730100	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[miR-760/FOXA1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In the current research, we showed that LOC730100 expression was increased in glioma tissues and cell lines.  In conclusion, our findings revealed that LOC730100 promoted glioma progression through regulating miR-760/FOXA1 axis.		Yes	 Loss-of-function assays showed that LOC730100 knockdown inhibited proliferation, migration and invasion of glioma cells, but increasing apoptosis. 	30914197
LOXL1-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms		Regulation[ LOXL1-AS1/miR-28-5p/SEMA7A axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Our findings constitute the first report to delineate that lncRNA LOXL1-AS1/miR-28-5p/SEMA7A axis facilitates PC progression. According to our experimental results, we found the expression of miR-28-5p was downregulated in PC cells and miR-28-5p overexpression inhibited cell proliferation and migration in PC. LOXL1-AS1 could sponge miR-28-5p and then upregulate the expression of SEMA7A. Thus, LOXL1-AS1/miR-28-5p/SEMA7A axis facilitated PC progression. This initially proposed point might provide a novel molecular target for PC treatment.		Yes	Therefore, the function of LOXL1-AS1 was further explored in PC, presenting that LOXL1-AS1 suppression inhibited cell proliferation and migration.	31732974
LOXL1-AS1	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	Interaction(miR-374b-5p/MMP14 axis)	In Vivo Experiment//Western Blot//Transfection//Tube Formation Assay//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	In this study, low levels of TIAR and high levels of LOXL1-AS1 were found in glioma cells and tissues.  In summary, we demonstrated that TIAR combined with LOXL1-AS1 modulates VM in glioma via the miR-374b-5p/MMP14 axis, revealing novel targets for glioma therapy.		Yes	 LOXL1-AS1 acted like a miRNA sponge towards miR-374b-5p so that downregulation of the former greatly inhibited cell proliferation, migration, invasion and VM. 	34890108
hsa_circ_0005358	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction(PTBP1/CDCP1)	RNA Pull-Down//Northern Blot//Western Blot//ISH//Transfection//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//RIP//RNA-seq//PCR//Cell Proliferation Assay//Invasion Assay	In this study, we identified a downregulated circRNA derived from the host gene Gli1 (hsa_circ_0005358) in cervical cancer tissues, which was expressed at lower levels in tissues with extracervical metastasis than in those without extracervical metastasis. RNA-pull-down assay, mass spectrometry, and RNA immunoprecipitation validated the findings that hsa_circ_0005358 functions via its 215-224 sequence, which interacts with polypyrimidine tract-binding protein 1 (PTBP1). RNA-sequencing profiling revealed that CUB-domain-containing protein 1 (CDCP1) is a common target for hsa_circ_0005358 and PTBP1. 		Yes	Upregulation of hsa_circ_0005358 significantly suppressed the migration and invasion of cervical cancer cells in vitro, and downregulation of hsa_circ_0005358 had the opposite effect. A mouse model revealed that cervical cancer cells overexpressing hsa_circ_0005358 possessed weaker metastatic potential in vivo.	34976440
LOXL1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cells and tissues	Interaction( LOXL1-AS1/miR-423-5p/ENC1 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//IF	The results of RT-qPCR demonstrated that LOXL1-AS1 and ectodermal-neural cortex 1 (ENC1) expression levels were upregulated in CC cells and tissues, while microRNA-423-5p (miR-423-5p) level was downregulated. As subcellular fractionation assays, RNA pull down assays and luciferase reporter assays revealed, LOXL1-AS1 bound to miR-423-5p and miR-423-5p targeted ENC1. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, wound healing and colony formation assays demonstrated that miR-423-5p upregulation and LOXL1-AS1 downregulation inhibited CC cell proliferation and migration, while ENC1 upregulation attenuated the inhibitory effects of miR-423-5p upregulation on the malignant phenotypes of CC cells. Western blotting was conducted to measure protein levels and the results showed that ENC1 knockdown inhibited the activation of ERK/MEK pathway. 		Yes	The in vivo experiments demonstrated that LOXL1-AS1 downregulation inhibited tumor growth and metastasis and proliferation of CC cells. 	35015607
hsa_circ_0000135	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction( circ_0000135/miR-140-3p/PDZK1)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Transwell Assay	 circ_0000135 and PDZK1 expressions were increased, while those of miR-140-3p were decreased in cervical cancer tissues and cells (both P < 0.05).  circ_0000135 had conserved target of miR-140-3p. There was a direct interaction between circ_0000135 and miR-140-3p. miR-140-3p might have direct interaction with PDZK1. sh-circ_0000135 and/or miR-140-3p treatment showed obviously decreased PDZK1 expression, decreased cell activity, arrested cells in G0/G1 phase, downregulated cell migration and invasion; sh-circ_0000135 and/or miR-140-3p mimic treatment showed obviously decreased tumor volume, tumor weight, and Ki67 expression (all P < 0.05).		Yes	sh-circ_0000135 group had decreased cell viability, arrested cells in G0/G1 phase, decreased CyclinD1 expression, inhibited cell migration and invasion; sh-circ_0000135 group showed reduced tumor volume, weight, and lower Ki67 expression (all P < 0.05). 	35066758
LOXL1‑AS1	LncRNA	Homo sapiens	Thymoma	thymoma and thymic carcinoma tissues	Interaction(miR-525-5p-HSPA9)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	 LOXL1-AS1 and HSPA9 were overexpressed in thymoma and thymic carcinoma; high levels of LOXL1-AS1 and HSPA9 were associated with poor prognosis, and there was a significant positive correlation between their levels. miR‑525‑5p inhibited the expression of HSPA9 protein by targeting the 3'‑untranslated region (UTR) of HSPA9 mRNA. LOXL1‑AS1 promoted the expression of HSPA9 as a sponge targeting miR‑525‑5p.	LOXL1-AS1 and HSPA9 were overexpressed in thymoma and thymic carcinoma; high levels of LOXL1-AS1 and HSPA9 were associated with poor prognosis, and there was a significant positive correlation between their levels. Downregulation of miR?525?5p expression was also associated with poor prognosis of patients. 	Yes	Animal experiment results also showed that knockdown of miR?525?5p promoted cancer by promoting the expression of HSPA9. 	33907842
LOXL1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[miR-142-5p/PIK3CA Axis]	CCK8//qRT-PCR//Western Blot//Transwell Assay	LOXL1-AS1 expression in GC samples was significantly increased, which was correlated with unfavorable pathological indexes.Additionally, overexpressed LOXL1-AS1 notably reduced the expression of miR-142-5p, but enhanced the expression level of PIK3CA.	 Highly expressed LOXL1-AS1 was closely linked to shorter overall survival time and post-progression survival time of the patients.	Yes	Additionally, overexpressed LOXL1-AS1 notably reduced the expression of miR-142-5p, but enhanced the expression level of PIK3CA. In vivo experiments further validated that knockdown of LOXL1-AS1 inhibited the growth and metastasis of GC cells via regulating miR-142-5p and PIK3CA.	31908498
LOXL1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	Interaction[miR-708-5p/USF1 pathway]	RNA Pull-Down//ChIP//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	LOXL1-AS1 was highly expressed in tissues and cells of gastric cancer.Rescue experiments testified the stimulative role of LOXL1-AS1/miR-708-5p/USF1 pathway in gastric cancer progression. 		Yes	Our findings demonstrated that LOXL1-AS1 accelerated the deterioration of gastric cancer by inducing cell proliferation, migration, EMT and stemness.	31468594
LOXL1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer and adjacent normal tissues,cell lines(MCF42,MDA-MB-7)	Interaction[Antagonizing miR-708-5p ]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay//Transwell Assay	The results showed that LOXL1-AS1 expression levels were significantly higher in breast cancer samples than those in corresponding normal tissues.Overall, LOXL1-AS1 upregulation facilitates breast cancer invasion and metastasis by blocking miR-708-5p expression and activity. 	  Increased LOXL1-AS1 expression is correlated with tumor stage and lymph node metastasis in breast cancer patients.	Yes	Biologically, overexpression of LOXL1-AS1 enhances and knockdown of LOXL1-AS1 suppresses breast cancer cell migration and invasion. In vivo studies demonstrate that depletion of LOXL1-AS1 inhibits breast cancer metastasis.	31945728
LOXL1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction[regulating miR-143-3p]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	In this study, we found that LOXL1-AS1 expression was induced while miR-142-3p expression was decreased in breast cancer tissues and cells, implying that LOXL1-AS1 and miR-143-3p play an important role in cell progression of breast cancer.The analysis of luciferase reporter assay determined that LOXL1-AS1 directly targeted miR-143-3p in breast cancer cells. The rescue experiments further proved that miR-143-3p reversed the inhibited effects of si- LOXL1-AS1 on breast cancer cells.		Yes	Further investigation showed that silencing LOXL1-AS1 inhibited proliferation, promoted cell apoptosis and decreased the capacity of cell migrated and invasive in breast cancer cells.	31841194
LOXL1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer tissues and cells	regulation[ miR-3128/RHOXF2 Axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 LncRNA LOXL1-AS1 was higher expressed in lung cancer tissues and cells.LOXL1-AS1 promotes the progression of NSCLC by regulating miR-3128/RHOXF2 axis, which might be a new potential target for the diagnosis and treatment of NSCLC.	Moreover, LOXL1-AS1 expression was upregulated in tumor tissues with advanced stages and metastasis. 	Yes	After knocking down LOXL1-AS1, proliferation, invasion and migration of H1299 and A549 cells were inhibited. 	32636639
LOXL1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	Regulation(DESC1)	Migration Assay//CCK8//qRT-PCR//Cell Cycle Assay//Invasion Assay	Here we validated that LOXL1-AS1 was significantly upregulated in ESCC tissues compared with the corresponding adjacent non-neoplastic tissues, and LOXL1-AS1 expression was positively correlated with ESCC patients' lymph node metastasis.  From high throughput RNA sequencing (RNA-seq) analysis, we identified that differentially expressed in squamous cell carcinoma 1 (DESC1) was a critical downstream target of LOXL1-AS1. 	Here we validated that LOXL1-AS1 was significantly upregulated in ESCC tissues compared with the corresponding adjacent non-neoplastic tissues, and LOXL1-AS1 expression was positively correlated with ESCC patients' lymph node metastasis. 	Yes	LOXL1-AS1 knockdown impaired ESCC cells proliferation, migration and invasion capabilities in vitro. Furthermore, inhibiting LOXL1-AS1 in ESCC cells increased the percentage of cells at the G1 phase, accompanied by reducing in S phase in contrast to scramble control, and silencing of LOXL1-AS1 evoked ESCC cell apoptosis. 	33391449
hsa_circ_0000190	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells and  tisuuses	Interaction(miR-1252-5p/EIF4EBP2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0000190 functioned through the modulation of miR-1252-5p/EIF4EBP2 axis.		Yes	 Overexpressed circ_0000190 attenuated CC progression in vitro and in vivo.	35414334
LOXL1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines 	regulation[miR-708-5p/CD44-EGFR Axis]	Western Blot//Wound Healing Assay//qRT-PCR//IF//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	This study demonstrated that lncRNA LOXL1-AS1 enhances multiplication, migration, invasion, and progression of CRC by sponging miR-708-5p to regulate the CD44-EGFR signal pathway.	 In this study, we reveal that the regulation of lncRNA LOXL1-AS1 occurs within CRC based on the correlation with poor clinical outcomes.	Yes	LOXL1-AS1 knockdown along with miR-708-5p overpresentation in CRC cell lines inhibited cell multiplication, migration, and invasion. 	32821123
LOXL1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Regulation(miR-1224-5p/miR-761/HK2 Axis)	Western Blot//Wound Healing Assay//qRT-PCR//Colony Formation Assay//Transwell Assay	LOXL1-AS1 and HK2 levels were increased, while miR-1224-5p and miR-761 levels were reduced in CRC tissues and cells. Knockdown of LOXL1-AS1 suppressed CRC cell proliferation, invasion, migration, and glycolysis, and induced cell apoptosis. Silencing of LOXL1-AS1 blocked tumor growth in vivo. Moreover, LOXL1-AS1 accelerated CRC cell progression by absorbing miR-1224-5p/miR-761. Besides, miR-1224-5p and miR-761 inhibited CRC cell progression via targeting HK2. LOXL1-AS1 contributed to CRC progression via modulating miR-1224-5p/miR-761/HK2 pathway.		Yes	Knockdown of LOXL1-AS1 suppressed CRC cell proliferation, invasion, migration, and glycolysis, and induced cell apoptosis. Silencing of LOXL1-AS1 blocked tumor growth in vivo.	35441953
LOXL1-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC tissues and cells	interaction[sponges miR-589-5p]	qRT-PCR//Western Blot	 LOXL1-AS1 was highly expressed in RCC tissues and cells. LncRNA LOXL1-AS1 sequestered miR-589-5p to augment CBX5 expression in RCC cells, opening a new way for potential development in RCC treatment.		Yes	Moreover, knockdown of LOXL1-AS1 hampered RCC cell proliferation and migration.	33185692
LOXL1-AS1	LncRNA	Homo sapiens	Osteoarthritis	OA cartilage tissues	regulation[miR-423-5p/KDM5C axis]	qRT-PCR	LOXL1-AS1 was up-regulated in OA cartilage tissues.LncRNA LOXL1-AS1 is transcriptionally activated by JUND and facilitates the proliferation and inflammation of chondrocytes via elevating miR-423-5p-mediated KDM5C in OA, which may provide potential therapeutic target for OA.		Yes	Silencing LOXL1-AS1 hampered proliferation and inflammation, yet promoting apoptosis in chondrocytes.	32679142
LOXL1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(LOXL1-AS1/miR-3614-5p/YY1 signal axis)	qRT-PCR	We discovered that LOXL1-AS1 was high expressed in HCC cells. Inhibition of LOXL1-AS1 repressed cell proliferation, migration and invasion, but enhanced cell apoptosis in HCC. Further, miR-3614-5p was proven to be sponged by LOXL1-AS1. Additionally, Yin Yang 1 (YY1) was proven as the target gene of miR-3614-5p, and YY1 depletion could repress HCC cell malignant behaviors. YY1 could also transcriptionally activate LOXL1-AS1 expression. In rescue assays, we confirmed that overexpression of YY1 or miR-3614-5p inhibition could reverse the suppressive effects of LOXL1-AS1 silence on the malignant behaviors of HCC cells.		Yes	Inhibition of LOXL1-AS1 repressed cell proliferation, migration and invasion, but enhanced cell apoptosis in HCC.	34863279
hsa_circ_0119412	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical tumor tissues and cancer cells	Interaction( miR-217/AGR2 pathway)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	 circ_0119412 expression was highly enhanced in cervical tumor tissues and cancer cells. AGR2 was upregulated in cervical cancer by the public bioinformatics data. circ_0119412 bound to miR-217, and miR-217 bound to AGR 3'UTR. The promoting effects of circ_0119412 overexpression on cancer cell malignant phenotypes were reversed by miR-217 enrichment. In addition, increased expression of miR-217 suppressed AGR2 expression, thus weakening the functional effects of AGR2.		Yes	circ_0119412 overexpression aggravated cervical cancer cell proliferation, migration, and adhesion, and its overexpression was also conducive to tumor formation and growth in animal models.	35274779
LOXL1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian carcinoma tissue	regulation[miR-18b-5p/VMA21 axis]	Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	LOXL1-AS1 is significantly overexpressed in ovarian carcinoma tissue compared with adjacent non-cancerous sample.These findings suggest that lncRNA LOXL1-AS1 promotes ovarian cancer cell growth, migratory and invasiveness via modulating miR-18b-5p/VMA21 axis.		Yes	Transfection of LOXL1-AS1 siRNA or miR-18b-5p mimics inhibits the growth and aggressive phenotypes of SKOV3 and OVCAR3 cell. 	32058209
LOXL1-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction[PI3K-AKT pathway]	qRT-PCR//MTT//Western Blot//Transwell Assay	In our study, we found LOXL1-AS1 expression levels were higher in osteosarcoma tissues and cell lines than normal bone tissues and normal osteoblast cell line, respectively.The loss-of-function studies showed knockdown of LOXL1-AS1 dramatically inhibited osteosarcoma cell proliferation, migration, and invasion through suppressing PI3K-AKT pathway. In conclusion, LOXL1-AS1 predicts clinical progression and poor prognosis in osteosarcoma patients and functions as oncogenic lncRNA to regulate cell proliferation, cell cycle, migration, and invasion.	Moreover, high-expression of LOXL1-AS1 was correlated with Enneking stage, tumor size, distant metastasis, histological grade, and overall survival time in osteosarcoma patients.	Yes	 The loss-of-function studies showed knockdown of LOXL1-AS1 dramatically inhibited osteosarcoma cell proliferation, migration, and invasion through suppressing PI3K-AKT pathway. 	30944201
LOXL1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-526b-5p /LYPLA1 Axis)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Tube Formation Assay//qRT-PCR//RIP//FISH//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	In this study, LOXL1-AS1 was found elevated in CC tissues and cells.  Furthermore, we found that LOXL1-AS1 upregulated Lysophospholipase 1 expression via sequestering miR‐526b-5p. Rescue assays revealed that overexpression of LYPLA1 reversed the LOXL1-AS1 silencing-induced inhibitory effects on the malignant phenotypes of CC cells. 		Yes	LOXL1-AS1 depletion restrained CC cell proliferation, migration, invasion, and angiogenesis in vivo. 	34984578
hsa_circ_0000228	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells 	Interaction(miR-337-3p / TGFBR1 Axis)	Western Blot//Transfection//BrdU//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	Circ_0000228 expression in the CC tissues and cells was up-modulated.  MiR-337-3p could be adsorbed by circ_0000228. TGFBR1 was identified as a target gene of miR-337-3p that indirectly and positively modulated bycirc_0000228 in the CC cells.		Yes	Circ_0000228 overexpression markedly enhanced cell proliferation, migration, and invasion, while knocking down circ_0000228 remarkably repressed cell proliferation, migration, and invasion. 	35279965
circRNF121	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-153-3p/ATF2 axis and wnt/β-catenin pathway)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Our results showed that circRNF121 was highly expressed in CC tissues and cells. For mechanism investigation, circRNF121 could affect activating transcription factor 2 (ATF2) expression by decoying miR-153-3p, thereby accelerating CC cell development. In conclusion, circRNF121 exerted the tumor-suppressive role in CC progression by altering miR-153-3p/ATF2 axis. 		Yes	 Knockdown of circRNF121 suppressed cell growth, metastasis, epithelial-mesenchymal transition (EMT), autophagy, and wnt/β-catenin pathway in CC cells in vitro and blocked tumor formation in vivo. 	34981843
hsa_circ_0072995	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cancer tissues	Interaction(miR-29a/WDR5 axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//IHC//Invasion Assay//IF	 Circ_0072995 was significantly up-regulated in cancer tissues, and its level was markedly correlated with the International Federation of Gynecology and Obstetrics system (FIGO) staging.  In conclusion, circ_0072995 promoted cervical cancer development by inducing miR-29a-mediated WDR5 expression.	 Circ_0072995 was significantly up-regulated in cancer tissues, and its level was markedly correlated with the International Federation of Gynecology and Obstetrics system (FIGO) staging. 	Yes	 In vitro studies revealed that circ_0072995 interacts with miR-29a to induce WD repeat domain 5 (WDR5) expression and promotes the proliferation and invasion of cells, but inhibits apoptosis of cells. Knockdown of circ_0072995 or WDR5, or overexpression of miR-29a significantly inhibited tumour growth in vivo. 	36168936
hsa_circ_0003221	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cancer tissues and cells	Interaction(miR-139-3p/S100A14 Pathway)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Tube Formation Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 Circ_0003221 was highly expressed in cancer tissues and cells, and its downregulation suppressed cancer cell proliferation, migration, invasion, and angiogenesis and also delayed tumor growth in vivo. Circ_0003221 downregulation restrains cervical cancer cell growth, metastasis, and angiogenesis by governing the miR-139-3p/S100A14 pathway.		Yes	 Circ_0003221 was highly expressed in cancer tissues and cells, and its downregulation suppressed cancer cell proliferation, migration, invasion, and angiogenesis and also delayed tumor growth in vivo.	35023052
hsa_circ_0000069	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells and tissues	Interaction(miR-4426)	In Vivo Experiment//IHC//MeRIP//Wound Healing Assay//CCK8//qRT-PCR//IF//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 We found that circ0000069 was upregulated in CC cells and tissues, and that N6-methyladenosine (m6A) modification maintained circ0000069 stability. miR-4426 specifically binds circ0000069 and mediates its functions in CC development. 		Yes	Gain- and loss-of-function assays revealed that circ0000069 promoted CC cell proliferation and migration. 	33725572
LOC644135	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	CD8+ T cell	Expression(highly expressed)	Bioinformatics Analysis	Pan-cancer analysis indicated that LOC644135 was most highly expressed in AML across 33 types of cancer. Patients with high expression of LOC644135 had poor overall prognosis in both TCGA-AML cohort and the TARGET-AML cohort. Especially, high expression of LOC644135 indicated inferior overall survival and event-free survival in CN-AML patients in the TCGA-AML cohort. Besides, CN-AML patients had higher expression of LOC644135 than normal samples. Multivariable analysis suggested that LOC644135 was an independent prognostic factor in AML. GSEA analysis showed that LOC644135 was associated with some immune-related pathways. Besides, high expression of LOC644135 was associated with less infiltration of CD8+ T cell.	Patients with high expression of LOC644135 had poor overall prognosis in both TCGA-AML cohort and the TARGET-AML cohort. 	Yes	Multivariable analysis suggested that LOC644135 was an independent prognostic factor in AML. GSEA analysis showed that LOC644135 was associated with some immune-related pathways. Besides, high expression of LOC644135 was associated with less infiltration of CD8+ T cell.	35713000
circCCDC66	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tumor tissues	Interaction(miR-452-5p/REXO1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	 The expression of circ-CCDC66 was upregulated in cervical cancer tumor tissues in comparison with normal tissues, and correlated with later tumor stage and larger tumor size.Circ-CCDC66 was an efficient molecular sponge for miR-452-5p, and negatively regulated miR-452-5p expression. MiR-452-5p directly targeted to REXO1. Circ-CCDC66 regulated REXO1 expression to modulate cervical cancer progression via miR-452-5p. 		Yes	Downregulated circ-CCDC66 inhibited cervical cancer cell proliferation, migration, and invasion. Moreover, downregulated circ-CCDC66 was found to suppress tumor growth in vivo.	33407514
hsa_circ_0000326	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	Cervical cancer cells and tissues	Interaction(microRNA-338-3p/CDK4)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Colony Formation Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//IHC//EdU Staining//Transwell Assay	Cervical cancer cells and tissues were also observed to have elevated levels of circ_0000326 and the upregulation of circ_0000326 depended on the stage of cancer.  Interestingly, we confirmed that circ_0000326 served as a sponge for microRNA-338-3p and that the miRNA bound to Cyclin-dependent kinase 4. In the presence of microRNA-338-3p mimic or silencing of circ_0000326, Cyclin-dependent kinase 4 expression was decreased. 		Yes	. Transfection with siRNA of circ_0000326 resulted in the inhibition of proliferation, migration and cell cycle of cancer cells. 	33735107
hsa_circ_0019435	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells 	Regulation(DKK1 and PTEN)	ChIP//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The present study uncovered that circ_0019435 was upregulated in CC cells by qRT-PCR. Furthermore, it was disclosed that circ_0019435 binds to EZH2 to silence DKK1 and PTEN. Finally, rescue assays corroborated that DKK1 and PTEN were involved in circ_0019435-mediated CC cell progression. 		Yes	 Then, it was unveiled by a series of functional assays including colony formation, trypan blue staining, and transwell invasion assays in that circ_0019435 ablation induced the suppression of proliferation, invasion, and EMT of HeLa and SiHa cells. 	34037956
LOC550643	LncRNA	Homo sapiens	Breast Neoplasms	cell lines and 36 breast cancer tissues	Interaction(miR-125b-2-3p)	qRT-PCR//Luciferase Report Assay	Among the cell lines, a novel lncRNA, LOC550643, was highly expressed in breast cancer cells.Furthermore, LOC550643 could inhibit miR-125b-2-3p expression to promote breast cancer cell growth and invasiveness.  	 Furthermore, the high expression of LOC550643 was significantly correlated with the poor prognosis of breast cancer patients, especially those with triple-negative breast cancer.	Yes	 Knockdown of LOC550643 inhibited cell proliferation of breast cancer cells by blocking cell cycle progression at S phase. LOC550643 promoted important in vitro metastatic traits such as cell migration and invasion. In addition, by using a xenograft mouse model, we demonstrated that depletion of LOC550643 suppressed the lung metastatic potential of breast cancer cells.	34354991
LOC550643	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue and cells	Interaction( miR-29b-2-5p)	qRT-PCR//Colony Formation Assay//Western Blot	In this study, we assessed the clinical impacts of LOC550643 on CRC through the analysis of The Cancer Genome Atlas database, which revealed the significant upregulation of LOC550643 in CRC. Furthermore, miR-29b-2-5p interacted with the LOC550643 sequence. Ectopic miR-29b-2-5p significantly suppressed colon cancer cell growth and motility and induced cell apoptosis. 	Moreover, the high expression of LOC550643 was associated with poor survival in patients with CRC (p = 0.001). Multivariate Cox regression analysis indicated that LOC550643 overexpression was an independent prognostic factor for shorter overall survival in patients with CRC (adjusted hazard ratio, 1.90; 95% confidence interval, 1.21-3.00; p = 0.006). 	Yes	A biological function analysis revealed that LOC550643 knockdown reduced colon cancer cell growth by hindering cell cycle progression. In addition, LOC550643 knockdown significantly induced cell apoptosis through the inhibition of signaling activity in phosphoinositide 3-kinases. Moreover, LOC550643 knockdown contributed to the inhibition of migration and invasion ability in colon cancer cells. F	35406629
hsa_circ_0001400	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction(miR-326-Akt network)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//circRNA-seq//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Colony Formation Assay//Bioinformatics Analysis	 In the present study, we showed that hsa_circRNA_0001400 was highly expressed in cervical cancer tissues relative to in matched normal tissue. We showed that hsa_circRNA_0001400_siRNA can inhibit the protein expression of Akt and that the inhibition of miR-326 could rescue the inhibition of Akt in cervical cancer cells. 		Yes	We found that hsa_circRNA_0001400_siRNA significantly promoted the apoptosis of cervical cancer cells and arrested the cell cycle and migration of cervical cancer cells. 	34976014
LOC441461	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Regulation(TRAIL/RUNX1)	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	LOC441461 expression was lower in stage IV than in stages I, II, and III. LOC441461 downregulation increased the epithelial-to-mesenchymal transition, as indicated by increased TRAIL signaling and decreased RUNX1 interactions. The interaction of the transcription factors RELA, IRF1, ESR1, AR, POU5F1, TRIM28, and GATA1 with LOC441461 affected the degree of the malignancy of gastric cancer by modulating gene transcription. 		Yes	The depletion of LOC441461 promoted cell proliferation, cell cycle progression, apoptosis, cell motility, and invasiveness. 	35267457
LOC441461	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	regulation[RhoA/ROCK signaling]	qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Western Blot	This study determined that LOC441461 expression was significantly higher in CRC tissues than in adjacent normal mucosa. Overall, LOC441461 was discovered to play an oncogenic role in CRC cell growth and motility through RhoA/ROCK signaling. 		Yes	Knockdown of the LOC441461 expression significantly suppressed colon cancer cell growth by impairing cell cycle progression and inducing cell apoptosis. 	33126743
hsa_circ_0000520	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction(miR-1296)	In Vivo Experiment//Western Blot//Transfection//EdU Staining//Colony Formation Assay//CCK8//qRT-PCR//FISH//RIP//Flow Cytometry//Luciferase Report Assay//IHC//Bioinformatics Analysis	Hsa_circ_0000520 and cyclin-dependent kinase 2 (CDK2) were highly expressed in cervical cancer tissues.Binding sites between microRNA-1296 (miR-1296) and hsa_circ_0000520 or CDK2 were verified. Antibody to Argonaute 2 (Ago2) could precipitate hsa_circ_0000520, indicating that hsa_circ_0000520 could competitively bind to miR-1296 via Ago2. 		Yes	Silencing hsa_circ_0000520 inhibited cervical cancer cell proliferation and promoted the inhibitory effects of miR-1296 on CDK2, thereby blocking cell cycle progression and promoting apoptosis.	34284793
LOC441178	LncRNA	Homo sapiens	esophageal carcinoma	ESCC cells	regulation[LOC441178/miR-182 axis]	Flow Cytometry//qRT-PCR//Wound Healing Assay//Transwell Assay	In this study, we found that LOC441178 negatively regulated miR-182 expression in ESCC cells.These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC.		Yes	 In addition, overexpression of LOC441178 inhibited the proliferation and migration and induced apoptosis in ESCC cells via downregulation of miR-182. 	33173314
LOC441178	LncRNA	Homo sapiens	esophageal carcinoma		Regulation	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//ELISA//Transwell Assay	The results revealed that LOC441178 overexpression notably suppressed the metastasis of EC cells. Exosomal LOC441178 also suppressed macrophage M2 polarization, and the polarized macrophages decreased EC cell invasion. Exosomes containing LOC441178 notably inhibited the growth of EC in mice. 		Yes	The results revealed that LOC441178 overexpression notably suppressed the metastasis of EC cells. Exosomal LOC441178 also suppressed macrophage M2 polarization, and the polarized macrophages decreased EC cell invasion. Exosomes containing LOC441178 notably inhibited the growth of EC in mice. 	36250676
hsa_circ_0043280	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CCa tissues 	Interaction(miR-203a-3p/PAQR3 axis)	In Vivo Experiment//Western Blot//ISH//Transfection//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//migration assay//RNA-seq//H&E Staining//Luciferase Report Assay//IHC//EdU Staining	Herein, we demonstrated that a circRNA derived from the TADA2A gene (hsa_circ_0043280) was significantly downregulated in CCa and that this reduction in expression was correlated with a poor prognosis.  Mechanistically, hsa_circ_0043280 competitively sponges miR-203a-3p and prevents miR-203a-3p from reducing the levels of PAQR3. 		Yes	Furthermore, our results demonstrated that hsa_circ_0043280 functions as a tumor suppressor to inhibit tumor growth and metastasis in CCa. 	34588429
hsa_circ_000543	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-567/ZNF268 Axis)	Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Hsa_circ_000543 was over-expressed in CC tissues and cells. Hsa_circ_000543 directly targeted miR-567/ZNF268 in CC cell lines. In CC tumor tissues and cells, the hsa_circ_000543 expression was negatively correlated with miR-567 expression and showed a positive correlation with ZNF268 expression. 	The high expression of hsa_circ_000543 indicated poor prognosis of CC patients. 	Yes	Hsa_circ_000543 promoted cell proliferation, colony formation, migration and invasion, as well as inhibited cell apoptosis in CC cells.	34234564
circEPSTI1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Interaction(miR-375/409-3P/515-5p-SLC7A11 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. 		Yes	Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro.	33534779
LOC440173	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	regulation[miR-30d-5p/HDAC9 axis ]	qRT-PCR	The expression level of LOC440173 was significantly increased in ESCC tissues and esophageal carcinoma cells.In conclusion, LOC440173 exerts a promotive role in ESCC tumorigenesis by targeting the miR-30d-5p/HDAC9 axis and regulating the EMT process.	High LOC440173 expression was correlated with histological grade, tumor invasion depth, lymph node metastasis, and TNM stage.	Yes	Overexpression of LOC440173 promoted esophageal cancer cell proliferation, migration, and invasion, as well as the epithelial-mesenchymal transition (EMT) process in vitro, and facilitated tumor growth in vivo. 	33079409
circZNF609C	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cell lines	Interaction(miR-197-3p/E2F6 axis)	In Vivo Experiment//Transfection//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	In the present study, it was found that circ-ZNF609 was elevated in CC tissues and cell lines, circ-ZNF609 was identified to negatively regulate miR-197-3p expression in CC cells.  Additionally, we further demonstrated that circ-ZNF609 upregulated E2F6 by interacting with miR-197-3p. 		Yes	 circ-ZNF609 deletion repressed cell viability, migration and invasion in CC. 	33734009
LOC645166	LncRNA	Homo sapiens	Atherosclerosis	T cells	Regulation(Decreasingly Blocking Recruitment of the IKK Complex to K63-Linked Polyubiquitin Chains)	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//Microarray	we have identified that the levels of lncRNA, LOC645166, in T cells of AS patients were reduced. Overexpression of LOC645166 in Jurkat cells down-regulated the IL-23p19 expression and suppressed the JAK2/STAT3 signaling in response to stimulation by phorbol 12-myristate 13-acetate. Suppression of STAT3 activation by LOC645166 was also observed when Jurkat cells or T cells of AS patient were treated with anti-CD3/CD28 antibodies. In order to explore the role of LOC645166 in the pathogenesis of AS, RNA pull-down assay plus proteomic approach and western blotting were performed and identified that LOC645166 prefers binding the K63-linked polyubiquitin chains. LOC645166 can suppress recruitment of the IKK complex to K63-linked polyubiquitin chains and diminish IKK2 activation, leading to down-regulation of NF-κB activation. Down-regulation of LOC645166 expression in T cells of AS patients up-regulates NF-kB activation via decreasingly impeding recruitment of the IKK complex to K63-linked polyubiquitin chains, allowing AS patients to exhibit more sensitivity to stimulation by the proinflammatory cytokines or by TLR ligands.		Yes	Overexpression of LOC645166 in Jurkat cells down-regulated the IL-23p19 expression and suppressed the JAK2/STAT3 signaling in response to stimulation by phorbol 12-myristate 13-acetate.	33717069
circFAT1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction(miR-409-3p/CDK8 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircFAT1 was highly expressed in CC, and closely associated with poor prognosis.Mechanistic analysis showed that circFAT1 directly sponged miR-409-3p and then relieved the repressive effect of miR-409-3p on its target CDK8. CircFAT1 promoted CC progression via activating ERK1/2 and p38 MAPK pathway through the miR-409-3p/CDK8 axis, suggesting a promising prognostic biomarker and therapeutic target for CC.	CircFAT1 was highly expressed in CC, and closely associated with poor prognosis.	Yes	CircFAT1 knockdown resulted in the suppression of proliferation, migration and invasion, and promotion of apoptosis in CC cells via the inactivation of ERK1/2 and p38 MAPK pathway; also, circFAT1 silencing could inactivate this pathway and repressed CC tumor growth in vivo. 	33818788
hsa_circ_0000730	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	50 CC patients and CC cell lines	Interaction(miR-942-5p/PTEN axis)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	Circ_0000730 was significantly down-regulated in the cancer tissues of 50 CC patients and CC cell lines. Mechanistically, miR-942-5p was identified as a downstream target of circ_0000730, and circ_0000730 could positively regulate PTEN expression via repressing miR-942-5p in CC cells.Circ_0000730 inhibits the proliferation, migration, and invasion of CC cells via regulating miR-942-5p/PTEN axis.	Additionally, underexpression of circ_0000730 was associated with the shorter survival time of CC patients. 	Yes	 Gain- and loss-of-function assays highlighted that circ_0000730 significantly inhibited the proliferation, migration, and invasion of CC cells. 	34562344
circTPCN	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells	Regulation(circTPCN/miR-634/mTOR regulatory pathway)	Transfection//Wound Healing Assay//qRT-PCR//Cell Apoptosis Assay//Microarray//Cell Proliferation Assay//Invasion Assay//Transwell Assay	The expression patterns, obtained using a microarray assay, revealed a total of 192 differentially expressed circRNAs, of which 106 were upregulated and 86 were downregulated, in cervical cancer samples compared with normal cervical samples. The differential expression of circRNAs was validated using quantitative real-time polymerase chain reaction. Two circRNAs (circTPCN and circFAM185A) were confirmed to be significantly upregulated in cervical cancer samples, indicating that they represent potential biomarkers of cervical cancer. The role and the potential molecular mechanism of circTPCN in cervical cancer tumorigenesis were further investigated. Knockdown of circTPCN significantly suppressed proliferation, migration, and invasion and increased apoptosis of cervical cancer cells in vitro. Molecular analysis revealed that circTPCN acted as a sponge of miR-634 to enhance mTOR expression. Thus, the circTPCN/miR-634/mTOR regulatory pathway might be involved in cervical cancer tumorigenesis, and circTPCN is a potential therapeutic target in cervical cancer.		Yes	Knockdown of circTPCN significantly suppressed proliferation, migration, and invasion and increased apoptosis of cervical cancer cells in vitro	34029698
hsa_circ_0000263	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tumor tissues	Interaction(miR-1179/ABL2 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining	 Circ_0000263 was highly expressed in CC tumor tissues. Circ_0000263 served as a sponge for miR-1179, and miR-1179 inhibitor reversed the regulation of si-circ_0000263 on CC cell proliferation and apoptosis. ABL2 could be targeted by miR-1179, and circ_0000263 could sponge miR-1179 to regulate ABL2. Overexpression of ABL2 reversed the anti-proliferation and pro-apoptosis roles of miR-1179 in CC cells. In addition, circ_0000263 knockdown reduced CC tumor growth by miR-1179/ABL2 axis.		Yes	 Silencing of circ_0000263 suppressed CC cell proliferation and increased apoptosis. 	35355231
circCDK17	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues or cells	Interaction( miR-1294/YWHAZ)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 CircCDK17 expression and the mRNA and protein expression levels of YWHAZ were dramatically upregulated, while miR-1294 expression was obviously downregulated in CC tissues or cells compared with control groups. Additionally, circCDK17 was a sponge of miR-1294 and miR-1294 bound to YWHAZ.		Yes	 CircCDK17 silencing suppressed cell proliferation, migration, invasion and glycolysis, and induced cell apoptosis in CC; however, miR-1294 inhibitor restrained these effects.Furthermore, circCDK17 knockdown inhibited tumor formation in vivo.	35168653
hsa_circ_0001627	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cancerous tissues and cells	Interaction(miR-1225-5p/FNDC3B/PI3K/mTOR axis )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	Analyzing circRNA microarray dataset (GSE102686) and clinical specimens, a novel circRNA termed hsa_circ_0001627, was identified and it was highly expressed in CC cancerous tissues and cells, and was associated with poor clinical outcomes. Mechanistically, hsa_circ_0001627 acted as a miR-1225-5p sponge, thus indirectly regulating FNDC3B and leading to the activation of PI3K/mTOR signaling pathway.	Analyzing circRNA microarray dataset (GSE102686) and clinical specimens, a novel circRNA termed hsa_circ_0001627, was identified and it was highly expressed in CC cancerous tissues and cells, and was associated with poor clinical outcomes. 	Yes	 Functionally, hsa_circ_0001627 silencing impaired the malignant progression of CC cells and the growth of CC xenografts in nude mice. 	36357650
hsa_circ_0000212	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	ervical cancer tissues	Interaction(miR-625-5p/PTP4A1)	In Vivo Experiment//Western Blot//Transfection//Tube Formation Assay//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//IHC//Invasion Assay	 Circ_0000212 and PTP4A1 were highly expressed and miR-625-5p expression level was decreased in cervical cancer. MiR-625-5p was targeted by circ_0000212, and miR-625-5p inhibition reversed the effects of circ_0000212 knockdown. MiR-625-5p directly targeted PTP4A1, and the inhibitory effect of miR-625-5p on the malignant progression of cervical cancer was reversed after PTP4A1 overexpression.		Yes	 Circ_0000212 silencing suppressed cervical cancer cell proliferation, migration, invasion and angiogenesis while promoting apoptosis. In-vivo assays validated that circ_0000212 promoted cervical cancer tumor growth in vivo .	36729102
hsa_circ_0000285	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tumor tissues	Interaction(miR-654-3p/)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	The expression levels of circRNA_0000285 and miR-654-3p were analyzed in CC and the corresponding normal tissues, as well as in SiHa, HeLa, and NC104 cells using reverse transcription-quantitative polymerase chain reaction (RT-qPCR).. The results verified that miR-654-3p directly targeted circRNA_0000285 expression. circRNA_0000285 was overexpressed and miR-654-3p expression was downregulated in CC tissues and cells compared to that in control. 		Yes	In addition, the effect of circRNA_0000285 inhibition on cell viability, apoptosis, and the expression of apoptosis-related markers was assessed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), flow cytometry, and Western blotting assays, respectively. 	35166172
hsa_circ_0001823	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cells and tissues.	Interaction(microRNA-613/RAB8A axis)	RNA Pull-Down//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	 The circ_0001823 and RAB8A expressions were increased, and miR-613 were decreased in the CC cells and tissues. Knockdown of circ_0001823 inhibited the malignant behavior of the CC cells, which was antagonized by miR-613 inhibitor. Over-expressed RAB8A reversed the miR-613 effects in the CC cells. Knockdown of circ_0001823 inhibited the malignant behaviors of the CC cells via regulating the miR-613/RAB8A axis.		Yes	Knockdown of circ_0001823 inhibited the malignant behavior of the CC cells, which was antagonized by miR-613 inhibitor. Over-expressed RAB8A reversed the miR-613 effects in the CC cells. Knockdown of circ_0001823 inhibited the malignant behaviors of the CC cells via regulating the miR-613/RAB8A axis.	35435110
circLMO1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues 	Interaction(miR-4291/ACSL4)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The level of circLMO1 was down-regulated in cervical cancer tissues and was associated with the International Federation of Gynecology and Obstetrics (FIGO) staging.Mechanistically, circLMO1 acted as a competing endogenous RNA (ceRNA) by sponging miR-4192 to repress target gene ACSL4. CircLMO1 promoted cervical cancer cell ferroptosis through up-regulating ACSL4 expression. Overexpression of miR-4291 or knockdown of ACSL4 reversed the effect of circLMO1 on facilitating ferroptosis and repressing cervical cancer cell proliferation and invasion.		Yes	 Functionally, circLMO1 overexpression inhibited cervical cancer growth and metastasis both in vitro and in vivo, whereas circLMO1 depletion promoted cervical cancer cell proliferation and invasion. 	35321435
hsa_circ_0107593	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and CC cell lines	Interaction(hsa-miR-20a-5p/93-5p/106b-5p)	Bioinformatics Analysis//Transfection//Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 The results revealed that hsa_circ_0107593 has low expression in CC tissues and CC cell lines. Mechanistically, hsa_circ_0107593 serves as a sponge of hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p. Collectively, our study implies that hsa_circ_0107593 has tumor-suppressing activity in CC by physically binding with hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p.	Moreover, negative correlations of hsa_circ_0107593 expression were found against tumor diameter, FIGO stage, and myometrial invasion. 	Yes	Also, hsa_circ_0107593 impedes CC cell proliferation, migration, and invasion.	33585208
hsa_circ_0018289	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cells	Interaction(miR-183-5p/TMED5 regulatory network)	In Vivo Experiment//Western Blot//Transfection//Tube Formation Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis	 Circ_0018289 was overexpressed in cervical cancer tissues and cells.  Mechanistically, circ_0018289 targeted and regulated miR-183-5p by binding to miR-183-5p, and circ_0018289 regulated cervical cancer development and angiogenesis partially through miR-183-5p. 		Yes	Circ_0018289 silencing impeded cell proliferation, enhanced cell apoptosis, and suppressed angiogenesis in vitro, as well as diminished tumor growth in vivo.	34404391
hsa_circ_0000511	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Interaction(hsa-mir-296-5p/HMGA1)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//IHC//Transwell Assay	 hsa_circ_0000511 had the highest expression in SiHa and HeLa cells, and the expression in the cytoplasm was significantly higher than that in the nucleus, and its expression was not affected by RNase R. Our results indicate that the upregulated hsa_circ_0000511 can inhibit the proliferation, invasion, and migration of SiHa and HeLa cells by regulating hsa-mir-296-5p/HMGA1, suggesting that the hsa_circ_0000511/hsa-mir-296-5p/HMGA1 pathway may be a potential target for the treatment of cervical cancer.		Yes	When hsa_circ_0000511 was silenced, its expression in SiHa and HeLa cells was significantly decreased; the proliferation, invasion, and migration abilities of the two kinds of cells were significantly enhanced; and the protein expression of E-cadherin was significantly upregulated, while the protein expression of N-cadherin was significantly downregulated. 	34136582
LOC648987	LncRNA	Homo sapiens	Carcinoma, Renal Cell	50 primary renal cell carcinoma samples and corresponding adjacent tissues 	Expression [highly expressed]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The RT-PCR results showed that the lncRNA LOC648987 levels were highly expressed in RCC as compared to in the adjacent tissues.		Yes	The results showed that the knockdown of LOC648987 inhibited the proliferation of ACHN and 786-O cells and colony formation. The knockdown of LOC648987 significantly inhibited the progression of ACHN and 786-O cells from G0/G1 to S phase and promoted cell apoptosis. Finally, the promotion of LOC648987 on RCC tumorigenesis was evaluated in BALb/c nude mice. 	33858283
circSAMD11	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cells	Interaction(miR-503/SOX4 axis )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	CircSAMD11 and SOX4 levels were elevated, while miR-503 level was reduced in CC tissues and cells.  CircSAMD11 was localised in cytoplasm and directly targeted miR-503. Also, circSAMD11 sponged miR-503 to modulate SOX4 expression. 		Yes	 Knockdown of circSAMD11 suppressed CC cell proliferation, migration and invasion and accelerated apoptosis. 	34546569
circACACA	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	Interaction(miR-582-5p/ERO1A signaling axis)	Western Blot//Transfection//Wound Healing Assay//Tunel//qRT-PCR//MTT//Luciferase Report Assay//cell invasion assay//Colony Formation Assay	The results revealed that circ-ACACA expression was significantly upregulated in CC cells and silencing of circ-ACACA significantly reduced the proliferation, invasion and migration, and promoted the apoptosis of CC cells. The results suggested that circ-ACACA may promote CC tumorigenesis and glycolysis by targeting the miR-582-5p/ERO1A signaling axis. 		Yes	The results revealed that circ-ACACA expression was significantly upregulated in CC cells and silencing of circ-ACACA significantly reduced the proliferation, invasion and migration, and promoted the apoptosis of CC cells.  Knockdown of circ-ACACA markedly inhibited glycolysis in CC cells. 	34584570
hsa_circ_0101119	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(EIF4A3/TCEAL6 )	RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Flow Cytometry//RIP//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	It was found that hsa_circ_0101119 was highly expressed in CC tissues and cells, while TCEAL6 was lowly expressed. It was also demonstrated that hsa_circ_0101119 could recruit EIF4A3 to inhibit TCEAL6 expression in CC. Furthermore, knockdown of TCEAL6 could reverse the effects of silencing hsa_circ_0101119 on the proliferation, apoptosis, migration and invasion of HeLa cells.		Yes	Knockdown of hsa_circ_0101119 or TCEAL6 overexpression significantly inhibited the proliferation, migration and invasion of SiHa and HeLa cells, but facilitated apoptosis.	34278492
hsa_circ_0009035	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cells	Interaction(miR-889-3p/HOXB7 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//Survival Analysis//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	We found that hsa_circ_0009035 was highly expressed in CC tissues and cells, and it was associated with the radioresistance of CC patients.Mechanistically, hsa_circ_0009035 directly targeted miR-889-3p by binding to miR-889-3p, and hsa_circ_0009035 modulated HOXB7 expression through miR-889-3p. HOXB7 was a functional target of miR-889-3p in regulating CC progression and radioresistance in vitro, and hsa_circ_0009035 modulated CC progression and radioresistance in vitro by miR-889-3p. 		Yes	Moreover, the silencing of hsa_circ_0009035 inhibited CC cell proliferation, migration, invasion, and it enhanced apoptosis and radiosensitivity in vitro and weakened tumor growth in vivo. 	33782039
circE2F3	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Interaction(miR-296-5p/STAT3 )	In Vivo Experiment//Northern Blot//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//Cell Proliferation Assay//IHC//Transwell Assay	Circ-E2F3 was upregulated in both CC tissues and cell lines, and this correlated with the clinicopathological features and poor prognosis of CC patients. . It was also observed that circ-E2F3 promoted the nuclear translocation of STAT3 through inhibition of miR-296-5p, thus affecting the expression of cyclin D1. 	Circ-E2F3 was upregulated in both CC tissues and cell lines, and this correlated with the clinicopathological features and poor prognosis of CC patients. 	Yes	Moreover, circ-E2F3 promoted the proliferation, invasion, and migration of CC cells and tumor growth in vivo.	34468993
hsa_circ_0003221	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction(miR-758-3p/CPEB4 Axis)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Circ_0003221 was upregulated in cervical cancer tissues and cells. MiR-758-3p was a direct target of circ_0003221, and miR-758-3p inhibition reversed the effects of circ_0003221 knockdown in cervical cancer cells. Moreover, CPEB4 was identified as a direct target of miR-758-3p, and miR-758-3p exerted its anti-cancer role by targeting CPEB4.		Yes	 Knockdown of circ_0003221 suppressed cell proliferation, migration, invasion, and EMT and induced cell cycle arrest in cervical cancer cells. 	34262342
lncR-SMAL	LncRNA	Homo sapiens	Cardiac Mitophagy	serum of human at an age of 60, mice	Regulation(Parkin protein )	Western Blot//Co-IP//Flow Cytometry//RIP//FISH//qRT-PCR//IF	 The heart-enriched lncR-SMAL reached the expression crest in the serum of human at an age of 60. Exogenously overexpression of lncRNA SMAL deteriorated cardiac function exactly as natural ageing and inhibited the associated cardiomyocytes mitophagy by depressing Parkin protein level.Besides, we found the interaction between lncR-SMAL and Parkin protein through computational docking analysis, pull-down and RIP assay. This would contribute to the promotive effect of lncR-SMAL on Parkin ubiquitination and decrease Parkin protein stability.		Yes	Improved heart ageing and mitophagy caused by Parkin overexpression were reversed by lncR-SMAL in mice. In contrast, the loss of lncR-SMAL in AC16 cells induced the upregulation of Parkin protein and ameliorated mitophagy and mitochondrial dysfunction, resulting in alleviated cardiac senescence.	35758595
lncROR	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancers tissues	interaction[miR-223-3p]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 In the present study, Lnc-ROR was highly expressed in colorectal cancers compared with adjacent non-cancerous normal tissues. The findings of this study first revealed that ROR was upregulated in colorectal cancer cells and can promote cell proliferation and invasion by inhibiting tumor suppressor gene NF2 through interacting with miR-223-3p.		Yes	CCK8 assay and invasion assay suggested that ROR can promote cell proliferation and invasion.	32196591
LINC02932	LncRNA	Homo sapiens	Unexplained Recurrent Spontaneous Abortion	 lymphocytes and monocytes of human peripheral blood	Interaction(HNRNPH3/HSP70)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//RNA-seq//Microarray//ELISA	 RP11-115N4.1 was identified as the most differentially expressed lncRNA which was highly upregulated in peripheral blood of non-pregnant URSA patients (P = 3.63E-07, Fold change = 2.96), and this dysregulation was further validated in approximately 26.67% additional patients (4/15). Our results demonstrated that the activation of RP11-115N4.1 can significantly increase the protein level of HSP70 via binding to HNRNPH3, which may modulate the immune responses and related to URSA. 		Yes	 RP11-115N4.1 expression was detected in both lymphocytes and monocytes of human peripheral blood, and in vitro overexpression of RP11-115N4.1 decreased cell proliferation in K562 cells significantly.	34484222
lnc34977	LncRNA	Homo sapiens	Mammary Neoplasms, Animal	CMTs	Expression(lower expressed)	In Vivo Experiment//Wound Healing Assay//CCK8//qRT-PCR//RNA-seq//Colony Formation Assay//Bioinformatics Analysis	lnc40589 was significantly upregulated and lnc34977 was significantly downregulated in CMTs.		Yes	In addition, lnc40589 inhibits cell proliferation, migration and invasion, while lnc34977 promotes cell proliferation, migration and invasion.  In addition, lnc34977 promotes the development of mammary tumors in animals. 	35202335
Lnc00152	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tumour tissues	regulation[miR-30d/SOX9/ZEB2 pathway]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 We found that Lnc00152 was significantly up-regulated in retinoblastoma tumour tissues, and was a risk factor for tumour invasion, metastasis and recurrence.		Yes	Lnc00152 overexpressing retinoblastoma cells exhibited a tendency to transform into mesenchymal cells, with significantly increased migration and invasion capacities, significantly decreased E-cadherin expression levels, and significantly increased N-cadherin, SOX9 and ZEB2 expression levels.	32488851
LNC_AL139002.1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines (MKN-45, AGS, BGC823, SGC7901, MGC803, MKN-74)	Interaction(miR-490-3p/HAVCR1 axis)	Western Blot//Bioinformatics Analysis//Migration Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	The results showed that lncRNA AL139002.1 was highly expressed in GC cells. Functional examining indicated that lncRNA AL139002.1 regulated HAVCR1 expression by competitively binding miR-490-3p. In addition, lncRNA AL139002.1/miR-490-3p/HAVCR1 regulated EMT and metastasis through MEK/ERK signaling. 		Yes	 lncRNA AL139002.1 knockdown induced apoptosis, while suppressed cell proliferation, migration, invasion, and EMT. 	34002670
LNC_691	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cell lines and tissues	regulation[PTEN/PI3K/AKT signal pathway]	Flow Cytometry//qRT-PCR//Colony Formation Assay	 In our study, we disclosed that lncRNA 691 had low expression levels in osteosarcoma cell lines and tissues.LncRNA 691/miR-9-5p could regulate the tumorigenesis by regulating the PTEN/PI3K/AKT signal pathway in osteosarcoma.		Yes	 Overexpression of lncRNA 691 could suppress the cell proliferation and induce cell apoptosis in MG-63 cell line.	32547090
LNC_554	LncRNA	Homo sapiens	Myocardial Infarction	heart tissues	regulation[TGF-β1 Pathway]	qRT-PCR//Wound Healing Assay//H&E Staining//FISH	We found that lncRNA 554 was significantly up-regulated in the mouse hearts following MI. This suggests that the effects of lncRNA 554 on cardiac fibrosis is TGF-β1 dependent.		Yes	In vitro knockdown of lncRNA 554 by siRNA suppressed fibroblasts migration and expression of extracellular matrix (ECM); while overexpression of lncRNA 554 promoted expression of ECM genes. Consistently, lentivirus mediated in vivo knockdown of lncRNA 554 could inhibit cardiac fibrosis and improve cardiac function in mouse model of MI.	33390954
LNC_01977	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cells	Regulation(SDF-1/CXCR4 pathway)	qRT-PCR//Western Blot//Transwell Assay	In vitro assays demonstrated that LncRNA01977 can significantly promote the progression of LUAD and that stromal cells in tumor microenvironment secrete chemokine CXCL12, also known as stromal derived factor-1 (SDF-1), and its receptor CXCR4 is low expressed in normal tissues and high expressed in LUAD tissues. Lung cancer patients with high expression of CXCR4 are more prone to metastasis.		Yes	In vitro assays demonstrated that LncRNA01977 can significantly promote the progression of LUAD and that stromal cells in tumor microenvironment secrete chemokine CXCL12, also known as stromal derived factor-1 (SDF-1), and its receptor CXCR4 is low expressed in normal tissues and high expressed in LUAD tissues. Lung cancer patients with high expression of CXCR4 are more prone to metastasis.	35402179
LNC_00312	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC cells,RCC tissues	regulation[miR-34a-5p/ASS1 Axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	lncRNA was significantly downregulated in RCC cells such as A498 and ACHN; the expression of lncRNA 00312 in RCC tissues was significantly lower than that in adjacent normal tissues. Our study demonstrated that the lncRNA 00312/miR-34a-5p/ASS1 axis may play a functional role in the progression of RCC.	Patients with low expression of lncRNA 00312 have worse prognosis regarding pathological grade, tumor size, and TNM stage.	Yes	 Overexpression of lncRNA 00312 suppressed A498 and ACHN cell proliferation and invasion, while promoting apoptosis.	32308805
LNC_00152	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[JAK2/STAT3 pathway]	Flow Cytometry//qRT-PCR//EdU Staining//Western Blot	The expression of lncRNA 00152 in HCC tissues was significantly higher than that of matched para-cancerous tissues and normal liver tissues. Similarly, lncRNA 00152 was highly expressed in HCC cell lines when compared with that of normal liver cells.High expression of lncRNA 00152 promotes the development of HCC by activating the JAK2/STAT3 pathway.	LncRNA 00152 expression was positively correlated with tumor stage and tumor size, whereas negatively correlated with the overall survival of HCC patients. 	Yes	 Knockdown of lncRNA 00152 in MHCC97 cells remarkably decreased the proliferative ability and arrested cell cycle. Overexpression of lncRNA 00152 in HB611 cells significantly promoted cell proliferation and cell cycle.	30779070
LNC_001089	LncRNA	Homo sapiens	Glioma	glioma tissues	Expression[lower expressed]	CCK8//qRT-PCR//Transwell Assay	LncRNA001089 was downregulated in glioma tissues, evaluated by qRT-PCR.	Kaplan-Meier analysis indicated that the downregulation of LncRNA001089 expression was associated with poor prognoses in glioma patients. Multivariate analysis demonstrated that LncRNA001089 downregulation and WHO high-grade glioma were independent factors that both predicted poor outcomes for glioma patients.	Yes	Cells with LncRNA001089 stable overexpression exhibited decreased capacities for proliferation, migration, and invasion in vitro, and restrained nude mouse tumorigenesis in vivo, but LncRNA001089 overexpression enhanced apoptosis.	30868865
LNC_000898	LncRNA	Mus musculus	Myocardial Infarction	marginal tissue of MI 	regulation[miR-375/PDK1 Axis]	qRT-PCR//Western Blot	The results indicated that LNC_000898 expression was downregulated in marginal tissue of MI and in NMCMs exposed to hypoxia.These data not only demonstrate that LNC_000898 could protect the heart against MI injury by regulating miR-375/PDK1 but also provide a new understanding to better protection of MI injury through the LNC_000898/miR-375/PDK1 axis.		Yes	Overexpression of LNC_000898 decreased cardiomyocyte apoptosis both in vivo and in vitro. 	32398474
lnc_000231	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells and tumour tissues	regulation[ KDM5C/lnc_000231/miR-497-5p/CCNE1 signalling pathway ]	RNA Pull-Down//Northern Blot//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Recent studies with genome-wide sequencing on cervical squamous cell carcinoma and matched adjacent non-tumour tissues showed that a newly identified lncRNA-lnc_000231 was highly expressed in cervical cancers. E6 hijacked KDM5C/lnc_000231/miR-497-5p/CCNE1 signalling pathway is a promising target for cervical cancer treatment in the future.		Yes	 In vitro and in vivo results showed that lnc_000231 promotes cervical cancer cell proliferation and tumour formation by acting as miR-497-5p sponge and maintaining cyclin E1 (CCNE1) expression.	32818316
LMCD1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(LMCD1-AS1/miR-526b-3p/OSBPL5 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 This paper was the first to probe the molecular regulatory mechanism of OSBPL5 involving the LMCD1-AS1/miR-526b-3p axis in NSCLC and our results revealed that the LMCD1-AS1/miR-526b-3p/OSBPL5 axis facilitates NSCLC cell proliferation, migration, invasion and EMT, which may offer a novel therapeutic direction for NSCLC.		Yes	Moreover, from rescue assays, we observed that OSBPL5 overexpression offset LMCD1-AS1 knockdown-mediated inhibition in cell proliferation, migration, invasion and EMT in NSCLC.	35000595
LMCD1-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	interaction[miR-106b-5p]	qRT-PCR	We found that LMCD1-AS1 and SP1 were highly expressed in osteosarcoma tissues and cell lines. Mechanistic studies revealed that LMCD1-AS1 was a sponge of miR-106b-5p activity. 	High levels of LMCD1-AS1 were correlated with positively metastasis and poor clinical prognosis.	Yes	Functionally, silencing of LMCD1-AS1 suppressed the proliferation, migration, invasion and EMT progress of osteosarcoma cells.	32248969
LMCD1-AS1	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues,cell lines	Interaction[miR-345-5p/COL6A3 pathway]	Immunoblotting//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay//ChIP	In our study, we confirmed that LMCD1-AS1 expression was significantly higher in CCA tissues and cell lines than in normal tissues and HIBEC, respectively.  In addition, LMCD1-AS1 could sponge miR-345-5p in CCA cells. Moreover, collagenVI-alpha3 chain (COL6A3) was found as a downstream target of miR-345-5p by bioinformatic prediction and dual luciferase reporter assay. Furthermore, we demonstrated that the oncogenic role of LMCD1-AS1 is partly dependent on COL6A3 expression. 		Yes	Function study showed depletion of LMCD1-AS1 suppressed cell proliferation, clone formation and invasion, and induced apoptosis of CCA cells.	30876691
LL22NC03-N64E9.1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues	regulation[LL22NC03-N64E9.1/EZH2/KLF2 pathway]	qRT-PCR//RIP//Transwell Assay	We identified that LL22NC03-N64E9.1 is an oncogene, upregulated in BC, which was verified in a cohort of 48 pairs of BC tissues. Relying on the LL22NC03-N64E9.1/EZH2/KLF2 pathway, the lncRNA LL22NC03-N64E9.1 was significantly associated with BC development and could, therefore, be a potential therapeutic target to block BC growth.		Yes	Based on the loss-of-function experiments, silencing LL22NC03-N64E9.1 expression significantly inhibited malignancy progression.	33149681
LL22NC03-N64E9.1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissue,lung cancer cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Colony Formation Assay	In clinical tissue samples, the level of LL22NC03-N64E9.1 in patients with lung cancer was significantly increased compared with adjacent normal lung tissues (P<0.001). 	The level of LL22NC03-N64E9.1 in patients with lung cancer was significantly correlated with tumor size and TNM stage (P<0.05), but not with age, sex and the presence of lymph node metastasis (P>0.05). 	Yes	In the H292 cells, following knockdown of LL22NC03-N64E9.1, cell proliferation and cloning were reduced. 	29935018
LL22NC03-N14H11.1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[H-RAS/MAPK pathway]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Results showed that LL22NC03-N14H11.1 was upregulated in HCC tissues and cells. In conclusion, this study firstly revealed that lncRNA LL22NC03-N14H11.1 promoted HCC progression through activating H-RAS/MAPK pathway to induce mitochondrial fission, indicating LL22NC03-N14H11.1 as a novel potential biomarker for HCC treatment.		Yes	Functionally, LL22NC03-N14H11.1 contributed to cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in HCC. 	33028809
LIT3527	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation(AKT/ERK/mTOR signaling pathway)	In Vivo Experiment//Northern Blot//Wound Healing Assay//Immunoblotting//Migration Assay//CCK8//qRT-PCR//MTT//Cell Cycle Assay//Transwell Assay//IF	 Here, we screened differentially expressed lncRNAs in gastric cancer tissues and matched adjacent tissues and found that lncRNA LIT3527, a 486-nucleotide (nt) sense transcript, was frequently upregulated in gastric cancer tissues.Mechanistically, we uncovered that depletion of LIT35227 induced significant cell apoptosis and autophagy through inhibiting AKT/ERK/mTOR signaling pathway. 		Yes	 Knockdown of LIT3527 dramatically suppressed proliferation and migration of gastric cancer cells through inducing severe cell death but not affecting cell cycle.	34234860
LIPH-4	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-216b/IGF2BP2 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	We identified a novel lncRNA, LIPH-4, which showed elevated amounts in ESCC tissues and positive correlations with increased tumor size and poor prognosis in ESCC patients. In terms of mechanism, LIPH-4 could bind to miR-216b and act as a competing endogenous RNA (ceRNA) to induce the expression of miR-216's target gene IGF2BP2. LIPH-4 played an oncogenic role in ESCC through the miR-216b/IGF2BP2 axis.	We identified a novel lncRNA, LIPH-4, which showed elevated amounts in ESCC tissues and positive correlations with increased tumor size and poor prognosis in ESCC patients. 	Yes	Functional studies showed that LIPH-4 promoted the growth, mediated cell cycle progression and inhibited apoptosis in ESCC cells in vitro, and promoted tumor growth in mice. 	35971159
LNC11649	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells 	Interaction(MALAT1)	RNA-seq	 Both northern blot and quantitative PCR analyses confirmed the presence of LNC11649 in NSCLC tissues and cells with high expression.  Its sequence was found to be highly homologous to lncRNA MALAT1. Knocking down MALAT1 could lead to a significant downregulation of LNC11649 content, revealing the possibility that LNC11649 could originate from MALAT1 reprocessing.		Yes	Further experiments revealed that LNC11649 promoted the cytoplasmic distribution of MSI1 through its interaction with MSI1 and then activated the Akt signaling pathway to regulate the proliferation and migration of NSCLC cells. 	36264775
lnc40589	LncRNA	Homo sapiens	Mammary Neoplasms, Animal	CMTs	Expression(highly expressed)	In Vivo Experiment//Wound Healing Assay//CCK8//qRT-PCR//RNA-seq//Colony Formation Assay//Bioinformatics Analysis	lnc40589 was significantly upregulated and lnc34977 was significantly downregulated in CMTs.		Yes	In addition, lnc40589 inhibits cell proliferation, migration and invasion, while lnc34977 promotes cell proliferation, migration and invasion.  In addition, lnc34977 promotes the development of mammary tumors in animals. 	35202335
LINP1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	FISH assay showed that LINP1 was expressed at low levels in normal esophageal tissues (Figure 2D), whereas it was highly expressed in ESCC and mainly expressed in the cytoplasm (Figure 2E).	High LINP1 expression had close correlation with larger tumor size (P=0.009), tumor invasion (P=0.015), lymph nodes metastasis (P=0.044), and advanced TNM stage (P=0.010). LINP1 overexpression was an independent prognostic factor of ESCC patients (P=0.034). 	Yes	LINP1 knockdown decreased the proliferative and migratory abilities of EC9706 cells, and promoted apoptosis and cell cycle arrest at the G2/GM phase. In the xenograft model, knockdown of LINP1 suppressed ESCC tumorigenesis in vivo.	32617295
Lnc408	LncRNA	Homo sapiens	Breast Neoplasms	BCSCs	Regulation(CBY1)	Flow Cytometry//qRT-PCR//IHC//Western Blot	The lnc408 is high expressed in BCSCs in vitro and in vivo. The enhanced lnc408 is critical to BCSC characteristics and tumorigenesis. Lnc408 can recruit transcript factor SP3 to CBY1 promoter to serve as an inhibitor in CBY1 transcription in BCSCs.  In shortly, these findings highlight that the novel lnc408 functions as an oncogenic factor by recruiting SP3 to inhibit CBY1 expression and β-catenin accumulation in nucleus to maintain stemness properties of BCSCs. 		Yes	 In shortly, these findings highlight that the novel lnc408 functions as an oncogenic factor by recruiting SP3 to inhibit CBY1 expression and β-catenin accumulation in nucleus to maintain stemness properties of BCSCs. 	33934099
lnc-Chaer	LncRNA	Mus musculus	acute myocardial infarction	 oxygen-glucose deprivation (oxygen-glucose deprivation)-treated cardiomyocytes in vitro and AMI heart	Regulation(AMPK Activation)	CCK8//qRT-PCR//Western Blot	 Importantly, lncRNA Chaer is significantly downregulated in both oxygen-glucose deprivation (oxygen-glucose deprivation)-treated cardiomyocytes in vitro and AMI heart.  Interestingly, overexpression of lncRNA Chaer promotes the phosphorylation of AMPK, and AMPK inhibitor Compound C reverses the overexpression of lncRNA Chaer effect of reducing cardiomyocyte apoptosis under OGD-treatment. 		Yes	 In vitro, overexpression of lncRNA Chaer with adeno virus reduces cardiomyocyte apoptosis induced by OGD-treated while silencing of lncRNA Chaer increases cardiomyocyte apoptosis instead. In vivo, forced expression of lncRNA Chaer with AAV9 attenuates cardiac apoptosis, reduces infarction area and improves mice heart function in AMI. 	34335241
lnc-CES1-1	LncRNA	Homo sapiens	Abortion, Habitual	 URPL patients and decidua-associated cell lines (DACs).	Regulation(FUS/PPARγ )	Western Blot//qRT-PCR//RIP//IF//RNA-seq//migration assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//ELISA//ChIP	Through comprehensive screening and validation, we identified a decidua-enriched eRNA long noncoding-CES1-1 (lnc-CES1-1) enriched in URPL patients and studied its function in decidua-associated cell lines (DACs).Upon activation by signal transduction and activation of transcription 4 (STAT4), lnc-CES1-1 interacted with the transcription factor fused in sarcoma (FUS) to upregulate the expression of PPARγ and affected cell migration. 		Yes	Higher expression of lnc-CES1-1 increased the level of inflammatory factors tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) and impaired the cell migration ability, which was attenuated by downregulating peroxisome proliferators-activated receptor γ (PPARγ). 	33738142
lnc-CCNL1-3:1	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	human luteinized granulosa cells	Interaction(FOXO1)	Transfection//Immunoblotting//Tunel//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//IF	 The interaction of CCNL with FOXO1 might prevents FOXO1 exclusion from the nucleus and subsequent degradation in the cytosol. 		Yes	 In KGN cells and hLGCs, CCNL overexpression upregulated FOXO1 expression, promoted cell apoptosis, reduced glucose transport capability, and impaired mitochondrial function, and these effects were partially abolished by silencing FOXO1. 	33552682
lncCCLM	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues 	Expression(lower expressed)	RNA Pull-Down//Transfection//Tube Formation Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Microarray//ELISA//Transwell Assay//Bioinformatics Analysis//IF	Herein, through RNA screening, we identified a novel long noncoding RNA (lncRNA), LncCCLM, that was downregulated in cervical cancer tissues and closely associated with lymphatic metastasis in cervical cancer patients.  Mechanistically, LncCCLM localized in the cytoplasm and interacted with staufen double-stranded RNA binding protein 1 (STAU1), promoting the binding of the STAU1 protein to the 3' untranslated region (3'UTR) of insulin-like growth factor 1 (IGF-1) mRNA, which accelerated the degradation of IGF-1 mRNA and decreased the IGF-1 protein level, ultimately reducing lymphangiogenesis and lymphatic metastasis in cervical cancer. 	Herein, through RNA screening, we identified a novel long noncoding RNA (lncRNA), LncCCLM, that was downregulated in cervical cancer tissues and closely associated with lymphatic metastasis in cervical cancer patients. 	Yes	Gain-of-function and loss-of-function studies in CC cells demonstrated that LncCCLM inhibited cervical cancer-associated lymphangiogenesis, and CC cell migration and invasion in vitro and suppressed LN metastasis in vivo, but did not affect the growth of CC cells. 	34273467
lnc-CCAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa and corresponding adjacent normal prostate tissues	Interaction(miR-490-3p/FRAT1 axis)	Western Blot//Bioinformatics Analysis//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	qRT-PCR results showed that CCAT1 was upregulated in PCa tissues and cells.  We also found that CCAT1 negatively regulated miR-490-3p expression and subsequently regulated FRAT1 expression. Inhibition of miR-490-3p or up-regulation of FRAT1 reversed the suppressive effects of CCAT1 knockdown on the PCa cells.		Yes	Functional assays demonstrated that CCAT1 knockdown suppressed cell proliferation, migration, invasion, yet promoted apoptosis, while CCAT1 promotion showed the opposite results. 	34319909
lncCCAT1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,Breast cancer stem cells	Regulation[WNT/β-catenin Signaling]	RIP//ChIP//Microarray	 LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. Mechanistic investigation suggests that LncCCAT1 can interact with miR-204/211, miR-148a/152 and Annexin A2(ANXA2), then upregulate T-cell factor 4 (TCF4) or promote translocation of β-catenin to the nucleus where it activates TCF4, leading to the activation of wingless/integrated (Wnt) signaling. 	 LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. 	Yes	 Overexpression of LncCCAT1 contributes to the proliferation, stemness, migration and invasion capacities of BCSCs. 	31695775
lncCCAT1	LncRNA	Homo sapiens	Osteosarcoma	HeLa cells & human OS cell line	Interaction(PKM2)	qRT-PCR//Western Blot	Peak calling analysis revealed that PKM2 binds to long noncoding RNAs (lncRNAs), which are associated with cancer pathogenesis and development. Validation of the PKM2‑lncRNA interaction in the human OS cell line revealed that lncRNA colon cancer associated transcript‑1 (lncCCAT1) interacted with PKM2, which upregulated the phosphorylation of sterol regulatory element‑binding protein 2 (SREBP2). These factors promoted the Warburg effect, lipogenesis, and OS cell growth. PKM2 appears to be a key regulator in OS by binding to lncCCAT1. This further extends the biological functions of PKM2 in tumorigenesis and makes it a novel potential therapeutic for OS.	Peak calling analysis revealed that PKM2 binds to long noncoding RNAs (lncRNAs), which are associated with cancer pathogenesis and development. 	Yes	Validation of the PKM2‑lncRNA interaction in the human OS cell line revealed that lncRNA colon cancer associated transcript‑1 (lncCCAT1) interacted with PKM2, which upregulated the phosphorylation of sterol regulatory element‑binding protein 2 (SREBP2).	35244192
LNCBRM	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	regulation[microRNA-331-3p/SLC25A1 axis]	CCK8//qRT-PCR//Transwell Assay//Western Blot	Reverse transcription-quantitative PCR assays revealed that lncBRM was upregulated in PTC tissues and cells. In conclusion, the present study suggests that lncBRM promotes PTC by regulating miR-331-3p and targeting SLC25A1.	 Furthermore, high expression of lncBRM was associated with poor overall survival time in patients with PTC.	Yes	lncBRM knockout significantly suppressed cell proliferation, migration and invasion.	32218861
lncAY927529	LncRNA	Homo sapiens	Prostatic Neoplasms	 PC3 and DU145 cells	Interaction(CXCL14 )	RNA Pull-Down//Western Blot//qRT-PCR//Cell Apoptosis Assay//ELISA	RT-qPCR assay indicated that lncAY927529 level was downregulated in PC3 and DU145 cells, exosomes derived from PCa cells (PCa-Exo) and ST2-CM treated with PCa-Exo with low expression of lncAY927529, and overexpression of lncAY927529 had the opposite results. In addition, Western blot assay showed that the autophagy related protein LC3II level was increased in ST2 cells treated with exosomes derived from DU145 cells with high expression of lncAY927529, and LC3I protein level was decreased. CXCL14 acted as a RNA-binding protein of lncAY927529, and exosome-mediated lncAY927529 positively regulated CXCL14 levels in ST2 cells. 		Yes	In general, exosome-mediated lncAY927529 could promote PCa cell proliferation and invasion by regulating bone microenvironment, suggesting that exosomal lncAY927529 may be a potential molecular diagnostic marker of PCa.	34724861
lnc-ATB	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	interaction[binding to EZH2]	qRT-PCR//RNA Pull-Down//RIP	 In our research, lnc-ATB expression in OC tissues was elevated compared with adjacent normal tissues and high expression of lnc-ATB was associated with poor outcomes of OC patients. RNA immunoprecipitation and RNA pull-down results showed that lnc-ATB positively regulated the expression of EZH2 via directly interacting with EZH2.	 In our research, lnc-ATB expression in OC tissues was elevated compared with adjacent normal tissues and high expression of lnc-ATB was associated with poor outcomes of OC patients.	Yes	The silencing of lnc-ATB blocked cell proliferation, invasion and migration in SKOV3 and A2780 cells. 	33336896
lnc-ATB	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues,cell lines	Interaction[PIK3R2/Sox2 signals ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The expression of Lnc-ATB is up-regulated in tumor tissues and EC cell lines.These data demonstrate the tumorigenic role of Lnc-ATBs in endometrial cancer via abrogation of tumor suppressor miR-126 signals.		Yes	Knockdown of Lnc-ATB in RL95 and HEC1A cell lines increased the miR-126 level and impaired the cell vitality, induced caspase-3-related tumor apoptosis and G1/S arrest. Knockdown of Lnc-ATB in vivo remarkably induced tumor regression via restoration of tumor suppressor miR-126	30601064
LNCARSR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues 	regulation[lncARSR/miR-34a-5p/HK1 ]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Here, we analyzed specimens from 89 patients with CRC and demonstrated that lncARSR was highly expressed in CRC tissues and negatively associated with survival.Collectively, we identified lncARSR as an onco-lncRNA in CRC and demonstrated that the combination of lncARSR/miR-34a-5p/HK1 may be a potential prognostic biomarker of CRC.	Here, we analyzed specimens from 89 patients with CRC and demonstrated that lncARSR was highly expressed in CRC tissues and negatively associated with survival.	Yes	Functionally, ectopic expression of lncARSR promoted the invasion, metastasis, and glycolysis metabolic reprogramming of CRC cells in vitro and in vivo, while these activities were inhibited by silencing lncARSR expression.	32798250
LNCARSR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	exosomes	Interaction(miR-34/miR- 449/STAT3 )	qRT-PCR//RNA Pull-Down//FISH	 Further study revealed high amount of a recently discovered lncRNA called lncARSR in RCC-derived exosomes.  LncARSR interacts directly with miR-34/miR- 449 to increase STAT3 expression and mediate macrophage polarization in RCC cells.		Yes	Overexpression of lncARSR induced phenotypic and functional changes of macrophages in vitro and promoted tumor growth in vivo, while knockdown of lncARSR by siRNA disrupted the exosomes-mediated macrophage polarization. 	35637970
LNCARSR	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	Bca tissue	regulation[SOX4 ]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	In this study, we discovered that lncARSR was significantly up-regulated in bladder cancer. Mechanistically, lncARSR was mainly located in the cytoplasm and acted as a miRNA sponge to positively modulate the expression of Sex-determining region Y-related high-mobility-group box transcription factor 4 (SOX4) via sponging miR-129-5p and subsequently promoted the proliferation and metastasis of Bca cells, thus playing an oncogenic role in Bca pathogenesis.	 In addition, increased expression of lncARSR was positively correlated with higher histological grade and larger tumor size.	Yes	Further experiments demonstrated that suppression of lncARSR attenuated the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of Bca cells.	31892841
LNCARSR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[PTEN/Akt]	qRT-PCR//Western Blot	 In the present study, it was demonstrated that lncARSR expression was higher in NSCLC tissues than in noncancerous tissues.  Furthermore, we demonstrated that overexpression of lncARSR induced NSCLC cell growth and migration via regulating the PTEN/Akt signaling pathway.		Yes	 Further investigation demonstrated that increased lncARSR expression promoted NSCLC cell migration and growth and induced epithelial-mesenchymal transition in A549 cells.	32269718
lnc-AGER-1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues 	interaction[sponging miR-182]	qRT-PCR	 We found that the expression of lnc-AGER-1 in the tumor tissues was significantly down-regulated, while compared with adjacent normal tissues (0.0115 ± 0.0718 vs. 0.0347 ± 0.157; P < 0.0001).  Further research proved that lnc-AGER-1 altered the expression of its neighbor gene, AGER, through acting as a competing endogenous RNA for miR-182 in colorectal cancer.	Also, lnc-AGER-1 was observably associated with clinical T status (r = -0.184, P = 0.024). Patients with advanced T status exerted a significantly lower level of lnc-AGER-1 than those with early T status (20.0% vs. 40.7%, P = 0.021). 	Yes	Over-expression of lnc-AGER-1 inhibited cell proliferation and migration efficiency, and induced cell cycle arrest at the G0/G1 phase, and promoted cell apoptosis. 	32031046
lnc-ADD3-AS1	LncRNA	Homo sapiens	Liver Cirrhosis	 LX-2 cell	Regulation	Transfection//Wound Healing Assay//Flow Cytometry//Cell Proliferation Assay//Transwell Assay	Our results show that lnc-ADD3-AS1 significantly promoted LX-2 cell proliferation and attenuated apoptosis. More importantly, lncRNA-ADD3-AS1 significantly accelerated the migration of LX-2 cells.		Yes	Our results show that lnc-ADD3-AS1 significantly promoted LX-2 cell proliferation and attenuated apoptosis. More importantly, lncRNA-ADD3-AS1 significantly accelerated the migration of LX-2 cells. 	35246014
lnc-ABCA12-3	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tumor tissues and cell lines	Regulation[regulate FN1]	qRT-PCR	We showed that lnc-ABCA12-3 was upregulated in ESCC tumor tissues and cell lines. Further studies indicated that lnc-ABCA12-3 acted as a competing endogenous RNA for miR-200b-3p to regulate FN1 expression. 		Yes	The knockdown of lnc-ABCA12-3 inhibited the cell migration, invasion, and proliferation abilities of KYSE-510 and Eca-109 cells.	31512786
Lnc-408	LncRNA	Homo sapiens	Breast Neoplasms	BC cells undergoing EMT and in BC tumor with lymphatic metastases	Interaction(miR-654-5p/LIMK1 axis)	Western Blot//Migration Assay//IF//Luciferase Report Assay//Invasion Assay//Transwell Assay	Here, we found that Lnc-408, a novel long noncoding RNA (lncRNA), is significantly upregulated in BC cells undergoing EMT and in BC tumor with lymphatic metastases compared with those without lymphatic metastases.  In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.		Yes	 Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1.	34079084
LIPCAR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC blood samples and HCC cell lines	Expression(highly expressed)	qRT-PCR	LIPCAR was significantly upregulated in HCC blood samples and HCC cell lines compared to their respective normal ones.		Yes	 Its overexpression promoted hepatocellular carcinoma cell proliferation, and migration, while inhibiting apoptosis. Its overexpression also promoted epithelial-mesenchymal transformation in hepatocellular carcinoma cells, and metastasis in vivo.	36336923
LINP1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and PTC cells	regulation[AMPK signaling pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	 It was shown in qRT-PCR results that LINP1 expression was upregulated in 42 out of 53 cases of PTC tissues and in all PTC cells. The transcription factor STAT1 promotes the expression of LINP1 in PTC, and highly expressed LINP1 facilitates the proliferation and inhibits the apoptosis of PTC by suppressing the AMPK signaling pathway.		Yes	After interference in the expression of LINP1 in PTC cells, the results of CCK-8 and colony formation assays indicated that the proliferative capacity of the cells was repressed. 	32964981
lncROR	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	PCOS patients 	Interaction(miR-206/VEGF )	Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	Highly expressed lncROR indirectly up-regulated the expression of VEGF by down-regulating the expression of miR-206, thereby promoting the proliferation of KGN cells and inhibiting apoptosis, and further promoting the development of PCOS.		Yes	Highly expressed lncROR indirectly up-regulated the expression of VEGF by down-regulating the expression of miR-206, thereby promoting the proliferation of KGN cells and inhibiting apoptosis, and further promoting the development of PCOS.	34148561
LINC-PINT	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues 	Interaction[PTCSC3 ]	CCK8//qRT-PCR	PTCSC3 and lncRNA Linc-pint were both downregulated in tumor tissues than in adjacent healthy tissues of gastric cancer patients.  PTCSC3 and Linc-pint overexpression inhibited tumor growth and cancer cell stemness, while Linc-pint knockdown played an opposite role an attenuated the effects of PTCSC3 overexpression. Expression levels of PTCSC3 and Linc-pint were significantly correlated in tumor tissues but not in adjacent healthy tissues. Overexpression of PTCSC3 and Linc-pint upregulated the expression of each other.	Low levels of PTCSC3 and Linc-pint were closely correlated with poor survival.	Yes	 PTCSC3 and Linc-pint overexpression inhibited tumor growth and cancer cell stemness, while Linc-pint knockdown played an opposite role an attenuated the effects of PTCSC3 overexpression.	31849528
LINC-PINT	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Interaction(miRNA-21)	qRT-PCR	downregulation of LINC-PINT participated in the recurrence of ESCC possibly by interacting with miRNA-21.	LINC-PINT expression was further downregulated in recurrent patients but not in nonrecurrent patients.	Yes	Overexpression of LINC-PINT could inhibit the expression of miRNA-21 in human ESCC cells, whereas LINC-PINT expression was not altered by miR-21 overexpression.	32401035
LINC-PINT	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues,cell lines (A2780, SKOV3, OVCAR3 and HO-8910)	interaction[targeting miR-374a-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Low expression of LINC-PINT was observed in OC tissues and cells, noticeably, LINC-PINT expression was even lower in OC tissues with higher FIGO stage.The current study aimed to explore the role of LINC-PINT in the progression of ovarian cancer (OC) and found that LINC-PINT inhibited cell proliferation, migration invasion and EMT process of OC cell via regulating miR-374a-5p; it might be a potential target for OC treatment.	Low expression of LINC-PINT was observed in OC tissues and cells, noticeably, LINC-PINT expression was even lower in OC tissues with higher FIGO stage.	Yes	Increased LINC-PINT expression significantly inhibited cell proliferation, promoted apoptosis and suppressed migration, invasion and EMT process, while silencing of LINC-PINT caused the opposite results.	32638404
LINC-PINT	LncRNA	Homo sapiens	Osteosarcoma	Osteosarcoma tissues	Interaction[Downregulating miRNA-21]	qRT-PCR	In this study, we found that LncRNA LINC-PINT was inhibited, whereas miRNA-21 was promoted in tumor tissues than in adjacent healthy tissues of patients with osteosarcoma. LncRNA LINC-PINT and miRNA-21 were significantly and reversely correlated in both tumor cells and adjacent healthy tissues. LncRNA LINC-PINT overexpression led to downregulated miRNA-21 expression in cancer cells, whereas miRNA-21 overexpression did not significantly affect LINC-PINT expression. 	Expression levels of LncRNA LINC-PINT were affected by both tumor size and tumor metastasis.	Yes	Overexpression of LncRNA LINC-PINT inhibited whereas miRNA-21 overexpression promoted cancer cell proliferation, migration, and invasion.	31070482
LINC-PINT	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	blood	Regulation[TGF-β pathway ]	CCK8//qRT-PCR//ELISA	The results demonstrated that Linc-pint plasma levels were significantly lower in patients with stage 0-1 PDAC compared with healthy controls.  In conclusion, results from the present study suggested that Linc-pint may inhibit early stage PDAC growth through TGF-β pathway activation.		Yes	Linc-pint overexpression and TGF-β1 both inhibited PDAC cell proliferation, whereas treatment with a TGF-β inhibitor reduced their inhibitory effects on cell proliferation.	30944652
LINC-PINT	LncRNA	Homo sapiens	Glioblastoma	cell lines	regulation[Wnt/β-Catenin Signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//IF//Colony Formation Assay//Transwell Assay	LINC-PINT was downregulated in GBM cell lines.LINC-PINT suppressed cell proliferation, invasion, and EMT by blocking Wnt/β-catenin signaling in GBM.		Yes	LINC-PINT suppressed cell progression, invasion, and EMT in GBM. LINC-PINT blocked Wnt/β-catenin signaling in GBM. 	33505307
LINC-PINT	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues	regulation[miR-767-5p/TET2 axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	LINC-PINT expression was downregulated in thyroid cancer relative to adjacent normal tissues (p = 0.0002). Taken together, LINC-PINT functions as a tumor suppressor in thyroid cancer via the miR-767-5p/TET2 axis, representing a potential therapeutic target for thyroid cancer.	 Low expression of LINC-PINT was significantly associated with advanced tumor node metastasis (TNM) stage (p = 0.0306) and lymph node metastasis (p = 0.0359). 	Yes	 Ectopic expression of LINC-PINT suppressed the proliferation, invasion, and tumorigenesis of thyroid cancer cells. 	33230437
LINC-PINT	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	Hep-2 and TU-177 cells	Interaction(ZEB1/AKT/mTOR pathway)	qRT-PCR//Western Blot	 LINC-PINT expression was inhibited in LSCC tissues and in Hep-2 and TU-177 cells, whose downregulation was associated with unsatisfactory prognosis.LINC-PINT enriches EZH2 to silence ZEB1 and thus inhibits the proliferative, migratory, and invasive capacities of Hep-2 and TU-177 cells. In addition, LINC-PINT might exert its biological function through the AKT/mTOR pathway.	 LINC-PINT expression was inhibited in LSCC tissues and in Hep-2 and TU-177 cells, whose downregulation was associated with unsatisfactory prognosis.	Yes	LINC-PINT overexpression suppressed the proliferative, migratory and invasive capacities of Hep-2 and TU-177 cells.	34257531
LINC-PINT	LncRNA	Homo sapiens	Retinoblastoma	cell lines	regulation[inhibits miR-523-3p ,upregulating Dickkopf-1 (DKK1)]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	Mechanistically, Linc-PINT was low-expressed, while miR-523-3p was high-expressed in RB cells, compared to the normal retinal epithelial cells (ARPE-19).In general, analysis of the data suggested that Linc-PINT inhibited miR-523-3p to upregulate DKK1, resulting in the inhibition of RB, and we demonstrated that Linc-PINT and miR-523-3p could be utilized as potential diagnostic and therapeutic biomarkers for RB in clinic.		Yes	 Further gain- and loss-function experiments verified that both upregulation of Linc-PINT and miR-523-3p downregulation slowed down cell growth, invasion and migration, and promoted cell apoptosis in RB cells, but Linc-PINT ablation and miR-523-3p overexpression promoted malignant phenotypes in RB cells. 	32828314
LINC-PINT	LncRNA	Homo sapiens	Melanoma	melanoma tissues	Interaction[downregulating lncRNA BANCR]	CCK8//qRT-PCR	LINC-PINT was downregulated, while BRAF-activated non-coding RNA (BANCR) was upregulated in melanoma tissues compared with normal adjacent tissues. LINC-PINT was downregulated, while BRAF-activated non-coding RNA (BANCR) was upregulated in melanoma tissues compared with normal adjacent tissues. Expression levels of LINC-PINT decreased, while expression levels of BANCR increased with increasing tumor thickness. The expression levels of LINC-PINT and BANCR were inversely associated in melanoma tissues but not in healthy adjacent tissue. LINC-PINT overexpression downregulated BANCR expression in melanoma cells, while BANCR overexpression did not significantly affect LINC-PINT expression. 		Yes	 LINC-PINT overexpression inhibited melanoma cell proliferation in vitro compared to controls.	31452772
LINC-PINT	LncRNA	Homo sapiens	Melanoma	cell lines	Interaction[Recruiting EZH2]	CCK8//qRT-PCR//Flow Cytometry//Microarray//Colony Formation Assay//ChIP	 LINC-PINT was significantly downregulated in melanoma tissues and cell lines. In conclusion, LINC-PINT inhibits the tumorigenicity of melanoma through recruiting EZH2 to the promoter of its target genes, leading to H3K27 trimethylation and epigenetic silencing of target genes.		Yes	The overexpression of LINC-PINT in tumor cells resulted in significant tumor growth reduction and migration inhibition in A375, Mum2B and CRMM1 cells. Results based on the in vivo xenograft model were further consistent with the in vitro findings that LINC-PINT impeded growth and metastasis of melanoma cells. 	31921860
LINC-PINT	LncRNA	Homo sapiens	Diabetes Mellitus	blood	Expression 	qRT-PCR	A comparison was made in this study, where LINC-PINT did not experience significant downregulation level in the majority of those suffering diabetes complications when in contrast to healthy controls, while LINC-PINT expression was found in diabetics. 		Yes	 While the overexpression of LINC-PINT increased the viability of ARPE-19 and AC16 cells, siRNA-mediated silencing of LINC-PINT elicited the opposite effect.	31711064
Linc8087	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Expression(lower expressed)	Wound Healing Assay//qRT-PCR//Cell Viability Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 We found that linc8087 expression was obviously decreased in both NSCLC tissues and cell lines compared with paired normal tissues and a normal bronchial epithelium cell line. The result of RT2 Profiler PCR Array showed that overexpressed linc8087 upregulated the expression of the COL4A2, CST7 and FAT1 genes and led to the downregulation of SERPINE1.	Low expression of linc8087 was significantly associated with poor survival. In addition, linc8087 was an independent risk factor for survival. 	Yes	Overexpressed linc8087 inhibited cell migration and invasion in A549 and PC9 cell lines. Knockdown of linc8087 promoted cell migration and invasion. 	34391179
LINC0638	LncRNA	Homo sapiens	Melanoma	blood	Expression[highly expressed]	qRT-PCR	 LINC01638 lncRNA was significantly upregulated in patients with melanoma compared with the other two groups of patients, and upregulation of LINC01638 lncRNA distinguished patients with melanoma from patients with benign skin lesions and healthy controls.		Yes	LINC01638 lncRNA overexpression promoted, while knockdown inhibited proliferation of cells of melanoma cell lines, C32 and SK-MEL-28, in vitro. 	31289478
LINC03047	LncRNA	Homo sapiens	Breast Neoplasms	clinical breast cancer tissues	Interaction(IGF2BP1/c-Myc axis)	qRT-PCR//Bioinformatics Analysis	Here, using RNA sequencing (RNA-seq) analysis, we identified a hypoxia-induced long noncoding RNA (lncRNA) KB-1980E6.3, which is aberrantly upregulated in clinical breast cancer tissues and closely correlated with poor prognosis of breast cancer patients. Mechanistically, lncRNA KB-1980E6.3 recruited insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) to form a lncRNA KB-1980E6.3/IGF2BP1/c-Myc signaling axis that retained the stability of c-Myc mRNA through increasing binding of IGF2BP1 with m6A-modified c-Myc coding region instability determinant (CRD) mRNA. 	Here, using RNA sequencing (RNA-seq) analysis, we identified a hypoxia-induced long noncoding RNA (lncRNA) KB-1980E6.3, which is aberrantly upregulated in clinical breast cancer tissues and closely correlated with poor prognosis of breast cancer patients. 	Yes	 The enhanced lncRNA KB-1980E6.3 facilitates breast cancer stem cells (BCSCs) self-renewal and tumorigenesis under hypoxic microenvironment both in vitro and in vivo. 	33469161
LINC03047	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells 	Regulation(PI3K/AKT signalling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 The levels of KB-1980E6.3 are significantly upregulated in breast cancer tissues and cells and are related to the poor prognosis. In terms of the mechanism, KB-1980E6.3 is involved in the activation of the PI3K/AKT signalling pathway. Knockdown of KB-1980E6.3 reduced the expression of the p-PI3K and p-AKT proteins, whereas KB-1980E6.3 overexpression showed the opposite result. 	 The levels of KB-1980E6.3 are significantly upregulated in breast cancer tissues and cells and are related to the poor prognosis. 	Yes	 Functional research both in vivo and in vitro revealed that the downregulation of KB-1980E6.3 expression significantly decreased cell proliferation, invasion and migration, while ectopic KB-1980E6.3 expression obviously promoted these biological phenotypes. 	35461041
LINC03046	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[MicroRNA-432-3p/ZEB1 Axis and the Wnt/β-Catenin Signaling Pathway]	Western Blot//ISH//qRT-PCR//IF//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The current study aimed to explore the function and molecular mechanism of lncRNA AC010789.1 in CRC progression. AC010789.1 found to be overexpressed in CRC tissues and cells.In summary, these results reveal that silencing AC010789.1 suppresses CRC progression via miR-432-3p-mediated ZEB1 downregulation and suppression of the Wnt/β-catenin signaling pathway, highlighting a potentially promising strategy for CRC treatment.	 High expression of AC010789.1 was associated with lymph node metastasis and poor prognosis. 	Yes	Moreover, AC010789.1 silencing inhibited proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro as well as tumorigenesis and metastasis in vivo.	33178684
LINC02990	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue specimens and cells	Interaction(miR-767-3p)	CCK8//qRT-PCR//Invasion Assay	LncRNA RP11-909N17.2 has an ascendant expression while miR-767-3p has descended one in NSCLC tissue specimens and cells.	Over-expression of lncRNA RP11-909N17.2 can shorten the overall survival period of NSCLC patients when compared with low expression. 	Yes	 Knockdown of lncRNA RP11-909N17.2 suppressed biology function of NSCLC cell including proliferation, migration, and invasion.	34957995
LINC02987-201	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial cancer cell lines	Interaction(miR-424/E2F6/E2F7 Axis)	CCK8//qRT-PCR//Wound Healing Assay	Combined with the results of the previous study, PCR analysis confirmed that lncRNA E27 was significantly upregulated in endometrial cancer cell lines. Furthermore, based on bioinformatics predictions, dual-luciferase assay and RT-qPCR analysis confirmed that miR-424, as its downstream molecule, competitively regulates the expression of E2F6/E2F7. Rescue experiments further supported that lncRNA E27 inhibited proliferation, migration, invasion, and promoted apoptosis of endometrial cancer through miR-424/E2F6/E2F7 signaling axis.		Yes	 The results of CCK-8, wound healing assay, and transwell experiments showed that lncRNA E27 could significantly inhibit cell proliferation, migration, and invasion. Flow cytometry results confirmed that lncRNA E27 could promote apoptosis.	36525235
LINC-PINT	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues	interaction[sponging miR-543 and inducing PTEN]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Firstly, in our study, we implied that LINC-PINT was obviously decreased in NSCLC. All these findings concluded that LINC-PINT exerted crucial biological roles in NSCLC through sponging miR-543 and inducing PTEN.		Yes	As exhibited, LINC-PINT repressed cell proliferation and cell colony formation of A549 and H1299 cells. 	31981466
LINC-PINT	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[miR-21]	qRT-PCR	In the present study, we found that lncRNA LINC-PINT was downregulated, while microRNA-21 (miR-21) was upregulated in tumor tissues than in adjacent healthy tissues of gastric cancer patients. LINC-PINT overexpression casued miR-21 inhibition in cells of human gastric cancer cell lines, while miR-21 overexpression did not alter LINC-PINT expression.. Effects of LINC-PINT overexpression on cellular behaviors of gastric cancer cells were attenuated by miR-21 overexpression. Therefore, LINC-PINT may participate in gastric cancer through the crosstalk with miR-21.		Yes	LINC-PINT overexpression led to inhibited, while miR-21 overexpression led to promoted proliferation, migration, and invasion of gastric cancer cells.	30569513
LINP1	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic tumor tissue	interaction[adsorbing microRNA-491-3p]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	QRT-PCR revealed that lncRNA LINP1 showed a significantly higher expression in pancreatic tumor tissue samples than in adjacent normal ones. LncRNA LINP1 is able to enhance the proliferation and metastasis of PCa cells by modulating microRNA-491-3p, thus affecting the incidence of lymph node or distant metastasis and prognosis of patients with PCa.	Compared with patients with low expression of lncRNA LINP1, patients with highly expressed lncRNA LINP1 showed a higher incidence of distant metastasis, but a lower overall survival rate.	Yes	In addition, compared to the sh-NC group, the proliferation, invasion, and migration ability of PCa cells decreased remarkably in LINP1 knockdown group. 	33015772
LincRNA00494	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues	regulation[SRCIN1 ]	CCK8//qRT-PCR	 LincRNA00494 was downregulated in the tumor tissues compared with the adjacent non-tumor tissues.Functional experiments revealed that LincRNA00494 inhibited NSCLC cell proliferation, which might be related to the suppression of SRCIN1, a tumor suppressor gene, by acting as a decoy for miR-150-3p.		Yes	Tumor growth from LincRNA00494-overexpressing xenografts was significantly decreased; additionally, LincRNA00494 silencing substantially increased tumor growth compared with that of the control cells.	32117734
LINP1	LncRNA	Homo sapiens	Endometrial Neoplasms	 EC tissues and normal tissues	Regulation[PI3K/AKT signaling pathway]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 LINP1 was proved to be Expression[Expression[up-expression]-expression]-regulated in EC cell lines and tissues by qRT-PCR assay. CCK-8 assay and colony formation assay were conducted and the results indicated that LINP1 over-expression can promote cell proliferation in EC in vitro. The data of transwell and Matrigel assays indicated that Expression[Expression[up-expression]-expression]-regulated LINP1 can facilitate cell migration and invasion. The results of Western blotting validated that LINP1 can activate PI3K/AKT signaling. Besides, the tumor formation assay verified that LINP1 can promote tumor formation in vivo.		Yes	CCK-8 assay and colony formation assay were conducted and the results indicated that LINP1 over-expression can promote cell proliferation in EC in vitro. The data of transwell and Matrigel assays indicated that Expression[Expression[up-expression]-expression]-regulated LINP1 can facilitate cell migration and invasion. 	31486482
Linc-UROD	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cells	Regulation(GF2BP3/METTL3/ENO1 and PKM)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	 The expression of linc-UROD was found to be upregulated in PC cells. Through mechanistic experiments, we found that IGF2BP3 stabilized linc-UROD through METTL3-mediated m6A modification. In addition, linc-UROD enhances the stability of ENO1 and PKM through interacting with them to inhibit ubiquitination. Detection on glucose consumption, pyruvate kinase activity and lactate production indicated that linc-UROD accelerated glycolysis of PC cells through PKM/ENO1-mediated pathway. 		Yes	The results of loss-of-function assays demonstrated that linc-UROD knockdown suppressed cell proliferation and migration, induced cell cycle G0/G1 arrest, and accelerated apoptosis of PC cells.	36413861
LINC-ROR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-212-3p/FGF7 Axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	We found that Linc-ROR were overexpressed in GC tissues compared to the adjacent tissues.Overexpression of miR-212-3p facilitated GC cells' migration and invasion, while the silencing of miR-212-3p attenuated GC cell migratory and invasive abilities. Fibroblast growth factor 7 (FGF7), a downstream molecule of miR-212-3p, was overexpressed in GC cells. 	High Linc-ROR predicts poor prognosis of GC patients. 	Yes	Moreover, Linc-ROR knockdown significantly suppressed the proliferation, migration, and invasion of GC cells, whereas miR-212-3p antagomir partially reversed Linc-ROR knockdown-induced phenotypes. 	33564265
LINC-ROR	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	 Interaction(MLL1)	RNA Pull-Down//ChIP//Western Blot//ISH//Flow Cytometry//FISH//RIP//IP//CHIP//EdU Staining//Transwell Assay	LncRNA ROR overexpresses in breast cancer tissues		Yes	Silencing of lncRNA ROR inhibits cell proliferation and invasion, promotes apoptosis in breast cancer	33653378
LINC-ROR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tumor tissues and cells	Interaction(miR-145/FSCN1)	Western Blot//Migration Assay//qRT-PCR//Invasion Assay//Transwell Assay	ROR expression in ESCC tumor tissues was significantly higher than in the adjacent tissues, p<0.001.  ROR overexpression could downregulate miR-145 by up to 50% was proven by RIP, DLR assay, and qRT-PCR. Two effective binding sites of ROR to miR-145 were verified by DLR assay. One of the sites has never been cited in the literature. The Western blotting results showed that FSCN1 was a downstream target of ROR/miR-145 (p<0.05). 	 The survival rate of ESCC patients with high ROR expression levels was lower than that of patients with low ROR expression levels (p<0.001). 	Yes	Transwell assays were used to show that overexpression of ROR enhanced migration and invasion behavior of ESCC and miR-145 hindered these effects.	29430188
LINC-ROR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cell lines and tissues	regulation[miR-6833-3p/SMC4 pathway]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//RIP	In this study, we found that LINC-RoR was upregulated in CRC cell lines and tissues.We concluded that LINC-RoR functions as an oncogene in CRC through the miR-6833-3p/SMC4 pathway.	High expression of LINC-RoR was associated with poorer survival time and multivariate analysis results showed that LINC-RoR was an independent risk factor of tumor malignancy progression.	Yes	Overexpression of LINC-RoR promoted the cell proliferation and knocked down it can reverse the effect in vitro. 	32273727
LINC-ROR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Regulation(TESC/ALDH1A1/TUBB3/PTEN axis)	qRT-PCR//MTT//Colony Formation Assay//Western Blot	LncRNA ROR, TESC, ALDH1A1, and TUBB3 were highly expressed in PTC tissues and cells.Overexpression of lncRNA ROR activated TESC by inhibiting the G9a recruitment on the promoter of TESC and histone H3-lysine 9me methylation. Moreover, TESC upregulated ALDH1A1 expression to increase TUBB3 expression, which then reduced PTEN expression.		Yes	Overexpression of lncRNA ROR, TESC, ALDH1A1 or TUBB3 and silencing of PTEN promoted PTC cell viability, colony formation, migration, and invasion while suppressing apoptosis. Moreover, overexpression of lncRNA ROR increased tumor growth by inhibiting PTEN in vivo.	35173149
LINC-ROR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Regulation[miR‑206/VEGF axis]	qRT-PCR	In the present study, ROR was found to be upregulated and microRNA (miR)‑206 was found to be downregulated in RCC tissues and cells.  In summary, the results of the present study revealed that ROR was upregulated in RCC tissues, which promoted tumor progression by regulating the miR‑206/VEGF axis. The present findings provided a novel insight into the potential functions of ROR in RCC, and the ROR/miR‑206/VEGF pathway may be a promising therapeutic target for the treatment of patients with RCC.		Yes	Furthermore, the knockdown of ROR inhibited the proliferation, migration and invasion of RCC cells. 	31485634
LINC-ROR	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Regulation[miR-145/FLNB regulatory axis]	Western Blot//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	In our study, we demonstrated that LncRNA-ROR was high expression in ovarian cancer tissues than in normal ovarian tissues.Functionally, LncRNA-ROR could induce epithelial-mesenchymal transition (EMT), and regulated ovarian cancer cell migration and invasion by decreasing the expression of tumor suppressive miR-145 and its target gene FLNB. Moreover, the binding site for miR-145 within LncRNA-ROR contributed to the reciprocal negative regulation of LncRNA-ROR and miR-145. Taken together, LncRNA-ROR promoted EMT by the miR-145/FLNB regulatory axis in ovarian cancer, providing a potential therapeutic target for ovarian cancer.	 In our study, we demonstrated that LncRNA-ROR was high expression in ovarian cancer tissues than in normal ovarian tissues, and LncRNA-ROR level was positively associated with clinical stages and the differentiation grades of malignant cells. 	Yes	 Functionally, LncRNA-ROR could induce epithelial-mesenchymal transition (EMT), and regulated ovarian cancer cell migration and invasion by decreasing the expression of tumor suppressive miR-145 and its target gene FLNB.	31829305
LINC-ROR	LncRNA	Homo sapiens	Osteosarcoma	OS tissue	Interaction[targeting miR-206]	IHC//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Here, we found that ROR expression level was significantly up-regulated in OS tissue samples compared to adjacent normal tissues.In addition, miR-206 was verified to be a target miRNA of ROR using bioinformatics online program and luciferase report assay. miR-206 inhibition partially rescued the inhibitory effects on OS cells induced by ROR knockdown. In conclusion, these results suggested that ROR function as an oncogene in OS by sponging miR-206 and might be a potential therapeutic target for patients with OS.	Here, we found that ROR expression level was significantly up-regulated in OS tissue samples compared to adjacent normal tissues, and the elevated ROR was closely correlated with advanced tumour-node-metastasis (TNM) stage and lymph node metastasis and poor overall survival rate.	Yes	Functional assays showed that ROR knockdown suppressed the OS cell proliferation, colony formation, migration and invasion in vitro, and retarded tumour growth in vivo.	30565392
LINC-ROR	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells 	regulation[LncRNA-ROR/microRNA-185-3p/YAP1 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Up-regulated lncRNA-ROR and YAP1 and down-regulated miR-185-3p were found in osteosarcoma.This work illustrates that lncRNA-ROR down-regulation or miR-185-3p up-regulation inhibits osteosarcoma progression via YAP1 repression.		Yes	 LncRNA ROR knockdown or miR-185-3p overexpression inhibited osteosarcoma cell progression while lncRNA ROR elevation or miR-185-3p inhibition presented the opposite effects.	32898639
LINC-ROR	LncRNA	Homo sapiens	Esophageal Neoplasms	EC tissues and cells	regulation[miR-145/LMNB2 signal axis]	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	ROR and LMNB2 were up-regulated and miR-145 was down-regulated in EC tissues and cells. LMNB2 which is regulated by ROR and miR-145 was highly expressed in EC and promoted the proliferation and migration of EC in vitro and in vivo. 		Yes	The proliferation and migration of EC cells were promoted by overexpression of of ROR or LMNB2. 	33312362
LINC-ROR	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	serum exosomes	Regulation( p-AKT/p-VEGFR2 pathway )	Western Blot//Transfection//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//EdU Staining//Transwell Assay	This study demonstrates that linc-ROR is substantially expressed in serum exosomes from NPC and can be taken up by HUVECs.  Thus, the p-AKT/p-VEGFR2 pathway is the mechanism by which linc-ROR affects the aforementioned biological activities. By stimulating angiogenesis, linc-ROR appears to play a significant role in the course of NPC and could account for a therapeutic target.		Yes	 Using qRT-PCR, the CCK8 test, the transwell migration assay, the wound healing assay, and the tube formation assay, we demonstrated that linc-ROR increases proliferation, migration, and angiogenesis in vitro. Similar to prior research, our results have shown that linc-ROR can stimulate tumor angiogenesis in the zebrafish model. 	36183926
LINC-ROR	LncRNA	Homo sapiens	Glioblastoma	cancer stem cell	Expression(highly expressed)	Transfection//Flow Cytometry//qRT-PCR//RNA-seq//Cell Proliferation Assay	 Here, we investigated linc-RoR (long intergenic non-protein coding RNA, regulator of reprogramming) using GBM neurospheres obtained from 12 different patients. We demonstrated that the highest level of this transcript is detected in cells with increased EGFR expression.  Analysis of RNA sequencing data revealed that linc-RoR affects expression of genes involved in the regulation of mitosis. In agreement with this observation, we have showen that the highest level of linc-RoR is detected in the G2/M phase of the cell cycle, when linc-RoR is localized on the chromosomes of dividing cells. 		Yes	 According to our data, linc-RoR knockdown decreases cell proliferation, increases sensitivity to DNA damage, and downregulates the level of cancer stem cell (CSC) markers. On the other hand, linc-RoR overexpression promote cell growth and increases the proportion of CSCs. 	35654242
LINC-ROR	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cells	Regulation(mTORC2)	In Vivo Experiment//Western Blot//qRT-PCR//Cell Proliferation Assay//IHC//EdU Staining	We found that LincRNA-RoR was markedly reduced in GBM tissues compared with adjacent non-tumor tissues from 10 cases of GBM patients. Consistently, LincRNA-RoR expression in GBM cells was significantly lower than that in normal glial cells.  Mechanistically, LincRNA-RoR inhibited the expression of Rictor, the key component of mTORC2 (mammalian target of rapamycin complex 2), to suppress the activity of Akt pathway and impair the expression of glycolytic effectors, including Glut1, HK2, PKM2 and LDHA. 		Yes	The aerobic glycolysis of GBM cells, as determined by the measurement of glucose uptake and lactate production, was impaired by LincRNA-RoR overexpression. Finally, enforced expression of LincRNA-RoR reduced the proliferation of GBM cells in vitro, restrained tumor growth in vivo, and repressed the expression of glycolytic molecules in GBM xenografts. 	29581766
LINC-ROR	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tissues	Interaction(miR-32/H3K27 acetylation )	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//ChIP	We showed that lincRNA-ROR was significantly upregulated in retinoblastoma tissues, and overexpression of lincRNA-ROR was significantly correlated with optic nerve invasion, nodal or distant metastasis, and recurrence.  Further, we demonstrated that lincRNA-ROR activates the Notch signaling pathway by acting as a sponge of miR-32-5p. Upregulation of lincRNA-ROR was attributed to the CBP-mediated H3K27 acetylation at the promoter region.	We showed that lincRNA-ROR was significantly upregulated in retinoblastoma tissues, and overexpression of lincRNA-ROR was significantly correlated with optic nerve invasion, nodal or distant metastasis, and recurrence. 	Yes	 We also showed that lincRNA-ROR is a critical promoter of retinoblastoma cell metastasis, both in vivo and in vitro. 	32439866
LINC-ROR	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	regulation[Notch1 pathway]	CCK8//qRT-PCR//Tunel//Western Blot	Both lncRNA ROR and Notch1 were highly expressed in EC tissues (p<0.05). LncRNA ROR regulates the proliferation and apoptosis of EC cells via promoting the expression of Notch1 protein.		Yes	After overexpression of lncRNA ROR, HEC-1A cells had significantly enhanced proliferation (p<0.05) and weakened apoptosis (p<0.05). 	32572910
LINC-ROR	LncRNA	Homo sapiens	Osteoporosis	OP patients	Interaction(miR-145-5p axis )	Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	LncRNA ROR was downregulated, and miR-145-5p was overexpressed in OP patients. Luciferase reporting assay verified the target relationship between ROR and miR-145-5p. MiR-145-5p downregulation reversed ROR silence mediated effect on MC3T3-E1 cell proliferation and apoptosis. LncRNA ROR is downregulated and miR-145-5p is highly expressed in OP patient	 The combined diagnosis of ROR and miR-145-5p showed good diagnostic value for OP.	Yes	ROR knockdown promoted the MC3T3-E1 cell apoptosis and inhibited cell proliferation. 	34617877
lincRNA-01317	LncRNA	Homo sapiens	Stomach Neoplasms	cancer tissue 	Interaction(KCNQ1)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//Cell Viability Assay//Colony Formation Assay//Invasion Assay	Here, we found significantly decreased lincRNA-01317 levels in cancer tissue compared with paracancer tissue of patients with gastric cancer, and lincRNA-01317 expression levels positively correlated with clinical survival rate. Finally, we demonstrated that lincRNA-01317 may target KCNQ1, as KCNQ1 was downregulated after transfection of cells with lincRNA-01317. 	Here, we found significantly decreased lincRNA-01317 levels in cancer tissue compared with paracancer tissue of patients with gastric cancer, and lincRNA-01317 expression levels positively correlated with clinical survival rate. 	Yes	Furthermore, using a gastric cancer cell line and a xenograft mouse model, we found that transfection of a gastric cancer cell line with lincRNA-01317 significantly inhibited the proliferation, migration, and invasion of gastric cancer cells. 	33594325
lnc-CHAF1B-3	LncRNA	Homo sapiens	renal fibrosis	human renal proximal tubular cells 	Expression(highly expressed)	Western Blot//Transfection//qRT-PCR//RNA-seq//Microarray	Microarray assays showed that expression of the lncRNA lnc-CHAF1B-3 (also called claudin 14 antisense RNA 1) was significantly upregulated in human renal proximal tubular cells by both transforming growth factor-β1 (TGF-β1) and hypoxic stimulation, accompanied with increased expression of EMT-related genes.		Yes	Knockdown of lnc-CHAF1B-3 significantly suppressed TGF-β1-induced upregulated expression of collagen type I alpha 1, cadherin-2, plasminogen activator inhibitor-1, snail family transcriptional repressor I (SNAI1) and SNAI2. 	36700051
lncCIRBIL	LncRNA	Rattus norvegicus	Esophageal Neoplasms	Cardiomyocyte	Interaction(Bclaf1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//FISH//RIP//IF	 The level of lncCIRBIL is reduced in I/R hearts. Cardiomyocyte-specific transgenic overexpression of lncCIRBIL reduces infarct area following I/R injury. Knockout of lncCIRBIL in mice exacerbates cardiac I/R injury. Qualitatively, the same results are observed in vitro. LncCIRBIL directly binds to BCL2-associated transcription factor 1 (Bclaf1), to inhibit its nuclear translocation. Cardiomyocyte-specific transgenic overexpression of Bclaf1 worsens, while partial knockout of Bclaf1 mitigates cardiac I/R injury. Meanwhile, partial knockout of Bclaf1 abrogates the detrimental effects of lncCIRBIL knockout on cardiac I/R injury.		Yes	Knockout of lncCIRBIL in mice exacerbates cardiac I/R injury.Qualitatively, the same results are observed in vitro. LncCIRBIL directly binds to BCL2-associated transcription factor 1 (Bclaf1), to inhibit its nuclear translocation. Cardiomyocyte-specific transgenic overexpression of Bclaf1 worsens, while partial knockout of Bclaf1 mitigates cardiac I/R injury. Meanwhile, partial knockout of Bclaf1 abrogates the detrimental effects of lncCIRBIL knockout on cardiac I/R injury. 	33483496
lncCSMD1-1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	liver tissues	regulation[MYC signaling pathway]	qRT-PCR//RNA Pull-Down//RIP	With microarray, we identified a highly upregulated lncRNA, lncCSMD1-1, which was associated with tumor progression and poor prognosis in the Discovery Cohort, and validated in another 3 HCC cohorts.  lncCSMD1-1 is upregulated in HCC and promotes progression of HCC by activating the MYC signaling pathway.		Yes	Consistently, ectopic expression of lncCSMD1-1 notably promotes cell proliferation, migration, invasion, tumor growth and metastasis of HCC cells in in vitro and in vivo experiments. 	32685003
LncRNA-CTS	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues,cell lines(HeLa, SiHa, Ca-Ski, C-33A, and HT-3)	Regulation[miR-505/ZEB2 axis]	qRT-PCR//Luciferase Report Assay//Transwell Assay//Western Blot	Data also showed that lncRNA-CTS could function as a competing endogenous RNA for miR-505 in CC cells. Further investigations disclosed that ZEB2 was demonstrated as a Expression[down-expression]stream target of miR-505, and subsequently exerted its metastatic effects via the lncRNA-CTS/miR-505/ZEB2 axis in CC cells. Finally, lncRNA-CTS activated the SMAD/TGF pathway via miR-505 in CC cells. Collectively, our results demonstrate the importance of the lncRNA-CTS/miR-505/ZEB2 axis in CC. LncRNA-CTS can predispose CC patients to metastases and may represent a promising therapeutic target for CC.	The expression levels of lncRNA-CTS and miR-505 were correlated with the metastasis-associated clinicopathological features of CC patients. Moreover, lncRNA-CTS was associated with a poor prognosis in CC patients.	Yes	In vitro and in vivo experiments, along with gain- and loss-of-function studies, showed that lncRNA-CTS enhanced cell migration, invasion, and the transforming growth factor (TGF)-β1-induced-EMT process. 	31499118
lncRNA-CCHE1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 PTC tissues 	Expression [highly expressed]	Western Blot//Transfection//CCK8//qRT-PCR//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	A higher expression of lncRNA-CCHE1 was found in PTC tissues than in adjacent tissues. 	High expression of lncRNA-CCHE1 was positively correlated with the number of tumors, extra-glandular invasion, and tumor stage. 	Yes	In addition, the down-regulation of lncRNA-CCHE1 reduced the proliferation and invasion of PTC cell lines and promoted cell apoptosis, while its up-regulation caused the opposite effect. 	35116712
lncRNACASC9	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer cells and tissues	Interaction(CASC9/miR-195-5p/TK1 axis)	qRT-PCR//RNA Pull-Down	CASC9 was highly expressed in bladder cancer cells and tissues, and the prognosis of bladder cancer patients with high expression of CASC9 was poor. Mechanistically, through FISH experiments, luciferase reporter experiments, and RIP experiments, we proved that CASC9 regulated the expression of TK1 by adsorbing miR-195-5p, thereby exerting an oncogenic effect in bladder cancer. 	CASC9 was highly expressed in bladder cancer cells and tissues, and the prognosis of bladder cancer patients with high expression of CASC9 was poor.	Yes	 The results of colony formation assays, CCK-8 assays, EdU assays, transwell assays, mouse xenograft models, and tail vein injection lung metastasis model showed that CASC9 could promote bladder cancer cells growth and metastasis both in vitro and in vivo. 	35578597
lncRNA-CASC15	LncRNA	Homo sapiens	Osteosarcoma	 clinical samples and OS cells	Interaction(Wnt/β-catenin signaling pathway)	CCK8//qRT-PCR//Western Blot	 The results revealed that lncRNA-CASC15 was highly expressed in clinical samples and OS cells. Rescue experiments demonstrated that CASC15 affected the cell cycle by activating the Wnt/β-catenin pathway, thereby promoting cell proliferation. 		Yes	 In vitro verification experiments revealed that CASC15 promoted the growth of OS cells.	33760218
lncRNA-ATB	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[activating YAP and increasing ATG5]	qRT-PCR//RIP//Western Blot	The expression of lncRNA-ATB was higher in HCC tissues than in normal liver tissues. LncRNA-ATB promoted autophagy by activating Yes-associated protein (YAP). Moreover, lncRNA-ATB interacted with autophagy-related protein 5 (ATG5) mRNA and increased ATG5 expression.	lncRNA-ATB expression was positively correlated with tumor size, TNM stage, and poorer survival of patients with HCC.	Yes	 Moreover, ectopic overexpression of lncRNA-ATB promoted cell proliferation and clonogenicnity of HCC cells in vitro. 	31558875
lncRNA-ATB	LncRNA	Homo sapiens	Liver Neoplasms	HBV-related liver cancer and non-HBV infected liver cancer tissues	 Interaction[TGF‑β ]	qRT-PCR//Western Blot	These results suggested that increased expression of lncRNA-ATB in primary liver cancer may be associated with HBV infection and advanced tumor development.Bx‑induced autophagy could upregulate the expression of TGF‑β and lncRNA‑ATB. Mechanistically, PGM5-AS1 was transcriptionally activated by p53 and it could directly interact with and sequester miR-466 to elevate PTEN expression, thereby inhibiting ESCC progression. 		Yes	In addition, the invasive and migration abilities of HBx‑HepG2 cells were increased compared with HepG2 cells, while knockdown of lncRNA‑ATB or TGF‑β could reduce these abilities.	31746419
lncRNA-ANRIL	LncRNA	Homo sapiens	Glioma	142 glioma patients	Interaction(SOX9 )	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 ANRIL and SOX9 were evidently higher in RG than in CG (P<0.01).The receiver operating characteristic (ROC) curve revealed that the diagnostic sensitivity of ANRIL combined with SOX9 for glioma was 81.62%, and the specificity was 90.83% (P<0.01). ANRIL and SOX9 were closely related to tumor grade, tumor diameter, distant metastasis, and family history of glioma (P<0.01).ANRIL and SOX9 were markedly higher in glioma cell lines (U251 and U87) than in normal brain cells (P<0.01).  Bcl-2 expression was markedly increased in lncRNA-ANRIL-inhibitor and SOX9-inhibitor (P<0.01), while bax expression was markedly reduced in lncRNA-ANRIL-inhibitor and SOX9-inhibitor (P<0.01).	The receiver operating characteristic (ROC) curve revealed that the diagnostic sensitivity of ANRIL combined with SOX9 for glioma was 81.62%, and the specificity was 90.83% (P<0.01). ANRIL and SOX9 were closely related to tumor grade, tumor diameter, distant metastasis, and family history of glioma (P<0.01).	Yes	The proliferation and invasion of U251 cells were notably reduced after the transfection of ANRIL and SOX9 inhibitory sequences (P<0.01), but the apoptosis was notably increased (P<0.01).	34556140
lncRNA-AK001903	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	Cervical cancer (CC) tissues and cell lines(Hela, Siha, Ca Ski, C33a, H8)	Expression [highly expressed]	ISH//CCK8//qPCR//Transwell Assay	In the present study, lncRNA microarrays were conducted to investigate the differentially expression lncRNAs in cervical cancer (CC) tissues compared with peritumoral tissues. Then, the most significantly upregulated lncRNA, which was lncRNA-AK001903 was selected to conduct further experiments. Real-time Quantitative polymerase chain reaction was conducted to investigate lncRNA-AK001903 expression in CC tissues and Hela, Siha, Ca Ski, C33a, H8 (HPV-immortalized cervical epithelial cell line) cell lines, and in situ hybridization histochemistry (ISHH) was performed to detect lncRNA-AK001903 expression level in different CC stages. The effect of lncRNA-AK001903 on cell proliferation, invasion and migration was assessed after knockdown of lncRNA-AK001903.	LncRNA-AK001903 is upregulated in CC tissues and cells and related to FIGO stage in patients with CC Among the 20 most significantly differentially expressed lncRNAs (DE lncRNAs) in the CC tissues vs. CP (peritumoral tissues), the most notably upregulated one was lncRNA-AK001903.	Yes	 The effect of lncRNA-AK001903 on cell proliferation, invasion and migration was assessed after knockdown of lncRNA-AK001903.	33363614
LncRNAAirsci	LncRNA	Rattus norvegicus	Spinal Cord Injuries	SCI rats	Regulation	In Vivo Experiment//Western Blot//qRT-PCR//RNA-seq//Bioinformatics Analysis	 LncRNA Airsci was the most significantly expressed among the five lncRNAs involved in the NF-κB signaling pathway. LncRNA Airsci-siRNA reduced the inflammatory response by inhibiting the NF-κB signaling pathway, alleviated spinal cord tissue injury, and promoted the recovery of motor function in SCI rats. 		Yes	LncRNA Airsci-siRNA reduced the inflammatory response by inhibiting the NF-κB signaling pathway, alleviated spinal cord tissue injury, and promoted the recovery of motor function in SCI rats. 	33063741
LncRNA-Airn	LncRNA	Homo sapiens	Acute Liver Injury	 liver tissue and primary hepatocytes	Regulation(p65 and IκBα)	Western Blot//Transfection//Tunel//qRT-PCR//Luciferase Report Assay//H&E Staining	In this study, we show that Airn is upregulated in liver tissue and primary hepatocytes from an acute liver injury mouse model. Consistently, Airn is also overexpressed in serum samples of patients with acute-on-chronic liver failure and is negatively correlated with the Model for End-Stage Liver Disease (MELD) score.  Mechanistically, we reveal that Airn represses CCl 4- and H 2O 2-induced enhancement of phosphorylation of p65 and IκBα, suggesting that Airn inhibits hepatocyte apoptosis by inactivating the NF-κB pathway.		Yes	Moreover, gene knockout and rescue assays reveal that Airn alleviates CCl 4-induced liver injury by inhibiting hepatocyte apoptosis and oxidative stress in vivo. Further investigation reveals that Airn decreases H 2O 2-induced hepatocyte apoptosis in vitro. 	36604144
lncRNA-ABHD11-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 serum of PTC patients	Expression [highly expressed]	qRT-PCR	 According to the data, the expression levels of serum ABHD11-AS1 in the PTC patients were remarkably higher than those in the healthy controls, and the area under the curve (AUC) for distinguishing the patients from the controls was 0.920. 	 In the analysis of prognosis, the levels in patients with a poor prognosis were remarkably higher than those in patients with a good prognosis. 	Yes	In the cell experiments, knocking down ABHD11-AS1 remarkably inhibited PTC cells from proliferation, arrested them in G0/G1 phase, and induced their apoptosis, negatively affecting their survival indices. Overexpressing this RNA had positive effects on the survival indices.	34102210
lncRNA93358	LncRNA	Rattus norvegicus	Myocardial Infarction	model rats	Regulation(SLC8A1)	In Vivo Experiment//Western Blot//Tunel//qRT-PCR//Luciferase Report Assay//H&E Staining	 lncRNA 93358 and Bax were found significantly upregulated, and Bcl-2 and SLC8A1 were greatly downregulated in model rats, which were dramatically reversed by the knockdown of lncRNA 93358, accompanied by the decline area of myocardial necrosis and decreased apoptotic myocardial cells.		Yes	 lncRNA 93358 and Bax were found significantly upregulated, and Bcl-2 and SLC8A1 were greatly downregulated in model rats, which were dramatically reversed by the knockdown of lncRNA 93358, accompanied by the decline area of myocardial necrosis and decreased apoptotic myocardial cells.	35845941
LncRNA-6395	LncRNA	Mus musculus	Myocardial Reperfusion Injury	infarct area of mouse hearts and NMVCs	Interaction(p53)	Other	We showed that lncRNA KnowTID_00006395, termed lncRNA-6395 was significantly upregulated in the infarct area of mouse hearts following I/R injury as well as in H2O2-treated neonatal mouse ventricular cardiomyocytes (NMVCs).  We demonstrated that lncRNA-6395 directly bound to p53, and increased the abundance of p53 protein through inhibiting ubiquitination-mediated p53 degradation and thereby facilitated p53 translocation to the nucleus. More importantly, overexpression of p53 canceled the inhibitory effects of lncRNA-6395 knockdown on cardiomyocyte apoptosis, whereas knockdown of p53 counteracted the apoptotic effects of lncRNA-6395 in cardiomyocytes. 		Yes	Overexpression of lncRNA-6395 led to cell apoptosis and the expression change of apoptosis-related proteins in NMVCs, whereas knockdown of lncRNA-6395 attenuated H2O2-induced cell apoptosis. LncRNA-6395 knockout mice (lncRNA-6395+/-) displayed improved cardiac function, decreased plasma LDH activity and infarct size following I/R injury. 	34493812
LncRNA-5657	LncRNA	Rattus norvegicus	Brain Injuries	glial cells and rat models of septic encephalopathy	Regulation	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//H&E Staining//ELISA//IHC	The sh-LncRNA-5657 treatment reduced the level of neuronal degeneration and necrosis in the rat hippocampus, reduced the immunoreactivities of aquaporin 4, heparanase, and metallopeptidase-9, and lowered the level of tumor necrosis factor-alpha. These findings suggested that LncRNA-5657 expression can significantly reduce the inflammatory reaction during septic encephalopathy and induce protective effects against this disease. 		Yes	The sh-LncRNA-5657 treatment reduced the level of neuronal degeneration and necrosis in the rat hippocampus, reduced the immunoreactivities of aquaporin 4, heparanase, and metallopeptidase-9, and lowered the level of tumor necrosis factor-alpha. Sh-LncRNA-5657 transfection decreased the expression of LncRNA-5657 in lipopolysaccharide-treated glial cells and decreased the mRNA and protein levels of tumor necrosis factor-alpha, interleukin-1β, and interleukin-6. 	33318407
lncRNA-45	LncRNA	Homo sapiens	Breast Neoplasms	4T1-LG12 cells	Expression(highly expressed)	Western Blot//Wound Healing Assay//Tunel//Migration Assay//qRT-PCR//RNA-seq//Invasion Assay//Transwell Assay	 We found that many differently expressed lncRNAs greatly correlated to the metastatic propensity of 4T1-LG12 cells, particularly lncRNA-45, a new lncRNA without functional annotations, which was found to be the most upregulated lncRNA transcribed by an internal region within the regulatory associated with protein of mechanistic target of rapamycin kinase (mTOR) complex 1 (Rptor) gene.Molecular mechanistic investigation showed that reduced activity of mTORC1-associated pathway led to a decrease of total ribosomal protein S6 kinase, polypeptide 1 (S6K1) content and enhancement of autophagy, consequently compromising the metastatic propensity in lncRNA-45 knockdown cells.		Yes	LncRNA-45 was uncovered to be involved in the epithelial-to-mesenchymal transition process of breast cancer cells, as evidenced by the observation that lncRNA-45 knockdown significantly suppressed the invasive capability of parental 4T1-LG12 cells.	36502630
LncRNA4344	LncRNA	Rattus norvegicus	Cognitive Dysfunction	hippocampal tissues of LPS-treated rats and RM cells	Interaction( miR-138-5p)	In Vivo Experiment//Western Blot//Tunel//qRT-PCR//Cell Apoptosis Assay//ELISA//Bioinformatics Analysis	 The expression levels of lncRNA 4344 and NLRP3 were upregulated in the hippocampal tissues of LPS-treated rats and RM cells, and showed a strong positive correlation between each other.  Subsequently, the results of the animal experiments showed that the lncRNA 4344/miR-138-5p/NLRP3 axis plays an essential role in regulating the cognitive behavior, pathological changes and apoptosis of hippocampal neurons, expression of inflammation-related factors (NLRP3, caspase-1, IL-1β, and IL-18), and microglial activation in LPS-induced cognitive impairment rats.		Yes	LncRNA 4344 overexpression further enhanced the expression of NLRP3 and its downstream genes (caspase-1, IL-1β, and IL-18), as well as neuronal apoptosis in LPS-stimulated RM cells, whereas lncRNA 4344 silencing attenuated the inflammatory injuries. 	34455059
lncRNA‐422	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissue and cell line	Interaction(SFPQ)	qRT-PCR	Mechanistically, lncRNA‐422 could interact directly with splicing factor proline and glutamine rich (SFPQ) to activate downstream pathways. SFPQ drives cancer progression through diverse roles in RNA transcriptional activity, mRNA processing, splicing regulation and innate immune response in hepatocellular carcinoma, 1 breast cancer, 2 ovarian cancer 3 and colorectal cancer. 4 Moreover, SFPQ promoted the proliferation and onset of colorectal cancer.		Yes	In this study, the biological function of lncRNA‐422 was investigated in colorectal cancer, which suggested that down‐regulated lncRNA‐422 suppressed cell proliferation and inhibited tumor growth in cellular and xenograft models. 	35075799
lnc-RAB11B-AS1	LncRNA	Homo sapiens	Lung Neoplasms	LC tissues 	Expression[highly expressed]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The results showed that lnc-RAB11B-AS1 was significantly overexpressed in LC tissues compared to the corresponding non-tumor tissues.	Patients with a higher level of lnc-RAB11B-AS1 expression showed a poorer overall survival rate. 	Yes	Functionally, overexpression of lnc-RAB11B-AS1 promotes cell proliferation, migration and invasion abilities of LC cell lines, which suggests lnc-RAB11B-AS1 may play an oncogenic role in LC. 	32566609
LNCPOIR	LncRNA	Homo sapiens	Epithelial-Mesenchymal Transition	HCC cells	Interaction(miR-182-5p)	Cell Proliferation Assay//qRT-PCR//Transfection//Luciferase Report Assay	Together, these pieces of data suggest that lncRNA-POIR promotes EMT progression and suppresses SOR sensitivity simultaneously by sponging miR-182-5p. 		Yes	 Furthermore, loss- or gain-of-function approaches were used to demonstrate the role of lncRNA-POIR/miR-182-5p on EMT and SOR sensitivity in HCC. 	32951268
lnc-PKMYT1AR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Interaction(miR-485-5p/PKMYT1 axis)	Migration Assay//CCK8//Flow Cytometry//qRT-PCR//IP//Colony Formation Assay	Here, we identify a human-specific long non-coding RNA (lncRNA, ENST00000595422), termed PKMYT1AR (PKMYT1 associated lncRNA), that is induced in NSCLC by Yin Yang 1 (YY1) factor, especially in cancerous cell lines (H358, H1975, H1299, H1650, A549 and SPC-A1) compared to that in normal human bronchial epithelium cell line (BEAS-2B). Bioinformatic analysis and a luciferase assay demonstrate that PKMYT1AR directly interacts with miR-485-5p to attenuate the inhibitory role on its downstream oncogenic factor PKMYT1 (the protein kinase, membrane-associated tyrosine/threonine 1) in NSCLC. 	We show that PKMYT1AR high expression correlates with worse clinical outcome, and knockdown of PKMYT1AR inhibits tumor cell proliferation, migration and xenograft tumor formation abilities. 	Yes	We show that PKMYT1AR high expression correlates with worse clinical outcome, and knockdown of PKMYT1AR inhibits tumor cell proliferation, migration and xenograft tumor formation abilities. 	34856993
lncRNA-CCRR	LncRNA	Homo sapiens	Breast Neoplasms	64 breast cancer patients 	Interaction(CX43)	qRT-PCR//IHC//Western Blot	Compared with the non-metastasis group, the mRNA expression of tissue lncRNA-CCRR, cerebrospinal fluid (CSF) lncRNA-CCRR, tissue CX43 and tissue protein expression of CX43 were both evidently up-regulated in metastasis patients, especially in patients with brain metastasis.The expression of lncRNA-CCRR was positively correlated with the up-regulated expression of CX43. 		Yes	Also, the overexpression of lncRNA-CCRR evidently increased dye transfer rate from astrocytes to MDA-MB-231BR/BT-474BR cells but reduced lncRNA-CCRR expression and suppressed the transmigration of MDA-MB-231BR/BT-474BR cells in a blood-brain barrier (BBB) model. 	33793070
lncRNA-DANCR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[highly expressed ]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	 The expression of lncRNA-DANCR in CRC tissues and HT-29 cells was significantly higher than that in non-CRC tissues and FHC cells.		Yes	Silencing lncRNA-DANCR could significantly inhibit the proliferation, invasion and metastasis of HT-29 cells. Western blot showed that the expression of E-cadherin increased significantly and vimentin decreased significantly after silencing lncRNA-DANCR. The same results were observed in immunofluorescence experiment. Silence of lncRNA-DANCR markedly sExpression[Expression[up-expression]-expression]pressed the growth and metastasis of CRC.	35117008
lnc-CTSLP4	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tumor tissues	Interaction(Hsp90α and recruiting E3 ubiquitin ligase ZFP91/HNRNPAB-dependent Snail transcription)	In Vivo Experiment//RNA Pull-Down//Western Blot//Co-IP//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//IP//IHC//Invasion Assay//ChIP	 We found that lnc-CTSLP4 was significantly downregulated in GC tumor tissues compared with adjacent non-tumor tissues, and its levels in GC tumor tissues were closely correlated with tumor local invasion, TNM stage, lymph node metastasis, and prognosis of GC patients. Mechanistic analysis demonstrated that lnc-CTSLP4 could bind with Hsp90α/heterogeneous nuclear ribonucleoprotein AB (HNRNPAB) complex and recruit E3-ubiquitin ligase ZFP91 to induce the degradation of HNRNPAB, thus suppressing the transcriptional activation of Snail and ultimately reversing EMT of GC cells. 	 We found that lnc-CTSLP4 was significantly downregulated in GC tumor tissues compared with adjacent non-tumor tissues, and its levels in GC tumor tissues were closely correlated with tumor local invasion, TNM stage, lymph node metastasis, and prognosis of GC patients. 	Yes	 Loss- and gain-of-function assays indicated that lnc-CTSLP4 inhibited GC cell migration, invasion, and EMT in vitro, as well as peritoneal dissemination in vivo. 	33717650
lncRNA-DAW	LncRNA	Homo sapiens	Liver Neoplasms	hepatocellular carcinoma (HCC) specimens	Interaction(EZH2/Wnt2/Wnt/β-catenin pathway)	In Vivo Experiment//Western Blot//Co-IP//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	Our results revealed that lncRNA-DAW was driven by a liver-specific super-enhancer and transcriptionally activated by HNF4G, leading to frequent elevation in hepatocellular carcinoma (HCC) specimens. By using RNA sequencing, Wnt2 was screened out as a downstream effector of lncRNA-DAW. We next found that lncRNA-DAW physically interacted with EZH2, a negative regulator of Wnt2.  This interplay subsequently potentiated CDK1-EZH2 interaction, leading to the phosphorylation and ubiquitination of EZH2. 		Yes	Ectopic expression of lncRNA-DAW promoted both in vivo and in vitro tumor growth. 	34853732
LncRNA-ZXF1	LncRNA	Mus musculus	endometrial endometrioid adenocarcinoma, secretory variant	(EEC) cells	Interaction(miR-378a-3p/PCDHA3 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Transfection//qRT-PCR//RIP//migration assay//Luciferase Report Assay//IP//IHC	 This regulation may be achieved by the lncRNA-ZXF1-mediated alteration in the expression of P21 through two mechanisms. One is that lncRNA-ZXF1 functions as a molecular sponge of miR-378a-3p to regulate PCDHA3 expression and then modulate the expression of P21. The other is that lncRNA-ZXF1 inhibits CDC20-mediated degradation of ubiquitination by directly binding to P21. 		Yes	We found that lncRNA-ZXF1 altered the migration and invasion of endometrioid endometrial cancer (EEC) cells. Furthermore, our results suggest that lncRNA-ZXF1 regulates EEC cell proliferation.	33751805
LncRNA-UCA1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 tumor tissues and cells 	Interaction( miR-383/VEGFA)	In Vivo Experiment//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Colony Formation Assay//Transwell Assay	The expression of lncRNA-UCA1 was significantly increased in tumor tissues and cells compared with adjacent tissues or HBE cells. Silencing lncRNA-UCA1 expression in cells resulted in a reduction in lung cancer cell viability. 		Yes	 Silencing lncRNA-UCA1 expression in cells resulted in a reduction in lung cancer cell viability. 	35980157
lncRNA-u50535	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues,cell line( HBE,A549, H1299 and SPC-A1)	Regulation[CCL20/ERK signaling]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results demonstrated that lncRNA‑u50535 expression was Expression[Expression[up-expression]-expression]regulated in lung cancer tissues and cell lines compared with normal tissues and cells.Western blot and luciferase reporter gene assays demonstrated that lncRNA‑u50535 overexpression increased the translation and transcription of CCL20. In addition, knockExpression[down-expression] of lncRNA‑u50535 decreased CCL20, CCR6 and p‑ERK levels. The effects of lncRNA‑u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced.		Yes	KnockExpression[down-expression] of lncRNA‑u50535 decreased lung cancer cell proliferation and migration, induced G0/G1 phase arrest and promoted cell apoptosis. 	31545478
lncRNA-SRA	LncRNA	Homo sapiens	Cardiovascular Diseases	blood	Expression[Expression[lower expressed]-expression]	qRT-PCR//MTT	 The clinicopathological features of these patients are summarized in Table I. As presented in Fig. 1, the plasma levels of lncRNA-SRA were significantly decreased in patients with type II diabetic cardiovascular disease compared with type II diabetic patients without any obvious complications and healthy controls (P<0.05). 	A total of 172 type II diabetic patients without any obvious complications on the day of admission completed the 5-year follow-Expression[Expression[up-expression]-expression]. According to the median relative plasma level of lncRNA-SRA (1.44), these patients were divided into a high (n=86) and a low (n=86) expression groExpression[Expression[up-expression]-expression]. During the follow-Expression[Expression[up-expression]-expression], cardiovascular disease occurred in 41 cases, including 29 cases in the low expression groExpression[Expression[up-expression]-expression] and 12 cases in the high expression groExpression[Expression[up-expression]-expression]. As presented in Fig. 3, the incidence of cardiovascular disease was significantly higher in the low expression groExpression[Expression[up-expression]-expression] compared with that in the high expression groExpression[Expression[up-expression]-expression] (P<0.05).	Yes	In addition, lncRNA-SRA overexpression significantly increased the viability of VSMCs compared with the untransfected control cells and negative control-transfected cells in the presence of D-glucose, but not in the absence of glucose (P<0.05; Fig. 5B).	30988713
lncRNASNHG1	LncRNA	Mus musculus	Breast Neoplasms	cell lines	Expression [highly expressed]	qRT-PCR//FISH	Here we reported that lncRNA SNHG1 functioned as a modulator of M2 macrophage polarization and regulated tumor growth and angiogenesis. We indicated that knockdown of SNHG1 inhibited M2 macrophage polarization by suppression of STAT6 phosphorylation.		Yes	We indicated that knockdown of SNHG1 inhibited M2 macrophage polarization by suppression of STAT6 phosphorylation.	34618681
lncRNASLC26A4‐AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cells	Regulation( ETS1 to promote ITPR1‐mediated autophagy)	qRT-PCR//RIP//Luciferase Report Assay//IHC//ChIP	Then, Western blot and RT‐qPCR were conducted to determine the expression of ITPR1 and SLC26A4‐AS1 in PTC tissues and cells, both of which were found to be poorly expressed in PTC tissues and cells.  In conclusion, our study elucidated that SLC26A4‐AS1 overexpression promoted ITPR1 expression through recruiting ETS1 and thereby promotes autophagy, alleviating PTC progression.		Yes	Then, we constructed ITPR1‐overexpressing cells and revealed that ITPR1 overexpression could trigger the autophagy of PTC cells. Further, we performed a series of gain‐ and loss‐of function experiments. The results suggested that silencing of SLC26A4‐AS1 led to declined ITPR1 level, up‐regulation of ETS1 promoted ITPR1 expression, and either ETS1 knockdown or autophagy inhibitor Bafilomycin A1 could mitigate the promoting effects of SLC26A4‐AS1 overexpression on PTC cell autophagy. In vivo experiments also revealed that SLC26A4‐AS1 overexpression suppressed PTC tumour growth.	34378314
LncRNA-ROR	LncRNA	Homo sapiens	Osteosarcoma	Fifty-one patients with the first diagnosis of osteosarcoma 	Interaction(microRNA-185-3p/YAP1 axis)	qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	Up-regulated lncRNA-ROR and YAP1 and down-regulated miR-185-3p were found in osteosarcoma. Function of lncRNA ROR was rescued by miR-185-3p and regulated the growth and metastasis of osteosarcoma cells via modulating YAP1, the target gene of miR-185-3p.		Yes	LncRNA ROR knockdown or miR-185-3p overexpression inhibited osteosarcoma cell progression while lncRNA ROR elevation or miR-185-3p inhibition presented the opposite effects.	32898639
lncRNARAMS11	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissue samples	Interaction(CBX4/Top2α axis)	Western Blot//qRT-PCR//RIP//Microarray//Transwell Assay	The expression of lncRNA RAMS11 was up-regulated in prostate cancer tissue samples. We also demonstrated that lncRNA RAMS11 bound to CBX4 to activate expression of Top2α. 		Yes	 LncRNA RAMS11 promoted cell growth and metastasis of prostate cancer cells. Down-regulation of lncRNA RAMS11 attenuated cell growth and metastasis of prostate cancer cells.	33564266
LncRNA-PVT1	LncRNA	Homo sapiens	Glioma	glioma patients	Interaction(miR-1207-3p/HNF1B signaling axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Microarray//Cell Proliferation Assay//IHC//Transwell Assay	 Our data showed that the expression of lncRNA-PVT1 was increased obviously and associated with advanced tumor stage, metastasis, invasion ability, and poor prognosis in glioma patients.Online software (TargetScan, miRDB and miR TarBase) were used to predict the regulating mechanisms of lncRNA-PVT1, miR-1207-3p and HNF1B, which were validated by dual-luciferase reporter gene system.  Therefore, we suggested that lncRNA-PVT1/miR-1207-3p/HNF1B axis might play critical roles in glioma progression, indicating that lncRNA-PVT1/miR-1207-3p/HNF1B signaling axis may serve as novel molecular targets for glioma prevention and treatment.	 Our data showed that the expression of lncRNA-PVT1 was increased obviously and associated with advanced tumor stage, metastasis, invasion ability, and poor prognosis in glioma patients.	Yes	 Up-regulation of lncRNA-PVT1 was observed to promote glioma cells proliferation, and invasion abilities in vitro as well as tumor growth in vivo by regulating miR-1207-3p expression. In vivo tumor-bearing mice models were established to validate the cellular results. 	34475987
lncRNA-PACER	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(COX-2)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qPCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	RT-qPCR analysis revealed that PACER was highly expressed in CRC tissues and cells, and a high PACER-expression level was associated with poor prognosis. RT-qPCR showed that PACER increased mRNA levels of COX-2. Luciferase assay revealed that PACER modulated the COX-2 promoter region. Mouse xenograft models of CRC revealed that PACER promoted colorectal tumorigenesis in vivo. ELISA revealed that PACER knock-down inhibited PGE2 production.	RT-qPCR analysis revealed that PACER was highly expressed in CRC tissues and cells, and a high PACER-expression level was associated with poor prognosis. 	Yes	MTT assay, wound-healing assay, colony-formation assay, and transwell assay revealed that PACER enhanced CRC-cell proliferation, invasion, and metastasis in vitro. 	34316376
LncRNA-p21	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell line 	Interaction(miR-514b-3p/ARHGEF9 pathway)	Luciferase Report Assay//Bioinformatics Analysis	 LncRNA-p21 overexpression in GC cell line somatic gastric cancer (SGC)-7901 and human gastric cancer (HGC)-27 suppressed cell proliferation and enhanced apoptosis, while lncRNA-p21 knockdown caused the opposite effects. Our study reveals a novel lncRNA-p21/miR-514b-3p/ARHGEF9 pathway that can be targeted for GC therapy.		Yes	 LncRNA-p21 overexpression in GC cell line somatic gastric cancer (SGC)-7901 and human gastric cancer (HGC)-27 suppressed cell proliferation and enhanced apoptosis, while lncRNA-p21 knockdown caused the opposite effects. 	35947460
LncRNA-MSC-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	Interaction(miR-425-5p)	qRT-PCR//MTT//Luciferase Report Assay//Tunel	MSC-AS1 expression level was lowly expressed, while miR-425-5p level was highly in ovarian cancer tissues and cells. Moreover, MSC-AS1 targeted and negatively modulated miR-425-5p. MiR-425-5p up-regulation has been proved to partially reverse the tumor suppressive function of MSC-AS1 overexpression 		Yes	Elevation of MSC-AS1 has the ability to significantly inhibit cell proliferation and facilitate cell apoptosis in SKOV3 and A2780 cells. 	34454554
LncRNAMORT	LncRNA	Mus musculus	Myocardial Infarction	 plasma and heart tissues 	regulation[downregulating miR-93]	qRT-PCR	In the present study we found that MORT expression levels were higher, while expression levels of miR-93 were lower in both plasma and heart tissues of mice MI mice models compared with Sham mice.  Therefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.		Yes	 MORT overexpression promoted cardiomyocyte apoptosis, while miR-93 overexpression played and opposite role and attenuated the effects of MORT overexpression.	32450811
LncRNA-KAT7	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-10a)	Cell Proliferation Assay//qRT-PCR//Transfection	The results showed that KAT7 was downregulated in NSCLC and predicted poor survival. KAT7 negatively correlated with miR-10a in NSCLC. In NSCLC cells, overexpression of KAT7 led to downregulated miR-10a, whereas silencing of KAT7 led to upregulated miR-10a. Methylation-specific polymerase chain reaction revealed that KAT7 positively regulated the methylation of miR-10a.	The results showed that KAT7 was downregulated in NSCLC and predicted poor survival. 	Yes	Cell proliferation assay showed that overexpression of miR-10a led to increased proliferation rate of NSCLC cells. In addition, overexpression of KAT7 played an opposite role and reduced the effects of the overexpression of miR-10a. 	32423237
LncRNA-IMAT1	LncRNA	Homo sapiens	Meningioma	meningioma cell	Interaction(KLF4/hsa-miR22-3p/Snai1 Pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay	Our studies indicated that IMAT1 was highly expressed in invasive meningiomas compared with non-invasive meningiomas.  In vitro studies showed that IMAT1 promoted meningioma cell invasion through the inactivation of the Krüppel-like factor 4 (KLF4)/hsa-miR22-3p/Snai1 pathway by acting as a sponge for hsa-miR22-3p, and IMAT1 knockdown effectively restored the tumor suppressive properties of KLF4 by preserving its tumor suppressor pathway. 		Yes	 In vitro studies showed that IMAT1 promoted meningioma cell invasion through the inactivation of the Krüppel-like factor 4 (KLF4)/hsa-miR22-3p/Snai1 pathway by acting as a sponge for hsa-miR22-3p, and IMAT1 knockdown effectively restored the tumor suppressive properties of KLF4 by preserving its tumor suppressor pathway.  In vivo experiments confirmed that IMAT1 silencing could significantly inhibit the growth of subcutaneous tumors and prolong the survival period of tumor-bearing mice. 	35680373
LncRNA-HCG18	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction(miR-106a-5p/PPP2R2A)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 It was found that HCG18 was down-regulated in PTC.HCG18 interacted with miR-106a-5p, the expression of which was upregulated in PTC. Upregulating miR-106a-5p expression by lentivirus infection promoted viability, migration and invasion and inhibited apoptosis of PTC cells, reversed the effect of HCG18 on the biological behaviors of PTC cells, and promoted the expressions of MMP-2, MMP-9, E-cadherin, and Vimentin and downregulated E-cadherin expression in PTC cells. PPP2R2A, a direct target of miR-106a-5p, was downregulated in PTC, and HCG18 promoted PPP2R2A expression in PTC cells by sponging miR-106a-5p. 		Yes	 Overexpressing HCG18 suppressed viability, migration, and invasion, promoted apoptosis, and inhibited miR-106a-5p expression in PTC cells.	33798913
LncRNA-HAGLR	LncRNA	Homo sapiens	Breast Neoplasms	 TNBC tissues and cell lines	Interaction(miR-335-3p/WNT2 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	HAGLR was increased in TNBC tissues and cell lines. Furthermore, HAGLR acted as a sponge of miR-335-3p and inhibited its expression. And miR-335-3p directly targeted WNT2. 		Yes	Silencing of HAGLR inhibited viability, proliferation, migration, and invasion of BT549 cells. Functionally, forced expression of miR-335-3p or knockdown of WNT2 removed the promoted effects of lncRNA HAGLR on TNBC development. In vivo tumorigenesis experiments indicated HAGLR accelerated tumor growth via miR-335-3p/WNT2 axis.	34375306
LncRNA-H19	LncRNA	Homo sapiens	Glioma	 U251 and U87-MG cells	Regulation	In Vivo Experiment//Wound Healing Assay//Migration Assay//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Transwell Assay	 Knocking down lncRNA-H19 gene could effectively suppress the proliferation of U251 and U87-MG cells. The knockdown of lncRNA-H19 remarkably inhibited the migration and blocked cycle progressions of U251 and U87-MG cells, yet, no obvious changes were observed in cell apoptosis. Besides, inhibiting lncRNA-H19 expression could attenuate sphere-forming function of U251 and U87-MG cells. 		Yes	Knocking down lncRNA-H19 gene could effectively suppress the proliferation of U251 and U87-MG cells. The knockdown of lncRNA-H19 remarkably inhibited the migration and blocked cycle progressions of U251 and U87-MG cells.	34477331
lncRNA-FTX	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cell lines	Interaction(miR-513b-5p)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//Cell Cycle Assay//Invasion Assay	The expression levels of FTX were increased in PC cell lines, and silencing of FTX remarkably suppressed the invasion ability and cell viability. Besides, FTX could bind to miR-513b-5p as a competitive endogenous RNA, thus promoting the invasion and proliferation ability of PC cells.		Yes	silencing of FTX remarkably suppressed the invasion ability and cell viability. Moreover, knockdown of FTX inhibited the tumor growth and increased the expression levels of miR-513b-5p and apoptosis-related proteins in vivo.	33736615
lnc-PKD2-2-3	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues, CCA cell lines	Interaction(Lnc-PKD2-2-3/miR-328/GPAM )	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	 Lnc-PKD2-2-3 and GPAM were higher, whereas miR-328 was lower in CCA tissues versus adjacent tissues and also in CCA cell lines versus control cells; meanwhile, they were correlated with each other (all P <0.05). MiR-328 knockdown induced CCA cell proliferation and invasion and also attenuated the effect of lnc-PKD2-2-3-knockdown in these functions (all P <0.05). Subsequently, GPAM knockdown reduced CCA cell proliferation and invasion and also weakened the effect of miR-328-knockdown in these functions (all P <0.05). Additionally, lnc-PKD2-2-3 positively regulated GPAM while negatively regulating miR-328. MiR-328 negatively modified GPAM in CCA cells. Luciferase gene reporter assays verified that lnc-PKD2-2-3 directly bound miR-328 and miR-328 directly bound GPAM. Finally, the lnc-PKD2-2-3/miR-328/GPAM network also regulated the 5-FU chemosensitivity of CCA cells.		Yes	 Lnc-PKD2-2-3 knockdown decreased CCA cell proliferation, invasion, and increased apoptosis (all P <0.05), but lnc-PKD2-2-3 overexpression exhibited the opposite and weaker effect. In vivo experiments further revealed that lnc-PKD2-2-3 overexpression promoted tumor volume and weight but repressed tumor apoptosis in xenograft mice; meanwhile, it increased GPAM expression but decreased miR-328 expression (all P <0.05). Conversely, lnc-PKD2-2-3 knockdown exhibited the opposite effects (all P <0.05).	35965521
lncPENG	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	interaction[PDZK1,miR-15b]	RNA Pull-Down//Western Blot//ISH//CCK8//qRT-PCR//FISH//RIP//Colony Formation Assay	Conversely, a novel lncRNA (lncPENG) was expressed at a lower level in ccRCC tissues, and its downregulation was associated with the same effects as upregulation of miR-15b.Thus, lncPENG may function as a ceRNA to attenuate miR-15b-dependent PDZK1 downregulation and inhibit cell proliferation, suggesting that it may be clinically valuable as a therapeutic target and a prognostic biomarker of ccRCC.		Yes	Downregulation of miR-15b and upregulation of lncPENG resulted in a significant increase in PDZK1 level and inhibition of proliferation in vitro and in vivo.	32341409
lnc-PCIR	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TCGA(One hundred and ten paired TNBC and neighboring noncancerous tissues)	Interaction(TAB3 and PABPC4)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Invasion Assay	 Here, we report a lncRNA RP11-214F16.8, which renamed Lnc-PCIR, is upregulated and higher RNA level of Lnc-PCIR was positively correlated to the poor survival of patients with triple negative breast cancer (TNBC) tissues. Mechanistically, higher Lnc-PCIR level of blocks PABPC4 proteasome-dependent ubiquitination degradation; stable and highly expressed PABPC4 can further increase the stability of TAB3 Mrna.	 Here, we report a lncRNA RP11-214F16.8, which renamed Lnc-PCIR, is upregulated and higher RNA level of Lnc-PCIR was positively correlated to the poor survival of patients with triple negative breast cancer (TNBC) tissues. 	Yes	 Lnc-PCIR overexpression significantly promoted cell proliferation, migration, and invasion in vitro and in vivo.	34012913
LNCOC1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues 	regulation[Lnc-OC1/miR-34a/PD-L1 axis ]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay	Our results suggested that Lnc-OC1 was significantly upregulated in EC tissues comparing with normal tissues.Concisely, our results proved that Lnc-OC1/miR-34a/PD-L1 axis might serve as a therapeutic target of EC.		Yes	Moreover, knockdown of Lnc-OC1 leaded to an inhibition of cell viability and a raise of cell apoptosis.	32748220
lnc-IUR	LncRNA	Homo sapiens	pancreatic adenocarcinoma	PAAD tissue 	Interaction(miR-34a/CD44 Signaling Pathway )	qRT-PCR//Western Blot	The results demonstrated that IUR was downregulated in PAAD tissue compared with adjacent non-tumor tissue samples and that low expression levels of IUR correlated with poor survival in patients with PAAD. In PAAD tissue samples, the expression of IUR positively correlated with miR-34a expression but negatively correlated with CD44 expression, which is a target of miR-34a. 	The results demonstrated that IUR was downregulated in PAAD tissue compared with adjacent non-tumor tissue samples and that low expression levels of IUR correlated with poor survival in patients with PAAD. 	Yes	In PAAD cells, overexpression of IUR resulted in miR-34a upregulation and CD44 downregulation. miR-34a overexpression did not affect the expression of IUR but downregulated CD44. In PAAD cells, overexpression of IUR and miR-34a led to decreased invasive and migratory abilities. However, CD44 overexpression played an opposite role and attenuated the effects of IUR and miR-34a overexpression.	34113395
lncINS-IGF2	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues	Expression[highly expressed]	Wound Healing Assay//CCK8//qRT-PCR//Microarray//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	Among the dysregulated long noncoding RNAs, we identified INS-IGF2 readthrough, transcript variant 1, noncoding RNA (NR_003512.3) is upregulated in non-small-cell lung cancer tissues, the cis gene of which is insulin-like growth factor 2 gene hinted by bioinformatics analysis. 		Yes	 Furthermore, INS-IGF2 readthrough, transcript variant 1, noncoding RNA downregulation suppresses non-small-cell lung cancer cell proliferation and migration. 	30803359
LncIHAT	LncRNA	Homo sapiens	Breast Neoplasms		interaction[HIF1]	qRT-PCR	 Hypoxia-inducible factor 1 (HIF1) but not HIF2 bound to the hypoxia response element at the promoter of lncIHAT to activate its transcription in hypoxic TNBC cells.This study systematically identified hypoxia-induced lncRNA transcriptome in TNBC and sheds light on multiple layers of regulatory mechanisms of gene expression under hypoxia.		Yes	LncIHAT promoted TNBC cell survival in vitro and tumor growth and lung metastasis in mice.	33380467
lncHUPC1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa cells and 70 PCa cases	Interaction( miR-133b/SDCCAG3)	In Vivo Experiment//Western Blot//qPCR//CCK8//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//ChIP	 Using q-PCR, lncHUPC1 and SDCCAG3 were found to be up-regulated in PCa cells, while miR-133b was down-regulated.  The same results were found in tissue samples from 70 PCa cases.In conclusion, the ceRNA network of lncHUPC1/miR-133b/SDCCAG3 affected the growth and apoptosis of PCa cells, and FOXA1 may be involved in the process as a transcription factor of lncHUPC1.		Yes	 It was confirmed that the knockdown of lncHUPC1 increased the expression of miR-133b and decreased that of SDCCAG3, which further increased apoptosis and inhibited cell growth, while the miR-133b inhibitor partially reversed these effects. After transfection with miR-133b mimic after lncHUPC1-knockdown, the expression of miR-133b increased while that of SDCCAG3 reduced, and the apoptosis of the cells was more obvious and the growth of the cells was slower.	35812058
lnc-HSD17B11-1:1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC primary tissues	regulation[lnc-HSD17B11-1:1/miR-338-3p/MACC1 axis]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Evidently up-regulation of lnc-HSD17B11-1:1 in CRC primary tissues was correlated with the depth of invasion (p = 0.043), clinical stage (p = 0.027), distant metastasis (p = 0.003) and poor prognosis of patients with CRC.These findings suggest that lnc-HSD17B11-1:1 promotes CRC progression through lnc-HSD17B11-1:1/miR-338-3p/MACC1 axis and this might serve as a new diagnostic marker or target for treatment of CRC.	Evidently up-regulation of lnc-HSD17B11-1:1 in CRC primary tissues was correlated with the depth of invasion (p = 0.043), clinical stage (p = 0.027), distant metastasis (p = 0.003) and poor prognosis of patients with CRC.	Yes	lnc-HSD17B11-1:1 promoted CRC cell proliferation, mobility and invasion in vitro and in vivo.	32595704
lnc-HLX-2-7	LncRNA	Homo sapiens	Medulloblastoma	MB cell line	Expression(highly expressed)	In Vivo Experiment//qRT-PCR//Colony Formation Assay//EdU Staining	Lnc-HLX-2-7 is highly upregulated in Group 3 MB cell lines, patient-derived xenografts, and primary MBs compared with other MB subgroups as assessed by quantitative real-time, RNA-seq, and RNA fluorescence in situ hybridization. Depletion of lnc-HLX-2-7 significantly reduced cell proliferation and 3D colony formation and induced apoptosis. Lnc-HLX-2-7-deleted cells injected into mouse cerebellums produced smaller tumors than those derived from parental cells. Pathway analysis revealed that lnc-HLX-2-7 modulated oxidative phosphorylation, mitochondrial dysfunction, and sirtuin signaling pathways. The MYC oncogene regulated lnc-HLX-2-7, and the small-molecule bromodomain and extraterminal domain family‒bromodomain 4 inhibitor Jun Qi 1 (JQ1) reduced lnc-HLX-2-7 expression.		Yes	 Depletion of lnc-HLX-2-7 significantly reduced cell proliferation and 3D colony formation and induced apoptosis.	33844835
LNC-HCG11	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-224-3p/c-caspase-3 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	 Lnc-HCG11 was significantly reduced in NSCLC.Lnc-HCG11 could inhibit the progression of NSCLC by modulating the miR-224-3p/caspase-3 axis, and Lnc-HCG11 may be a potential therapeutic target for NSCLC.		Yes	Lnc-HCG11 significantly inhibited cell proliferation of NSCLC cells and induced apoptosis. 	32694917
LNC-HC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatic tumors	regulation[Sequestering hsa-miR-183-5p]	qRT-PCR//Wound Healing Assay//MTT	 In this study, we identified a novel human lncRNA, LNC-HC, with significantly reduced levels in hepatic tumors from patients with HCC.Overall, human LNC-HC was identified as a novel tumor suppressor that could inhibit HCC cell proliferation in vitro and suppress tumor growth in vivo by competitively binding hsa-miR-183-5p as a competing endogenous RNA (ceRNA). 		Yes	Xenograft transplantation of LNC-HC-overexpressing Huh7 cells in nude mice resulted in the production of smaller tumors. 	32278306
lnc-H2AFV-1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues and cells	Regulation(m6A methylases METTL3/14 and FTO)	CCK8//qRT-PCR	The present study evaluated the expression of lnc-H2AFV-1 in HNSCC tissues using quantitative real-time PCR (qPCR) and associated abundant lnc-H2AFV-1 expression with tumor size. Thus, our findings suggested that lnc-H2AFV-1 might be a biomarker that alters m6A modification by regulating the m6A methylases METTL3/14 and FTO and then mediating the downstream target IFT80 to promote HNSCC progression.		Yes	Functionally, lnc-H2AFV-1 significantly promoted the proliferation of HNSCC cells in vitro and in vivo. 	35403343
lnc-GNAT1-1	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues, cell lines	regulation[inhibiting EMT]	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	Downregulation of lnc-GNAT1-1 was observed in cancerous tissues from patients with liver cancer and in liver cancer cell lines, and low expression levels of lnc-GNAT1-1 were related to advanced TNM stage. Mechanistic experiments revealed that lnc-GNAT1-1 exerted anti-tumor effects in liver cancer cells by inhibiting EMT.	Downregulation of lnc-GNAT1-1 was observed in cancerous tissues from patients with liver cancer and in liver cancer cell lines, and low expression levels of lnc-GNAT1-1 were related to advanced TNM stage. 	Yes	Lnc-GNAT1-1 knockdown promoted invasion, migration, and proliferation of liver cancer cells and inhibited apoptosis, while lnc-GNAT1-1 upregulation exerted the opposite effects. 	33193591
lnc-GLRX3	LncRNA	Homo sapiens	Atherosclerosis	carotid plaque 	Regulation	RNA Pull-Down//Transfection//RIP//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	Next, lncRNA_FGF7-5 and lncRNA_GLRX3 targeted miR-2681-5p directly to upregulate ERCC4 expression.Taken together, these findings indicated that lncRNA_FGF7-5 and lncRNA_GLRX3 together reduced atherosclerosis-induced apoptosis of HUVECs via targeting miR-2681-5p to increase ERCC4 expression, thereby preventing the formation of carotid plaque and finally inhibiting atherosclerosis progression.		Yes	Silencing of lncRNA_FGF7-5 and lncRNA_GLRX3 promoted apoptosis and TP53 expression in HUVECs treated with ox-LDL; however, these effects were reversed by ERCC4-overexpression. 	36071684
lncGHET1	LncRNA	Homo sapiens	Osteosarcoma	OS cell lines	regulation[Wnt/β-catenin signaling pathway]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	lncGHET1 expression was significantly upregulated in OS cell lines compared with in an osteoblastic cell line according to the RT?qPCR assay. The results of a knockdown functional experiment suggested that inhibition of lncGHET1 attenuated cell proliferation, migration, invasion and epithelial‑to‑mesenchymal transition, and promoted apoptosis, partly through regulating the Wnt/β‑catenin signaling pathway in OS.		Yes	The results of a knockdown functional experiment suggested that inhibition of lncGHET1 attenuated cell proliferation, migration, invasion and epithelial?to?mesenchymal transition, and promoted apoptosis, partly through regulating the Wnt/β?catenin signaling pathway in OS.	32319657
lnc-GAN1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	HCC tissues	Interaction(miR-26a-5p/PTEN)	Western Blot//Co-IP//Colony Formation Assay//qRT-PCR//Luciferase Report Assay//IHC//ChIP	lnc-GAN1 is downregulated in HCC tissues and associated with larger tumor size and poor overall survival and disease-free survival.  Mechanistically, lnc-GAN1 acts as a sponge for miR-26a-5p by two seed sequences, and the two non-coding RNAs have a negative relationship in NSCLC tissues; we further prove that PTEN is a direct target of miR-26a-5p and lnc-GAN1 inhibits cell cycle signaling pathway by activating PTEN, whose expression level correlated negatively with miR-26a-5p level but positively with lnc-GAN1 level in NSCLC samples.	lnc-GAN1 is downregulated in HCC tissues and associated with larger tumor size and poor overall survival and disease-free survival	Yes	 its ectopic expression suppresses cell proliferation, colony formation, and cell cycle progression and induces apoptosis in NSCLC cells; it also inhibits tumor growth in the NSCLC xenograft model. 	33407724
lnc-FoxD2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR‑4306)	CCK8//qRT-PCR//Western Blot	Compared with normal samples and cells, FoxD2‑AS1 expression was increased and miR‑4306 expression was decreased in CRC tissues and cells. Furthermore, investigations into the underling mechanism revealed that FoxD2‑AS1 functioned as a molecular sponge of miR‑4306.		Yes	 Functional experiments demonstrated that silencing FoxD2‑AS1 inhibited proliferation and induced cell arrest at G0/G1 phase in CRC cells, while the overexpression of FoxD2‑AS1 showed opposite results. Ki‑67 and proliferating cell nuclear antigen expression levels were decreased after transfection with small interfering RNA FoxD2‑AS1, but were increased after transfection with FoxD2‑AS1 overexpression plasmid. 	34396433
lncFGD5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	30 gastric cancer patients' cancer tissue and para-cancer tissue	Interaction(miR-196a-5p/SMAD6/BMP axis )	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Bioinformatics Analysis	 LncFGD5-AS1 served as a ceRNA of miR-196a-5p to release its inhibition on SMAD6, a conventional inhibitor on the BMP pathway. 		Yes	Comparing with normal gastric cancer cells, FGD5-AS1 overexpressed group had fewer migration cells, lower cell viability, and lower EMT transformation rate. Meanwhile, xenografts nude mice injecting with overexpressed-FGD5-AS1 cells also shown smaller tumor weight and volume.	33892661
lncDQ	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction（EZH2）	qRT-PCR	 LncDQ was upregulated in both HCC tissue samples and serum and was correlated with low survival rate and adverse clinical pathological characteristics. Mechanistically, LncDQ regulated the epithelial-mesenchymal transition pathway by interacting with EZH2, to epigenetically repress the expression of E-cadherin in HCC cells.	 LncDQ was upregulated in both HCC tissue samples and serum and was correlated with low survival rate and adverse clinical pathological characteristics. Multivariate analysis demonstrated that LncDQ expression was an independent prognostic factor for HCC. The area under the receiver operating characteristic curve was 0.804 with a sensitivity of 0.72 and a specificity of 0.8.	Yes	Knockdown of LncDQ induced inhibition of cell proliferation, migration, and invasion in vitro and in vivo.	29669339
lnc-DILC	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	Interaction[WWP2 and USP11]	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//RIP	 Here, we identified that lnc-DILC levels were dramatically downregulated in ccRCC tissues.In summary, our research revealed a novel mechanism by which lnc-DILC regulates PTEN stability via WWP2 and USP11, and shed light on potential therapeutic strategies by the restoration of lnc-DILC expression in patients with ccRCC.	Loss of lnc-DILC expression was correlated with larger tumor size, advanced tumor grade and lymph node metastasis, and also predicted worse prognosis in patients with ccRCC.	Yes	Functionally, knockdown and overexpression experiments demonstrated that lnc-DILC inhibited cell proliferation, migration and invasion in ccRCC cells. 	31592114
lnc-DILC	LncRNA	Homo sapiens	gallbladder carcinoma	GBC tissues,cell lines	Regulation[Wnt/β-catenin signaling]	Western Blot//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//migration assay//Luciferase Report Assay//cell invasion assay	 Herein, we show that lnc-DILC is upregulated in gallbladder CSCs and GBC patients' tissues. In conclusion, lnc-DILC drives gallbladder CSCs self-renewal, tumorigenicity, proliferation and metastasis by activating Wnt/β-catenin signaling, and may therefore prove to be a potential therapeutic target for GBC patients.		Yes	Knockdown of lnc-DILC attenuates the self-renewal, tumorigenicity, proliferation and metastasis of gallbladder CSCs.	30716440
LncDBH-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines and tissue samples	Interaction(miR-155/AXIN1 axis)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	The DBH-AS1 expression was significantly down-regulated in NSCLC cell lines and tissue samples. The mechanism was that DBH-AS1 regulated AXIN1 expression by sponging miR-155 in NSCLC cell lines. Importantly, LncDBH-AS1 might inhibit WNT/β-CATENIN activation in NSCLC cells.		Yes	Decreased DBH-AS1 levels promoted the in vitro proliferation of the NSCLC cells. 	33506901
lnc-KIAA1244-2	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Expression[highly expressed]	qRT-PCR//Microarray	Furthermore, we investigated the function and potential mechanism of a novel highly expressed lncRNA, lnc-KIAA1244-2, and found that its expression is associated with tumor size, N classification and clinical stage.	Furthermore, we investigated the function and potential mechanism of a novel highly expressed lncRNA, lnc-KIAA1244-2, and found that its expression is associated with tumor size, N classification and clinical stage.	Yes	 Knockdown of lnc-KIAA1244-2 inhibited the cell proliferation and inhibited the TNFAIP3 expression in Eca-109 cells.	31235759
LncKLHDC7B	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	tumor tissues	Interaction[RUNX3]	qRT-PCR//Microarray	We discovered that LncKLHDC7B (ENSG00000226738) acts as a transcriptional modulator of its neighboring coding gene KLHDC7B in the immunomodulatory subtype. Furthermore, LncKLHDC7B knockExpression[down-expression] enhanced migration and invasion, and promoted resistance to cellular death. Our findings confirmed the contribution of LncKLHDC7B to induction of apoptosis and inhibition of cell migration and invasion, suggesting that TNBC tumors with enrichment of LncKLHDC7B may exhibit distinct regulatory activity, or that this may be a generalized process in breast cancer. Additionally, in silico analysis confirmed for the first time that the low expression of KLHDC7B and LncKLHDC7B is associated with poor prognosis in patients with breast cancer.		Yes	The knockExpression[down-expression] of LncKLHDC7B was achieved with ~ 75% silencing efficiency (Fig. 4B) and a 50% inhibition of the expression of KLHDC7B gene 	30648789
lncKRT16P6	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues and cell lines	Interaction(miR‑3180/GATAD2A )	In Vivo Experiment//qRT-PCT//Western Blot//CCK8//Flow Cytometry//FISH//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	Through RNA screening, the present study identified a novel long noncoding RNA (lncRNA), keratin 16 pseudogene 6 (lncKRT16P6), which was upregulated in TSCC tissues and cell lines and associated with TSCC tumor stage and differentiation grade. lncKRT16P6 sponged microRNA (miR)‑3180 and upregulated GATA zinc finger domain containing 2A (GATAD2A) expression. miR‑3180 inhibition reversed the lncKRT16P6 depletion‑induced attenuation of TSCC malignancy and GATAD2A depletion reversed the miR‑3180 silencing‑induced enhancement of TSCC malignancy. 	Through RNA screening, the present study identified a novel long noncoding RNA (lncRNA), keratin 16 pseudogene 6 (lncKRT16P6), which was upregulated in TSCC tissues and cell lines and associated with TSCC tumor stage and differentiation grade.	Yes	 Inhibition of lncKRT16P6 expression reduced TSCC cell migration, invasion and proliferation. 	35904180
LncNAP1L6	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa cells	Interaction(HNRNPC/NAP1L2)	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//MeRIP//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Firstly, RT-qPCR analysis was to detect lncNAP1L6 expression and suggested that lncNAP1L6 was markedly upregulated in PCa cells. It turned out that METTL14/METTL3 complex mediated m6A methylation of NAP1L2 mRNA. Besides, lncNAP1L6 recruited HNRNPC to m6A-modified NAP1L2, leading to stabilization of NAP1L2 mRNA. Moreover, NAP1L6 interacted with YY1 to promote the transcription of MMP2 and MMP9 and activate MMP signaling pathway. 		Yes	Functional assays manifested that silencing of lncNAP1L6 hampered cell migration, invasion, and epithelial-mesenchymal transition (EMT) while overexpression of lncNAP1L6 exacerbated cell migration, invasion and EMT. 	36195720
LNCOC1	LncRNA	Homo sapiens	Melanoma	 65 melanoma patients	Interaction(miR-124)	qRT-PCR//Transwell Assay	 LNCOC1 was accumulated to high levels in melanoma, and it was significantly correlated with the low survival rate of melanoma patients. Our bioinformatics data showed that miR-124 could target LNCOC1. Overexpression of miR-124 could downregulate LNCOC1. However, up-regulated the expression of LNCOC1 did not affect the expression of miR-124. 	LNCOC1 was accumulated to high levels in melanoma, and it was significantly correlated with the low survival rate of melanoma patients.	Yes	However, overexpression of LNCOC1 promoted melanoma cell invasion and migration.	35502349
LncNORAD	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[CXCR4 and RhoA/ROCK signaling pathway]	CCK8//qRT-PCR//Western Blot	NORAD has elevated the levels in NSCLC tissues and cells. This study revealed that the downregulation of lncRNA NORAD could slow down the progression of NSCLC by regulating CXCR4 and RhoA/ROCK signaling pathway.		Yes	 NORAD interference dramatically inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion by downregulating CXCR4 and CXCL12 expression.	32495879
lncNNT-AS1	LncRNA	Homo sapiens	Glioma	cell lines 	regulation[miR-494-3p/PRMT1 axis]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//BrdU//Transwell Assay	In particular, high levels of NNT-AS1 are observed in glioma cell lines compared to human astrocyte (HA) cells.Collectively, our results indicated that the miR-494-3p-PRMT1 axis is involved the tumor-suppressive effects of NNT-AS1 inhibition, which sheds new light on lncRNA-directed diagnostics and the therapeutics of glioma.		Yes	Furthermore, the inhibition of lnc-NNT-AS1 by siRNA interfere attenuates the cell viability, proliferation, migration and invasion of glioma cell lines.	32420808
lnc-NLC1-C	LncRNA	Homo sapiens	Glioma	U87MG glioma cells	Interaction(miR-383/PRDX-3 axis )	Western Blot//Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Cell Cycle Assay//Invasion Assay	The highest expression levels of lnc-NLC1-C were identified in U87MG glioma cells. Mechanistically, miR-383 could bind to lnc-NLC1-C to regulate PRDX-3 expression and improve its oncogenic effect. Rescue experiments confirmed that the lnc-NLC1-C/miR-383/PRDX-3 axis was involved in the molecular mechanism of glioma progression. 		Yes	 Overexpression of lnc-NLC1-C expression promoted cell proliferation, G1 phase blocking, migration and invasion, while inhibiting apoptosis and autophagy in U87MG cells.	34386062
LNCNEF	LncRNA	Homo sapiens	Osteosarcoma	blood	Interaction[downregulating miRNA-21]	qRT-PCR//Transwell Assay	The present study revealed that plasma lncRNA-NEF was downregulated, while miRNA-21 was Expression[up-expression]regulated in patients with osteosarcoma compared with healthy controls.lncRNA-NEF overexpression mediated the inhibition of miRNA-21 expression in osteosarcoma cell lines, while miRNA-21 overexpression did not significantly affect the expression of lncRNA-NEF. miRNA-21 overexpression partially compensated the inhibitory effects of lncRNA-NEF overexpression on osteosarcoma cell migration and invasion.		Yes	lncRNA-NEF overexpression inhibited, while miRNA-21 overexpression promoted, migration and invasion of osteosarcoma cell lines in vitro. 	31186758
Lnc-NEAT1	LncRNA	Homo sapiens	Hepatic Ischemia/Reperfusion Injury	Human liver cells (HL-7702)	Expression(highly expressed)	Western Blot//Transfection//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//ELISA	Lnc-NEAT1 expression was elevated in the I/R group compared with the normal group. 		Yes	 Cell proliferation was decreased in the NEAT1(+) group compared with the NC(+) group but increased in NEAT1(-) compared with NC(-). The apoptosis rate increased in the NEAT1(+) group compared with the NC(+) group but decreased in NEAT1(-) compared with NC(-). Western blot assay (detection of apoptosis-related proteins) showed similar results. Expression of interleukin-1β, interleukin-6, and tumor necrosis factor-α increased in the NEAT1(+) group compared with NC(+) but decreased in NEAT1(-) compared with NC(-).	33682508
lnc-NEAT1	LncRNA	Mus musculus	Parkinson Disease	 PD mouse models and cell models	Interaction(MiR-212-3p/AXIN1 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA	NEAT1 was upregulated in PD mouse models and cell models. MiR-212-3p was downregulated in PD, and its inhibitor could reverse the suppression effect of NEAT1 knockdown on PD progression. Additionally, AXIN1 was a target of miR-212-3p, and its overexpression could invert the inhibition effect of miR-212-3p mimic on PD progression. 		Yes	 Function experiments confirmed that NEAT1 knockdown could promote the viability, suppress the apoptosis and inflammation of MPP+-stimulated SK-N-SH cells to restrain PD progression. 	33241432
lnc-n339260	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miRNA30e-5p/TP53INP1)	qRT-PCR	 LncRNA n339260 promotes the development of VM, and lncRNA n339260 may enhance Snail expression by decreasing the expression of miRNA30e-5p, thereby reducing TP53INP1 expression. Therefore, a potential lncRNA n339260- miRNA30e-5p- TP53INP1 regulatory axis was associated with HCC progression.	LncRNA n339260 and miRNA30e-5p were found to be associated with VM formation, metastasis and survival time in HCC patients. 	Yes	In vivo experiment showed lncRNA n339260 promoted tumor growth and VM formation.	35802258
lnc-LIFR-AS1	LncRNA	Homo sapiens	stomach carcinoma	GC tissues and cells	Interaction(miR‑4698 /MTUS1)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//cell invasion assay//Bioinformatics Analysis	Decreased lncRNA LIFR‑AS1 expression was observed in GC tissues and cells.  Upregulated miR‑4698 and downregulated MTUS1 were identified in GC tissues and cells. Upregulated miR‑4698 and downregulated MTUS1 were identified in GC tissues and cells. The inhibitory interaction between lncRNA LIFR‑AS1 and miR‑4698 was confirmed. Additionally, MTUS1 was predicted as a target gene of miR‑4698 positively regulated by lncRNA LIFR‑AS1. The MEK/ERK pathway was inhibited by lncRNA LIFR‑AS1 via regulating MTUS1.		Yes	Upregulated lncRNA LIFR‑AS1 inhibited GC cell proliferation, migration and invasion.	33355363
lnc-MTX2-6	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	80 paired ESCC tissues and matched adjacent tissues 	Interaction(miR-574-5p/SMAD4 axis)	Tunel//CCK8//qRT-PCR//RIP//IHC	In this study, we first reported that lncRNA MTX2-6 was significantly downregulated in ESCC tissues and cell lines. Further studies showed that MTX2-6 exerts as a competing endogenous RNA (ceRNA) by binding miR-574-5p and elevates the expression of SMAD4 in ESCC. 	The decreased expression of MTX2-6 is closely related to larger tumor and worse prognosis of ESCC patients.	Yes	Through a series of functional experiments, we detected that overexpressed MTX2-6 inhibited cell proliferation and promoted cell apoptosis of ESCC in vitro and in vivo. 	33869216
lnc-MPEG1-1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cell lines	Interaction(papillary thyroid cancer)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//H&E Staining//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Microarray//Colony Formation Assay//EdU Staining//Transwell Assay	In particular, in vivo and in vitro experiments showed that overexpression of lnc-MPEG1-1:1 in PTC cell lines promoted the proliferation and migration of PTC. lnc-MPEG1-1:1 is overexpressed in the cytoplasm of PTC cells and functionally promotes cellular proliferation and migration and functions as a competitive endogenous RNA (ceRNA) by competitively occupying the shared binding sequences of miR-766-5p. lnc-MPEG1-1:1 knockdown suppressed epithelial-mesenchymal transition by miR-766-5p in PTC cells. 		Yes	lnc-MPEG1-1:1 knockdown suppressed epithelial-mesenchymal transition by miR-766-5p in PTC cells.	35505969
lncMMPA	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor cells 	Interaction(miR-548)	qRT-PCR	Mechanistically, lncMMPA not only could polarize M2 macrophage, but also could act as an microRNA sponge to interact with miR-548 s and increase the mRNA level of ALDH1A3, then further promote glucose metabolism and cell proliferation in HCC. Moreover, lncMMPA increased HCC cell multiplication through interacting with miR-548 s in vivo. Clinically, lncMMPA expression associates with glycolysis in TAMs and reduced survival of HCC patients.		Yes	Mechanistically, lncMMPA not only could polarize M2 macrophage, but also could act as an microRNA sponge to interact with miR-548 s and increase the mRNA level of ALDH1A3, then further promote glucose metabolism and cell proliferation in HCC. Moreover, lncMMPA increased HCC cell multiplication through interacting with miR-548 s in vivo. Clinically, lncMMPA expression associates with glycolysis in TAMs and reduced survival of HCC patients.	35986343
lnc-MEG3	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Regulation(SQSTM1)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Transwell Assay	Downregulated lnc-MEG3 expression and upregulated SQSTM1 expression were found in NPC tissues and cells.Overexpression of lnc-MEG3 reduced the expression level of SQSTM1, and SQSTM1 expression was inversely correlated with lnc-MEG3 level in NPC tissues. Besides, overexpression of SQSTM1 reversed the effects of lnc-MEG3 overexpression. 		Yes	 Overexpression of lnc-MEG3 inhibited invasion, migration, and epithelial-mesenchymal transition in NPC cells. 	34704649
Lnc-MAP6-1:3	LncRNA	Homo sapiens	Osteosarcoma	cell lines	regulation[Bax/Bcl-2 and Wnt/β-catenin pathways]	qRT-PCR//Western Blot	 As a result, we were able to find a novel lncRNA Lnc-MAP6-1:3 which is highly expressed in osteosarcoma. For the first time, we have identified that Lnc-MAP6-1:3 potentially influence the malignant behavior of osteosarcoma via Bax/Bcl-2 and Wnt/β-catenin signaling pathways.		Yes	Using a set of approaches including gene knockdown, RT-PCR, oncogenic function assay and western blotting, we observed that knockdown of Lnc-MAP6-1:3 expression suppressed cell proliferation and colony formation, and promoted apoptosis in vitro.	32922188
lnc-MAP3K13-7:1	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	granulosa cell	regulation[CDKN1A/p21 expression]	Western Blot//Co-IP//CCK8//qRT-PCR//RIP//Cell Apoptosis Assay//Cell Cycle Assay//IF	We observed that lnc-MAP3K13-7:1 was highly expressed in GCs from patients with PCOS.Our work uncovered a novel and essential mechanism through which lnc-MAP3K13-7:1-dependent DNMT1 inhibition regulates CDKN1A/p21 expression and inhibits GC proliferation.		Yes	In KGN cells, lnc-MAP3K13-7:1 overexpression resulted in cell cycle arrest in the G0/G1 phase, as well as the molecular inhibition and genetic silencing of DNMT1.	33212300
lnc-LOC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients	Expression [highly expressed]	qRT-PCR	LOC101926913 (LOC) was further characterized because it is the most highly differentially expressed amongst those that are associated with the most number of clinical features (tumor-stage, vascular and tumor invasion and poorer overall survival). Experimental gain- and loss-of-function manipulation of LOC in liver cell-lines highlight LOC as a potential onco-lncRNA promoting cell proliferation, anchorage independent growth and invasion. 		Yes	Experimental gain- and loss-of-function manipulation of LOC in liver cell-lines highlight LOC as a potential onco-lncRNA promoting cell proliferation, anchorage independent growth and invasion. 	33976720
LPAL2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 hepatocellular carcinoma (HCC) tissues	Interaction(MMP9 )	qRT-PCR	 In the current study, we found that the pseudogene-derived lncRNA LPAL2 is downregulated in hepatocellular carcinoma (HCC) tissues, and further showed that elevated LPAL2 expression is positively correlated with survival outcome.  Metalloproteinase 9 (MMP9) was identified as an LPAL2-regulated target gene, consistent with clinical findings that LPAL2 expression is significantly associated with MMP9 expression. Furthermore, patients with a higher expression of LPAL2 and lower expression of MMP9 (LPAL2-high/MMP9-low) had a higher survival rate than those with other combinations.	 In the current study, we found that the pseudogene-derived lncRNA LPAL2 is downregulated in hepatocellular carcinoma (HCC) tissues, and further showed that elevated LPAL2 expression is positively correlated with survival outcome. 	Yes	 The knockdown of LPAL2 in hepatoma cells induced tumor formation, migration, invasion, sphere formation, and drug resistance. 	36010685
circCDK17	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cells	Interaction(circCDK17/miR-122-5p/ASF1B axis )	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	CircCDK17 and anti-silencing function 1B histone chaperone (ASF1B) were highly expressed in CC tissues and cells. MiR-122-5p was a target of circCDK17. Silencing circCDK17 inhibited the malignant behaviors of CC cells by releasing miR-122-5p. Moreover, ASF1B was a target of miR-122-5p. Overexpression of ASF1B partially restored the inhibitory effects of circCDK17 silencing on cell proliferation, migration and invasion.		Yes	Silencing circCDK17 reduced the proliferation, migration and invasion of CC cells. Animal experiments confirmed the anti-tumor effect of circCDK17 knockdown in vivo.	36178207
circACAP2	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells,  clinical cervical cancer samples	Interaction(miR-193a-5p/GPX4)	RNA Pull-Down//Western Blot//Transfection//CCK8//Luciferase Report Assay	 The circACAP2 served as a ceRNA of miR-193a-5p and directly interacted with miR-193a-5p in cervical cancer cells. miR-193a-5p was able to target GPX4 and circACAP2 promoted GPX4 expression by sponging miR-193a-5p in cervical cancer cells.  Clinically, the expression of circACAP2 and GPX4 was upregulated, and miR-193a-5p expression was downregulated in clinical cervical cancer samples. The expression of miR-193a-5p was negatively correlated with circACAP2 and GPX4, while the circACAP2 expression was positively correlated with GPX4 in the samples. 		Yes	The cervical cancer cell viability was inhibited by circACAP2 knockdown as well. The levels of lipid ROS, iron, and Fe2+ were reduced by circACAP2 depletion in cervical cancer cells.  The knockdown of circACAP2 inhibited the cervical cancer cell viability, but the miR-193a-5p inhibitor or GPX4 overexpression could reverse the effect in the cells. The inhibition of miR-193a-5p or GPX4 overexpression repressed the circACAP2 depletion-induced levels of lipid ROS, iron, and Fe2+ in cervical cancer cells.	35847361
MALAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	cell lines	Interaction[sponging miR‑1‑3p]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In the present study, it was demonstrated that MALAT1 was increased while microRNA (miR/miRNA)‑1‑3p was decreased in prostate cancer cell lines.Dual‑luciferase reporter assay results demonstrated that miR‑1‑3p bound to MALAT1 and coronin 1C (CORO1C) 3' untranslated region, and MALAT1 competed with CORO1C for the binding sites of miR‑1‑3p. MALAT1 inhibited the expression of miR‑1‑3p and vice versa. MALAT1 knockdown induced the decline of CORO1C, which was subsequently recovered by the miR‑1‑3p inhibitor. In addition, by inhibiting miR‑1‑3p or overexpressing CORO1C, the silencing of MALAT1‑induced phenotypic alterations were restored. In conclusion, MALAT1 serving as a degradable miRNA sponge, may sequester miR‑1‑3p from CORO1C and by silencing MALAT1, migration, invasion and epithelial‑mesenchymal transition may be inhibited in prostate cancer cells. MALAT1 and CORO1C may serve as novel clinical therapeutic targets for prostate cancer.		Yes	The silencing of MALAT1 inhibited migration, invasion and epithelial‑mesenchymal transition, when epithelial (E)‑cadherin expression level was increased, and neural (N)‑cadherin, vimentin, Slug and Snail expression levels were decreased. 	31485645
MALAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	 LNCaP cell lines and CWR22Rv1 cell lines	Interaction(miR-145)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//IHC//Invasion Assay	 The expression of MALAT1 was upregulated in both LNCaP cell lines and CWR22Rv1 cell lines (F=2.882, t=13.370, P<0.001; F=2.268, t=15.859, P<0.001).  Using direct binding, MALAT1 suppressed the antitumor function of miR-145, which in turn upregulated transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) via SMAD3 and TGFBR2 (F=2.097, t=5.389, P=0.006; F=1.306, t=4.155, P=0.014).		Yes	Knockdown of MALAT1 reduced the migratory and invasive capabilities of PCa cells (F=0.017, t=12.212, P<0.001; F=10.723, t=6.016, P=0.002). 	34295718
circCCDC66	CircRNA	Homo sapiens	Glioma	12 pairs of glioma samples	Interaction(miR-320a /FOXM1 signaling pathway)	CCK8//Transfection//Luciferase Report Assay//Transwell Assay	The results showed circCCDC66 was overexpressed in glioma and acted as an oncogene.  In mechanism study, circCCDC66 could sponge miR-320a, thereby increasing the expression of FOXM1.		Yes	CircCCDC66 knockdown suppressed the proliferation, migration, and invasion of glioma cells. 	34252882
MALAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cells	Interaction( MYBL2/mTOR Axis)	qRT-PCR//RNA-seq//Colony Formation Assay	 In the present study, our findings revealed that MALAT1 plays a critical part in regulating PCa proliferation and glucose metabolism.  Silencing MALAT1/MYBL2/mTOR axis in PCa cell lines affects their glycolysis and lactate levels, and we verified these findings in mice. 	 Furthermore, we explored the underlying tumorigenesis functions of MYBL2 in PCa and found that high expression of MYBL2 was positively associated with TNM stage, Gleason score, PSA level, and poor survival rate in PCa patients. 	Yes	 Knockdown of MALAT1 affects the protein and mRNA levels of MYBL2. In addition, MALAT1 enhances the phosphorylation level of mTOR pathway by upregulating MYBL2. Knockdown of MALAT1 or MYBL2 in PCa cell lines significantly inhibits their proliferation capacity. 	35557985
MALAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PC cells	Expression(highly expressed)	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	 MALAT1 is highly expressed in PC cells.Overall, data suggest that MALAT1 overexpression in PC helps metastasis and tumorigenesis. Also, MALAT1 knockout can be considered a therapeutic and diagnostic target in PC.		Yes	MALAT1 Knockout in DU-145 cells increases apoptosis and prevents proliferation and migration, and DU-145 transfected cells were unable to migrate based on the scratch recovery test. 	36163080
hsa_circ_0037655	CircRNA	Homo sapiens	Glioma	glioma samples and cells	Interaction(miR-1229-3p/ITGB8 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Upregulation of circ_0037655 was affirmed in glioma samples and cells. miR-1229-3p acted as a target of circ_0037655, and its upregulation was responsible for the function of si-circ_0037655 in glioma cells. miR-1229-3p functioned as a tumor inhibitor in glioma progression by targeting ITGB8.		Yes	Tumor formation and metastasis of glioma were inhibited after circ_0037655 was downregulated. 	34017919
circGLIS3	CircRNA	Homo sapiens	Glioma	28 glioma samples and 5 non-tumor brain tissues	Expression [highly expressed]	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//RIP//RNA-seq//Microarray//IHC//Invasion Assay//IF	We found that upregulation of circGLIS3 promoted glioma cell migration and invasion and showed aggressive characteristics in tumor-bearing mice. Mechanistically, we found that circGLIS3 could promote the Ezrin T567 phosphorylation level.		Yes	CircGLIS3 Enhances Migration and Invasion of Glioma Cells in vitro and in vivo	34540823
circASPH	CircRNA	Homo sapiens	Glioma	GM specimens and cells	Interaction(miR-599/AR/SOCS2-AS1)	RNA Pull-Down//Transfection//Immunoblotting//Wound Healing Assay//CCK8//qRT-PCR//circRNA-seq//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	circ-ASPH levels were upregulated in GM specimens and cells. Mechanistically, circ-ASPH counteracted microRNA (miR)-599-mediated androgen receptor (AR) suppression by acting as a sponge for miR-599. 	The prognostic role of circ-ASPH was identified in patients with GM. 	Yes	Loss/gain of function assays demonstrated that circ-ASPH increased cell proliferation, migration and invasion in GM cells. 	33777211
circPTN	CircRNA	Homo sapiens	Glioma	glioma cells	regulation[circ_PTN/miR-122/SOX6 axis]	qRT-PCR//Luciferase Report Assay//Western Blot	 Circ_PTN was overexpressed in glioma cells, and its knockdown induced cell proliferation inhibition, cell cycle arrest and apoptosis in glioma cells.  In addition, mitogen activated kinase-like protein (MAPK)/ERK pathway was involved in circ_PTN/miR-122/SOX6 axis.		Yes	 Circ_PTN was overexpressed in glioma cells, and its knockdown induced cell proliferation inhibition, cell cycle arrest and apoptosis in glioma cells. 	31609809
hsa_circ_101064	CircRNA	Homo sapiens	Glioma	glioma tissues and glioma cells	regulation[miR-154-5p/ PIWIL1 axis]	CCK8//qRT-PCR//Western Blot//Transwell Assay	The expression level of Circ_101064 was significantly upregulated in glioma tissues compared with control, and was closely associated with tumor grading and diameter. Furthermore, increased Circ_101064 expression was detected in human glioma cell lines.  More importantly, Circ_101064/miR-154-5p/PIWIL1 axis could be a promising therapeutic target for the treatment of this disease.		Yes	In addition, knockdown of Circ_101064 remarkably suppressed cell proliferation, invasion and migration in glioma cells in vitro. 	31941603
MALAT1	LncRNA	Homo sapiens	Thyroid Neoplasms	ATC tissues and cell lines	Interaction[miR-200a-3p/FOXA1]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Results showed that MALAT1 expression was enhanced and miR-200a-3p was reduced in ATC tissues and cells.		Yes	Knockdown of MALAT1 or overexpression of miR-200a-3p inhibited cell proliferation, migration and invasion but increased apoptosis and autophagy formation in ATC cells.	31500506
hsa_circ_0005075	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[SIRT1]	qRT-PCR	Circ_0005075 was significantly up-regulated in glioma tissues and cell lines. Furthermore, it aggravates the malignant progression of glioma by down-regulating SIRT1.	Meanwhile, its expression level was significantly higher in glioma patients with lymphatic metastasis or distant metastasis when compared with those with negative metastasis.	Yes	Knockdown of circ_0005075 decreased the viability, migration, and wound closure percentage of T98-G cells. However, overexpression of circ_0005075 in U87 cells yielded the opposite trends. 	31957839
MALAT1	LncRNA	Homo sapiens	Retinoblastoma	 RB tissues and cell lines	regulation[miR-20b-5p,STAT3]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining	Both RB tissues and cells showed highly expressed MALAT1.  MALAT1 could increase proliferation and reduce apoptosis by sponging miR-20b-5p to upregulate STAT3 in RB cells. 		Yes	When MALAT1 was downregulated, RB cell proliferation was hindered and apoptosis was accelerated.	32336590
MALAT1	LncRNA	Homo sapiens	Retinoblastoma	RB tissues and cells	Interaction(miR-655-3p/ATAD2)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	MALAT1 was upregulated in RB tissues and cells, and it served as a competing endogenous RNA (ceRNA) and inhibited miRNA-655-3p (miR-655-3p) expression, which eventually regulated the expression of miR-655-3p downstream target ATPase Family AAA Domain Containing 2 (ATAD2). The level of ATAD2 significantly increased, while that of miR-655-3p remarkably decreased in RB tissues and cells. 		Yes	MALAT1 depletion inhibited cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT), but promoted apoptosis in vitro and blocked xenograft tumor growth in vivo. MALAT1 exerted its oncogenic functions in RB by regulating miR-655-3p/ATAD2 axis.	34222668
MALAT1	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma cell 	Interaction(miR-124/STX17)	qRT-PCR//Luciferase Report Assay//Western Blot	 In the present study, we investigated the roles of MALAT1 and miR-124 in the regulation of retinoblastoma cell autophagy through evaluating the changes of autophagy-related proteins. Further, we investigated whether Syntaxin 17 (STX17), a Soluble NSF Attachment Protein receptor (SNARE) of the autophagosome, is involved in MALAT1/miR-124 regulation of retinoblastoma cell autophagy, and the underlying mechanism. 		Yes	Through direct targeting miR-124, MALAT1 promotes retinoblastoma cell autophagy. 	29073720
hsa_circ_0037655	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines (U251 and SHG-44)	regulation[ miR-214/PI3K signaling]	CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Transwell Assay	 The circRNA circ_0037655 was highly expressed in both glioma tissues and cell lines (U251 and SHG-44) compared to control. This study identified circRNAs expression profile in gliomas and revealed that circ_0037655 could promote glioma progression by regulating miR-214/PI3K signaling, which may provide new therapeutic approach for gliomas.		Yes	Inhibition of circ_0037655 could suppress the viability and invasion of glioma cells.	32001271
MALAT1	LncRNA	Homo sapiens	Melanoma	melanoma tissue	regulation[Downregulating miR-23a]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Compared with corresponding non-tumor normal tissues, lncRNA MALAT1 in melanoma tissue increased while miR-23a decreased. lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.		Yes	Downregulating lncRNA MALAT1 or upregulating miR-23a inhibited cell proliferation, migration and invasion and promoted apoptosis.	32801893
hsa_circ_0088732	CircRNA	Homo sapiens	Glioma	glioma tissues	regulation[miR-661/RAB3D Axis]	Western Blot//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay	We verified that hsa_circ_0088732 is circular and highly expressed in glioma tissues.We demonstrated that hsa_circ_0088732 facilitated glioma progression by sponging miR-661 to increase RAB3D expression. 		Yes	 Knockdown of hsa_circ_0088732 induced glioma cell apoptosis and inhibited glioma cell migration, invasion, and epithelial-mesenchymal transition (EMT).	32154171
circKIF4A	CircRNA	Homo sapiens	Glioma	glioma cells and tissues	regulation[miR-139-3p/Wnt5a axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 circKIF4A and Wnt5a were up-regulated and miR-139-3p was down-regulated in both glioma cells and tissues.  circKIF4A was overexpressed in glioma, and knockdown of circKIF4A suppressed glioma progression via miR-139-3p/Wnt5a axis. 		Yes	Knockdown of circKIF4A inhibited the colony formation ability, migration and invasion, and promoted the apoptosis of glioma cells by regulating miR-139-3p.	32268875
MALAT1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	tongue cancer tissues,blood	Interaction[downregulating MMP-9]	Western Blot//CCK8//qRT-PCR//Invasion Assay//Transwell Assay	The expression level of MALAT1 was remarkably higher in tumor tissues than that in adjacent healthy tissues. Serum MALAT1 was significantly higher in tongue cancer patients than in healthy controls.MALAT1 knockdown also reduced the phosphorylation level of Akt as well as the expression level of MMP-9. It showed no significant effects on Akt expression, while PI3K activator treatment reduced the inhibitory effects of MALAT1 knockdown on the proliferation, migration and invasion of tongue cancer cells.		Yes	MALAT1 knockdown markedly inhibits the proliferation, migration and invasion of tongue cancer cells. 	30657561
MALAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tumor tissues and cell lines	regulation[miR-140/BIRC6 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//EdU Staining//Transwell Assay	MALAT1 and BIRC6 were highly expressed in human PCa tumor tissues and cell lines. MALAT1 knockdown hindered PCa progression by regulating miR-140/BIRC6 axis in vitro and in vivo, hinting the potential value of MALAT1 in the management of PCa.		Yes	MALAT1 or BIRC6 knockdown inhibited cell proliferation, migration and invasion and induced cell apoptosis in PCa.	31935634
MALAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	n this study, we demonstrated that lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was increased in prostate cancer cells after androgen stimulation, as well as AR. MALAT1 bound to miR-320b and negatively regulated its expression, and vice versa. AR is a target of miR-320b. The phenotypic changes induced by silencing of MALAT1 were abolished by miR-320b inhibition or AR overexpression.		Yes	The silencing of MALAT1 inhibited dihydrotestosterone (DHT) administration-induced acceleration of proliferation and cell cycle progression, and increase of AR expression in prostate cancer cells. Additionally, MALAT1 knockdown also suppressed the tumorigenesis of prostate cancer cells in nude mice.	30642743
MALAT1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 OSCC tissue	Expression[highly expressed]	CCK8//qRT-PCR	MALAT-1 levels were significantly higher in the OSCC tissue than in the normal tissues (p < 0.004); no significant differences in UCA1, BC200 or SRA RNA levels were observed.		Yes	Knockdown of MALAT-1 by siRNA significantly suppressed proliferation of SSC4 cells (p < 0.004) and enhanced their apoptosis (p < 0.001). 	31360193
MALAT1	LncRNA	Homo sapiens	Intervertebral Disc Degeneration	IDD tissues	regulation[MALAT1-miR-503-MAPK pathway]	qRT-PCR	We validated the decreased expression of MALAT1 in the IDD tissues, which was associated with decreased Collagen II and Aggrecan expression.Our data suggested that the MALAT1-miR-503-MAPK pathway plays a critical role in NPCs, which may be a potential strategy for alleviating IDD.		Yes	In vitro, overexpressed MALAT1 could attenuate the effect of IL-1β on NPC proliferation, apoptosis, and Aggrecan degradation. In vivo, MALAT1 overexpression attenuated the severity of disc degeneration in IDD model rats.	32228440
MALAT1	LncRNA	Homo sapiens	Thyroid Neoplasms		regulation[miR-204/IGF2BP2/m6A-MYC Signaling]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Our data indicated that MALAT1 and IGF2BP2 were highly expressed, while miR-204 was poorly expressed in TC.Altogether, the central findings of our study suggest that MALAT1 contributes to TC progression through the upregulation of IGF2BP2 by binding to miR-204.		Yes	MALAT1 was found to upregulate IGF2BP2 and enhance MYC expression via m6A modification recognition by competitively binding to miR-204, conferring a stimulatory effect on proliferation, migration, and invasion of TC cells, which was accompanied by weakened tumor growth and cell apoptosis.	33312756
circITCH	CircRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Interaction(miR-106a-5p/SASH1 Axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we performed quantitative real-time polymerase chain reaction analysis and identified that circ-ITCH was significantly downregulated in glioma tissues and cell lines. Moreover, miR-106a-5p was found serving as a target of circ-ITCH and miR-106a-5p mimics could reverse the inhibitory effect of circ-ITCH on glioma cell proliferation and invasion. Moreover, miR-106a-5p was found serving as a target of circ-ITCH and miR-106a-5p mimics could reverse the inhibitory effect of circ-ITCH on glioma cell proliferation and invasion.		Yes	he function assays showed that upregulation of circ-ITCH inhibited glioma cell proliferation and invasion in vitro as well as reduced cell growth in vivo. 	33571015
MALAT1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	regulation[miR-146b-5p]	qRT-PCR//Luciferase Report Assay	The expression of MALAT1 was upregulated in PTC tissues and cells, while a MALAT1 knockdown counteracted cellular activity, migration, and invasion of B-CPAP and K1 cells.  The microRNA miR-146b-5p can promote a MALAT1 expression by negatively regulating DNMT3A in PTC.		Yes	 The expression of MALAT1 was upregulated in PTC tissues and cells, while a MALAT1 knockdown counteracted cellular activity, migration, and invasion of B-CPAP and K1 cells. 	32343601
MALAT1	LncRNA	Homo sapiens	Multiple Myeloma	 cell lines	Regulation[Hippo-YAP signaling pathway]	CCK8//qRT-PCR//ELISA//Flow Cytometry	LncRNA MALAT1 was increased in MM cells and LncRNA MALAT1 interference could inhibit cell proliferation and promote cell apoptosis with the changes in the related proteins.  In conclusion, this study showed that LncRNA MALAT1 interference inhibited the proliferation and adhesion of myeloma cells by the up-regulation of miR-181a-5p through activating the Hippo-YAP signaling pathway.		Yes	LncRNA MALAT1 interference could inhibit cell proliferation and promote cell apoptosis with the changes in the related proteins.	31397203
MALAT1	LncRNA	Homo sapiens	Multiple Myeloma	MM serums and cells	regulation[miR-1271-5p/SOX13 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The up-regulation of MALAT1 and the down-regulation of miR-1271-5p were found in MM serums and cells. LncRNA MALAT1 expedited MM tumorigenesis, invasion, and glycolysis via miR-1271-5p/SOX13 axis.		Yes	 MALAT1 knockdown suppressed cell viability, invasion, and glycolysis while expedited cell apoptosis in MM cells.	31953613
MALAT1	LncRNA	Homo sapiens	Multiple Myeloma	four main MM cell lines	Interaction(miR-188-5p)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Transfection//Tunel//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//IHC//EdU Staining	Moreover, MALAT1 was shown to be inversely correlated with miR-188-5p expression through direct binding to miR-188-5p, and in turn, miR-188-5p could mediate the MM cell proliferation and apoptosis regulated by MALAT1. 		Yes	Moreover, MALAT1 was shown to be inversely correlated with miR-188-5p expression through direct binding to miR-188-5p, and in turn, miR-188-5p could mediate the MM cell proliferation and apoptosis regulated by MALAT1. 	33944676
MALAT1	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer cells	Regulation	qRT-PCR//Transfection//Bioinformatics Analysis//Western Blot	 Notably, METTL3 positively regulates the expression of lncRNA MALAT1 in pancreatic cancer cells. Strikingly, lncRNA MALAT1 increased the expression of PD-L1 in pancreatic cancer cells. This finding indicated that METTL3 regulated the expression of PD-L1 possibly via targeting lncRNA MALAT1 in pancreatic cancer cells. Lastly, MALAT1 governed the viability of pancreatic cancer cells. Taken together, lncRNA MALAT1 is involved in METTL3-mediated promotion of PD-L1 expression in pancreatic cancer.		Yes	This finding indicated that METTL3 regulated the expression of PD-L1 possibly via targeting lncRNA MALAT1 in pancreatic cancer cells. Lastly, MALAT1 governed the viability of pancreatic cancer cells.	36212476
MALAT1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LAC tissues	Interaction[miR-429]	qRT-PCR//MTT//Transwell Assay//Western Blot	In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells).In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. 	The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues.	Yes	"To evaluate the effect of LncRNA MALAT1 on LAC cell proliferation, we inhibited MALAT1 in human lung adenocarcinoma cells PG49 and A549 by si-MALAT1-1 or si-MALAT1-2, and RT-qPCR was used to confirm this, as shown in Figure 3A. The cell growth of PG49 and A549 were monitored by MTT assays after LncRNA MALAT1 knockdown in PG49 and A549, and we found that (Figure 3B, ​,3C)3C) the proliferation of PG49 and A549 after LncRNA MALAT1 knockdown were significantly suppressed (P<0.05).
"	31933847
circSEPT9	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-432-5p/LASP1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	CircSEPT9 was highly expressed in glioma tissues and cell lines. MicroRNA-432-5p (miR-432-5p) was a target of circSEPT9, and circSEPT9 silencing-mediated effects in glioma cells were largely alleviated by the addition of anti-miR-432-5p. MiR-432-5p bound to the 3' untranslated region (3'UTR) of LIM and SH3 protein 1 (LASP1), and LASP1 overexpression largely overturned miR-432-5p-induced effects in glioma cells. 		Yes	CircSEPT9 interference inhibited the proliferation, migration, invasion and glycolytic metabolism and triggered the apoptosis of glioma cells.  CircSEPT9 silencing suppressed xenograft tumor growth in vivo.	33915163
circitga7	CircRNA	Homo sapiens	Glioma	glioma tissues and glioma cells	Interaction(miR-34a-5p/VEGFA axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In our research, we found that the expression of circITGA7 in glioma tissues and glioma cells increased significantly. Through analysis and dual-luciferase report assay, we found that circITGA7 acts as a sponge for miR-34a-5p targeting VEGFA in glioma. 		Yes	Knocking down circITGA7 can significantly inhibit the proliferation of glioma cells and reduce cell metastasis. 	33962397
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	interaction[miR-206,Akt/mTOR signaling]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	MALAT1 was significantly up-regulated in both NSCLC tissues and cell lines.lncRNA MALAT1 promotes migration and invasion of NSCLC by targeting miR-206 and activating Akt/mTOR signaling.	High expression of MALAT1 correlated positively with tumor size and lymphatic metastasis in NSCLC, whereas no correlation was found between MALAT1 expression and sex, age, clinical stage, and histological grade.	Yes	 We also showed that MALAT1 promoted epithelial-mesenchymal transition, cell migration, and invasion by activating Akt/mTOR signaling in A549 and H1299 cells.	29916897
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[miR-124]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	LncRNA MALAT-1 expression was higher in NSCLC tissues than that in adjacent tissues, but a lower expression of miR-124 was detected in the former tissues than in the latter tissues.By competitively regulating miR-124, MALAT-1 can promote epithelial-mesenchymal transition, thus accelerating the development of NSCLC.		Yes	Compared with 16HBE cells, MALAT-1 was highly expressed in NSCLC tissues. Compared with the blank group, E-cadherin and cell apoptosis were increased, but vimentin, cell variability, cell invasion, and migration ability in the si-MALAT-1 and miR-124 mimics groups were reduced. 	29782349
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[Down-Regulating miR-202 Expression]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	MALAT1 was overexpressed in NSCLC samples and cell lines.Next, we verified that MALAT1 could act as a competing endogenous RNA (ceRNA) by sponging miR-202 in NSCLC and there is a negative correlation between MALAT1 and miR-202. Besides, overexpression of miR-202 inhibited cell proliferation and invasive ability in MALAT1-overexpressed cells.	 High expression of MALAT1 was related to large tumor size (>3 cm), poor histological grade, advanced cancer and tumor metastasis in NSCLC. 	Yes	In vitro assays exhibited that knockdown of MALAT1 remarkably decreased A549 cell growth and invasion capacity, while overexpression of MALAT1 significantly enhanced NCI-H292 cell proliferation and invasion ability.	31863664
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-515-3p/ TRIM65 Axis]	RNA Pull-Down//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	MALAT1 and TRIM65 expression was upregulated, and miR-515-5p expression was downregulated in NSCLC tissues and cells. Our findings demonstrated that MALAT1 depletion inhibited the growth of NSCLC cells by regulating miR-515-5p/TRIM65 axis, providing the theoretical basis for the therapy of NSCLC.		Yes	Both MALAT1 knockdown and TRIM65 depletion suppressed cell proliferation, migration, and invasion and induced apoptosis in NSCLC cells.	33395541
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[MALAT1/miR-374b-5p/SRSF7 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	We first observed that the levels of MALAT1 and SRSF7 were upregulated while miR-374b-5p was downregulated in NSCLC tissues; meanwhile, the expression level of MALAT1 was negatively correlated with miR-374b-5p and positively correlated with SRSF7. Our results demonstrated that MALAT1 contributed to NSCLC progression through the MALAT1/miR-374b-5p/SRSF7 axis.		Yes	Both knockdown of MALAT1 and miR-374b-5p overexpression inhibited proliferation, migration and invasion and induced apoptosis in NSCLC cells. 	32141554
hsa_circ_0030018	CircRNA	Homo sapiens	Glioma	Thirty five cases of glioma tissues	Interaction(miR-34b-6p targets HuR)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Cell Apoptosis Assay//Colony Formation Assay//Invasion Assay	circ_0030018 was overexpressed in glioma tissues and cells, and its silencing could inhibit glioma cell proliferation, migration, invasion, and accelerate apoptosis.  Our data showed that circ_0030018 enhanced glioma progression by sponging miR-194-5p to regulate TRIM44, indicating that circ_0030018 might be a potential treatment target for glioma.		Yes	circ_0030018 was overexpressed in glioma tissues and cells, and its silencing could inhibit glioma cell proliferation, migration, invasion, and accelerate apoptosis. Animal experiments suggested that circ_0030018 knockdown could reduce glioma tumor growth through regulating miR-194-5p and TRIM44.	34150336
circMMP1	CircRNA	Homo sapiens	Glioma	Clinical Samples	Interaction( miR-195-5p/TGIF2 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	CircMMP1 and TGIF2 expression were upregulated, and miR-195-5p expression was downregulated in glioma tissues and cells. The mechanical analysis discovered that circMMP1 acted as a sponge of miR-195-5p to regulate TGIF2 expression.		Yes	And the knockdown of circMMP1 could block colony formation, migration, and invasion and expedite apoptosis and autophagy in glioma cells. 	34471941
MALAT1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cells	Regulation[miR-140-5p-PAK1 pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The expression of MALAT1 and p21 (RAC1)-activated kinase 1 (PAK1) was upregulated and microRNA-140-5p (miR-140-5p) expression was downregulated in TSCC tissues and cells. MALAT1 contributed to TSCC progression via miR-140-5p-PAK1 regulatory axis, highlighting a potential target for TSCC management.		Yes	Moreover, MALAT1 knockdown inhibited proliferation, migration, and invasion by upregulating miR-140-5p expression in TSCC cells.	30863103
circCSPP1	CircRNA	Homo sapiens	Glioma	GC tissues and cells	Expression[highly expressed]	CCK8//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	Circ-CSPP1 expression was significantly up-regulated both in GC tissues and cells. 		Yes	GC cells with low expression of circ-CSPP1 showed significantly reduced proliferation, invasion, and migration abilities. 	32495924
LPP-AS2	LncRNA	Homo sapiens	Glioma	glioma tissues	regulation[miR-7-5p/EGFR/PI3K/AKT/c-MYC feedback loop]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	The results of high-throughput RNA-seq indicated lncRNA LPP-AS2 was upregulated in glioma tissues and further confirmed by RT-qPCR. Thus, lncRNA LPP-AS2 promoted glioma tumorigenesis via a miR-7-5p/EGFR/PI3K/AKT/c-MYC feedback loop.	 Higher LPP-AS2 expression was related to a poor prognosis in glioma patients. 	Yes	Based on functional studies, LPP-AS2 depletion inhibited glioma cell proliferation, invasion and promoted apoptosis in vitro and restrained tumor growth in vivo, overexpression of LPP-AS2 resulted in the opposite effects.	32962742
circCPA4	CircRNA	Homo sapiens	Glioma	 glioma tissues	regulation[miR-760/MEF2D Axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	e found circCPA4 was highly expressed in glioma, and circCPA4 knockdown suppressed tumor cell proliferative, migratory and invasive behaviors, but enhanced cell apoptosis and radiosensitivity in glioma. In conclusion, circCPA4 knockdown suppressed cell malignant phenotypes in glioma via miR-760/MEF2D axis to impede the progression of glioma, suggesting potential therapeutic targets for glioma treatment.		Yes	We found circCPA4 was highly expressed in glioma, and circCPA4 knockdown suppressed tumor cell proliferative, migratory and invasive behaviors, but enhanced cell apoptosis and radiosensitivity in glioma.	33068224
circELF2	CircRNA	Homo sapiens	Glioma	GM tissues	regulation[MiR-510-5p/MUC15 Signaling]	CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay	We observed that circ-ELF2 was significantly upregulated in GM tissues, which was analyzed by circRNA microarray and qRT-PCR.This study indicates that circ-ELF2/miR-510-5p/MUC15 signaling plays a key role in promoting the occurrence and development of GM.	 Upregulation of circ-ELF2 was associated with poor prognosis and high recurrence rate for GM patients after surgery.	Yes	The collapse of circ-ELF2 caused growth arrest and downregulation of cell migratory and invasive potential of GM cells and promoted cell apoptosis. In contrast, elevated expression of circ-ELF2 led to the opposite effect.	33116591
circVPS18	CircRNA	Homo sapiens	Glioma	glioma tissues,cells	regulation[MiR-370/RUNX1 Axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 Circ-VPS18 expression and the mRNA and protein levels of RUNX1 were dramatically upregulated, and miR-370 expression was significantly downregulated in glioma cells, TMZ-resistant glioma tissues, or tissue compared with control groups.Circ-VPS18 knockdown improved TMZ sensitivity and repressed glioma progression by sponging miR-370 to downregulate RUNX1 expression, which provided a new insight in further studying glioma resistance to TMZ.		Yes	Functionally, circ-VPS18 knockdown improved TMZ sensitivity, induced cell apoptosis, whereas repressed cell viability, migration and invasion in U251/TR and LN229/TR cells, which was reversed by miR-370 inhibitor.	33188501
MALAT1	LncRNA	Homo sapiens	Pulmonary Arterial Hypertension	PA tissues,cell lines	Interaction[sponges miR‑124‑3p.1/KLF5]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay	The results revealed that MALAT1 expression levels were significantly upregulated in the pulmonary arteries (PAs) and HPASMCs obtained from patients with PAH compared with adjacent normal PA tissues and HPASMCs. Bioinformatics analysis predicted complementary binding of hsa‑microRNA (miR)‑124‑3p.1 with the 3'‑untranslated region of MALAT1. Luciferase reporter assays and RNA immunoprecipitation experiments demonstrated molecular binding between MALAT1 and hsa‑miR‑124‑3p.1. This resulted in the formation of an RNA‑induced silencing complex. In addition, Kruppel‑like factor 5 (KLF5) was confirmed to be a target gene of MALAT1/hsa‑miR‑124‑3p.1. MALAT1 silencing did not inhibit the proliferation and migration of HPASMCs following knockdown of hsa‑miR‑124‑3p.1. In addition, MALAT1 knockdown was demonstrated to attenuate the expression of KLF5. Following MALAT1 knockdown, the expression level of KLF5 was rescued by inhibition of hsa‑miR‑124‑3p.1 expression. The results of the current study indicate that the MALAT1/hsa‑miR‑124‑3p.1/KLF5 axis may serve a key role in HPASMCs.		Yes	Knockdown of MALAT1 suppressed the viability and proliferation of HPASMCs and prevented cells entering the G0/G1 cell cycle phase. MALAT1 overexpression exerted the opposite effects.	31257528
MALAT1	LncRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	blood	regulation[miR-205-PTK7 pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	The levels of MALAT1 and PTK7 were upregulated in ALL samples. Our results suggest that MALAT1-miR-205-PTK7 axis participates in the proliferation and apoptosis of ALL, which may provide a potential treatment target for ALL.		Yes	Moreover, MALAT1 silencing or miR-205 overexpression restrained proliferation and promoted apoptosis of ALL cells.	32754978
MALAT1	LncRNA	Homo sapiens	Adrenal Cortex Neoplasms	ACC tissues	Interaction[miR-497-MALAT1/EIF4E]	qRT-PCR//Luciferase Report Assay//RIP	 Recent contributions of high-throughput transcriptomic profiling identified microRNA-497 (miR-497) as significantly underexpressed, while lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) as overexpressed in ACC.Furthermore, MALAT1 directly binds to SFPQ (splicing factor proline and glutamine rich) protein, indicating its multifaceted roles in ACC pathophysiology. This is the first study to identify the feedback axis of miR-497-MALAT1/EIF4E in ACC tumourigenesis, providing novel insights into the molecular functions of noncoding RNAs in ACC.		Yes	We showed that overexpression of miR-497 and silencing of MALAT1 suppressed cellular proliferation and induced cell cycle arrest through downregulation of EIF4E expression.	31085769
circPTPRZ1	CircRNA	Homo sapiens	Glioma		Regulation[MiR-1261/circ-PTPRZ1/PAK1 pathway ]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	Therefore, in glioma cells, the expression of circ-PTPRZ1/PAK1 is regulated by miR-1261, which affects the proliferation, apoptosis, and invasion. This finding provides another powerful evidence for the role of circRNAs in glioma.		Yes	 Biological behaviors of glioma cells were detected, circ-PTPRZ1 enhanced cell proliferation and invasion, and inhibited cell apoptosis; miR-1261 had the opposite effects, and could terminate the above effects of circ-PTPRZ1. 	31364003
MALAT1	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues	Interaction[sponging miR-195]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	MALAT1, PD-L1 and CD8 were up-regulated in DLBCL tissues while miR-195 was down-regulated.MALAT1 could sponge miR-195 to regulate the expression of PD-L1. shMALAT1 treatment increased miR-195 level and decreased PD-L1 level. It also inhibited cell proliferation, migration and immune escape ability while increased apoptosis ratio of OCI-Ly10 cells. shMALAT1 treatment in OCI-Ly10 cells also promoted proliferation and inhibited apoptosis of CD8 T cells. Knocking down of MALAT1 also suppressed EMT-like process via Ras/ERK signaling pathway. These effects were all rescued by miR-195 inhibitor. +		Yes	 shMALAT1 treatment increased miR-195 level and decreased PD-L1 level. It also inhibited cell proliferation, migration and immune escape ability while increased apoptosis ratio of OCI-Ly10 cells.	30898647
circHIPK3	CircRNA	Homo sapiens	Glioma	cell lines	Interaction[binding to miR-124-3p]	CCK8//qRT-PCR//Flow Cytometry//EdU Staining	QRT-PCR data showed that circ-HIPK3 and STAT3 are highly expressed, whereas miR-124-3p is lowly expressed in glioma cells than those of negative control cell. In summary, we found that overexpression of circ-HIPK3 promotes proliferative and invasive capacities of glioma cells by sponging miR-124-3p to upregulate STAT3 expression.		Yes	Knockdown of circ-HIPK3 in U87 and U251 cells inhibited their proliferative and invasive capacities.	30576808
hsa_circ_0034642	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Regulation[miR-1205/BATF3 axis]	qRT-PCR//Luciferase Report Assay	As the results demonstrated, hsa_circ_0034642 was boosted in glioma tissues and cells.Mechanistically, hsa_circ_0034642 sponges miR-1205. miR-1205 regulates BATF3 level through targeting its 3'-untranslated region.	Overexpression of hsa_circ_0034642 was associated with clinical severity and poor prognosis. 	Yes	What is more, elevated hsa_circ_0034642 strikingly facilitated cell proliferation, migratory and invasive capacities, and decreased apoptotic cells.	30938850
circZNF264	CircRNA	Homo sapiens	Glioma	cell lines	Interaction[miR-4493 ]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	Detection of circRNAs in glioma cells revealed that the expression of circ-ZNF264 was upregulated. Therefore, in glioma cells, circ-ZNF264 can inhibit the function of miR-4493 and then upregulate its target gene apelin expression, thus regulating glioma cell proliferation, apoptosis, and invasion.		Yes	Biological behaviors of glioma cells were detected; circ-ZNF264 promoted cell proliferation and invasion and inhibited apoptosis.	31114952
MALAT1	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive		Regulation(MALAT1/miR-146a/COX2 signaling axis.)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//ELISA	we found that forced vital capacity, volume that has been exhaled at the end of the first second of forced expiration, and diffusion capacity for carbon monoxide were the highest in the MALAT1 HYPO + miR-146a HYPER group and lowest in the MALAT1 HYPER + miR-146a HYPO group, and COPD patients with hypermethylated MALAT1 showed lower expression of MALAT1 than that in the COPD patients with hypomethylated MALAT1. Meanwhile, miR-146a was the most significantly upregulated in the MALAT1 HYPER + miR-146a HYPO group and the most significantly downregulated in the MALAT1 HYPO + miR-146a HYPER group. Both prostaglandin E1 and cyclooxygenase 2 (COX2) expression were the highest in the MALAT1 HYPO + miR-146a HYPER group and the lowest in the MALAT1 HYPER + miR-146a HYPO group. In conclusion, our results established a MALAT1/miR-146a/COX2 signaling axis. The overexpression of MALAT1 could increase the expression of COX2 by inhibiting the expression of miR-146a, thus affecting the pulmonary function of COPD patients.		Yes	The overexpression of MALAT1 could increase the expression of COX2 by inhibiting the expression of miR-146a, thus affecting the pulmonary function of COPD patients.	34604205
hsa_circ_001350	CircRNA	Homo sapiens	Glioma	Glioma Tissue,cell lines	Interaction[sponges miR-1236]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Microarray//Transwell Assay	 circ_001350 level was significantly enhanced in glioma tissue specimens and cells. Collectively, circ_001350 directly sponges miR-1236, thus contributing to malignant progression of glioma.		Yes	Knockdown of circ_001350 could inhibit cell proliferation and metastatic properties and increase apoptotic cells. 	31020693
circTTBK2	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[miR-520b/EZH2 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The levels of circ-TTBK2 and EZH2 were markedly augmented, whereas miR-520b expression level was notably reduced in glioma tissues and cell lines.Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.		Yes	Either circ-TTBK2 or EZH2 detection could clearly facilitate cell apoptosis and block proliferation and invasion in A172 and U251 cells, while the effect of circ-TTBK2 or EZH2 deficiency was reverted by co-transfecting with miR-520 inhibitor. 	31858557
MALAT1	LncRNA	Homo sapiens	Skin Neoplasms		Regulation[MALAT1-KTN1-EGFR regulatory axis]	qRT-PCR	 Further, MALAT1 was identified to regulate epidermal growth factor receptor (EGFR) protein expression but did not affect EGFR mRNA expression. Transcriptomic sequencing identified kinectin 1 (KTN1) as the key mediator for MALAT1 regulation of EGFR. Mechanistic study revealed that MALAT1 interacts with c-MYC to form a complex and directly binds to the promoter region of KTN1 gene and enhances its transactivation to positively regulate EGFR protein expression. Our findings, therefore, establish a novel c-MYC-assisted MALAT1-KTN1-EGFR axis, which contributes to cSCC development and may serve as novel target for therapeutic intervention.		Yes	In this study, functional studies using in vitro cellular and in vivo xenograft models confirmed the pro-carcinogenic roles of MALAT1 in cSCC.	30683916
MALAT1	LncRNA	Homo sapiens	Pre-Eclampsia	placenta 	Regulation[ miR-206/IGF-1 axis]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that MALAT1 was decreased but miR-206 was increased in the placenta of patients with PE.Further, miR-206 was confirmed as a direct target of MALAT1. Besides, miR-206 inhibited IGF-1 expression by directly binding to the 3'UTR. Mechanistically, our study demonstrated that MALAT1 regulates IGF-1/PI3K/Akt signaling via miR-206. Together, these results suggest that MALAT1 and miR-206 play important roles in PE. MALAT1 regulates miR-206/IGF-1 axis, thereby modulating trophoblast cells migration and invasion through PI3K/Akt signal pathway. These results show light on the underlying mechanisms of PE and provide potential targets for PE therapy.		Yes	Inhibition of MALAT1, knockdown IGF-1, or miR-206 mimics suppressed the trophoblast cells migration and invasion, while overexpression of MALAT1, IGF-1 or miR-206 inhibitors exhibited opposite effects.	31774373
MALAT1	LncRNA	Homo sapiens	Pre-Eclampsia	 placenta of patients with severe preeclampsia	Expression [lower expressed]	Transfection//Tube Formation Assay//Immunoblotting//Migration Assay//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay	The expression of lncRNA MALAT1 was downregulated in the placenta of patients with severe preeclampsia. Moreover, MALAT1 inhibited the expression of angiogenic factors in umbilical vein endothelial cells co-cultured with trophoblasts. 		Yes	MALAT1 smart silencer significantly inhibited HTR-8/SVneo trophoblast cell proliferation, invasion, migration and tube formation in vitro.	33547935
MALAT1	LncRNA	Homo sapiens	Coronary Artery Disease	blood,cell line	Regulation[mTOR signaling pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	MALAT1 was overexpressed in CAD blood samples and EPCs. LncRNA MALAT1 inhibited EPCs autophagy and increased cell viability while repressed apoptosis of CAD via activating mTOR signaling pathway.		Yes	Knockdown of MALAT1 and MAPK1 promoted cell viability, autophagy and further suppressed the development of CAD. 	30787203
circMAN2B2	CircRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Regulation[miR-1205/S100A8 axis]	CCK8//qRT-PCR//Transwell Assay	In our study, we found that circMAN2B2 has a higher expression in glioma tissues and cells. In conclusion, circMAN2B2 could improve cell proliferation, invasion, and migration of the glioma by inhibiting miR-1205 and promoting the expression of S100A8.	In our study, we found that circMAN2B2 has a higher expression in glioma tissues and cells, which was negatively related to the overall survival of glioma patients.	Yes	The cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine labeling assay, transwell assay, and the nude mice assay indicated that knockdown of circMAN2B2 inhibited the cell proliferation, invasion, migration and decreased tumor size. 	31131447
circPITX52	CircRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Interaction[sponging miR-518a-5p]	qRT-PCR	 Quantitative reverse-transcription polymerase chain reaction was carried out to measure the expression of circ-PITX1, which was upregulated in matched cancerous tissues and adjacent noncancerous tissues from 52 patients and four cell lines of GM.What's more, circ-PITX1 sponges miR-518a-5p to release its repression on 3'-untranslated region (3'UTR) of interleukin 17 receptor D (IL17RD) messenger RNA to exert its oncogenic functions in GM cells proved by dual-luciferase reporter and rescue assays. 		Yes	 Gain and loss-of-function assays demonstrated that circ-PITX1 could facilitate the growth, migration, and invasion and inhibit cell apoptosis in GM cell lines.	31069865
hsa_circ_0000215	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	interaction[Sponging miR-495-3p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Circ_0000215 and CXCR2 were remarkably upregulated in glioma tissues and cells.These data demonstrated that circ_0000215 functions as a competitive endogenous RNA by sponging miR-495-3p, thus accelerating glioma progression through CXCR2 axis.		Yes	Overexpression of circ_0000215 notably promoted the proliferation, invasion and epithelial-mesenchymal transition (EMT) but inhibited apoptosis of glioma cells, while knocking down circ_0000215 had the opposite effects. 	33089764
MALAT1	LncRNA	Homo sapiens	lung carcinoma	 lung carcinoma cells	Interaction(miR-491-5p/UBE2C Axis)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	 The results indicated that the expression of MALAT1 was often augmented in lung carcinoma cells. Collectively, MALAT1 downregulation suppressed lung carcinoma progression by regulating the miR-491-5p/UBE2C axis. 		Yes	 Suppression of MALAT1 blocked the proliferation, invasion and migration ability of cancer cells and inhibited the expression of UBE2C.  UBE2C restoration attenuated the MALAT1 knockdown-induced anti-cancer effects. 	34257576
hsa_circ_0079586	CircRNA	Homo sapiens	Glioma	GM samples and cells	regulation[miR-183-5p/ MDM4 Signaling Pathway]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The expression of circ_0079586 was elevated in GM samples and cells and correlated with the clinical severity and unfavorable prognosis of the patients.In summary, circ_0079586 was found to be up-regulated in GM that increased the proliferation, migration and invasion in GM cells via interaction with the miR-183-5p/MDM4 axis.		Yes	 The elevated expression of circ_0079586 led to an increase in cell growth, migration and invasion but inhibited apoptosis in U251 cells, whereas its down-regulation reversed these effects in the LN229 cells.	32606734
MALAT1	LncRNA	Homo sapiens	Endometriosis	endometrium tissues	regulation[PI3K/AKT pathway]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI3K/AKT pathway. 		Yes	Knockdown of MALAT1 or CREB1 restrained proliferation and induced apoptosis as confirmed by upregulating cleaved caspase-3 and Bax, and down-regulating Bcl-2 in HESCs, while inhibition of miR-126-5p presented the opposite results. 	32809092
circPTN	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-432-5p/RAB10 axis]	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 circ-PTN expression was enhanced and miR-432-5p abundance was reduced in glioma tissues and cells.circ-PTN knockdown repressed cell proliferation, invasion and glycolysis in glioma via modulating miR-432-5p and RAB10.		Yes	 circ-PTN silence suppressed cell proliferation, invasion and glycolysis.	32629066
circABCB10	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-620/FABP5 axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The expression levels of circ-ABCB10 and FABP5 in glioma tissues and cells were significantly higher than those in their normal counterparts. These data suggest that circ-ABCB10 affects glioma progression by regulating the miR-620/FABP5 axis, and circ-ABCB10 might be used as a potential target for the treatment of glioma.		Yes	Silencing of circ-ABCB10 in glioma cells significantly inhibited the proliferation, migration and invasion of glioma cells.	32633377
MALAT1	LncRNA	Homo sapiens	Crohn Disease	intestine mucosa of CD patients and mice 	Interaction(miR-146b-5p-CLDN11/NUMB Pathway)	Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Microarray	MALAT1 was aberrantly downregulated in the intestine mucosa of CD patients and mice with experimental colitis. MALAT1 regulated the intestinal mucosal barrier and regained intestinal homeostasis by sequestering miR-146b-5p and maintaining the expression of the AJC proteins NUMB and CLDN11.		Yes	 MALAT1 knockout mice were hypersensitive to DSS-induced experimental colitis.	33677577
circFANCL	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-337-3p/HMGB1 signal axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	CircFANCL was signally increased in glioma tissues and cells, and the up-regulated circFANCL could predict poor prognosis in clinical glioma patients. Through the illustration of oncogenic function of circFANCL in glioma by the miR-337-3p/HMGB1 axis, we believed that circFANCL might be a great target in the early diagnosis and late treatment of glioma.	CircFANCL was signally increased in glioma tissues and cells, and the up-regulated circFANCL could predict poor prognosis in clinical glioma patients.	Yes	Down-regulated circFANCL induced the proliferation inhibition, cell cycle arrest and apoptosis promotion of glioma cells in vitro, and inhibited tumor growth in vivo.	32683852
MALAT1	LncRNA	Homo sapiens	Diabetic Nephropathies	 DN tissues, HK-2 cells	Interaction(LIN28A/Nox4/AMPK/TOR signaling)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//MTT//ELISA	MALAT1, LIN28A and Nox4 were upregulated in DN tissues and HG-treated HK-2 cells. Furthermore, MALAT1 directly interacted with LIN28A. Moreover, MALAT1 facilitated the interaction between LIN28A and Nox4 to increase Nox4 stability. Knockdown of Nox4 relieved HG-induced injury by suppressing the AMPK/mTOR signaling in HK-2 cells. Knockdown of MALAT1 alleviated renal tubular epithelial injury by suppressing LIN28A and the Nox4/AMPK/TOR signaling in DN.		Yes	Overexpression of MALAT1, LIN28A or Nox4 reduced cell viability and enhanced cell apoptosis, ROS generation and secretion of inflammatory cytokines in HG-treated HK-2 cells, whereas knockdown of MALAT1, LIN28A or Nox4 exerted opposite effects.	35813614
MALAT1	LncRNA	Homo sapiens	Diabetes, Gestational	Gestational diabetes mellitus placental tissues	regulation[TGF-β/NF-κB signaling pathway]	Western Blot//qRT-PCR//MTT//ELISA//Transwell Assay	Gestational diabetes mellitus placental tissues showed higher lncRNA MALAT1 expression compared to a normal control group (p < 0.05). Downregulation of lncRNA MALAT1 inhibits inflammation and suppresses the proliferation, invasion and migration of GDM placental trophoblastic cells, possibly by modulating the TGF-β/NF-κB signaling pathway.		Yes	After siRNA intervention, lncRNA MALAT1 showed decreased expression in the trophoblastic layer; inhibited trophoblastic cell proliferation, migration, or invasion; decreased the secretion of inflammatory factors TNF-α and IL-6; and suppressed the expression of TGF-β and NF-κB compared to that of the control and siRNA-NC groups (p < 0.05).	32783409
circPOSTN	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[CircPOSTN/miR-361-5p/TPX2 axis ]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	CircPOSTN was overexpressed in glioma tissues and cells.Mechanistically, circPOSTN regulated cell growth, apoptosis, and aerobic glycolysis in glioma through miR-361-5p/TPX2 axis.		Yes	In vivo study revealed that deficiency of circPOSTN restrained tumor growth.	32774168
hsa_circ_0082374	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-326/SIRT1]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We found circ0082374 expression was elevated in glioma tissues and cells. Collectively, silence of circ0082374 repressed the viability, migration, invasion and glycolysis in glioma cells by regulating miR-326 and SIRT1 in a ceRNA mechanism, providing a new mechanism for the pathogenesis of glioma.		Yes	 Knockdown of circ0082374 suppressed the viability, migration, invasion and glycolysis in glioma cells.	32896523
circMMP1	CircRNA	Homo sapiens	Glioma	exosomal 	regulation[circMMP1/miR-433/HMGB3 signaling]	CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	The results showed that high serum exosomal circMMP1 level might predict poor prognosis of glioma patients.Targeting circMMP1/miR-433/HMGB3 signaling might be a novel insight for glioma treatment.	The results showed that high serum exosomal circMMP1 level might predict poor prognosis of glioma patients.	Yes	 CircMMP1 promoted the proliferation and motility and impeded the apoptosis of glioma cells.CircMMP1 silencing suppressed the progression of glioma in vivo.	32918539
MALAT1	LncRNA	Homo sapiens	laryngeal carcinoma	cell lines	Expression[highly expressed]	CCK8//Cell Cycle Assay//qRT-PCR//Transwell Assay	MALAT1 was significantly up-regulated in laryngeal and hypopharyngeal carcinoma cells. 		Yes	MALAT1 down-regulation induced the increased apoptosis of both cell lines and suppressed cells' proliferation. Cells were arrested in G1/G2 phase and cells of S phase were significantly decreased. 	31792655
MALAT1	LncRNA	Homo sapiens	gastric adenocarcinoma	blood,cell lines	Regulation[MALAT1/miR-181a-5p/AKT3 axis]	CCK8//qRT-PCR//Western Blot	Our results showed that MALAT1 was highly expressed in the serum of patients with gastric adenocarcinoma and in cell lines. Our research proposes a novel mechanism where the role of MALAT1 is dependent on the MALAT1/miR-181a-5p/AKT3 axis. 		Yes	 Downregulating MALAT1 inhibited proliferation and promoted apoptosis of MGC-803 cells. 	31480991
MALAT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical tumor cell lines	Interaction(miR-124)	In Vivo Experiment//qRT-PCR//Transfection//Cell Proliferation Assay	We observed that miR-124 was the potential target of LncRNA MALAT1 in cervical tumor cell lines (Hela, C-33A, Caski, and SiHa), the expression level of which is negatively correlated with LncRNA MALAT1 in cervical tumor cells, tissues of cervical patients, and mice. In conclusion, LncRNA MALAT1 disabled the effects of miR-124 as an inhibitory sponge, accelerating the progression of cervical carcinoma.		Yes	Gain- or loss-of-function analyses in cervical tumor cells have further verified the regulatory role of MALAT1 on miR-124. Additionally, the proliferation of cervical carcinoma was inhibited by miR-124 overexpression, whereas it was blocked by LV-MALAT1 transfection. In vivo assays, overexpression of miR-124, or knockdown of MALAT1 exhibited beneficial effects on tumor weight, size, and volume, together with elevating the survival rate, tightly related with the progression of cervical cancer. 	34221014
MALAT1	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	cell line	Interaction(MDM2)	Transfection//Immunoblotting//Flow Cytometry//FISH//qRT-PCR//Cell Proliferation Assay//IP//IF	We identified that MALAT1 interacted with MDM2 and PARP1 in the cell nucleus. MDM2 binds to the 3' segment of MALAT1, containing the ENE domain through the ring finger domain.		Yes	Knockdown of MALAT1 in KGN cells and primary GCs increased apoptosis and reduced proliferation.	34883204
MALAT1	LncRNA	Homo sapiens	capillary hemangioma	IH tissues	Interaction[MEKK3/NF-κB pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In IH tissues, MALAT1 and MEKK3 were overexpressed while miR-424 was down-regulated. Knockdown of MALAT1 suppressed the expression of MEKK3 and inactivated the IKK/NF-κB pathway by sponging miR-424. Overexpression of MEKK3 in HemEcs reversed the impact of knockdown of MALAT1 and overexpression of miR-424 on the cell proliferation, apoptosis, migration, invasion and tube formation rate. The tumor xenografts experiments demonstrated that silencing MALAT1 significantly inhibited the tumor growth in vivo and Ki-67 in the tumor tissues was also significantly suppressed.		Yes	 Silencing MALAT1 or overexpression of miR-424 significantly inhibited the IH cell proliferation, migration and tube formation, but promoted the cell apoptosis. 	31610202
MALAT1	LncRNA	Homo sapiens	capillary hemangioma	IH tissues	regulation[MiR-206 / VEGFA axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results showed that MALAT1 and VEGFA were high-expressed and miR-206 was low-expressed in IH tissues. Knock-down of MALAT1 inhibits the growth of HemECs through regulating miR-206/VEGFA axis, indicating that MALAT1 is a potential therapeutic mechanism for the treatment of IH.		Yes	SiMALAT1 negatively affected the cell proliferation, migration, invasion and vasoformation of HemECs and promoted apoptosis of HemECs.	32084582
MALAT1	LncRNA	Homo sapiens	Laryngeal Neoplasms	 tissues and cell	Interaction(miR-125b/HMGA1.)	Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In laryngocarcinoma tissues and cells, lncRNA MALAT1 expression was significantly increased compared to normal tissues and cells.LncRNA MALAT1 upregulates HMGA1 expression by acting as a competitive endogenous RNA (ceRNA) for miR-125b. Rescue experiments showed that microRNA-125b inhibitor reversed the change in cell viability and invasion induced by sh-MALAT1. Down regulation of lncRNA MALAT1 inhibits laryngocarcinoma proliferation and invasion by modulating miR-125b/HMGA1.		Yes	 LncRNA MALAT1 promotes proliferation and migration of laryngocarcinoma cells. 	34183954
MALAT1	LncRNA	Homo sapiens	Laryngeal Neoplasms	laryngocarcinoma cells	Interaction(miR-708-5p/BRD4 )	In Vivo Experiment//Western Blot//Transfection//Migration Assay//CCK8//Flow Cytometry//qRT-PCR//Transwell Assay	MALAT1 suppression inhibited the malignant phenotypes of laryngocarcinoma cells, such as decreased proliferation, promoted apoptosis, suppressed migration, and inhibited the CSC properties.Suppression of MALAT1 increased miR-708-5p expression and decreased the expression of BRD4 and YAP1 and inhibited EMT. Moreover, there were target relationships between MALAT1 and miR-708-5p as well as between miR-708-5p and BRD4. miR-708-5p overexpression and MALAT1 suppression had synergistic inhibitory effects on the malignant phenotypes of laryngocarcinoma cells and the expression of BRD4, YAP1, and EMT. 		Yes	MALAT1 suppression inhibited the malignant phenotypes of laryngocarcinoma cells, such as decreased proliferation, promoted apoptosis, suppressed migration, and inhibited the CSC properties.Furthermore, in vivo experiments confirmed that MALAT1/miR-708-5p regulated tumorigenicity by regulating BRD4 and YAP1-mediated EMT.	35601153
circHIPK3	CircRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	interaction[sponging miR-124]	CCK8//qRT-PCR//Transwell Assay	Our results showed that circHIPK3 expression was significantly up-regulated in glioma tissues and cell lines. In summary, our results indicated that circHIPK3 had carcinogenic effects by regulating the expression of CCND2 in glioma by sponging miR-124. 		Yes	In vitro, the down-regulation of circHIPK3 significantly inhibited the proliferation, migration and invasion of glioma cells.	33005182
MALAT1	LncRNA	Homo sapiens	Endometriosis	endometriosis granulosa cells	Interaction[ERK/MAPK pathway]	qRT-PCR	We first found that MALAT1 lncRNA was significantly down-regulated in endometriosis GCs and was associated with the antral follicle count (R = 0.376, P < 0.001 versus control).MALAT1 knockdown induced an increase in both the mRNA and protein levels of P21, and of P53, phosphorylated ERK1/2 (p-ERK1/2) and phosphorylated c-Jun N-terminal protein kinase (p-JNK) protein levels, as well as causing a decrease in cyclin dependent kinase 2 (CDK2), cyclin D1 and p-P38 MAPK protein levels. Furthermore, inhibition of the ERK/MAPK pathway with U0126, the up-regulation of p-ERK1/2, P21 and P53, and the down-regulation of CDK2 and cyclin D1 by the knockdown of MALAT1 were all attenuated by MALAT1 knockdown. 		Yes	MALAT1 knockdown in KGN cells inhibited cell proliferation and cell-cycle progression.	30371869
hsa_circ_0001445	CircRNA	Homo sapiens	Glioma	glioma cells	Interaction(miRNA-127-5p/SNX5 pathway)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Cell Apoptosis Assay//RNA-seq//Invasion Assay//Transwell Assay	The results demonstrated that exosomes derived from glioma cells promoted glioma progression. Also, exosomal circRNA 0001445 was taken up and upregulated in glioma cells treated with exosomes.  In addition, exosomal circRNA 0001445 acted as a sponge for miRNA-127-5p to upregulate the expression of sorting nexin 5 (SNX5). Lastly, the effect of exosomal circRNA 0001445 was mediated by miRNA-127-5p/ SNX5 signaling pathway.		Yes	 In addition, exosomal circRNA 0001445 acted as a sponge for miRNA-127-5p to upregulate the expression of sorting nexin 5 (SNX5). Lastly, the effect of exosomal circRNA 0001445 was mediated by miRNA-127-5p/ SNX5 signaling pathway.	33982667
MALAT1	LncRNA	Homo sapiens	Glioblastoma		Regulation[MALAT1/miR-199a/ZHX1 Axis]	FISH//RNA Pull-Down//Luciferase Report Assay//RIP	Elevated ZHX1 expression correlated with poor prognosis in GBM patients, and in vitro studies demonstrated that ZHX1 attenuated GBM cell apoptosis by downregulation of pro-apoptotic protein (Bax) and upregulation of anti-apoptotic protein (Bcl-2). Finally, we demonstrated that MALAT1 promoted ZHX1 expression via acting as a competing endogenous RNA by sponging miR-199a. The MALAT1/miR-199a/ZHX1 axis promotes GBM cell proliferation and progression in vitro and in vivo, and its expression negatively correlates with GBM patient survival. Blocking the MALAT1/miR-199a/ZHX1 axis can serve as a novel therapeutic strategy for treating GBM.		Yes	Furthermore, knockdown of MALAT1 inhibited GBM proliferation and progression in vitro and reduced tumor volume and prolonged survival in an orthotopic GBM murine model.	31648104
MALAT1	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(miR-613)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Cell Proliferation Assay//Transwell Assay	The results of qRT-PCR showed that LncRNA MALAT1 was up-regulated and miR-613 was down-regulated in glioma tissues and cells, and LncRNA MALAT1 was negatively correlated with miR-613. Bioinformatics prediction and subsequent experiments proved that miR-613 was the direct target of LncRNA MALAT1. 		Yes	Cell tests confirmed that LncRNA MALAT1 played a role in promoting oncogene, including promoting proliferation and invasion of glioma cells and promoting apoptosis. 	34268963
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumor tissues	Expression[highly expressed]	CCK8//qRT-PCR//Wound Healing Assay//Invasion Assay	MALAT1 expression was significantly increased in NSCLC samples compared with expression in adjacent non-cancerous tissues. 		Yes	The proliferative, migratory and invasive abilities of MALAT1-silenced A549 cells were significantly decreased compared with those of control cells. 	29805668
hsa_circ_0067934	CircRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(microRNA miR-7/ Wnt/β-catenin axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay//IF	The results of qRT-PCR indicated that circRNA_0067934 was over-expressed in glioma tissues, and down regulation of circRNA_0067934 reduced the tumor progression by inhibiting cell proliferation, invasion, and migration. In conclusion, our results revealed that circRNA_0067934 regulates glioma cells progression by targeting miR-7/ Wnt/β-catenin axis.		Yes	The results of qRT-PCR indicated that circRNA_0067934 was over-expressed in glioma tissues, and down regulation of circRNA_0067934 reduced the tumor progression by inhibiting cell proliferation, invasion, and migration.	35213267
hsa_circ_0001367	CircRNA	Homo sapiens	Glioma	glioma tissues	Interaction(miR-431/NRXN3 axis)	In Vivo Experiment//IHC//Western Blot//Transfection//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In this study, we found that circ_0001367 was downregulated in glioma tissues and showed a close correlation with glioma patient survival. Functional assays demonstrated that upregulation of circ_0001367 could suppress the proliferation, migration and invasion of glioma cells in vitro and inhibit glioma growth in vivo. Furthermore, bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation assay indicated that circ_0001367 can serve as a sponge for miR-431 and that miR-431 acts as an oncogene by regulating neurexin 3 (NRXN3). In addition, rescue experiments verified that circ_0001367 could regulate both the expression and function of NRXN3 in a miR-431-dependent manner.	we found that circ_0001367 was downregulated in glioma tissues and showed a close correlation with glioma patient survival. 	Yes	Functional assays demonstrated that upregulation of circ_0001367 could suppress the proliferation, migration and invasion of glioma cells in vitro and inhibit glioma growth in vivo. Furthermore, bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation assay indicated that circ_0001367 can serve as a sponge for miR-431 and that miR-431 acts as an oncogene by regulating neurexin 3 (NRXN3).	34035217
hsa_circ_0001017	CircRNA	Homo sapiens	Glioma	glioma tissue and cells	Interaction(let-7g-3p/NDST3 axis)	Western Blot//Transfection//Wound Healing Assay//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	In glioma tissues and cells, hsa_circ_0001017 expression was decreased. The overexpression of hsa_circ_0001017 inhibited glioma cell proliferation, EMT, migration, and invasion and promoted glioma cell apoptosis, while the knockdown of hsa_circ_0001017 caused the opposite results. Mechanistically, hsa_circ_0001017 sponged hsa-let-7g-3p and NDST3 was the target gene of hsa-let-7g-3p. Moreover, the tumour-suppressive role of circ_0001017 was associated with hsa-let-7g-3p and NDST3.		Yes	The overexpression of hsa_circ_0001017 inhibited glioma cell proliferation, EMT, migration, and invasion and promoted glioma cell apoptosis, while the knockdown of hsa_circ_0001017 caused the opposite results. 	34284545
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-613/COMMD8 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	MALAT1 and COMMD8 were aberrantly upregulated in NSCLC tissues and cells.MALAT1 promoted malignant activities of NSCLC cells through targeting miR-613/COMMD8 axis, and exosome-mediated transfer of NSCLC might be a novel approach for NSCLC treatment.		Yes	MALAT1 or COMMD8 knockdown blocked cell proliferation, colony formation and glycolysis but accelerated cell apoptosis in vitro. Besides, MALAT1 knockdown reduced tumor growth in vivo.	33149680
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-185-5p/MDM4 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	We found MALAT1 and MDM4 were upregulated and MALAT1 positively regulated the MDM4 expression. Collectively, MALAT1 contributed to proliferation, migration, invasion, and impeded apoptosis by regulating the MDM4 expression mediated by miR-185-5p in NSCLC cells. Besides, knockdown of MALAT1 inhibited tumor growth in vivo through miR-185-5p/MDM4 axis in NSCLC.		Yes	MALAT1 and MDM4 deletion significantly hindered the proliferation, metastasis, and expedited the apoptosis of NSCLC cells.  Besides, knockdown of MALAT1 inhibited tumor growth in vivo through miR-185-5p/MDM4 axis in NSCLC.	33146951
circBRAF	CircRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(miR-1290/FBXW7 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Expression of circBRAF and FBXW7 was decreased in glioma tissues and cells. MiR-1290 was upregulated in glioma, which was sponged by circBRAF. Besides, circBRAF elevated FBXW7 expression by targeting miR-1290. Introduction of miR-1290 or FBXW7 knockdown could counteract the inhibitory effects of circBRAF upregulation on the malignant phenotypes of glioma cells. 		Yes	 Upregulation of circBRAF inhibited glioma cell proliferation and metastasis in vitro.  Overexpression of circBRAF repressed the tumor growth in vivo.	33650075
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	serum and cell exosomes	regulation[miR-515-5p/EEF2 Axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 MALAT1 was highly expressed in serum and cell exosomes from NSCLC patients. MALAT1 knockdown repressed NSCLC tumorigenicity by inhibiting cell proliferation, invasion and promoting apoptosis through regulating miR-515-5p/EEF2, besides, MALAT1 was highly enriched in exosomes of NSCLC, suggesting a possible molecular-targeted therapy for NSCLC patients.		Yes	 MALAT1 knockdown repressed cell proliferation, invasion and induced cell apoptosis in vitro as well as inhibited tumor growth in vivo in NSCLC.	32943920
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC clinical tissues & NSCLC cell lines	Interaction(MALAT1/microRNA-503-5p/SEPT2 axis)	ChIP//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Augmented JMJD2C, MALAT1, and SEPT2 and reduced miR-503-5p levels were found in NSCLC. Depleting JMJD2C or MALAT1, or restoring miR-503-5p exerted anti-tumor effects on NSCLC cells in vitro and in vivo. JMJD2C is bound to the promoter of MALAT1. MALAT1 bound to miR-503-5p and miR-503-5p targeted SEPT2. Knocking down MALAT1 or SEPT2, or elevating miR-503-5p mitigated the pro-tumor effects of upregulated JMJD2C on NSCLC. It is evident that the JMJD2C-mediated MALAT1/miR-503-5p/SEPT2 axis takes part in the process of NSCLC and even worsens NSCLC.		Yes	Knocking down MALAT1 or SEPT2, or elevating miR-503-5p mitigated the pro-tumor effects of upregulated JMJD2C on NSCLC.	35046387
circTOP2A	CircRNA	Homo sapiens	Glioma	GM tissue specimens and cells	Interaction(miR-346/SUSD2 signaling)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The present study demonstrated that circ-TOP2A was elevated in GM tissue specimens and cells and that circ?TOP2A levels indicated an unfavorable clinical prognosis in GM. Circ‑TOP2A acted as a competing endogenous RNA to upregulate sushi domain‑containing 2 (SUSD2) expression by sponging microRNA (miR) 346. 	The present study demonstrated that circ?TOP2A was elevated in GM tissue specimens and cells and that circ?TOP2A levels indicated an unfavorable clinical prognosis in GM. 	Yes	Functionally, circ?TOP2A knockdown reduced viability, migration and invasion and triggered apoptosis in LN229 cells. 	33537815
MALAT1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cell lines	Interaction[YAP ]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	In this study, we found that MALAT1 expression was remarkably increased in ESCC cells compared to normal human esophageal epithelial cells. We also established that MALAT1 binds directly to Yes-associated protein (YAP), thereby enhancing YAP protein expression and increasing YAP transcriptional activity. Overexpression of YAP partially rescued the effect of MALAT1 knockdown on stemness and radiosensitivity of ESCC cells. Overall, this study has identified that a novel MALAT1-YAP axis promotes the stemness of ESCC cells, and thus could be a potential target for treatment of ESCC.		Yes	 In addition, knockdown of MALAT1 attenuated the stemness of ESCC cells, as evidenced by a decrease in spheroid formation capacity, stemness marker expression and aldehyde dehydrogenase 1 activity. Moreover, MALAT1 knockdown decreased the migration ability of ESCC cells. Notably, knockdown of MALAT1 enhanced the radiosensitivity and chemosensitivity of ESCC cells. 	31116509
hsa_circ_0007534	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction( miR-22-3p/PROX1 )	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	Circ_0007534 was highly expressed in glioma tissues and cell lines relative to that in normal tissues and NHA cell line. . Circ_0007534 negatively regulated miR-22-3p level through targeting it in glioma cells. Circ_0007534 interference-induced influences in glioma cells were partly overturned by the silencing of miR-22-3p. PROX1 was a target of miR-22-3p, and circ_0007534 interference-mediated effects in glioma cells were largely diminished by the overexpression of PROX1. 		Yes	Circ_0007534 knockdown suppressed the proliferation and motility while induced the apoptosis of glioma cells.  Circ_0007534 interference restrained glioma development in vivo. 	34536179
hsa_circ_0091581	CircRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(miR-1243-5p/RMI1 )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 This study demonstrated that hsa_circ_0091581 is upregulated in glioma tissues and cells. The results of the luciferase reporter and RNA immunoprecipitation assays indicated that the mechanism of the effects of hsa_circ_0091581 on glioma cells involves sponging miR-1243-5p to regulate RMI1. 		Yes	The results of the CCK-8, EdU, and transwell assays indicated that hsa_circ_0091581 promotes proliferation, migration, and invasion of glioma cells. 	33976734
circCREBBP	CircRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(miR-375/glutaminase axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-CREBBP was highly expressed in glioma tissues and cells, and high expression of circ-CREBBP predicted poor prognosis.  Mechanistically, circ-CREBBP indirectly regulated GLS expression through sponging miR-375. In all, circ-CREBBP expedited glioma tumorigenesis and glutamine metabolism through miR-375/GLS axis, suggesting a promising target for combined glioma therapy.	Circ-CREBBP was highly expressed in glioma tissues and cells, and high expression of circ-CREBBP predicted poor prognosis. 	Yes	Circ-CREBBP knockdown suppressed cell proliferation, migration, invasion and glutamine metabolism while expedited cell apoptosis in glioma in vitro, as well as impeded tumor growth in vivo.	34813772
MALAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues,cell lines	Interaction[sponging miR-363-3p]	qRT-PCR//Luciferase Report Assay//Western Blot	We observed that MALAT1 was highly expressed in colorectal cancer tissues and cells.Moreover, miR-363-3p functions as a downstream target of MALAT1, meanwhile EZH2 was a target of miR-363-3p, suggesting MALAT1 might regulate miR-363-3p and/or EZH2 expression. Collectively, we concluded that MALAT1 functioned as a ceRNA to promote colorectal cancer development and EZH2 expression through sponging miR-363-3p in vitro and in vivo.		Yes	We observed that MALAT1 was highly expressed in colorectal cancer tissues and cells, and MALAT1 knockdown inhibited cell proliferation as well as expression levels of EZH2 by upregulated miR-363-3p in cell models and in vivo.	30972996
circNCAPG	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-200a-3p/RAB5A axis)	Cell Proliferation Assay	 Expression of circNCAPG and RAB5A was upregulated, and miR-200a-3p was decreased in glioma tissues and cells, while their expression presented an opposite trend in Pro-treated glioma cells. Mechanically, circNCAPG could regulate RAB5A expression by sponging miR-200a-3p. Pro blocked glioma tumor growth in vivo by modulating circNCAPG.		Yes	Moreover, circNCAPG overexpression could abolish Pro-mediated proliferation, apoptosis, migration, and invasion in glioma cells in vitro. 	34129971
circUBAP2	CircRNA	Homo sapiens	Glioma	glioma tissues	Interaction(miR-1205 or miR-382 /GPRC5A )	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	 Circ-UBAP2 expression was upregulated in glioma. Mechanistically, circ-UBAP2 directly bound to miR-1205 and miR-382. miR-1205 and miR-382 mediated the regulation of circ-UBAP2 silencing on glioma cell behaviors. Moreover, GPRC5A was a functional target of miR-1205 and miR-382 in regulating glioma cell behaviors.Furthermore, circ-UBAP2 mediated GPRC5A expression through miR-1205 or miR-382 in glioma cells.		Yes	The reduced level of circ-UBAP2 hampered cell proliferation, migration, invasion, and enhanced apoptosis in vitro and weakened tumor growth in vivo.	33543830
circEGFR	CircRNA	Homo sapiens	Glioma	glioma samples	Interaction(miR-183-5p/TUSC2 Axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The qRT-PCR showed the downregulation of circ-EGFR and TUSC2 but the upregulation of microRNA-183-5p (miR-183-5p) in glioma samples. Circ-EGFR was identified as a sponge of miR-183-5p and circ-EGFR-mediated glioma progression inhibition was abolished by miR-183-5p downregulation. Additionally, miR-183-5p targeted TUSC2 and miR-183-5p inhibitor impeded the development of glioma by upregulating the expression of TUSC2. Furthermore, circ-EGFR could regulate the TUSC2 level by sponging miR-183-5p. Glioma growth in vivo was also reduced by circ-EGFR via targeting the miR-183-5p/TUSC2 axis. 		Yes	 In vitro assays revealed that circ-EGFR overexpression induced the repression of cell proliferation, migration, and invasion but the promotion of apoptosis. 	33993369
MALAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Expression[highly expressed]	qRT-PCR	We observed increased expression of MALAT1 in six CRC cell lines compared to that in normal cells, suggesting its involvement in CRC progression. 		Yes	Downregulation of MALAT1 inhibited cell migration and induced apoptosis in vitro and inhibited tumor growth and metastasis in nude mice. 	30716387
circTLK1	CircRNA	Homo sapiens	Glioma	glioma tissues 	Interaction(miR-17-5p-PANX1 )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Transwell Assay	We found that Circ-TLK1 was conspicuously up-regulated in glioma tissues compared with adjacent normal tissues, and the up-regulated Circ-TLK1 was significantly correlated with glioma patients' larger tumor volume and higher grades. In addition, bioinformatics analysis showed that miR-17-5p was a potential target of Circ-TLK1 and targeted at PANX1. Furthermore, through dual luciferase viability assay, Circ-TLK1 acted as a competing endogenous RNA by sponging miR-17-5p, which targeted and inhibited PANX1/MAPK/ERK expression. 	We found that Circ-TLK1 was conspicuously up-regulated in glioma tissues compared with adjacent normal tissues, and the up-regulated Circ-TLK1 was significantly correlated with glioma patients' larger tumor volume and higher grades.	Yes	Functionally, Circ-TLK1 over-expression facilitated glioma growth, migration and invasion, inhibited cell apoptosis, and accelerated PANX1/MAPK/ERK expression, while Circ-TLK1 low expression had the opposite effects. 	34181173
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[miR-200a-3p/PDL1 axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	In this study, we demonstrated that in NSCLC tissues, the expression level of MALAT1 was negatively correlated with that of miR-200a-3p, while positively correlated with PD-L1. Besides, MALAT1 promoted proliferation, mobility, migration, and invasion of NSCLC cells via sponging miR-200a-3p. PD-L1 was validated as a target of miR-200a-3p, and indirectly modulated by MALAT1.		Yes	Subsequently, CCK8 assay were conducted. The proliferation rate of CAL-12T cells with low-expressed MALAT1 significantly decreased than that of the control groExpression[Expression[up-expression]-expression], and the proliferation of CAL-12T cells with lowly expressed MALAT1 significantly increased after transfection of miR-200a-3p inhibitors (Figure 3(d)). 	31240979
hsa_circ_0008344	CircRNA	Homo sapiens	Glioma	glioma tumors and cells	Interaction(miR-638/SZRD1 Pathway)	In Vivo Experiment//Bioinformatics Analysis//Transfection//Tube Formation Assay//qPCR//CCK8//Luciferase Report Assay//EdU Staining//Transwell Assay	Abundances of circ_0008344 and SUZ RNA binding domain containing 1 (SZRD1) were highly elevated, while miR-638 was downregulated in glioma tumors and cells. Circ_0008344 might contribute to glioma progression through miR-638/SZRD1 axis, which might be a novel pathology and treatment target in glioma.		Yes	 Circ_0008344 was identified as a stable circRNA with a circular structure. Silencing circ_0008344 could restrain glioma proliferation, migration, invasion, and angiogenesis. Also, circ_00008344 knockdown suppressed glioma tumor growth. 	35394558
MALAT1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction( miR-124)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//MTT//Cell Apoptosis Assay//Cell Cycle Assay//IHC	In the present study, we found that the expression of MALAT1 was aberrantly increased in both human glioma tissues and cells and associated with poor prognosis in glioma patients. 	In the present study, we found that the expression of MALAT1 was aberrantly increased in both human glioma tissues and cells and associated with poor prognosis in glioma patients. 	Yes	We further found that MALAT1 silencing significantly inhibited glioma cell proliferation while induced cell cycle arrest and apoptosis. In parallel, knockdown of MALAT1 decreased tumor volume in vivo. 	33078370
hsa_circ_0000285	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-197-3p/CKS1B axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	We noted that circ_0000285 was highly expressed in glioma tissues and cells and that circ_0000285-silencing retarded tumor growth both in vitro and in vivo.  This effect was mediated by the binding of circ_0000285 to miR-197-3p, which silenced CKS1B, an essential driver of glioma cell proliferation and invasion.		Yes	We noted that circ_0000285 was highly expressed in glioma tissues and cells and that circ_0000285-silencing retarded tumor growth both in vitro and in vivo. 	35174774
MANCR	LncRNA	Homo sapiens	Lymphoma, Mantle-Cell	blood	Interaction[RUNX2]	qRT-PCR	 We found that serum MANCR and Runt-related transcription factor 2 (RUNX2) were upregulated in MCL patients when compared with those in healthy controls. Therefore, we conclude that downregulation of MANCR may inhibit cancer cell proliferation in MCL possibly by interacting with RUNX2.		Yes	MANCR overexpression promoted the proliferation of MCL cells, while MANCR silencing inhibited the proliferation of MCL cells. 	31650163
hsa_circ_0076931	CircRNA	Homo sapiens	Glioma	NBT tissues and cells	Interaction(miR-6760-3p/CCBE1)	cell invasion assay//qRT-PCR//migration assay	Hsa_circ_0007694 and hsa_circ_0008016 were memorably increased whereas hsa_circ_0076931 and hsa_circ_0076948 decreased in glioma compared with those in NBT. In addition, elevated hsa_circ_0076931 levels induced the expression of CCBE1 while suppressing miR-6760-3p expression. miR-6760-3p can bind to hsa_circ_0076931. 	 Additionally, hsa_circ_0076931 expression was negatively correlated with histological grade.	Yes	Overexpression of hsa_circ_0076931 inhibited proliferation, migration, and invasion while promoting apoptosis of glioma cells. 	34931668
MALR	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCC cells	Interaction(ILF3)	qRT-PCR//RNA Pull-Down	TAM-mediated secretion of TNFα drove MALR upregulation in ESCC cells.  Mechanistically, MALR bound the dsRBD1 domain of interleukin enhancer-binding factor 3 (ILF3), promoting ILF3 protein stability and ILF3-mediated liquid–liquid phase separation (LLPS), thereby enhancing HIF1α mRNA stability by preventing PARN-mediated degradation.	Clinically, high expression of MALR positively correlated with HIF1α target gene expression and indicated poor prognoses for patients with esophageal cancer. 	Yes	MALR promoted aerobic glycolytic activity and facilitated angiogenesis by activating the HIF1α signaling pathway.  Loss of MALR suppressed cell line–based and patient-derived xenograft tumor growth.	36264156
MALINC1	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer cells	Regulation	Cell Proliferation Assay//qRT-PCR//RNA-seq//Migration Assay	We determined that MALINC1 is an estrogen-estrogen receptor-modulated lncRNA enriched in the cytoplasmic fraction of luminal A/B breast cancer cells that is associated with worse overall survival in patients with primary invasive breast carcinomas. 	We determined that MALINC1 is an estrogen-estrogen receptor-modulated lncRNA enriched in the cytoplasmic fraction of luminal A/B breast cancer cells that is associated with worse overall survival in patients with primary invasive breast carcinomas. 	Yes	We determined that MALINC1 induces premalignant phenotypic changes by increasing cell migration in normal breast cells. Moreover, high MALINC1 expression in invasive carcinomas was associated with a pro-tumorigenic immune environment and a favorable predicted response to immunotherapy both in luminal and basal-like subtypes compared with low-MALINC1-expression tumors. 	35740485
MALAT2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cell lines	Expression[highly expressed]	CCK8//Cell Cycle Assay//qRT-PCR//Transwell Assay	MALAT1 was significantly up-regulated in laryngeal and hypopharyngeal carcinoma cells. 		Yes	MALAT1 down-regulation induced the increased apoptosis of both cell lines and suppressed cells' proliferation. Cells were arrested in G1/G2 phase and cells of S phase were significantly decreased. 	31792655
MALAT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[PI3K/AKT pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	In the present study, MALAT1 expression was significantly upregulated in gastric tumors compared with adjacent healthy tissue in patients with gastric cancer.	 Furthermore, MALAT1 plasma expression was higher in patients with gastric cancer compared with healthy controls and was found to have prognostic and diagnostic value independent of patients' lifestyle choices. 	Yes	Cell proliferation assay and Transwell migration and invasion results indicated that the overexpression of MALAT1 resulted in increased proliferation, migration and invasion of gastric cancer cells in vitro, possibly through activation of the phosphoinositide 3-kinase/protein kinase B pathway.	31186750
MALAT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[downregulating microRNA-204 ]	qRT-PCR//MTT//Colony Formation Assay//Western Blot	 To the best of our knowledge, the present study was the first to demonstrate that upregulated MALAT1 was associated with increased autophagy activation in GC tissues.In addition, the results revealed that MALAT1 inhibited microRNA (miR)-204 expression in GC cells. The present study also demonstrated that miR-204 repressed autophagy through the downregulation of LC3B and transient receptor potential melastatin 3 expression in GC cells. These results indicated that MALAT1 activated autophagy and promoted cell proliferation by downregulating miR-204 expression in GC.		Yes	Furthermore, this study reported that MALAT1 increased cell proliferation and enhanced autophagy activation in GC cells. 	31897197
MALAT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Expression[highly expressed]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//Colony Formation Assay//Transwell Assay	Higher expression of MALAT1 was detected in GC tissues than that of adjacent normal tissues, high MALAT1 expression is an independent risk for overall survival of gastric cancer patients. 	Higher expression of MALAT1 was detected in GC tissues than that of adjacent normal tissues, high MALAT1 expression is an independent risk for overall survival of gastric cancer patients. 	Yes	Knockdown of MALAT1 inhibited proliferation, migration and invasion of GC cells, while overexpression of MALAT1 Overexpression of MALAT1 yielded opposite results.	32214850
MALAT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[microRNA-22-3p-Mediated ErbB3]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 MALAT1 was significantly upregulated in GC tissues and cells and negatively associated with the survival of GC patients.Silencing of MALAT1 inhibited the proliferation and promoted the apoptosis of GC cells through upregulating miR-22-3p and downregulating ErbB3.	MALAT1 was significantly upregulated in GC tissues and cells and negatively associated with the survival of GC patients. 	Yes	Overexpression of MALAT1 significantly promoted the proliferation and inhibited the apoptosis of SGC-7901 cells, while silencing of MALAT1 exerts contrary effects on BGC-823 cells. Silencing of MALAT1 also significantly inhibited the tumor growth in mice. 	32021298
hsa_circ_0001982	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-1205/E2F1 axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 Circ_0001982 expression level was increased in glioma tissues and correlated with larger tumor size. Circ_0001982 directly targeted miR-1205, and miR-1205 directly targeted E2F1. Besides, circ_0001982 could up-regulate E2F1 expression via repressing miR-1205 expression. 	 Circ_0001982 expression level was increased in glioma tissues and correlated with larger tumor size. 	Yes	 Circ_0001982 overexpression enhanced glioma cell proliferation, migration, and invasion, and accelerated cell cycle progression while knocking down circ_0001982 exerted opposite effects.	35994229
MALAT1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissue 	Regulation[miR-145]	qRT-PCR	To investigate the role of MALAT1 in human BC progression, we detected MALAT1 expression levels based on tissue samples from 20 BC cases and 20 healthy controls and found MALAT1 expression levels to be significantly high (P<0.05).  This outcome revealed that MALAT1 promoted angiogenesis in BC, which may be related to the expression of miR‑145.		Yes	 The results revealed that MALAT1 knockdown could significantly inhibit proliferation, migration, and tube formation in vitro. 	30226550
circNEIL3	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(IGF2BP3 )	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	We identified circNEIL3, which could be cyclized by EWS RNA-binding protein 1(EWSR1), to be upregulated in glioma tissues and to correlate positively with glioma malignant progression.Mechanistically, circNEIL3 stabilizes IGF2BP3 (insulin-like growth factor 2 mRNA binding protein 3) protein, a known oncogenic protein, by preventing HECTD4-mediated ubiquitination. Moreover, circNEIL3 overexpression glioma cells drives macrophage infiltration into the tumour microenvironment (TME). 		Yes	Functionally, we confirmed that circNEIL3 promotes tumorigenesis and carcinogenic progression of glioma in vitro and in vivo. 	35031058
circABCC1	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-591/HMGA2 signaling)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//FISH//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//H&E Staining//Cell Proliferation Assay//Transwell Assay	CircABCC1 was highly expressed, and miR-591 was downregulated in glioma tissues and cells.Through the ceRNA mechanism, circABCC1 interacts with miR-591 to regulate the expression of HMGA2. CircABCC1 functions as an oncogene to promote the progression of glioma via the regulation of miR-591/HMGA2 signaling. 		Yes	Suppression of circABCC1 repressed the malignant behaviors of glioma cells and tumor growth.	35000195
hsa_circ_0001588	CircRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction(miR-1281/ERBB4 pathway)	In Vivo Experiment//IHC//Western Blot//Transfection//Tube Formation Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	Circ_0001588 and ERBB4 expressions were significantly upregulated, while miR-1281 was downregulated in glioma tissues and cells compared with control groups.Decreased expression of circ_0001588 in glioma cells led to significant decreases of cell proliferation, migration, invasion, and tube formation and an increase of cell apoptosis. 	 Circ_0001588 expression was closely related to tumor size and WHO grade of glioma.	Yes	Decreased expression of circ_0001588 in glioma cells led to significant decreases of cell proliferation, migration, invasion, and tube formation and an increase of cell apoptosis. Furthermore, circ_0001588 depletion suppressed tumor formation in vivo. 	34982356
MALAT1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues	Expression[highly expressed]	qRT-PCR//MTT//Transwell Assay	 MALAT1 was highly expressed in BC tissues compared with normal tissues adjacent to cancer as well as in BC cells.		Yes	In addition, inhibition the expression of MALAT1 could significantly suppress the proliferation, migration and invasion of BC cells.	35410813
hsa_circ_0008922	CircRNA	Homo sapiens	Glioma	 glioma tissues	Expression(highly expressed)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RNA-seq//Bioinformatics Analysis//Transwell Assay	We found that the expression of hsa_circ_0008922 in glioma tissues was 3.4 times higher than that in normal tissues. 	The expression of has_circ_0008922 was correlated with WHO tumor grade.	Yes	After down-regulating the expression of hsa_circ_0008922, malignant biological behavior of glioma cells was inhibited, such as cell proliferation, colony formation, migration, and invasion.  At the same time, it also induced apoptosis of glioma cells.	36570001
MALAT1	LncRNA	Homo sapiens	Breast Neoplasms	36 pairs of breast cancer and adjacent tissues	Interaction(miR‑26a/26b/ST8SIA4 axis)	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Invasion Assay//IF	Upregulated MALAT1 was a crucial predictor of poor breast cancer prognosis. Altered MALAT1 modulated cell progression in breast cancer. Moreover, miR‑26a/26b was confirmed as a direct regulator of MALAT1, and ST8SIA4 was predicted as a target of miR‑26a/26b. 		Yes	Functional analysis in human breast cancer cell lines demonstrated that MALAT1 modulated breast cancer cell tumorigenicity by acting as a competing endogenous lncRNA (ceRNA) to regulate ST8SIA4 levels by sponging miR‑26a/26b. 	34278507
MALAT1	LncRNA	Homo sapiens	Breast Neoplasms	71 intraoperative tumor specimens from BC patients and matched normal specimens 	Interaction(miR101-3p/mTOR/PKM2 pathway )	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The MALAT1 overexpressions in the BC tissues and cells were considered to be a predictor of poor prognosis. MALAT1 was anticipated to be an miR-101-3p target according to the dual-luciferase reporter gene assay results. Additionally, the mTOR/PKM2 pathway was directly targeted by miR-101-3p. 		Yes	Therefore, MALAT1 downregulation significantly inhibited BC progression, including cell growth, invasion, and migration. 	34650695
MALAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues 	interaction[sponging miR-508-5p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, we reported that MALAT1 expression is significantly upregulated in CRC and correlated with advanced TNM stage, lymph node metastasis, and worse prognosis in patients. Collectively, our findings indicated that MALAT1 could promote CRC progress by sponging miR-508-5p and enhancing RAB14 expression, which provides a therapeutic target in CRC treatment.	In the present study, we reported that MALAT1 expression is significantly upregulated in CRC and correlated with advanced TNM stage, lymph node metastasis, and worse prognosis in patients.	Yes	Functional assays revealed that MALAT1 knockdown reduced CRC cell growth and invasion abilities in vitro.	33344634
circHECTD1	CircRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Interaction(miR-296-3p/SLC10A7 axis)	In Vivo Experiment//Transfection//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	Then we confirmed that the level of circHECTD1 was significantly increased both in glioma tissues and cell lines, which is negatively correlated with the overall survival of patients. Luciferase reports and RNA immunoprecipitation data indicated that miR-296-3p was a direct target of circHECTD1 and that the miR-296-3p expression negatively regulated SLC10A7. Rescue experiments showed that the overexpression of SLC10A7 could impede the effects of circHECTD1 silencing on the proliferation and invasion of glioma cells. 	Then we confirmed that the level of circHECTD1 was significantly increased both in glioma tissues and cell lines, which is negatively correlated with the overall survival of patients. 	Yes	Knockdown of circHECTD1 inhibited proliferation and invasion in vitro, and also reduced the growth of tumor and prolonged the prognosis in vivo. Knockdown of circHECTD1 significantly elevated the miR-296-3p expression in LN229 and T98G cells.	33561315
circGFRA1	CircRNA	Homo sapiens	Glioma	 glioma specimens	Interaction(miR-99a)	Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay	 The results showed that circGFRA1 expression was overexpressed in glioma specimens. Moreover, circGFRA1 acts as a microRNA sponge for miR-99a. Furthermore, miR-99a was involved in the circGFRA1-regulated glioma cell behaviors. Silencing circGFRA1 reduced p/t-AKT, p/t-FOXO1 and p/t-mTOR expression levels via upregulating miR-99a expression.		Yes	Knockdown circGFRA1 declined viability, colony formation, proliferation and migrative potential, but enhanced U251 cell apoptosis. 	33994521
MALAT1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	regulation[miR-21]	qRT-PCR//Wound Healing Assay//Transwell Assay	 Compared with paracancerous tissues, MALAT1 expression was significantly increased in colon cancer tissues.MALAT1 can regulate miR-21 to regulate the migration and invasion of colon cancer cells.		Yes	 Inhibition of MALAT1 could inhibit colon cancer cell invasion and migration ability, and tumor formation in nude mice showed that the tumor volume and weight of the tumor-bearing mice were reduced after inhibiting the expression of MALAT1.	32521885
MALAT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC and matched adjacent non-tumor tissues，cell lines (HT-1376, RT112, 253J and T24)	Interaction[miR‑34a;CCND1]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	As indicated in Fig. 1A, the expression levels of MALAT1 were significantly increased in the BC tissues compared with the adjacent non-tumour tissues. The expression of MALAT1 in the BC cell lines (HT-1376, RT112, 253J and T24) and the normal urinary tract epithelial cell line SV-HUC-1 were also assessed. MALAT1 was also significantly Expression[Expression[up-expression]-expression]regulated in the BC cell lines compared with the SV-HUC-1 cells (Fig. 1D). knockExpression[down-expression] of MALAT1 significantly inhibited BC cell proliferation and migration by targeting microRNA (miR)‑34a. The expression levels of miR‑34a were significantly decreased in BC tissues and cell lines compared with that of adjacent non‑tumour tissues and SV‑HUC‑1 cells. In addition, the expression of miR‑34a was inversely correlated with the expression of MALAT1 in BC tissues. The present study revealed that cyclin D1 (CCND1) was identified as a target gene of miR‑34a, and its expression was negatively mediated by miR‑34a in BC cells. 	Furthermore, the expression levels of MALAT1 were significantly increased in the BC tissues at stage III-IV compared with that in the tissues at stage I-II (Fig. 1B). These patients with BC were subsequently divided into high- and low-MALAT1 expression groExpression[Expression[up-expression]-expression]s based on the mean expression value in the BC tissues. As indicated in Table I, high expression of MALAT1 was significantly associated with advanced Tumour, Node, Metastases (TNM) stage and positive lymph node metastasis. Furthermore, patients with high MALAT1 expression exhibited a shorter survival time when compared with those with a low MALAT1 expression (Fig. 1C).	Yes	Furthermore, knockExpression[down-expression] of MALAT1 significantly inhibited BC cell proliferation and migration by targeting microRNA (miR)‑34a. 	30387807
MALAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines (HSC3, SCC9, SCC15 and SCC25)	regulation[miR-101/EZH2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	qPCR analysis indicated that MALAT1 expression was obviously increased, and miR-101 was decreased in the OSCC tissues and cell lines.Collectively, these findings revealed that upregulation of MALAT1 facilitated OSCC proliferation and invasion by targeting the miR-101/EZH2 axis.		Yes	 Functional studies revealed that overexpression of MALAT1 promoted OSCC cell proliferation and invasion. 	32934732
MALAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	regulation[miR-143-3p/MAGEA9 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 QRT-PCR results showed that MALAT1 and MAGEA9 were expressed at higher levels and miR-143-3p was expressed at lower levels in OSCC tissues.Taken together, our results suggest that MALAT1 functions as a competing endogenous RNA (ceRNA) in promoting OSCC cell proliferation and migration abilities through the miR-143-3p/MAGEA9 axis, thus providing new therapeutic targets for treatment of OSCC.		Yes	 Dramatic suppression of cell proliferation and migration abilities were caused by MALAT1 knockdown or miR-143-3p overexpression in CAL-27 cells.	32879299
hsa_circ_0073237	CircRNA	Homo sapiens	Glioma	glioma cell lines	Interaction(miR-345/HDGF pathway)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	 Previous studies found that circRNA-hsa_circ_0073237 was upregulated in gliomas. Our further analyses of the biological function and molecular mechanism of hsa_circ_0073237 showed that hsa_circ_0073237 was also upregulated in glioma cell lines and could combine with miR-345 to inhibit its expression. Therefore, hsa_circ_0073237 can regulate the biological functions of glioma cells through miR-345/HDGF, thereby affecting the progression of tumors, indicating that the hsa_circ_0073237/miR-345/HDGF pathway may be a key target for the treatment of glioma.		Yes	Hsa_circ_0073237 siRNA, miR-345, and HDGF siRNA effectively inhibited cell viability and invasion and promoted cell apoptosis. When expression of hsa_circ_0073237 and miR-345 was inhibited simultaneously, cell viability, apoptosis, and invasion did not change significantly	34348265
MALAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(MALAT1/miR-224-5p/ KDM2A)	CCK8//qRT-PCR//MeRIP	METTL14 and lncRNA MALAT1 were upregulated, and miR-224-5p was downregulated in OSCC tissues and cells. Overexpression of MALAT1 and KDM2A or miR-224-5p downregulation reversed the inhibition of silencing METTL14 on OSCC cell proliferation. METTL14 induced m6A modification of MALAT1 to upregulate MALAT1. MALAT1 is comparatively bound to miR-224-5p to promote KDM2A transcription. In vivo, METTL14 promoted tumor growth via regulating MALAT1/miR-224-5p/ KDM2A.		Yes	Silencing METTL14 repressed OSCC cell viability and colony formation.	35467063
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Regulation[PI3K-Akt Signaling Pathway]	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. Our data revealed for the first time that MALAT1 increases stem cell-like properties by up-regulating RET via sponging miR-129-5p, and thus activates the PI3K-Akt signaling pathway and provides potential therapeutic targets for osteosarcoma treatment.		Yes	Overexpression of MALAT1 promoted osteosarcoma cell proliferation, migration, and invasion in vitro and enhanced tumor growth in a tumor xenograft mouse model.	30481748
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Regulation[miR‑34a/cyclin D1 axis]	qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	The results demonstrated that MALAT1 and CCND1 mRNA expression levels were upregulated and miR‑34a was downregulated in OS tissues and cells.  Moreover, MALAT1 functioned as a ceRNA to suppress miR‑34a expression and in turn upregulate CCND1 in OS cells. Rescue experiments further demonstrated that MALAT1 knockdown partially reversed anti‑miR‑34a‑mediated promotion on OS cell viability, migration and invasion; overexpression of CCND1 partially reversed the effects of MALAT1 silencing on OS progression. Furthermore, in vivo experiments also revealed that MALAT1 promoted OS tumor growth via miR‑34a inhibition and upregulating the expression of CCND1. In conclusion, the present study suggested that MALAT1 exerted its oncogenic function in OS by regulating the miR‑34a/CCND1 axis in OS, which may provide novel insight into the diagnosis and therapy for OS.	Additionally, MALAT1 expression was correlated with tumor size, clinical stage and distant metastasis in patients with OS. 	Yes	In addition, MALAT1 promoted OS cell viability, invasion and migration, while MALAT1 silencing exhibited opposing effects.	30365098
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction[binding to miR-34a/c-5p and miR-449a/b]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay	We found that MALAT1 was frequently upregulated in osteosarcoma samples and cell lines and a high level of MALAT1 predicted poor overall survival in osteosarcoma patients. Mechanistic investigations demonstrated that MALAT1, as a competing endogenous RNA (ceRNA), regulated osteosarcoma proliferation and metastasis through competitively binding to miR-34a/c-5p and miR-449a/b.	We found that MALAT1 was frequently upregulated in osteosarcoma samples and cell lines and a high level of MALAT1 predicted poor overall survival in osteosarcoma patients. 	Yes	Knockdown of MALAT1 inhibited proliferation, migration, and invasion of osteosarcoma cells. 	30793707
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	OS cell	Interaction(miR-150-5p/VEGFA signaling )	qRT-PCR//ELISA//Western Blot	MALAT1 expression in OS cells was significantly higher than in normal osteoblasts. Mechanistically, silencing MALAT1 downregulated vascular endothelial growth factor A (VEGFA) expression and upregulated miR-150-5p expression in OS cells, and MALAT1-mediated angiogenic induction by VEGFA in OS microenvironment. Moreover, MALAT1 directly targeted miR-150-5p and miR-150-5p directly target VEGFA in OS. Overexpression of miR-150-5p downregulates VEGFA expression in OS.		Yes	The functional analysis indicated that MALAT1 appears to enhance OS-induced angiogenesis, in vitro and in vivo analyses, endothelial cell proliferation and migration, chick embryo angiogenesis assay, and zebrafish xenograft model. 	34692524
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-485-3p/AKT3/mTOR signalling)	qRT-PCR//Western Blot	miR-485-3p was decreased while c-MET, AKT3, and MALAT1 were increased in human OS tissues and cells.  In addition, MALAT1 interacted with miR-485-3p and disinhibited c-MET and AKT3/mTOR signalling.		Yes	Knockdown MALAT1 or overexpression of miR-485-3p restrained OS tumour growth and lung metastasis in vivo.	33358903
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	OS cell lines and tissue specimens	Interaction(miR-124-3p/SphK1 signaling pathway )	CCK8//qRT-PCR	 MALAT1 was overexpressed in OS cell lines and tissue specimens, and knockdown of MALAT1 significantly inhibited cell proliferation and migration and increased cell apoptosis and the percentage of G0/G1 phase. Furthermore, MALAT1 could directly bind to miR-124-3p and inhibit miR-124-3p expression. Moreover, MALAT1 overexpression significantly relieved the inhibition on OS cell proliferation mediated by miR-124-3p overexpression, which involved the derepression of sphingosine kinase 1 (SphK1).		Yes	 MALAT1 was overexpressed in OS cell lines and tissue specimens, and knockdown of MALAT1 significantly inhibited cell proliferation and migration and increased cell apoptosis and the percentage of G0/G1 phase.	34373692
MALAT1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-590-3p)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	 The results indicated that MALAT1 was highly expressed in OS tissues and cell lines.  In addition, MALAT1 knockdown upregulated the expression of miR-590-3p in OS cells. In conclusion, MALAT1 was demonstrated to suppress cell apoptosis and induce cell proliferation, migration, invasion and EMT by inhibiting miR-590-3p in OS, which indicated that MALAT1 has potential value in the diagnosis and treatment of OS.		Yes	MALAT1 knockdown promoted apoptosis and suppressed proliferation, migration, invasion and epithelial- mesenchymal transition (EMT) of OS cells. Overexpression of miR-590-3p increased cell apoptosis and hampered cell proliferation, migration, invasion and EMT in OS cells. 	36277152
MALAT1	LncRNA	Homo sapiens	Parkinson Disease	serum	Expression(highly expressed)	qRT-PCR//Genotyping	The results showed that PD patients with high serum level of MALAT1 were associated with lower MMSE score and higher serum levels of IL-1β, IL-6, TNF-α and IFN-γ than patients carrying low serum level of MALAT1 (p < .05). Mutant alleles of SNPs in MALAT1, including rs3200401 (C>T) and rs4102217 (G>C), tended to elevate PD susceptibility and facilitate cytokine production, as compared with their wild alleles (p < .05). 		Yes	And LPS-exposed PC12 cells secreted larger amounts of inflammation cytokines in the pcDNA3.1-MALAT1 group than in the Mock group (p < .05). 	34291564
MALAT1	LncRNA	Homo sapiens	Parkinson Disease	Parkinson's disease cell model	Interaction(miR-135b-5p/GPNMB axis)	qRT-PCR//Luciferase Report Assay//Western Blot	 MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP+-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis.		Yes	 MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP+-stimulated cells. 	33726823
MALAT1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients and  HL-60 cells	Interaction( miR-146a/CXCR4 )	qRT-PCR//Western Blot	 Firstly, MALAT1 and CXCR4 were upregulated while miR-146a was downregulated in AML patients compared with healthy controls. We observed a negative correlation between miR-146a and MALAT1 or CXCR4, but a positive correlation between MALAT1 and CXCR4 in AML patients. 		Yes	Our results showed that MALAT1 regulates migration, proliferation and apoptosis by sponging miR-146a to regulate CXCR4 expression in AML cells, providing novel insights into the role of MALAT1 as a therapeutic target in AML.	33382018
MALAT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Regulation[MALAT1/miR-429 axis ]	qRT-PCR	We observed that MALAT1 was significantly upregulated in human cervical cancer cell lines compared with the ectocervical epithelial cells. In conclusion, we indicated that the MALAT1/miR-429 axis was involved in cervical cancer development.		Yes	Silencing of MALAT1 obviously reduced cervical cell viability, induced cell apoptosis, and repressed cell invasion capacity. Conversely, overexpression of MALAT1 exhibited an opposite phenomenon. 	30515786
hsa_circ_0001367	CircRNA	Homo sapiens	Glioma	Glioma Cells	Interaction(miR-545-3p/LUZP1 Axis )	In Vivo Experiment//Western Blot//Transfection//Tunel//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	 First, qRT-PCR was conducted, which showed that circ_0001367 level was downregulated in glioma tissues and cells. Taken together, the results of this study demonstrate that the circ_0001367/miR-545-3p/LUZP1 axis may be a novel target for glioma therapy.		Yes	Next, gain-of-function and loss-of-function assays were performed, which indicated that circ_0001367 inhibited the proliferation, migration and invasion of glioma cells. 	34869035
MALAT1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[miR-384/GOLM1 axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	MALAT1 was highly expressed in glioma tissues and cells. The MALAT1/miR-384/GOLM1 axis was first proposed in our report, enriching the action mechanism of MALAT1 in glioma.		Yes	MALAT1 knockdown inhibited autophagy, migration and invasion of glioma cells. 	32196610
hsa_circ_0001162	CircRNA	Homo sapiens	Glioma	 glioma tissues	Interaction(miR-936/ERBB4 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_0001162 was an overexpressed circRNA in glioma.  These results indicated that circ_0001162 contributed to the glioma progression via regulating the miR-936/ERBB4 axis, which laid a foundation for the pathomechanism and molecular treatment of glioma.		Yes	 Circ_0001162 promoted glioma cell proliferation, colony formation, migration and invasion in vitro. Tumorigenesis of glioma in vivo was also enhanced by circ_0001162. 	34057019
MALAT1	LncRNA	Homo sapiens	Ovarian Neoplasms	cell line	Interaction[targeting miR-503-5p]	RNA Pull-Down//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining	MALAT1 expression in OC cells was elevated compared with HOSE cells.  The expression of lncRNA-MALAT1 was negatively associated with the expression of miR-503-5p in OC cells, while luciferase assay and RNA pull-down together supported the direct binding of MALAT1 with miR-503-5p. Knockdown of MALAT1 was able to inhibit the activation of JAK2/STAT3 signal pathway, and MALAT1 overexpression was accompanied by activation of these factors.		Yes	MTT assay and EdU assay supported that si-MALAT1 could inhibit cell proliferation in OC cells.Treatment of si-MALAT1 results in increased cell apoptosis rate in both SKOV3 cells and OVCAR3 cells.	31496733
MALAT1	LncRNA	Homo sapiens	Ovarian Neoplasms	cell lines (HEY, OVCA420, OVARY1847, OVCA433, CAOV3, and SKOV3) 	Interaction[RBFOX2]	qRT-PCR//Microarray	SExpression[up-expression]pression of MALAT1 also resulted in decreased expression of RBFOX2, and alternative processing of the pro-apoptotic tumor sExpression[up-expression]pressor gene KIF1B. RBFOX2 sExpression[up-expression]pression resulted in preferential splicing of the pro-apoptotic isoform of KIF1B (KIFB1B-beta) and increased anoikis. The lncRNA MALAT1 facilitates a pro-metastatic phenotype in ovarian cancer by promoting alternative RNA processing and differential expression of anti-apoptosis and epithelial to mesenchymal transition (EMT)-related genes.		Yes	 MALAT1 knockdown resulted in decreased proliferation, invasion, anchorage-independent growth, and increased anoikis.	30294913
MALAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC clinical samples and cell lines	Interaction(miR-429)	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 Data found that MALAT1 was overexpressed in RCC clinical samples and cell lines. RT-PCR showed that miR-429 expression was downregulated in RCC cell lines, which was negatively correlated with that of MALAT1. Bioinformatics analysis suggested that miR-429 had complementary binding sequences with MALAT1, which was confirmed by dual-luciferase reporter assay.		Yes	Moreover, loss-of-functional experiments showed that MALAT1 knockdown suppress the proliferation, migration, and invasion abilities of RCC cells. 	29588438
circCHAF1A	CircRNA	Homo sapiens	Glioma	GSCs	Interaction(miR-211-5p/HOXC8 feedback loop)	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Bioinformatics Analysis//Transfection//Colony Formation Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//IHC//EdU Staining//IF	CircCHAF1A was overexpressed in glioma and related to the low survival rate. Mechanistically, circCHAF1A upregulated transcription factor HOXC8 expression in GSCs through miR-211-5p sponging. Then, HOXC8 can transcriptionally upregulate MDM2 expression and inhibited the antitumor effect of p53. 	CircCHAF1A was overexpressed in glioma and related to the low survival rate.	Yes	Functionally, it was found that no matter in vitro or in vivo, circCHAF1A can facilitate the proliferation and tumorigenesis of TP53wt GSCs. 	34017077
MALAT1	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues	regulation[miR-101-3p/STC1 Axis]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The expression of MALAT1 was elevated in CC tissues compared with adjacent normal tissues and was associated with lymph node metastasis, depth of invasion and tumor-node-metastasis (TNM) stage. MALAT1 may function as an oncogene in CC progression by affecting the miR-101-3p/STC1 axis, providing a hopeful therapeutic option for CC.	The expression of MALAT1 was elevated in CC tissues compared with adjacent normal tissues and was associated with lymph node metastasis, depth of invasion and tumor-node-metastasis (TNM) stage.	Yes	Up-regulation of MALAT1 promoted the proliferation, migration, and invasion and inhibited the apoptosis of CC cells; while MALAT1 knockdown exhibited opposite results. 	32431516
MALAT1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	regulation[Wnt/β-catenin signaling pathway]	Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry	MALAT1 expression was significantly higher in colon cancer vs. para-carcinoma tissues.Inhibition of MALAT1 expression in colon cancer may promote apoptosis and hinder cell proliferation by suppressing the activation of Wnt/β-catenin signaling pathway.		Yes	 Knockdown of MALAT1 by siRNA increased the number of apoptotic cells and the apoptosis rate at 24 h post-transfection in SW480 cells.	31733641
MALAT1	LncRNA	Homo sapiens	Colonic Neoplasms	 human colon cancer cell lines	Interaction(miR-129-5p/HMGB1 axis)	colony Formation Assay//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	In our study, it was demonstrated that MALAT1 was upregulated in human colon cancer cell lines including Lovo, HCT116, SW480, and HT29 cells compared to the normal human intestinal epithelial HIEC cells. Moreover, we observed that miR-129-5p was downregulated in colon cancer cells with a significant increase of HMGB1 expression. Inhibition of MALAT1 can inhibit the proliferation of colon cancer SW480 and HCT116 cells and next, bioinformatics analysis was used to predict the target microRNA of MALAT1. Taken together, our results indicated that MALAT1/miR-129-5p/HMGB1 axis could be provided as an important prognostic biomarker in colon cancer development.		Yes	 Inhibition of MALAT1 can inhibit the proliferation of colon cancer SW480 and HCT116 cells and next, bioinformatics analysis was used to predict the target microRNA of MALAT1. 	29226325
MALAT1	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	clinical carcinoma tissues	Expression [highly expressed]	qRT-PCR//Wound Healing Assay	Herein, we observed the consistent upregulation of MALAT1 in MYST4-overexpressing cell lines, while MALAT1 was frequently found to be upregulated in various types of clinical carcinoma tissues, especially EOC. 		Yes	We found that MALAT1 overexpression in EOC cell lines significantly increased drug resistance, cell migration, and invasion. Furthermore, the concomitant overexpression of MALAT1 in EOC cells and CAFs dramatically increased EOC cell invasion. Accordingly, a mechanistic investigation of MALAT1 overexpression in EOC cells showed that expressions of the cytokines interleukin (IL)-1β and p-P38/p-NFκB/Cox2/prostaglandin E2 (PGE2) signaling were significantly increased, which stimulated inflammatory responses, whereas cell apoptosis was inhibited due to increased Bcl-2 levels and reduced Caspase3 levels. 	34638541
MALAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction[PI3K/Akt pathway]	Western Blot//CCK8//RIP//EdU Staining//ChIP	MALAT1 was highly expressed and the expression of miR‑22‑3p was suppressed in RCC tissues and cell lines. In conclusion, lncR‑MALAT1 affected the proliferation and migration of RCC cells by targeting miR‑22‑3p through the inactivation of the PI3K/Akt signaling pathway.		Yes	ShRNA‑mediated knockdown of MALAT1 significantly inhibited the viability and mobility of RCC cells in vitro and in vivo.	30431104
MALAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction[BIRC5]	qRT-PCR	The expression levels of BIRC5 and MALAT1 were higher in RCC tissues and cell lines than in adjacent normal tissues and a normal renal cortex proximal tubule epithelial cell line. Our study demonstrated that MALAT1 functions as a miR-203 decoy to increase BIRC5 expression in RCC.		Yes	BIRC5 and MALAT1 promoted cell proliferation yet decreased the percentage of RCC cells at G0/G1 phase.	31250518
MALAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 786‑O‑EVs on RCC cells	Regulation	Western Blot//qRT-PCR//MTT//Colony Formation Assay//Invasion Assay	MALAT1 knockdown attenuated the promotive effect of sole 786‑O‑EVs on RCC cells. MALAT1 located ETS1 in the TFCP2L1 promoter and negatively regulated TFCP2L1, and ETS1 protein could specifically bind to MALAT1. 		Yes	MALAT1 knockdown attenuated the promotive effect of sole 786?O?EVs on RCC cells. 	34278501
MALAT1	LncRNA	Homo sapiens	Osteoarthritis	cartilage tissues 	Regulation[MALAT1/miR-145 axis ]	Flow Cytometry//qRT-PCR	 MALAT1 was upregulated, and miR-145 was downregulated in OA samples and IL-1β-induced chondrocytes. An MALAT1/miR-145 axis contributes to ECM degradation in IL-1β-induced chondrocytes through targeting ADAMTS5, suggesting that MALAT1/miR-145/ADAMTS5 signaling may underlie human OA pathogenesis.		Yes	Functionally, overexpression of MALAT1 inhibited chondrocyte viability and promoted cartilage ECM degradation in IL-1β-induced chondrocytes. 	31637891
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	Expression(highly expressed)	qRT-PCR	The expression of MALAT1 was markedly upregulated in HCC tissues compared with PANTs. 	High MALAT1 expression was associated with mutations in two genes leading to poor prognosis and may upregulate some prognostic risk genes through methylation. 	Yes	 MALAT1 was significantly co-expressed with various signatures of genes involved in HCC progression, including the cell cycle, DNA damage repair, mismatch repair, homologous recombination, molecular cancer m6A, exosome, ferroptosis, infiltration of lymphocyte (p < 0.05). 	36685103
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Interaction[sponging miR-140]	qRT-PCR	 We revealed that the expression of MALAT1 and VEGF-A was significantly increased in HCC cells.Mechanistically, the interaction between MALAT1 and miR-140 or between miR-140 and VEGF-A was confirmed by multiple assays. Besides, a negative correlation between MALAT1 and miR-140 was found in HCC tissues. Furthermore, miR-140 inhibition significantly increased VEGF-A expression, promoted angiogenesis of HUVECs, and redirected the polarization of macrophages toward the M2 subset. In addition, in vivo studies also verified the regulatory network of the MALAT1/miR-140 axis on VEGF-A in HCC progression. In summary, this study revealed the mechanism that MALAT1 worked as a putative HCC promotor via inhibiting miR-140. Therefore, targeting MALAT1 or miR-140 might alleviate the progression of HCC in the future.		Yes	 Knockdown of MALAT1 in HCC cells suppressed the production of VEGF-A, impaired the angiogenesis of HUVECs, and facilitated the polarization of macrophage toward the M1 subset.	31693399
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[MALAT1/miR-124-3p/Slug axis]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//IHC//Transwell Assay	 MALAT1 expression was upregulated in HCC tissues and positively correlated with Slug expression.MALAT1 and miR-124-3p bind directly and reversibly to each other. MALAT1 silencing inhibited cell migration and invasion. miR-124-3p inhibited HCC metastasis by targeting Slug.		Yes	MALAT1 silencing inhibited cell migration and invasion.	31466138
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[BRG1 ]	RNA Pull-Down//Western Blot//qPCR//CCK8//RIP//Cell Cycle Assay//ELISA//IHC	Here, we found that lncRNA metastasis associated lung adenocarcinoma transcript1 (MALAT1) was upregulated in HCC tumor tissues. Mechanistically, MALAT1 recruited Brahma-related gene 1 (BRG1), a catalytic subunit of chromatin remodeling complex switching/sucrose non-fermentable (SWI/SNF), to the promoter region of IL-6 and CXCL8, and thus facilitated NF-κB to induce the expression of these inflammatory factors. 		Yes	 Here, we found that lncRNA metastasis associated lung adenocarcinoma transcript1 (MALAT1) was upregulated in HCC tumor tissues, and knockdown of MALAT1 suppressed proliferation, cell cycle and invasion of HCC cells in response to lipopolysaccharide (LPS) stimulation.Importantly, in vivo silencing of MALAT1 in HCC tissues inhibited growth of HCC xenografts, and also suppressed the expression of pro-inflammatory factors in HCC tissues accordingly.	30546959
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[ sponging miR-125a-3p]	qRT-PCR//Luciferase Report Assay//Western Blot	 HCC tissues exhibited MALAT1 upregulation.These results indicate that MALAT1 modulates FOXM1 expression via being a miR-125a-3p sponge, thus promoting HCC progression.		Yes	MALAT1 knockdown disrupted proliferation and invasion, whereas miR-125a-3p knockdown partially reversed this phenotype.	31777593
circPOSTN	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction( miR-185-5p/KIF1B)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 CircPOSTN was highly expressed in glioma tissues and cells. Mechanistically, circPOSTN acted as miR-185-5p sponge to up-regulate the expression of its target KIF1B. Moreover, miR-185-5p inhibition reversed the anticancer effects of circPOSTN knockdown on glioma tumorigenesis, and miR-185-5p re-expression suppressed the malignant phenotype of glioma cells via targeting KIF1B.		Yes	Knockdown of circPOSTN restrained glioma cell proliferation, migration and invasion in vitro, as well as hindered glioma xenograft growth in vivo. 	34974134
hsa_circ_0002109	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-129-5P/EMP2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Invasion Assay//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//EdU Staining	In this study, we found that circRNA-0002109 was highly expressed in glioma tissues and cell lines.  Investigations into the relevant mechanisms showed that circRNA-0002109 upregulated the expression of EMP2 through endogenous competitive binding of microRNA-129-5P (miR-129-5P), which partially alleviated the inhibitory effect of miR-129-5P on epithelial membrane protein-2 (EMP2) and ultimately promoted the malignant development of glioma. 		Yes	Downregulation of circRNA-0002109 expression inhibited the proliferation, migration, and invasion of glioma cells and inhibited the malignant progression of tumors in vivo. 	34938603
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[microRNA-146a/PI3K/Akt/mTOR axis]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	MALAT1 expression was higher in HCC tissues than in normal tissues. Moreover, effects of MALAT1 downregulation on HCC cells were abolished by miR-146a inhibition. miR-146a directly targeted the 3'-untranslated region of PI3K, and PI3K protein level was clearly decreased upon miR-146a mimic transfection.		Yes	 MALAT1 upregulation promoted HCC cell proliferation, whereas MALAT1 downregulation promoted HCC apoptosis and autophagy.	32435156
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	doxorubicin-resistant HCC tissues and cells	Interaction(miR-3129-5p/Nova1 axis)	In Vivo Experiment//Western Blot//qRT-PCR//migration assay//Cell Viability Assay//Luciferase Report Assay//Invasion Assay	MALAT1 and Nova1 were upregulated, while miR-3129-5p expression was decreased in doxorubicin-resistant HCC tissues and cells. Elevation of LncRNA MALAT1 mediated doxorubicin resistance and the progression of HCC via a MALAT1/miR-3129-5p/Nova1 axis. 		Yes	Knockdown of MALAT1 regulated doxorubicin resistance of HCC cells through inhibiting cell proliferation, migration, invasion and promoting apoptosis, but antisense miR-3129-5p released the functional effect of MALAT1 knockdown. Xenograft tumor model suggested that dysregulation of MALAT1 regulated tumor growth and Nova1 to mediate doxorubicin resistance of HCC cells by as a sponge for miR-3129-5p in vivo.	34058824
circNFIX	CircRNA	Homo sapiens	Glioma	glioma tissues and cells	Regulation[miR-378e/RPN2 axis ]	RNA Pull-Down//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 The expression of circNFIX was enhanced in glioma tissues and cells compared with matched controls and high expression of circNFIX indicated poor outcomes of patients.  Knockdown of circNFIX inhibits progression of glioma in vitro and in vivo by increasing miR-378e and decreasing RPN2, providing a novel mechanism for understanding the pathogenesis of glioma.		Yes	 Knockdown of circNFIX led to arrest of cell cycle, inhibition of glycolysis, migration and invasion and promotion of apoptosis in glioma cells. 	31888753
MALAT1	LncRNA	Homo sapiens	Diabetic Retinopathy	cell lines	Regulation[miR-125b/VE-cadherin axis ]	Western Blot//qRT-PCR//MTT//ELISA//Transwell Assay	 MALAT1 and VE-cadherin were up-regulated while miR-125b was down-regulated in hRMECs treated with HG. Knockdown of MALAT1 inhibited cell proliferation, migration and angiogenesis of hRMECs via suppressing the VE-cadherin/β-catenin complex through targeting miR-125b. Inhibition of MALAT1 may serve as a potential target for anti-angiogenic therapy for DR.		Yes	Knockdown of MALAT1 inhibited the proliferation, migration, tube formation and vascular permeability of hRMECs induced by HG through up-regulating miR-125b. 	30988072
MALAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	Regulation(MALAT1-FOXP3-GINS1 axis)	RNA Pull-Down//Western Blot//Co-IP//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//IF	In this study, the clinicopathologic significance of MALAT1 and GINS1 in NSCLC was investigated, a positive correlation in their expression was found. The silencing of MALAT1 decreased GINS1 expression and inhibited NSCLC proliferation in vitro and in vivo. The upregulation of GINS1 reversed NSCLC proliferation inhibited by MALAT1 knockdown. FOXP3 (forkhead box protein 3) was identified as the critical transcription factor for GINS1 transcription. In addition, MALAT1 could stabilize FOXP3 by binding to zinc finger (ZF) domain and leucine zipper (LZ) domain of FOXP3. Interestingly, these two domains were also interaction domains for FOXP3 binding with E3 ligase STUB1 (STIP1 homology and U-box containing protein 1). In this way, MALAT1 masked the protein-interacting domain, and inhibited FOXP3 ubiquitination by STUB1. 		Yes	The silencing of MALAT1 decreased GINS1 expression and inhibited NSCLC proliferation in vitro and in vivo. The upregulation of GINS1 reversed NSCLC proliferation inhibited by MALAT1 knockdown. FOXP3 (forkhead box protein 3) was identified as the critical transcription factor for GINS1 transcription. 	33972684
LY6E-DT	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	Expression[highly expressed]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//IP//Colony Formation Assay	 LOC100133669 was upregulated in ESCC tissues compared with adjacent non-tumour tissues. 	High LOC100133669 expression was associated with poor prognosis of patients with ESCC.	Yes	Knockdown of LOC100133669 inhibited ESCC cell proliferation and cell cycle progression, while overexpression of LOC100133669 showed the opposite effects. 	32130753
LURAP1L-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(LURAP1L/IKK/IκB/NF-κB signaling pathway)	qRT-PCR//IF	Therefore, LURAP1L-AS1 was selected and PDGF-BB was demonstrated to upregulate the expression of LURAP1L-AS1 and LURAP1L, which was reversed by a PDGFR-β inhibitor. The present study indicates that LURAP1L-AS1/LURAP1L/IKK/IĸB/NF-κB plays an important regulatory role in PDGF-BB-induced fibroblast activation and may become a potential target for the treatment of OSCC.		Yes	Subsequently, knocking down LURAP1L-AS1 suppressed the expression of PDGF-BB-induced fibroblast activation marker protein α-smooth muscle actin, fibroblast activation protein-α, PDGFR-β and phosphorylated (p)-PDGFR-β. IKKα, p-IĸB and p-NF-κB were downregulated by the knockdown of LURAP1L-AS1 and upregulated by overexpression of LURAP1L-AS1. 	34079593
LUNAR1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[suppress IGF1]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Significantly increased expression of LUNAR1 in clinical CRC specimens was detected compared with that in matching normal tissues.Moreover, the inhibition of LUNAR1 can significantly suppress IGF1 signalling in CRC. 	LUNAR1 expression in CRC was found to be associated with the tumour aggressiveness, disease-free survival and overall survival of patients. 	Yes	 The downregulation of LUNAR1 in SW620 cells inhibited cell proliferation, migration, invasion and tumour growth while inducing apoptosis.	31882986
LUNAR1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[miR-495-3p/MYCBP axis]	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	RT?qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients.In conclusion, LUNAR1 accelerates CRC progression via the miR‑495‑3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.	RT?qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients.	Yes	Moreover, CCK?8, clone formation, wound?healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis.	33300052
LUCRC	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[Expression[Expression[highly expressed]-expression]-expression]	qRT-PCR//Wound Healing Assay//RNA-seq//Transwell Assay	It was found that LUCRC was nearly undetectable in six out of seven healthy control donors, but it was expressed in a significantly higher level in all seven colorectal cancer patients (Figure 5).		Yes	We then tested whether these lncRNAs affect colorectal cancer cell proliferation by using HCT116 as a model cell line. HCT116 cells were transfected with control siRNA (siCTL) or siRNA specifically targeting each individual lncRNA, followed by cell proliferation assay. Out of the 10 lncRNAs being tested, knockExpression[down-expression] of several of them resulted in growth defects of HCT116 cells and lncRNA LOC105371049 seemed to affect HCT116 cell growth the most (Figure 2F). The knockExpression[down-expression] efficiency of siRNAs targeting the 10 lncRNAs was examined by RT-qPCR analysis (Figure S2F). We named lncRNA LOC105371049 as LUCRC (LncRNA Expression[Expression[up-expression]-expression]regulated in Colorectal Cancer).	32082365
circERBB2	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Interaction(miR-136-5p)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	We observed that circ-ERBB2 was overexpressed in TNBC, and TNBC patients with high circ-ERBB2 expression levels had a poor prognosis.	We observed that circ-ERBB2 was overexpressed in TNBC, and TNBC patients with high circ-ERBB2 expression levels had a poor prognosis.	Yes	 Functionally, circ-ERBB2 knockdown constrained TNBC growth in vivo, reduced the Warburg effect, accelerated apoptosis, and repressed the proliferation, migration, and invasion of TNBC cells in vitro. Mechanically, circ-ERBB2 sponged microRNA 136-5p (miR-136-5p) to elevate pyruvate dehydrogenase kinase 4 (PDK4) expression. 	34370552
LUCAT1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and paracancer tissues 	Regulation[miR-134-5p/YWHAZ axis ]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	the expression of lncRNA LUCAT1 in gastric cancer tissue was significant higher than that in adjacent tissues. LncRNA LUCAT1 could promote proliferation and invasion of gastric cancer by regulating miR-134-5p/YWHAZ axis.	 Patients with high LUCAT1 level displayed short overall survival and disease-free survival periods. 	Yes	LUCAT1 knockdown or miR-134-5p overexpression decreased the proliferation, colony formation, migration and invasion of SGC7901 cells.	31545227
LUCAT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines and tissues 	regulation[CXXC4 and SFRP2 ]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Colony Formation Assay	LUCAT1 expression in GC cell lines and tissues was significantly elevated, compared to that in normal gastric cells and adjacent non-tumor tissues (p<0.001). We concluded that LUCAT1 induces methylation of CXXC4 and SFRP2, thereby regulating Wnt/β-catenin signaling in GC.		Yes	Two different siRNAs for LUCAT1 reduced cell proliferation, invasion, and migration, compared to siCT (p<0.05), and these reductions were restored by pcDNA-LUCAT1 (p<0.05).	33107235
LUCAT1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues ,cell lines	Interaction[lnc-LUCAT1/miR-7-5p-SOX2]	Western Blot//CCK8//qRT-PCR//EdU Staining//Transwell Assay	Our results indicated that the expression of lnc-LUCAT1 was highly up-regulated in breast cancer tissues and cell lines.Moreover, lnc-LUCAT1 was found to be a target of miR-7-5p. There was a negative correlation between lnc-LUCAT1 and miR-7-5p. The reduction of miR-7-5p was required in the augmentation of breast cancer development induced by lnc-LUCAT1 over-expression. In addition, SOX2 acted as a target of miR-7-5p. SOX2 was an oncogene in breast cancer through promoting cell proliferation, migration and invasion. The in vivo study confirmed the role of lnc-LUCAT1 in promoting tumor growth, accompanied with down-regulated SOX2 expression, whereas up-regulated miR-7-5p.		Yes	Over-expression of lnc-LUCAT1 enhanced cell proliferation, migration and invasion in breast cancer cell lines. 	31635802
circGNB1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	cell lines	regulation[ miR-141-5p-IGF1R Axis]	Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Microarray	Validating by qRT-PCR, circGNB1 was overexpressed in TNBC cell lines and high expression of circGNB1 was associated with worse clinical features and survival outcomes. Altogether, our study demonstrated the pivotal role of circGNB1-miR-141-5p-IGF1R axis in TNBC growth and metastasis though the mechanism of competing endogenous RNAs.	Validating by qRT-PCR, circGNB1 was overexpressed in TNBC cell lines and high expression of circGNB1 was associated with worse clinical features and survival outcomes.  The expression of circGNB1 was positively correlated with tumor size and clinical stage, and high expression of circGNB1 was an independent risk factor for TNBC patients.	Yes	Both in vitro and in vivo assays revealed that knockdown of circGNB1 significantly suppressed cell proliferation, migration and tumor growth.	32194644
LUCAT1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	regulation[LUCAT1/miR-181a-5p axis]	qRT-PCR//Luciferase Report Assay	qRT-PCR analysis indicated that, compared with the adjacent tissues and MCF-10A normal breast epithelial cells, LUCAT1 was markedly up-regulated in the breast cancer tissues and five BC cell lines, including MDA-MB-231, MDA-MB-468, MDA-MB-435, SKBR3, and MCF-7.  Our data indicate that LUCAT1/miR-181a-5p axis can serve as a novel therapeutic target in breast cancer.		Yes	 The knockdown of LUCAT1, through the transfection of small interfering RNA (siRNA) specific to LUCAT1, resulted in inhibition of proliferation in breast cancer cells. 	32998707
LUCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[RPL40-MDM2-p53 pathway]	qRT-PCR//Microarray	Among them, we found that the lncRNA lung cancer-associated transcript 1 (LUCAT1) was upregulated in CRC tissues and was closely associated with poor overall survival of CRC patients, through analysis of clinical data and The Cancer Genome Atlas.  Mechanistically, bioinformatic analysis indicated that low expression of LUCAT1 was associated with the p53 signaling pathway. Chromatin isolation by RNA purification followed by mass spectrometry and RNA immunoprecipitation revealed that LUCAT1 bound with UBA52, which encodes ubiquitin and 60S ribosomal protein L40 (RPL40). We found that RPL40 functions in the ribosomal protein-MDM2-p53 pathway to regulate p53 expression. Taken together, our findings indicate that suppression of LUCAT1 induces CRC cell cycle arrest and apoptosis by binding UBA52 and activating the RPL40-MDM2-p53 pathway. These results implicate LUCAT1 as a potential prognostic biomarker and therapeutic target for CRC.	Among them, we found that the lncRNA lung cancer-associated transcript 1 (LUCAT1) was upregulated in CRC tissues and was closely associated with poor overall survival of CRC patients, through analysis of clinical data and The Cancer Genome Atlas. 	Yes	Functional studies indicated that LUCAT1 promoted CRC cell proliferation, apoptosis, migration, and invasion in vitro and in vivo. Furthermore, knockdown of LUCAT1 rendered CRC cells hypersensitive to oxaliplatin treatment.	30690837
LUCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[ regulate MYC expression]	qRT-PCR	LUCAT1 is identified as a putative oncogene, which is significantly upregulated in CRC and is associated with poor prognosis. Our results suggest that LUCAT1 plays a critical role in CRC cell proliferation by inhibiting the function of NCL via its G-quadruplex structure and may serve as a new prognostic biomarker and effective therapeutic target for CRC.		Yes	 Loss of LUCAT1 restricts CRC proliferative capacities in vitro and in vivo.	33097685
LUCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(MiR-133b)	RIP//Luciferase Report Assay//Transwell Assay	MiR-133b was expressed at low levels in CRC tissues, and LUCAT1 was highly expressed, with an inverse correlation between them. However, the dual luciferase assay showed that miR-133b did not directly target LUCAT1.		Yes	LUCAT1 promoted the migration and invasion of HCT116 and SW620 cells. Overexpression of LUCAT1 attenuated the inhibition of cell migration and invasion induced by miR-133b. 	33541136
LUCAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[ inhibiting ANXA2 ]	RNA Pull-Down//Northern Blot//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//FISH//Invasion Assay	Our results demonstrated that LUCAT1 was up-regulated in HCC tissues and cells. Furthermore, RNA pulldown and Western blot assays indicated that LUCAT1 inhibited the phosphorylation of Annexin A2 (ANXA2) to reduce the degradation of ANXA2-S100A10 heterotetramer (AIIt), which in turn accelerated the secretion of plasminogen into plasmin, thereby resulting in the activation of metalloprotease proteins. 		Yes	Loss- and gain-of-function studies revealed that LUCAT1 promotes the proliferation and metastasis of HCC cells in vitro and in vivo.	30588744
LUCAT1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cell lines	interaction[miR-199a-5p]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	LncRNA LUCAT1 was highly expressed in three human ovarian cancer cell lines compared to that in normal ovarian surface epithelial cell line (p<0.05).LncRNA LUCAT1 is overexpressed in ovarian cancer cells, which may target miR-199a-5p to exert its effects on driving the malignant development of ovarian cancer.		Yes	The cell proliferation rate in SK-OV-3 cells with lncRNA LUCAT1 knockdown was remarkably lower in comparison to that in control group. 	32141534
LUCAT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder carcinoma tissue and cells	regulation[Targeting miR-181c-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The results demonstrated that LUCAT1 was overexpressed in bladder cancer tissue and cells, while miR-181c-5p showed a low expression pattern as compared to normal bladder cells and tissues. Collectively, this study reveals that knockdown of LUCAT1 inhibits the migration and invasion of bladder cancer cells in a miR-181c-5p-dependent manner, which may be related to KRAS downregulation.		Yes	Cell proliferation, migration, and invasion capacities were significantly impaired, and cell apoptosis was enhanced when LUCAT1 was silenced in UM-UC-3 and T24 cell lines, but this effect was abolished by miR-181c-5p downregulation. 	33282949
LUCAT1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	pancreatic ductal adenocarcinoma tissues	Interaction[sponging miR-539]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	 The qRT-PCR analysis and in situ hybridization staining showed that lncRNA LUCAT1 expression was significantly increased in tumorous tissues compared with adjacent normal tissues.Mechanistic studies uncovered that lncRNA LUCAT1 acted as a molecular sponge of miR-539 and that miR-539 mediated the effects of lncRNA LUCAT1 on PDAC cell proliferation, cell cycle progression, and motility. Collectively, our findings may offer some novel insights into understanding lncRNA LUCAT1 in PDAC.		Yes	unctional studies demonstrated that lncRNA LUCAT1 knockdown dramatically sExpression[up-expression]pressed PDAC cell proliferation, induced cell cycle arrest and inhibited cell migration and invasion. Tumor xenograft in vivo assays displayed that lncRNA LUCAT1 inhibited tumorigenecity of PDAC cells. 	31789465
LUCAT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction[sponging miR-181a]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//ChIP	In this study, we, first, confirmed that LUCAT1 acted as an up-regulated lncRNA by analyzing the data from GCTA dataset and RT-PCR in both CC tissues and cell lines. Mechanistically, Bioinformatic tools predicted that miR-181a may target LUCAT1, which was confirmed using luciferase reporter assay and RNA immunoprecipitation (RIP) assays. Overall, our findings showed that SP1-activated LUCAT1 exerts an oncogenic function in CC by binding to miR-181a, suggesting that miR-181a may be a ponderable and promising therapeutic target for CC.	 Then, clinical assays showed that LUCAT1 was associated with advanced clinical progression and poor prognosis of CC patients.Importantly, multivariate Cox model confirmed that LUCAT1 expression was an independent prognostic factor for both 5-year overall survival in CC. 	Yes	Then, lost-function assays revealed that knockdown of LUCAT1 significantly suppressed CC cells proliferation, colony formation, migration, invasion and EMT by a series of cells experiments. 	30831032
LUCAT1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues, cell lines	Interaction[modulating miR-5702]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	In our study, we identified that LUCAT1 expression was dramatically enhanced in TNBC samples and cells.	High LUCAT1 expression was strongly associated with advanced stages and poor prognosis of TNBC.	Yes	Moreover, miR-5702 was proved to directly bind to LUCAT1 and be negatively modulated by LUCAT1. Knockdown of miR-5702 reversed the suppressing influences of LUCAT1 depletion on TNBC progression. In conclusion, it was the first investigation to shed light on the significant function and underlying regulatory mechanism of LUCAT1 in TNBC tumorigenesis. 	31399501
LVBU	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Regulation(BCL6-p53 signaling axis)	RNA Pull-Down//ChIP	Here, we characterized a hypoxia-induced lncRNA LVBU (lncRNA regulation via BCL6/urea cycle) that is highly expressed in colorectal cancer (CRC) and correlates with poor cancer prognosis. Mechanistically, overexpression of LVBU competitively bound miR-10a/miR-34c to protect BCL6 from miR-10a/34c-mediated degradation, which in turn allows BCL6 to block p53-mediated suppression of genes (arginase1 ARG1, ornithine transcarbamylase OTC, ornithine decarboxylase 1 ODC1) involved in UC/polyamine synthesis. Taken together, elevated LVBU can regulate BCL6-p53 signaling axis for systemic UC/polyamine synthesis reprogramming and confers a predilection toward CRC development.	Here, we characterized a hypoxia-induced lncRNA LVBU (lncRNA regulation via BCL6/urea cycle) that is highly expressed in colorectal cancer (CRC) and correlates with poor cancer prognosis. 	Yes	 Increased LVBU expression promoted CRC cells proliferation, foci formation and tumorigenesis. Further, LVBU regulates urea cycle and polyamine synthesis through BCL6, a negative regulator of p53. 	35906392
hsa_circ_102229	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-152-3p/PFTK1 pathway)	In Vivo Experiment//Western Blot//ISH//Transfection//EdU Staining//Tunel//CCK8//qRT-PCR//Flow Cytometry//IF//FISH//Luciferase Report Assay//Microarray//IHC//Bioinformatics Analysis//Transwell Assay	In TNBC tissues and cells, hsa_circ_102229 was remarkably up-regulated. Furthermore, hsa_circ_102229 directly targeted miR-152-3p and could regulate the expression of PFTK1 by targeting miR-152-3p.	Patients with TNBC presenting high hsa_circ_102229 exhibited poor prognosis. 	Yes	Moreover, hsa_circ_102229 could promote the migration, proliferation and invasion, whereas it inhibited the apoptosis of TNBC cells.	34031947
MAGI2-AS3	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC tissues	Interaction[ upregulating CDK6]	CCK8//qRT-PCR	qRT-PCR results showed that CDK6 and MAGI2-AS3 were both up-regulated in CSCC and positively correlated with each other.In CCK-8 assay, MAGI2-AS3 and CDK6 over-expression led to increased proliferation rate of CSCC cells by reducing CDK6 levels, while MAGI2-AS3 siRNA didn't. 	High levels of MAGI2-AS3 were associated with the poor survival of CSCC patients.	Yes	In CCK-8 assay, MAGI2-AS3 and CDK6 over-expression led to increased proliferation rate of CSCC cells by reducing CDK6 levels, while MAGI2-AS3 siRNA didn't. 	31832086
circBACH2	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	The 38 pairs of TNBC cancerous tissues and adjacent normal tissues 	Interaction(miR-186-5p and miR-548c-3p)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//FISH//Luciferase Report Assay//H&E Staining//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	Among them, circBACH2 was most significantly elevated in TNBC cancerous tissues and its high expression was positively correlated to the malignant progression of TNBC patients. Mechanistically, circBACH2 sponged miR-186-5p and miR-548c-3p, thus releasing the C-X-C chemokine receptor type 4 (CXCR4) expression. 	Among them, circBACH2 was most significantly elevated in TNBC cancerous tissues and its high expression was positively correlated to the malignant progression of TNBC patients.	Yes	In normal human mammary gland cell line, the overexpression of circBACH2 facilitated epithelial to mesenchymal transition and cell proliferation. In TNBC cell lines, circBACH2 knockdown suppressed the malignant progression of TNBC cells. 	33875646
MAGI2-AS3	LncRNA	Homo sapiens	Liver Neoplasms	tumor tissues	Interaction(miRNA-23a-3p/PTEN axis)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//IF//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Microarray//Invasion Assay//Transwell Assay	The expression of lncRNA MAGI2-AS3 was significantly downregulated in tumor tissues.  Through WB assay, MAGI2-AS3 could increase PTEN and depress p-AKT and MMP-9 protein expressions via miRNA-23a-3p suppression. 	MAGI2-AS3 expression was closely correlation with HCC patient's clinicopathology and prognosis and prognosis.	Yes	In the cell experiment, compared with the negative control (NC) group, MAGI2-AS3 overexpression reduced cell proliferation, invasion, and migration and increased cell apoptosis in Bel-7402 and Huh-7 cell lines. However, when Bel-7402 and Huh-7 cells were transfected with miRNA-23a-3p, their biological activities (proliferation, invasion, and migration) were significantly increased. 	34026068
hsa_circ_0041732	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells 	Interaction(miR-149-5p/FGF5 pathway)	In Vivo Experiment//IHC//Western Blot//Transfection//Wound Healing Assay//Tube Formation Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Invasion Assay//Transwell Assay	Circ_0041732 and FGF5 expression were significantly upregulated, whereas miR-149-5p was downregulated in TNBC tissues and cells compared with normal breast tissues and cells, respectively. Additionally, circ_0041732 regulated TNBC cell tumor properties by binding to miR-149-5p. MiR-149-5p also modulated TNBC cell tumor properties by targeting FGF5. Furthermore, circ_0041732 knockdown hindered tumor formation in vivo.		Yes	Circ_0041732 silencing inhibited TNBC cell proliferation, migration, invasion, and tube formation, but induced apoptosis.	35341378
circWHSC1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	BC tissues and cells	Interaction(miR-212-5p/AKT3 axis.)	qRT-PCR	 CircWHSC1 was upregulated in BC tissues and cells. Also, circWHSC1 could discriminate BC tissues and paracancerous normal tissues. CircWHSC1 regulated AKT3 expression by sponging miR-212-5p. Silencing of miR-212-5p overturned circWHSC1 knockdown-mediated impacts on malignancy and glycolysis of TNBC cells. AKT3 overexpression reversed the inhibitory effect of miR-212-5p mimic on malignancy and glycolysis of TNBC cells.	 TNBC patients with high circWHSC1 possessed a poor prognosis. 	Yes	CircWHSC1 silencing reduced TNBC cell growth in vivo and repressed proliferation, migration, invasion, glycolysis, and induced apoptosis of TNBC cells in vitro.	34624276
MAGI1-IT1	LncRNA	Homo sapiens	Stomach Neoplasms	120 pairs of GC patient tumor, paracancerous tissues, human GES-1 control cells and human AGS, MKN-74, MKN-45, and MGC-803 GC cell lines	Interaction(miR-302d-3p/IGF1 Axis)	In Vivo Experiment//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ELISA	Elevated MAGI1-IT1 expression was detected in GC cell lines and tissues, and was linked to poorer patient overall survival. Knocking down this lncRNA disrupted GC cell proliferation in vitro and in vivo, and miR-302d-3p was identified as a MAGI1-IT1 target. IGF1 was subsequently identified as a miR-302d-3p target gene that was upregulated by MAGI1-IT1 through miR-302d-3p.	Elevated MAGI1-IT1 expression was detected in GC cell lines and tissues, and was linked to poorer patient overall survival. 	Yes	Knocking down this lncRNA disrupted GC cell proliferation in vitro and in vivo, and miR-302d-3p was identified as a MAGI1-IT1 target. 	33833579
hsa_circ_0000520	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC tissues and cell lines	Interaction( miR-1296/ZFX axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//H&E Staining//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	 Circ_0000520 expression was upregulated in TNBC tissues and cell lines.miR-1296 was verified as a target of circ_0000520, and circ_0000520 silencing-mediated suppressive effects on the malignant potential of TNBC cells were partly overturned by miR-1296 knockdown. miR-1296 interacted with the 3' untranslated region (3'UTR) of ZFX, and ZFX overexpression partly reversed miR-1296 overexpression-mediated effects in TNBC cells. 		Yes	Circ_0000520 knockdown suppressed the proliferation, migration, and invasion whereas induced the apoptosis of TNBC cells. 	34324278
circPDCD11	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-432-5p/LDHA )	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Transfection//qRT-PCR//Luciferase Report Assay//Microarray//EdU Staining	The results revealed that circPDCD11 expression was significantly upregulated in TNBC tissues and cells.  Mechanistically, circPDCD11 acted as a miRNA sponge to enhance LDHA expression by sponging miR-432-5p.	Clinical data demonstrated that the high expression of circPDCD11 was closely correlated with a poor prognosis and acted as an independent risk factor for TNBC prognosis.	Yes	Functionally, in vitro gain- and loss-of-function experiments revealed that circPDCD11 accelerated glucose uptake, lactate production, ATP generation, and the extracellular acidification rate in TNBC cells. In vivo, circPDCD11 silencing repressed tumor growth. 	34420029
circEIF6	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC cells 	Regulation	In Vivo Experiment//Western Blot//Wound Healing Assay//Invasion Assay//Co-IP//Migration Assay//FISH//circRNA-seq//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining	 Mechanistically, we found that circ-EIF6 contains a 675-nucleotide (nt) open reading frame (ORF) and that the -150-bp sequence from ATG functioned as an internal ribosome entry site (IRES), which is required for translation initiation in 5' cap-independent coding RNAs.	 By intersecting circRNA sequencing data from clinical samples and cell lines, we identified a circRNA, termed circ-EIF6, which predicted a poorer prognosis and correlated with clinicopathological characteristics in a cohort of TNBC patients. 	Yes	Functionally, we showed that circ-EIF6 promoted the proliferation and metastasis of TNBC cells in vitro and in vivo. 	34450253
circHIF1A	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 breast cancer tissues	Regulation(NFIB/FUS positive feedback loop)	In Vivo Experiment	In our present study, we found that the novel circRNA circHIF1A was significantly overexpressed in breast cancer tissues and that it was associated with metastasis, poor prognosis, and the TNBC subtype. Mechanistically, circHIF1A modulated the expression and translocation of NFIB through posttranscriptional and posttranslational modifications, resulting in the activation of the AKT/STAT3 signaling pathway and inhibition of P21. 	In our present study, we found that the novel circRNA circHIF1A was significantly overexpressed in breast cancer tissues and that it was associated with metastasis, poor prognosis, and the TNBC subtype.	Yes	Overexpression of circHIF1A significantly promoted TNBC growth and metastasis in vitro and in vivo, while knockdown of circHIF1A exerted the opposite effects. 	33714984
circCD44	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Interaction( miR-502-5p/KRAS and IGF2BP2/Myc axes)	In Vivo Experiment//RNA Pull-Down//Northern Blot//IHC//Western Blot//Flow Cytometry//FISH//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//EdU Staining	CircCD44 is an uncharacterized circRNA, which is highly expressed in TNBC, and its expression is negatively correlated with the prognosis of TNBC patients. CircCD44 promotes TNBC proliferation, migration, invasion and tumorigenesis at least partially by sponging miR-502-5p and interacting with IGF2BP2.	CircCD44 is an uncharacterized circRNA, which is highly expressed in TNBC, and its expression is negatively correlated with the prognosis of TNBC patients. 	Yes	CircCD44 promotes TNBC proliferation, migration, invasion and tumorigenesis at least partially by sponging miR-502-5p and interacting with IGF2BP2.	34696797
circPSMA1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC cells,  exosomes, and serum exosomes samples from TNBC patients.	Interaction( miR-637/Akt1/β-catenin (cyclin D1) axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Transwell Assay	"We identified increased circRNA circPSMA1 in TNBC cells, their exosomes, and serum exosomes samples from TNBC patients. Mechanistically, circPSMA1 acted as a ""miRNAs sponge"" to absorb miR-637; miR-637 inhibited TNBC cell migration and metastasis by directly targeted Akt1, which recognized as a key immune-related gene and affected downstream genes β-catenin and cyclin D1. "		Yes	 The overexpression of circPSMA1 promoted TNBC cell proliferation, migration, and metastasis both in vitro and in vivo. 	33911067
MACC1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells 	regulation[SMAD2/MACC1-AS1 axis]	Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//ChIP	 In this work, it was shown that lncRNA MACC1-AS1 was highly expressed in NPC tissues and cells relative to the adjacent tissues and nasal mucosa cells, respectively.Therefore, these results demonstrate a novel MACC1-AS1/miR-145/Smad2 negative loop responsible for NPC cell stemness.	Additionally, MACC1-AS1 expression was positively correlated with the high rate of lymph node metastasis and large tumor size. 	Yes	in vitro and in vivo experiments revealed that MACC1-AS1 knockdown reduced the stemness of NPC cells, which was indicated by the decrease of sphere-forming ability, ALDH1 activity, stemness marker expression and tumor-initiating capacity.	32058221
MACC1-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	regulation[Downregulating PTEN]	CCK8//qPCR//Western Blot	MACC1-AS1 was upregulated in LUAD and inversely correlated with the expression of PTEN. The authors' results demonstrated that MACC1-AS1 promoted cell proliferation by downregulating PTEN in LUAD cells.	High expression levels of MACC1-AS1 in LUAD tissues were closely correlated with poor survival rate of LUAD patients.	Yes	In LUAD cells, overexpression of MACC1-AS1 led to decreased expression of PTEN and increased proliferation rate of LUAD cells, while MACC1-AS1 silencing led to increased expression of PTEN and decreased proliferation rate of LUAD cells.	32109147
MACC1-AS1	LncRNA	Homo sapiens	Pancreatic Carcinoma	PC tissues	Regulation[PAX8/NOTCH1 signaling pathway]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	 Numbers of differentially expressed lncRNAs in PC were identified via lncRNA microarrays, among which MACC1-AS1 was revealed as the most abundant lncRNA. The upregulation of MACC1-AS1 in PC was further confirmed in two expanded PC cohorts, which showed that MACC1-AS1 expression was upregulated in those PC patients with poor survival.Meanwhile, MACC1-AS1 upregulated the expression of PAX8 protein, which promoted aerobic glycolysis and activated NOTCH1 signaling. Additionally, PAX8 was upregulated in PC tissues, which was correlated with the expression of MACC1-AS1 and the overall survival of PC patients.		Yes	unctionally, knockdown of MACC1-AS1 inhibited the proliferation as well as metastasis of PC cells. 	31391063
MACC1-AS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC tissues and cells	interaction[microRNA-34a,CDK6]	CCK8//qRT-PCR//Cell Cycle Assay//Western Blot	It was observed that MACC1-AS1 was upregulated in CSCC, and its expression levels were elevated with the increase in clinical stage.Therefore, the lncRNA MACC1-AS1 may serve as a sponge of miR-34a to upregulate CDK6, thereby promoting cell cycle progression and cell proliferation.	It was observed that MACC1-AS1 was upregulated in CSCC, and its expression levels were elevated with the increase in clinical stage.	Yes	Cell cycle and proliferation analyses demonstrated that MACC1-AS1 and CDK6 promoted cell cycle progression and cell proliferation. 	32194733
hsa_circ_0006220	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 BC tissues and cell lines	Interaction(miR-197-5p/CDH19)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Hsa_circ_0006220 was more downregulated in TNBC than other subtypes of BC tissues and cell lines. Further, hsa_circ_0006220 was confirmed to be a sponge of miR-197-5p, and to indirectly regulate CDH19 expression. A rescue assay indicated the biological function of the hsa_circ_0006220/miR-197-5p/CDH19 pathway in TNBC cells.		Yes	 In vitro data showed that hsa_circ_0006220 remarkably inhibited the proliferation, migration, and invasion of TNBC cells. 	34532373
LYPLAL1-DT	LncRNA	Homo sapiens	Type 2 Diabetes With Macrovascular Complication	EC	Interaction(miR-204-5p/SIRT1 axis)	Western Blot//Transfection//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Transwell Assay	Furthermore, these DE-lncRNAs were shown to be significantly related to hypoxia, HG, and IS in EC, especially lncRNA LYPLAL1-DT. LYPLAL1-DT overexpression results in the promotion of the proliferation, and migration of EC, as well as an elevation of autophagy. Overexpressed LYPLAL1-DT reduces the adhesion of monocytes to EC, boosts anti-inflammation, and suppresses inflammatory molecules secreted in the medium.Mechanistically, LYPLAL1-DT acts as competing endogenous RNA (ceRNA) by downregulating miR-204-5p, therefore enhancing SIRT1 and protecting EC autophagy function; thus, alleviating apoptosis. Finally, exosome sequencing revealed LYPLAL1-DT expression was 4 times lower in DMC cells than in healthy samples.		Yes	Furthermore, these DE-lncRNAs were shown to be significantly related to hypoxia, HG, and IS in EC, especially lncRNA LYPLAL1-DT. LYPLAL1-DT overexpression results in the promotion of the proliferation, and migration of EC, as well as an elevation of autophagy. Overexpressed LYPLAL1-DT reduces the adhesion of monocytes to EC, boosts anti-inflammation, and suppresses inflammatory molecules secreted in the medium.	35508613
LYPLAL1-2	LncRNA	Homo sapiens	Glioma	glioma tumor tissue	regulation[miR-217/YWHAG]	qRT-PCR//Western Blot//Transwell Assay	 LncRNA-LYPLAL1-2 was significantly downregulated in glioma tumor tissue.LncRNA-LYPLAL1-2 suppressed glioma metastasis via the miR-217/YWHAG axis and is expected to be a potential target for early diagnosis and treatment of gliomas.		Yes	LncRNA-LYPLAL1-2 overexpression suppressed migration and invasion in vitro and in vivo. 	32913498
circNR3C2	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer tissues/cell lines	Interaction(miR-513a-3p/HRD1/Vimentin axis)	In Vivo Experiment//RNA Pull-Down//cell invasion assay//Wound Healing Assay//Immunoblotting//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//IF	 CircNR3C2 (hsa_circ_0071127) is also remarkably downregulated in TNBC, negatively correlated with the distant metastasis and lethality of invasive breast carcinoma. Collectively, we elucidated a bona fide circNR3C2/miR-513a-3p/HRD1/Vimentin axis that negatively regulates the metastasis of TNBC, suggesting that circNR3C2 and HRD1 can act as potential prognostic biomarkers. 		Yes	Overexpressing circNR3C2 in vitro and in vivo leads to a crucial enhancement of the tumor-suppressive effects of HRD1 through sponging miR-513a-3p.	33530981
LY6K-AS	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung adenocarcinoma (LUAD) patients	Expression(highly expressed)	RNA-seq	We identified an antisense transcript, LY6K-AS, with elevated expression in lung adenocarcinoma (LUAD) patients, and its higher expression in LUAD patients predicts poor survival outcomes. 	We identified an antisense transcript, LY6K-AS, with elevated expression in lung adenocarcinoma (LUAD) patients, and its higher expression in LUAD patients predicts poor survival outcomes. 	Yes	LY6K-AS abrogation interfered with the mitotic progression of lung cancer cells resulting in unfaithful chromosomal segregation. LY6K-AS interacts with and stabilizes 14-3-3 proteins to regulate the transcription of kinetochore and mitotic checkpoint proteins.	33674747
LUCAT1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells	Interaction(ELAVL1/LIN28B/SOX2 Positive Feedback Loop)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Bioinformatics Analysis//ChIP	 LUCAT1 is significantly overexpressed in TNBC cells. SRY-box transcription factor 2 (SOX2) is an active transcription factor of LUCAT1. LUCAT1 recruits ELAV-like RNA binding protein 1 (ELAVL1) protein to stabilize lin-28 homolog B (LIN28B) mRNA, thereby further modulating SOX2 expression, which forms a positive feedback loop.		Yes	LUCAT1 interference impedes cell stemness in TNBC cells. 	35711895
LUCAT1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-375)	Transfection//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	 In the present study, we showed that LUCAT1 was substantially upregulated in glioma tissues and cells. Subsequently, DIANA showed that miR-375 was predicted to contain the complementary binding sites to LUCAT1. Luciferase reporter assay showed that miR-375 directly targeted LUCAT1. In addition, we found that miR-375 was downregulated in glioma tissues and negatively correlated with LUCAT1 expression in glioma tissues. Furthermore, the results showed that miR-375 could rescue the function of LUCAT1 in glioma progression. The lncRNA LUCAT1 was critical for the proliferation and invasion of glioma cells by regulating miR-375. 		Yes	LUCAT1 inhibition significantly suppressed the proliferation and invasion of glioma cells.	29089067
LUCAT1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	papillary thyroid carcinoma tissues 	Expression[highly expressed]	CCK8//qRT-PCR//cell invasion assay//Western Blot	Quantitative reverse transcription PCR was performed to detect the expression levels of 84 lncRNAs in 61 papillary thyroid carcinoma tissues and their adjacent non-tumor tissues. The highest fold-change was obtained for lung cancer associated transcript 1 LUCAT1, and thus, this study determines the expression and biological implication of lncRNA LUCAT1 through different in vitro and ex vivo approaches in this tumor. 		Yes	. Furthermore, LUCAT1 knockdown significantly reduced both cell proliferation and invasion ex vivo and induced cell-cycle arrest and apoptosis. 	31591432
circSEPT9	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	regulation[circSEPT9/miR-637/LIF axis]	RNA Pull-Down//ISH//qRT-PCR//FISH//RIP//ChIP	 Increased expression of circSEPT9 was found in TNBC tissues, which was positively correlated with advanced clinical stage and poor prognosis. Our data reveal that the circSEPT9 mediated by E2F1 and EIF4A3 facilitates the carcinogenesis and development of triple-negative breast cancer through circSEPT9/miR-637/LIF axis. 	 Increased expression of circSEPT9 was found in TNBC tissues, which was positively correlated with advanced clinical stage and poor prognosis.	Yes	Knockdown of circSEPT9 significantly suppressed the proliferation, migration and invasion of TNBC cells, induced apoptosis and autophagy in TNBC cells as well as inhibited tumor growth and metastasis in vivo.	32264877
LTSCCAT	LncRNA	Homo sapiens	tongue squamous cell carcinoma	CAL27 cells	Interaction(miR-103a-2-5p/SMYD3/TWIST1 axis)	In Vivo Experiment//IHC//ChIP//Western Blot//ISH//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//IF	. LTSCCAT was upregulated in P.g-LPS-treated CAL27 cells compared with untreated CAL27 cells. We predicted through an online database and confirmed by dual-luciferase reporter assays that LTSCCAT is a competitive endogenous RNA for the regulation of miR-103a-2-5p. Another dual-luciferase reporter assay confirmed that miR-103a-2-5p has a binding site at the 3'-UTR of the histone methylation transferase SMYD3 and inhibits its translation.  Chromatin immunoprecipitation experiments demonstrated that SMYD3 binds directly to the promoter region of TWIST1 and promotes its transcription, which is related to H3K4 trimethylation. 	LncRNA LTSCCAT was upregulated in TSCC patients with periodontitis and was correlated with metastasis and poor prognosis. 	Yes	 LTSCCAT induced epithelial-mesenchymal transition and promoted the invasion and metastasis of TSCC in vitro and in vivo. 	33542221
circAHNAK1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues,cell lines	Interaction[modulating miR-421 and RASA1]	Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 We found that circAHNAK1 was significantly down-regulated in TNBC.Mechanistic analysis indicated that circAHNAK1 acted as a miR-421 ceRNA (competitive endogenous RNA) to attenuate the inhibitory effect of miR-421 on its target gene RASA1.	We found that circAHNAK1 was significantly down-regulated in TNBC, and its expression was negatively associated with RFS and OS.	Yes	Overexpression of circAHNAK1 can inhibit TNBC proliferation, migration and invasion in vitro. In vivo studies confirmed that circAHNAK1 inhibited TNBC tumor growth and metastasis.	31857500
LSINCT5	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-30a/Wnt/β-catenin axis]	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LSINCT5 was significantly up-regulated in BC tissues and cells.The present results uncovered that LSINCT5 knockdown suppressed BC growth and metastasis via the miR-30a/Wnt/β-catenin axis, and it served as a potential therapeutic target for early diagnosis and treatment of BC patients.		Yes	 LSINCT5 knockdown suppressed proliferation, invasion, and epithelial-mesenchymal transition (EMT) in vitro and in vivo.	33490147
LSINCT5	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Regulation[LSINCT5/HMGA2 axis]	qRT-PCR//RIP	This novel LSINCT5/HMGA2 axis can modulate lung cancer progression and might be a promising target for pharmacological intervention.	Increased LSINCT5 expression positively correlates with malignant clinicopathological features and poor survival. 	Yes	LSINCT5 can promote migration and viability of various NSCLC cells in vitro and also enhance lung cancer progression in vivo. 	29883241
LSINCT5	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC specimens 	Interaction(miRNA-185-5p/ZNF703 axis)	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 LSINCT5 was upregulated in OSCC specimens and correlated to poor prognosis of OSCC. LSINCT5 is abnormally upregulated in OSCC specimens and drives its malignant progression through the miR-185-5p/ZNF703 axis.	 LSINCT5 was upregulated in OSCC specimens and correlated to poor prognosis of OSCC.	Yes	Knockdown of LSINCT5 inhibited proliferative and migratory capacities of OSCC. 	33721442
LSINCT5	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial carcinoma tissue	Regulation[LSINCT5-HMGA2-Wnt/β-catenin signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	The authors observed positively correlated and aberrantly up-regulated LSINCT5 and HMGA2 in EC. Our data uncovered the oncogenic activities and highlighted the mechanistic contributions of the LSINCT5-HMGA2-Wnt/β-catenin signaling pathway in EC.		Yes	LSINCT5 deficiency significantly inhibited cell proliferation, cell cycle progression, and induced apoptosis. Meanwhile, cell migration and invasion were greatly compromised by the LSINCT5 knockdown.	31632465
LSINCT5	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	interaction[EZH2 ]	CCK8//qRT-PCR//ChIP//Transwell Assay	 In our study, we found that LSINCT5 was significantly upregulated in OS tissues than in adjacent normal tissues. Mechanistic exploration revealed that LSINCT5 interacted with EZH2 to suppress the expression of APC, a negative regulator of the Wnt/β-catenin pathway. 	Additionally, the expression of LSINCT5 was inversely associated with the prognosis of patients with OS.	Yes	LSINCT5 knockdown dramatically inhibited OS cell proliferation in vitro and tumor growth in vivo. 	30420287
LSINCT5	LncRNA	Homo sapiens	Glioma	glioma tissue	Regulation[PI3K/AKT, Wnt/β-catenin and NF-κB pathways]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	LSINCT5 was highly expressed while miR-451 low expressed in glioma tissues when compared to normal controls. Down-regulation of LSINCT5 represses glioma cells growth and metastasis in vitro likely through targeting miR-451 and thereby inhibiting Rac1-regulated PI3K/AKT, Wnt/β-catenin and NF-κB pathways.		Yes	Down-regulating LSINCT5 effectively declined GL15 cells viability, migration and invasion, but accelerated apoptosis. 	31213092
LSAMP-1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	170 cases of NSCLC tissues	Interaction(LSAMP/TKI )	CCK8//qRT-PCR//Western Blot	We found that Lnc-LSAMP-1 was significantly down-regulated in 170 cases of NSCLC tissues when compared to their adjacent non-cancerous tissues.  Chemotherapy sensitization experiments showed that over-expressed Lnc-LSAMP-1 enhanced the inhibition of cell proliferation induced by TKI. Mechanistically, Lnc-LSAMP-1-LSAMP formed a complex which could protect the degradation of LSAMP gene, and thus exerted crucial roles in NSCLC progression and TKI targeted treatment.	Loss expression of Lnc-LSAMP-1 was notably correlated with unfavorable prognosis of NSCLC patients. 	Yes	 The ectopic expression of Lnc-LSAMP-1 drastically inhibited lung cancer cell proliferation, viability, invasion and migration ability, arrested cell cycle and facilitated apoptosis. 	35524253
circITCH	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues,cell lines	Interaction[Wnt/β-catenin pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we characterized the role of circ-ITCH in TNBC and found that circ-ITCH was significantly Expression[down-expression]-regulated in TNBC tissues and cell lines and closely associated with poor prognosis.Mechanistically, we found that circ-ITCH acts as a sponge for miR-214 and miR-17 to increase expression of its ITCH linear isoform, thereby inactivating Wnt/β-catenin signaling.		Yes	 Most importantly, over-expression of circ-ITCH remarkably inhibited TNBC proliferation, invasion and metastasis both in vitro and in vivo. 	30509108
hsa_circ_069718	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Interaction[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	We found that circRNA_069718 expression was significantly increased in TNBC tissues and cell lines.Mechanically, we found that circRNA_069718 inhibition reduced the expression levels of Wnt/β-catenin pathway-related genes (β-catenin, c-myc, and cyclin D1).	High circRNA_069718 expression was significantly correlated with advanced TNM stage, lymph node metastasis, and poor overall survival of TNBC patients. 	Yes	. Functionally, we showed that circRNA_069718 inhibition significantly reduced TNBC cells proliferation and invasion ability in vitro.	31298383
hsa_circ_0004543	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction( hsa_circ_0004543/hsa-miR-217/HIF-1α axis)	RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	Our results revealed that the hsa_circ_0004543 expression was considerably increased in CC tissues and cells.The investigation of the mechanism showed that hsa-miR-217 silencing or HIF-1a overexpression rescued hsa_circ_0004543, and silencing inhibited malignant phenotypes of CC cells. hsa_circ_0004543 upregulated the HIF-1α expression by sponging hsa-miR-217 in CC development. 		Yes	Its silencing repressed proliferation and metastasis, while it increased apoptosis of CC cells. 	35310917
hsa_circ_0001495	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Interaction(miR-526b-3p/TMBIM6/mTOR axis)	In Vivo Experiment//Western Blot//Transfection//EdU Staining//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//IHC//Invasion Assay	Our finding showed that hsa_circ_0001495 and TMBIM6 expression were upregulated, while miR-526b-3p was downregulated in CC tissues and cell lines. Hsa_circ_0001495 knockdown or TMBIM6 knockdown suppressed cell proliferation, migration, glycolysis, while promoted cell apoptosis in vitro, and hsa_circ_0001495 silence curbed tumor growth in vivo. 		Yes	Hsa_circ_0001495 knockdown or TMBIM6 knockdown suppressed cell proliferation, migration, glycolysis, while promoted cell apoptosis in vitro, and hsa_circ_0001495 silence curbed tumor growth in vivo. 	35533615
circASAP1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction(miR-338-3p/RPP25)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	CircASAP1 was overexpressed in cervical cancer tissues and cells compared with negative groups. Mechanistically, circASAP1 could function as a sponge for miR-338-3p to increase the expression of RPP25, and further regulated proliferation, migration, invasion, apoptosis, and cell cycle program of cervical cancer cells, which might be potential markers for cervical cancer diagnosis.		Yes	Additionally, the loss-of-functional experiments implied that knockdown of circASAP1 impeded proliferation, migration, and invasion while induced apoptosis and cell cycle arrest in cervical cancer cells along with repressed tumor growth in vivo through regulation of miR-338-3p.	34407047
hsa_circ_0084904	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Interaction(miR-802/MAL2 axis)	In Vivo Experiment//Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0084904 was markedly up-regulated in CC tissues and cell lines. Mechanistically, circ_0084904 targeted miR-802, and the effects of circ_0084904 silencing were mediated by miR-802. MAL2 was directly targeted and inhibited by miR-802, and MAL2 was a functional target of miR-802. Moreover, circ_0084904 modulated MAL2 expression via miR-802. 		Yes	 Silencing endogenous circ_0084904 impeded cell colony formation, cell cycle progression, migration, invasion, epithelial-mesenchymal transition (EMT), and promoted apoptosis in vitro, as well as diminished tumor growth in vivo. 	35033901
LRP11-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells 	Interaction( miR-149-3p/NRP2 axis)	Western Blot//Wound Healing Assay//qPCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	LRP11-AS1 was found to be significantly overexpressed in TNBC cells compared to the non-TNBC cells and normal mammary epithelial cells. Mechanistically, LRP11-AS1 was found to act as a competing endogenous RNA (ceRNA) to sponge miR-149-3p. Silencing of LRP11-AS1 increased the expression of miR-149-3p and overexpression of miR-149-3p suppressed the expression of LRP11-AS1. Inhibition of miR-149-3p could reverse the anticancer effect of LRP11-AS1 deficiency in TNBC cells. Moreover, Neuropilin-2 (NRP2) was found to be the target of miR-149-3p. Rescue experiments revealed that NRP2 overexpression could rescue the anticancer effect of LRP11-AS1 deficiency in TNBC cells.		Yes	Knockdown of LRP11-AS1 could inhibit the growth and metastasis of TNBC cells and regulate cell cycle. 	35279146
hsa_circ_0009035	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	 tumor cells and tissues	Interaction(miR-1305/CREBRF axis)	In Vivo Experiment//IHC//Western Blot//Transfection//Tube Formation Assay//Invasion Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	First, we found that circ_0009035 expression was significantly upregulated in tumor cells and tissues; second, knockdown of circ_0009035 could inhibit cell proliferation, migration and invasion and promote cell apoptosis. Subsequently, circ_0009035 was found to be able to target miR-1305, and the expression of miR-1305 in tumor tissues and cells was significantly lower. MiR-1305 inhibitor could restore cell-related progression of cervical cancer inhibited by si-circ_0009035. Finally, miR-1305 could target CREBRF, and circ_0009035 could regulate CREBRF expression by targeting miR-1305, thereby affecting cervical cancer tumorigenesis.		Yes	First, we found that circ_0009035 expression was significantly upregulated in tumor cells and tissues; second, knockdown of circ_0009035 could inhibit cell proliferation, migration and invasion and promote cell apoptosis.	35389936
hsa_circ_0060551	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells	Regulation(TPD52)	qRT-PCR//Western Blot	 According to the results, circ_0060551 was upregulated in cervical cancer cells and could promote the migration and invasion of cells via TPD52. In addition, circ_0060551 could up-regulate TPD52 expression through a ceRNA model to target miR-520a-5p. Moreover, circ_0060551 could stabilize the mRNA expression of TPD52 via recruiting ELAVL1.		Yes	 According to the results, circ_0060551 was upregulated in cervical cancer cells and could promote the migration and invasion of cells via TPD52. 	35716110
LUADT1	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	SCLC tissues	Interaction[miR-15a-3p]	qRT-PCR//Transwell Assay//Western Blot	We found that LUADT1 and Twist1 were upregulated in SCLC, while miR-15a-3p was downregulated in SCLC.However, LUADT1 was posively correlated with Twist1 but was not significnatly correlated with miR-15a-3p. Overexpression experiments showed that and LUADT1 and miR-15a-3p did not significantly affect the expression of each other. 		Yes	 Transwell assays showed that LUADT1 and Twist1 overexpression mediated the increased rate of cell invasion and migration, while miR-15a-3p overexpression mediated the decreased rate of cell invasion and migration. 	31842825
LUADT1	LncRNA	Homo sapiens	Melanoma	melanoma tissues 	interaction[miR-28-5p,RAP1B]	qRT-PCR//Western Blot	We found that LUADT1 was upregulated in melanoma and high levels of LUADT1 predicted poor survival.  LUADT1 in melanoma and may sponge miR-28-5p to upregulate RAP1B, thereby promoting cancer cell proliferation.	We found that LUADT1 was upregulated in melanoma and high levels of LUADT1 predicted poor survival. 	Yes	Cell proliferation assay showed that LUADT1 and RAP1B overexpression mediated the increased proliferation rate of melanoma cells. 	32191497
LUADT1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC tissues and cell lines	Interaction(miR-1207-5p)	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Initially, the expression of lncRNA-LUADT1 and TEAD1 were significantly up-regulated in NPC tissues and cells, while miR-1207-5p was significantly down-regulated. 		Yes	The results showed that interfering with lncRNA-LUADT1 expression could inhibit the proliferation, invasion, and migration of NPC cells.	34738862
circIFI30	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC tissues and cells	regulation[circIFI30/miR-520b-3p/CD44 axis]	RNA Pull-Down//qRT-PCR//RIP//FISH//Luciferase Report Assay	We found that circIFI30 was significantly up-regulated in TNBC tissues and cells using quantitative real-time PCR and in situ hybridization. Therefore, our work uncovers the mechanism by which circIFI30 could promote TNBC progression through circIFI30/miR-520b-3p/CD44 axis and circIFI30 could be a novel diagnostic/prognostic marker and therapeutic target for TNBC patients.	High circIFI30 expression was positively correlated with clinical TNM stage, pathological grade and poor prognosis of TNBC patients.	Yes	Functionally, a series of in vivo and in vitro experiments showed that knockdown of circIFI30 could markedly inhibit TNBC cell proliferation, migration, invasion and cell cycle progression, induce apoptosis as well as suppress tumorigenesis and metastasis. 	32497020
LUCAT1	LncRNA	Homo sapiens	Multiple Myeloma	cancer tissues,blood	regulation[TGF-β Signaling Pathway]	qRT-PCR//Western Blot	 Long noncoding RNA lung cancer-associated transcript 1 was increased in cancer tissues and serum of patients with multiple myeloma as well as multiple myeloma cells, which was correlated with dismal prognosis of patients with multiple myeloma.This study suggests that suppression of long noncoding RNA lung cancer-associated transcript 1 inhibits the activation of transforming growth factor-β signaling pathway, thereby inhibiting the growth of multiple myeloma cells.		Yes	Overexpression of long noncoding RNA lung cancer-associated transcript 1 promoted the activity of U266 and H929 cells, while inhibition of long noncoding RNA lung cancer-associated transcript 1 suppressed the activity of U266 and H929 cells. 	32812490
LUCAT1	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer cell lines	Expression [highly expressed]	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//BrdU	In comparison to normal cells, LUCAT1 was highly expressed in human pancreatic cancer cell lines (p<0.05). 		Yes	The higher expression of LUCAT1 resulted in enhanced pathogenesis of PDA cells and motivated the development to S phase by regulation of cyclin D1, CDK4. Furthermore, LUCAT1 promoted PDA cells development by inducing AKT's and p38 MAPK's phosphorylation.	33577028
LUCAT1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD serum exosomes, tumor tissues, and LUAD cells	Interaction(iR-4316/VEGFA axis)	In Vivo Experiment//Western Blot//ISH//Transfection//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay	Our findings revealed that lncRNA LUCAT1 was significantly up-regulated in LUAD serum exosomes, tumor tissues, and LUAD cells in comparison with corresponding controls.  Furthermore, mechanistic investigations revealed that LUCAT1 elevated LUAD cell metastasis and glycolysis by sponging miR-4316, which further led to the upregulation of VEGFA. Finally, the regulatory axis LUCAT1-miR-4316-VEGFA was verified in LUAD.	High expression of LUCAT1 in LUAD patient tissues was associated with enhanced Lymph Node Metastasis (LNM), advanced Tumor Node Metastasis (TNM) stage and poorer clinical outcome in LUAD patients.	Yes	Knockdown of LUCAT1 inhibited LUAD cell metastasis and glycolysis in vitro as well as tumor metastasis in vivo, while overexpression of LUCAT1 induced a promoted LUAD metastasis and glycolysis.	35646922
LUCAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cell line	regulation[inhibition of miR-493]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	The results of the present study revealed that the expression levels of LUCAT1 were upregulated in AMC?HN?8 cells. In conclusion, these results suggested that LUCAT1 may facilitate tumorigenesis in LSCC through the targeted inhibition of miR‑493, which provides evidence for a novel target for the treatment of LSCC.		Yes	The genetic knockdown of LUCAT1 expression levels significantly suppressed the cell proliferation, alongside downregulating the expression levels of CDK2 and cyclin E1 and upregulating p21 expression levels. In addition, the knockdown of LUCAT1 inhibited cell migration and invasion, as demonstrated using the wound healing and Transwell assays, respectively. 	33215214
LUCAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues 	Regulation[AKT/GSK-3β Signaling Pathway]	qRT-PCR//Western Blot	We found that LUCAT1 was significantly upregulated in both clinical ccRCC tissues (n = 90) and TCGA ccRCC tissues (n = 448) compared with normal tissues.These findings indicate that the CXCL2/LUCAT1/AKT/GSK-3β axis is a potential therapeutic target and molecular biomarker for ccRCC.	Statistical analysis revealed that the LUCAT1 expression level positively correlated with tumor T stage (P < 0.01), M stage (P < 0.01), and TNM stage (P < 0.01). Overall survival and disease-free survival time were significantly shorter in the high-LUCAT1-expression group than in the low-LUCAT1-expression group (log-rank P < 0.01).	Yes	 LUCAT1 knockdown inhibited ccRCC cell proliferation and colony formation, induced cell cycle arrest at G1 phase, and inhibited cell migration and invasion. Overexpression of LUCAT1 promoted proliferation, migration, and invasion of ccRCC cells.	30032137
LUCAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction(microRNA-375/YAP1 axis)	Northern Blot//Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay	The results revealed that LUCAT1 and YAP1 were upregulated and miR-375 was downregulated in ccRCC tissues and cells. LUCAT1 knockdown suppressed cell proliferation, migration and invasion, which were reversed by the inhibition of miR-375. 		Yes	LUCAT1 knockdown suppressed cell proliferation, migration and invasion, which were reversed by the inhibition of miR-375. 	34035851
LUCAT1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC cells and tissues 	Interaction(miR-375 )	Cell Proliferation Assay//qRT-PCR//Cell Cycle Assay//Migration Assay	We showed that the expression of LUCAT1 was up-regulated in the TSCC cells and tissues and the higher LUCAT1 expression was associated with the poor overall survival (OS).  In summary, this study suggested the tumorigenic effect of lncRNA LUCAT1 in TSCC cells by targeting miR-375 expression.	We showed that the expression of LUCAT1 was up-regulated in the TSCC cells and tissues and the higher LUCAT1 expression was associated with the poor overall survival (OS). 	Yes	Knockdown expression of LUCAT1 suppressed TSCC cell proliferation, cycle and migration. 	33787082
LUCAT1	LncRNA	Homo sapiens	Diabetic Lung Disease	blood	Interaction[iNOS]	qRT-PCR//Western Blot	The serum expression level of lncRNA SACL1 was significantly decreased in diabetic patients with diabetic lung disease compared with diabetic patients without lung disease and healthy controls (P<0.05; Fig. 1). 	ROC curve analysis determined that the area under the curve (AUC) was 0.9233 (95% confidence interval: 0.8679–0.9769) with a standard error of 0.02735 (Fig. 2A). In addition, ROC analysis was used to evaluate the diagnostic value of serum lncRNA SCAL1 in discriminating diabetic patients with diabetic lung disease from diabetic patients without diabetic lung disease. The AUC was 0.8876 (95% confidence interval: 0.8254–0.9498) with a standard error of 0.03174 (Fig. 2B). An AUC>0.65 indicates the potential diagnostic value of a certain indicator for a disease (11). Therefore, serum levels of lncRNA SCAL1 can be used to effectively distinguish diabetic lung patients from healthy controls and diabetic patients without lung disease.	Yes	Furthermore, the overexpression of SCAL1 inhibited iNOS protein expression and reduced NO production in cells treated with high glucose. 	31410144
LUADT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cells	Interaction(microRNA-1207-5p)	In Vivo Experiment//Western Blot//Transfection//Invasion Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Bioinformatics Analysis//Transwell Assay	In this study we found that LUADT1 is highly expressed in CC tissues and cells.  Mechanistically, LUADT1 binds to miR-1207-5p and inhibits miR-1207-5p expression in CC cells. Septin 9 (SEPT9) is identified as a miR-1207-5p target which is negatively regulated by LUADT1. Overexpression of SEPT9 abrogates the suppressed proliferation of CC cells induced by LUADT1 knockdown. 	Up-regulated LUADT1 is significantly correlated with the more aggressive status and poorer survival of CC patients. 	Yes	studies show that LUADT1 depletion suppresses CC proliferation, and leads to cell apoptosis and cell cycle arrest. Furthermore, the xenograft mouse assay demonstrates that LUADT1 knockdown remarkably suppresses tumor growth. 	35538030
LUCAT1	LncRNA	Homo sapiens	Hepatoblastoma	HB tissues, cell lines	Regulation[miR-301b/STAT3 axis]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Quantitative reverse transcription polymerase chain reaction analysis showed that LUCAT1 was highly expressed in both HB tissues and cell lines. Luciferase assays indicated that STAT3 was a transcription activator of LUCAT1 and that LUCAT1 could increase STAT3 expression by competitively binding to miR-301b. 		Yes	Loss-of function assays to identify the biological function of LUCAT1 in HB showed that LUCAT1 knockExpression[down-expression] inhibited cell proliferation, migration, and invasion but reversed epithelial-mesenchymal transition.	30479162
LUCAT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	blood,cell lines	interaction[targeting miR-199a-5p and miR-199b-5p]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	 In the present study, LUCAT1 was up-regulated in the serum samples of MIBC patients and bladder cancer cell lines, as assessed using real-time PCR. Moreover, LUCAT1 directly targeted miR-199a-5p and miR-199b-5p, as affirmed using the luciferase reporter assay, and manipulation of LUCAT1 significantly suppressed miR-199a-5p and miR-199b-5p.		Yes	 Our in vitro data (including wound healing and trans-well assays) showed that LUCAT1 was required for the proliferation, EMT, migration and invasion processes of T24 cells.	32844284
hsa_circ_0131242	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	cancer tissues and cell lines	interaction[Sponging hsa-miR-2682]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Hsa_circ_0131242 was highly expressed in both cancer tissues and cell lines compared to control. Our study identified hsa_circ_0131242 expression in TNBC for the first time and found that hsa_circ_0131242 may promote triple-negative breast cancer progression by sponging hsa-miR-2682.	Subsequently, statistical analyses revealed that high expression of hsa_circ_0131242 was positively correlated with advanced tumor stages and poorer clinical features in cancer patients. 	Yes	Hsa_circ_0131242 knockdown could suppress the progression of breast cancer cells.	32547106
circRPPH1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer tissues and cell lines	regulation[miR-556-5p/YAP1 axis]	qRT-PCR//Luciferase Report Assay//RIP	PCR results showed that circRPPH1 levels were significantly upregulated in tumor tissues and breast cancer cells. Our data reveal that circRPPH1 plays a vital regulatory role in breast cancer via the miR-556-5p/YAP1 axis and may serve as a promising therapeutic target for breast cancer treatment.		Yes	Functionally, circRPPH1 promoted the proliferation, migration, invasion, and angiogenesis of breast cancer cell lines and tumor growth in vivo. 	33194025
LUCAT1	LncRNA	Mus musculus	Myocardial Oxidative	 AMI patient	Interaction(miR-181a-5p)	Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	LUCAT1 was lowly expressed in the AMI patients. After H2O2 induction, the expression of LUCAT1 in H9c2 cells lessened significantly, while the expression of miR-181a-5p elevated significantly (P < 0.001).  LUCAT1 targeted miR-181a-5p and negatively regulated miR-181a-5p expression (P < 0.001). 		Yes	Transfection of p-LUCAT1 significantly reversed the decreased SOD levels, the increased MDA and ROS content, and the elevated tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) in H2O2-stimulated cells (P < 0.001). Upregulation of LUCAT1 contributed to the mitigation of H2O2 injury by promoting viable cells and repressing apoptotic cells (P < 0.01). 	34414854
LUCAT1	LncRNA	Mus musculus	Glioma	glioma cells	Regulation(RAS pathway)	Western Blot//Transfection//Migration Assay//FISH//qRT-PCR//MTT//IHC//Transwell Assay	The expression of LUCAT 1 was up-regulated with an increase in WHO grade, and the lncRNA-mRNA co-expression analysis showed that the expression of ABCB1 was low. LUCAT 1 gene knockout reduced the mRNA and protein levels of Ras signaling pathway related factors (Ras, Raf-1, p-AKT, and p-ERK) as regulating ABCB1 expression and inhibiting the ability of tumor in proliferation and invasion no matter in vitro or in vivo. For overexpressing of LUCAT 1, the opposite was true. After we knocked out ABCB1, the LUCAT1 expression was reversely regulated while the level of RAS signaling pathway related factors increased, and the ability of tumors in proliferation and invasion was enhanced. The abnormal LUCAT1 expression affected the biological behaviors of glioma cells, such as proliferation, invasion, etc. by regulating ABCB1 and promoting the activation of the RAS signaling pathway. This provided a new drug target and therapeutic approach for gene therapy of glioma, which is expected to significantly improve the prognosis of relevant patients.		Yes	LUCAT 1 gene knockout reduced the mRNA and protein levels of Ras signaling pathway related factors (Ras, Raf-1, p-AKT, and p-ERK) as regulating ABCB1 expression and inhibiting the ability of tumor in proliferation and invasion no matter in vitro or in vivo. For overexpressing of LUCAT 1, the opposite was true.	36270516
circRAD18	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cell lines	Regulation[ circRAD18-miR-208a/3164-IGF1/FGF2 axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Expression of circRAD18 was found significantly upregulated in TNBC compared with normal mammary tissues and cell lines.Altogether, our research revealed the pivotal role of circRAD18-miR-208a/3164-IGF1/FGF2 axis in TNBC tumorigenesis and metastasis though the mechanism of competing endogenous RNAs.	circRAD18 was positively correlated with T stage, clinical stage and pathological grade and was an independent risk factor for TNBC patients. 	Yes	 Knockdown of circRAD18 significantly suppressed cell proliferation and migration, promoted cell apoptosis and inhibited tumor growth in functional and xenograft experiments. 	31001629
circKIF4A	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer cell lines and tissues	Expression[highly expressed]	qRT-PCR//Microarray	qRT-PCR analyses verified that circKIF4A was significantly upregulated and positively associated with poorer survival of TNBC.Luciferase reporter assay and RNA immunoprecipitation assay revealed that circKIF4A and KIF4A could bind to miR-375 and that circKIF4A regulated the expression of KIF4A via sponging miR-375.	qRT-PCR analyses verified that circKIF4A was significantly upregulated and positively associated with poorer survival of TNBC.	Yes	The inhibition of circKIF4A suppressed cell proliferation and migration in TNBC.	30744636
MAGI2-AS3	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC clinical samples and cell lines	regulation[miRNA-233/EPB41L3 Axis]	qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that MAGI2-AS3 and EPB41L3 were both downregulated in CSCC and the expression of this two was positively correlated. MAGI2-AS3 may sponge miR-233 to upregulate EPB41L3, thereby inhibiting CSCC cell invasion and migration.		Yes	In addition, overexpression of MAGI2-AS3 and EPB41L3 led to inhibited cancer cell invasion and migration, while overexpression of miR-233 played an opposite role and attenuated the effects of overexpressing MAGI2-AS3.	32581592
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Regulation[miRNA-23a-3p/PTEN axis]	qRT-PCR//Luciferase Report Assay	LncRNA MAGI2-AS3 was downregulated in NSCLC tissues and cell lines.MiRNA-23a-3p was verified to be the target gene of MAGI2-AS3, and furthermore, PTEN was the target of miRNA-23a-3p. Overexpression of miRNA-23a-3p could reverse the inhibited viability and invasion in NSCLC cells overexpressing MAGI2-AS3.	Its level was closely related to tumor size, Tumor Node Metastasis (TNM) stage and distant metastasis of NSCLC patients. The worse prognosis was identified in NSCLC patients with low expression of MAGI2-AS3 relative to those with a high expression.	Yes	Overexpression of MAGI2-AS3 markedly attenuated viability and invasive ability of A549 and PC9 cells. 	31539127
MALAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HSCC tissues	regulation[microRNA-429,ZEB1]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	MALAT1 and ZEB1 expression in HSCC was upregulated while miR-429 expression was downregulated. Inhibition of MALAT1 was able to elevate miR-429 to suppress the progression of HSCC via reducing ZEB1. Our research provided a potential therapeutic target for HSCC.		Yes	Reduced MALAT1 and ZEB1, and upregulated miR-429 inactivated the PI3K/Akt/mTOR signaling pathway, suppressed in vitro viability, colony formation ability, migration and invasion, as well as cell growth in vivo, and promoted the apoptosis of FaDu cells. 	32980391
hsa_circ_0079593	CircRNA	Homo sapiens	Glioma	cancerous tissues,cell lines(U118、U251、U87MG 、LN229)	Interaction[miR-182,miR-433]	Wound Healing Assay//qPCR//CCK8//Luciferase Report Assay//Transwell Assay	Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to measure the relative expression of circ_0079593, which was Expression[Expression[up-expression]-expression]regulated in matched cancerous tissues from 60 patients and four cell lines of glioma. Mechanistically, bioinformatics analysis, qRT-PCR, and dual-luciferase reporter assays showed that microRNA 182 (miR-182) and miR-433 could be sponged and negatively regulated by circ_0079593. Further, rescue assays demonstrated that the biological functions of circ_0079593 are dependent on its inhibition of miR-182 and miR-433. 	A higher level of circ_0079593 in glioma specimens was linked to larger tumor size, higher WHO grade, and worse survival rate for patients with glioma. 	Yes	Exogenous Expression[down-expression]regulation of circ_0079593 expression significantly sExpression[Expression[up-expression]-expression]pressed glioma cell proliferation by increasing cell apoptosis in vitro, and retarded the migratory and invasive potential.	31148222
MALAT1	LncRNA	Homo sapiens	bronchopulmonary dysplasia		Interaction(miR-206)	In Vivo Experiment//Transfection//Tunel//qRT-PCR//RIP//Luciferase Report Assay//ELISA	In our study, we first found that serum MALAT1 was up-regulated in neonatal BPD and severe BPD.  Further, through receiver operating characteristic curve (ROC) analysis, it was found that the area under the curve of MALAT1 for differentiating neonatal BPD from severe BPD was 0.943 and 0.866, respectively. Pathological evaluation confirmed that down-regulating MALAT1 or up-regulating miR-206 might improve the pathological condition of BPD. Furthermore, we also found that MALAT1 has a targeted relationship with miR-206, and miR-206 is down-regulated in BPD in vivo and in vitro. Down-regulating miR-206 could also eliminate the anti-BPD effect after knocking down MALAT1.		Yes	Then, we established BPD models in vivo and in vitro with C57BL/6J mice and BEAS-2B cells, and found that MALAT1 was also highly expressed in them and increased with the induction time of the models. Obvious inflammatory response, oxidative stress and up-regulated apoptosis were observed in BPD models in vivo and in vitro. However, after MALAT1 knockdown treatment, the above abnormal phenomena were alleviated to varying degrees. 	33594304
MALAT1	LncRNA	Homo sapiens	Coronary Slow Flow Endothelial Dysfunction	 peripheral blood of the CSF patient	(miR-181b-5p-MEF2A-ET-1 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//ELISA//EdU Staining//ChIP	MALAT1 and ET-1 were increased, and miR-181b-5p was decreased in the peripheral blood of the CSF patients, and could be used as predictors of CSF. While MEF2A was highly enriched in CSF-induced HUVECs, MEF2A knockdown reduced ET-1 and increased the endothelial function of CSF-induced HUVECs as a transcriptional regulator of ET-1. MALAT1 modulated MEF2A expression positively by sponging miR-181b-5p.		Yes	In the CSF-induced HUVECs, MALAT1 was highly expressed, and MALAT1 knockdown improved endothelial function.  In contrast, miR-181b-5p was downregulated in the CSF-induced HUVECs, and miR-181b-5p overexpression improved endothelial function. 	33545365
hsa_circ_0034642	CircRNA	Homo sapiens	Glioma	glioma tissues,cell lines (U118, U251, LN229, and U87MG)	Interaction[ circ_0034642/miR-1205/BATF3 pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_0034642 was Expression[Expression[up-expression]-expression]regulated in glioma tissues and cell lines. For the mechanism investigation, circ_0034642 was proved to be a sponge of miR-1205, and miR-1205 could regulate BATF3 expression via targeting 3'UTR of BATF3.	Overexpressed circ_0034642 was correlated with adverse phenotypes in the patients with glioma. In addition, circ_0034642 could be regarded as a prognostic predictor for glioma patients. 	Yes	As shown in Fig. 2E, overexpressed circ_0034642 represses cell apoptosis in U251 cells and knockExpression[down-expression] of circ_0034642 increases apoptosis rate in LN229 cells. What's more, transwell assays uncovered that silencing of circ_0034642 attenuated LN229 cell migration and invasion capacities. While Expression[Expression[up-expression]-expression]regulation of circ_0034642 promoted the migration and invasion potential in U251 cells (Fig. 2F). Collectively, circ_0034642 affects cell proliferation, apoptosis, migration and invasion in glioma cells.	30551880
MALAT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	tissue and cell lines	Interaction(miR-485-5p / MAT2A)	Western Blot//ISH//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	In the current study, we documented that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA, is upregulated in HPV16-positive cervical cancer tissue and cell lines. Mechanistically, our results suggested that MALAT1 upregulates Methionine adenosyltransferase 2A (MAT2A) by sponging miR-485-5p. 		Yes	Functionally, the proliferation of cervical cancer was detected by Cell Counting Kit-8 (CCK-8) and colony formation assay in MALAT1 overexpression or knockdown cells, our data showed that MALAT1 promotes the proliferation of cervical cancer cells. 	34610246
MALAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(MiRNA-613)	qRT-PCR//Luciferase Report Assay//Transwell Assay	 CEUS of HCC and Pearson correlation analysis showed that CEUS grading and lncRNA MALAT1 were positively correlated in patients with HCC. In HCC tissues of patients with HCC, lncRNA MALAT1 expressed high and miRNA-613 expressed low.  The results of bioinformatic analysis showed the targeting of lncRNA MALAT1 and miRNA-613.	 CEUS of HCC and Pearson correlation analysis showed that CEUS grading and lncRNA MALAT1 were positively correlated in patients with HCC. 	Yes	 Knocking down lncRNA MALAT1 could increase miRNA-613 expression significantly, and reduce the migration of HCC cells. Inhibiting miRNA-613 based on knocking down lncRNA MALAT1 could increase the survival and migration of HCC cells.	35706002
MALAT1	LncRNA	Homo sapiens	Thymus Neoplasms	cells	Interaction(miR-145-5p/HMGA2 pathway)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	Among the four cell lines evaluated, IU-TAB-1 showed the highest expression of MALAT1; thus, IU-TAB-1 cells were selected for subsequent experiments.  After treatment with si-MALAT1 in combination with miR-145-5p mimics or inhibitors, cell proliferation and apoptosis were respectively enhanced and inhibited in IU-TAB-1 cells. miR-145-5p inhibited the luciferase activity of IU-TAB-1 cells transfected with the MALAT1 or HMGA2 3' untranslated region. In conclusion, si-MALAT1 significantly attenuated cell proliferation and apoptosis via the miR-145-5p/HMGA2 pathway in thymic cancer cells.		Yes	 Compared with the findings in the control group, si-MALAT1 significantly decreased the cell proliferation of IU-TAB-1 cells, whereas the apoptosis levels and number of cells in G2 phase were increased. The protein expression levels of cyclin D1, cyclin E, Bcl-2 and HMGA2 were significantly decreased in the si-MALAT1 group compared with those in the control group, while Bax levels were significantly increased. 	34122636
MALAT1	LncRNA	Homo sapiens	Vitiligo		Interaction(MALAT1-miR-211-SIRT1 signalling axis)	Transfection//Luciferase Report Assay	sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated microRNA in lesional epidermis. Inhibition of SIRT1 with EX-527 downregulated keratin 10 and involucrin, suggesting that SIRT1 promotes keratinocyte differentiation. Overexpression of miR-211 mimic led to a significant increase in γ-H2AX positivity and cyclobutane pyrimidine dimer (CPD) formation, hallmarks of UVB-mediated DNA damage. These effects could be ameliorated by the addition of resveratrol, a SIRT1 activator. Furthermore, a long noncoding RNA, MALAT1, was identified as a negative upstream regulator of miR-211. Overexpression of MALAT1 resulted in increased expression of SIRT1 and a concomitant removal of UVB-induced CPDs in primary keratinocytes.		Yes	Overexpression of MALAT1 resulted in increased expression of SIRT1 and a concomitant removal of UVB-induced CPDs in primary keratinocytes.	33152110
MALAT1	LncRNA	Homo sapiens	Chronic Periodontitis	PDLCs	Interaction(miR-769-5p/HIF3A Axis)	Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//ELISA	The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro.		Yes	MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. 	33604388
MALAT1	LncRNA	Homo sapiens	Myocarditis	mice with AVMC	Expression(highly expressed)	Flow Cytometry//qRT-PCR//ELISA	In the present study, we found that MALAT1 was highly expressed in mice with AVMC, and the expression was correlated positively with cardiac pathological scores, cardiac IL-17 mRNA expression, and the percentages of splenic Th17 cells. In conclusion, our results suggest that MALAT1 knockdown alleviates CVB3-induced AVMC in mice, which may be partially attributable to the decline in Th17 cells responses. 	In the present study, we found that MALAT1 was highly expressed in mice with AVMC, and the expression was correlated positively with cardiac pathological scores, cardiac IL-17 mRNA expression, and the percentages of splenic Th17 cells. 	Yes	We further demonstrated that MALAT1 knockdown could significantly alleviate the severity of disease and inhibit the differentiation of Th17 cells, accompanying the reduced mRNA expression of RORγt and productions of Th17-related pro-inflammatory cytokines in vivo. Additionally, in vitro analysis showed that MALAT1 knockdown suppressed na?ve CD4+ T cells differentiation towards Th17 cells. 	35088199
hsa_circ_0000177	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[Wnt signaling]	qRT-PCR//Luciferase Report Assay//Transwell Assay	In our study, we found that circRNA hsa_circ_0000177 was upregulated in glioma tissues and cell lines.Through upregulating FZD7 expression, hsa_circ_0000177 activated Wnt signaling and facilitated glioma growth. 	Also, hsa_circ_0000177 overexpression was associated with poor prognosis in glioma patients. 	Yes	Through functional experiments, we found that hsa_circ_0000177 knockdown dramatically inhibited glioma cell proliferation and invasion in vitro. Consistently, hsa_circ_0000177 knockdown significantly repressed glioma growth in vivo. 	30010402
hsa_circ_0001649	CircRNA	Homo sapiens	Glioma	glioma specimens and cell lines	Expression[lower expressed]	qRT-PCR	 The data documented a decrease of hsa_circ_0001649 expression in glioma specimens and cell lines.	 In addition, down-regulated hsa_circ_0001649 is linked to larger tumor size (p = 0.002) and advanced WHO grade (p = 0.023). Additionally, hsa_circ_0001649 may be an independent prognostic marker for glioma patients after surgery (p = 0.046).	Yes	Moreover, up-regulated hsa_circ_0001649 inhibits glioma cell growth in vitro and in vivo. 	30016668
circNFIX	CircRNA	Homo sapiens	Glioma	glioma tissue	Regulation[miR-34a-5p,Notch Signaling Pathway]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Flow Cytometry	Of those, circNFIX was the sole circRNA to be overexpressed in glioma among the five methods of finding circRNAs. CircNFIX was markedly upregulated in glioma cells. CircNFIX could regulate NOTCH1 and the Notch signaling pathway to promote glioma progression by sponging miR-34a-5p via the Notch signaling pathway. 		Yes	Downregulation of circNFIX and upregulation of miR-34a-5p both inhibited cell propagation and migration.	30072869
hsa_circ_0074362	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[miR-1236-3p/HOXB7 pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Results demonstrated that hsa_circ_0074362 was significantly upregulated in glioma tissues compared with normal tissues, and hsa_circ_0074362 overexpression was correlated with clinical severity and poor prognosis in patients with glioma. Thus, hsa_circ_0074362 played a crucial role in glioma progression by regulating the miR-1236-3p/HOXB7 pathway.	Results demonstrated that hsa_circ_0074362 was significantly upregulated in glioma tissues compared with normal tissues, and hsa_circ_0074362 overexpression was correlated with clinical severity and poor prognosis in patients with glioma.	Yes	Moreover, hsa_circ_0074362 knockdown remarkably suppressed glioma cell proliferation, migration, and invasion.	30388035
circPTK2	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cell lines	Interaction(miR-136/NFIB )	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	CircPTK2 were downregulated in TNBC tissues and cell lines. CircPTK2 significantly promoted the proliferation, migration, and invasion of TNBC cells. CircPTK2 was confirmed to be a sponge of miR-136, and directly regulated NFBI and AKT/PI3K pathway. A rescue assay validated circPTK2/miR-136/NFIB axis in TNBC cells.		Yes	 CircPTK2 significantly promoted the proliferation, migration, and invasion of TNBC cells	35234989
circCSNK1G1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC tissues and cells	Interaction(miR-28-5p/LDHA)	In Vivo Experiment//IHC//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ-CSNK1G1 was upregulated in TNBC tissues and cells. Mechanism analysis showed that circ-CSNK1G1 positively regulated LDHA expression by suppressing miR-28-5p. Rescue experiments presented that circ-CSNK1G1 played functions by targeting miR-28-5p, and miR-28-5p participated in TNBC progression by degrading LDHA.		Yes	 Circ-CSNK1G1 knockdown suppressed cancer cell proliferation, migration, invasion and glycolysis energy metabolism, promoted cell apoptosis in vitro, and blocked tumor growth in vivo. 	36109751
MALAT1	LncRNA	Homo sapiens	Lymphoma, T-Cell, Cutaneous	CTCL cells	Interaction(miR-124)	Cell Proliferation Assay//qRT-PCR//ELISA	CTCL patients had higher circulating levels of IL-6, IL-8, IL-10, TGFβ, PGE2 and MMP7 which are factors released by tumor-associated macrophages in tumor microenvironment. MALAT1 sponged miR-124 as this tumor suppressive miRNA was de-repressed upon MALAT1 silencing. Moreover, downregulation of miR-124 attenuated MALAT1 silencing effects. Our study provides a rationale for further studies focused on an evaluation of MALAT1-miR-124 in CTCL progression.		Yes	Such silencing of MALAT1 resulted in reversal of EMT and inhibition of cancer stem cell phenotype, along with reduced cell growth and proliferation.	36059695
circTRIO	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-432-5p/CCDC58 axis)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Invasion Assay//Migration Assay//qRT-PCR//circRNA-seq//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining	Mechanistically, a dual luciferase reporter assay and RNA immunoprecipitation were performed and indicated that circ-TRIO could combine with miR-432-5p to regulate the expression of coiled-coil domain containing 58 (CCDC58). 		Yes	Functionally, the knockdown of circ-TRIO inhibited the proliferation, migration and invasion of TNBC cells, while the overexpression of circ-TRIO resulted in the opposite impacts.	36075896
hsa_circ_0000732	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells 	Interaction(miR-1184)	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 Our present study found that ERβ2 is upregulated in some TNBC cells and promotes TNBC cell growth, migration and invasion by regulating hsa_circ_0000732 targeting miR-1184.		Yes	ERβ2 was up-regulated in TNBC tissues and promoted the growth, migration, and invasion of TNBC cells. ERβ2 regulated hsa_circ_0000732 expression by binding to SCARF1 promoter. Knockdown of hsa_circ_0000732 inhibited TNBC cell proliferation, migration, and invasion by upregulating miR-1184.	35064304
Malat1	LncRNA	Mus musculus	acute myocardial infarction		Interaction[miR-125b-5p]	qRT-PCR//Western Blot	Downregulation of MALAT1 by siRNA transfection attenuated heart damage in an AMI model rat. The mouse cardiomyocyte cell line HL-1 was used to show that downregulation of nucleotide binding and oligomerization domain-like receptor C5 (NLRC5) and upregulation of miR-125b-5p were the results of MALAT1 silencing. TargetScan and a dual-luciferase reporter assay indicated that NLRC5 is a direct target of miR-125b-5p. Overexpression of miR-125b-5p significantly reduced hypoxia/reperfusion-induced apoptosis of HL-1 cells, an effect that could be blocked by NLCR5 overexpression. Taken together, these results suggest that MALAT1 reduced the protective effect of miR-125b-5p on injured cells through upregulation of NLCR5. This study highlights the role of MALAT1 in the pathogenesis of AMI and may guide future genetic therapeutic strategies for AMI treatment.		Yes	Interestingly, knockdown of MALAT1 strongly decreased the myocardial infarction area in AMI rats as compared with the NC-siRNA group (Fig. 1B). 	32010261
MALAT1	LncRNA	Homo sapiens	Glaucoma	RGCs	Interaction(miR-149-5p)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay	The level of MALAT1 was significantly down-regulated, and the level of miR-149-5p was distinctly up-regulated in RGCs under pressure in a dose-dependent manner. The interaction between MALAT1 and miR-149-5p was predicted by starBase v2.0 online database, and dual luciferase reporter assay, RIP assay and RNA pull-down assay validated the interaction. 		Yes	 Functionally, MALAT1 overexpression or miR-149-5p inhibitor alleviated the inhibitory effect on cell viability and the promoted effect on apoptotic rate of RGCs in EIOP. 	33108931
hsa_circ_001160	CircRNA	Homo sapiens	Glioma	cell line	Regulation[CircRNA_001160/miR-195-5p/ETV1 axis]	Northern Blot//ChIP//Western Blot//FISH//qRT-PCR//RIP//Luciferase Report Assay//IF	In this study, we found that polypyrimidine tract binding protein 1 (PTBP1) and circRNA_001160 were remarkably Expression[up-expression]regulated in GECs.As a molecular sponge of miR-195-5p, circRNA_001160 attenuated its negative regulation of the target gene ETV1 by adsorbing miR-195-5p. In addition, ETV1 was overexpression in GECs. ETV1 bounded to the promoter regions of tight junction-related proteins and increased the promoter activities, which significantly promoted the expression levels of tight junction-related proteins. The present study showed that the combined application of PTBP1, circRNA_001160, and miR-195-5p with the anti-tumor drug Dox effectively promoted Dox through BTB and extremely induced the apoptosis of glioma cells. 		Yes	Knockdown of PTBP1 or circRNA_001160 significantly increased BTB permeability, respectively. 	31862871
MAGI2-AS3	LncRNA	Homo sapiens	lung squamous cell carcinoma		regulation[miR-374a/b-5p/CADM2 Axis]	Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In conclusion, lncRNA MAGI2-AS3 suppressed LUSC by regulating miR-374a/b-5p/CADM2 axis, which might potentially serve as a therapeutic marker for LUSC patients.		Yes	MAGI2-AS3 inhibited the proliferative, migratory and invasive capability of LUSC cells with upregulated expression. 	32021443
hsa_circ_0005198	CircRNA	Homo sapiens	Glioma	GM tissue,cell line	Interaction[miR-1294]	qRT-PCR//Luciferase Report Assay	The expression of circ_0005198 was enhanced in GM tumors and cells. What's more, circ_0005198 could directly sponge miR-1294 to exert oncogenic functions.	Its expression in tumor specimens was related to clinical severity and poor prognosis.	Yes	Functionally, circ_0005198 could remarkably boost cell growth, clone-forming ability, and metastatic properties and attenuate cell apoptosis in GM cells.	31038801
hsa_circ_0037251	CircRNA	Homo sapiens	Glioma	cell lines	Interaction[Sponging miR-1229-3p and Regulating mTOR]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Through in vitro experiments, we discovered that high expression of hsa_circ_0037251 was related to low expression of the microRNA miR-1229-3p and high expression of mTOR. Then, hsa_circ_0037251 was observed to directly sponge miR-1229-3p, and mTOR was identified as a direct target of miR-1229-3p. In addition, knockdown of hsa_circ_0037251 up-regulated the expression of miR-1229-3p and inhibited the expression of mTOR. And overexpression of miR-1229-3p or low-expressed mTOR inhibited the glioma cell progression. Furthermore, transfection with mTOR overexpression vectors can restore the abilities of glioma cell progression even if hsa_circ_00037251 was knocked down using siRNAs. These results indicated that hsa_circ_0037251 may act as a tumour promoter by a hsa_circ_0037251/miR-1229-3p/mTOR axis, and these potential biomarkers may be therapeutic targets for glioma.		Yes	 The over-expressed hsa_circ_0037251 promoted cell proliferation, invasion and migration in glioma, while knockdown of hsa_circ_00037251 promoted cell apoptosis and induced G1 phase arrest. In vivo experiments revealed that hsa_circ_00037251 promoted the growth of xenografted tumours and shortened the survival period. 	31875034
circCDC45	CircRNA	Homo sapiens	Glioma	GM tissues,cell lines  	Interaction[sponging miR-516b and miR-527]	qRT-PCR//Luciferase Report Assay	High circ-CDC45 expression was found in GM specimens and cells.Stepwise mechanism studies indicated that circ-CDC45 sponged and regulated the expression of miR-516b and miR-527 to promote cell growth and invasion. Briefly, the regulatory network of circ-CDC45/miR-516b/miR-527 plays a pivotal role in GM tumorigenesis and may act as a potential target for GM treatment.	High circ-CDC45 expression was found in GM specimens and cells, which was tightly related to a larger tumor size, higher world health organization (WHO) stages, and worse survival for patients with GM.	Yes	Functionally, manipulation of circ-CDC45 expression strongly affected cell growth, apoptosis, migration and invasion, which suggests the oncogenic function of circ-CDC45 in GM oncogenesis.	31407396
MALAT1	LncRNA	Homo sapiens	Arthritis, Juvenile	sJIA patients	Interaction(miR-150-5p/ZBTB4 / JAK/STAT signal pathway)	Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//ELISA	 We found that the expression of MALAT1, the plasma level of pro-inflammatory cytokines (IL-6, IL-17, IL-1β, and TNF-α) as well as MMP-8 and MMP-9 production were significantly elevated in sJIA patients.Furthermore, bioinformatics analysis predicted that MALAT1 might bind to miR-150-5p and ZBTB4 was a downstream target gene of miR-150-5p. Besides, rescue assays revealed that MALAT1 knockdown-mediated suppressive effects on cytokine production could be reversed by ZBTB4 overexpression. In addition, MALAT1 activated the JAK/STAT signaling by upregulating ZBTB4 expression. 		Yes	Moreover, we observed that the production of these cytokines in peripheral blood mononuclear cells (PBMCs) from sJIA patients were reduced after MALAT1 knockdown. 	33341002
circPRKCI	CircRNA	Homo sapiens	Glioma	glioma tissue and cell lines	Interaction[inhibiting miR-545]	Western Blot//qPCR//CCK8//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	Our results show that circPRKCI is upregulated in human glioma tissues and glioma cells, correlating with downregulation of its potential target, microRNA-545 (miR-545). miR-545 is the primary target of circPRKCI in glioma cells. Forced overexpression of miR-545 mimicked circPRKCI shRNA-induced actions, inhibiting glioma cell survival and proliferation. In contrast, miR-545 inhibition, by a lentiviral antagomiR-545 construct, reversed circPRKCI shRNA-induced anti-A172 cell activity. Importantly, neither circPRKCI shRNA nor circPRKCI overexpression was effective in miR-545-knockout (Cas9 method) A172 cells. Importantly, the subcutaneous and orthotopic A172 xenograft growth was significantly inhibited by circPRKCI silencing. Collectively, circPRKCI promotes human glioma cell progression possibly by inhibiting miR-545. Targeting circPRKCI-miR-545 cascade could efficiently inhibit human glioma cells.		Yes	In A172 and primary human glioma cells, shRNA-mediated silencing of circPRKCI inhibited cancer cell growth, survival, proliferation, and migration. Conversely, ectopic circPRKCI overexpression promoted A172 cell progression. 	31409777
circU2AF1	CircRNA	Homo sapiens	Glioma	glioma tissues and glioma cell lines	Interaction[circ-U2AF1/hsa-miR-7-5p/NOVA2 regulatory pathway]	qRT-PCR//Luciferase Report Assay	We found that the expression levels of circ-U2AF1 and NOVA2 were upregulated, while hsa-miR-7-5p was downregulated in human glioma tissues and glioma cell lines.Our data and bioinformatic analysis indicated the association of these molecules with glioma grade, a positive correlation between circ-U2AF1 and NOVA2 expression levels and a negative correlation of hsa-miR-7-5p with both circ-U2AF1 and NOVA2, respectively. In addition, silencing of circ-U2AF1 expression resulted in increased hsa-miR-7-5p expression and decreased NOVA2 expression both in vitro and in vivo. Luciferase assay confirmed hsa-miR-7-5p as a direct target of circ-U2AF1 and NOVA2 as a direct target of hsa-miR-7-5p. Functionally, silencing of circ-U2AF1 inhibits glioma development by repressing NOVA2 via upregulating hsa-miR-7-5p both in vitro and in vivo. Thus, we assumed that circ-U2AF1 promotes glioma malignancy via derepressing NOVA2 by sponging hsa-miR-7-5p. Taken together, we suggest that circ-U2AF1 can be a prognostic biomarker and the circ-U2AF1/hsa-miR-7-5p/NOVA2 regulatory pathway may be a novel therapeutic target for treating gliomas.		Yes	Functionally, silencing of circ-U2AF1 inhibits glioma development by repressing NOVA2 via upregulating hsa-miR-7-5p both in vitro and in vivo. 	30341906
MALAT1	LncRNA	Homo sapiens	Venous Thrombosis	DVT tissues	regulation[Wnt/β-catenin pathway]	qRT-PCR//MTT//Transwell Assay//Western Blot	The results revealed that MALAT1 was upregulated in DVT tissues. In summary, the data indicated the roles of MALAT1 in the pathogenesis of DVT, and the MALAT1/Wnt/β-catenin axis could be a novel therapeutic target for the treatment of DVT.		Yes	 Furthermore, MALAT1 was able to regulate the biological behaviors of EPCs, including proliferation, migration, cell cycle arrest and apoptosis.	32855682
MALAT1	LncRNA	Homo sapiens	Venous Thrombosis	vascular endothelial cell 	Interaction(microRNA-383-5p/BCL2L11 axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	There was an interaction between MALAT1 and miR-383-5p. Compared to the control siRNA group, MALAT1-siRNA increased the cell viability, reduced cell apoptosis, upregulated Bcl-2 expression, and suppressed Bax expression. These changes were reversed by the miR-383-5p inhibitor. Additionally, we verified that BCL2L11 is a target of miR-383-5p. miR-383-5p improved the cell proliferation, while decreasing cell apoptosis in HUVECs by targeting BCL2L11.		Yes	 Compared to the control vector group, MALAT1-plasmid suppressed the viability and induced apoptosis of HUVECs, while improving Bcl-2-associated X protein (Bax) expression and decreasing Bcl-2 expression. 	35706417
hsa_circ_0001730	CircRNA	Homo sapiens	Glioma	glioblastoma cell lines and tissues	Regulation[miR-326/Wnt7B axis]	RNA Pull-Down//FISH//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining	The levels of circ_0001730 were elevated in glioblastoma cell lines and tissues. SP1 bounds to the promoter of circ_0001730 host gene EPHB4 thereby increasing the expression of circ_0001730. circ_0001730 activated the Wnt/β-catenin pathway via the miR-326/Wnt7B axis.		Yes	 circ_0001730 downregulation suppressed migration and proliferation in glioblastoma cells.	31304776
circPCMTD1	CircRNA	Homo sapiens	Glioma	cell lines	Interaction[sponging miR-224-5p]	Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	In this study, circPCMTD1 upregulation promoted the cell viability, migration and invasion dramatically, while the inhibition of circPCMTD1 led to a significant reduction of tumor growth in vivo.MiRNAs microarray analyses on circPCMTD1 silencing models in U251 and U118MG cells were performed, and the results suggested that circPCMTD1 knockdown could upregulate the expression of miR-224-5p and downregulate the expression of mTOR, one of miR-224-5p targets, in both cell lines. According to the prediction from circular RNA interactome and Targetscan, there was a complementary sequence in circPCMTD1 for miR-224-5p. Dual-luciferase reporter assay demonstrated that circPCMTD1 were targets of miR-224-5p. RIP assay was also performed to further confirm their directly interaction. Overexpression of miR-224-5p inhibited the viability and proliferation, migration, and invasion of U251 and U118MG glioma cells. In conclusion, circPCMTD1 could contribute to the promotion of glioma progression, and it may serve as the sponge of miR-224-5p to exert its function.		Yes	In this study, circPCMTD1 upregulation promoted the cell viability, migration and invasion dramatically, while the inhibition of circPCMTD1 led to a significant reduction of tumor growth in vivo.	31179240
circEZH2	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[sponging miR-1265]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We identified that circ-EZH2 was overexpressed in glioma tissues and cell lines. Additionally, we found circ-EZH2 served as a miRNA sponge for miR-1265 to release its suppression on DDAH1 and CBX3. Rescue assays further revealed that the oncogenic function of circ-EZH2 was partly dependent on its modulation of DDAH1 and CBX3. 		Yes	 Further studies revealed that ectopic expression of circ-EZH2 significantly promoted cell growth, migration and invasion but inhibited cell apoptosis.By contrast, silencing of circ-EZH2 induced the opposite effects. 	31669648
MALAT1	LncRNA	Homo sapiens	Esophageal Neoplasms	EC tissues	regulation[miR-1-3p/CORO1C/TPM3 axis]	qRT-PCR//Luciferase Report Assay	 MALAT1 level was downregulated, while miR-1-3p level was upregulated in EC specimens. The suppressed level of miR-1-3p not only induced the activity of CORO1C/TPM3 signaling, but also upregulated MALAT1 expression, indicating the reciprocal regulation between the two factors. 		Yes	The inhibition of MALAT1 suppressed the viability, migration, and invasion in EC cell lines. 	32468237
circPTN	CircRNA	Homo sapiens	Glioma	cell lines	Interaction[sponges miR-145-5p/miR-330-5p ]	RNA Pull-Down//CCK8//qRT-PCR//FISH//Flow Cytometry//EdU Staining	We demonstrated circPTN was significantly higher expression in glioma tissues and glioma cell lines, compared with NBT and HEB (human astrocyte).Furthermore, we performed dual-luciferase reporter assays and RNA pull-down assays to verify that circPTN acts through sponging miR-145-5p and miR-330-5p. Increasing expression of circPTN rescued the inhibition of proliferation and downregulation of SOX9/ITGA5 in glioma cells by miR-145-5p/miR-330-5p. In addition, we found that circPTN promoted self-renewal and increased the expression of stemness markers (Nestin, CD133, SOX9, and SOX2) via sponging miR-145-5p. Moreover, this regulation was disappeared when circPTN binding sites in miR-145-5p were mutated.		Yes	In gain- and loss-of-function experiments, circPTN significantly promoted glioma growth in vitro and in vivo. 	31511040
hsa_circ_0076248	CircRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[sponging miR-181a to modulate SIRT1]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	The quantitative real-time polymerase chain reaction results showed that the expression of miR-181a was significantly decreased in glioma tissues and cell lines compared with normal brain tissues and normal gliocyte, respectively, and the expression of hsa_circ_0076248 and SIRT1 demonstrated the opposite.The experiment also showed that downregulating hsa_circ_0076248 or upregulating miR-181a could remarkably promote the temozolomide chemotherapy sensitivity. Furthermore, Western blot analysis testified that downregulating hsa_circ_0076248 or upregulating miR-181a could promote the expression of p53 and SIRT1. In summary, our study sheds light on the regulatory mechanism of hsa_circ_0076248 in glioma growth and invasion via sponging miR-181a, which downregulates the SIRT1 expression and also suggests that hsa_circ_0076248, miR-181a, and SIRT1 may serve as potential therapeutic targets for glioma.		Yes	Our results verified that downregulating hsa_circ_0076248 or upregulating miR-181a could depress the proliferation and invasion of glioma in vitro and in vivo. 	30506951
circSCAF11	CircRNA	Homo sapiens	Glioma	Glioma Tissue,cell lines	Regulation[ miR-421/SP1/VEGFA Axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	circSCAF11 expression was found to be significantly upregulated in the glioma tissue specimens and cell lines. Mechanically, circSCAF11 positively regulated the SP1 expression through sponging miR-421. Moreover, transcription factor SP1 activated the transcription of VEGFA, constructing the circSCAF11/miR-421/SP1/VEGFA axis in the glioma genesis.	The ectopic overexpression of circSCAF11 was closely correlated with the poor clinical outcome of glioma patients.	Yes	Functionally, knockdown of circSCAF11 inhibited the proliferation, invasion, and tumor growth and induced the G0/G1 phase arrest. 	31400609
MALAT1	LncRNA	Homo sapiens	Cerebral Ischaemia/Reperfusion Injury	PC12 cells	Interaction(miR-182-5p/TLR4 axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining	 MiR-182-5p was validated to be a downstream target gene of MALAT1, and MALAT1 could increase the expression of TLR4 by suppressing miR-182-5p. The effects of PPF on the injury of the mice brain and PC12 cells were partly counteracted by the restoration of MALAT1. PPF protects the brain against I/R-induced injury by regulating MALAT1/miR-182-5p/TLR4 axis.		Yes	 MiR-182-5p was validated to be a downstream target gene of MALAT1, and MALAT1 could increase the expression of TLR4 by suppressing miR-182-5p. The effects of PPF on the injury of the mice brain and PC12 cells were partly counteracted by the restoration of MALAT1. PPF protects the brain against I/R-induced injury by regulating MALAT1/miR-182-5p/TLR4 axis.	34427851
hsa-circ-0014359	CircRNA	Homo sapiens	Glioma	glioma tissues，cell lines	Regulation[miR-153/PI3K signaling]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	The expression of circ-0014359 was increased in T98G and SHG44 cancer cell lines and glioma tissues from patients, when compared with control cells and tissue. Further, our observations indicated that circ-0014359 acted as a miRNA-153 (miR-153) sponge in glioma cells. Transfection of miR-153 inhibitor significantly suppressed si-circ-0014359-induced inhibition of cell viability, cell migration, and invasion. The increased expression of circ-0014359 levels in glioma cells was correlated with downregulated expression of miR-153. Overexpression of miR-153 reduced p-AKTser473 (a PI3K pathway indicator) and the rescue experiment showed enhanced p-AKTser473 expression. 		Yes	 SiRNA-mediated silencing of circ-0014359 potently inhibited cell viability, migration, invasion, and apoptosis of glioma cells. 	30745107
MALAT1	LncRNA	Homo sapiens	Her2-receptor positive breast cancer	cells and tissues	Expression [highly expressed]	Other	As a result, MALAT1 was remarkably up-regulated in HER2-positive breast cancer both in cells and tissues. In addition, the silencing of MALAT1 inhibited the proliferation of HER2-positive breast cancer cells both in vitro and in vivo. Furthermore, knockdown of MALAT1 by shRNA down-regulated DNMT1, DNMT3a, and DNMT3b, while up-regulated BRCA1 and PTEN in HER2-positive breast cancer both in cell lines and mouse xenograft models.		Yes	In addition, the silencing of MALAT1 inhibited the proliferation of HER2-positive breast cancer cells both in vitro and in vivo. Furthermore, knockdown of MALAT1 by shRNA down-regulated DNMT1, DNMT3a, and DNMT3b, while up-regulated BRCA1 and PTEN in HER2-positive breast cancer both in cell lines and mouse xenograft models.	34148540
MALAT1	LncRNA	Homo sapiens	Acute Kidney Injury	serum samples from AKI patients	Interaction(miR-204/APOL1 pathway)	RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 From the results, lncRNA MALAT1 was strongly elevated in serum samples from AKI patients, with the high sensitivity and specificity concerning differentiating AKI patients from healthy controls.After co-transfection with MALAT1 silencing and miR-204 inhibition, we found that miR-204 could counteract the effects of MALAT1 on HK-2 cell progression and inflammation after under hypoxic conditions. Finally, NF-κB signaling was inactivated while APOL1 expression was increased in HK-2 cells after hypoxia treatment, and lncRNA MALAT1 inhibition reactivated NF-κB signaling while suppressed APOL1 expression by sponging miR-204.		Yes	Silencing of MALAT1 could reverse hypoxia-triggered promotion of HK-2 cell apoptosis. Meanwhile, the increase of IL-1β, IL-6, and TNF-α after hypoxia treatment could be repressed by MALAT1 knockdown as well. 	34240756
circCPA4	CircRNA	Homo sapiens	Glioma	glioma tissues	Regulation[circCPA4/let-7/CPA4 axis]	Microarray	We found that circCPA4 (hsa_circ_0082374) up-regulated the most in glioma tissues and high levels of circCPA4 were positively related to poor outcome of glioma. Moreover, circCPA4 interacts with let-7 and serves as a sponge for let-7. Through the competitive endogenous RNA (ceRNA) mechanism, circCPA4 sponges let-7 to regulate the expression of CPA4 and glioma progression. The circCPA4/let-7/CPA4 axis regulates glioma progression by ceRNA mechanism, and circCPA4 could be a novel prognostic biomarker and target for glioma treatment.		Yes	And knockdown of circCPA4 suppresses cell proliferation and metastasis in glioma.	31424161
Malat1	LncRNA	Mus musculus	Myocardial Infarction	MI mice	Interaction(MicroRNA-25-3p/CDC42 Axis)	In Vivo Experiment//Transfection//Flow Cytometry//FISH//qRT-PCR//MTT//Luciferase Report Assay//IHC//IF	MALAT1 was highly expressed in MI mice, OGD-treated MMECs, M1-BMMs, and EVs. MALAT1 sponged miR-25-3p to upregulate CDC42. miR-25-3p overexpression promoted OGD-treated cell viability, proliferation, and angiogenesis. The MEK/ERK pathway was activated after EV treatment. 		Yes	Silencing MALAT1 weakened the inhibition of EV treatment on OGD-treated cells.	34745428
hsa_circ_0001777	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cell line	Interaction(miR-95-3p/AKAP12 Axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//Invasion Assay//Migration Assay//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining	The expression of circ_0001777 and AKAP12 was decreased in TNBC tissues, while the expression of miR-95-3p was increased.  Circ_0001777 can sponge miR-95-3p, and AKAP12 is the target of miR-95-3p.Mechanically, circ_0001777 regulates AKAP12 expression in TNBC cells by sponge miR-95-3p. 		Yes	 In vitro complement experiments, overexpression of circ_0001777 significantly decreased the malignant behavior of TNBC, while co-transfection of miR-95-3p partially up-regulated this change. In addition, AKAP12 knockdown increased the proliferation, migration, and invasion of TNBC cells inhibited by overexpression of circ_0001777. 	36513585
Malat1	LncRNA	Mus musculus	Sepsis	skeletal muscle tissues	Interaction[BRCA1,EZH2]	Western Blot//FISH//qRT-PCR//RIP//ELISA//ChIP	 High expression of lncRNA MALAT1 along with low expression of breast cancer susceptibility gene 1 (BRCA1) were identified in septic mice and human skeletal muscle cells of sepsis.		Yes	Silencing lncRNA MALAT1 resulted in reduced serum levels of interleukin (IL)-6, IL-8, and tumor necrosis factor alpha (TNF-α), neutrophil migration, skeletal muscle cell apoptosis, and AKT-1 phosphorylation. 	31830649
Malat1	LncRNA	Mus musculus	Sepsis	mice model	Interaction(MALAT1-METTL16-MAT2A interactive axis)	qRT-PCR//MeRIP	. In cultured macrophages, LPS treatment significantly induced MALAT1 expression, while genetic ablation of MALAT1 greatly reduced proinflammatory cytokine levels. Furthermore, MALAT1-ablated mice had significantly increased survival rates in cecal ligation and puncture (CLP)-induced sepsis and LPS-induced endotoxemia. We showed a mechanism for MALAT1 ablation leading to enhanced antioxidant capacity is through activation of methionine cycle by epitranscriptomical regulation of methionine adenosyltransferase 2A (MAT2A). MAT2A 3'UTR can be methylated by METTL16 which was known to directly bind to MALAT1. MALAT1 ablation was found to reduce methylation in MAT2A hairpin1 and increase MAT2A protein levels. 		Yes	. In cultured macrophages, LPS treatment significantly induced MALAT1 expression, while genetic ablation of MALAT1 greatly reduced proinflammatory cytokine levels. Furthermore, MALAT1-ablated mice had significantly increased survival rates in cecal ligation and puncture (CLP)-induced sepsis and LPS-induced endotoxemia. 	35763934
circDHDDS	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and  TNBC cell lines	Interaction(miR-362-3p/DDX5 )	In Vivo Experiment//IHC//Western Blot//Transfection//Tube Formation Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	The contents of circDHDDS and DDX5 were increased, and miR-362-3p level was decreased in TNBC. Furthermore, miR-362-3p was validated to exert a tumor repressive effect in TNBC cells by suppressing DDX5. Moreover, DDX5 could regulate the development of TNBC. The experimental data exposed that levels of miR-362-3p presented noteworthy negative correlation with circDHDDS and DDX5, while circDHDDS and DDX5 exhibited significant positive correlation. In mechanism, circDHDDS bound to miR-362-3p to modulate DDX5 expression. In addition, circDHDDS knock-down also attenuated tumor growth.		Yes	 CircDHDDS deficiency reserved cell proliferation, migration, invasion and angiogenesis, while facilitated cell apoptosis in TNBC cells. 	35343646
MAGI2-AS3	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Expression[highly expressed]	qRT-PCR//Wound Healing Assay//Migration Assay	The results showed that the expression level of lncRNA MAGI2-AS3 was significantly increased in diffuse gastric cancer tissues compared with intestinal gastric cancer tissues (p < 0.0001; Figure 1B).	Moreover, lncRNA MAGI2-AS3 was overexpressed in poorly differentiated gastric cancer tissues compared with moderately or highly differentiated gastric cancer tissues (p < 0.0001; Figure 1C). Furthermore, lncRNA MAGI2-AS3 was more highly expressed in tumors extending beyond the gastric mucosa layer (T2+T3+T4) compared with tumors detected only in the gastric mucosa (T1), and more highly expressed in tumors with a high degree of malignancy (stage II+III+IV) compared with tumors with a low degree of malignancy (stage I; Figures 1D and 1E). 	Yes	 Loss-of-function and gain-of-function studies showed that lncRNA MAGI2-AS3 could positively regulate ZEB1 expression and the process of cell migration and invasion in gastric cancer. 	31837602
hsa_circ_0062558	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells 	Interaction(miR-876-3p/SLC1A5 axis)	In Vivo Experiment//Western Blot//Transfection//Invasion Assay//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//H&E Staining//Cell Proliferation Assay//IHC//EdU Staining//Transwell Assay	TNBC tissues and cells showed the higher level of circ_0062558 when compared with control samples. MiR-876-3p was confirmed as a target of circ_0062558, and circ_0062558 knockdown repressed TNBC cell malignant behaviors by increasing miR-876-3p. Furthermore, miR-876-3p inhibited malignant behaviors of TNBC cells by down-regulating SLC1A5, a newly identified target of miR-876-3p.		Yes	 Downregulation of circ_0062558 inhibited proliferation, migration, invasion, and glutamine metabolism, while enhanced apoptosis of TNBC cells, and silencing of circ_0062558 also inhibited the growth of tumor in vivo. 	35284960
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	interaction[sponge miR-25,upregulate RECK]	qRT-PCR	 We found that MAGI2-AS3 and RECK were upregulated and positively correlated in NSCLC.Therefore, MAGI2-AS3 may sponge miR-25 to upregulate RECK, thereby inhibiting NSCLC cell invasion and migration.		Yes	Cell invasion and migration analysis showed decreased NSCLC cell invasion and migration rates after MAGI2-AS3 and RECK overexpression.	32138716
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumor tissues	interaction[ Sponging miR-155]	qRT-PCR	The authors found that MAGI2-AS3 and suppressor of cytokine signaling 1 (SOCS-1) were both downregulated in NSCLC.	During follow-up, low levels of MAGI2-AS3 and SOCS-1 were found to be significantly correlated with patients' poor survival.	Yes	Cell proliferation revealed decreased cell proliferation rate of NSCLC cells after MAGI2-AS3 and SOCS-1 overexpression.	31910343
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-629-5p/TXNIP axis)	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Transwell Assay	MAGI2-AS3 was found to be downregulated in NSCLC tissues.The bioinformatics analysis and luciferase report assay revealed that MAGI2-AS3 functioned as competing endogenous RNA to suppress microRNA (miR)-629-5p expression, while miR-629-5p suppressed thioredoxin-interacting protein (TXNIP) expression by targeting its 3' untranslated region. 		Yes	The gain-of-function in vitro studies showed that the overexpression of MAGI2-AS3 suppressed NSCLC cell proliferation and invasion. Conversely, the knockdown of MAGI2-AS3 had the opposite effects. 	35071487
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[miR-374b-5p/SMG1 signaling pathway]	qRT-PCR	In the current study, we found that MAGI2-AS3 expression is downregulated in HCC tissues and closely associated with some clinical characteristics (tumor size, lymph node metastasis, and TNM stage) and poor overall survival.Taken together, we reveal a functional MAGI2-AS3/miR-374b-5p/SMG1 axis that suppresses HCC progression, potently suggesting a new road for HCC treatment.	In the current study, we found that MAGI2-AS3 expression is downregulated in HCC tissues and closely associated with some clinical characteristics (tumor size, lymph node metastasis, and TNM stage) and poor overall survival.	Yes	Overexpression of MAGI2-AS3 inhibits HCC cell proliferation and migration in vitro, while impedes tumor growth in vivo accordantly.	30924168
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction[KDM1A ,H3K4me2 ,RACGAP1  ]	Western Blot//Tunel//qRT-PCR//FISH//RIP//IHC//EdU Staining//Transwell Assay	MAGI2-AS3 was found to be under-expressed in HCC tissues and cell lines. Interaction between MAGI2-AS3 and KDM1A was identified. KDM1A recruited by MAGI2-AS3 was found to promote H3K4me2 demethylation at the RACGAP1 promoter, which ultimately decreased the expression of RACGAP1. We also identified that RACGAP1 knockdown eliminated the stimulatory effects of MAGI2-AS3 silencing on the malignant phenotypes of HCC cells.		Yes	The restoration of MAGI2-AS3 was identified to markedly inhibit HCC cell growth, migrating ability, and invasiveness, and promote cell apoptosis. Additionally, the expression of MAGI2-AS3 reduced tumor weight and size in HCC transplanted nude mice. 	31629962
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	blood 	regulation[ROCK2]	Flow Cytometry//qRT-PCR//Western Blot//Transwell Assay	We found that MAGI2-AS3 was downregulated in plasma of early stage HCC patients compared to healthy controls. Our study indicated that MAGI2-AS3 was downregulated in the distant recurrence of HCC after surgical resection and affected the invasion and migration of HCC cells via ROCK2.		Yes	Cell invasion and migration assay showed that overexpression of MAGI2-AS3 mediated the decreased cell invasion and migration rate, while ROCK2 played an opposite role and attenuated the effects of overexpression of MAGI2-AS3.	32546442
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Regulation(miR-519c-3p/TXNIP Axis)	qRT-PCR	 MAGI2-AS3 levels were elevated, and miR-519c-3p decreased in HCC. MAGI2-AS3 overexpression inhibits while its knockdown stimulates HCC cell growth through miR-519c-3p. Moreover, miR-519c-3p overexpression stimulates HCC cell growth. MAGI2-AS3 serves as competing endogenous RNA (ceRNA) of miR-519c-3p to regulate TXNIP in HCC. And, TXNIP upregulation weakened the influence of MAGI2-AS3 knockdown on HCC cell behaviors. Additionally, MAGI2-AS3 overexpression suppressed HCC tumor growth in vivo.		Yes	MAGI2-AS3 overexpression inhibits while its knockdown stimulates HCC cell growth through miR-519c-3p.	34484334
MAGI2-AS3	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell lines 	regulation[miR-31-5p/TNS1 axis]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//IHC//Transwell Assay	Furthermore, we observed significantly lower MAGI2-AS3 and TNS1 mRNA expression and higher miR-31-5p expression in the BCa tissues and cell lines (T24 and J82) compared with their corresponding controls.In conclusion, our study demonstrates that the MAGI2-AS3/miR-31-5p/TNS1 axis regulates BCa progression.	Moreover, immunohistochemical staining of paired BCa and normal urothelial tissues showed that low expression of TNS1 correlated with advanced tumor (T) stages and lymph node metastasis in BCa.	Yes	Functional and biochemical experiments in BCa cell lines including luciferase reporter assays showed that MAGI2-AS3 upregulated TNS1 by sponging miR-31-5p. Transwell assays showed that the MAGI2-AS3/miR-31-5p/TNS1 axis regulated migration and invasion ability of BCa cell lines. 	33231563
MAGI2-AS3	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	Bca tissues	Regulation(MAGI2/PTEN/epithelial-mesenchymal transition (EMT) axis)	qRT-PCR//Western Blot	MAGI2-AS3 expression was significantly downregulated in Bca, compared with normal tissues, and negatively associated with tumor stage and a poor prognosis. MAGI2-AS3 overexpression inhibited Bca cell progression by regulating the MAGI2/PTEN/epithelial-mesenchymal transition, offering novel insights into the mechanism of Bca progression.	MAGI2-AS3 expression was significantly downregulated in Bca, compared with normal tissues, and negatively associated with tumor stage and a poor prognosis.	Yes	The expression of MAGI2 and its downstream gene, PTEN, increased in Bca cells overexpressing MAGI2-AS3, and interference by MAGI2 expression reversed the migration and invasion inhibited by MAGI2-AS3 overexpression.	33104021
MAGI2-AS3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	rOSCC and OSCC-LNM	Regulation(PI3K-AKT-mTOR pathway)	qRT-PCR//Western Blot//Transwell Assay	 The expressions of the lncRNAs, namely MAGI2-AS3 and CCDC144NL-AS1, were significantly upregulated in rOSCC and OSCC-LNM. MAGI2-AS3 was overexpressed in cancer tissue compared to other control groups. MAGI2-AS3 and CCDC144NL-AS1 might promote cell proliferation, invasion, and migration in OSCC cells by regulating the PI3K-AKT-mTOR pathway.		Yes	MAGI2-AS3 and CCDC144NL-AS1 might promote cell proliferation, invasion, and migration in OSCC cells by regulating the PI3K-AKT-mTOR pathway.	36401978
hsa_circ_0000851	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	BC cell lines and tissue samples	Interaction( miR-1183/PDK1/p-AKT)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Proliferation Assay//IHC//Invasion Assay	 Our study showed that hsa_circ_0000851 was mainly located in the cytoplasm of BC cells and upregulated in BC cell lines and tissue samples. We found that hsa_circ_0000851 bound directly to miR-1183, accelerating the expression of its target gene PDK1, which facilities BC cell proliferation and migration through PDK1/p-AKT.		Yes	Higher hsa_circ_0000851 expression levels resulted in increased proliferation of BC cells both in vitro and in vivo, while treatment of BC cells with hsa_circ_0000851 siRNA decreased their proliferation. 	36241055
MAGI2-AS3	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cell lines	Expression[highly expressed]	qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay			Yes	Moreover, MAGI2-AS3 knockdown-suppressed NPC progression in vitro and in vivo.	32450008
circAR-E2E4	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells	Interaction(miR-665-STAT3 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//PCR//Bioinformatics Analysis	Collectively, the regulatory network circAR-E2E4-miR-665-STAT3 axis we constructed was associated with TNBC progression, providing a promising diagnostic, prognostic, and therapeutic target in future treatment for TNBC.		Yes	CCK-8 assay showed circAR-E2E4 regulated TNBC cell proliferation. 	36691537
MAGI2-AS3	LncRNA	Homo sapiens	Prostatic Neoplasms	 prostate cancer serum samples and cells	Interaction( miR-142-3p)	Luciferase Report Assay//Transwell Assay	MAGI2-AS3 has descended expression while miR-142-3p has an ascendant one in prostate cancer serum samples and cells. 	ROC curve analysis revealed that the AUC was 0.953 for MAGI2-AS3, with a sensitivity of 91.5% and specificity of 84.7%.	Yes	Overexpression of MAGI2-AS3 in LNCaP and PC3 cells suppressed the biological function of the cell including proliferation capacity, migration level, and invasion. 	35944561
MAGI2-AS3	LncRNA	Homo sapiens	Prostatic Neoplasms	clinical samples, PC-3 and DU145 cell line	Interaction(miR-424-5p/COP1 )	Western Blot//RIP//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Bioinformatics Analysis	We found that MAGI2-AS3 was one of the most downregulated lncRNAs in prostate tumors, which was further confirmed in our collected clinical samples. Elevation of MAGI2-AS3 decreased the activity of STAT3 in PC-3 and DU145. In addition, microRNA-424-5p (miR-424-5p), a positive regulator of STAT3 pathway, was predicted as a target of MAGI2-AS3, furthermore, the interaction between MAGI2-AS3 and miR-424-5p was confirmed via reverse-transcript polymerase chain reaction (RT-qPCR), dual luciferase reporter assay and RNA immunoprecipitation (RIP). MAGI2-AS3 upregulated miR-424-5p and downregulated COP1 in PC-3 and DU145. More importantly, IL6-induced activation of STAT3 pathway could attenuate the biological effect of MAGI2-AS3 in PC-3 and DU145. In clinical samples, MAGI2-AS3 levels were negatively correlated with miR-424-5p expression, while positively correlated with COP1 mRNA expression.		Yes	 The function assays showed that MAGI2-AS3 overexpression decreased cell viability and led to obvious cell apoptosis in PC-3 and DU145 prostate cancer cells. 	34976194
MAGI2-AS3	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	Regulation( HEY1/ACY1 pathway)	In Vivo Experiment//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay//ChIP	MAGI2-AS3 and ACY1 expression was downregulated in ccRCC tissues, and low expression of MAGI2-AS3 was associated with poor patient survival. The present study demonstrates that MAGI2-AS3 exerts tumor-suppressive, anti-angiogenic activities in ccRCC by modulating the HEY1/ACY1 pathway.	MAGI2-AS3 and ACY1 expression was downregulated in ccRCC tissues, and low expression of MAGI2-AS3 was associated with poor patient survival. 	Yes	Overexpression of MAGI2-AS3 could reduce ccRCC cell viability and migration, inhibit vessel-like tube formation of HUVECs in vitro, and repress tumor growth and angiogenesis in vivo. 	34002044
MAILR	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	cells	Regulation(PDGFA )	qRT-PCR//Luciferase Report Assay//Western Blot	Bioinformatics analysis and luciferase assay revealed that H22954 targeted the 3' untranslated region (UTR) of the platelet-derived growth factor subunit A (PDGFA) gene. In transfected cells, H22954 overexpression reduced PDGFA expression and protein levels.  These findings indicate that H22954 inhibits angiogenesis in AML through the down-regulation of PDGFA expression. 		Yes	Overexpression of H22954 inhibited angiogenesis in mouse xenograft tumors and cultured acute myeloid leukemia (AML) cells.	35319391
MAILR	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	Bone marrow	Expression[lower expressed]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Microarray	In this study, we analyzed differentially expressed genes in CD34 hematopoietic cells and identified a novel lncRNA, H22954, which was down-regulated in acute myeloid leukemia (AML) patients. Bioinformatic analysis and RNA antisense purification assay indicated that H22954 targeted the 3' untranslated region of the BCL2 gene. In luciferase assays, H22954 expression inhibited BCL2 expression. In transfected K562 cells and mouse xenograft tumors, H22954 overexpression reduced BCL-2 protein levels and promoted cell death. In AML patients, H22954 expression inversely correlated with BCL-2 protein levels in bone marrow cells, blast cell numbers and disease prognosis. These results indicate that H22954 is a novel regulator of BCL-2 and that reduced H22954 expression may play an important role in the pathogenesis of AML. +		Yes	In cultured AML cells and mouse xenograft models, H22954 expression inhibited cell proliferation and tumor growth, respectively.	30959078
MAILR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells and tissues	regulation[Regulating MiR-513b-5p and DUSP11]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	AZIN1-AS1 was up-regulated in NSCLC cells and tissues, while miR-513b-5p was significantly down-regulated.AZIN1-AS1 acts as a tumor promoter in NSCLC, which is ascribed to the regulation of miR-513b-5p and DUSP11.		Yes	Silencing of AZIN1-AS1 or overexpression of miR-513b-5p markedly inhibited proliferation, migration and invasion of NSCLC cells, while overexpression of AZIN1-AS1 or inhibition of miR-513b-5p functioned oppositely.	33116570
Malat1	LncRNA	Mus musculus	Diabetic Gastroparesis	DGP model mice	Interaction(miR-449a/DLL1 Axis )	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//RNA-seq//migration assay//Luciferase Report Assay//Cell Proliferation Assay	 We show that MALAT1 expression was upregulated in the gastric tissues of DGP model mice, the adjacent healthy tissues collected from diabetic gastric cancer patients with DGP symptoms, and in HGSMCs cultured under HG conditions.  Collectively, our data highlight a novel regulatory signaling pathway, the MALAT1/miR-449a/DLL1 axis, in the context of DGP.		Yes	 Functionally, MALAT1 knockdown in vitro impacted the viability, proliferation, migration and promoted the phenotypic switch of HGSMCs under HG conditions. 	34385927
Malat1	LncRNA	Mus musculus	Neuralgia	spinal cord tissue,cell line	Regulation[miR‑154‑5p/AQP9 axis]	qRT-PCR//ELISA//Luciferase Report Assay//Western Blot	The results of the present study identified that the expression levels of MALAT1 and AQP9 were upregulated, while miR‑154‑5p was downregulated in spinal cord tissue and microglia of CCI rats. The present study also identified that miR‑154‑5p was the target gene of MALAT1, and AQP9 was the target gene of miR‑154‑5p. AQP9 knockdown promoted the occurrence of neuropathic pain. In conclusion, lncRNA MALAT1 promotes the progression of neuropathic pain in rats by reducing miR‑154‑5p and increasing AQP9. The MALAT1/miR‑154‑5p/AQP9 axis can be used as a new therapeutic target for neuropathic pain.		Yes	MALAT1 knockdown in CCI model rats significantly induced the occurrence of neuropathic pain, while the upregulation of miR‑154‑5p could reverse this process. 	31746418
Malat1	LncRNA	Mus musculus	Lung Injury	 lung tissues	Interaction[p38 MAPK/p65 NF-κB pathway]	qRT-PCR//Western Blot	The expression of lncRNA MALAT1 in lung tissues of mice with septic lung injury was significantly increased (p<0.05).The immunohistochemical results manifested that the knockdown of lncRNA MALAT1 could inhibit the LPS-induced up-regulation of p38 in lung tissues in mice. According to the results of Western blotting, the p38 MAPK/p65 NF-κB signaling pathway was significantly activated in lung tissues in LPS group (p<0.05), while it was significantly suppressed after inhibition on lncRNA MALAT1 (p<0.05).		Yes	 After knockdown of lncRNA MALAT1, the LPS-induced pathological injury of lungs could be improved, and the wet weight/dry weight ratio of lungs could be reduced (p<0.05).	30779099
circEIF3H	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer tissues and cells 	Interaction( IGF2BP2 and HuR /HSPD1, RBM8A, and G3BP1)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//Invasion Assay//Co-IP//Migration Assay//FISH//qRT-PCR//RIP//MTT//RNA-seq//Cell Cycle Assay//Colony Formation Assay//EdU Staining//IF	a novel circRNA, circEIF3H, which was upregulated in breast cancer tissues. Large cohort survival analysis confirmed the association between high circEIF3H expression and poor prognosis of TNBC,Further experiments showed that circEIF3H did not function as a microRNA sponge as in the most well-established pathway, but as a scaffold for IGF2BP2 and HuR to regulate the mRNA stability of HSPD1, RBM8A, and G3BP1.	a novel circRNA, circEIF3H, which was upregulated in breast cancer tissues. Large cohort survival analysis confirmed the association between high circEIF3H expression and poor prognosis of TNBC,	Yes	 Then we conducted both in vitro and in vivo experiments which illustrated that circEIF3H was essential for TNBC proliferation and metastasis.	35568705
hsa_circ_0076611	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	 (TNBC) cells and tissues	Regulation	Western Blot//Transfection//Wound Healing Assay//qPCR//RNA-seq//Cell Proliferation Assay//ELISA//Colony Formation Assay//Bioinformatics Analysis//invasion assay	Circ_0076611 is detectable in triple-negative breast cancer (TNBC) cells and tissues, in exosomes released from TNBC cells and in the serum of breast cancer patients.Circ_0076611 interacts with a variety of proliferation-related transcripts, included MYC and VEGFA mRNAs, and increases cell proliferation and migration of TNBC cells. Mechanistically, circ_0076611 favors the expression of its target mRNAs by facilitating their interaction with components of the translation initiation machinery. 		Yes	Circ_0076611 interacts with a variety of proliferation-related transcripts, included MYC and VEGFA mRNAs, and increases cell proliferation and migration of TNBC cells. 	35710947
Malat1	LncRNA	Mus musculus	Brain Injuries, Traumatic	endothelial cell 	Regulation	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Tube Formation Assay//qRT-PCR//FISH//Cell Proliferation Assay	The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced.  Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.		Yes	The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. 	35017438
circDUSP1	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-761/DACT2 signaling axis)	In Vivo Experiment//RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay	 We identified the circRNA named circDUSP1 that was inversely correlated with tumorigenesis and progression in TNBC. In-depth mechanism analysis indicated that circDUSP1 acts as an endogenous sponge of miR-761 to reduce its suppression on target gene DACT2 expression in TNBC. Upregulation of miR-761 or downregulation of DACT2 partially reversed the biological process of TNBC and the prognosis of paclitaxel affected by circDUSP1. Taken together, our findings revealed a role for the regulation of the miR-761/DACT2 axis by circDUSP1 in the biological process of TNBC.		Yes	 Overexpression of circDUSP1 significantly attenuated cell proliferation, migration, invasion, and epithelial-mesenchymal transition, while increased the sensitivity of TNBC cells to paclitaxel.	36562476
Malat1	LncRNA	Mus musculus	Reperfusion Injury	myocardial tissues	Regulation[PI3K/AKT signaling pathway ]	qRT-PCR//Western Blot//Tunel//H&E Staining	The expression level of lncRNA MALAT1 in myocardial tissues was significantly higher in the I/R group than that in the Control group (p<0.05). The MALAT1 knockdown can markedly improve the I/R-induced myocardial injury and promote the cardiac function of rats, whose mechanism may be related to the activation of the AKT signaling pathway by MALAT1 siRNA. 		Yes	The MALAT1 knockdown could significantly improve the cardiac insufficiency caused by I/R injury, and increase both EF% and FS% in rats (p<0.05).In addition, the MALAT1 knockdown could markedly inhibit myocardial infarction caused by I/R injury and reduce the infarction area from (62.12 ± 1.29) to (27.66 ± 3.58; p<0.05).	31841208
Malat1	LncRNA	Mus musculus	Cerebral Ischaemia/Reperfusion Injury	MCAO/reperfusion model and OGD/RX model	regulation[miR-145,AQP4]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	We found that the level of MALAT1 was significantly upregulated in both the MCAO/reperfusion model and OGD/RX model. Taken together, our study confirmed that MALAT1 promotes cerebral ischemia-reperfusion injury by affecting AQP4 expression through competitively binding miR-145, indicating that MALAT1 might be a new therapeutic target for treatment cerebral ischemic stroke.		Yes	Knockdown of MALAT1 increased cell viability and reduced cell apoptosis in MA-C cells, while an AQP4 siRNA combined with a siRNA targeting MALAT1 could not enhance this effect. 	32138732
Malat1	LncRNA	Mus musculus	Brain Injuries, Traumatic	 brain microvascular endothelial cells	Regulation(Ang1)	Western Blot//Migration Assay//qRT-PCR//FISH//Cell Proliferation Assay//IHC	Our results indicated that 1) MALAT1 RNA was localized in cerebral endothelium, enhanced by OGD stimuli. 2) Inhibition of MALAT1 by siRNA suppressed angiogenesis, as indicated by endothelial viability, tube formation, migration, and functional vessel density. 3) MALAT1 inhibition further decreased Ang1 expression in the endothelium. 4) Mice with MALAT1 inhibition exhibited worse behavioral performances (NSS, wire grip, Morris water maze), as compared to control. MALAT1 could promote angiogenesis, subsequently contributing to the Ang1 synthesis from active vasculature. It may eventually benefit to functional recovery following TBI.		Yes	 Inhibition of MALAT1 by siRNA suppressed angiogenesis, as indicated by endothelial viability, tube formation, migration, and functional vessel density.	34808123
MALAT1	LncRNA	Rattus norvegicus	Esophageal Neoplasms	PMVECs	Interaction(MALAT1/microRNA-144/GSK3β axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Tunel//Flow Cytometry//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC//Bioinformatics Analysis	Our experimental data revealed that Propofol treatment could decrease the elevated expression of MALAT1 following I/R injury or H/R induction, indicating its protection against lung I/R injury. Additionally, overexpressing MALAT1 or GSK3β promoted the activation of autophagosomes, proinflammatory factor release, and cell apoptosis, suggesting that overexpressing MALAT1 or GSK3β may reverse the protective effects of Propofol against lung I/R injury. MALAT1 was identified to negatively regulate miR-144 to upregulate the GSK3β expression.		Yes	overexpressing MALAT1 or GSK3β promoted the activation of autophagosomes, proinflammatory factor release, and cell apoptosis, suggesting that overexpressing MALAT1 or GSK3β may reverse the protective effects of Propofol against lung I/R injury. MALAT1 was identified to negatively regulate miR-144 to upregulate the GSK3β expression.	34266379
Malat1	LncRNA	Mus musculus	Cardiomyopathies	cardiomyocytes	Regulation(EZH2/miR-22/ABCA1 signaling cascade)	In Vivo Experiment//Northern Blot//Western Blot//Tunel//Flow Cytometry//RIP//Luciferase Report Assay//ChIP	Silencing of MALAT1 was found to attenuate cardiac dysfunction and inhibit cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes. MALAT1 recruited the histone methyltransferase EZH2 to the miR-22 promoter region and inhibited its expression. EZH2 induced an increased in the expression of ATP-binding cassette transporter A1 (ABCA1), which was identified to be a target gene of miR-22. Silencing of EZH2 was found to improve cardiac function and prevent cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes in the presence of MALAT1, suggesting that MALAT1 mediated myocardial damage by recruiting EZH2 to the miR-22 promoter. Taken together, this study's findings provide evidence confirming our hypothesis, suggesting the involvement of MALAT1 in the processes of cardiac function and cardiomyocyte apoptosis via the EZH2/miR-22/ABCA1 signaling cascade, which has potential therapeutic implications for the understanding of diabetic cardiomyopathy.		Yes	Silencing of MALAT1 was found to attenuate cardiac dysfunction and inhibit cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes.	33097254
Malat1	LncRNA	Mus musculus	Acute Lung Injury	 smoke-induced ALI in mice	Regulation( SOCS-1 )	In Vivo Experiment//qRT-PCR//ELISA//Western Blot	 In conclusion, the results pointed out that HA1600 exerted a protective effect against smoke-induced ALI through increasing the MALAT1 level and the subsequent SOCS-1 expression. 		Yes	 Next, we overexpressed MALAT1 in the lungs by intratracheal administration of adenovirus cloned with MALAT1 cDNA and found that the survival of mice after smoke exposure was improved. Moreover, pulmonary overexpression of MALAT1 ameliorated smoke-induced ALI in mice and elevated the level of SOCS-1 in the lungs. 	35807375
Malat1	LncRNA	Mus musculus	Renal Ischemia/Reperfusion Injury	murine hypoxic kidney tissue, hypoxic endothelial cells and tubular epithelial cells	Expression [highly expressed]	In Vivo Experiment	Malat1 was upregulated in kidney biopsies and plasma of patients with AKI, in murine hypoxic kidney tissue as well as in cultured and ex vivo sorted hypoxic endothelial cells and tubular epithelial cells. 		Yes	In vitro, Malat1 inhibition reduced proliferation and the number of endothelial cells in the S-phase of the cell cycle. In vivo, Malat1 knockout and wildtype mice showed similar degrees of outer medullary tubular epithelial injury, proliferation, capillary rarefaction, inflammation and fibrosis, survival and kidney function.	29467431
circUBR5	CircRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(circUBR5/miR-1179/UBR5 axis )	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	 In this study, we detected higher expressions of both circUBR5 and UBR5 in TNBC tissues, which were associated with worse prognosis, and also in a panel of breast cancer cells, particularly in TNBC cells.  Mechanistically, the oncogenic phenotypes of circUBC5 were mediated through sponging miR-1179 and up-regulating UBR5. 	 In this study, we detected higher expressions of both circUBR5 and UBR5 in TNBC tissues, which were associated with worse prognosis, and also in a panel of breast cancer cells, particularly in TNBC cells. 	Yes	 Functionally, circUBR5 was crucial for sustaining the malignant growth and metastasis of TNBC cells both in vitro and in vivo. 	35812044
MALAT1	LncRNA	Rattus norvegicus	Acute Lung Injury	LPS-induced ALI rat model	Interaction(miR-146a)	In Vivo Experiment//qRT-PCR//RIP//Luciferase Report Assay//ELISA	 The results revealed that MALAT1 knockdown played a protective role in the LPS-induced ALI rat model.  This study found that MALAT1 acts as a molecular sponge for miR-146a and MALAT1 negatively regulated miR-146a expression. Mechanistically, MALAT1 overexpression alleviated the inhibitory effect of miR-146a on LPS-induced inflammatory response in MH-S.		Yes	In addition, knockdown of MALAT1 in vitro inhibited LPS-induced inflammatory response in murine alveolar macrophages cell line MH-S and murine alveolar epithelial cell line MLE-12. 	29649906
MALAT1	LncRNA	Rattus norvegicus	Subarachnoid Hemorrhage	mouse primary neurons	Interaction(miR-499-5p/SOX6 axis)	In Vivo Experiment//Western Blot//Transfection//Tunel//qRT-PCR//RIP//MTT//Luciferase Report Assay	MALAT1 was found upregulated in brain tissues of SAH mice and OxyHb-stimulated neurons. In addition, knockdown of MALAT1 attenuated apoptosis and decreased reactive oxygen species (ROS) production in OxyHb-stimulated neurons. Mechanistically, we demonstrated that MALAT1 bound with miR-499-5p. Furthermore, our findings indicated that miR-499-5p bound to SOX6 3' untranslated region (UTR) and negatively regulated SOX6 mRNA and protein levels. Rescue assays suggested that SOX6 overexpression counteracted the effects of MALAT1 knockdown on neurocyte apoptosis, and ROS production in OxyHb-stimulated neurons. The in vivo assays indicated that knockdown of MALAT1 improved brain injury of SAH mice.		Yes	knockdown of MALAT1 attenuated apoptosis and decreased reactive oxygen species (ROS) production in OxyHb-stimulated neurons.Rescue assays suggested that SOX6 overexpression counteracted the effects of MALAT1 knockdown on neurocyte apoptosis, and ROS production in OxyHb-stimulated neurons. The in vivo assays indicated that knockdown of MALAT1 improved brain injury of SAH mice. 	34709490
MALAT1	LncRNA	Rattus norvegicus	Cerebral Small Vessel Diseases	A rat model of diabetes	Interaction(miR-7641/TPR axis )	In Vivo Experiment//qPCR//Bioinformatics Analysis	High blood glucose level induced the increase of lncRNA MALAT1 and regulated the expression of TPR by activating miR-7641 to promote the initiation of apoptosis of microvascular endothelial cells, aggravating the neurological dysfunction caused by CSVD.		Yes	High blood glucose level induced the increase of lncRNA MALAT1 and regulated the expression of TPR by activating miR-7641 to promote the initiation of apoptosis of microvascular endothelial cells, aggravating the neurological dysfunction caused by CSVD.	35071456
LINC02933	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction(RAD54B/PI3K/AKT Axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Our data showed high expression of lncRNA AC012213.3 in breast cancer tissues and cell lines. The high expression of the AC012213.3 was associated with the worse prognosis and clinical features. Besides, in vitro assays demonstrated that downregulation of AC012213.3 suppresses the proliferation and invasion of breast cancer cells. Further analysis showed that RAD54B is a downstream AC012213.3 target gene and was upregulated in breast cancer. 	lncRNA AC012213.3 is upregulated in breast cancer and could enhance breast cancer progression through RAD54B/PI3K/AKT axis.	Yes	Besides, in vitro assays demonstrated that downregulation of AC012213.3 suppresses the proliferation and invasion of breast cancer cells. 	34557038
LINC02925	LncRNA	Homo sapiens	Glioblastoma	GBM tumor 	Interaction(miR-139-5p/NR5A2 axis.)	Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	NR5A2 was upregulated in the three independent GBM tumor cohorts.  Further in vitro experiments revealed that RP3-439F8.1 acts as a competing endogenous RNA (ceRNA) to regulate NR5A2 by sponging the microRNA miR-139-5p. 		Yes	In vitro, NR5A2 overexpression enhanced GBM cell proliferation, colony formation, invasiveness, and G0-G1 cell cycle phase shift via co-activating β-catenin/TCF4 signaling, with no apparent effect upon apoptosis. In contrast, RP3-439F8.1 knockdown produced the opposite effects. RP3-439F8.1 knockdown reduced tumor progression in vivo, increasing overall survival in model mice.	33991848
LINC00294	LncRNA	Homo sapiens	Glioma	GBM tissues and glioma cell lines	interaction[miR-1278]	CCK8//qRT-PCR//EdU Staining//RIP	A new lncRNA, LINC00294, was highly expressed in normal brain tissues. However, it was markedly down-regulated in GBM tissues and glioma cell lines.Collectively, our observations demonstrate the tumor-suppressive function of LINC00294 in glioma development by sponging miR-1278 and promoting NEFM, suggesting a potential use in therapy for glioma.		Yes	Overexpression of LINC00294 abates glioma cell proliferation but induces apoptosis.	32450002
LINC00665	LncRNA	Homo sapiens	lung non-small cell carcinoma	(NSCLC) tissues	Interaction(EZH2 )	IHC//Western Blot//Transfection//qPCR//Flow Cytometry//RIP//migration assay//Cell Proliferation Assay//Colony Formation Assay//EdU Staining//ChIP	Herein, we report that lncRNA linc00665 is significantly upregulated in non-small cell lung cancer (NSCLC) tissues compared with adjacent normal tissues. Further work revealed that linc00665 could recruit enhancer of zeste homolog 2 (EZH2) to the promoter region of cyclin-dependent kinase inhibitor 1C (CDKN1C) to inhibit its transcription and thus carry out its tumorigenic role. 		Yes	 Functional experiments showed that linc00665 enhanced the proliferation and migration of NSCLC cells in vivo and in vitro, and knocking down linc00665 could enhance the drug sensitivity of NSCLC cells to DDP.	33664990
LINC00662	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cell lines and tissue	regulation[miR-497-5p/EglN2 axis]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that LINC00662 was overexpressed in both breast cancer cell lines and tissue compared to normal breast cell lines and healthy breast tissue. Overall, our results demonstrated that overexpression of LINC00662 accelerated the malignant growth of breast cancer cells via sponging miR-497-5p and upregulating EglN2 expression, and indicate that targeting LINC00662 may represent a novel strategy for breast cancer therapy.		Yes	Furthermore, LINC00662 silencing reduced cell viability and inhibited the proliferation, migration and invasion of MDA-MB-157 cells.	32558530
LINC00662	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	plasma exosome of NSCLC patients	Interaction(miR-320d/E2F1 axis)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Significantly, we revealed that the expression of lncRNA LINC00662 was elevated in the plasma exosome of NSCLC patients. Exosomal LINC00662 promoted proliferation, invasion, and migration, and inhibited apoptosis and cell cycle arrest of NSCLC cells. 		Yes	Exosomal LINC00662 contributed to the progression of NSCLC by miR-320d/E2F1 axis in vitro. Remarkably, exosomal LINC00662 enhanced the tumor growth of NSCLC in vivo. 	33589572
LINC00662	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation(EZH2/BIK cell axis)	qRT-PCR//ChIP//RIP//Western Blot	Here, through systematic bioinformatics analysis and screening, we identified a long noncoding RNA LINC00662 with high copy number amplification in NSCLC.  Mechanically, we obtained global expression profile that respond to LINC00662 knockdown through RNA-Seq analysis. And we found that LINC00662 could bind to EZH2 and recruit EZH2 to the promoter regions of BIK, regulating the level of H3K27me3 in the BIK promoter, thus epigenetically repressing BIK expression.	High expression of LINC00662 predicted a poorer survival. 	Yes	The exact sequence full-length of LINC00662 was determined by rapid amplification of cDNA ends (RACE). We also found that LINC00662 could regulate lung cancer cell proliferation both in vitro and in vivo. 	35371316
LINC00662	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	regulation[miR-340-5p,HOXB2]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Upregulation of LINC00662 was found in ESCC and associated with worse clinical outcomes in ESCC patients.LncRNA LINC00662 promotes the progression of ESCC by upregulating HOXB2 by sponging miR-340-5p.		Yes	More importantly, knockdown of LINC00662 restrained cell proliferation, migration and invasion in ESCC.	32633082
LINC00662	LncRNA	Homo sapiens	Lung Neoplasms		regulation[miR-145-5p-PAFAH1B2 axis]	qRT-PCR	The lncRNA linc00662 is overexpressed in lung cancer.We further show that linc00662 binds with miR-145-5p, and that miR-145-5p binds to the 3'UTR of PAFAH1B2. miR-145-5p negatively regulates PAFAH1B2 both at the mRNA and the protein level. 		Yes	We knocked-down the expression of linc00662 using siRNA, and found that silencing linc00662 significantly inhibited the proliferation and colony formation of the lung cancer cell lines A549 and H460. 	33108738
LINC00662	LncRNA	Homo sapiens	Colorectal Neoplasms	colon cancer tissues and cell lines	interaction[CLDN8/IL22,miR-340-5p]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC00662 was up-regulation in colon cancer tissues and cell lines.  LINC00662 overexpression promoted the occurrence and development of colon cancer by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.	Univariate Cox regression analysis showed that the LINC00662 expression level was related to the poor prognosis. 	Yes	LINC00662 overexpression promoted cell proliferation, invasion and migration, and inhibited cell apoptosis in colon cancer.	31900207
LINC00662	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[Wnt/β-catenin signaling]	RNA Pull-Down//Northern Blot//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//ELISA//IHC//Invasion Assay//IF	LINC00662 was found to be upregulated in HCC, and high LINC00662 levels correlated with poor survival of HCC patients.Through inducing WNT3A secretion, LINC00662 activated Wnt/β-catenin signaling in HCC cells in an autocrine manner and further promoted HCC cell proliferation, cell cycle, and tumor cell invasion, while repressing HCC cell apoptosis.	LINC00662 was found to be upregulated in HCC, and high LINC00662 levels correlated with poor survival of HCC patients.	Yes	 Via activating Wnt/β-catenin signaling and M2 macrophages polarization, LINC00662 significantly promoted HCC tumor growth and metastasis in vivo. 	31785055
LINC00662	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cells	regulation[miR- 375/HIF-1α axis ]	qRT-PCR//Luciferase Report Assay//RIP	Results showed that LINC00662 was highly expressed in OC tissues and cells, and patients with increased expression of LINC00662 were associated with shorter overall survival. 	Results showed that LINC00662 was highly expressed in OC tissues and cells, and patients with increased expression of LINC00662 were associated with shorter overall survival. 	Yes	Furthermore, functional assays proved that LINC00662 was essential for OC cell proliferation and glycolysis. 	32476381
LINC00662	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC patients 	Interaction(GRP78/p38 pathway)	qRT-PCR//Western Blot	 LINC00662 overexpression is highly associated with malignant features in OC patients and is a prognostic indicator. Mechanistically, LINC00662 is stabilized by heterogeneous nuclear ribonucleoprotein H1 (HNRNPH1). Moreover, LINC00662 exerts oncogenic effects by interacting with glucose-regulated protein 78 (GRP78) and preventing its ubiquitination in OC cells, leading to activation of the oncogenic p38 MAPK signaling pathway.	 LINC00662 overexpression is highly associated with malignant features in OC patients and is a prognostic indicator. 	Yes	 LINC00662 significantly promotes OC cell proliferation and metastasis in vitro and in vivo.	34148056
LINC00662	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Regulation[Wnt/β-catenin signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//EdU Staining//Transwell Assay	We found that the expression of LINC00662 was significantly increased in OSCC tissues. Furthermore, LINC00662 regulated the Wnt/β-catenin pathway.	We found that the expression of LINC00662 was significantly increased in OSCC tissues, and a higher expression of LINC00662 was detected in larger tumor size, higher stage tumors and with lymph node metastasis. 	Yes	Moreover, overexpression of LINC00662 induced OSCC cell proliferation, increased migration and invasion abilities, and suppressed cell apoptosis. Knockdown of LINC00662 decreased the proliferation, migration, and invasion abilities of OSCC cell, and induced apoptosis. 	30705593
LINC00662	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Interaction(miR-144-3p/EZH2 Axis)	qRT-PCR//Luciferase Report Assay//Transwell Assay	The expression of LINC00662, positively associated with the increased TNM stage and lymph node metastasis of the patients, was up-regulated in OSCC tissues and cells. MiR-144-3p could bind to LINC00662, and the promoting effect of LINC00662 overexpression was counteracted by miR-144-3p mimic. Moreover, EZH2 expression was negatively regulated by miR-144-3p and positively regulated by LINC00662. 	The expression of LINC00662, positively associated with the increased TNM stage and lymph node metastasis of the patients, was up-regulated in OSCC tissues and cells. 	Yes	The overexpression of LINC00662 facilitated the proliferation, migration, and invasion of OSCC cells. The silencing of EZH2 attenuated the promoting effects of overexpression of LINC00662 on cell proliferation, migration, invasion, and epithelial-mesenchymal transition.	34164962
LINC00662	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[ miR-15a-5p/Notch2 axis]	Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 The expression of LINC00662 and Notch2 was found to be upregulated in OS, but the expression of miR-15a-5p was downregulated. The study demonstrated that LINC00662 could be a potential biomarker for OS therapy, and LINC00662 knockdown suppressed the proliferation, migration, and invasion of OS cells by regulating the miR-15a-5p/Notch2 axis.		Yes	The results demonstrated that LINC00662 knockdown attenuated the proliferation, migration, and invasion of OS cells and suppressed tumor growth in mice. 	32848412
LINC00662	LncRNA	Homo sapiens	Osteosarcoma	 OS cells	Interaction(miR-103a-3p/SIK2 axis)	qRT-PCR//RIP//Western Blot	In this study, we found that LINC00662 displayed high expression in OS cells.Subsequently, miR-103a-3p was proven to bind with LINC00662 and overexpression of miR-103a-3p inhibited OS cell proliferation, migration and invasion. Then, SIK2, the downstream of miR-103a-3p, was up-regulated in OS cells and positively regulated by LINC00662. 		Yes	LINC00662 down-regulation negatively affected OS cell malignant behaviors and tumor growth. 	34559955
LINC00662	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-16-5p/ITPR1 Axis)	qRT-PCR//Western Blot	 In the present study, our findings demonstrated the upregulation of LINC00662 expression in OS tissues and cells, and high expression of LINC00662 predicted a poor clinical prognosis of patients' iNOS.Further mechanistical investigations indicated that LINC00662 functioned as a competing endogenous RNA (ceRNA) for sponging microRNA-16-5p (miR-16-5p) to upregulate the expression of IP receptor type 1 (ITPR1) in OS cells. Restoration assays validated the involvement of ITPR1 in LINC00662-mediated regulation of cell functions in OS.	 In the present study, our findings demonstrated the upregulation of LINC00662 expression in OS tissues and cells, and high expression of LINC00662 predicted a poor clinical prognosis of patients' iNOS.	Yes	Through a series of in vivo assays, LINC00662 knockdown suppressed OS cell proliferation, invasion, migration, and stemness property maintenance.	34621314
LINC00662	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	Interaction(miR-30b-3p/ELK1 )	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//IHC//Transwell Assay	 LncRNA LINC00662 and ELK1 were significantly increased, while miR-30b-3p was reduced in osteosarcoma tissues.  LncRNA LINC00662 also appeared to sponge miR-30b-3p in order to affect the expression of ELK1. Simultaneously, there were weak negative correlations between the expression of miR-30b-3p and LINC00662/ELK1 in osteosarcoma tissues. Rescue experiments suggested that ELK1 overexpression and downregulation of miR-30b-3p reversed the suppressive effects of sh-LINC00662 on the cell migration, invasion, and proliferation in osteosarcoma.		Yes	 The results of functional experiments indicated that transfection of small hairpin (sh)-LINC00662 and miR-30b-3p mimics repressed the migration, invasion, and proliferation of osteosarcoma cells. 	35123530
LINC00662	LncRNA	Homo sapiens	Glioma	glioma tissues	regulation[miR-34a-5p/LMAN2L Axis]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Our study was the first to report that LINC00662 acted as a competing endogenous RNA (ceRNA) to regulate glioma progression by targeting miR-34a-5p/LMAN2L axis, providing a new therapeutic target for glioma.	High LINC00662 level predicted poor overall survival of glioma patients.	Yes	Functional studies revealed that suppression of LINC00662 remarkably inhibited cell proliferation, clonogenicity and EMT pathway.	33116598
LINC00662	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines	Interaction[targeting miR-34a]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC00662 was significantly upregulated in PCa tissues and cell lines compared with adjacent normal tissue and a normal prostate epithelial cell line. Also, the results of RT-PCR showed that knockdown of LINC00662 suppressed the expression levels of miR-34a.		Yes	 Furthermore, LINC00662 silencing inhibited the proliferation, migration, and invasion of PC-3 and LNCaP cells, and promoted apoptosis in vitro. 	31114993
LINC00662	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissue and cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	The expression of Linc00662 in the PCa tissue and cell lines was significantly up-regulated compared with that in the adjacent normal prostatic tissue and epithelial cells (P < 0.01), and the high expression of Linc00662 was positively correlated with the tumor stage (P = 0.002), primary tumor size (P = 0.006), lymph node metastasis (P = 0.001) and distant metastasis (P = 0.001). 	The expression of Linc00662 in the PCa tissue and cell lines was significantly up-regulated compared with that in the adjacent normal prostatic tissue and epithelial cells (P < 0.01), and the high expression of Linc00662 was positively correlated with the tumor stage (P = 0.002), primary tumor size (P = 0.006), lymph node metastasis (P = 0.001) and distant metastasis (P = 0.001). 	Yes	Compared with the normal control, the PC-3 and DU145 cells in the Linc00662 interference group showed remarkably decreased proliferation, invasion and migration abilities (P < 0.01), but an increased rate of apoptosis (P < 0.01).	33377712
LINC00663	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Regulation(AKT/mTOR pathway)	Western Blot//Bioinformatics Analysis//Transfection//CCK8//qRT-PCR//EdU Staining//Transwell Assay	LINC00663 expression was higher in both glioma tissues and cell lines than that in the normal brain tissues and human astrocytes. 	High expression of LINC00663 led to the low overall survival rate of patients with glioma. 	Yes	LINC00663 knockdown notably restrained cell proliferation, migration, and invasion abilities by decreasing the activation of AKT and mTOR. 	33830405
LINC00665	LncRNA	Homo sapiens	Melanoma	melanoma cells	Interaction(miR-224-5p/VMA21 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	LINC00665 was abnormally highly expressed in melanoma cells. LINC00665 sponged miR-224-5p to upregulate VMA21. VMA21 knockdown exerted similarly interfering effects on above biological processes in melanoma cells. However, VMA21 overexpression abolished the in vitro and in vivo outcomes of LINC00665 silencing. LINC00665 promotes proliferative and migrating abilities of melanoma cells via targeting miR-224-5p/VMA21 axis.		Yes	Silencing LINC00665 could inhibit the proliferation and migration of melanoma cells.	33247967
LINC00659	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Expression [highly expressed]	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Invasion Assay	LINC00659 expression was significantly upregulated in GC tissues and cell lines.	Increased levels of LINC00659 were associated with advanced tumor stage and unfavorable prognosis of patients with GC. 	Yes	Additionally, upregulated LINC00659 expression promoted the migration and invasion of GC cells	34084224
LINC00667	LncRNA	Homo sapiens	Breast Neoplasms	 BC cell and patients	Interaction(m6A/KIAA1429 positive feedback loop)	Western Blot//Migration Assay//RIP//qRT-PCR//Luciferase Report Assay//Cell Viability Assay	 In the current study, we found that LINC00667 was m6A-modified lncRNA, which was up-regulated upon the overexpression of KIAA1429. Mechanistic assays illustrated that KIAA1429 targeted the m6A modification site of LINC00667 and enhanced its mRNA stability. Moreover, LINC00667 positively regulated the KIAA1429 via sponging miR-556-5p, forming a KIAA1429/m6A/LINC00667/miR-556-5p feedback loop.	 The high expression of LINC00667 was correlated with the prognosis of BC patients. 	Yes	 Bio-functional assays indicated that LINC00667 promoted the proliferation and migration of BC cells. 	36700472
LINC00667	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		regulation[stabilizing VEGFA by EIF4A3]	qRT-PCR	Our study was the first to illustrate that LINC00667 was upregulated in NSCLC and LINC00667 silence refrained the proliferation, migration, and angiogenesis of NSCLC cells in vitro.  Eventually, rescue assays implied that LINC00667 modulated NSCLC progression via EIF4A3-stabilized VEGFA.		Yes	Our study was the first to illustrate that LINC00667 was upregulated in NSCLC and LINC00667 silence refrained the proliferation, migration, and angiogenesis of NSCLC cells in vitro. 	32281700
LINC00667	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miRNA-130a-3p/AR signal pathway)	Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	We found that the expression of LINC00667 was upregulated in HCC tissues and cell lines. This inhibitory effect could be counteracted by miR-130a-3p inhibitor. LINC00667 reduced the inhibition of AR expression by miR-130a-3p, which correlated with the progression of HCC. Our finding suggests LINC00667 is a molecular sponge in the miR-130s-3p/AR signal pathway in the progression of HCC, in which it relieves the repressive function of miR-130a-3p on the AR expression. 	Upregulation of LINC00667 was significantly associated with the unfavorable prognosis of HCC in our study patients. 	Yes	On the other hand, low expression of LINC00667 significantly inhibited the cell proliferation, cell migration and cell invasion of HCC in vitro and tumor growth in vivo. 	34907204
LINC00667	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC cells	Interaction(miR-200b-3p/SLC2A3 Axis)	Flow Cytometry//qRT-PCR//Western Blot	In this work, we found that LINC00667 expression was up-regulated in EC cell lines, and LINC00667 knockdown inhibited cell proliferation, migration, and invasion in EC cells. In addition, it showed that LINC00667 functioned as competitive endogenous RNA for miR-200b-3p by the DIANA-LncBase database.  Moreover, we used targetscan online software to predict SLC2A3 as a target gene of miR-200b-3p. Subsequently, rescue experiments confirmed that knocking out SLC2A3 could reverse the inhibitory effect of miR-200b-3p on EC cells transfected with sh-LINC00667.		Yes	In this work, we found that LINC00667 expression was up-regulated in EC cell lines, and LINC00667 knockdown inhibited cell proliferation, migration, and invasion in EC cells. 	34313922
LINC00667	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	regulation[YY1/LINC00667/miR-200c-3p/PDK1 axis ]	qRT-PCR//Luciferase Report Assay//RIP//ChIP	Our data indicated that LINC00667 was highly expressed in CCA tissues and cells, and transcription factor Yin Yang 1 (YY1) induced LINC00667 expression in CCA cells.Targeting the YY1/LINC00667/miR-200c-3p/PDK1 axis may provide a new therapeutic strategy for CCA treatment.	Up-regulated LINC00667 was significantly associated with lymph node metastasis, advanced TNM stage, and poor prognosis. 	Yes	 Knockdown of LINC00667 suppressed the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of CCA cells, while overexpression of LINC00667 acquired opposite effects.	33040228
LINC00665	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissue	Regulation[miR-149-3p/RNF2 axis]	qRT-PCR//Luciferase Report Assay	 In the present study, we found that LINC00665 expression was significantly elevated in GC tissues and cell lines.	 High LINC00665 expression was associated with TNM stage, histological grade, and poor prognosis of GC patients. 	Yes	 Function assays showed that LINC00665 suppression significantly reduced GC cells viability and invasion ability in vitro. 	31695413
LINC00665	LncRNA	Homo sapiens	Breast Neoplasms	 BCa tissues and cell lines	regulation[triggering EMT]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	 LINC00665 was highly expressed in BCa tissues and cell lines, and the high expression of LINC00665 could be used to predict a poor prognosis of BCa patients. In addition, LINC00665 may promote the malignant metastasis of BCa cells by affecting the EMT process.	 LINC00665 was highly expressed in BCa tissues and cell lines, and the high expression of LINC00665 could be used to predict a poor prognosis of BCa patients. 	Yes	In addition, the results of in vitro cell experiments showed that the migration and invasion ability of BCa cells were remarkably attenuated after downregulation of LINC00665. 	32271427
LINC00665	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC lung tissues and cells	regulation[miR-138-5p/E2F3 signaling pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	As a result, LINC00665 expression was upregulated in NSCLC lung tissues and cells.  In conclusion, dysregulation of LINC00665 plays a vital role in NSCLC progression, indicating that its downregulation may confer decreased cell proliferation and invasion via the miR-138-5p/E2F3 signaling pathway.		Yes	Downregulated LINC00665 could arrest A549 and H1299 cell proliferation and invasion in vitro, and this finding was recapitulated in vivo.	32403047
LINC00665	LncRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer cell lines	Interaction(miR-181a-5p/FHDC)	qRT-PCR//Luciferase Report Assay//Transwell Assay//Western Blot	We found that LINC00665 was upregulated in ovarian cancer cell lines. LINC00665 downregulated the miR-181a-5p in SKOV-3 and OVCAR-3 cells. The knockdown of miR-181a-5p evidently reverses the inhibitory effect of sh-LINC00662. Besides, FH2 domain containing 1 (FHDC1) has been proved to deed as an effective target of miR-181a-5p. 		Yes	Besides, a series of assays including flow cytometry, wound-healing, transwell, cell counting Kit-8 (CCK-8), and EdU assay confirmed that the knockdown of LINC00665 could reduce the viability, proliferation, and migration of SKOV-3 and OVCAR-3 cells. 	35524876
LINC00665	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-708 and miR-142-5p/RAP1B )	qRT-PCR//RIP//FISH	In this study, we found that LINC00665 was highly expressed in OS tissues and cell lines, and its high expression was associated with malignant feature and poor prognosis of OS.Mechanistically, LINC00665 served as a sponge for miR-708 and miR-142-5p and positively mediated the expression of their target RAP1B. Finally, we confirmed that LINC00665 exercised its biological functions by mediating RAP1B. 		Yes	In OS cells, LINC00665 could facilitate the proliferation, migration, and invasion to play an oncogenic role. 	34306997
LINC00665	LncRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(LINC00665/miR-1249-5p/WNT2B/Wnt)	qRT-PCR//Luciferase Report Assay	 LINC00665 was significantly up-regulated in OS cells. Mechanically, LINC00665 acted as a competing endogenous RNA (ceRNA) to sponge miR-1249-5p and thereby modulated Wnt family member 2B (WNT2B) to activate Wnt pathway. Wnt pathway activated LINC00665 expression transcriptionally.		Yes	LINC00665 silence facilitated OS cell proliferation, migration, invasion, and EMT while inhibiting cell apoptosis. 	36387061
LINC00665	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	HeLa cells	Activation(WNT-CTNNB1/β‑catenin signaling pathway)	In Vivo Experiment//Western Blot//qRT-PCR//IF//RNA-seq//Cell Proliferation Assay//Transwell Assay	The results showed that silencing LINC00665 reduced cell viability of Hela cells, up-regulated protein expression level of E-cadherin, down-regulated protein expression levels of N-cadherin, Vimentin and CTNNB1, and inhibited cell migration and invasion of HeLa cells. Bioinformatics analysis results showed that LINC00665 might promote EMT by activating WNT-CTNNB1/β‑catenin signaling pathway. 		Yes	The results showed that silencing LINC00665 reduced cell viability of Hela cells, up-regulated protein expression level of E-cadherin, down-regulated protein expression levels of N-cadherin, Vimentin and CTNNB1, and inhibited cell migration and invasion of HeLa cells. 	33903885
LINC00665	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR‑34a‑5p/AGTR1)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Microarray//Cell Proliferation Assay//IHC//Invasion Assay	High expression of LINC00665 was marked in glioma tissues and cells, which correlated with an unsatisfactory prognosis. LINC00665 acted as a competing endogenous RNA by sponging miR‑34a‑5p to upregulate angiotensin II receptor type 1 (AGTR1). LINC00665 promoted the progression of glioma by acting as a competitive endogenous RNA to competitively bind to miR‑34a‑5p and mediate AGTR1 expression.	High expression of LINC00665 was marked in glioma tissues and cells, which correlated with an unsatisfactory prognosis. 	Yes	Upregulation of LINC00665 significantly promoted the proliferation and invasion of glioma cells. 	33650673
LINC00665	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-129-5p/HMGB1 )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	INC00665 expression was markedly increased in glioma. Mechanistically, LINC00665 could decoy miR-129-5p, and indirectly increased HMGB1 expression.	High LINC00665 expression in glioma was closely linked to larger tumor diameter, higher pathologic grade, heterogeneous MRI signal of the tumor, increased peritumoral edema, and stronger MRI enhancement characteristics.	Yes	LINC00665 overexpression facilitated the malignant behavior of glioma cells, while LINC00665 knockdown played the reverse role. 	35702084
LINC00665	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Regulation[ AKR1B10-ERK signaling]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Herein, we reported the identification of a novel lncRNA, linc00665 (ENST00000590622), which was markedly upregulated in lung adenocarcinoma (LUAD) tissues and might serve as an independent predictor for poor prognosis.Mechanistically, transcription factor SP1 induced the transcription of linc00665 in LUAD cells, which exerted its oncogenic role by functioning as competing endogenous RNA (ceRNA) for miR-98 and subsequently activating downstream AKR1B10-ERK signaling pathway. Together, our study elucidates oncogenic roles of linc00665-miR98-AKR1B10 axis in LUAD tumorigenesis, which may serve as potential diagnostic biomarkers and therapeutic targets.		Yes	 Functional assays indicated that linc00665 reinforced LUAD cell proliferation and metastasis in vitro and in vivo.	30692511
LINC00665	LncRNA	Homo sapiens	Adenocarcinoma of Lung	Eighty-four cases of clinical human LUAD tissue samples and the adjacent paired normal lung tissues 	Interaction(miR-181c-5p/ZIC2 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results showed that LINC00665, HOXA1, ZIC2, and HOXA11 levels were increased in LUAD tissues, while miR-181c-5p level was decreased when compared to the adjacent normal tissues.  In summary, the present study reveals that silencing of LINC00665 suppresses LUAD progression through targeting miR-181c-5p/ZIC2 axis.	High expression levels of LINC00665, ZIC2, HOXA1 and HOXA11, and low expression of miR-181c-5p were closely linked to poor prognosis of LUAD patients.	Yes	Knockdown of LINC00665 induced obvious inhibitions in cell viability, clone formation, invasion and tumorigenesis in LUAD cells, whereas miR-181c-5p downregulation significantly neutralized these effects. 	34232917
LINC00665	LncRNA	Homo sapiens	Adenocarcinoma of Lung	clinical samples and cell lines	Interaction( miR-195-5p/MYCBP axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay//EdU Staining	Based on pan-cancer screening analyses, we identified that the noncoding RNA LINC00665 was up-regulated in lung adenocarcinoma, which was subsequently confirmed in clinical samples and cell lines. The results of bioinformatics prediction and RNA pull-down assay indicated that LINC00665 directly interacted with miR-195-5p. This was also confirmed by fluorescence colocalization. Furthermore, luciferase reporter assay demonstrated that Myc binding protein (MYCBP, also called AMY-1), which enhanced c-Myc transcriptional activity, was the target gene of LINC00665 dependent on miR-195-5p.	Higher expression of LINC00665 was positively associated with poor prognosis and advanced T stage. 	Yes	Next, using gain- and loss- of function approaches, we revealed that LINC00665 promotes cell proliferation, cell migration, invasion, and suppresses cell apoptosis in LUAD through in vitro and in vivo experiments. 	34277412
LINC00665	LncRNA	Homo sapiens	Prostatic Neoplasms	 PC samples	regulation[ miR-1224-5p/SND1 Axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC00665 expression was increased in PC samples in contrast to control tissues, according to bioinformatics analysis and qRT-PCR validation.  LINC00665 is a novel oncogenic gene in PC by targeting miR-1224-5p/SND1 pathway and may be a therapeutic target.	LINC00665 high expression was related to a poor prognosis. 	Yes	 LINC00665 knockdown markedly attenuated growth and metastasis of PC cells and impaired tumor propagation in vivo. 	32273723
LINC00659	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	regulation[promoting the expression of SUZ12]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	As a result, LINC00659 expression was increased in gastric cancer tissues, which was closely associated with tumour stage and lymph node metastasis, but was not correlated with age, gender and tissue differentiation. Additionally, LINC00659 could regulate cell cycle and invasion of gastric cancer by promoting the expression of SUZ12.	As a result, LINC00659 expression was increased in gastric cancer tissues, which was closely associated with tumour stage and lymph node metastasis, but was not correlated with age, gender and tissue differentiation.Survival curve analysis showed that patients with low expression of LINC00659 harboured higher overall survival. 	Yes	 In vitro, the level of LINC00659 was increased in gastric cancer cells. Afterwards, the expression of LINC00659 was down-regulated in SGC-7901 and BGC-823 cells by plasmid-mediated si-LINC00659 transfection. Consequently, the cell invasion ability was weakened, the cell cycle was inhibited, and cell viability was also suppressed.	33145980
LINC00659	LncRNA	Homo sapiens	Stomach Neoplasms	GC specimens and cells 	Interaction(miR-370/AQP3 Axis)	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	We firstly demonstrated that LINC00659 levels were distinctly up-regulated in both GC specimens and cells using bioinformatics analysis and RT-PCR.  The results of ChIP assays and luciferase reporter assays confirmed that upregulation of LINC00659 was activated by SP1 in GC. Mechanistic investigation indicated that LINC00659 served as a competing endogenous RNA (ceRNA) for miR-370, thereby resulting in the upregulation of leading to the depression of its endogenous target gene AQP3. 	Clinical assays revealed that higher levels of LINC00659 were associated with TNM stage, lymphatic metastasis, and poorer prognosis. 	Yes	Lost-of-function assays indicated that knockdown of LINC00659 suppressed the proliferation, metastasis, and EMT progress of GC cells in vitro. 	35957833
LINC00525	LncRNA	Homo sapiens	spinal chordoma	spinal chordoma tissues	interaction[ targeted miR-31-5p and miR-125a-5p]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 After LINC00525 was downregulated in spinal chordoma cells, there were inhibitory effects on cell proliferation, migration, invasion and EMT but a promoting effect on cell apoptosis.All these results suggested that LINC00525 targeted miR-31-5p and miR-125a-5p to promote the tumorigenesis and progression of spinal chordoma. 		Yes	Tumorigenesis of spinal chordoma in vivo was also inhibited by knockdown of LINC00525 via the promotion of miR-31-5p and miR-125a-5p.	33370717
LINC00623	LncRNA	Homo sapiens	Pancreatic Neoplasms	PDAC cells	Interaction(LINC00623/NAT10 signaling axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//FISH//RIP//RNA-seq//IP//IHC//IF	 A novel lncRNA, LINC00623, was identified, and its diagnostic value was confirmed, as it could discriminate patients with PDAC from patients with benign pancreatic neoplasms and healthy individuals. Mechanistically, LINC00623 bound to N-acetyltransferase 10 (NAT10) and blocked its ubiquitination-dependent degradation by recruiting the deubiquitinase USP39. As a key regulator of N4-acetylcytidine (ac4C) modification of mRNA, NAT10 was demonstrated to maintain the stability of oncogenic mRNAs and promote their translation efficiency through ac4C modification.		Yes	 Moreover, LINC00623 was shown to promote the tumorigenicity and migratory capacity of PDAC cells in vitro and in vivo.	35978332
LINC00612	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	Interaction[sponging miR-590 to upregulate PHF14]	RNA Pull-Down//Western Blot//qRT-PCR//FISH//Luciferase Report Assay	LINC00612 was upregulated in BC tissues and cell lines.Our results indicate that LINC00612 enhances the proliferation and invasion ability of BC cells by sponging miR-590 to upregulate PHF14 expression and promote BC cellular EMT, suggesting that LINC00612 may act as a potential biomarker and therapeutic target for BC.		Yes	Functionally, downregulation of LINC00612 inhibited cell proliferation and invasion in vitro and in vivo, whereas overexpression of LINC00612 resulted in the opposite effects. 	30940184
LINC00612	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	interaction[miR-214-5p]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 LINC00612 was found to be significantly upregulated in osteosarcoma cells and metastatic osteosarcoma. Our study shows that LINC00612 plays an important role in regulating the proliferation and invasion of osteosarcoma by endogenously competing with miR-214-5p and mediating EMT.		Yes	 LINC00612 overexpression promoted the proliferation, invasion and in vivo explant growth of osteosarcoma.	32311343
LINC00607	LncRNA	Homo sapiens	Osteosarcoma	cell lines	interaction[ miR-607,E2F6 ]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//CCK8//FISH//Luciferase Report Assay//Colony Formation Assay	Based on the RNA-sequencing results, LINC00607 expression was significantly upregulated in pulmonary metastasis within OS. This work revealed that LINC00607 worked as an miR-607 sponge to upregulate E2F6 expression, which promoted tumor proliferation in OS.		Yes	Functional experiments revealed that LINC00607 promoted migration and invasion of endothelial cells to exacerbate epithelial-mesenchymal transition (EMT). Finally, we found that LINC00607 promoted OS progression in vivo. 	33585204
LINC00607	LncRNA	Homo sapiens	Thyroid Neoplasms	TC cell lines and tissues	Interaction(CASP9)	Western Blot//Flow Cytometry//FISH//RIP//qRT-PCR//Colony Formation Assay	LINC00607 expression was up-regulated in the doxorubicin-resistant TC cell lines and tissues and negatively correlated to the poor prognosis of TC patients. Notably, it was also revealed that LINC00607 down-regulated the CASP9 expression by promoting CASP9 promoter methylation. 	LINC00607 expression was up-regulated in the doxorubicin-resistant TC cell lines and tissues and negatively correlated to the poor prognosis of TC patients. 	Yes	Knockdown of LINC00607 suppressed doxorubicin resistance, proliferation and colony formation, and promoted cell apoptosis of TC cells in vitro, as well as suppressed tumour growth in vivo, whereas LINC00607 overexpression was observed to exercise the opposite effects. 	34232553
LINC00589	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	Interaction(hnRNPA1/ PKM to PKM2)	H&E Staining	We revealed that LINC00589 was downregulated in GC tissues and suppressed the metastatic ability of GC cells.  Mechanistically, LINC00589 exerted tumor suppressive function by promoting hnRNPA1 protein ubiquitination and proteasomal degradation, thus blocking alternative splicing of PKM to PKM2.		Yes	 Furthermore, LINC00589 delivered by PMSNs could suppress the peritoneal metastasis of GC in vivo and in vitro. 	36126899
LINC00589	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Regulation[miR-214-3p/FOXP2 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	TSLNC8 is significantly increased in breast cancer tissues and cell lines. Further analysis indicated that TSLNC8 could directly bind to miR-214-3p. Up-regulation of miR-214-3p may attenuate the suppressive role of TSLNC8 on the proliferation capacity of breast cancer cells. Moreover, miR-214-3p was found to directly interact with the 3'-untranslated region (UTR) of Forkhead box P2 (FOXP2) in luciferase assays, suggesting that FOXP2 may be one of the downstream targets of miR-412-3p.		Yes	TSLNC8 is significantly increased in breast cancer tissues and cell lines. 	31646574
LINC00589	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 cell lines	Regulation[IL-6/STAT3/HIF-1alpha signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//IF//Transwell Assay	The results revealed that TSLNC8 was significantly downregulated in lung cancer cells compared to normal bronchial epithelial cells.lncRNA TSLNC8 remarkably inhibited the proliferation and migration and accelerated apoptosis of lung cancer cells by targeting the IL-6/STAT3/HIF-1alpha signaling pathway. TSLNC8 may be a potential therapeutic target for the diagnosis and treatment of NSCLC.		Yes	Further experiments showed that overexpression of TSLNC8 in A549 cells significantly inhibited proliferation in a time-dependent manner and promoted cell apoptosis. We found that TSLNC8 overexpression suppressed cell migration and invasion	31601776
LINC00589	LncRNA	Homo sapiens	Glioma	glioma tissues,cells	Expression[lower expressed]	qRT-PCR//Wound Healing Assay//MTT//Transwell Assay	It was initially reported that the relative transcript levels of TSLNC8 were significantly decreased in human glioma tissues and cultured glioma cells, as evidenced by RT?qPCR.	Among clinical variables, the expression of TSLNC8 was negatively associated with tumor size, distant metastasis, and tumor, node and metastasis stage.	Yes	Furthermore, cell apoptotic rate was upregulated in TSLNC8 plasmid?treated U251 and SWO38 cells, and inhibited by siRNA against TSLNC8 in SHG?44 and BT325 cells by cell apoptotic assay. 	30387847
LINC00589	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	regulation[CTNNB1,HuR]	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our results showed a significant increase of TSLNC8 expression in PC tissues and cell lines.Taken together, our present study revealed that oncogenic lncRNA TSLNC8 positively regulate PC growth and metastasis via HuR-mediated mRNA stability of CTNNB1, extending the understanding of PC pathogenesis regulated by lncRNAs.	Upregulation of TSLNC8 expression in PC tissues was closely correlated with TNM stage, distant and lymph node metastasis, and poor prognosis of PC patients.	Yes	Functional experiments demonstrated that TSLNC8 promoted PC cells proliferation and invasion in vitro, and enhanced PC growth and metastasis in vivo. 	32951177
LINC00588	LncRNA	Homo sapiens	Osteosarcoma		regulation[LINC00588/miRNA-1072/TP53 axis]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	Using information from GEO Datasets, we found that the lncRNA LINC00588 was downregulated in osteosarcoma (OS) in bone but was upregulated in the metastatic tumor present in the lung. Hence, we believe that the LINC00588/miRNA-1072/TP53 axis could potentially serve as a therapeutic target or diagnostic biomarker for osteosarcoma.		Yes	Overexpression of LINC00588 appeared to inhibit cell proliferation, viability, migration, invasion, endothelial cell function, EMT, and tumor growth but not apoptosis, while we got the opposite result when we knocked down LINC00588. 	32265694
LINC00578	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and serums	Expression[highly expressed]	qRT-PCR//MTT	The results showed that LINC00346, LINC00578, and LINC00673 were highly expressed, whereas LINC00671, LINC00261, and SNHG9 were lowly expressed in PC tissues and serums, and their expression levels were correlated with clinical stages. 	Survival analysis indicated that patients with high expression of LINC00346, LINC00578, or LINC00673 had significantly lower survival rate, while patients with high expression of LINC00671, LINC00261, and SNHG10 had significantly higher survival rate.	Yes	In addition, we also found that silence of LINC00346, LINC00578 and LINC00673 inhibited PC cell proliferation, and silence of LINC00671, LINC00261, and SNHG10 promoted PC cell proliferation.	30210701
LINC00551	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCC tissues	regulation[HSP27 phosphorylation]	qRT-PCR	 Three paired ESCC and normal tissues were subjected to next-generation sequencing and we identified 82 upregulated and 60 downregulated lncRNAs, including LINC00551, which was confirmed to markedly downregulated in 78 ESCC tissues and in the Gene Expression Profiling Interactive Analysis data set. RNA pull-down and mass spectrometry assays identified the potential LINC00551 binding proteins, and HSP27 was a promising LINC00551 targeting proteins after RNA immunoprecipitation assay. At the protein level, LINC00551 bound to and decreased HSP27 phosphorylation, and in turn, downregulated ESCC cell proliferation and invasion.	Downregulated LINC00551 expression was associated with lymph node metastasis, advanced TNM stage, and tumor size. Moreover, downregulated LINC00551 expression was also associated with poor progression-free survival and overall survival of ESCC patients. 	Yes	 In vitro and in vivo, LINC00551 overexpression inhibited ESCC cell proliferation and invasion, whereas knockdown of LINC00551 expression promoted ESCC cell proliferation and invasion. 	32677057
LINC00536	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Regulation[Wnt3a/β-Catenin signaling]	Western Blot//CCK8//qRT-PCR//IHC//EdU Staining//Transwell Assay	In the present study, we found LINC00536 expression was highly expressed in BC tissues compared with controls and negatively associated with survival rate in BC patients. In summary, our findings demonstrated that LINC00536 promoted BC progression by modulating the Wnt3a/β-Catenin signaling.	In the present study, we found LINC00536 expression was highly expressed in BC tissues compared with controls and negatively associated with survival rate in BC patients. 	Yes	Gain-of-function assays indicated that LINC00536 overexpression promoted the proliferation, migration and invasion, whereas LINC00536 knockdown attenuated the cell phenotypes above in BC cell lines. In vivo assay illustrated that LINC00536 knockdown inhibited BC growth in vivo. 	30851243
LINC00526	LncRNA	Homo sapiens	Glioma	glioma tissues 	Interaction[AXL]	RNA Pull-Down//ChIP//Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	In this study, we identified a novel lncRNA LINC00526, which is significantly low expressed in glioma. Low expression of LINC00526 is correlated with aggravation and poor survival in glioma.Mechanistically, we found that LINC00526 directly interacts with EZH2, represses the binding of EZH2 to AXL promoter, attenuates the transcriptional activating roles of EZH2 on AXL, and therefore represses AXL expression. Via repressing AXL, LINC00526 further represses PI3K/Akt/NF-κB signalling. Intriguingly, we identified that NFKB1 and NFKB2 directly binds LINC00526 promoter and represses LINC00526 transcription. We further found that via activating NF-κB signalling, AXL represses LINC00526 transcription. Therefore, LINC00526/EZH2/AXL/PI3K/Akt/NF-κB form a feedback loop in glioma.	In this study, we identified a novel lncRNA LINC00526, which is significantly low expressed in glioma. Low expression of LINC00526 is correlated with aggravation and poor survival in glioma.	Yes	Functional assays revealed that ectopic expression of LINC00526 inhibits glioma cell proliferation, migration, and invasion. LINC00526 silencing promotes glioma cell proliferation, migration and invasion. 	31240814
LINC00526	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-5581-3p/BEX1)	In Vivo Experiment//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	LINC00526 was found to be decreased in glioma tissues and cell lines compared with their normal counterparts. Mechanism analyses showed LINC00526 functions as a sponge for microRNA-5581-3p (miR-5581-3p) to regulate brain-expressed X-linked 1 (BEX1) expression and, in the end, affects glioma progression. Collectively, our study indicated LINC00526 serves as a tumor-suppressive lncRNA and directly regulates miR-5581-3p/BEX1 axis in glioma.		Yes	 Silencing the expression of LINC00526 promotes, while forcing its expression, inhibits glioma cell growth and invasion. 	33613672
LINC00525	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	Interaction(miR-338-3p / UBE2Q1 / β-catenin axis)	qRT-PCR//FISH//Western Blot	It was found that LINC00525 was up-regulated, and promoted cell proliferation in colorectal cancer in vitro and in vivo. In colorectal cancer cells, hypoxia increasedLINC00525 expression, whereas knocking down LINC00525 reduced hypoxia-enhanced glycolysis. For specific molecular mechanisms, it was found that LINC00525 promoted UBE2Q1 expression by binding miR-338-3p, and UBE2Q1-stabilized β-catenin enhances hypoxia-enhanced glycolysis by activating HIF-1α.		Yes	It was found that LINC00525 was up-regulated, and promoted cell proliferation in colorectal cancer in vitro and in vivo. 	35156520
LINC00619	LncRNA	Homo sapiens	Osteosarcoma	 Osteosarcoma tissues 	Regulation(HGF-mediated PI3K-Akt signalling pathway)	qRT-PCR//Transwell Assay	 Osteosarcoma tissues presented with elevated positive expression rate of HGF, up-regulated expression levels of PCNA, HGF, PI3K, Akt, Bcl-2, ALP and OPN, and down-regulated expressions of Bax and LINC00619.HGF was verified as a target gene of lncRNA LINC00619. LINC00619 was found to down-regulate the expressions of PCNA, HGF, PI3K, Akt, Bcl-2, ALP, and OPN in osteosarcoma cells. 		Yes	Up-regulation of lncRNA LINC00619 decreased cell growth, migration intensity, and invasion ability, but enhanced the apoptosis rate of osteosarcoma cells.	33797312
LINC00624	LncRNA	Homo sapiens	Liver Neoplasms	cell lines	Regulation(HDAC6-TRIM28-ZNF354C)	Bioinformatics Analysis	Mechanistically, higher levels of LINC00624 strengthen the interaction between histone deacetylase 6 (HDAC6) and tripartite motif containing 28 (TRIM28), which accelerates HDAC6 ubiquitination and degradation. Moreover, LINC00624 binds to the RBCC domain of TRIM28, inhibits trimer formation, and weakens the interaction between TRIM28 and zinc finger protein 354C (ZNF354C). 		Yes	Overexpression of LINC00624 enhances tumor growth and metastasis in vitro and in vivo. 	32869873
LINC00659	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(miR-342-3p/ANXA2 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of LINC00659 in CAF-derived exosomes was significantly increased, and fibroblasts could transfer exosomal LINC00659 to CRC cells. Mechanistically, LINC00659 interacts directly with miR-342-3p to increase ANXA2 expression in CRC cells.		Yes	We further revealed that transfection of miR-342-3p mimic or sh-ANXA2 could obviously reverse the promotion effect of exosomal LINC00659 on CRC progression. Functional studies reveal that LINC00659 is transferred from CAFs to the cancer cells via exosomes, where it promotes CRC cell proliferation, invasion, migration and EMT progression in vitro. 	33407563
LINC00628	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Regulation[PI3K/Akt signaling pathway]	Flow Cytometry//qRT-PCR//Western Blot	LINC00628 expression was significantly decreased in osteosarcoma tissues compared with adjacent tissues. LINC00628 expression was decreased in osteosarcoma. The overexpression of LINC00628 inhibited the proliferation, invasion and migration and promoted cell apoptosis in osteosarcoma cells through the inactivation of PI3K/Akt signaling pathway. 	Meanwhile, osteosarcoma tissues with metastasis were significantly associated with a low expression level of LINC00628 and the low expression level of LINC00628 has a lower overall survival rate. 	Yes	 LINC00628 expression was increased in osteosarcoma cell lines after transfection with lncRNA-LINC00628 and the cell proliferation, invasion and migration in osteosarcoma cells after transfection with lncRNA-LINC00628 were significantly inhibited. 	30280767
LINC00657	LncRNA	Mus musculus	Chronic Constriction Injury	spinal cord tissues	Regulation[miR-136/ZEB1 axis]	qRT-PCR//Luciferase Report Assay//Western Blot	A chronic constriction injury (CCI) rat model was established, and we found that LINC00657 was greatly increased in CCI rats associated with a decrease of miR-136. In conclusion, it was implied that LINC00657 can induce the neuropathic pain development via regulating miR-136/ZEB1 axis.		Yes	Inhibition of LINC00657 suppressed neuropathic pain via alleviating mechanical and thermal hyperalgesia.	30203524
LINC00649	LncRNA	Homo sapiens	Stomach Neoplasms	 54 paired cancerous and non-cancerous tissues	Interaction(miR-16-5p/YES-associated protein 1 (YAP1)/Hippo pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay	 we found that LINC00649 tended to be enriched in cancerous tissues and cells but not in their normal counterparts,Finally, we proved that LINC00649 exerted its tumor-promoting effects in GC by regulating the miR-16-5p/YES-associated protein 1 (YAP1)/Hippo pathway. 		Yes	Next, by performing the gain- and loss-of-function experiments, we expectedly found that LINC00649 acted as an oncogene to accelerate GC cell proliferation, migration and epithelial-mesenchymal transition (EMT) in vitro and promote its tumorigenesis in vivo	33975517
LINC00649	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC clinical samples and cells	Interaction(NF90/NF45 complex)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	LINC00649 increased hypoxia-inducible factor 1α (HIF-1α) mRNA stability and protein expression by interacting with the nuclear factor 90 (NF90)/NF45 complex.  We demonstrated that LINC00649 interacts with the NF90/NF45 complex to increase the mRNA stability of HIF-1α and up-regulate HIF-1α expression, thereby inducing the proliferation, invasion, and migration of TNBC cells as well as tumor growth and metastasis.	LINC00649 was found to be a key molecule involved in the occurrence and development of TNBC by screening of public databases and detection of TNBC clinical samples.	Yes	 In vitro, interference with LINC00649 inhibits MDA-MB-231 and BT549 cell proliferation, migration, and invasion, and the addition of HIF-1α revised this effect. In vivo experiments showed that LINC00649 promoted the growth and metastasis of TNBC. 	35188449
LINC00649	LncRNA	Homo sapiens	lung squamous cell carcinoma	LUSC cells	Interaction(E2F7/LINC00649/TAF15/MAPK6/MAPK signaling pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 As a result, LINC00649 was discovered to be with high expression in LUSC cells. Results of mechanism assays validated that E2F transcription factor 7 (E2F7) was a transcription activator of LINC00649 and induced its up-regulation in LUSC cells. Furthermore, LINC00649 recruited TAF15, which is TATA-box binding protein associated factor 15 to stabilize mitogen-activated protein kinase 6 (MAPK6) expression and activate the transcription of MAPK6, thereby enhancing MAPK6 expression to activate the MAPK signaling pathway.  In summary, our research determined the E2F7/LINC00649/TAF15/MAPK6/MAPK signaling pathway in regulating LUSC development, which made LINC00649 a potential biomarker for LUSC treatment.		Yes	Moreover, it was confirmed through functional assays that the knockdown of LINC00649 hindered the occurrence and progression of LUSC.	35228660
LINC00645	LncRNA	Homo sapiens	Glioma	GBM tissues and cell lines	Regulation[linc00645/miR-205-3p/ZEB1 signaling axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay//IF	In the present study, linc00645 expression was significantly upregulated in GBM tissues and cell lines. Furthermore, linc00645 directly interacted with miR-205-3p and upregulated of miR-205-3p impeded efficiently the increase of ZEB1 induced by linc00645 overexpression. Moreover, knockdown of linc00645 significantly suppressed the progression of glioma cells in vivo. miR-205-3p was a target of linc00645 and linc00645 modulates TGF-β-induced glioma cell migration and invasion via miR-205-3p. Taken together, our findings identified the linc00645/miR-205-3p/ZEB1 signaling axis as a key player in EMT of glioma cells triggered by TGF-β. These data elucidated that linc00645 plays an oncogenic role in glioma and it may serve as a prognostic biomarker and a potential therapeutic target for the treatment of glioma in humans.	High level of linc00645 was associated with poor overall survival in GBM patients.	Yes	 Knockdown of linc00645 suppressed the proliferation, stemness, migration, invasion, and reversed transforming growth factor (TGF)-β-induced motility of glioma cell lines.	31558707
LINC00641	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues	Interaction[sponging miR-194-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 This study shows that LINC00641 expression level was decreased in BC tissues.  In conclusion, LINC00641 inhibits BC cell proliferation, migration, as well as invasion by sponging miR-194-5p.	 LINC00641 expression level was negatively related to tumor size, lymph-node metastasis, as well as clinical stage. 	Yes	LINC00641 overexpression inhibited cell proliferation, migration, and invasion but stimulated apoptosis in BC cells. LINC00641 overexpression also remarkably reduced BC growth and metastasis in vivo.	31490021
LINC00641	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	Interaction[sponging miR-424-5p to upregulate PLSCR4]	qRT-PCR	At first, downregulation of LINC00641 was identified in NSCLC cells. Through mechanism investigation, we determined that LINC00641 acted as a competing endogenous RNA (ceRNA) in NSCLC by sponging miR-424-5p to upregulate phospholipid scramblase (PLSCR4) expression. Further rescue assays indicated that miR-424-5p and PLSCR4 could reverse LINC00641-mediated cellular processes. Taken together, it is demonstrated in our study that LINC00641 can function as a tumor suppressor in NSCLC via a ceRNA network.		Yes	Functionally, LINC00641 suppressed cell proliferation and induced cell apoptosis in NSCLC, indicating that LINC00641 exerted tumor-suppressive role in NSCLC.	31322545
LINC00641	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction(microRNA-340-5p)	Wound Healing Assay//CCK8//qRT-PCR//RNA-seq//Colony Formation Assay//Transwell Assay	The expression of LINC00641 was overexpressed in RCC tissues and cell lines, and high LINC00641 expression was correlated with tumor-node-metastasis stage. Mechanistically, miR-340-5p was validated to be targeted by LINC00641 and knockdown of miR-340-5p counteracted LINC00641 silencing-mediated inhibition of RCC progression. 	The expression of LINC00641 was overexpressed in RCC tissues and cell lines, and high LINC00641 expression was correlated with tumor-node-metastasis stage.	Yes	 Furthermore, Silencing of LINC00641 remarkably inhibited the ability of cell proliferation, colony formation, and invasive capacities, as well as increasing the apoptotic rates of RCC cells in vitro. 	33853611
LINC00641	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-320d/MCL1 )	qRT-PCR//Tunel	The data displayed, LINC00641 was prominently elevated in OS tissues and cells, especially in DDP-resistant tumors and cell lines.  On the grounds of bioinformatics prediction, a direct binding of LINC00641 with miR-320d existed, whose target was MCL1. Meanwhile, LINC00641 modulated MCL1 via targeting miR-320d. Additionally, repressive LINC00641 blocked MCL1 via emulative interaction with miR-320d, thus expediting DDP-sensitivity of OS cells. 		Yes	 Knock-down LINC00641 was able to attenuate progression of DDP-resistant OS cells thus dampening their drug resistance toward DDP. Moreover, knock-downing LINC00641 gene was also able to manifest antagonism toward DDP-resistance in vivo. 	35266447
LINC00641	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	blood,cell lines	Regulation[miR-378a/ZBTB20 axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	We found that LINC00641 was highly expressed in AML specimens and cell lines. The results using bioinformatics assays predicted the complementary binding sites within LINC00641 and miR-378a, which was demonstrated by the use of the Luciferase reporter assays. In addition, we also demonstrated that ZBTB20 was a direct target of miR-378a. Moreover, the inhibition of miR-378a could rescue the ZBTB20 protein level decrease induced by LINC00641 knockdown.		Yes	Functionally, the silence of LINC00641 inhibited the proliferation, migration, invasion, and cell cycle arrest in AML cells while inducing their apoptosis.	31539138
LINC00641	LncRNA	Homo sapiens	Prostatic Neoplasms	23 paired PCa tumor tissues and adjacent  tissues 	Interaction(miR-365a-3p/VGLL4 axis)	RNA Pull-Down//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	We found LINC00641 and VGLL4 was reduced, while miR-365a-3p was elevated expression in PCa tissues compared with normal tissues. Functional assays revealed that miR-365a-3p/VGLL4 pair was the downstream targets of LINC00641.		Yes	LINC00641 overexpression inhibited growth and invasion abilities of PCa cells in vitro. 	33506898
LINC00638	LncRNA	Homo sapiens	Arthritis, Rheumatoid	PBMCs 	Expression(lower expressed)	CCK8//Transfection	Compared with the healthy control subjects, RA patients had significantly increased ESR, CRP, RF, anti-CCP, IgA, and C4 levels (P < 0.05) and significantly decreased Linc00638 expression in the PBMCs (P < 0.01). 	 The area under the receiver-operating characteristic (ROC) curve of Linc00638 was 91.86% with the best cut-off value of 0.74 for diagnosis of RA. Spearman correlation analysis showed that Linc00638 expression level was negatively correlated with age, course of disease, DAS28, ESR, CRP, RF and anti-CCP, and positively correlated with IL-4 and SOD levels (P < 0.05). 	Yes	In RA-FLS, overexpression of Linc00638 significantly inhibited while Linc00638 interference obviously enhanced the cell viability. Over-expression of Linc00638 also significantly increased the levels of IL-4 and SOD (P < 0.05) and decreased the expressions of IL-6 and ROS (P < 0.05), while interference of Linc00638 produced the opposite effects in the cells (P < 0.05).	34308844
LINC00638	LncRNA	Homo sapiens	Arthritis, Rheumatoid	48 RA patients 	Expression(lower expressed)	qRT-PCR//ELISA//IF	Compared with the control group, the expression of LINC00638 in the RA group was lower (P<0.01). 		Yes	 Compared with siRNA-control group, LINC00638, IL-10, SOD2 and HO-1 in the siRNA-LINC00638 group were significantly decreased (all P<0.01), and TNF-α was significantly increased (P<0.01).	35545408
LINC00638	LncRNA	Homo sapiens	Arthritis, Rheumatoid	PBMCs,  RA-FLS	Regulation(Nrf2/HO-1 pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//IF//ELISA//Transwell Assay	LINC00638 expression was found to be significantly decreased in PBMCs of RA patients, and it was negatively correlated with erythrocyte sedimentation rate, interleukin (IL)-17, reactive oxygen species (ROS), and disease activity scores for 28 joints (DAS28). Overexpression of LINC00638 activated the Nrf2/HO-1 pathway, markedly decreased the expressions of IL-6, IL-17, IL-23, ROS, as well as malondialdehyde, increased the total antioxidant capacity, and attenuated the proliferation and migration of RA-FLS, while silencing of LINC00638 reversed these manifestations.		Yes	Overexpression of LINC00638 activated the Nrf2/HO-1 pathway, markedly decreased the expressions of IL-6, IL-17, IL-23, ROS, as well as malondialdehyde, increased the total antioxidant capacity, and attenuated the proliferation and migration of RA-FLS, while silencing of LINC00638 reversed these manifestations.	35759235
LINC00632	LncRNA	Homo sapiens	Lung Neoplasms	NSCLC tissues	regulation[downregulating miR-1203]	qRT-PCR//Luciferase Report Assay	 LINC00632 was lowly expressed in NSCLC tissues.  LINC00632 is downregulated in NSCLC samples, which is closely linked to metastasis and prognosis in NSCLC patients. It inhibits the malignant development of NSCLC by negatively regulating miR-1203 level.	Low level of LINC00632 indicated high rates of lymph node metastasis and distant metastasis, as well as poor prognosis in NSCLC.	Yes	 Overexpression of LINC00632 suppressed in vitro proliferative and migratory abilities in NSCLC. Moreover, overexpression of LINC00632 inhibited tumor growth in nude mice bearing NSCLC. 	32862599
LINC00632	LncRNA	Homo sapiens	Glioma	gliomas tissues	Interaction(ALDOA)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Co-IP//Flow Cytometry//FISH//qRT-PCR//RIP//IF//Cell Proliferation Assay//Transwell Assay	 In this study, we reported that ARST was downregulated in the gliomas. We further demonstrated that the tumor suppressive effects of ARST could be mediated by a direct binding to a glycolytic enzyme aldolase A (ALDOA), which together with cofilin, keeping the polymerization and depolymerization of actin filaments in an orderly dynamic equilibrium.		Yes	Overexpression of ARST in the glioma cells significantly suppressed various cellular vital abilities such as cell growth, proliferation, migration and invasion. The tumorigenic capacity of these cells in vivo was reduced as well. 	34099027
LINC00630	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cultured cells	Interaction(miR-199a/FGF7 axis)	Western Blot//Migration Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	 In the present study, lncRNA long intergenic non-protein coding RNA 630 (LINC00630) was found to be significantly upregulated in CCA tissues and cultured cells.  Further investigations found that LINC00630 could interact with microRNA (miR)-199a, which specifically targeted fibroblast growth factor 7 (FGF7) for degradation. FGF7 overexpression restored the sh-LINC00630 transfection-induced decrease in CCA cell proliferation, migration and invasion. 	 LINC00630 expression was positively associated with histological differentiation, TNM stage and lymph node invasion. 	Yes	Short hairpin RNA (sh)-LINC00630 transfection could effectively decrease CCA cell proliferation, migration and invasion. 	35154463
LINC00630	LncRNA	Homo sapiens	colon carcinoma	colon carcinoma tissues and cell lines	Interaction(miR-409-3p/HK2 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	In this study, we found that the expression of LINC00630 was remarkably upregulated in colon carcinoma tissues and cell lines compared with that in adjacent tissues and the NCM-460 cell lines. In addition, we confirmed the direct interaction between LINC00630 and miR-409-3p in colon carcinoma cells using bioinformatics methods and dual luciferase reporter gene assay. Finally, we demonstrated that LINC00630 could promote cell growth and glycolysis and inhibit apoptosis by functioning as a miR-409-3p sponge, and further regulate hexokinase 2 (HK2) in colon carcinoma cells. 		Yes	Knocking out LINC00630 resulted in inhibition of proliferation and glycolysis but increase in apoptosis. 	35273690
LINC00629	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[binding to miR-196b-5p]	qRT-PCR	In gastric cancer, expression of LINC00629 and AQP4 was downregulated, and expression of miR-196b-5p was upregulated.LINC00629 competitively bound to miR-196b-5p, while AQP4 was a target of miR-196b-5p. Either downregulating miR-196b-5p or upregulating AQP4 could restrain the development of gastric cancer in vitro. LINC00629 overexpression repressed the growth of transplanted tumors in vivo. Taken together, LINC00629 competitively bound to miR-196b-5p to upregulate AQP4 expression, thereby inhibiting gastric cancer progression. Therefore, understanding of this mechanism may help to improve gastric cancer treatment.		Yes	Proliferation, invasion, and migration of gastric cancer cells were reduced after overexpression of LINC00629. 	31674022
LINC00668	LncRNA	Homo sapiens	lung squamous cell carcinoma	 LUSC patients, LUSC cell lines	Expression(highly expressed)	qRT-PCR	 LINC00668 expression was significantly up-regulated in LUSC patients and high expression level of LINC00668 was associated with advanced tumor-node-metastasis (TMN) stage. 	 LINC00668 expression was significantly up-regulated in LUSC patients and high expression level of LINC00668 was associated with advanced tumor-node-metastasis (TMN) stage. Moreover, the expression of LINC00668 significantly increased in smoking patients, and was a prognostic indicator for overall survival (OS) of smoking patients with LUSC.	Yes	In vitro experiments showed that LINC00668 has significantly higher expression level in LUSC cell lines and tissues compared to normal bronchial epithelial cell and para-tumor tissues; meanwhile, functional assay indicated knockdown of LINC00668 effectively inhibited the migration and invasion of LUSC cells.	35477186
LINC00668	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and HCC tissues	regulation[miR-532-5p/YY1 axis]	qRT-PCR//Western Blot//Transwell Assay	 LINC00668 was significantly up-regulated in HCC tissues and cell lines. Mechanistically, LINC00668 positively modulates the expression of YY1 by competitively binding to miR-532-5p. 		Yes	LINC00668 knockdown inhibited cell proliferative, migratory and invasion abilities and slowed down the epithelial-mesenchymal transition (EMT) process.	32249890
LINC00668	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Interaction[sponging miR-188-5p and regulating USP47]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//EdU Staining//Transwell Assay	LINC00668 was significantly upregulated in CRC tissues and cells.Conclusively, our findings demonstrated that lncRNA LINC00668 acted as an oncogenic role in CRC cells by sponging miR-188-5p and upregulating USP47 and may represent a potential marker for CRC patients.		Yes	Knockdown of LINC00668 suppressed cell proliferation and migration potential and induced cell apoptosis, but inhibition of miR-188-5p which was predicted to bind with LINC00668 reversed these effects.	31233752
LINC00887	LncRNA	Homo sapiens	lung carcinoma	 lung carcinoma tissues and cells	Interaction(microRNA-206/NRP1 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay	 The expression levels of LINC00887 were upregulated in lung carcinoma tissues and cells compared with adjacent tissues or normal cells (BEAS-2B).Furthermore, LINC00887 was identified as a competing endogenous RNA and to directly interact with miR-206. Mechanistically, miR-206 was demonstrated to regulate neuropilin-1 (NRP1) expression by targeting the NRP1 3'-untranslated region. 		Yes	Knockdown LINC00887 significantly inhibited the proliferation, migration and invasion of lung carcinoma A549 and NCI-H460 cells. 	33376520
LINC00885	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Expression[highly expressed]	qRT-PCR//RNA Pull-Down//Western Blot	Long intergenic non-protein coding RNA 885 (LINC00885) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS).		Yes	We determined that LINC00885 induces premalignant phenotypic changes by increasing cell proliferation, motility, migration and altering 3D growth in normal and DCIS breast cell lines. 	33049922
LINC00882	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression[highly expressed]	qRT-PCR	 LncRNA 882 (LINC00882) is one of the lncRNAs that was significantly upregulated in HCC tissues compared with normal liver tissues.	We found that upregulation of LINC00882 is correlated with poorer prognosis of HCC patients. 	Yes	In vitro cell experiments demonstrated that knockdown of LINC00882 inhibits proliferation, migration and invasion of HCC cell lines.	30271163
LINC00882	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells and clinical specimens	Interaction(miR-214-3p/CENPM)	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC00882 was markedly upregulated in HCC cells and clinical specimens. . Mechanistically, LINC00882 adsorbed miR-214-3p, thus promoting the expressions of CENPM. Rescue assays demonstrated that functions of LINC00882 deficiency in HCC cells were reversed through suppressing miR-214-3p.		Yes	Additionally, ATF2 could bind directly to the LINC00882 promoter region and activate its transcription. Loss-of-function studies further demonstrated that LINC00882 knockdown inhibited proliferation, invasion, and migration of HCC cells. 	34513693
LINC00861	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	regulation[PTEN/AKT/mTOR signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The results of the present study discovered that LINC00861 expression levels were significantly downregulated in cervical cancer tissues and CaSki and ME?180 cell lines. In conclusion, the findings of the present study indicated that the LINC00861/miR‑513b‑5p axis may inhibit the progression of cervical cancer cells through the PTEN/AKT/mTOR signaling pathway to suppress the EMT process.	Downregulated LINC00861 expression levels were identified to be associated with an advanced?stage, lymph node metastasis and the poor survival of patients with cervical cancer.	Yes	The overexpression of LINC00861 reduced cervical cancer cell proliferation, migration, invasion and epithelial?mesenchymal transition (EMT) processes, upregulated PTEN protein expression levels and downregulated phosphorylated (p)?AKT and p?mTOR protein expression levels. 	33179755
LINC00858	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	Expression[highly expressed]	qRT-PCR	 The results showed that LINC00858 had a high level of expressions in GC tissues as demonstrated by both online data and qRT-PCR assay.		Yes	Also, the knockdown of LINC00858 reduced the proliferation and migration of BGC823 and MGC803 cells in vitro. 	33112114
LINC00858	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-363-3p/FOXP4 axis]	CCK8//qRT-PCR//Transwell Assay	Our findings revealed that LINC00858 expression was markedly upregulated in GC tissues and cell lines. Collectively, LINC00858 acted as an oncogene in GC via regulating miR-363-3p/FOXP4 axis, which indicated that LINC00858 might be a novel therapeutic target for the treatment of GC.		Yes	 Loss-of-function experiments demonstrated that LINC00858 silencing inhibited the proliferation, migration and invasion of GC cells.	33015780
LINC00858	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[miR-22-3p/YWHAZ axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay//Transwell Assay	In this study, we firstly found that LINC00858 expression was significantly up-regulated in both CRC tissues and cell lines by both online data and RT-PCR assay. Mechanistically, bioinformatics analysis, dual-luciferase reporter assays, and western blot assays showed that LINC00858 functioned as competing endogenous RNA to repress miR-22-3p, which controlled its down-stream target YWHAZ. Then, we suggested that LINC00858 exerted its function through the miR-22-3p/YWHAZ axis.	Then, clinical assay revealed that high LINC00858 expression was significantly associated with advanced clinical progression and poor prognosis. Multivariate analysis demonstrated that high LINC00858 expression was an independent poor prognostic factor for CRC patients.	Yes	Moreover, lost-of-function assay indicated that knockdown of LINC00858 suppressed CRC cells proliferation, migration and invasion, and promoted apoptosis.	30931636
LINC00858	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues	regulation[microRNA-25-3p/SMAD7 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	The present study aimed to reveal the role and possible molecular mechanisms of a new LNCRNA, LINC00858, in CRC. LINC00858 was increased in CRC tumor tissues, and patients with high LINC00858 expression had a shorter survival time. 	The present study aimed to reveal the role and possible molecular mechanisms of a new LNCRNA, LINC00858, in CRC. LINC00858 was increased in CRC tumor tissues, and patients with high LINC00858 expression had a shorter survival time. 	Yes	Knockdown of LINC00858 expression suppressed cell proliferation and induced G0/G1 cell cycle arrest and apoptosis in TP53?wild?type CRC cells. 	32323793
LINC00858	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC patients	interaction[miR-4766-5p,PAK2]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//BrdU//Transwell Assay	With a predicted poor prognosis, LINC00858 was upregulated in CRC patients. LINC00858 promoted CRC progression by sponging miR-4766 to upregulate PAK2, shedding lights on LINC00858 as a potential therapeutic target candidate in CRC treatment from bench to clinic.		Yes	LINC00858 knockdown suppressed cell proliferation, invasion, and migration abilities, meanwhile induced cell apoptosis.	31902050
LINC00858	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues,cell lines	Interaction[ upregulating HNF4α and downregulating WNK2]	RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	We found that LINC00858 was highly expressed in primary colon cancer tissues and colon cancer cell lines, and was mainly located in the nucleus. In addition, we found that LINC00858 can bind to and upregulate the nuclear transcription factor HNF4α, leading to WNK2 expression downregulation. This, in turn, resulted in the promotion of colon cancer cell growth.	High LINC00858 expression was found to correlate with a poor differentiation, advanced TNM stages and lymph node metastasis.	Yes	Exogenous overexpression of LINC00858 promoted cell proliferation, invasion and migration of colon cancer cells, and facilitated angiogenesis and tumor growth.	31884577
LINC00858	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cell	regulation[WNK2]	qRT-PCR//RNA Pull-Down//RIP//FISH	There was high expression of LINC00858 and low expression of WNK2 in colon cancer tissues and cell lines.  In summary, LINC00858 acts as a tumor-promoting lncRNA in colon cancer by downregulating WNK2.		Yes	Silencing of LINC00858 promoted apoptosis, senescence, and autophagy in colon cancer cells. 	32768499
LINC00858	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-153-3p/Rabl3 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our results showed that LINC00858 was highly expressed in both HCC tissues and cell lines. In summary, these findings showed that LINC00858 exerted an ontogenetic role in HCC via regulating miR-153-3p/Rabl3 axis. 		Yes	 Knockdown of LINC00858 inhibited the proliferation and invasion of HCC cells. 	33015775
LINC00858	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	regulation[miR-134-5p/RAD18 signaling]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	LINC00858 were up-regulated in ovarian cancer tissues and cells, and its expression was elevated in advanced samples compared to early ones.		Yes	Knocking down LINC00858 inhibited cell proliferation, motility and EMT, but accelerated cell apoptosis in ovarian cancer. 	32875345
LINC00858	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Interaction(miR-134-5p/TRIM44 axis)	qRT-PCR//Western Blot	Our results showed that LINC00858 was highly expressed in human ovarian cancer tissues and cell lines. Mechanistic studies revealed that LINC00858 acted as a sponge of miR-134-5p and then regulated TRIM44 expression in SKOV3 cells. 		Yes	Knockdown of LINC00858 inhibited cell proliferation, migration and invasion of SKOV3 cells, and suppressed tumor growth in mouse xenograft models.	34423728
LINC00858	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	Interaction(miR‑3064‑5p/CTGF axis)	qRT-PCR//RIP	 The results revealed that the expression level of LINC00858 was upregulated in bladder cancer tissues and cell lines including T24, J82 and 5637. Mechanistically, LINC00858 functioned as a competitive RNA to increase the expression level of oncogene CTGF by sequestering miR-3064-5p.		Yes	 Moreover, knockdown of LINC00858 suppressed cell proliferation, migration and invasion in vitro. 	34132366
LINC00858	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cells	Interaction(miR-3064-5p/ VMA21 axis)	RNA Pull-Down//Transfection//Tunel//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	The up-regulated LINC00858 was detected in CC cells.LINC00858 was determined to bind with miR-3064-5p and up-regulate VMA21 in CC cells. In rescue assays, miR-3064-5p down-regulation and VMA21 up-regulation were able to counteract the effect caused by LINC00858 decrease on CC cell proliferation and apoptosis.		Yes	Reduction of LINC00858 effectively subdued CC cells proliferation and stimulated cell apoptosis. 	34275889
LINC00857	LncRNA	Homo sapiens	Lung Neoplasms		regulation[LINC00857-YBX1-MET/p-AMPKa signaling]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP	Collectively, LINC00857-YBX1-MET/p-AMPKa signaling is critical to regulate cell proliferation, apoptosis, and autophagy, which may provide a potential clinically therapeutic target in lung cancer.		Yes	The cell apoptosis and autophagy were induced upon LINC00857 silencing in lung cancer cells.	33312753
LINC00857	LncRNA	Homo sapiens	Colorectal Neoplasms	cell 	Interaction(miR-122-5p/SLC1A5/ASCT2 )	Western Blot//qRT-PCR//FISH//RIP//ChIP	We screened out an HSF1-mediated super enhancer, lncRNA-LINC00857, which exerts its characteristics in promoting cell growth via regulating glutamine metabolism. Notably, HSF1 could stimulate the super-enhancer activity of LINC00857 by the enrichment of acetyltransferase P300 to its gene loci, contributing to LINC00857 transcription. In turn, nuclear LINC00857 cooperated with HSF1 to promote ANXA11 transcription, which modulated SLC1A5/ASCT2 protein expression by binding competitively to miR-122-5p. 		Yes	We screened out an HSF1-mediated super enhancer, lncRNA-LINC00857, which exerts its characteristics in promoting cell growth via regulating glutamine metabolism. The knockout of ANXA11 attenuated colorectal cancer formation in vivo. 	36010849
LINC00857	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-455-5p/LRP4 axis )	qRT-PCR	 In our study, the level of HUMT was enhanced in HCC tissues and cells.  MiR-455-5p was a target of HUMT. Lowexpression of miR-455-5p reversed the inhibitive influence on HCC cells induced by of HUMT silencing. LRP4 was a target of miR-455-5p and was negatively regulated by miR-455-5p. In addition, LRP4 expression was positively modified by HUMT, and LRP4 inhibited the inhibitory effects on HCC cells induced by HUMT silencing.		Yes	Cell proliferation, invasion, and migration in HCC cells were repressed by knockdown of HUMT, and knockdown of HUMT arrested cells in G1 phase and decreased the levels of PCNA, MMP-2, and MMP-9. 	35293286
LINC00886	LncRNA	Homo sapiens	laryngeal carcinoma	tumor tissues and laryngeal cancer cell lines	Expression[lower expressed]	qRT-PCR//Western Blot	The remarkable downregulation of LINC00886 was observed in tumor tissues and laryngeal cancer cell lines. 		Yes	 Over-expression of LINC00886 dramatically mitigated cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo.	32111441
LINC00668	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[miR-193a/KLF7 axis]	ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In this study, we found that LINC00668 expression was significantly up-regulated in both NSCLC tissues and cell lines.Our findings suggested that STAT3-induced LINC00668 contributed to NSCLC progression through upregulating KLF7 expression by sponging miR-193a, and may serve as a prognostic biomarker and a potential target for NSCLC.	Clinical investigation demonstrated that high expression level of LINC00668 was associated with advanced TNM stage, histological grade and lymph node metastasis.	Yes	Functional assays indicated that knockdown of LINC00668 suppressed NSCLC cells proliferation, migration and invasion, and promoted apoptosis. 	31150989
LINC00887	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC patients 	Expression(highly expressed)	Western Blot//Flow Cytometry//qRT-PCR//IHC//Transwell Assay	As suggested by bioinformatics analysis, LINC00887 was markedly upregulated in ccRCC patients and associated with expression of immune-suppression molecule, thereby abating the immune infiltration level of CD8+ cells in tumor tissue. 		Yes	As revealed by cellular assay, LINC00887 was upregulated in ccRCC cells, and knockdown of LINC00887 resulted in a decreased PD-L1 expression, increased CD8+ T cell toxicity, decreased apoptotic levels, and enhanced chemotaxis. 	36060659
LINC00924	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Interaction( miR-6755-5p/NDRG2 )	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Transwell Assay	 The LINC00924 downregulation in HBV-related HCC tissues and cells was revealed by reverse transcription-quantitative polymerase chain reaction. The binding site between LINC00924 and miR-6755-5p was determined by luciferase reporter assays. miR-6755-5p was confirmed to target NDRG2. miR-6755-5p upregulation decreased NDRG2 messenger RNA (mRNA) and protein levels. The mRNA and protein levels of NDRG2 were downregulated in tissues and cells. NDRG2 knockdown attenuated the inhibition induced by LINC00924 overexpression on invasion and EMT of HCC cells. 	Based on the bioinformatics analysis, LINC00924 downregulation is positively related to unfavorable outcomes in patients with HBV-related HCC.	Yes	Functionally, as Transwell assays and western blotting indicated, LINC00924 elevation inhibited HCC cell invasion and epithelial-mesenchymal transition (EMT). 	34997970
LINC00922	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction( miR-204-5p/HMGA2 axis)	IHC//Western Blot//Wound Healing Assay//Tunel//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	LINC00922 was upregulated in GC, and high LINC00922 expression was associated with poor prognosis.Besides, LINC00922 was markedly located in the cytoplasm. The mechanistic analysis demonstrated that LINC00922 acted as a sponge of miR-204-5p, thereby inhibiting the expression of the target gene-High Mobility Group AT-hook 2 (HMGA2).	LINC00922 was upregulated in GC, and high LINC00922 expression was associated with poor prognosis.	Yes	Inhibition of LINC00922 suppressed GC cell proliferation, migration, invasion, and activated cell apoptosis in vitro and inhibited tumorigenesis in vivo. 	35428261
LINC00922	LncRNA	Homo sapiens	Breast Neoplasms	Breast cancer tissues	regulation[promoting NKD2 methylation]	qRT-PCR//RIP//ChIP	The RNA extraction and quantification and immunohistochemical staining characterized the high expression of LINC00922 and low expression of NKD2 in breast cancer tissues in comparison to its adjacent counterparts.  The current study provides evidence that LINC00922 acts as a tumor promoter by promoting NKD2 methylation. Hopefully, it provides a novel potential gene target for the treatment of breast cancer.		Yes	The ectopically expressed LINC00922 activated the Wnt signaling pathway, promoted epithelial-mesenchymal transition, cell proliferative, invasive and migratory capacities, tumor growth and metastasis.	33045317
LINC00922	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	Interaction(miR-361-3p/CLDN1)	CCK8//qRT-PCR//Luciferase Report Assay//FISH	 LINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. This study suggested that LINC00922 could competitively bind with miR-361-3p to promote the CLDN1 expression and activate Wnt/β-catenin signaling in OC progression, which providing a promising therapeutically target for OC.	 LINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. 	Yes	 LINC00922 knockdown inhibited proliferation and tumorigenesis of OC cells in vitro and vivo. In addition, LINC00922 knockdown suppressed migration, invasion, and EMT of OC cells in vitro. 	34116704
LINC00922	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues	Interaction(miR-424-5p/ARK5)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Bioinformatics Analysis//Transwell Assay	 MiR-424-5p was low expressed, whereas LINC00922 and ARK5 were high expressed in HCC tissues.  MiR-424-5p was negatively associated with LINC00922 and ARK5 that was positively associated with LINC00922. Interestingly, LINC00922 partially shared an identical binding site of miR-424-5p with ARK5. 		Yes	 LINC00922 its overexpression partially offset the inhibitory effect of miR-424-5p on cancer cell functions. ARK5 silencing repressed the malignant phenotype of cancer cells and inhibited the expressions of epithelial-to-mesenchymal transition (EMT)-related molecules (Vimentin, Snail and N-Cadherin). However, these effects were partially neutralized by miR-424-5p inhibitors. 	34097192
LINC00922	LncRNA	Homo sapiens	Colorectal Cancer Liver Metastasis	CRC cell 	Interaction(Lnc-LALC/ LZTS1 axis)	In Vivo Experiment//ChIP//Western Blot//Wound Healing Assay//Transfection//Migration Assay//qRT-PCR//RIP//H&E Staining//cell invasion assay//IHC//MSP	We found that upregulated Lnc-LALC in CRC was negatively correlated with LZTS1 expression, and Lnc-LALC could regulate LZTS1 expression in both mRNA and protein level in our study.  Furthermore, the precise mechanisms exploration showed that lnc-LALC could recruit DNA methyltransferases (DNMTs) to the LZTS1 promoter by combining with Enhancer of zeste homolog 2(EZH2) and then altered the expression of LZTS1 via DNMTs-mediated DNA methylation. 		Yes	 Functionally, Lnc-LALC enhanced the CRC cells metastasis ability in vitro and vivo through inhibiting the expression of LZTS1. 	33637680
LINC00921	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC cells and tissues	Interaction(miR-9-5p/LZTS2 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	 Low expression of linc00921 was observed in 49 of 95 TNBC tissues.  A luciferase reporter assay showed that linc00921 could sponge miR-9-5p in TNBC. Moreover, linc00921 and miR-9-5p occupied the same Argonaute-2 (Ago2) protein in TNBC cells. Leucine zipper tumor suppressor 2 (LZTS2) was recognized as a target gene of miR-9-5p, and thereby a linc00921/miR-9-5p/LZTS2 axis was identified in TNBC cells. 	 Low expression of linc00921 was correlated with poor postoperative disease-free survival (DFS) and overall survival (OS) of TNBC patients.	Yes	Overexpression of linc00921 with lentivirus suppressed the proliferation, migration and invasion of TNBC cells. Overexpression of linc00921 promoted nuclear export of β-catenin, neutralized its function, and subsequently promoted epithelial-to-mesenchymal transition (EMT) in TNBC. A xenograft tumor mouse model showed that the miR-9-5p inhibitor upregulates LZTS2 expression and induce nuclear export of β-catenin in TNBC. 	35179718
LINC00920	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(microRNA-10a)	CCK8//qRT-PCR	LINRIS expression was upregulated in NSCLC tissues.LINRIS were positively correlated with mature (miR-10a) levels but not miR-10a precursor. Overall, LINRIS silencing may inhibit NSCLC cell proliferation by suppressing miR-10a maturation.	High LINRIS levels predicted poor survival of NSCLC patients.	Yes	 In NSCLC cells, LINRIS silencing showed no role in miR-10a precursor accumulation but downregulated mature miR10a level. Moreover, LINRIS silencing inhibited cell proliferation, while miR-10a overexpression increased cell proliferation and inhibited the role of LINRIS silencing. 	35137650
LINC00920	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[highly expressed]	qRT-PCR//RNA Pull-Down//RIP	LINRIS was upregulated in CRC tissues from patients with poor overall survival (OS), and LINRIS inhibition led to the impaired CRC cell line growth.		Yes	 In vivo experiments showed that the inhibition of LINRIS suppressed the proliferation of tumors in orthotopic models and in patient-derived xenograft (PDX) models.	31791342
LINC00920	LncRNA	Homo sapiens	Prostatic Neoplasms		regulation[14-3-3ε-FOXO Pathway]	Western Blot//Immunoblotting//qRT-PCR//RIP//Luciferase Report Assay//ChIP	Here, we leverage the International Cancer Genome Consortium-Early Onset Prostate Cancer transcriptome and identify the previously uncharacterized lncRNA LINC00920 to be upregulated in prostate tumors.Chromatin isolation by RNA purification-mass spectrometry revealed the interaction of LINC00920 with the 14-3-3ε protein, leading to enhanced sequestration of tumor suppressive FOXO1. 		Yes	Phenotypic characterization of LINC00920 revealed its positive impact on cellular proliferation, colony formation, and migration. 	32646965
LINC00908	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissue	regulation[KLF5 ]	qRT-PCR	We found that LINC00908 was significantly upregulated in CRC. Mechanistically, miR-143-3p directly targets LINC00908. The KLF5 inhibitor ML264 affected proliferation and apoptosis, indicating that LINC00908 may act as a competing endogenous RNA to facilitate the expression of the miR-143-3p target gene KLF5. 		Yes	 Inhibition of LINC00908 resulted in reduced cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, cyclin-dependent kinase 4, and phosphorylated retinoblastoma.	33020901
LINC00899	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction[inhibiting miR-425]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Here, we found that LINC00899 is downregulated in breast cancer tissues and cell lines.These findings highlight the important role of the LINC00899-miR-425-DICER1 axis in breast cancer cell proliferation and invasion, and could potentially lead to new lncRNA-based diagnostics or therapeutics for breast cancer.		Yes	Functional assays indicated that LINC00899 overexpression suppresses proliferation, migration and invasion of breast cancer cells in vitro. 	31739288
LINC00899	LncRNA	Homo sapiens	acute myeloid leukemia	AML cells	regulation[miR-744-3p/YY1 signalling]	qRT-PCR	Here, we demonstrated that lncRNA LINC00899 was upregulated in acute myeloid leukaemia (AML) cells and was quite correlated with poor prognosis of AML patients.YY1 is the downstream target of LINC00899/miR-744-3p signalling.	Here, we demonstrated that lncRNA LINC00899 was upregulated in acute myeloid leukaemia (AML) cells and was quite correlated with poor prognosis of AML patients.	Yes	 LncRNA LINC00899 mediates cell proliferation and apoptosis of acute myeloid leukaemia cells. Knockdown of LINC00899 inhibited the growth of xenograft glioma tumour in vivo. 	32157707
LINC00891	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines 	Interaction(miR-128-3p/GATA2 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay//ChIP	Here, we found that LINC00891 expression is downregulated in lung cancer tissues and cell lines compared with that in adjacent normal tissues and normal lung epithelial cells. Mechanistic research showed that GATA2 directly binds to LINC00891 promoter and transcriptionally regulates LINC00891 expression. Meanwhile, GATA2 was identified as a target of miR-128-3p, and it is negatively regulated by miR-128-3p. Moreover, overexpression of GATA2 suppresses lung cancer cell proliferation, invasion, migration, and EMT process.		Yes	 LINC00891 overexpression impedes cell proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT) process in lung cancer cells.	35538035
LINC00888	LncRNA	Homo sapiens	Laryngeal Neoplasms	 laryngeal cancer cells 	Interaction(miR-378g/TFRC)	Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	We observed that LINC00888 expression was notably increased in laryngeal cancer and associated with death, recurrence, and prognosis.  Interestingly, we discovered that LINC00888 functioned as an miRNA sponge to suppress the effect of miR-378g on laryngeal cancer cells behaviors, as well as positively regulate TFRC expression. 	. We observed that LINC00888 expression was notably increased in laryngeal cancer and associated with death, recurrence, and prognosis. 	Yes	Depletion of LINC00888 repressed the proliferative and motile abilities of laryngeal cancer cells in vitro. 	34472153
LINC00887	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and the serum 	Expression[highly expressed]	qRT-PCR	We found that LINC00887 expression is significantly increased in early-stage RCC tissues and the serum of early-stage RCC patients compared to matched normal tissues and the serum of healthy subjects, respectively.		Yes	 Furthermore, we found that LINC00887 promotes RCC cell proliferation in vitro.	32654370
LINC00887	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues or human cervical cancer cell lines (Hela, C33A)	Interaction( miR-454-3p/FRMD6-Hippo axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	Linc00887 was downregulated in cervical cancer tissues or human cervical cancer cell lines (Hela, C33A) compared with normal tissues or cell lines. Linc00887 bound with miR-454-3p, and overexpression of miR-454-3p rescued linc00887-induced inhibition proliferation and invasion of HeLa cells. MiR-454-3p targeted and suppressed the expression of FRMD6, and linc00887 suppressed tumorigenesis of cervical cancer through activating the FRMD6-Hippo signaling pathway.		Yes	Overexpression of linc00887 inhibited proliferation and invasion HeLa and C33A cells, while linc00887 knockdown had the opposite effect.	33413358
LINC00857	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	regulation[miR-486-5p,YAP1 ]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	The upregulation of LINC00857 was further determined in 50 ovarian cancer tissues by comparing their corresponding non‐tumor tissues (Figure S1B). In a word, this study unveiled that LINC00857 regulates YAP1 by competitively binding to miR-486-5p and accelerates ovarian cancer progression.		Yes	 Functional experiments revealed that LINC00857 silencing led to the inhibition on cell proliferation, migration, invasion, and glycolysis but accelerated cell apoptosis in ovarian cancer.	32918541
LINC00857	LncRNA	Homo sapiens	pancreatic adenocarcinoma	pancreatic adenocarcinoma cells	Expression(highly expressed)	qRT-PCR//Luciferase Report Assay	 LINC00857 upregulation promoted the proliferation and clone formation abilities of PAAD cells. Afterwards, the downstream miRNA and mRNA targets of LINC00857 were picked up to construct a ceRNA network. Further study revealed that TGFA expression was positively regulated by LINC00857 and negatively regulated by miR-340-5p. Besides that, the inhibitory effect of miR-340-5p on PAAD cells growth and movement can be blocked by LINC00857 upregulation.	By enquiring TCGA database, we got that LINC00857 was highly expressed in patients with PAAD and positively associated with worse prognosis in PAAD patients.	Yes	the malignant behavior of PAAD cells induced by TGFA overexpression can be eliminated by LINC00857 knockdown.	33661995
LINC00857	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cells	Regulation(STAT3/CREB)	Cell Proliferation Assay//qRT-PCR//qPCR//Western Blot	We revealed that the knockdown of LINC00857 in PC cell lines inhibited the proliferation of the PC cells.  We found that LINC00857 downregulation was followed by the downregulation of oncogenic proteins mesenchymal-epithelial transition (MET), signal transducer and activator of transcription 3 (STAT3), and cAMP response element-binding protein (CREB).		Yes	We revealed that the knockdown of LINC00857 in PC cell lines inhibited the proliferation of the PC cells.	35070392
LINC00857	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cells	Interaction( p53-LINC00857/FOXM1/OTUB1)	RNA Pull-Down//ChIP//Wound Healing Assay//Co-IP//FISH//RIP//Luciferase Report Assay//Transwell Assay	In the present study, we demonstrated that the lncRNA LINC00857 exhibits a significantly elevated level in PC and that it is associated with poor prognosis; furthermore, TCGA data showed that LINC00857 expression was significantly upregulated in the mutant p53 group compared with the wild-type p53 group.Mechanistically, LINC00857 bound simultaneously to FOXM1 and to the deubiquitinase OTUB1, thereby serving as a protein scaffold and enhancing the interaction between FOXM1 and OTUB1, which inhibits FOXM1 degradation through the ubiquitin-proteasome pathway. 		Yes	 Gain- and loss-of-function experiments showed that LINC00857 promotes the metastasis of PC cells. We further found that LINC00857 upregulates FOXM1 protein expression and thus accelerates metastasis in vitro and in vivo. 	36272615
LINC00680	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cell	Interaction(GATA6-SOX12 axis )	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//FISH//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	LINC00680 has been characterized as a novel oncogenic lncRNA in LUAD,  In summary, this study revealed a novel LINC00680-GATA6-SOX12 axis in promoting LUAD cell cycle progression and proliferation. 		Yes	Results showed LINC00680 depletion resulted in G0/G1 phase arrest of LUAD cells and reduced CDK4 and cyclin D1 expression in H1650 and H1299 cells. LINC00680 overexpression promoted A549 cell proliferation and increased CDK4 and cyclin D1 expression.	34029572
LINC00680	LncRNA	Homo sapiens	Myasthenia Gravis	 peripheral blood mononuclear cells of patients with MG	Interaction(miR-320a/MAPK1)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Bioinformatics Analysis	Compared with control subjects, the expression levels of LINC00680 and mitogen-activated protein kinase 1 (MAPK1) in peripheral blood mononuclear cells of patients with MG were both upregulated; the levels of miR-320a were downregulated. A positive correlation was detected between LINC00680 expression and the severity of MG. Luciferase reporter assays identified that LINC00680 acts as a target for miR-320a. The in vitro analysis confirmed that LINC00680 regulates the expression of MAPK1 by sponging miR-320a. Finally, the functional analysis indicated that LINC00680 promoted Jurkat cell proliferation and inhibited cellular apoptosis by sponging miR-320a.		Yes	Finally, the functional analysis indicated that LINC00680 promoted Jurkat cell proliferation and inhibited cellular apoptosis by sponging miR-320a.	35800083
Linc00673	LncRNA	Homo sapiens	Stomach Neoplasms	cell line MGC-803	Regulation(PI3K/Akt signaling pathway)	Flow Cytometry//MTT//Colony Formation Assay//Western Blot	 The expressions of Linc00673 in gastric cancer cell line MGC-803, BGC-823 and AGS were significantly higher than that in normal gastric mucosa cell line GES-1 (P＜0.05). MGC-803 cell line with stable overexpression of LINC00673 was established, and the expression level of LincC00673 was 200 times higher than that of the control empty carrier group.  Western blot showed that Linc00673 overexpression not only promoted the expressions of the key molecule pAkt in PI3K / Akt signaling pathway and its downstream target NF-κ B and Bcl-2 protein, but also up regulated the expressions of tumor related factors β-catenin and EZH2 proteins. 		Yes	Overexpression of Linc00673 promoted proliferation of MGC-803 cells (P＜0.05) and clone formation (P＜0.05), inhibited cell apoptosis and affected the G1→S phase progression of cell cycle (P＜0.01). Overexpression of Linc00673 could affect the expressions of cell cycle regulatory gene CCNG2, P19 and CDK1 in MGC-803. 	35634670
LINC00673	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[B7-H6 ]	qRT-PCR//Western Blot	We discovered that LINC00673 is significantly upregulated in breast cancer tissues compared to paired adjacent non-tumor tissues by RT-qPCR and highly expressed LINC00673 is positively correlated with lymph node metastasis and clinical stage in the validated cohort.Gene expression profiling results indicated that LINC00673 could influence NCR3LG1(B7-H6) expression in transcriptional level.	We discovered that LINC00673 is significantly upregulated in breast cancer tissues compared to paired adjacent non-tumor tissues by RT-qPCR and highly expressed LINC00673 is positively correlated with lymph node metastasis and clinical stage in the validated cohort.	Yes	Knocking down LINC00673 inhibited cell proliferation and metastasis, whereas upregulated LINC00673 had the opposite effect.	30094100
LINC00673	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	Regulation[miR-515-5p/MARK4/Hippo signaling pathway]	qRT-PCR//Luciferase Report Assay//RNA-seq//ChIP	 In the present study, LINC00673 displayed a trend of remarkably increased expression in breast cancer tissues and was associated with poor prognosis in breast cancer patients. YY1-activated LINC00673 may exert an oncogenic function by acting as a sponge for miR-515-5p to upregulate the MARK4 and then inhibit Hippo signaling pathway, and may serve as a potential therapeutic target.	 In the present study, LINC00673 displayed a trend of remarkably increased expression in breast cancer tissues and was associated with poor prognosis in breast cancer patients. 	Yes	Importantly, LINC00673 depletion inhibited breast cancer cell proliferation by inhibiting the cell cycle and increasing apoptosis. Furthermore, ASO therapy targeting LINC00673 substantially suppressed breast cancer cell proliferation in vivo. 	31623640
LINC00673	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues,cell lines	regulation[EZH2-Mediated H3K27 Trimethylation]	Western Blot//Flow Cytometry//qRT-PCR//FISH//ChIP	Up-regulated LINC00673 was associated with poor prognosis in ESCC patients and promoted the proliferation of ESCC cells both in vitro and in vivo.The present findings are the first to reveal that LINC00673 represses CDKN2C expression and promotes ESCC cell proliferation by elevating EZH2-mediated H3K27me3 levels. 	Up-regulated LINC00673 was associated with poor prognosis in ESCC patients and promoted the proliferation of ESCC cells both in vitro and in vivo.	Yes	Up-regulated LINC00673 was associated with poor prognosis in ESCC patients and promoted the proliferation of ESCC cells both in vitro and in vivo.Compared to the control group, depletion of LINC00673 in ESCC cells arrested the cell cycle, at least, at the G1/S checkpoint. 	33014799
LINC00673	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Interaction[EZH2 and DNMT1]	Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay//ChIP	LINC00673 expression in PTC tissues was significantly higher than that of the adjacent normal tissues.  RIP and ChIP assay demonstrated that LINC00673 could bind to EZH2 and DNMT1. Besides, Western blot analysis showed that LINC00673 negatively regulated p53 expression. In addition, the knockdown of p53 in K1 and TPC-1 cells partially reversed the inhibitory effect of LINC00673 deficiency on the proliferation and metastasis of PTC cells.	Besides, higher expression of LINC00673 indicated worse prognosis of PTC.	Yes	The knockdown of LINC00673 in K1 and TPC-1 cells markedly reduced the proliferative rate. Meanwhile, LINC00673 down-regulation remarkably inhibited the migratory and invasive capacities of K1 and TPC-1 cells.	30915752
LINC00673	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cancer cell lines 	regulation[PTEN/PI3K/AKT signaling pathway]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 It was confirmed that the relative mRNA expression of LINC00673 was promoted in cervical cancer tissues and cancer cell lines compared with its corresponding normal tissues and cells (P < 0.05).These results provide the evidence that LINC00673 overexpression promotes cervical cancer cells progression through regulating miR-126-5p and activating the PTEN/PI3K/AKT signaling pathway, indicating that LINC00673 may be a potential therapeutic target for cervical cancer treatment.	 Higher LINC00673 expression was associated with tumor size, lymph node metastasis, and International Federation of Gynecology and Obstetrics (FIGO) stage (P < 0.05). Survival analysis showed higher LINC00673 expression predicted poor OS of cervical cancer patients, and Multivariate Cox analysis demonstrated that higher LINC00673 expression was identified as an independent risk factor for OS. 	Yes	LINC00673 overexpression promoted cell proliferation and cell cycle progression, but LINC00673 knockdown inhibited cell proliferation and cell cycle progression significantly (P < 0.05). 	32950808
LINC00673	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer patients	Expression(highly expressed)	In Vivo Experiment//Western Blot//qRT-PCR//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay	Our results revealed that serum LINC00673 levels were highest in cervical cancer patients, followed by patients with CIN and healthy controls. Western blotting showed that cell cycle-related proteins cyclin A2 and cyclin E and interstitial-associated proteins Snail and N-cadherin were upregulated and p53 signaling pathway-related proteins were downregulated in LINC00673-overexpressing HeLa and SiHa cells.	Our results revealed that serum LINC00673 levels were highest in cervical cancer patients, followed by patients with CIN and healthy controls. 	Yes	 In vitro experiments demonstrated that overexpression of LINC00673 enhanced the proliferation and cell cycle progression of HeLa and SiHa cells. In vivo experiments showed that the tumor weight and volume of nude mice subcutaneously injected with LINC00673-overexpressing HeLa cells were larger than those of nude mice injected with control cells (P < 0.05). 	34094965
LINC00673	LncRNA	Homo sapiens	Glioma	glioma cells 	Regulation(PI3K/AKT signaling pathway)	Western Blot//Transfection//Migration Assay//qRT-PCR//Invasion Assay	 In this study, we examined its expression in glioma cells by quantitative real-time PCR and found higher expression of LINC00673 in glioma cells compared with that in normal human astrocytes.  Furthermore, LINC00673 silencing inhibited the migration and invasion of U87MG and U118MG cells, phosphoinositide 3-kinase (PI3K) expression, and AKT phosphorylation. Moreover, activation of the PI3K/AKT signaling pathway by insulin-like Growth factor-1 abolished the inhibitory effect of LINC00673 silencing on the migration and invasion of U87MG and U118MG cells.		Yes	 Furthermore, LINC00673 silencing inhibited the migration and invasion of U87MG and U118MG cells, phosphoinositide 3-kinase (PI3K) expression, and AKT phosphorylation. Moreover, activation of the PI3K/AKT signaling pathway by insulin-like Growth factor-1 abolished the inhibitory effect of LINC00673 silencing on the migration and invasion of U87MG and U118MG cells.	29621055
LINC00673	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and serums	Expression[highly expressed]	qRT-PCR//MTT	The results showed that LINC00346, LINC00578, and LINC00673 were highly expressed, whereas LINC00671, LINC00261, and SNHG9 were lowly expressed in PC tissues and serums, and their expression levels were correlated with clinical stages. 	Survival analysis indicated that patients with high expression of LINC00346, LINC00578, or LINC00673 had significantly lower survival rate, while patients with high expression of LINC00671, LINC00261, and SNHG11 had significantly higher survival rate.	Yes	In addition, we also found that silence of LINC00346, LINC00578 and LINC00673 inhibited PC cell proliferation, and silence of LINC00671, LINC00261, and SNHG11 promoted PC cell proliferation.	30210701
LINC00673	LncRNA	Homo sapiens	Adenocarcinoma of Lung	cell lines	Regulation[WNT/β-catenin signaling]	qRT-PCR	Here we reported that a long noncoding RNA, LINC00673, was up-regulated in LAD cells.Together, our data suggest that LINC00673-v4 is a driver molecule for metastasis via constitutively activating WNT/β-catenin signaling in LAD and may represent a potential therapeutic target against the metastasis of LAD.		Yes	In vitro and in vivo experiments demonstrated that LINC00673-v4 enhanced invasiveness, migration, and metastasis of LAD cells.	31235588
LINC00673	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues	Regulation[KLF2]	CCK8//qRT-PCR//Western Blot//Transwell Assay	The study revealed that long non?coding RNA LINC00673 was significantly upregulated in thyroid cancer tissues compared with paired adjacent non?tumor tissues using RT-qPCR and that high expression of LINC00673 is was associated with larger tumor size and lymph node metastasis in the validated cohort. The results showed that LINC00673 may influence EMT and the expression of Kruppel-like factor 2 (KLF2). 	The study revealed that long non?coding RNA LINC00673 was significantly upregulated in thyroid cancer tissues compared with paired adjacent non?tumor tissues using RT-qPCR and that high expression of LINC00673 is was associated with larger tumor size and lymph node metastasis in the validated cohort. 	Yes	Knockdown of LINC00673 inhibited cell proliferation and metastasis, whereas, LINC00673 overexpression had the opposite effect. 	30106140
LINC00673	LncRNA	Homo sapiens	Diabetic Retinopathy	plasma samples of DR patients 	Regulation(p53 )	Western Blot//Transfection//qRT-PCR//Cell Apoptosis Assay//ELISA	LINC00673 was downregulated in plasma samples of DR patients (n=60) in comparison with the healthy controls (n=60) and negatively correlated with p53 only across DR patients but not across the healthy controls.  In retinal pigment epithelial cells (RPECs), high glucose treatment downregulated LINC00673. Moreover, LINC00673 overexpression downregulated p53 and decreased RPEC apoptosis, while LINC00673 silencing upregulated p53 and increased RPEC apoptosis. In addition, p53 overexpression reduced the effects of LINC00673 overexpression.		Yes	LINC00673 was downregulated in plasma samples of DR patients (n=60) in comparison with the healthy controls (n=60) and negatively correlated with p53 only across DR patients but not across the healthy controls.  In retinal pigment epithelial cells (RPECs), high glucose treatment downregulated LINC00673. Moreover, LINC00673 overexpression downregulated p53 and decreased RPEC apoptosis, while LINC00673 silencing upregulated p53 and increased RPEC apoptosis. In addition, p53 overexpression reduced the effects of LINC00673 overexpression.	34675574
LINC00671	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and serums	Expression[lower expressed]	qRT-PCR//MTT	The results showed that LINC00346, LINC00578, and LINC00673 were highly expressed, whereas LINC00671, LINC00261, and SNHG9 were lowly expressed in PC tissues and serums, and their expression levels were correlated with clinical stages. 	Survival analysis indicated that patients with high expression of LINC00346, LINC00578, or LINC00673 had significantly lower survival rate, while patients with high expression of LINC00671, LINC00261, and SNHG12 had significantly higher survival rate.	Yes	In addition, we also found that silence of LINC00346, LINC00578 and LINC00673 inhibited PC cell proliferation, and silence of LINC00671, LINC00261, and SNHG12 promoted PC cell proliferation.	30210701
LINC00671	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells 	Interaction(miR-221-5p/SOCS1 axis)	Western Blot//Transfection//Invasion Assay//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	LINC00671 expression in RCC tissues and cells was significantly reduced.In terms of mechanism, miR-221-5p was identified as a target of LINC00671, and LINC00671 could up-regulate SOCS1 by repressing miR-221-5p.	Patients with low LINC00671 expression had relatively shorter disease-free survival and overall survival. Moreover, LINC00671 expression was linked to lymph node metastasis, tumor stage, and tumor size. 	Yes	 In Caki-1 and 769-P cell lines, LINC00671 overexpression restrained the multiplication, migration, invasion, as well as the EMT process of RCC cells in vitro. 	34377233
LINC00671	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer	Interaction( STAT3/LINC00671/LDHA axis)	In Vivo Experiment//Migration Assay//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//ChIP	Here, we identified a novel lncRNA LINC00671 negatively correlated with LDHA, downregulating LDHA expression and predicting good clinical outcome in thyroid cancer.  Our work established STAT3/LINC00671/LDHA as a critical axis to regulate PTC growth and progression. 		Yes	hypoxia inhibits LINC00671 expression and activates LDHA expression largely through transcriptional factor STAT3. STAT3/LINC00671/LDHA axis regulates thyroid cancer glycolysis, growth, and lung metastasis both in vitro and in vivo. 	34404767
LINC00668	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue and cells	Regulation(PKN2 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Bioinformatics Analysis//Transwell Assay	We found that LINC00668 level was upregulated in GC tissue and cells and predicted poor prognosis.  Mechanistically, HuR was predicted to bind with LINC00668 and protein kinase N2 (PKN2). RNA pull-down assays validated the binding between HuR and LINC00668 (or PKN2). Moreover, either silencing of LINC00668 or HuR could decrease PKN2 mRNA stability or reduce PKN2 mRNA and protein levels. 	We found that LINC00668 level was upregulated in GC tissue and cells and predicted poor prognosis. 	Yes	Functionally, LINC00668 knockdown suppressed GC cell migration and invasion. Additionally, LINC00668 knockdown inhibited epithelial to mesenchymal transition (EMT) process. PKN2 exerts similar effects with LINC00668 in GC cells. LINC00668 knockdown suppressed tumor growth and metastasis in vivo. 	33879018
LINC00668	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Expression[highly expressed]	Western Blot//Colony Formation Assay//CCK8//qRT-PCR//IHC//EdU Staining	Both TCGA data and BC tissues harvested from our hospital indicated the higher expression of LINC00668 in BC tissues. LINC00668 expression was negatively correlated to prognosis of BC patients. 		Yes	Besides, LINC00668 knockdown in BC cells induced apoptosis and arrested cell cycle.In vivo experiments demonstrated the decreased proliferative rate in tumor-bearing mice administrated with sh-LINC00668 transfected BC cells.	31371999
LINC00680	LncRNA	Homo sapiens	Osteoarthritis	chondrocytes	Interaction(SIRT1 )	CCK8//RIP	Here, we found that a m6A-related lncRNA LINC00680 upregulated in the OA tissue and IL-1β-induced isolated primary chondrocytes. Mechanistically, m6A methyltransferase METTL3 combined tithe the m6A site of LINC00680 to up-regulate its expression. Moreover, LINC00680 interacted with SIRT1 mRNA through binding at m6A site on SIRT1 mRNA 3'-UTR, thereby enhancing the stability of SIRT1 mRNA. 		Yes	Functionally, in IL-1β-induced chondrocytes, silencing of LINC00680 recovered the proliferation and repressed the extracellular matrix (ECM) degradation. 	35501316
LINC00680	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues or cell lines	Interaction(miR-423-5p/PAK6 axis)	CCK8//qRT-PCR	 Notably, LINC00680 was highly expressed, and upregulation of LINC00680 was associated with large tumor size, advanced tumor stage, and poor prognosis.  Mechanistically, LINC00680 was found to act as a ceRNA by sponging miR-423-5p to regulate PAK6 (p21-activated kinase 6) expression in ESCC cells. The cell viability and motility inhibition induced by LINC00680 knockdown was significantly reversed upon PAK6 restoration and miR-423-5p inhibition.		Yes	 Functionally, knockdown of LINC00680 restrained ESCC cell proliferation, colony formation, migration, and invasion in vitro and inhibited tumor growth in vivo. Furthermore, ASO targeting LINC00680 substantially suppressed ESCC both in vitro and in vivo.	35255921
LINC00682	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[miR-9-LMX1A signaling axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Results show that LINC00682 levels are significantly downregulated in cancer tissues (“Can”) (Figure 4L), when compared to those in the adjacent epithelial (“Epi”) tissues (Figure 4L). Therefore, LINC00682 downregulation correlates with miR-9 upregulation and LMX1A downregulation in GC tissues (see the results from same set of tissue samples [9]). In the primary human GC cells, forced LINC00682 overexpression similarly induced miR-9 downregulation and LMX1A upregulation, causing proliferation inhibition and apoptosis activation. Significantly, restoring miR-9 expression by a lentiviral construct reversed LINC00682-induced actions in GC cells. Furthermore, LINC00682 was ineffective in LMX1A KO AGS cells. Importantly, LINC00682 expression levels are significantly downregulated in human GC tissues. We conclude that LINC00682 inhibits GC cell progression via targeting miR-9-LMX1A signaling axis.		Yes	We show that ectopic overexpression of LINC00682 induced miR-9 downregulation but LMX1A upregulation, inhibiting AGS cell survival, proliferation, migration and invasion.	31822638
LINC00839	LncRNA	Homo sapiens	Neuroblastoma	NB tumor tissues and cells	Regulation(miR-454-3p to Up-Regulate NEUROD1)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining	LINC00839 was found as a potential driver of NB progression. LINC00839 expression was higher in NB tumor tissues and cells. Also, LINC00839 expression was positively correlated with MYCN amplification, advanced INSS stages, and worse prognosis. Silencing of LINC00839 suppressed cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, LINC00839 could act as a sponge of miR-454-3p to facilitate the expression of its target NEUROD1. Moreover, miR-454-3p was demonstrated to exert an anti-cancer activity in NB. More importantly, the tumor-suppressive properties mediated by LINC00839 knockdown were significantly counteracted by the inhibition of miR-454-3p or overexpression of NEUROD1. Our study demonstrates that LINC00839 exerts an oncogenic role in NB through sponging miR-454-3p to up-regulate NEUROD1 expression, deepening our comprehension of lncRNA involved in NB and providing access to the possibility of LINC00839 as a therapeutic target for NB.	Also, LINC00839 expression was positively correlated with MYCN amplification, advanced INSS stages, and worse prognosis. 	Yes	Silencing of LINC00839 suppressed cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, LINC00839 could act as a sponge of miR-454-3p to facilitate the expression of its target NEUROD1.	35606572
LINC00857	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues , cell lines(BEAS-2B)	Regulation[targeting miR-1179/SPAG5 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In this study, we explored the expression of LINC00857 in lung adenocarcinoma (LUAD) tissues and LUAD cell lines and found a dramatical upregulation of LINC00857 compared with the adjacent normal lung tissues and BEAS-2B cell line, respectively. 		Yes	Then, LINC00857 knockdown led to the cell proliferation and glycolysis was repressed, while the apoptosis was elevated in LUAD cell lines. 	31667785
LINC00852	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumors and NSCLC cell lines	Interaction( hsa-miR-145-5p/KLF4 axis)	qRT-PCR//Cell Cycle Assay//Luciferase Report Assay	 LINC00852 is up-regulated in both NSCLC tumors and NSCLC cell lines. Moreover, the hsa-miR-145-5p/KLF4 axis was demonstrated to be directly regulated by LINC00852 in NSCLC. Inhibiting hsa-miR-145-5p or overexpressing KLF4 could reverse the LINC00852-down-regulation-induced anti-cancer effects on NSCLC cancer cell proliferation and chemoresistance.	High LINC00852 expression was significantly correlated with NSCLC patients' short overall survival.	Yes	 In NSCLC cell lines, LINC00852 down-regulation had anti-cancer effects by suppressing cancer cell proliferation, cisplatin chemoresistance and cell-cycle transition in vitro, as well as explant growth in vivo. 	34342374
LINC00852	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cell 	Interaction(miR-625/E2F1 Axis)	qRT-PCR	LINC00852 bound miR-625 which further targeted E2F1. Overexpressing miR-625 or down-regulating E2F1 reversed the oncogenic effects of LINC00852.		Yes	Overexpression of LINC00852 was positively associated with HCC cell proliferation, invasion and migration while negatively associated with the cell apoptosis. 	35401844
LINC00847	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC samples and  cell lines	Interaction(miR-147a/IFITM1 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Increased expressions of LINC00847 were observed in NSCLC samples as well as cell lines. Additionally, E2F1 could be capable of directly binding to the LINC00847 promoter region, followed by promoting its expression. Mechanically, miR-147a/IFITM1 axis was a downstream target of LINC00847, and silencing of miR-147a could rescue the anti-cancer effects of LINC00847 knockdown on NSCLC cell behaviors. X	Clinically, LINC00847 high-expression could lead to poor prognosis of NSCLC patients. 	Yes	Functionally, LINC00847 knockdown noticeably repressed NSCLC cell growth and metastasis. Mechanically, miR-147a/IFITM1 axis was a downstream target of LINC00847, and silencing of miR-147a could rescue the anti-cancer effects of LINC00847 knockdown on NSCLC cell behaviors. 	33968966
LINC00844	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[MAPK signaling]	qRT-PCR//Transwell Assay//Western Blot	LINC00844 was found to be significantly decreased in HCC tissue and was correlated with poor tumor characteristics, such as portal vein invasion, high α-fetoprotein (AFP), and a high rate of tumor recurrence.Mechanistic analyses indicated that the mitogen-activated protein kinase (MAPK) signaling pathway was remarkably inactivated by LINC00844. Furthermore, the immunoprecipitation assay verified that LINC00844 can bind to zinc-alpha-2-glycoprotein (AZGP1) and interfere with its translocation. LINC00844 can also promote AZGP1 expression, leading to the suppression of the transforming growth factor-β1 (TGF-β1)-extracellular signal-regulated kinase (ERK) pathway.	LINC00844 was found to be significantly decreased in HCC tissue and was correlated with poor tumor characteristics, such as portal vein invasion, high α-fetoprotein (AFP), and a high rate of tumor recurrence.	Yes	Exotic LINC00844 expression in HCC cell lines significantly suppressed proliferation and migration, as well as invasiveness, whereas LINC00844 deletion had the opposite effect. LINC00844 overexpression significantly inhibited HCC tumorigenesis in vivo. 	33313110
LINC00839	LncRNA	Homo sapiens	Lung Neoplasms	 LC cells	Interaction(miR-519d-3p/JMJD6 axis )	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay//Transwell Assay	LINC00839 was upregulated in LC cells and its knockdown resulted in reduced cell viability, migratory ability and invasion with increased cell apoptosis.MiR-519d-3p was the target gene of LINC00839 and its expression was reduced by LINC00839 overexpression. JMJD6 was directly targeted and suppressed at the level of mRNA and protein expression by miR-519d-3p. 		Yes	LINC00839 was upregulated in LC cells and its knockdown resulted in reduced cell viability, migratory ability and invasion with increased cell apoptosis.	34734406
LINC00839	LncRNA	Homo sapiens	Liver Neoplasms	 liver cancer tissues and cell lines	Regulation(FMNL2)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Transwell Assay	 LINC00839 expression was up-regulated in liver cancer tissues and cell lines, and the patients with high LINC00839 expression had shortened overall survival. Mechanistically, LINC00839 bound multiple proteins that were primarily associated with the metabolism and RNA transport, and positively regulated the expression of Formin-like protein 2 (FMNL2). 	 LINC00839 expression was up-regulated in liver cancer tissues and cell lines, and the patients with high LINC00839 expression had shortened overall survival. 	Yes	 LINC00839 further overexpressed under hypoxia and promoted liver cancer cell proliferation, migration, and invasion.	36335129
LINC00839	LncRNA	Homo sapiens	Neuroblastoma	neuroblastoma tissues and cell lines	Interaction(miR-338-3p/GLUT1 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC00839 and GLUT1 abundances were increased in neuroblastoma tissues and cell lines. The high expression of LINC00839 and GLUT1 indicated the lower overall survival. LINC00839 interference constrained neuroblastoma cell proliferation, migration, invasion and glycolysis, and facilitated apoptosis. GLUT1 overexpression or miR-338-3p knockdown could mitigate the influence of LINC00839 silence on neuroblastoma cell processes. LINC00839 could regulate GLUT1 expression via miR-338-3p. LINC00839 knockdown reduced neuroblastoma cell growth in xenograft model.	The high expression of LINC00839 and GLUT1 indicated the lower overall survival.	Yes	GLUT1 overexpression or miR-338-3p knockdown could mitigate the influence of LINC00839 silence on neuroblastoma cell processes. LINC00839 could regulate GLUT1 expression via miR-338-3p. LINC00839 knockdown reduced neuroblastoma cell growth in xenograft model.	34188473
LINC00707	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[VAV3/F11R ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//migration assay	"In this study, we identified that LINC00707 was excessively expressed in GC tissues and correlated with advanced stage, larger tumor size, lymph node metastasis and poorer prognosis in GC patients. Mechanistically, LINC00707 could abundantly interact with mRNA stabilizing protein HuR; ""LINC00707-HuR"" coalition ulteriorly combined with VAV3/F11R mRNAs and increased their stability. "	In this study, we identified that LINC00707 was excessively expressed in GC tissues and correlated with advanced stage, larger tumor size, lymph node metastasis and poorer prognosis in GC patients. 	Yes	In vitro and in vivo assays showed that LINC00707 promote GC cell proliferation and metastasis.	30502359
LINC00689	LncRNA	Homo sapiens	Glioma	glioma cells	Interaction(miR-526b-3p/IGF2BP1 Axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	 LINC00689 was upregulated in glioma cells, while miR-526b-3p was downregulated.In conclusion, silencing of LINC00689 could inhibit the tumorigenesis of glioma via mediation of miR-526b-3p/IGF2BP1 axis. LINC00689 may serve as a new target for the treatment of glioma.		Yes	 Moreover, LINC00689 knockdown or upregulation of miR-526b-3p inhibited the proliferation of glioma cells and induced the apoptosis. Consistently, the migration and invasion of glioma cells were notably reduced by LINC00689 shRNA/miR-526-3p mimics. miR-526b-3p inhibitor or IGF2BP1 upregulation could reverse the effect of LINC00689 knockdown or miR-526b-3p mimics. Finally, knockdown of LINC00689 inhibited the tumor growth of glioma in vivo through regulating miR-526b-3p/IGF2BP1/MAPK axis. 	33389570
LINC00707	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	regulation[miR-30c/CTHRC1 regulatory loop]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 LINC00707 was significantly upregulated in BC tissues and cell lines. It promoted cell proliferation, invasion, and migration via miR-30c/CTHRC1 regulatory loop. 		Yes	The knockdown of LINC00707 inhibited proliferation, invasion, and migration in MDA-MB-231 cells, while the overexpression of LINC00707 achieved the opposite results in MDA-MB-468 cells. 	32432749
LINC00707	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue,cell lines	Interaction[(miR)-485-5p]	CCK8//qRT-PCR//Luciferase Report Assay	The expression level of LINC00707 was confirmed by RT-qPCR in 65 paired CRC tissues and matched NCTs. The results revealed that LINC00707 expression was significantly increased in tumor tissues compared with that in the corresponding NCTs (P<0.001; Fig. 1A and B).  Furthermore, bioinformatics analysis demonstrated that microRNA (miR)-485-5p could directly bind to LINC00707, which was confirmed by a dual-luciferase reporter assay.	 The upregulation of LINC00707 expression was significantly associated with tumor size, stage and poor survival in patients with CRC. 	Yes	 Functional analyses revealed that the knockdown of LINC00707 could inhibit CRC cell proliferation. 	32010320
LINC00707	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Regulation[ ERK/JNK/AKT pathway signaling pathway]	qRT-PCR//Colony Formation Assay	 We observed that LINC00707 was upregulated in HCC cell lines compared with normal liver cell lines.Taking the above results together, it was implied in our study that LINC00707 contributed to HCC progression through modulating the ERK/JNK/AKT pathway.		Yes	LINC00707 silencing could greatly repress the proliferation and colony formation of HCC cells in vitro. On the contrary, overexpression of LINC00707 induced HCC cell proliferation and colony formation. 	30317590
LINC00707	LncRNA	Homo sapiens	Glioma	glioma tissues,cell lines	regulation[ LINC00707/miR-613]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	LINC00707 was up-regulated in gliomas. The regulatory axis of LINC00707/miR-613 provides new insights into the mechanism and treatment of gliomas.		Yes	Up-regulated LINC00707 increased the proliferation, migration and invasion of glioma cells, and silenced LINC00707 reduced these abilities. 	33107401
LINC00691	LncRNA	Homo sapiens	Stomach Neoplasms	Clinical tissue and serum samples	regulation[JAK/STAT signalling pathway]	qRT-PCR//Western blot//Luciferase Report Assay	 Our data indicated that the expression of LINC00691 in GC was significantly higher than that in healthy controls and was associated with clinicopathological features and survival time.LINC00691 promotes the proliferation and invasion of GC cells by activating Lin28 transcription and facilitating EGF expression through the JAK/STAT signalling pathway, which provides new ideas for targeted therapy of GC.	 Our data indicated that the expression of LINC00691 in GC was significantly higher than that in healthy controls and was associated with clinicopathological features and survival time.	Yes	 In the GC cell lines MKN-45 and HGC-27, the knockdown of LINC00691 suppressed proliferation, colony formation, migration, and invasion. 	32330554
LINC00691	LncRNA	Homo sapiens	Osteosarcoma	cell lines	regulation[LINC00691/miR-1256/ST5 pathway]	CCK8//qRT-PCR//RNA Pull-Down//Transwell Assay	 Expression analysis showed that the levels of lncRNA LINC00691 in osteosarcoma cells were decreased compared to those of control cells. The LINC00691/miR-1256/ST5 pathway plays an important role in the progression and metastasis of osteosarcoma and represents a good therapeutic target.		Yes	Overexpression of LINC00691 could inhibit the proliferation, migration, invasion, and induction of G1 cell cycle arrest in osteosarcoma cells, which was shown through in vitro and in vivo studies.	33380807
LINC00689	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[ADAM9 ,miR-526b-3p]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We found that LINC00689 was upregulated in GC tissues and positively correlated with advanced tumor stage and tumor size, while miR-526b-3p was downregulated. Our study suggests that LINC00689 functions as a novel oncogenic lncRNA in the development of GC by promoting ADAM9 expression through suppression of miR-526b-3p.	We found that LINC00689 was upregulated in GC tissues and positively correlated with advanced tumor stage and tumor size, while miR-526b-3p was downregulated. 	Yes	Furthermore, gain- and loss-of-function experiments revealed that LINC00689 promoted the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of GC cells, while miR-526b-3p had the opposite effects. 	32581594
LINC00689	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[miR-338-3p/PKM2 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 The analysis of our data indicated that the expression of LINC00689 was up-regulated in glioma tissues and cell lines.		Yes	 Further investigation demonstrated that LINC00689 knockdown markedly repressed the proliferation, migration, invasion and glycolysis of glioma cells. Additionally, silencing of LINC00689 significantly suppressed the growth of glioma cells in vivo. 	31181442
LINC00525	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cells and tissues	Regulation( p21 / EZH2 and RBMS2)	Western Blot//Transfection//qPCR//Colony Formation Assay//FISH//qRT-PCR//Luciferase Report Assay//IHC	LINC00525 is highly expressed in LUAD cells and tissues. Survival analysis indicated that upregulation of LINC00525 was associated with poor prognosis in patients with LUAD patients. Knockdown of LINC00525 inhibited cell proliferation and cell cycle progression in vitro. In xenograft models, LINC00525 knockdown suppressed tumor growth and tumorigenesis of tumor-bearing mice. 	Survival analysis indicated that upregulation of LINC00525 was associated with poor prognosis in patients with LUAD patients.	Yes	Knockdown of LINC00525 inhibited cell proliferation and cell cycle progression in vitro. In xenograft models, LINC00525 knockdown suppressed tumor growth and tumorigenesis of tumor-bearing mice. Mechanistically, LINC00525 epigenetically suppressed p21 transcription by guiding Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) to the p21 promoter through an formation of RNA-DNA triplex with the p21 promoter, leading to increased trimethylation of lysine 27 on histone 3 (H3K27me3) of the p21 promoter.	34105888
LINC02908	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	 acute myeloid leukemia cell	Interaction(miR-24-3P/TAOK1 )	qRT-PCR//Western Blot	LncRNA C9ORF139 regulates TAOK1 by sponging miR-24-3P to promote the proliferation, invasion and migration of acute myeloid leukemiacell.In vivo experiments have confirmed that the expression of C9ORF139 can promote the growth of subcutaneous tumors in AML nude mice.		Yes	LncRNA C9ORF139 regulates TAOK1 by sponging miR-24-3P to promote the proliferation, invasion and migration of acute myeloid leukemiacell.In vivo experiments have confirmed that the expression of C9ORF139 can promote the growth of subcutaneous tumors in AML nude mice.	35196780
LINC00460	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(IGF2BP2 and DHX9 /HMGA1)	ISH//qRT-PCR//MeRIP//RNA Pull-Down	LINC00460 expression was increased in human CRC, and high LINC00460 expression was correlated with poor five-year overall survival and disease-free survival.In addition, LINC00460 enhanced the protein expression of high-mobility group AT-hook 1 (HMGA1) by directly interacting with IGF2BP2 and DHX9 to bind the 3′ untranslated region (UTR) of HMGA1 mRNA and increased the stability of HMGA1 mRNA. In addition, the N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC. 	LINC00460 expression was increased in human CRC, and high LINC00460 expression was correlated with poor five-year overall survival and disease-free survival.	Yes	LINC00460 overexpression sufficiently induced the epithelial–mesenchymal transition and promoted tumor cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo.Finally, it suggested that HMGA1 was essential for LINC00460-induced cell proliferation, migration, and invasion.	33526059
LINC00460	LncRNA	Homo sapiens	Colonic Neoplasms		Interaction[miR-433-3p,ANXA2 ]	Western Blot//CCK8//FISH//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	 We found that LINC00460 was expressed highly in CC.Moreover, LINC00460 was able to specifically bind to miR-433-3p to increase the expression of ANXA2. Furthermore, LINC00460 Expression[down-expression]regulated the E-cadherin expression and Expression[Expression[up-expression]-expression]regulated the vimentin and N-cadherin expression by Expression[Expression[up-expression]-expression]regulating ANXA2, therefore inducing epithelial-mesenchymal transition. 		Yes	Expression[down-expression]regulation of LINC00460 inhibited cell invasion and proliferation in vitro and restrained tumor growth in vivo.	32069703
LINC00460	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Interaction[sponging miR-613]	qRT-PCR	Our findings revealed that the level of LINC00460 was significantly upregulated in PTC tissues and cell lines.These findings suggested that LINC00460 could function as a competing endogenous RNA to regulate SphK2 expression by sponging miR-613 in PTC. 	Our findings revealed that the level of LINC00460 was significantly upregulated in PTC tissues and cell lines, which was positively correlated with advanced tumor-node-metastasis (TNM) stage and lymph node metastasis.	Yes	Cellular experiments exhibited that knockdown of LINC00460 decreased proliferative, migratory, and invasive abilities of PTC cells.	30478856
LINC00460	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell	Regulation(PI3K/AKT signaling pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining	We identified the significant up-regulated expression of LINC00460 both in RCC tissues and cell. We crucially identified that LNC00460 promotes development of RCC by influencing the PI3K/AKT pathway. Knockdown of LNC00460 decreased the phosphorylation of AKT and mTOR. The key finding of our study showed that LINC00460 functions as an oncogene in RCC pathogenesis by mediating the PI3K/AKT.	RCC patients with elevated LINC00460 expression have shorter survival. 	Yes	Up-expression of LINC00460 promoted cell proliferation, invasion and migration, meanwhile down-regulation of LINC00460 exerted inhibitory effect on these activities. 	35912013
LINC00460	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[LINC00460 / miR-342-3p / AGR2 axis ]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Transwell Assay	LINC00460 was up-regulated in HCC tissues and cell lines compared with the control.The LINC00460 / miR-342-3p / AGR2 axis exerts anti-tumor effect in HCC in vitro and in vivo, consolidating and expanding the research about targeted gene therapy for early diagnosis and treatment of HCC.		Yes	Then we revealed that knockdown of LINC00460 suppressed cell proliferation and cell mobility and induced cell apoptosis in HCC cells.	32493835
LINC00460	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues and cell lines	regulation[miR-342-3p/AGR2 Axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We firstly detected LINC00460 expression was significantly upregulated in both HCC tumor tissues and cell lines. LINC00460 promotes HCC progression by elevating AGR2 expression via sponging miR-342-3p, providing a promising therapeutic target for HCC treatment.		Yes	 Functionally, LINC00460 facilitated HCC cell proliferation, migration, and invasion capacities, which due to that LINC00460 could physically bind to and repress miR-342-3p to elevate the expression of AGR2.	32184630
LINC00460	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-503-5p/miR-654-3p and TCP1)	qRT-PCR	Our results showed that LINC00460 was markedly over-expressed in HCC and silencing LINC00460 impaired cell stemness.  In conclusion, LINC00460 aggravated cell stemness in HCC via targeting miR-503-5p/miR-654-3p and TCP1, suggesting that LINC00460 may work as a potential signature for cell stemness in HCC		Yes	 Additionally, LINC00460 knockdown curbed proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) and drove apoptosis of HCC cells.	34612153
LINC00460	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC cancer tissues and cell lines	Interaction[sponging miR-612 to up-regulate AKT2]	Western Blot//CCK8//FISH//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the current study, we discovered that LINC00460 was relatively up-regulated in both HNSCC cancer tissues and cell lines, and predicted a poor prognosis in HNSCC patients.Our results identified miR-612 as a novel target of LINC00460, whose expression suggested a negative correlation with LINC00460 in HNSCC tissues and cell lines. LINC00460 increased the expression of serine/threonine kinase AKT2 via sponging miR-612. Rescue experiments indicated that LINC00460 could promote HNSCC progression partially through inhibition of miR-612. Subcutaneous xenotransplanted tumor model confirmed that interference of LINC00460 suppressed in vivo tumorigenic ability of HNSCC via down-regulation of AKT2. In conclusion, our findings clarified the biologic significance of LINC00460/miR-612/AKT2 axis in HNSCC progression and provided novel evidence that LINC00460 may be a new potential therapeutic target for HNSCC.		Yes	Gain- and loss-of functional studies established that over-expression of LINC00460 promoted cell proliferation, invasion and migration of HNSCC cells in vitro, while the promotion abilities were suppressed via knockdown of LINC00460.	31737186
LINC00460	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Regulation[miR-1224-5p/FADS1 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Linc00460 was up-regulated in OS tissues and cells.In conclusion, this study recognized linc00460 as a new oncogenic lncRNA in OS and suggests that the linc00460/miR-1224-5p/FADS1 axis might be a potential therapeutic target for OS.	High linc00460 expression was positively correlated with distant metastasis and poor overall survival of OS patients.	Yes	 Knockdown of linc00460 suppressed OS cells proliferation and metastasis in vitro. 	31419446
LINC00460	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	serum of patients with AM	Interaction(miR-320b/PBX3 axis)	qRT-PCR//Western Blot	It was found that the expression of LINC00460 was significantly upregulated in the serum of patients with AML and those with CN-AML. LINC00460 was also a decoy of microRNA (miR)‑320b, which can further inhibit the expression of PBX homeobox 3 (PBX3). 	Furthermore, ROC curve analyses demonstrated that serum LINC00460 could differentiate patients with AML from healthy individuals with an area under the curve of 0.8488 (95% CI, 0.7697?0.9279). The serum LINC00460 expression was also significantly decreased when the patients achieved complete remission. Kaplan‑Meier analysis indicated that patients with high serum LINC00460 expression had a shorter overall survival time compared with the low serum LINC00460 expression group. 	Yes	 Knockdown of LINC00460 inhibited viability, while inducing cell cycle arrest and apoptosis in AML cells. 	33846790
LINC00460	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCA tissues and cell lines	regulation[linc00460/miR-1224-5p]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we discovered that lncRNA linc00460 was obviously over-expressed in ESCA, both in tissues and cell lines. Our findings suggest that linc00460/miR-1224-5p is a possible clinical target for ESCA.		Yes	Down-regulation of linc00460 significantly suppressed the metastatic potential (including cell migration and invasion) and EMT of ESCA cells. 	32534700
LINC00460	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues 	interaction[targeting microRNA-503-5p]	Flow Cytometry//qRT-PCR//MTT//Tunel	LINC00460 levels in CC tissues were higher than tumor-adjacent tissues.Hence, LINC00460 functioned as an oncogene in CC that affected cell proliferation and apoptosis via sponging miR-503-5p. This study provides a novel therapeutic target for CC.		Yes	LINC00460 silencing suppressed proliferation and promoted apoptosis of CC cells as evidenced by decreased cell viability, inhibited proliferation-related protein and cell cycle protein expressions and G1/S transition, increased apoptotic cells and Hoechst-positive cells, and enhanced apoptosis-related protein expressions. 	32740791
LINC00460	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	Interaction[miR-30a-3p/Rap1A]	RNA Pull-Down//IHC//Western Blot//ISH//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay//IF	LIN00460 expression was significantly higher in NPC tissues compared with noncancerous tissues.  We further demonstrated that LINC00460 regulated Rap1A expression through competitively binding to miR-30a-3p.		Yes	In NPC cell lines named C666-1 and 5-8F, LINC00460 overexpression promoted cancer cell migration, invasion and epithelial-mesenchymal transition (EMT), while depletion of LINC00460 exhibited opposite effects.LINC00460 knockdown suppressed NPC metastasis in a xenograft mouse model.	31414345
LINC00460	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	interaction[miR-539]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 LINC00460 expression was markedly up-regulated in PTC tissues and cells compared to their corresponding controls by quantitative real-time PCR (qRT-PCR).These findings indicated that LINC00460 can modulate MMP-9 expression to promote cell proliferation, invasion and apoptosis through targeting miR-539, suggesting act as an oncogenic RNA in PTC and provide a new therapeutic perspective.		Yes	Meanwhile, LINC00460 knockdown notably inhibited the proliferation capacity, accelerated the apoptosis and down-regulated the invasion-related proteins (MMP-2, MMP-9, ZEB1) expression.	32021436
LINC00460	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues	Expression[highly expressed]	qRT-PCR	The present bioinformatic analysis revealed that LINC00460 was upregulated in PC samples with a prognostic significance. 	The results of real-time quantitative PCR confirmed that LINC00460 was significantly upregulated in cancer tissues and was associated with poor survival of patients with PC.	Yes	Further in vitro experiments demonstrated that suppressing LINC00460 using small interfering RNA inhibited viability and colony formation of PC cells.	32724379
LINC00460	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer (PC) cells	Interaction(miR-320b/ARF1 axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	A marked increase in the level of long non-coding RNA LINC00460 was reported in PAAD patients, in comparison with the healthy controls.Moreover, miR-320b was targeted straight and its expression was downregulated by LINC00460, whose knockdown led to a reduction in ARF1 expression. Interestingly, miR-320b downregulation partly reversed the effect of LINC00460 knockdown on the proliferation, migration, invasion and apoptosis of SW1990 cells, as well as ARF1expression. 		Yes	. It was found in our study that LINC00460 knockdown inhibited SW1990 cell proliferation, migration and invasion and promoted its apoptosis. 	33345740
LINC00460	LncRNA	Homo sapiens	Pancreatic Neoplasms	 PC tissues and cells	Interaction(miR-503-5p/ANLN positive feedback loop)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//EdU Staining//Transwell Assay	 LINC00460 was up-regulated in PC tissues and cells.  LINC00460 silencing attenuates the development of PC by regulating the miR-503-5p/ANLN axis and exosomal LINC00460-induced M2 macrophage polarization accelerates the migration and invasion of PANC-1 cells, thus LINC00460 may act as a possible therapeutic target for treating PC.		Yes	 LINC00460 knockdown suppressed cell proliferation, migration, and invasion, facilitated cell apoptosis and G0/G1 phase arrest, and inhibited the tumor growth through anti-PD-1 therapy. 	36482354
LINC00460	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LC tissues and cell lines	Interaction[miR-302c-5p/FOXA1 signal pathway]	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	We observed that LINC00460 was increased in lung adenocarcinoma tissues and cells in comparison to their corresponding controls. Rescue assay confirmed that LINC00460 contributed to lung adenocarcinoma progression by regulating miR-302c-5p/FOXA1 signal pathway. In conclusion, LINC00460 promotes LC progression by competitively binding miR-302c-5p and regulating FOXA1 signal pathway. Our findings reveal that LINC00460 may be a potential prognostic biomarker and a candidate target for LC therapy.		Yes	In addition, silencing LINC00460 was able to suppress lung adenocarcinoma cell growth in vitro and in vivo.	30359741
LINC00460	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues & cell lines	Interaction(miR-149-5p)	RIP//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The results revealed that LINC00460 was significantly enhanced in ccRCC tissues, as well as in ccRCC cell lines. The overexpression of LINC00460 was significantly associated with lymph node metastasis and TNM stage, and lead to poor overall survival. Knockdown of LINC00460 reduces the cell ability of proliferation, migration, and invasion. LINC00460 could sponge to miR-149-5p.		Yes	Knockdown of LINC00460 reduces the cell ability of proliferation, migration, and invasion. 	34429655
LINC00460	LncRNA	Homo sapiens	bladder carcinoma	bladder carcinoma tissues and cell lines	regulation[miR-612/FOXK1 Axis]	Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 LINC00460 was elevated in bladder carcinoma tissues and cell lines. LINC00460 promoted bladder carcinoma progression via sponging miR-612 to facilitate FOXK1 expression, suggesting that LINC00460 might have the potential of being explored as a therapeutic target for treatment of bladder carcinoma.		Yes	Overexpression of LINC00460 promoted cell viability, proliferation, invasion, and migration, while silencing of LINC00460 indicated the opposite effect on bladder carcinoma progression. 	33027786
LINC00460	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	Interaction(miR-149-5p )	qRT-PCR//Western Blot	In the present study, lncRNA LINC00460 was shown to be upregulated in colorectal cancer tissues, and overexpression of LINC00460 significantly promoted metastasis of colorectal cancer in vitro.  Furthermore, miR-149-5p interacted with LINC00460, and they negatively regulated expression of each other. Transfection of miR-149-5p mimics partially counteracted the tumor metastasis-promoting effects induced by LINC00460 overexpression. Finally, overexpression of LINC00460 upregulated the expression levels of biglycan, a target gene of miR-149-5p, which has also been identified as an oncogenic driver in colorectal cancer.		Yes	 In the present study, lncRNA LINC00460 was shown to be upregulated in colorectal cancer tissues, and overexpression of LINC00460 significantly promoted metastasis of colorectal cancer in vitro. 	33472555
LINC00460	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue ,cell lines	Regulation[miR-939-3p/LIMK2 axial ]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that LINC00460 was upregulated and closely correlated to clinicopathological features and poor prognosis of patients with CRC.The findings of this study showed that LINC00460 works as an oncogene in CRC and promoted CRC cell metastasis via regulation of miR-939-3p/LIMK2 axial. 	We found that LINC00460 was upregulated and closely correlated to clinicopathological features and poor prognosis of patients with CRC.	Yes	 Functionally, we elucidated that LINC00460 promoted metastasis in CRC cell lines HT29 and LOVO.	30863183
LINC00460	LncRNA	Homo sapiens	Skin Neoplasms	CSCC tissues and cell lines	Interaction(ELAVL1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Invasion Assay//Migration Assay//CCK8//qRT-PCR//RIP//IHC//EdU Staining//Transwell Assay	LINC00460 was found to be significantly upregulated in CSCC tissues and cell lines.  Mechanistically, LINC00460 binds to embryonic lethal abnormal vision like RNA binding protein 1 (ELAVL1) and enhances its stability by inhibiting the β-transducin repeats-containing protein (β-TrCP)-mediated ubiquitination of ELAVL1. Moreover, the effect of LINC00460 silencing on the proliferation, migration, and invasion of CSCC cells could be reversed by overexpressing ELAVL1. 		Yes	Functionally, LINC00460 knockdown inhibited cell proliferation, migration, and invasion in vitro. Consistent with this, when LINC00460 expression decreased, CSCC tumorigenesis and metastasis in vivo were inhibited.	36513874
LINC00460	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Expression[highly expressed]	Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay	The expression of LINC00460 was significantly upregulated in CRC tissues and cells, associated with early stage CRC and low disease-free survival. 	The expression of LINC00460 was significantly upregulated in CRC tissues and cells, associated with early stage CRC and low disease-free survival. 	Yes	 The downregulated of LINC00460 expression increased cell proliferation by regulating the cell cycles of SW620 and HCT116 cells. LINC00460 knockdown did not affect cell migration or invasion in vitro. 	30123352
LINC00467	LncRNA	Homo sapiens	Glioma	glioma tissues	interaction[miRNA-485-5p]	qRT-PCR//Luciferase Report Assay	LINC00467 was upregulated in glioma. LINC00467 aggravates the progression of glioma by negatively regulating miRNA-485-5p, which may be a potential therapeutic target for glioma.		Yes	The knockdown of LINC00467 attenuated proliferative and invasive abilities, and induced apoptosis in U87 and U251 cells.	32016980
LINC00467	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Regulation[Linc00467/miR-20b-5p/CCND1 signaling pathway]	Western Blot//qPCR//CCK8//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining	Our data suggested that linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. Linc00467/miR-20b-5p/CCND1 signaling pathway may provide new insights into lung cancer treatment.	Our data suggested that linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. 	Yes	Linc00467 knockdown resulted in reduced proliferation rate in lung cancer cells.	31686834
LINC00467	LncRNA	Homo sapiens	Adenocarcinoma of Lung	cell lines	Regulation[Wnt/β-catenin signaling pathway]	ChIP//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 High expression of LINC00467 was further detected in LUAD cell lines. Collectively, we determined that STAT1-induced upregulation of LINC00467 promoted LUAD progression by epigenetically silencing DKK1 to activate Wnt/β-catenin signaling pathway.		Yes	Functionally, high expression level of LINC00467 promoted LUAD cell proliferation and migration, indicating that LINC00467 exerted oncogenic functions in LUAD progression. 	31027730
LINC00467	LncRNA	Homo sapiens	Prostatic Neoplasms	PC tissues and cells	Interaction(miR-494-3p/STAT3 Axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Cell Cycle Assay//Transwell Assay	We established that LINC00467 expression was upregulated in PC tissues and cells. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. 		Yes	Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo.	34094954
LINC00467	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC cells	regulation[ miR-299-5p/ubiquitin specific protease-48 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC. LINC00467 enhances HNSCC progression by serving as a sponge of miR-299-5p to increase USP48 expression.		Yes	LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC.	32159247
LINC00466	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	regulation[miR-508/CHEK1]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We report that LINC00466 expression is increased in glioma cells and tissues.LINC00466 may exhibit its anti-oncogenic roles through targeting the miR-508/CHEK1 axis.	Clinical studies revealed that the elevated expression of LINC00466 is closely correlated with an advanced World Health Organization grade (p = 0.008), Karnofsky Performance Status score (p = 0.004) and a short overall survival (p = 0.0035) of glioma patients.	Yes	Functional assays revealed that LINC00466 knockdown distinctly suppresses glioma cell proliferation, migration, invasion and epithelial-mesenchymal progress, and also promotes apoptosis. 	33037684
LINC00466	LncRNA	Homo sapiens	Glioma	 glioma tissues	Interaction(miR-137 /PPP1R14B )	In Vivo Experiment//IHC//Western Blot//Transfection//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	Highly expressed LINC00466 and PPP1R14B and lowly expressed miR-137 were eventually revealed in glioma tissues.  LINC00466 could bind to miR-137, and up-regulation of miR-137 could attenuate the enhancing effects caused by LINC00466 overexpression. We took a further step and found that miR-137 could bind to PPP1R14B. 		Yes	Overexpression of LINC00466 could promote proliferation, metastasis and drug sensitivity to TMZ of glioma cells. 	33642868
LINC00461	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Regulation[miR-30a-5p/integrin β3 axis ]	qRT-PCR	 In the current study, LINC00461 was found to be significantly upregulated in both BC tissues and cell lines.Taken together, LINC00461 exerts an oncogenic role in BC through miR-30a-5p/ITGB3 axis. 	Besides, we found that high LINC00461 expression was associated with TNM stage and differentiation. 	Yes	Furthermore, functional studies demonstrated that LINC00461 expedited BC cell migration and invasion.	30623482
LINC00461	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Interaction[targeting miR-323b-3p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that the expression of LINC00461 was significantly overexpressed in CRC tissues and different cell lines.Downregulation of LINC00461 expression significantly suppressed the proliferation, migration and invasion of CRC cells and promoted cell apoptosis. 	We found that the expression of LINC00461 was significantly overexpressed in CRC tissues and different cell lines	Yes	Downregulation of LINC00461 expression significantly suppressed the proliferation, migration and invasion of CRC cells and promoted cell apoptosis. 	31908480
LINC00461	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[LINC00461/miR-149-5p/LRIG2 axis ]	CCK8//qRT-PCR//RNA Pull-Down//Transwell Assay	Here, we found that LINC00461 was upregulated in HCC tissues and positively correlated with advanced stage and metastasis.In summary, our findings revealed that LINC00461 is an oncogene in HCC through regulating miR-149-5p/LRIG2 pathway.	Here, we found that LINC00461 was upregulated in HCC tissues and positively correlated with advanced stage and metastasis. Furthermore, LINC00461 overexpression in HCC patients predicts unfavorable prognosis.	Yes	 Loss-of-function assays showed that LINC00461 silencing suppressed the proliferation, migration and invasion of HCC cells in vitro, and impeded tumor growth in vivo. 	30879766
LINC00461	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[LINC00461/miR-216a/aquaporin 4 pathway]	qRT-PCR	 LINC00461 was upregulated, and miR-216a was downregulated in glioma tissues and cells, and LINC00461 upregulation was correlated with large tumor size, higher WHO grade and recurrence, and poor overall survival. Moreover, LINC00461 downregulation blocked the glioma tumor growth in vivo. In conclusion, LINC00461 knockdown inhibits glioma cell proliferation, migration, invasion, and TMZ resistance through miR-216a/AQP4 axis, suggesting LINC00461 as an oncogene in glioma progression.	 LINC00461 was upregulated, and miR-216a was downregulated in glioma tissues and cells, and LINC00461 upregulation was correlated with large tumor size, higher WHO grade and recurrence, and poor overall survival. 	Yes	 LINC00461 knockdown suppressed cell viability, abilities of cell cloning and migration and invasion, and TMZ resistance in glioma. 	33817241
LINC00461	LncRNA	Homo sapiens	Multiple Myeloma	blood	Interaction[microRNA/BCL-2 ]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	LINC00461 was highly expressed in MM. Our findings demonstrate that LINC00461, a sponge for miR-15a/16, is highly expressed in MSC-derived exosomes, and enhances MM cell proliferation, which may become an excellent candidate for therapeutic applications.		Yes	Knockdown of LINC00461 dramatically reduced MM cell proliferation and induced cell apoptosis. 	30409700
LINC00461	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[ miR-518a-3p/WDR1 pathway]	qRT-PCR	Our results demonstrated that LINC00461 was significantly up-regulated in NSCLC tissues and cell lines.aken together, we suggested an essential role of LINC00461/miR-518a-3p/WDR1 axis in NSCLC, which could be used as a potential therapeutic target for NSCLC treatment.		Yes	Furthermore, knockdown of LINC00461 inhibited NSCLC cell proliferation and invasion in vitro as well as suppressed tumor growth and metastasis in vivo. 	33233986
LINC00461	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL cells	Interaction(miR-411-5p/BNIP3 Pathway)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//IHC//Bioinformatics Analysis	The level of LINC00461 in DLBCL was significantly higher than that in normal cases, and the level in recurrence DLBCL was significantly higher than that in nonrecurrence. The results shown that miR-411-5p bound to LINC00461 and BNIP3 and was negatively correlated with LINC00461 and BNIP3 mRNA in blood of DLBCL patients.The inhibition of LINC00461 or overexpression of miR-411-5p reduced the expression of BNIP3 protein, thereby inducing apoptosis at the in vivo and in vitro levels.		Yes	Suppressing the level of LINC00461 inhibited cell proliferation and induced apoptosis. 	35783530
LINC00461	LncRNA	Mus musculus	Myocardial Reperfusion Injury	 I/R mice	Interaction(microRNA-185-3p/Myd88)	In Vivo Experiment//RNA Pull-Down//Western Blot//Tunel//qRT-PCR//Luciferase Report Assay//H&E Staining	 I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice.		Yes	Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice.	35272621
LINC00460	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues	regulation[CCNG2,EZH2/LSD1]	RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//RIP//MTT//ChIP	In this research, we discovered that LINC00460 is remarkably upregulated in GC tissues compared to the non-tumor tissues.In conclusion, our results suggested that LINC00460 acted as an oncogene in GC to inhibit the expression of CCNG2 at least partly by binding with EZH2 and LSD1. 		Yes	Functionally, proliferation of GC cells could be regulated by LINC00460 both in vitro and in vivo. 	32059342
LINC00460	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Regulation[miR-489-5p/FGF7/AKT axis]	RNA Pull-Down//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We demonstrated that lncRNA Linc00460 was upregulated in breast cancer, and its expression level was positively associated with lymphatic metastasis and poor overall survival.  Linc00460 was identified as a direct target of miR-489-5p, which further targeted FGF7 and exerted oncogenic functions in breast cancer. Mechanistically, Linc00460 served as a competing endogenous RNA of FGF-7 mRNA by sponging miR-489-5p, resulting in upregulated FGF7 expression and AKT activity. Notably, forced expression of miR-489-5p abrogated Linc00460-mediated oncogenic behavior and activation of the FGF7-AKT pathway in breast cancer cells.	We demonstrated that lncRNA Linc00460 was upregulated in breast cancer, and its expression level was positively associated with lymphatic metastasis and poor overall survival. 	Yes	Forced expression of Linc00460 increased, whereas Linc00460 silencing decreased, breast cancer cell viability, migration and invasion both in vitro and in vivo. 	31308741
LINC00460	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Regulation[LINC00460/miR-485-5p/Raf1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 LINC00460 was upregulated in PTC tissues and cells. Raf1 was upregulated in PTC tissues, but miR-485-5p was down-regulated.Bioinformatics prediction revealed that LINC00460 had binding sites with miR-485-5p, which was validated by luciferase reporter assay. In addition, miR-485-5p was confirmed to directly target Raf1 3'-UTR. Moreover, LINC00460 promoted PTC progression by sponging miR-485-5p to elevate the expression of Raf1. Knockdown of LINC00460 restrained tumor growth in vivo.	High LINC00460 expression was associated with poor prognosis.	Yes	 LINC00460 knockdown suppressed proliferation, migration, invation and EMT of PTC cells. 	31870440
LINC00520	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 (NSCLC) tissue and cells	Interaction(miR-577/CCNE2 axis)	qRT-PCR//ChIP//RIP//Western Blot	In this paper, our group first showed that LINC00520 level was elevated in non-small cell lung cancer (NSCLC) tissue and cells. Mechanistically, we found that LINC00520 serving as a competing endogenous RNA to be involved in the modulation of miR-577 expressions, and thus affected the expression of CCNE2 which was a target gene of miR-577.	Increased LINC00520 was distinctly correlated with advanced tumor stage and shorter survival time in NSCLC patients. 	Yes	Moreover, in NSCLC cells with si-LINC00520, up regulation of CCNE2 led to an increase of cell growth and invasion.	33728585
LINC00332	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation(MMP-13 )	Wound Healing Assay//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	The expressions of LINC00332 and MMP-13 were significantly downregulated and upregulated in GC tissues, respectively.  A significant inverse correlation between LINC00332 and MMP-13 mRNA expression was observed in tumor samples. 		Yes	The mRNA expression level of mesenchymal markers, stem cell factors, and MMP genes were significantly decreased after the LINC00332 ectopic expression, while epithelial markers expression was significantly increased. The LINC00332 overexpression markedly repressed proliferation, migration, and invasion and did not induce apoptosis in AGS cells.  In addition, LINC00332 overexpression notably promoted the E-cadherin protein expression.	35787995
LINC00324	LncRNA	Homo sapiens	Colorectal Neoplasms	 cell lines	Interaction[ targeting miR-214-3p]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 We first detected the expression of LIN00324 was increased while miR-214-3p was decreased in CRC cells. Moreover, overexpression of miR-214-3p also inhibited CRC cell proliferation, migration and invasion. Then, we identified miR-214-3p as directly target of LINC00324 and the expression of miR-214-3p was downregulated by LINC00324. In addition, inhibiting miR-214-3p reversed the effects of LINC00324 on CRC cell proliferation, migration and invasion.		Yes	 Knockdown of LIN00324 suppressed proliferation, migration and invasion in SW620 and HCT15 cells. 	31858541
LINC00324	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissue and cell lines	regulation[ downregulation of TRIM29 via upregulating microRNA-195-5p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ChIP	Levels of LINC00324 were markedly up-regulated in PTC. In short, this work demonstrates that LINC00324 knockdown inhibits the proliferation and invasion of PTC cells by decreasing TRIM29 expression via up-regulating miR-195-5p expression.		Yes	Silencing of LINC00324 significantly repressed the proliferation and invasion of PTC cells. 	33318312
LINC00324	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines 	Interaction[regulating WDR66]	qRT-PCR	We first validated the upregulation of LINC00324 in OS tissues and cell lines and established its correlation with OS tumor progression and metastasis.In conclusion, the present study proved that LINC00324 accelerated the proliferation and migration of osteosarcoma cells through regulating WDR66, providing a new prognostic target for osteosarcoma.	We first validated the upregulation of LINC00324 in OS tissues and cell lines and established its correlation with OS tumor progression and metastasis.	Yes	Gain- and loss-of-function assays revealed that LINC00324 accelerated cell proliferation and migration in OS. 	31225659
LINC00324	LncRNA	Homo sapiens	Ovarian Neoplasms	IOT tissues and cells	interaction[miR-214-5p-CDK6/CCND1/MDM2/MDM4 network]	qRT-PCR	According to the results, LINC00324 was upregulated in IOT tissues and cells, as determined by reverse transcription?quantitative PCR, and its depletion impaired cell proliferation ability and improved cell apoptosis ability in IOT. Taken together, these results demonstrated that LINC00324 could serve as a competing endogenous RNA to facilitate IOT cell proliferation by regulation of miR‑214‑5p‑CDK6/CCND1/MDM2/MDM4 network, which possibly provide a novel therapeutic target for IOT.		Yes	According to the results, LINC00324 was upregulated in IOT tissues and cells, as determined by reverse transcription?quantitative PCR, and its depletion impaired cell proliferation ability and improved cell apoptosis ability in IOT.	33416104
LINC00319	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Regulation[miR-423-5p/NACC1 pathway]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 In this study, LINC00319 expression was found to be upregulated in ovarian cancer tissues and cell lines.In conclusion, our findings demonstrated that LINC00319 promotes ovarian cancer progression through upregulating NACC1 expression by restraining miR-423-5p.		Yes	Cell Counting Kit-8 (CCK-8), colony formation and transwell assays indicated that LINC00319 upregulation promoted proliferation, migration and invasion of ovarian cancer cells.	30442370
LINC00319	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues	Regulation[miR-4492/ROMO1 axis]	qRT-PCR	In our research, LINC00319 was shown to be an upregulated lncRNA in BCa tissues.In addition, the data indicated LINC00319 was a sponge for miR-4492 and miR-4492 suppressed ROMO1 expression in BCa. Furthermore, our results illustrated miR-4492/ROMO1 axis regulates proliferation, migration, and invasion and LINC00319 exerts oncogenic roles through modulating miR-4492/ROMO1 axis. In sum, this study suggested that LINC00319 acts as oncogenic roles in BCa progression.		Yes	 Silencing of LINC00319 suppressed BCa proliferation and invasiveness.	31608995
LINC00319	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	regulation[miR-199a-5p/FZD4 axis]	Western Blot//CCK8//qRT-PCR//FISH//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The present study using lncRNA sequencing found LINC00319 to be significantly upregulated in OSCC cells subjected to rCCL18 stimulation. Taken together, these results evidenced a mechanism of CCL18 action in OSCC mediated through the LINC00319/miR-199a-5p/FZD4 signaling pathway, which may comprise a potential target for OSCC therapeutic development.		Yes	 Furthermore, LINC00319 knockdown was found to attenuate the carcinogenic function of CCL18 in OSCC, reducing OSCC proliferation, metastasis, epithelial-mesenchymal transition (EMT), and angiogenesis.Functionally, in vitro and in vivo experiments showed that LINC00319 promoted OSCC growth and metastasis via downregulating miR-199a-5p and upregulating FZD4.	32948745
LINC00319	LncRNA	Homo sapiens	Osteosarcoma	tumor cells and tissue	regulation[miR-455-3p/NFIB axis]	qRT-PCR//Luciferase Report Assay//FISH	PCR results showed that lncRNA LINC00319 exhibited high expression in tumor cells and tissue. lncRNA LINC00319 may promote OS progression by regulating the miR-455-3p/NFIB axis, which probably serves as an innovative potential indicator of prognosis and a target of therapy for OS.		Yes	Knockdown of lncRNA LINC00319/NFIB or overexpression of miR-455-3p blocked the migration of OS cells. 	32621625
LINC00319	LncRNA	Homo sapiens	Glioma	glioma tissues	Expression[highly expressed]	CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//ChIP	 In our study, LINC00319 was expressed at high levels in glioma and closely associated with poor prognosis of patients with glioma, whose knockdown impaired cell proliferation, arrested cell cycle and induced cell apoptosis of glioma.	 In our study, LINC00319 was expressed at high levels in glioma and closely associated with poor prognosis of patients with glioma, whose knockdown impaired cell proliferation, arrested cell cycle and induced cell apoptosis of glioma.	Yes	 In our study, LINC00319 was expressed at high levels in glioma and closely associated with poor prognosis of patients with glioma, whose knockdown impaired cell proliferation, arrested cell cycle and induced cell apoptosis of glioma.	31325436
LINC00319	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Regulation[LINC00319/miR-1207-5p/KLF12 pathway]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//IHC	It was indicated that LINC00319 was markedly increased in NPC tissues and cells in comparison to their corresponding controls. Taken together, our study discovered the oncogenic role of LINC00319 in clinical specimens and cellular experiments, showing the potential LINC00319/miR-1207-5p/KLF12 pathway.		Yes	Silence of LINC00319 was able to suppress NPC cell growth in vitro while overexpression of LINC00319 inversed this process.	30243935
LINC00313	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 H1299-derived exosomes	Interaction(miR-135a-3p /STAT6)	qRT-PCR//Luciferase Report Assay//Western Blot	LINC00313 was overexpressed in H1299-derived exosomes, and its knockdown abolished the effect of H1299-induced M2 macrophage differentiation. LINC00313 sponged miR-135a-3p to increase the STAT6 expression, resulting in the M2 macrophage differentiation. 		Yes	LINC00313 was overexpressed in H1299-derived exosomes, and its knockdown abolished the effect of H1299-induced M2 macrophage differentiation. LINC00313 sponged miR-135a-3p to increase the STAT6 expression, resulting in the M2 macrophage differentiation. 	35980503
LINC00313	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-342-3p/FOSL2 axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	 LINC00313 was upregulated and miR-342-3p was downregulated in OS tissues and cells. LINC00313 is upregulated in OS, and LINC00313 knockdown plays a vital anti-tumor role in OS cell progression through a miR-342-3p/FOSL2 axis. 	High expression of LINC00313 was associated with shorter overall survival.	Yes	LINC00313 knockdown suppressed tumor growth in vivo.	32390359
LINC00313	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical carcinoma tissues and cells	Interaction(miR-4677-3p/CDK6 Axis)	In Vivo Experiment//Western Blot//Transwell Assay//Wound Healing Assay//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//IF	Our data showed that the levels of LINC00313 in cervical carcinoma tissues and cells were significantly up-regulated. Luciferase reporter assay confirmed that miR-4677-3p/CDK6 regulatory axis is the direct downstream of LINC00313. Functional gain- and loss-of-function strategies further showed that LINC00313 induced the up-regulation of CDK6 expression through competitive binding with miR-4677-3p, leading to promote the progression of cervical carcinoma.		Yes	Functionally, LINC00313 accelerated the progression, migration, and EMT of SiHa and Hela cells. 	33824592
LINC00312	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Regulation[miR‑9/CDH1 axis]	qRT-PCR	 In the present study, LINC00312 was found to be downregulated in human BC tissues and cell lines by RT‑qPCR. Mechanistically, LINC00312 was found to induce suppression of cell migration and invasion by directly binding to miR‑9. Overexpression of LINC00312 increased the expression of cadherin 1 (CDH1), a direct target of miR‑9, and decreased the expression of vimentin (VIM), a major cytoskeletal component of mesenchymal cells as determined by western blot analysis. miR‑9 partly abrogated the upregulation of CDH1 and downregulation of VIM induced by LINC00312. Taken together, the results of the present study indicate a role for the LINC00312/miR‑9/CDH1 axis in the progression of BC, and suggest a novel lncRNA‑based diagnostic biomarker or therapeutic target for BC.		Yes	The findings of a functional study indicated that overexpression of LINC00312 suppressed the proliferation, colony forming ability, migration and invasiveness of BC cell lines.	31894332
LINC00312	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell	Regulation[LINC00312-miR-21-PTEN axis ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Here, we found that LINC00312 is underexpressed in CRC tissues and cell lines. Taken together, our results elucidate the role of the LINC00312-miR-21-PTEN axis in CRC cell proliferation and tumour progression and may lead to new lncRNA-based diagnostics or therapeutics for CRC.		Yes	 Functional experiments suggested that LINC00312 suppresses growth, migration and invasion of CRC cells in vitro and attenuates tumour proliferation and metastasis in vivo.	30134003
LINC00312	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tissues and cell lines	Regulation[ PI3K/Akt signaling pathway]	CCK8//qRT-PCR//EdU Staining//Transwell Assay	The expression of LINC00312 was significantly decreased in TC tissues and cell lines.LINC00312 can act as a tumor-suppressor in TC by attenuating the PI3K/Akt signaling pathway, and LINC00312 could be a novel diagnosis biomarker and a promising therapeutic target for TC patients.		Yes	 In an in vitro experiment, si-LINC00312 significantly promoted the invasion and proliferation of TC cells. Conversely, overexpression of LINC00312 decreased cell proliferation and invasion in vitro, and decreased tumorigenicity in TC xenograft models in nude mice. 	29969438
LINC00304	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues,cell lines	Interaction[regulating CCNA1]	qRT-PCR//Microarray	We observed higher expression of LINC00304 in PCa cells and samples compared with normal prostate cells and tissues.  Further, we identified androgen-inhibited lncRNA, LINC00304 as a direct target of AR. A series of functional studies revealed that overexpression of LINC00304 could significantly promote cell proliferation and cell cycle progression in PCa cells. We also find that LINC00304 can significantly promote CCNA1 expression in PCa cells.		Yes	 Functional analysis of LINC00304 showed it was related to regulating cell cycle process, cellular developmental process, and focal adhesion. 	31012142
LINC00301	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC clinical specimens or cell lines	regulation[FOXC1/LINC00301/EZH2/EAF2/pVHL/HIF1α and FOXC1/LINC00301/miR-1276/HIF1α pathways]	RNA Pull-Down//qRT-PCR//RIP//FISH//ChIP	LINC00301 is highly expressed in NSCLC and closely corelated to its prognosis by analyzing the relationship between differentially expressed lncRNAs and prognosis in NSCLC samples.  In summary, our present research revealed the oncogenic roles of LINC00301 in clinical specimens as well as cellular and animal experiments, illustrating the potential roles and mechanisms of the FOXC1/LINC00301/EZH2/EAF2/pVHL/HIF1α and FOXC1/LINC00301/miR-1276/HIF1α pathways, which provides novel insights and potential theraputic targets to NSCLC.		Yes	 in vitro and in vivo experiments revealed that LINC00301 facilitates cell proliferation, releases NSCLC cell cycle arrest, promotes cell migration and invasion, and suppresses cell apoptosis in NSCLC. 	32878637
LINC00299	LncRNA	Homo sapiens	Atherosclerosis	atherosclerotic plaques,blood	Regulation[Linc00299/miR-490-3p/AURKA axis ]	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//migration assay//Cell Apoptosis Assay	Expressions of Linc00299 and miR-490-3p were upregulated and downregulated in atherosclerosis patients, respectively.Our study reveals an important effect of Linc00299/miR-490-3p/AURKA axis on regulating cell proliferation and migration in atherosclerosis.		Yes	Both Linc00299 knockdown and miR-490-3p overexpression suppressed cell proliferation, increased apoptosis and inhibited migration of VSMCs and HUVECs. 	30734057
LINC00324	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	regulation[miR-139-5p/IGF1R axis]	qRT-PCR//MTT//Transwell Assay//Western Blot	 In NSCLC, the high expression of LINC00324 had correlation with the poor prognosis.Highly expressed LINC00324 in NSCLC through sponged miR-139-5p to elevate IGF1R expression and promoted cell proliferation and invasion. This research demonstrated that LINC00324 is a potential NSCLC diagnosis and therapy target.	 In NSCLC, the high expression of LINC00324 had correlation with the poor prognosis.	Yes	LINC00324 promoted the proliferation and invasion of NSCLC cells while miR-139-5p inhibited these behaviors. 	32734536
LINC00339	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	cell lines	Regulation[miR-377-3p/HOXC6 signaling pathway]	Western Blot//qPCR//Flow Cytometry//RIP//MTT//Luciferase Report Assay	 Linc00339 was increased in breast cancer cell lines compared with the normal epithelial cell.In conclusion, our results illuminated that the novel Linc00339/miR-377-3p/HOXC6 axis played a critical role in TNBC progression and might be a promising therapeutic target for TNBC treatment.		Yes	Through in vitro and in vivo experiments, Linc00339 overexpression promoted triple-negative breast cancer (TNBC) proliferation, inhibited cell cycle arrest, and suppressed apoptosis. Silencing of Linc00339 obtained the opposite effects.	30618083
LINC00459	LncRNA	Homo sapiens	Melanoma	melanoma cell lines and tissues	Interaction[sponging miR-218 to elevate DKK3]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	The results demonstrated decreased LINC00459 in melanoma cell lines and tissues.In conclusion, our analysis suggested that the LINC00459 could sponge miR-218 and increase the expression of DKK3 gene, thus inhibiting the invasion and proliferation of melanoma cells, which indicated that the LINC00459 could be an effective biomarker for melanoma and its potential as the therapeutic target.		Yes	 According to the in-vitro and in-vivo experiments, up-regulated LINC00459 had inhibitory effect on cell proliferation and invasion.	31844121
LINC00339	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Interaction[miR-148a-3p/ROCK1 axes]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	LINC00339 was overexpressed in ovarian cancer tissues, showed a poor prognosis in patients with ovarian cancer, and correlated with tumor size and advanced clinical stages. LINC00339 regulated ovarian cancer cell proliferation, migration, and invasion by targeting miR-148a-3p/ROCK1 axes, which provided novel insights for ovarian cancer diagnosis and therapy.	LINC00339 was overexpressed in ovarian cancer tissues, showed a poor prognosis in patients with ovarian cancer, and correlated with tumor size and advanced clinical stages. 	Yes	Upregulation of LINC00339 promoted cell proliferation, migration, and invasion, while downregulation of LINC00339 exhibited an opposite effect. LINC00339 promotedin vivo tumor growth.	31550677
LINC00452	LncRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer cells and tumor tissues 	interaction[ sponging miR-501-3p]	Co-IP//qRT-PCR//RIP//MTT//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	This study identified a novel lncRNA LINC00452 being elevated in both ovarian cancer cells and tumor tissues in patients. Irrespective of its miRNA sponge function, LINC00452 is capable of preventing ROCK1 protein from ubiquitin/proteasome-mediated degradation via their mutual physical interaction.	 Such aberrant expression of LINC00452 was negatively correlated with relapse-free survival of ovarian cancer patients.	Yes	Overexpression of LINC00452 potentiated CaOV3 cell viability, migration and invasion in vitro as well as xenograft tumor growth in vivo.	33168781
LINC00449	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues 	Expression[highly expressed]	qRT-PCR	 Among these, two lincRNAs (LINC01270 and LINC00449) were significantly associated with both worse overall survival and DFS and were expressed at significantly higher levels in tumor tissues compared with adjacent normal breast tissues (log2[Fold Change] > 0.5 and FDR < 0.05). 		Yes	We further evaluated the potential functions of LINC01270 and LINC00449 using in vitro functional experiments and found that siRNA-mediated knockdown of LINC01270 and LINC00449 expression significantly decreased cell viability, colony formation and cell migration ability in TNBC cells (P < 0.05).	33247132
LINC00423	LncRNA	Homo sapiens	Retroperitoneal liposarcoma	RLS tissues	Regulation[MAPK signaling pathway]	RNA Pull-Down//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay//IF	We found that long intergenic noncoding RNA 423 (linc00423) was downregulated in RLS tissues.Summing up, our findings demonstrated that linc00423 acted as the tumor suppressor in RLS cells through regulating the protein level of NFATC3 at a post-transcriptional level and negatively regulated the MAPK signaling pathway at a transcriptional level.		Yes	Gain-of-function assays revealed that overexpressed linc00423 obviously inhibited RLS cell growth in vitro and in vivo.	31160581
LINC00365	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[ NF-κB signaling]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	lncRNA LINC00365, which is expressed at a low level in breast cancer. Secretoglobin family 2A member 1 (SCGB2A1) was identified as a potential target protein regulated by LINC00365. The results of the present study demonstrated that the overexpression of LINC00365 and SCGB2A1 inhibited cell viability and induced cell apoptosis through the inhibition of the NF-κB signaling pathway in breast cancer cells. 		Yes	The results of the present study demonstrated that the overexpression of LINC00365 and SCGB2A1 inhibited cell viability and induced cell apoptosis through the inhibition of the NF-κB signaling pathway in breast cancer cells. 	31897191
LINC00365	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LAD patients and cells	Interaction(miR-429/KCTD12 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	 LINC00365 was low expressed in the LAD patients and cells, associating with poor outcome. LINC00365 inhibited KCTD12 expression by sponging miR-429. miR-429 up-regulation and KCTD12 down-regulation partial reversed LINC00365 inhibition on H1975 cells malignant phenotype. Thus, LINC00365 inhibited LAD progression and glycolysis via targeting miR-429/KCTD12 axis. LINC00365 might be a potential candidate for LAD target treatment clinically.	 LINC00365 was low expressed in the LAD patients and cells, associating with poor outcome. 	Yes	LINC00365 up-regulation attenuated H1975 cells proliferation, migration, invasion, glycolysis and in vivo growth. 	35426242
LINC00356	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		regulation[CDK1/CCNB1 Axis]	qRT-PCR//Luciferase Report Assay//RIP	The results showed that LINC00356, CDK1 and CCNB1 were highly expressed in HCC, while miR-199a-3p was lowly expressed.These results proved that LINC00346 could regulate the expression of CDK1/CCNB1 through the competitive adsorption of miR-199a-3p, thereby affecting the p53 signaling pathway and finally regulating the apoptosis, invasion and cell cycle of HCC cells. 		Yes	Overexpressing LINC00460 and silencing miR-199a-3p promoted cell invasion, inhibited apoptosis of HCC, and arrested the cell cycle in S phase while opposite results were obtained when silencing LINC00346, CDK1, and CCNB1. LINC00346 indirectly affects liver cancer by promoting the expression of CDK1/CCNB1 through competitive adsorption of miR-199a-3p. 	32133348
LINC00355	LncRNA	Homo sapiens	Stomach Neoplasms	cell lines,tissues 	regulation[P53]	Wound Healing Assay//CCK8//qRT-PCR//FISH//RNA-seq//IP//Transwell Assay	The results showed that LINC00355 was significantly increased in gastric cancer cell lines and patient tissues and closely correlated with late stages, distant metastasis, and poor prognosis of patients. These results indicated that LINC00355 induces gastric cancer cell proliferation and invasion by promoting transcription of RAD18 and UBE3C, which mediates ubiquitination of P53 and thereby plays a critical role in survival and tumorigenicity of gastric cancer cells. 	The results showed that LINC00355 was significantly increased in gastric cancer cell lines and patient tissues and closely correlated with late stages, distant metastasis, and poor prognosis of patients. 	Yes	High expression of LINC00355 promoted the proliferation and invasion of gastric cancer cells in vivo and in vitro.	33083020
LINC00355	LncRNA	Homo sapiens	Colonic Neoplasms	cell line	regulation[ GTF2B/IGFBP2 axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 LncRNA LINC00355 was highly expressed in colon cancer cells. In summary, downregulation of lncRNA LINC00355 in colon cancer inhibited tumor growth in colon cancer through effects on the GTF2B/IGFBP2 axis.		Yes	LncRNA LINC00355 was highly expressed in colon cancer cells, and overexpression of lncRNA LINC00355 increased the expression of IGFBP2 and GTF2B, and thereby promoted the proliferation, chemotaxis, invasion, and migration in colon cancer.	33227664
LINC00355	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[ MiR-6777-3p/Wnt10b axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	The present study revealed that LINC00355:8 was significantly upregulated in HCC, promoted HCC cell proliferation, migration and invasion in vitro and enhanced tumour growth in vivo. Our findings indicate that LINC00355:8 activates Wnt10b and promotes HCC progression via the suppression of miR-6777-3p, which may provide novel therapeutic targets for HCC.		Yes	The present study revealed that LINC00355:8 was significantly upregulated in HCC, promoted HCC cell proliferation, migration and invasion in vitro and enhanced tumour growth in vivo.	32913459
LINC00355	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer patients and cells	Interaction(miR-424-5p/HMGA2 axis)	qRT-PCR//RNA Pull-Down	LINC00355 was upregulated in bladder cancer patients, especially in patients with higher TNM stage. . Furthermore, LINC00355 could regulate HMGA2 expression by acting as a sponge for miR-424-5p. Overexpression of HMGA2 induced EMT of bladder cancer cells. Additionally, LINC00355 regulated the migration, invasion, and EMT ability of bladder cancer cells through modulating HMGA2 expression via sponging miR-424-5p.	LINC00355 was upregulated in bladder cancer patients, especially in patients with higher TNM stage. Elevated LINC00355 was correlated with the poor prognosis of bladder cancer patients. 	Yes	Besides, overexpressed LINC00355 promoted migration, invasion, and epithelial-mesenchymal transition (EMT) ability of bladder cancer cells.  Contrarily, decreased LINC00355 suppressed migration, invasion, and EMT ability of bladder cancer cells, and lung metastasis of xenograft tumors. 	34641698
LINC00355	LncRNA	Homo sapiens	Glioma	glioma cell lines and specimens	Interaction(miR-1225/FNDC3B)	Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 LINC00355 expression was increased in glioma cell lines and specimens, and higher LINC00355 expression predicted advanced clinical progress and reduced overall survival and disease-free survival in glioma patients. Mechanistic assays revealed that LINC00355 as a sponge for miR-1225 repressed fibronectin type III domain-containing 3B (FNDC3B) expressions.		Yes	Functionally, LINC00355 depletion promoted cell proliferation, invasion, and migration in glioma cells and induced apoptosis of glioma cells, whereas LINC00355 upregulation resulted in the opposite effects in vitro. 	34603558
LINC00355	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung adenocarcinoma tissues and cell lines	Interaction[down-regulating miR-195 and up-regulating the expression of CCNE1]	Other	Initially, we uncovered increased LINC00355 expressions in lung adenocarcinoma tissues and cells. Moreover, silencing LINC00355 by shRNA inhibited the cyclin E1 (CCNE1) gene expression via miR-195 in lung adenocarcinoma cells. Collectively, this study demonstrates the novel lncRNA LINC00355 in regulatory network of CCNE1 via miR-195 in lung adenocarcinoma, highlighting LINC00355 as a new target for the treatment of lung adenocarcinoma.		Yes	 Functionally, our findings demonstrated that LINC00355 silencing suppressed the proliferation in vitro and in vivo. Simultaneously, silencing LINC00355 by shRNA resulted in suppressed proliferation, colony formation and promoted cell cycle arrest and apoptosis via miR-195. 	31689506
LINC00342	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-545-5p/CNPY2 axis)	In Vivo Experiment//IHC//Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//IF	 LINC00342 was significantly upregulated in GC tissues and cell lines. Functional experiments showed that LINC00342 regulated the expression of canopy fibroblast growth factor signaling regulator 2 (CNPY2) by competitively sponging miR-545-5p. 		Yes	 Silencing of LINC00342 efficiently inhibited proliferation, migration and invasion of AGS cells in vitro, and also suppressed the tumorigenesis of GC in vivo.	34715819
LINC00342	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Interaction[targeting miR-203a-3p]	qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression of LINC00342 was increased in NSCLC tissues and cells compared with normal tissues and cells. Briefly, LINC00342 contributes to NSCLC cells growth and metastasis via targeting miR-203a-3p competitively.		Yes	Knockdown of LINC00342 suppressed cell proliferation, colony formation, migration, and invasion.	31539128
LINC00342	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-19a-3p/NPEPL1 axis)	qRT-PCR//Western Blot	 LINC00342 was highly expressed in CRC. Mechanistic investigation revealed that LINC00342 might sponge miR-19a-3p to regulate NPEPL1 expression. Further investigation indicated that the ontogenesis facilitated by LINC00342 was inhibited due to the depletion of NPEPL1.		Yes	Down-regulation of LINC00342 inhibited cell proliferation and metastasis of CRC cells. Moreover, knocking down LINC00342 inhibited the tumor growth in vivo. 	33588834
LINC00342	LncRNA	Homo sapiens	Adenocarcinoma of Lung	A549 cells & lung cancer cell lines	Interaction(miR-15b/TPBG)	Luciferase Report Assay//Bioinformatics Analysis	LINC00342 was found to be up-regulated in lung adenocarcinoma. The high expression of LINC00342 was also validated in lung cancer cell lines. LINC00342 induced invasion and epithelial-mesenchymal transition (EMT) process of A549 cells. By analyzing GEO datasets, TPBG was confirmed positively correlated to LINC00342 and highly expressed in lung adenocarcinoma. In addition, TPBG induced invasion and EMT process of A549 cells. Through bioinformatics analysis and luciferase assay, miR-15b was validated as a direct target of both LINC00342 and TPBG. Ectopic miR-15 expression repressed LINC00342 and TPBG. Interestingly, LINC00342 overexpression inhibited miR-15b and induced TPBG, whereas ectopic TPBG unchanged LINC00342 and miR-15b levels. In conclusion, LINC00342 promotes metastasis of lung adenocarcinoma through inducing TPBG targeted by miR-15b.		Yes	Interestingly, LINC00342 overexpression inhibited miR-15b and induced TPBG, whereas ectopic TPBG unchanged LINC00342 and miR-15b levels.	35452205
LINC00342	LncRNA	Homo sapiens	Carcinoma, Renal Cell	Eleven pairs of cancer tissues and adjacent normal tissues and  ccRCC cells	Expression [highly expressed]	qRT-PCR//Wound Healing Assay//Migration Assay	Clinical samples validated expression levels of three-glycolysis-related lncRNAs, and LINC00342 demonstrated the most significant aberrant expression.  in vitro, the general overexpression of LINC00342 was detected in ccRCC cells. 		Yes	After silencing LINC00342, the aberrant glycolytic levels and migration abilities in 786-O cells were decreased significantly, which might be explained by suppressed Wnt/β-catenin signaling pathway and reversed Epithelial mesenchymal transformation (EMT) process.	35083240
LINC00339	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Interaction[downregulating miR-218]	qRT-PCR//MTT	 LINC00339 expression was significantly increased in colorectal cancer tissues compared with adjacent colorectal tissues (4.69±1.52 vs 1.02±0.38, P<0.05).  LINC00339 expression was negatively correlated with miR-218 expression in colorectal cancer tissues (P<0.05). miR-218 mimics remarkably suppressed the fluorescence intensity of wild-type LINC00339 plasmid (P=0.001), but did not affect the fluorescence intensity of the mutant ones(P=0.88). Compared with cells transfected with LINC00339 siRNA only, downregulation of miR-218 elevated proliferation and decreased apoptosis of LoVoand HCT116 cells.	LINC00339 expression was not related to the age and gender of patients (P>0.05), but was associated with TNM stage, lymphatic metastasis, tumor maximum diameters, and differentiation degree (all P<0.05). 	Yes	Knockdown of LINC00339 remarkably inhibited proliferation, but promoted apoptosis of LoVo and HCT116 cells (all P<0.05).	31269584
LINC00339	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[miR-1182/SKA1 pathway]	ISH//qRT-PCR//CCK8//Transwell Assay	 LINC00339 overexpression was correlated with an advanced stage, metastasis, and bad prognosis in HCC patients.Mechanistically, LINC00339 could interact with miR-1182 to promote SKA1 expression. We also demonstrated that SKA1 acted as an oncogene and SKA1 upregulation reversed the effect of LINC00339 silencing.		Yes	Functional investigation showed that LINC00339 knockdown significantly suppressed HCC cell proliferation, migration, and invasion. Moreover, decreased LINC00339 expression inhibited HCC growth in vivo. 	31239716
LINC00467	LncRNA	Homo sapiens	Glioma	 tumor samples	regulation[p53 ,DNMT1]	CCK8//qRT-PCR//Flow Cytometry//RIP//EdU Staining//Transwell Assay	The expression of LINC00467 was significantly up-regulated in tumor samples than that in normal samples, which was not correlated with patient survival time.These results indicated that high expression of LINC00467 could promote proliferative and invasive abilities of glioma cells through targeting inhibition of p53 expression by binding to DNMT1.	The expression of LINC00467 was significantly up-regulated in tumor samples than that in normal samples, which was not correlated with patient survival time.	Yes	Upregulation of LINC00467 promoted proliferative and invasive abilities, and accelerated cell cycle in G0/G1 phase of U87 and LN229 cells. 	32226508
LINC00467	LncRNA	Homo sapiens	Glioma	cell lines	regulation[E2F3,miR-200a]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 LINC00467 was up-regulated in glioma cells. INC00467 promoted the development of glioma by inhibiting miR-200a and promoting E2F3 expression.		Yes	Knockdown of LINC00467 inhibited the viability, migration and invasion of glioma cells. 	32684096
LINC00467	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML specimens and cell lines	Interaction(miR-339/SKI pathway)	qRT-PCR//Western Blot	we find that LINC00467 expression is significantly increased in AML specimens and cell lines.  Interestingly, microRNA-339 (miR-339) is upregulated and its target gene SKI, an oncogene, is downregulated in AML cells after LINC00467 knockdown.  More importantly, inhibition of miR-339 can largely abolish the effect of LINC00467 knockdown on AML cells. 		Yes	 Further investigations show that knockdown of LINC00467 inhibits the malignant phenotypes of AML cells. Consistently, LINC00467 knockdown slows AML progression in immunodeficient mice.	33054480
LINC00511	LncRNA	Homo sapiens	Osteoarthritis	cell lines	regulation[LINC00511/miR-150-5p/SP1]	qRT-PCR	 Functionally, the functional experiments found that LINC00511 expression was upregulated in the IL-1β-stimulated chondrocyte (ATDC5).  In conclusion, our findings highlight the function and prognostic value of LINC00511/miR-150-5p/SP1 feedback loop in OA and extend the importance of lncRNA epigenetics in OA biology.		Yes	 Knockdown of LINC00511 facilitated proliferation, and repressed the apoptosis and extracellular matrix (ECM) synthesis of chondrocyte.	32635763
LINC00511	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction[sponging miR-618 ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC00511 overexpression was observed in OS tissues and cell lines.LINC00511 was confirmed to be beneficial for osteosarcoma development via sponging miR-618 and increasing MAEL expression and may thus be considered a potential target for osteosarcoma therapy.		Yes	Knockdown of LINC00511 in nude mice inhibited the tumorigenic ability of OS cells.Transfection-induced overexpression of LINC00511 and MAEL, as well as downregulation, highlighted the features of tumor cells, and LINC00511 overexpression reduced apoptosis in vitro.	31386627
LINC00511	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	regulation[miR-185-3p/E2F1 Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	It is significantly higher in the clinical samples of osteosarcoma patients than in normal adjacent cancer tissues. The dual-luciferase reporter assay verified the direct interaction between miR-185-3p and LINC00511 or E2F1.	 The present study shows the higher expression levels of LINC00511 correlates to a shorter overall survival and disease-free survival time in patients with sarcoma.	Yes	 The results showed that the LINC00511 knockdown significantly suppressed osteosarcoma cell growth and metastasis.	32964019
LINC00511	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC cell lines and patient specimens 	Interaction(miR-29b-3p/VEGFA)	qRT-PCR//Western Blot//FISH	The aberrant up-regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. Mechanistically, linc00511 could up-regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa-miR-29b-3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. 	An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis.	Yes	Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. 	28984028
LINC00511	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	Expression[highly expressed]	qRT-PCR	 In our study, we found LINC00511 expression levels were increased in cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cell line, respectively. 	 High LINC00511 expression was correlated with advanced clinical stage, large tumor size, histological type of adenocarcinoma, and present lymph node metastasis, distant metastasis, and poor overall survival in cervical cancer patients. 	Yes	The in vitro studies indicated that knockdown of LINC00511 inhibited cervical cancer cell proliferation, migration, and invasion. In conclusion, LINC00511 acts as oncogenic lncRNA in cervical cancer, and may be a novel biomarker and potential therapeutic target for cervical cancer patients.	31434692
LINC00511	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissue,cell lines 	regulation[miR-324-5p/DRAM1 Axis]	Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay	Herein, the results showed that LINC00511 was significantly up-regulated in cervical cancer and cell lines and mainly distributed in the cytoplasm of cervical cancer cells.  Collectively, these results suggest that LINC00511 functions as a competing endogenous RNA (ceRNA) to regulate the miR-324-5p/DRAM1 axis, leading to HPV-negative and HPV-positive cervical cancer aggravation.		Yes	Loss-of-function experiments indicated that silencing of LINC00511 inhibited the proliferation and invasion of both HPV-negative and HPV-positive cervical cancer cells, as well as promoted apoptosis by regulating the Bcl-2/Bax axis and Caspase 3 activation.	33116605
LINC00511	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	regulation[RXRA-regulated PLD1]	qRT-PCR	 LINC00511 and PLD1 expressions were remarkably high in cervical cancer tissues and cells.Collectively, this study suggests that LINC00511 acts as an oncogenic lncRNA in cervical cancer via the promotion of transcription factor RXRA-regulated PLD1.		Yes	 Si-LINC00511, si-RXRA or si-PLD1 triggered repression of proliferation and promotion of autophagy and apoptosis of cervical cancer cells. In vivo experiment, si-LINC00511, or si-PLD1 inhibited the tumorigenic ability of nude mice. 	32067228
LINC00511	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Interaction(miR-497-5p/MAPK1 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	 Up-regulation of LINC00511 expression in CC tissues and cell lines was observed, which was in association with tumor size, clinical stage and lymph node metastasis of the patients. Mechanistically, LINC00511 was capable of targeting miR-497-5p and up-regulating MAPK1 expression.	 Up-regulation of LINC00511 expression in CC tissues and cell lines was observed, which was in association with tumor size, clinical stage and lymph node metastasis of the patients. 	Yes	 LINC00511 overexpression facilitated the proliferation, migration and invasion of CC cells, while opposite effects were observed after knockdown of LINC00511. 	36103025
LINC00511	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LAC tissues and cell lines (H1299 and A549)	regulation[ LINC00511/miR-625-5p/PKM2 ]	CCK8//qRT-PCR//Transwell Assay	 Data from our study demonstrated that LINC00511 expression was increased in LAC tissues and cells in comparison to their corresponding controls.The present study showed that LINC00511 was involved in LAC progression by targeting miR-625-5p/PKM2, indicating that LINC00511/miR-625-5p/PKM2 may function as promising therapeutic targets for LAC.	Moreover, overexpression of LINC00511 indicated the poor prognosis of LAC patients.	Yes	Overexpression of LINC00511 promoted proliferation, invasion and migration capacities of LAC cells. 	32716147
LINC00511	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	Interaction(miR-195-5p/GCNT3 )	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//Transwell Assay	 LINC00511 and GCNT3 were found to be upregulated in LUAD, while miR-195-5p was downregulated.  Interference with miR-195-5p promoted malignant proliferation of cancer cells. miR-195-5p expression was affected by LINC00511and targeted GCNT3.		Yes	 Silencing LINC00511 or GCNT3 decreased the proliferation, migration, invasion, and Bcl-2 protein content in LUAD cells and increased the expression of Bax. 	35399076
LINC00511	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(miR-126-5p/miR-218-5p)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay	In the present work, we observed that Linc00511 was upregulated in LUAD tissues and cells.In addition, we determined that Linc00511 promoted COL1A1-mediated cell proliferation and cell motility by sponging miR-126-5p and miR-218-5p. Moreover, Linc00511 activated the PI3K/AKT signaling pathway through upregulation of COL1A1.		Yes	Loss/gain-of-function experiments indicated that knockdown of Linc00511 significantly inhibited LUAD cell proliferation, migration and invasion and promoted LUAD cell apoptosis, whereas overexpression of Linc00511 showed the opposite effects. Finally, silencing of Linc00511 inhibited LUAD tumor growth in vivo.	35842617
LINC00511	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(miR-4739/PYCR1 )	RNA Pull-Down//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//BrdU//Transwell Assay	The expression levels of LINC00511 and PYCR1 in LUAD were downregulated, whereas that of miR-4739 was upregulated. On the contrary, knockdown of miR-4739 had tumor-promoting effects. Mechanistically, LINC00511 prevented the miR-4739 led inhibition of PYCR1, resulting in PYCR1 overexpression.		Yes	 Functional studies showed that knockdown of LINC00511 or PYCR1 suppressed the proliferation and migration of LUAD cells, and promoted apoptosis. 	36371775
LINC00511	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Serum, NSCLC cell 	Interaction(miR-98-5p/TGFBR1)	CCK8//qRT-PCR//RNA Pull-Down//Western Blot	Serum Linc00511 level at admission was higher in patients than in healthy controls and decreased on the day of discharge than before surgical resection.During the 3-years of follow-up, plasma Linc00511 level was upregulated only in patients with distant recurrence.Linc00511 was predicted to interact with miR-98-5p, and Linc00511 overexpression inhibited miR-98-5p expression but upregulated TGFBR1, a downstream target for miR-98-5p. 		Yes	Moreover, the elevation of Linc00511 and TGFBR1 both promoted NSCLC cell proliferation, invasion, and migration. However, miR-98-5p overexpression had opposite effects, reversing the effects of TGFBR1. 	35993940
LINC00511	LncRNA	Homo sapiens	Melanoma	melanoma cells	Interaction(miR-625-5p/PKM2 axis)	qRT-PCR	Functional analysis of two SFPQ-enriched lncRNA, LINC00511 and LINC01234, demonstrated that these genes independently contribute to the melanoma phenotype and a more detailed analysis of LINC00511 indicated that this occurs in part via modulation of the miR-625-5p/PKM2 axis.		Yes	Functional analysis of two SFPQ-enriched lncRNA, LINC00511 and LINC01234, demonstrated that these genes independently contribute to the melanoma phenotype and a more detailed analysis of LINC00511 indicated that this occurs in part via modulation of the miR-625-5p/PKM2 axis.	34218270
LINC00511	LncRNA	Homo sapiens	lung squamous cell carcinoma		regulation[miR-150-5p,TADA1]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	 LINC00511 was upregulated in LUSC tissues in TCGA database compared to adjacent non-tumor counterparts, and its expression level was strongly associated with tumor stage. our study highlights that LINC00511 facilitates LUSC progression via sequestering miR-150-5p and targeting TADA1, suggesting a need for development of a strategy for therapeutic targeting of LINC00511 in LUSC.	 LINC00511 was upregulated in LUSC tissues in TCGA database compared to adjacent non-tumor counterparts, and its expression level was strongly associated with tumor stage.	Yes	 LINC00511 deficiency significantly suppressed LUSC cell proliferation and migration.	32953492
LINC00504	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction(miR-876-3p-HMGB3 axis )	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	LINC00504 was upregulated in breast cancer tissues and cell lines. Regarding the underlying mechanism, LIN00504 could function as a competing endogenous RNA in breast cancer by sponging microRNA-876-3p (miR-876-3p), resulting in the upregulation of high mobility group box 3 (HMGB3). 		Yes	Knocking down LINC00504 suppressed breast cancer cell proliferation, migration, and invasion and facilitated apoptosis in vitro. In addition, tumor growth in vivo was significantly inhibited by LINC00504 depletion.	33654429
LINC00504	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction(miR-140-5p/VEGFA)	In Vivo Experiment//Transwell Assay//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//IF//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//ChIP	We found that LINC00504 is upregulated in breast cancer.  In addition, we found that the transcription factor regulatory factor X5 (RFX5) can strongly bind to the LINC00504 promoter region and subsequently increase its transcriptional activity. We also found that the manipulation of RFX5 expression can significantly affect LINC00504 expression, which suggested that RFX5 can transcriptionally activate LINC00504 in breast cancer (BC).  We further found that LINCOO504 inhibits miR-140-5p, which decreases the levels of VEGFA. The further results showed that miR-140-5p was one of the target gene of LINC00504. 		Yes	Knockdown of LINC00504 inhibits cell proliferation, migration and invasion in vitro and in vivo. 	34239305
LINC00504	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues,cell lines	Interaction[c-Myc]	qRT-PCR	 The lncRNA LINC00504 was markedly upregulated in colon cancer cell lines and specimens. Mechanistic study showed that LINC00504 could interact with c-Myc to promote chromatin recruitment of c-Myc and enhance its transactivation activity. Collectively, our results showed that LINC00504 serves as an important transcriptional regulator for c-Myc in colon cancer cells. LINC00504 can reprogram central metabolism in colon cancer cells implying that LINC00504 may serve as a potential target for therapeutic intervention.		Yes	LINC00504 increases viability and migration of colon cells in vitro. Furthermore, LINC00504 also enhances colon cancer xenograft tumors in vivo. 	30998289
LINC00504	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	Interaction[ inhibition of miR-1244]	qRT-PCR//MTT//Luciferase Report Assay//ELISA//Colony Formation Assay	LINC00504 was upregulated in OC cell lines and specimens. Our study shows that LINC00504 promotes OC cell progression and stimulates aerobic glycolysis by interacting with miR-1244, which indicates that LINC00504 might act as a promising therapeutic target for OC treatment.		Yes	Knockdown of LINC00504 inhibited cell proliferation, enhanced apoptosis, decreased glycolysis-related gene (PKM2, HK2, and PDK1) expression, and altered aerobic glycolysis in OC cells and vice versa.	31691157
LINC00501	LncRNA	Homo sapiens	Lung Neoplasms		regulation[miR-129-5p/HMGB1]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Transwell Assay	LINC00501 was highly expressed in LC according to the database, and it was found that LINC00501 was upregulated in NSCLC specimens and cells, and the up-regulation indicated an unfavorable prognosis.  In addition, LINC00501 can inhibit the invasion and migration of LC by mediating miR-129-5p/HMGB1.		Yes	Besides, knockdown of LINC00501 hindered the proliferation and invasion of NSCLC cells and intensified their apoptosis, and LINC00501 could be adopted as competitive endogenous RNA to regulate HMGB1 and tumorigenesis through miR-129-5p.	32801746
LINC00511	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction[miR-424]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//EdU Staining//Transwell Assay	LINC00511 expression was significantly up-regulated in HCC tissues and cell lines, and its high expression was distinctly associated with nodal metastasis, vascular invasion, and clinical stage.  LINC00511 plays an important role in the malignant progression of HCC via modulation of miR-424.	LINC00511 expression was significantly up-regulated in HCC tissues and cell lines, and its high expression was distinctly associated with nodal metastasis, vascular invasion, and clinical stage. Furthermore, statistical assays revealed that HCC patients with higher LINC00511 expression levels had worse overall survival rates. 	Yes	Functionally, the inhibition of LINC00511 significantly suppressed the capability of proliferation, migration, and invasion in HCC cell lines.	31081082
LINC00511	LncRNA	Homo sapiens	Colonic Neoplasms	CC cells	Interaction(miR-625-5p/WEE1)	qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	 CC tissues and cells highly expressed LINC00511 and WEE1 and lowly expressed miR-625-5p.  LINC00511 was mainly localized in the cytoplasm. Deleted LINC00511 or restored miR-625-5p delayed cellular growth in CC. LINC00511 sponged miR-625-5p to target WEE1. Silenced miR-625-5p mitigated the role of depleted LINC00511, while inhibited WEE1 rescued the effect of silenced miR-625-5p on the biological functions of CC cells. 		Yes	LINC00511 sponged miR-625-5p to target WEE1. Silenced miR-625-5p mitigated the role of depleted LINC00511, while inhibited WEE1 rescued the effect of silenced miR-625-5p on the biological functions of CC cells. 	35477702
LINC00511	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miR-29c-3p/NFIA )	Transwell Assay//qRT-PCR//Colony Formation Assay//Western Blot	 Our results manifested that the expression level of LINC00511 was obviously upregulated in CRC tissues and cells and it accelerated CRC development through facilitating cell proliferation, metastasis and stemness.Molecular mechanism exploration uncovered that LINC00511 acted as a ceRNA competing with NFIA to bind with miR-29c-3p. 		Yes	 Our results manifested that the expression level of LINC00511 was obviously upregulated in CRC tissues and cells and it accelerated CRC development through facilitating cell proliferation, metastasis and stemness.	33536761
LINC00520	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cells	regulation[ inhibiting miR-3175 expression]	CCK8//qRT-PCR//RNA Pull-Down//Transwell Assay	 LINC00520 was highly expressed in lung cancer tissues and cells.LncRNA LINC00520 could predict poor prognosis and promote progression of lung cancer by inhibiting miR-3175 expression.	Patients at III+IV stage were always with higher LINC00520 level than patients at I+II stage.Patients with high expression of lncRNA LINC00520 have short survival time (hazard ratio=1.7). 	Yes	 Knockdown of LINC00520 inhibited proliferation, invasion and migration of lung cancer cells. 	32801856
LINC00520	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[LINC00520/miR-577/HSP27 axis ]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	In this study, high-LINC00520 expression was verified in CRC tissues and cell lines, and this high expression was associated with patients' unfavorable clinicopathological parameters and shorter overall survival and disease-free survival.LINC00520 functioned as an oncogenic lncRNA in CRC, and it facilitated CRC progression by regulating the miR-577/HSP27 axis, suggesting that the LINC00520/miR-577/HSP27 axis is an effective target in anticancer management.	In this study, high-LINC00520 expression was verified in CRC tissues and cell lines, and this high expression was associated with patients' unfavorable clinicopathological parameters and shorter overall survival and disease-free survival.	Yes	Functionally, interference of LINC00520 resulted in a significant decrease of CRC cell proliferation, migration, colony forming ability, and invasion.	32146708
LINC00520	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	regulation[LINC00520/miR-577/Sphk2 axis ]	qRT-PCR	High LINC00520 expression was verified in PTC tissues and cell lines, and this high expression was associated with the unfavorable clinicopathological parameters and short overall survival of patients.LINC00520 functioned as an oncogenic lncRNA in PTC, and it facilitated PTC progression by regulating the miR-577/Sphk2 axis, suggesting that the LINC00520/miR-577/Sphk2 axis is an effective target in anticancer management.	High LINC00520 expression was verified in PTC tissues and cell lines, and this high expression was associated with the unfavorable clinicopathological parameters and short overall survival of patients.	Yes	 Functionally, LINC00520 interference resulted in a significant decrease in PTC cell proliferation, migration, and in vitro invasion and an increase in cell apoptosis. Further, its downregulation impaired tumor growth in vivo.	32075502
LINC00520	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-4516/SOX5 axis)	Other	 The present study identified that LINC00520 was upregulated in HCC tissues and indicated poor patient survival. Furthermore, LINC00520 acted as a sponge of miR-4516 to regulate SRY-related high mobility group box 5 (SOX5). In addition, the inhibition of miR-4516 partly reversed the inhibitory effect of LINC00520 silencing on HCC cell proliferation, migration and invasion.	 The present study identified that LINC00520 was upregulated in HCC tissues and indicated poor patient survival.	Yes	Overexpression of LINC00520 promoted HCC cell proliferation, migration and invasion, while LINC00520 downregulation led to the opposite effects. Besides, LINC00520 knockdown was found to inhibit tumor growth in vivo.	35089659
LINC00520	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 HNSCC cells and tissues	regulation[LINC00520/miR-195/HOXA10]	qRT-PCR//RNA Pull-Down//RIP	 LINC00520 was upregulated while miR-195 was downregulated in HNSCC cells and tissues.LINC00520/miR-195/HOXA10 is involved in the radiosensitivity mediation, providing potential therapeutic target for HNSCC treatment.		Yes	Silencing LINC00520 or overexpressing miR-195 promoted radiosensitivity and inhibited cell proliferation, invasion, migration, and apoptosis in HNSCC.	32462956
LINC00520	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Regulation[miR-26b-3p/USP39 axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//IHC	Results indicated that LINC00520 was significantly increasing in NPC tissues and cells in comparison to their corresponding controls.Taken together, our study discovered the oncogenic role of LINC00520 in clinical specimens and cellular experiments, showing the potential LINC00520/miR-26b-3p/USP39 pathway. This results and findings provide a novel insight for NPC tumorigenesis.		Yes	Silence of LINC00520 was able to repress NPC cell growth in vitro while overexpression of LINC00520 inversed this process. 	30898716
LINC00520	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung ADC tissues and cell lines	Interaction(miR-1252-5p/FOXR2 pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	 We found that LINC00520 level was elevated in lung ADC tissues and cell lines. Besides, the LINC00520 expression had a negative connection with miR-1252-5p level in lung ADC tissues.  Additionally, our results demonstrated the reciprocal repression influence between LINC00520 and miR-1252-5p.  Additionally, the findings also demonstrated that FOXR2 was a target of miR-1252-5p; thus, LINC00520 could regulate FOXR2 level.		Yes	Furthermore, knockdown of LINC00520 inhibited lung ADC cells proliferation, migration and invasion, while co-transfection with a miR-1252-5p inhibitor inverted these influences.	33464477
LINC00520	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD specimens and adjacent non-tumor tissues	Expression(highly expressed)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//ChIP	We found that LINC00520 was upregulated in LUAD. Additionally, LINC00520 upregulation is associated with the poor prognosis for patients with LUAD. Furthermore, LINC00520 downregulation suppressed LUAD cell proliferation and migration and induced cell apoptosis. Forkhead box P3 (FOXP3) is identified as the transcription factor to transcriptionally activate LINC00520. Moreover, LINC00520 positively upregulated FOXP3 expression via sponging miR-3611 in LUAD cells. Subsequently, rescue experiments delineated that miR-3611 downregulation or FOXP3 overexpression reversed the effects of silenced LINC00520 on proliferative and migratory capabilities in LUAD cells.	Additionally, LINC00520 upregulation is associated with the poor prognosis for patients with LUAD.	Yes	function of LINC00520 in LUAD was verified by in vitro loss-of-function experiments.	34496829
LINC00519	LncRNA	Homo sapiens	lung squamous cell carcinoma	LUSC tissues and cell lines	regulation[miR-450b-5p/miR-515-5p/YAP1 axis]	RNA Pull-Down//qRT-PCR//RIP//FISH//Luciferase Report Assay	Elevated level of LINC00519 was identified in LUSC tissues and cell lines. H3K27ac-activated LINC00519 acts as a competing endogenous RNA (ceRNA) to promote LUSC progression by targeting miR-450b-5p/miR-515-5p/YAP1 axis.	High LINC00519 level predicted unsatisfactory prognosis. 	Yes	 Then, loss-of-function assays suggested the inhibitive role of silenced LINC00519 in cell proliferation, migration, invasion and tumour growth and promoting effect on cell apoptosis in LUSC.	32297697
LINC00518	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Regulation[JAK/STAT3 signaling]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	We found that LINC00518 was upregulated in CC tissues and associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, lymph node metastasis, depth of cervical invasion and poor survival of CC patients. The present work first suggests that LINC00518 acts as an oncogene in CC via regulation of the JAK/STAT3 signaling pathway. 	We found that LINC00518 was upregulated in CC tissues and associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, lymph node metastasis, depth of cervical invasion and poor survival of CC patients.	Yes	Furthermore, knocking down LINC00518 expression significantly suppressed CC cell proliferation, migration and invasion, and induced apoptosis in vitro. 	30720156
LINC00518	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD specimens and cell lines	Interaction(miR-185-3p/MECP2)	In Vivo Experiment//IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	We found that LINC00518 was highly expressed in LUAD specimens and the high-expression was negatively correlated with the overall survival rates. This finding was also proved in the LUAD cell lines. Through a series of in vitro and in vivo experiments, we proved that LICN00518 promoted the cell growth of LUAD by regulating the cell cycle. Moreover, LICN00518 upregulated the expression of MECP2 by mutagenesis of miR-185-3p.	We found that LINC00518 was highly expressed in LUAD specimens and the high-expression was negatively correlated with the overall survival rates.	Yes	Through a series of in vitro and in vivo experiments, we proved that LICN00518 promoted the cell growth of LUAD by regulating the cell cycle. 	33937054
LINC00518	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction(EIF4A3/MITF axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 In our study, LINC00518 was revealed to be upregulated in melanoma tissues and cells, and melanoma patients in high LINC00518 expression group had poorer prognosis as depicted in GEPIA database. Additionally, results of mechanism assays uncovered EIF4A3 could bind with LINC00518 and MITF, and LINC00518 recruited EIF4A3 to stabilize MITF mRNA. Finally, it was demonstrated that upregulation of MITF could partially abrogate the inhibitory impact of LINC00518 knockdown on melanoma cell malignant behaviors. 	 In our study, LINC00518 was revealed to be upregulated in melanoma tissues and cells, and melanoma patients in high LINC00518 expression group had poorer prognosis as depicted in GEPIA database.	Yes	Functional assays revealed that LINC00518 depletion inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).	35813236
LINC00518	LncRNA	Homo sapiens	Melanoma	 CMM tissues and cells	Interaction(miR-526b-3p/EIF5A2 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	LINC00518 and EIF5A2 were up-regulated and miR-526b-3p was down-regulated in CMM tissues and cells.  LINC00518 bound to miR-526b-3p and miR-526b-3p targeted EIF5A2. LINC00518 negatively regulated miR-526b-3p expression but positively regulated EIF5A2. Furthermore, EIF5A2 expression was negatively associated with miR-526b-3p expression.	CMM patients with highly expressed LINC00518 showed decreased survival time than those with lowly expressed LINC00518. 	Yes	Transfection of si-LINC00518, miR-526b-5p mimic or si-EIF5A2 weakened the proliferative, migratory, and invasive abilities of melanoma cells, while transfection of miR-526b-5p inhibitor or pcDNA-LINC00518 enhanced the progression of melanoma cells. Moreover, the proliferative, migratory, and invasive potentials of melanoma cells were decreased after co-transfection of si-EIF5A2 and pcDNA-LINC00518 compared with cells transfected with pcDNA-LINC00518 alone.	35189053
LINC00511	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	regulation[miR-124-3p/PDK4 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	 The expression of LINC00511 was remarkably upregulated in GC cells compared to that in corresponding normal cell lines. These data demonstrate that LINC00511 promotes gastric cancer cell growth by acting as a ceRNA to regulate the miR-124-3p/PDK4 axis, which may be a promising therapeutic target for GC.		Yes	 Compared to the controls, cell proliferation was inhibited, and cell apoptosis was increased upon LINC00511 knockdown, demonstrating that LINC00511 influenced GC cell growth. 	32368318
LINC00511	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-625-5p/STAT3 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	We reported that LINC00511 and STAT3 expressions in GC tissues and cell lines were observably up-regulated, while miR-625-5p expression was inhibited. 		Yes	High expression of LINC00511 could facilitate the proliferation and promote the migration of GC cells.  Additionally, knockdown of LINC00511 suppressed the growth and lung metastases of CRC cells in nude mice. 	34224294
LINC00511	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[LINC00511/miR-150/MMP13 axis]	qRT-PCR//Luciferase Report Assay	In this study, LINC00511 was significantly up-regulated in breast cancer, and its expression level was correlated to poor prognosis of patients with breast cancer.In conclusion, our data show that LINC00511 is a breast cancer promoter, and the LINC00511/miR-150/MMP13 axis may be a new therapeutic strategy for breast cancer patients.	In this study, LINC00511 was significantly up-regulated in breast cancer, and its expression level was correlated to poor prognosis of patients with breast cancer.	Yes	Cells transfected with siRNA-2 proliferated, and its metastasis was suppressed.	33031905
LINC00511	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer samples	Expression(highly expressed)	Bioinformatics Analysis	It was found that the role of LINC00511 was overexpressed in breast cancer samples, and this overexpression was ascribed to a poor prognosis.		Yes	It was found that the role of LINC00511 was overexpressed in breast cancer samples, and this overexpression was ascribed to a poor prognosis.	35790898
LINC00511	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues	Interaction(miR-625-5p/GSPT1)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	LINC00511 expression was clearly higher in the tumor tissues of the NSCLC patients than in normal tissues (P<0.001).  LINC00511 promoted GSPT1 expression via suppressing miR-625-5p.	High LINC00511 expression was related to larger tumor size, positive lymph node metastasis, advanced TNM stage, and a lower 5-year survival rate. 	Yes	Compared with those of the shNC group, the NSCLC cells of the shLINC00511 group had a prominently lower optical density (OD) 450 value at 72 h, a lower percentage of cells in S phase, a higher relative wound width, and a lower invasive cell number (P<0.01 or P<0.001).  Compared with those of the shNC group, the nude mice of the shLINC00511 group had a much lower subcutaneous tumor volume and weight (P<0.05 or P<0.001).	35116366
LINC00511	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue samples and cell lines	regulation[HIF-1α/LINC00511/miR-153-5p]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ChIP	Here, present research found that LINC00511 was significantly up-regulated in the CRC tissue samples and cell lines.In conclusion, this study identifies the roles of LINC00511 in CRC progression and uncovers the positive feedback loop of HIF-1α/LINC00511/miR-153-5p in CRC, providing a potential therapeutic target.	Consistently, LINC00011 overexpression was correlated with larger tumor size and advanced tumor stage. 	Yes	Functionally, LINC00511 promoted the proliferation and reduced the apoptosis of CRC cells in vitro, and LINC00511 knockdown repressed tumor growth in vivo.	32092829
LINC00494	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cells and tissues	regulation[NFκB1 and FBXO32]	RNA Pull-Down//ChIP//RIP//Luciferase Report Assay//Transwell Assay	 LINC00494 and NFκB1 were highly expressed whereas FBXO32 had low expression in ovarian cancer cells and tissues. Our work demonstrated that LINC00494 promoted ovarian cancer progression by modulating FBXO32 via binding with the transcription factor NFκB1.		Yes	 Overexpression of LINC00494 elevated NFκB1 expression and enhanced cell migration, invasion and tumorigenesis, but additional overexpression of FBXO32 interfered with the tumorgenicity of ovarian cancer cells in vitro and in vivo.	33585183
LINC00491	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	Expression [highly expressed]	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RNA-seq//Invasion Assay	The reverse transcription‑quantitative PCR results suggested that LINC00491 was upregulated in ESCC tissues and cells. 		Yes	The results showed that lower expression of LINC00491 resulted in decreased cell proliferation and migration and increased the apoptosis rate.	33537830
LINC00491	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(LINC00491/MTSS1/Wnt/β-catenin-signaling pathway )	In Vivo Experiment//Western Blot//Wound Healing Assay//FISH//Colony Formation Assay	Our results showed that LINC0491 was significantly upregulated in LUAD and positively correlated with poor survival. Using pull-down assay and mass spectrometry, MTSS1 was found binding to LINC00491, and the conducted experiments verified the direct interaction between LINC00491 and MTSS1. Meanwhile, LINC00491 was found to regulate MTSS1 degradation by promoting the MTSS1 ubiquitination level and then activating the Wnt/β-catenin-signaling pathway. LINC00491/MTSS1/β-catenin may act as a complex to facilitate tumor progression.	Our results showed that LINC00491 was significantly upregulated in LUAD and positively correlated with poor survival. 	Yes	 High LINC00491 expression promoted proliferation, migration and invasion, and resulted in a high metastatic burden in LUAD. 	36496997
LINC00472	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	several squamous cell carcinoma cancer tissues and OSCC cell lines	Interaction(miR-4311/GNG7 axis)	qRT-PCR//MTT//Western Blot	This study found that LncRNA LINC00472 was significantly down-regulated in several squamous cell carcinoma cancer tissues and OSCC cell lines.  Additionally, we confirmed that LINC00472 functioned as an hsa-miR-4311 sponge and regulated the expression of GNG7 (guanine nucleotide-binding protein, gamma 7). 		Yes	Over-expression of LINC00472 in OSCC cells inhibited OSCC progression and alleviated OSCC immune responses.Also, we found that LINC00472 over-expression could suppress xenograft tumor growth in vivo. 	35240924
LINC00472	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	interaction[miR-300 and FOXO1]	qRT-PCR	The expressions of LINC00472 were inhibited in OS tissues and cells, and were negatively related to the expressions of miR-300. From all the experiments and observations, we demonstrated that LINC00472 could be a potential tumor suppressor in OS through interacting with miR-300 and FOXO1.		Yes	 LINC00472 over-expressions decreased cell proliferation abilities and colony formation abilities.	32256209
LINC00472	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Expression [lower expressed]	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//qRT-PCR//RIP//H&E Staining//EdU Staining//Transwell Assay	 In this study, we found the lncRNA LINC00472 was poorly expressed in TNBC tissues and cells. LINC00472 induced site-specific DNA methylation and reduced the MCM6 expression by recruiting DNA methyltransferases into the MCM6 promoter. 		Yes	Overexpression of LINC00472 could inhibit the proliferation, invasion and migration of MDA-MB-231 cells. On the contrary, minichromosome maintenance complex component 6 (MCM6) was highly expressed in TNBC tissues and MDA-MB-231 cells due to suppressed methylation. 	33668040
LINC00472	LncRNA	Mus musculus	Acute Hepatic Injury	liver tissues	regulation[miR-373-3p/TRIM8 axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//ELISA	LINC00472 and TRIM8 were significantly upregulated in liver tissues and THLE-3 cells in sepsis-induced AHI models, while miR-373-3p was downregulated.Downregulation of LINC00472 ameliorates sepsis-induced AHI by regulating the miR-373-3p/TRIM8 axis.		Yes	Silencing of LINC00472 promoted cell viability and suppressed cell apoptosis in LPS-treated THLE-3 cells, whereas upregulation of LINC00472 had the opposite effect. 	33129786
LINC00470	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[PTEN ]	RNA Pull-Down//MeRIP//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	 In this study, our findings showed that LINC00470 was significantly upregulated in GC tissues and cell lines.Overexpression and knockdown experiments revealed its oncogenic functions on GC cell proliferation, migration and invasion.	In this study, our findings showed that LINC00470 was significantly upregulated in GC tissues and cell lines, and correlated with distant metastasis, TNM stage and poor prognosis.	Yes	Overexpression and knockdown experiments revealed its oncogenic functions on GC cell proliferation, migration and invasion.	31711642
LINC00470	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction[association with NF45/NF90 complex]	qRT-PCR	Here, we found that LINC00470 was upregulated in HCC cells and tissues.  Further investigation suggested that LINC00470 was associated with NF45/NF90 complex and increased its interaction with cyclin E1 mRNA, thus inhibiting the degradation of cyclin E1 mRNA. 	 High-level LINC00470 was significantly correlated with bigger tumor size, advanced TNM stage and poor prognosis in patients with HCC. 	Yes	Functional studies showed that knockdown of LINC00470 expression inhibited HCC cell proliferation and cell cycle progression, while overexpression of LINC00470 showed the opposite effects.	31612313
LINC00470	LncRNA	Homo sapiens	Glioma	serum derived exosome	Interaction(miR-580-3p/WEE1/PI3K/AKT/mTOR pathway)	Western Blot//Transfection//Colony Formation Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC	LINC00470 overexpressed in GBM-exo and associated with disease severity and postoperative survival time of glioma patients. The PI3K/AKT/mTOR pathway was activated. LINC00470 competitively bound to miR-580-3p with WEE1.	LINC00470 overexpressed in GBM-exo and associated with disease severity and postoperative survival time of glioma patients. GBM-exo deteriorated tumor progression in nude mice. 	Yes	Cells incubated with GBM-exo or transfected with pcDNA3.1-LINC00470/miR-580-3p inhibitor/pcDNA3.1-WEE1 had less autophagosome, downregulated LC3-II/LC3-I and Beclin1 expression levels and increased expression of p62 as well as strengthened proliferation ability	33663509
LINC00467	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	Expression [highly expressed]	Western Blot//Flow Cytometry//FISH//qRT-PCR//MTT//Colony Formation Assay//Bioinformatics Analysis	Levels of LINC00467 and ITGB3 were up-regulated in GC, and highly expressed LINC00467 was positively associated with tumor size, differentiation, N stage, and T stage in GC patients. 	Levels of LINC00467 and ITGB3 were up-regulated in GC, and highly expressed LINC00467 was positively associated with tumor size, differentiation, N stage, and T stage in GC patients. 	Yes	. LINC00467 was enriched in cytoplasm of GC cells, and overexpressed LINC00467 promoted the viability and proliferation as well as levels of ITGB3 and PCNA, while suppressing the apoptosis and levels of cleaved caspase-3 and cleaved PARP1 in GC cells.	34555778
LINC00467	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	Interaction(miR-138-5p and LIN28B)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	"A higher expression level of LINC00467 was observed in breast cancer tissues as compared to the adjacent normal counterparts and elevated LINC00467 predicted poor overall survival . LINC00467 down-regulated miR-138-5p by acting as a miRNA ""sponge"". Besides, LINC00467 also up-regulated the protein level of lin-28 homolog B (LIN28B) via a direct interaction. "		Yes	Silence of LINC00467 suppressed proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) of breast cancer cells in vitro, whereas forced expression of LINC00467 exhibited the opposite effects. Furthermore, we demonstrated overexpression of LINC00467 promoted tumor growth, while knockdown of LINC00467 inhibited pulmonary metastasis in vivo.	33996559
LINC00467	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[ Akt signal pathway]	qRT-PCR	 LINC00467 highly expressed in NSCLC tissues and associated with advanced clinical stages and poor outcome.  In conclusion, LINC00467 promotes NSCLC progression via Akt signal pathway.	 LINC00467 highly expressed in NSCLC tissues and associated with advanced clinical stages and poor outcome. 	Yes	Knockdown of LINC00467 inhibited cell growth and metastasis via regulating the Akt signaling pathway. 	32796958
LINC00467	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		regulation[miR-485-5p/DPAGT1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 According to experimental results, we found out upregulated LINC00467 improved cell proliferation, but hindered cell apoptosis. We proved that LINC00467 acted as an oncogene in ESCC by accelerating cell proliferation and preventing cell apoptosis via miR-485-5p/DPAGT1 axis. 		Yes	 Rescue assays suggested that DPAGT1 amplification was able to recover the influence of LINC00467 deficiency on cell proliferation and apoptosis. Furthermore, knockdown of LINC00467 suppressed tumor growth in vivo.	32720371
LINC00467	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[highly expressed]	qRT-PCR	 In this study, we report a novel lncRNA, LINC00467, which was significantly up-regulated in CRC; we investigated its function and mechanism in CRC. 	We used the Gene Expression Omnibus (GEO) and Gene Expression Profiling Interactive Analysis (GEPIA) databases for the analysis and measurement of clinical samples, and observed that the CRC patients with high LINC00467 expression levels showed poor overall survival (OS) and recurrent-free survival (RFS) rates.	Yes	Furthermore, following the short interfering RNA (siRNA) knockdown of LINC00467 in the CRC cell line, the results demonstrated that LINC00467 suppresses the proliferation, invasion and metastasis of CRC cells in vitro.	31772673
LINC00467	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	interaction[microRNA-451a]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	Consequently, linc00467 was revealed to be overexpressed in human CRC tissues, and its expression was significantly associated with metastasis and Tumor-Node-Metastasis stage.  In conclusion, the results of the present study indicate that increased linc00467 expression promotes metastasis by targeting miR-451a, which ultimately increases cellular proliferation and inhibits apoptosis in human CRC cells.	Consequently, linc00467 was revealed to be overexpressed in human CRC tissues, and its expression was significantly associated with metastasis and Tumor-Node-Metastasis stage. 	Yes	 In HT29 and HCT116 cells, linc00467-knockout was revealed to decrease cellular proliferation and increase apoptosis (P<0.05).	32934693
LINC00467	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Regulation[LINC00467/miR-9-5p/PPARA signalling]	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	It was found that LINC00467 was aberrantly decreased in HCC.Our data indicate the critical involvement of LINC00467/miR-9-5p/PPARA signalling in the incidence and progression of HCC.		Yes	The ectopic expression of LINC00467 significantly suppressed cell viability, proliferation, migration and invasion. 	31480990
LINC00467	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cell lines	regulation[inhibiting NR4A3]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Cell Apoptosis Assay//Cell Cycle Assay//Transwell Assay	Our findings revealed that LINC00467 was up-regulated in HCC tissues and HCC cell lines.Targeting LINC00467 or enhancing NR4A3 may be potential therapeutic strategies against HCC.		Yes	 In vitro functional experiments revealed that LINC00467 accelerated HCC cell proliferation, cell cycle progression and migration and reduced HCC cell apoptosis. In vivo functional assays revealed that LINC00467 drove HCC xenograft growth and HCC cell proliferation and repressed HCC cell apoptosis in vivo. 	32125766
LINC00467	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	regulation[miR-18a-5p/NEDD9 axis]	qRT-PCR	We observed that linc00467 was upregulated in HCC tissues and cells. In conclusion, our data highlighted the oncogenic role of linc00467 in HCC progression by regulating the miR-18a-5p/NEDD9 axis.		Yes	Silencing of linc00467 using small interfering RNA interference significantly inhibited the growth and motility of HCC cells, and increased cell apoptosis through regulating the Bcl-2/Bax axis and the caspase cascade, suggesting that linc00467 exerted oncogenic functions in the progression of HCC. 	31916278
LINC00467	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[IGF2BP3,TRAF5 ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	LINC00467 upregulation in HCC tissues and cells was observed.LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in HCC.		Yes	LINC00467 silencing suppressed cell proliferation and metastasis, whereas it facilitated cell apoptosis in HCC. 	31656043
LINC00467	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[HMGA1 ,miR-217]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Transwell Assay	The expression of LINC00467 and HMGA1 was increased in OS tissues and cells, while miR-217 expression was reduced. 	 High expression of HMGA1 led to the poor overall survival.	Yes	 Down-regulation of LINC00467 or up-regulation of miR-217 could accelerate cell apoptosis, and slump cell proliferation, migration, invasion and EMT.	32572906
LINC00472	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Mutation[miR-93-5p/PDCD4 pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	In the present study, we have demonstrated that long non-coding RNA (lncRNA) LINC00472 was low expressed in human HCC tissues and cell lines compared with adjacent non-tumor liver tissues and normal liver cell lines respectively.MiR-93-5p was a direct target of LINC00472, and miR-93-5p directly targeted PDCD4. The miR-93-5p/PDCD4 pathway mediated the suppressing role of LINC00472 in HCC cells.	 Expression level of LINC00472 was positively correlated with patient overall survival (OS) rate.	Yes	Forced expression of LINC00472 suppressed cell proliferation, migration, invasion and promoted cell apoptosis in HCC cells Huh-7 and SMMC-7721. 	30522853
LINC00472	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction[NF-κB]	Western Blot//Migration Assay//CCK8//RIP//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Analysis of LINC00472 transcriptome revealed ERα upregulation of LINC00472 expression, and an ERα-binding site in the LINC00472 promoter was identified.Evaluation of LINC00472 overexpression also indicated a possible link between LINC00472 and NF-κB. Cell experiments confirmed that LINC00472 suppressed the phosphorylation of p65 and IκBα through binding to IKKβ, inhibiting its phosphorylation.Tamoxifen treatment of ER-positive cells inhibited ERα and LINC00472 expression and increased p65 and IκBα phosphorylation. Meta-analysis showed that LINC00472 expression were higher in ER-positive than ER-negative tumors and that high expression was associated with better disease outcomes in ER-positive patients.		Yes	High LINC00472 expression inhibited tumor growth both in vitro and in vivo and suppressed aggressive tumor cell behaviors in vitro. Suppressing LINC00472 expression in ER-positive tumor cells increased cell aggressive behaviors. 	30830488
LINC00472	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	Expression[highly expressed]	qRT-PCR	Among them, the expression level of Linc00472 significantly decreased in gastric cancer tissues compared to adjacent normal tissues. 		Yes	Ectopic Linc00472 expression could significantly inhibit gastric cancer cell growth and migration.	31570433
LINC00473	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(miR-424-5p/CCNE1 Pathway)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	 LINC00473 expression was elevated in BC tissues and cell lines, which was associated with lymph node metastasis and higher clinical stage of the patients with BC.  LINC00473 proved to be a molecular sponge for miR-424-5p; LINC00473 knockdown impeded the growth, migration, invasion, and epithelial-mesenchymal transition of BC cells, while these effects were abolished by miR-424-5p inhibitors; miR-424-5p targeted CCNE1 to restrain its expression. LINC00473 positively regulated CCNE1 expression, and CCNE1 restoration counteracted the effects induced by LINC00473 knockdown in BC cells.	 LINC00473 expression was elevated in BC tissues and cell lines, which was associated with lymph node metastasis and higher clinical stage of the patients with BC. 	Yes	 LINC00473 proved to be a molecular sponge for miR-424-5p; LINC00473 knockdown impeded the growth, migration, invasion, and epithelial-mesenchymal transition of BC cells, while these effects were abolished by miR-424-5p inhibitors; miR-424-5p targeted CCNE1 to restrain its expression.	36305147
LINC00491	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer patients and cells&Xenograft tumor and lung tissues of mice	Interaction(miR-324-5p/ROCK1)	In Vivo Experiment//cell invasion assay//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay	LINC00491 was highly expressed in liver cancer cases, associating with poor prognosis. LINC00491 promoted ROCK1 expression by reducing miR-324-5p. miR-324-5p up-regulation or ROCK1 knockdown reversed LINC00491 promotion on liver SK-Hep-1 cells malignant phenotype. 	LINC00491 was highly expressed in liver cancer patients, associating with poor prognosis.	Yes	 si-LINC00491 inhibited proliferation, colony formation, invasion, migration, and induced cell cycle G1 arrest and apoptosis in HUH-7 and SK-Hep-1 cells. LINC00491 overexpression showed opposite effects.LINC00491 facilitated xenograft tumor growth and lung metastasis in mice.	34876144
LINC00485	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissue	regulation[miR-298/c-Myc axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this study, we found that the expression of Linc00485 was significantly increased in human lung cancer tissue and associated with malignant phenotypes, including tumour-node-metastasis (TNM) stage, metastasis and relapse. Overall, these findings indicate that Linc00485 overexpression down-regulates miR-298, resulting in the up-regulation of c-Myc and thereby promoting the development of lung cancer.	In this study, we found that the expression of Linc00485 was significantly increased in human lung cancer tissue and associated with malignant phenotypes, including tumour-node-metastasis (TNM) stage, metastasis and relapse.	Yes	 Furthermore, the proliferative, migratory and invasive abilities of lung cancer cells in vitro were significantly enhanced by overexpression of Linc00485 but inhibited by its silencing.	33237626
LINC00485	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cancer cells 	Interaction( miR-581/EDEM1 axis)	qRT-PCR//Colony Formation Assay//Western Blot	We found that LINC00485 expression was significantly lower in CRC tissues and cancer cells than in paired normal samples and human normal colonic epithelial cells.MicroRNA miR-581 was the downstream target of LINC00485, which was downregulated in CRC samples and cancer cells compared to normal tissues and normal colonic epithelial cells. MiR-581 overexpression induced proliferation, migration, and invasion of FHC cells, while miR-581 antagomir treatment produced opposite results. MiR-581 directly targeted the 3'UTR of EDEM1 and inhibited its expression and induction of epithelial-mesenchymal transition of CRC.	 Lower expression of LINC00485 predicted poor prognosis in CRC patients.	Yes	In mouse models, LINC00485 knockdown or down-regulation of miR-581 significantly repressed CRC cell growth and prevented CRC liver metastasis.  LINC00485 knockdown promoted the proliferation, migration, and invasion of FHC cells, while LINC00485 overexpression weakened these abilities of LoVo cells.	33461166
LINC00477	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	serum of PCOS patients	Interaction(miR-128 axis)	ISH//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	LINC00477 was significantly upregulated in the serum of PCOS patients as well as PCOS mouse models. Moreover, miR-128 mimics partially abrogated the effect of LINC00477 on granulosa cells.		Yes	LINC00477 overexpression inhibited the proliferation and promoted the apoptosis of granulosa cells, whereas knockdown of LINC00477 yielded the opposite effects. 	33622342
LINC00473	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue samples and GC cell lines	Expression[highly expressed]	qRT-PCR	In our results, LINC00473 expression was increased in GC tissue samples and GC cell lines compared with paired adjacent normal stomach tissue samples and normal gastric epithelial cell line, respectively. 	High-expression of LINC00473 was correlated with poor histological type, advanced clinical stage, more lymph node metastasis and present distant metastasis. 	Yes	 The study in vitro indicated that silencing of LINC00473 had no effect on GC cell viability, but inhibited GC cell migration and invasion through modulating MMP2 and MMP9 expression.	30071345
LINC00473	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction[CCND1 ]	qRT-PCR	Here, we found that lncRNA LINC00473 is significantly upregulated in breast cancer cells.Altogether, the activation effect of LINC00473 on CCND1 is a net effect of two antagonistic regulatory pathways. Our finding provides a novel lncRNA-mediated precise transcriptional control of CCND1.		Yes	 Loss- or gain-of-function experiments show that LINC00473 promotes cell proliferation. 	30848493
LINC00473	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells 	Interaction(miR-497-5p)	Western Blot//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression.A negative correlation between LINC00473 and miR-497-5p was observed in lung cancer tissues. Notably, it was demonstrated that LINC00473 could bind directly with miR-497-5p and inhibit its expression. miR-497-5p inhibitors reversed the effect of si-LINC00473. 	LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression.	Yes	Proliferation, migration and invasion as well as the related protein levels were increased in A549 and H1299 transfected with pcDNA3.1-LINC00473, while the opposite results were obtained in A549 and H1299 transfected with small interfering (si)-LINC00473.	33868467
LINC00473	LncRNA	Rattus norvegicus	Osteoarthritis	C28/I2 cells	Interaction(miR-424-5p/LY6E axis)	Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay//ELISA//Bioinformatics Analysis	The results indicated that, compared with the OA + adeno-associated virus si-NC group, LINC00473 knockdown significantly suppressed the degradation of chondrocyte extracellular matrix and the production of proinflammatory cytokines in OA model rats. Furthermore, bioinformatics analysis, luciferase reporter and RNA immunoprecipitation assays indicated that LINC00473 served as a microRNA (miR)-424-5p sponge in C28/I2 cells, and that lymphocyte antigen 6 locus E (LY6E) was the downstream target. In addition, the inhibitory effects of LINC00473 knockdown on chondrocyte apoptosis and the inflammatory response could be reversed by LY6E overexpression in IL-1β-stimulated C28/I2 cells. In summary, the findings indicated that LINC00473 contributed to OA progression by modulating the miR-424-5p/LY6E axis, which may serve as a potential therapeutic strategy for patients with OA.		Yes	LINC00473 knockdown significantly suppressed the degradation of chondrocyte extracellular matrix and the production of proinflammatory cytokines in OA model rats. Furthermore, bioinformatics analysis, luciferase reporter and RNA immunoprecipitation assays indicated that LINC00473 served as a microRNA (miR)-424-5p sponge in C28/I2 cells, and that lymphocyte antigen 6 locus E (LY6E) was the downstream target. In addition, the inhibitory effects of LINC00473 knockdown on chondrocyte apoptosis and the inflammatory response could be reversed by LY6E overexpression in IL-1β-stimulated C28/I2 cells. 	34539843
LINC00473	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cell lines	Regulation[miR-497-5p/PRKAA1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	 LINC00473 presented much higher expression and LINC00473 suppression restrained the proliferation, migration, and epithelial-mesenchymal transition (EMT) process in ESCC cells.LINC00473 regulates ESCC progression through miR-497-5p/PRKAA1 axis, which provides a new therapeutic strategy for ESCC patients.		Yes	 LINC00473 presented much higher expression and LINC00473 suppression restrained the proliferation, migration, and epithelial-mesenchymal transition (EMT) process in ESCC cells.	31584290
LINC00473	LncRNA	Homo sapiens	Colorectal Neoplasms	 colorectal cancer tissues from patients with distant metastasis 	Interaction(miR-195)	qRT-PCR//Luciferase Report Assay	The expression of LINC00473 in colorectal cancer tissues from patients with distant metastasis was higher than that from cases without distant metastasis.These data suggested that LINC00473 induced cell proliferation, cell cycle progression and EMT progression by acting as a ceRNA for miR-195 in colorectal cancer.	The higher expression level of LINC00473 was positively correlated with advanced clinical stage. 	Yes	 The elevated expression of LINC00473 accelerated colorectal cancer cell proliferation, cell cycle progression and invasion. Moreover, overexpression of LINC00473 induced epithelial to mesenchymal (EMT) progression in HT29 and SW480 cells. 	34306345
LINC00473	LncRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Regulation[YAP1‑TEAD1‑Hippo signaling]	Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the present study, LINC00473 was significantly increased in glioma tissues and in cell models, and predicted a poor prognosis in patients with glioma. Mechanistically, LINC00473 functioned as a competing endogenous (ce)RNA to decrease microRNA (miR)‑195‑5p expression. Moreover, Yes‑associated protein 1 (YAP1) and TEA domain family member 1 (TEAD1) were identified as downstream targets of miR‑195‑5p, whose expression levels were inhibited by miR‑195‑5p. LINC00473 knockdown suppressed glioma progression through the decrease of miR‑195‑5p and subsequent increase of YAP1 and TEAD1 expression levels.		Yes	Notably, LINC00473 knockdown not only suppressed cell proliferation, invasion and migration of glioma cells, but also blocked cell cycle progression and induced apoptosis. Subcutaneous xenotransplanted tumor model experiments revealed that reduced LINC00473 expression was able to suppress in vivo glioma growth. 	31894297
LINC00473	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[miR-637/CDK6 axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, LINC00473 was notably elevated in glioma tissues and cell lines. Thus, we demonstrated that LINC00473 could act as a ceRNA of miR-637 to promote glioma progression through regulating CDK6 expression, which provided a potential therapeutic target for treatment of glioma patients.	High LINC00473 expression was associated with advanced WHO grade (III-IV), low Karnofsky performance score (KPS), and poor prognosis. 	Yes	Loss function assays showed that LINC00473 knockdown decreased glioma cell proliferation, invasion and epithelial-mesenchymal transition (EMT) processes in vitro, and reduced tumor growth in vivo.	31561732
LINC00473	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung adenocarcinoma tissues and cells	regulation[miR-1294/ROBO1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results showed that LINC00473 was up-regulated and miR-1294 was down-regulated in lung adenocarcinoma tissues and cells.In conclusion, LINC00473 acts as a tumor promoter in lung adenocarcinoma by regulating the miR-1294/ROBO1 axis.		Yes	 Functionally, LINC00473 promoted cell proliferation and motility in lung adenocarcinoma by downregulating miR-1294. 	32351100
Linc00473	LncRNA	Homo sapiens	Cholangiocarcinoma	 CCA tissues and cell lines	regulation[DDX5,miR-506]	qRT-PCR//Luciferase Report Assay//RIP	Linc00473 was highly expressed in CCA tissues and cell lines. Furthermore, linc00473 acted as miR-506 sponge and regulated its target gene DDX5 expression. Rescue assays verified that linc00473 modulated the tumorigenesis of CCA by regulating miR-506.		Yes	 Linc00473 knockdown inhibited CCA growth and metastasis.	32694946
LINC00473	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer cells	regulation[miR-195-5p/SEPT2 axis ]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	In the present study, we discovered that prostate cancer cells presented high expression of LINC00473, and LINC00473 inhibition limited cell proliferation and the expression of proteins in JAK-STAT3 signaling pathway. All in all, LINC00473 contributed to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer, which provided a novel therapeutic tactic for prostate cancer patients.		Yes	In the present study, we discovered that prostate cancer cells presented high expression of LINC00473, and LINC00473 inhibition limited cell proliferation and the expression of proteins in JAK-STAT3 signaling pathway.	32440687
LINC00473	LncRNA	Homo sapiens	Molecular Epidemiology	IPA tissues	Interaction(miR-502-3p/KMT5A/cyclin D1 and CDK2)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RNA-seq//Luciferase Report Assay//IHC//EdU Staining	In our study, LINC00473 was identified as the most upregulated lncRNA in IPA by whole transcriptome RNA sequencing (RNA-Seq). LINC00473 is overexpressed in IPA and can promote PA cells proliferation. Mechanistically, overexpression of LINC00473 restricts miR-502-3p through the ceRNA mechanism, upregulates KMT5A expression, and promotes the expression of cyclin D1 and CDK2, which is conducive to the cell cycle process, thereby promoting the proliferation of PA cells, involving IPA progression.		Yes	LINC00473 is overexpressed in IPA and can promote PA cells proliferation. 	34091587
LINC00924	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(hnRNPC/Mnk2 )	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Colony Formation Assay//Invasion Assay//Transwell Assay	LINC00924 was highly expressed in GC, and its high expression is associated with a broad range of PM. Regarding the mechanism, LINC00924 regulated the alternative splicing (AS) of Mnk2 pre-mRNA by binding to hnRNPC. Specifically, LINC00924 enhanced the binding of hnRNPC to Mnk2 pre-mRNA at e14a, thus downregulating Mnk2a splicing and regulating the p38 MAPK/PPARα signaling pathway.		Yes	Via RNA sequencing, RNA pulldown assay, mass spectrometry, Seahorse, Lipidomics, spheroid formation and cell viability assays, we found that LINC00924 promoted fatty acid (FA) oxidation (FAO) and FA uptake, which was essential for matrix-detached GC cell survival and spheroid formation.	36418856
LINC00930	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Interaction(PFKFB3/RBBP5 and GCN5)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//qPCR//Co-IP//CCK8//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	 In this study, we identified and functionally characterized a novel metabolism-related lncRNA, LINC00930, which was upregulated and associated with tumorigenesis, lymphatic invasion, metastasis, and poor prognosis in nasopharyngeal carcinoma (NPC). Mechanistically, LINC00930 served as a scaffold to recruit the RBBP5 and GCN5 complex to the PFKFB3 promoter and increased H3K4 trimethylation and H3K9 acetylation levels in the PFKFB3 promoter region, which epigenetically transactivating PFKFB3, and thus promoting glycolytic flux and cell cycle progression.	 In this study, we identified and functionally characterized a novel metabolism-related lncRNA, LINC00930, which was upregulated and associated with tumorigenesis, lymphatic invasion, metastasis, and poor prognosis in nasopharyngeal carcinoma (NPC). 	Yes	 Functionally, LINC00930 was required for increased glycolysis activity and cell proliferation in multiple NPC models in vitro and in vivo. 	35209949
LINC00941	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cells	Regulation(Cadherin 6)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//RNA-seq//Cell Proliferation Assay//ChIP-seq//Invasion Assay//IF	Linc00941 expression was significantly higher in aggressive cancer both in the TCGA dataset and in a separate validation cohort from our institution. Loss of function assays for linc00941 showed that it promotes response to stimuli and invasiveness while restraining proliferation in PTC cells, a typical phenotype of metastatic cells. From the integration of TCGA data and linc00941 knockdown RNA-seq profiling, we identified 77 genes under the regulation of this lncRNA. Among these, we found the prometastatic gene CDH6. Linc00941 knockdown partially recapitulates the effects observed upon CDH6 silencing, promoting cell cytoskeleton and membrane adhesions rearrangements and autophagy. The combined expression of CDH6 and linc00941 is a distinctive feature of highly aggressive PTC lesions.		Yes	Loss of function assays for linc00941 showed that it promotes response to stimuli and invasiveness while restraining proliferation in PTC cells, a typical phenotype of metastatic cells. 	32495722
LINC01535	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction(LINC01535/miR-146b-5p/TRIM2 axis )	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	This study showed downregulation of LINC01535 in ccRCC.Furthermore, LINC01535 sponged miR-146b-5p which had a negative correlation with LINC01535, and TRIM2 was a direct target of miR-146b-5p and mediated by LINC01535. Mechanically, LINC01535/miR-146b-5p/TRIM2 axis affected ccRCC progression by mediating the PI3K/Akt signaling. 		Yes	Moreover, LINC01535 upregulation attenuated in vitro ccRCC development and hindered in vivo tumor growth. 	35342411
LINC01518	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Regulation[PIK3CA/Akt pathway ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	We found that LINC01518 expression was upregulated and miR-1-3p expression was downregulated in ESCC cells.In conclusion, LINC01518 knockdown inhibited tumorigenicity in ESCC cells by suppression of PIK3CA/Akt pathway through upregulating miR-1-3p.		Yes	LINC01518 knockdown inhibited cell proliferation and promoted apoptosis in ESCC cells.	31810385
LINC01515	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells 	Interaction(miR-325/CDCA5 pathway)	IHC//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC01515 expression was increased in NPC and that high LINC01515 expression was associated with a worse prognosis. Mechanistically, LINC01515 facilitated cell division cycle associated 5 (CDCA5) expression via serving as a sponge for miR-325. And more notably, miR-325 suppressed NPC progression in vitro by targeting CDCA5.	LINC01515 expression was increased in NPC and that high LINC01515 expression was associated with a worse prognosis. 	Yes	Functionally, depletion of LINC01515 resulted in an inhibition of cell proliferation, migration and invasion, while apoptosis was promoted. 	33770322
LINC01503	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	interaction[Wnt Signaling]	qRT-PCR//Western Blot//Transwell Assay	 LINC01503 was highly expressed in gastric cancer tissues and cell lines, which was correlated with poor prognosis.This research reported that the elevated expression of LINC01503 could promote proliferation and metastasis of gastric cancer through positively regulating the Wnt/β-catenin pathway.	 LINC01503 was highly expressed in gastric cancer tissues and cell lines, which was correlated with poor prognosis.	Yes	Knockdown of LINC01503 suppressed gastric cancer cell proliferation and invasion, whereas overexpression of LINC01503 showed a reverse trend. 	32207034
LINC01503	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[ DUSP5/CDKN1A]	qRT-PCR//FISH//RIP//ChIP	 Linc01503 was remarkably elevated in GC and tightly linked with the overall survival of patients with GC. EGR1-activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicating it as a prospective target for GC therapeutics.	 Linc01503 was remarkably elevated in GC and tightly linked with the overall survival of patients with GC. 	Yes	Functionally, linc01503 knockdown resulted in the activation of apoptosis and G1/G0 phase arrest in GC.	33145887
LINC01503	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		regulation[MAPK/ERK pathway]	CCK8//qRT-PCR//Flow Cytometry	LINC01503 was highly expressed in HCC and positively correlated with large tumor size, high tumor grade, advanced tumor stage, and poor prognosis of HCC patients.LINC01503 is highly expressed in HCC and promotes the progression of HCC via MAPK/ERK pathway, which maybe a new potential biomarker and therapeutic target for HCC.	LINC01503 was highly expressed in HCC and positively correlated with large tumor size, high tumor grade, advanced tumor stage, and poor prognosis of HCC patients.	Yes	Silencing LINC01503 with shRNA significantly restrained the proliferation of MHCC-97H HCC cells and strengthened the apoptosis, while up-regulation of LINC01503 in Huh7 HCC cells contributed to the contrary effects.	32547318
LINC01503	LncRNA	Homo sapiens	Glioma	glioma tissue and cell lines	Interaction[Wnt/β-catenin pathway]	qRT-PCR//Western Blot	We found that LINC01503 expression level was significantly up-regulated in glioma tissue and cells.Mechanistic investigation showed that LINC01503 can modulate Wnt/β-catenin signaling, as determined by that knockdown of LINC01503 decreased the TOP-FLASH activity and β-catenin, cyclin D1 and c-myc.	We found that LINC01503 expression level was significantly up-regulated in glioma tissue and cells, and that its overexpression was significantly correlated with KPS, tumor size and WHO grade in glioma patients. Kaplan-Meier analysis showed that patients with higher levels of LINC01503 had significantly poorer overall survival and disease-free survival than those with lower expression of this lncRNA in glioma patients.	Yes	 Functional assays with in vitro showed that knockdown of LINC01503 in the U251 and LN299 cell lines suppressed cells growth, colony formation, invasion and migration, and promoted apoptosis. 	30840283
LINC01503	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues 	regulation[ SFPQ-FOSL1 axis]	ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	Here, we verified that LINC01503 was highly expressed in NPC and correlated with poor prognosis.Taken together, our findings reveal that AR-induced LINC01503 can promote NPC progression through the SFPQ-FOSL1 axis, which represents a novel prognostic biomarker and therapeutic target for NPC patients.	Here, we verified that LINC01503 was highly expressed in NPC and correlated with poor prognosis.	Yes	 LINC01503 promoted NPC cell proliferation, migration, and invasion in vitro, and facilitated tumor growth and metastasis in vivo. 	32661324
LINC01503	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC samples and cell lines	interaction[miR-342-3p]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//EdU Staining//Transwell Assay	 We demonstrated that the expression of lncRNA LINC01503 and LIM and SH3 domain protein 1 (LASP1) were upregulated and miR-342-3p was downregulated in NSCLC samples and cell lines. In addition, LINC01503 could bind to miR-342-3p and affect the expression of LASP1.		Yes	 Functional experiments revealed that inhibiting the expression of LINC01503 or over-expression of miR-342-3p inhibited NSCLC growth and metastasis both in vitro and in vivo. 	32938459
LINC01503	LncRNA	Homo sapiens	gastric cardia adenocarcinoma	GCA tissues and cell lines	regulation[miR-133a-5p/VIM Axis and EMT Process]	qRT-PCR//Luciferase Report Assay//RIP	The expression level of LINC01503 was significantly elevated in GCA tissues and cell lines. LINC01503 serves as an oncogenic lncRNA to promote GCA progression via affecting LINC01503/miR-133a-5p/VIM axis and EMT process. 	High expression of LINC01503 was correlated with lymph node metastasis, TNM stage, and poor prognosis of GCA patients.	Yes	Knockdown of LINC01503 significantly reduced proliferation, migration, and invasion ability in GC cells.	33200343
LINC01494	LncRNA	Homo sapiens	Glioma	glioma tissue	Regulation[LINC01494/miR-122-5p/CCNG1 signaling ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC01494 was identified as a significantly upregulated lncRNA in glioma through bioinformatics analysis.Rescue assay further demonstrated that LINC01494/miR-122-5p/CCNG1 signaling cascade plays a critical role in regulating glioma cell proliferation, migration and invasion.	 Furthermore, LINC01494 upregulation indicated poor prognosis. 	Yes	 Meanwhile, in vitro investigation indicated that silencing LINC01494 with siRNAs obviously inhibited the proliferation, cell cycle, migration and invasion of glioma cells. 	31571916
LINC01485	LncRNA	Homo sapiens	Stomach Neoplasms	gastric tissues	regulation[EGFR/Akt Signaling]	RNA Pull-Down//Wound Healing Assay//qRT-PCR//FISH//Transwell Assay	LINC01485 was upregulated and associated with tumor size, lymphatic metastasis and advanced pathological stage in gastric cancer. LINC01485 promoted EGFR stabilization and activation of EGFR/Akt signaling in gastric cancer. 	LINC01485 was upregulated and associated with tumor size, lymphatic metastasis and advanced pathological stage in gastric cancer.	Yes	LINC01485 promoted gastric cancer cell proliferation, migration and invasion in vitro and in vivo. 	32904620
LINC01480	LncRNA	Homo sapiens	Coronary Artery Disease	CAD samples 	Regulation	Bioinformatics Analysis	 The immune cell infiltration analysis of ischemic cardiomyopathy (ICM; an advanced stage of CAD) samples revealed that the proportion of macrophage M2 was upregulated in the LINC01480 highly expressed samples, thus suggesting that LINC01480 plays a protective role in the progression of ICM.		Yes	 The immune cell infiltration analysis of ischemic cardiomyopathy (ICM; an advanced stage of CAD) samples revealed that the proportion of macrophage M2 was upregulated in the LINC01480 highly expressed samples, thus suggesting that LINC01480 plays a protective role in the progression of ICM.	35557532
LINC01451	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BLCa tissues	Interaction(LIN28/TGF-β/Smad pathway)	qRT-PCR//ChIP//Western Blot	LINC01451 was identified a novel functional lncRNA, whose expression level in BLCa tissues was significantly higher compared with the normal tissues. Mechanistically, LINC0145 was shown to depend on LIN28A and LIN28B, facilitated epithelial-mesenchymal transition (EMT) through activating the TGF-β/Smad signaling pathway, which subsequently aggravated BLCa progression.		Yes	Furthermore, it was found that LINC01451 directly docked LIN28A and LIN28B, and promoted the proliferation, invasion, and metastasis of BLCa.	33516780
LINC01448	LncRNA	Homo sapiens	Pancreatic Neoplasms		Interaction(miR-505)	Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	LINC01448 was identified as an oncogenic lncRNA that could reduce miR-505 expression. Subsequent studies confirmed that LINC01448 enhanced cell proliferation, invasion, sphere formation, glucose consumption, and lactate production by regulating the miR-505/HK2 pathway. 		Yes	Subsequent studies confirmed that LINC01448 enhanced cell proliferation, invasion, sphere formation, glucose consumption, and lactate production by regulating the miR-505/HK2 pathway. 	33520999
LINC01446	LncRNA	Homo sapiens	Glioblastoma	GBM tissues	Regulation[miR-489-3p/TPT1 axis]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Transwell Assay	 Our study revealed a novel lncRNA LINC01446 whose expression was elevated in GBM tissues.Taken together, this study demonstrates a novel singling pathway of LINC01446/miR-489-3p/TPT1 cascade that regulates GBM progression.	Besides, high expression of LINC01446 indicated a poor prognosis in GBM patients. 	Yes	 Functionally, LINC01446 knockdown dramatically inhibited GBM cell proliferation, arrested cell-cycle progression and attenuated invasion in vitro. Furthermore, the xenograft mouse model showed that LINC01446 silence led to impaired tumor growth in vivo.	30029885
LINC01436	LncRNA	Homo sapiens	Stomach Neoplasms	cancerous tissues of GC samples	regulation[ miR-585 and FBXO11]	qRT-PCR	We demonstrated that LINC01436 was significantly up-regulated in cancerous tissues of GC samples, and its overexpression was correlated with a worse prognosis for the patients.Collectively, these results suggested that LINC01436 was an oncogenic lncRNA in GC and promoted proliferation and metastasis of GC cell via regulating miR-585 and FBOX11.		Yes	In the GC cell line BGC823 cells, LINC01436 knockdown repressed the proliferation and metastasis of cancer cells; conversely, in GC cell line AGS cells, overexpression of LINC01436 showed the opposite effects. 	31829474
LINC01526	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells and tissues	Interaction(TARBP2/GNG7 )	RNA Pull-Down//Western Blot//CCK8//FISH//qRT-PCR//RIP//RNA-seq//Transwell Assay//IF	We found that LINC01526 was upregulated in gastric cancer cells and tissues.  Furthermore, LINC01526 interacted with TAR (HIV-1) RNA-binding protein 2 (TARBP2) and decreased the mRNA stability of G protein gamma 7 (GNG7) through TARBP2. Finally, the rescue assay showed that downregulating GNG7 partially rescued the cell proliferation inhibited by LINC01526 or TARBP2 silencing. 		Yes	The function experiments in vitro and the Xenograft mouse model in vivo proved that LINC01526 could promote gastric cancer cell proliferation and migration. 	36230863
LINC01535	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Interaction[miR‐214/EZH2]	RNA Pull-Down//IHC//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay//ChIP	Clinically, LINC01535 is significantly up-regulated in cervical cancer tissues and correlated with advanced clinical stage and poor prognosis. Activation of the miR-214/EZH2 regulatory loop by overexpression of miR-214 or silencing of EZH2 reverses the roles of LINC01535 in promoting cervical canc`er cell growth, migration and invasion in vitro and cervical cancer xenograft growth in vivo.	Clinically, LINC01535 is significantly up-regulated in cervical cancer tissues and correlated with advanced clinical stage and poor prognosis. 	Yes	 Functional experiments showed that enhanced expression of LINC01535 promotes cervical cancer cell growth, migration and invasion in vitro and cervical cancer xenograft growth in vivo. Reciprocally, LINC01535 knockdown suppresses cervical cancer cell growth, migration and invasion.	31273925
LINC01436	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-466)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	 LINC 01436 was upregulated in CRC and predicted poor survival.  LINC 01436 was inversely correlated with mature miR-466, but not miR-466 precursor. LINC 01436 was predicted to bind with miR-466 precursor. Their interaction was further verified by dual-luciferase activity assay. In CRC cells, LINC 01436 overexpression downregulated mature miR-466 but not miR-466 precursor. 	 LINC 01436 was upregulated in CRC and predicted poor survival. 	Yes	Cell proliferation analysis showed that LINC 01436 overexpression rescued cell proliferation reduced by miR-466. LINC 01436 is overexpressed in CRC and promotes cancer cell proliferation by suppressing miR-466 maturation.	35171402
LINC01535	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[miR-214-3p/KCNC4 Axis]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 The high expression of LINC01535 was presented in OS tissues and cell lines compared with adjacent normal tissues and human osteoblasts.  LINC01535, miR-214-3p and KCNC4 constituted an effective axis that exerted a pregnant regulation in OS development, which is a quite meaningful discovery for exploring potential therapeutic methods for OS patients.	 Moreover, OS patients with high LINC01535 expression exhibited poor prognosis.	Yes	 Loss-of-function assay revealed that silenced LINC01535 significantly attenuated cell proliferation, migration and invasion, and enhanced cell apoptosis in OS. 	32753970
LINC01606	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer cell and tissues	Interaction( SCD1-Wnt/β-catenin-TFE3 feedback loop signalling)	qRT-PCR//RIP//Transwell Assay	The expression of lncRNA LINC01606 was frequently upregulated in human colon cancer and strongly associated with a poor prognosis. Mechanistically, LINC01606 enhanced the expression of stearoyl-CoA desaturase 1 (SCD1), serving as a competing endogenous RNA to modulate miR-423-5p expression, subsequently activating the canonical Wnt/β-catenin signaling, and transcription factor binding to IGHM enhancer 3 (TFE3) increased LINC01606 transcription after recruitment to the promoter regions of LINC01606.	The expression of lncRNA LINC01606 was frequently upregulated in human colon cancer and strongly associated with a poor prognosis. 	Yes	LINC01606 functioned as an oncogene and promotes colon cancer cell growth, invasion and stemness both in vitro and in vivo. Moreover, LINC01606 protected colon cancer cells from ferroptosis by decreasing the concentration of iron, lipid reactive oxygen species, mitochondrial superoxide and increasing mitochondrial membrane potential.	35485210
LINC01605	LncRNA	Homo sapiens	Colorectal Neoplasms	CC tissues	Interaction(METTL3 and SPTBN2.)	RIP//MeRIP//RNA Pull-Down//Luciferase Report Assay	LINC01605, significantly highly expressed in CC, was a prognostic factor for patients with CC.Moreover, LINC01605 was regulated by SMYD2-EP300-mediated modifications of histone H3K4me3 as well as H3K27ac. 		Yes	Functional experiments revealed that LINC01605 knockdown inhibited the proliferatory and metastatic potential of CC cells in vitro and in vivo.	34544413
LINC01585	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues 	Regulation[CAMP/CREB signaling pathway]	RNA Pull-Down//CCK8//FISH//qRT-PCR//Cell Cycle Assay//Colony Formation Assay	Here, we report a novel lncRNA, LINC01585, is aberrantly down regulated during breast cancer (BC).  Mechanistically, LINC01585 was located in nuclear and binding with NONO protein. Interestingly, when LINC01585 was down-expressed, NONO separated from LINC01585 and then interacted with CRTC. The complex promotes CAMP/CREB target gene transcription and thus promotes the growth of breast cancer.		Yes	 Functionally, we found that LINC01585 overexpression inhibited breast cancer proliferation and growth by prototypical experiments.	30366079
LINC01572	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Interaction(miR-195-5p/PFKFB4 )	RNA Pull-Down//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	In this study, we profiled lncRNAs in HCC tissues and corresponding adjacent tissues from HCC patients with T2DM by RNA sequencing.  Our data showed that LINC01572 was aberrantly upregulated in HCC tissues as compared with control, especially in those with concurrent T2DM.  A mechanistic study revealed that LINC01572-regulated HCC progression via sponging miR-195-5p to increase the level of PFKFB4 and subsequent enhancement of glycolysis and activation of PI3K-AKT signaling.	The high level of LINC01572 was correlated with advanced tumor stage, increased blood HbA1c level, and shortened survival time. 	Yes	The overexpression of LINC01572 significantly promoted HCC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT), while the knockdown of LINC01572 had the opposite effects on HCC cells. 	34970545
LINC01572	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cell lines	Regulation	CCK8//qRT-PCR//Transfection//EdU Staining	 Then, we successfully created a risk model according to five ferroptosis-associated lncRNAs (LINC00472, MBNL1-AS1, LINC01572, ZFPM2-AS1, and TMPO-AS1). Our nominated model had good stability and predictive function. The expression patterns of five ferroptosis-associated lncRNAs were confirmed by polymerase chain reaction (PCR) in LUAD cell lines. 		Yes	Knockdown of LINC01572 significantly inhibited cell viability and induced ferroptosis in LUAD cell lines.	36686701
LINC01569	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-381-3p/RAP2A Axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	LINC01569 expression was distinctly increased in CRC.		Yes	Curiously, if LINC01569 is removed, CRC cells will not migrate, proliferate, and invade remarkably. 	34422671
LINC01564	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	Regulation(POU2F1 )	RNA Pull-Down//IHC//ChIP//Western Blot//qRT-PCR//FISH//RIP//MTT//Colony Formation Assay//Invasion Assay//IF	The results showed that LINC01564 complementary bound to the 3'UTR of POU2F1 to form an RNA duplex, whereby stabilizing POU2F1 mRNA and increasing the enrichment in cells.  The level of LINC01564 was also increased by POU2F1 through transcription activation.  In vitro assays showed that LINC01564 promoted the proliferation, invasion and migration of GC cells through increasing POU2F1. In vivo experiments indicate the promotion of GC proliferation and metastasis by the interaction between LINC01564 and POU2F1.		Yes	 In vitro assays showed that LINC01564 promoted the proliferation, invasion and migration of GC cells through increasing POU2F1. In vivo experiments indicate the promotion of GC proliferation and metastasis by the interaction between LINC01564 and POU2F1.	35562740
LINC01561	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	interaction[SHCBP1,miR-760]	qRT-PCR	 In this study, we first provided evidence that LINC01561 expressions were distinctly upregulated in NSCLC tissues and cell lines. In summary, our findings indicated that SOX2-induced overexpression of LINC01561 promoted the proliferation and metastasis by acting as a competing endogenous RNA to modulate SHCBP1 by sponging miR-760.	Clinical research revealed that upregulation of LINC01561 was related to poorer clinicopathologic features and shorter survival time.	Yes	 Functionally, suppression of LINC01561 exhibited tumor-suppressive functions through impairing cell proliferation, migration, and invasion as well as inducing apoptosis. 	32003010
LINC01559	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues	Interaction(miR-370-3p/miR-485-5p/miR-940)	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//EdU Staining//ChIP	LINC01559 was significantly increased in TNBC tissues as compared to matched normal tissues, which was due to high levels of H3K4Me3 and H3K27Ac in the promoter region. Mechanistically, LINC01559 served as a ceRNA that sponged miR-370-3p, miR-485-5p and miR-940, resulting in increasing the expression of a cohort of oncogenes, thus accelerating TNBC progression.		Yes	Knockdown of LINC01559 inhibited TNBC cell proliferation, migration and invasion in vitro, and also retarded tumor growth and reduced lung metastasis in vivo. 	35715331
LINC01559	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patient	Interaction(miR-511/SLC38A1 )	CCK8//qRT-PCR//Transwell Assay//Western Blot	LINC01559 was highly expressed, and related to poor prognosis in HCC patients. Furthermore, LINC01559 can function as a sponge for miR-511, which was downregulated in HCC patients. Downregulation of miR-511 significantly increased the cell viability, invasive and migratory capacities, and could abolish the suppressive effect of LINC01559-knockdown on these HCC cells. Moreover, SLC38A1 was a target of miR-511 and upregulated in HCC. K	LINC01559 was highly expressed, and related to poor prognosis in HCC patients.	Yes	LINC01559-knockdown restrained the proliferation and growth of HepG2 and Huh7 cells. 	33588099
LINC01559	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic tissues ,cell lines	Interaction[YAP-mediated pathway]	qRT-PCR	Further, our results showed that LINC01559 was stimulated in PC cell lines relative to normal controls. Collectively, our findings unmasked that LINC01559 accelerates PC progression through relying on YAP, providing a new potential target for clinical treatment of patients with PC.		Yes	Furthermore, we validated that LINC01559 facilitated PC cell proliferation and migration in vitro. Also, silencing LINC01559 obstructed PC cell growth in vivo.	31608998
LINC01559	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues 	Expression [highly expressed]	Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//IF//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	We found high expression of LINC01559 indicates lymph node metastasis and poor prognosis. 		Yes	Besides, LINC01559 promotes lung cancer cell proliferation and migration in vitro, by enhancing autophagy signal pathway via sponging hsa-miR-1343-3p.	34823534
LINC01555	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The Cancer Genome Atlas (TCGA) dataset showed that LINC01555 was highly expressed in CRC tissue when compared with adjacent normal colorectal tissue.	LINC01555 expression was positively correlated with tumor stage, but negatively correlated with disease-free survival (DFS) and overall survival (OS) and was an independent risk factor for CRC.	Yes	 Knockdown of LINC01555 inhibited cell proliferation, migration, and invasion of CRC cells. Functional studies showed that knockdown of NmU reduced cell migration and invasion of CRC cells that overexpressed LINC01555.	31144675
LINC01555	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	SCLC tissues and cells	Interaction(microRNA-122-5p/clic1 axis )	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	 Linc01555 was elevated in SCLC tissues and cells, and in H446/DDP cells or DMS-53/DDP vs. its parental cells; Restraining linc01555 or elevating miR-122-5p repressed the proliferation and metastasis of H446/DDP or DMS-53/DDP cells and vasculogenic mimicry (VM) formation. CLIC1 mediated miR-122-5p to influence the occurrence and development of SCLC. Linc01555 competitively combined with miR-122-5p, which targeted CLIC1.		Yes	 Linc01555 was elevated in SCLC tissues and cells, and in H446/DDP cells or DMS-53/DDP vs. its parental cells; Restraining linc01555 or elevating miR-122-5p repressed the proliferation and metastasis of H446/DDP or DMS-53/DDP cells and vasculogenic mimicry (VM) formation. 	36045598
LINC01554	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Regulation[ Akt/mTOR Signaling Pathway]	RNA Pull-Down//Northern Blot//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay	LINC01554 was frequently downregulated in HCC, which was significantly associated with tumor invasion (P = 0.005), tumor size (P = 0.041), tumor staging (P = 0.023) and shorter survival (P = 0.035) of HCC patients.LINC01554 promoted the ubiquitin-mediated degradation of PKM2 and inhibited Akt/mTOR signaling pathway to abolish aerobic glycolysis in HCC cells. Further study found that LINC01554-knockout could effectively reverse the tumor-suppressive effect of LINC01554. 	LINC01554 was frequently downregulated in HCC, which was significantly associated with tumor invasion (P = 0.005), tumor size (P = 0.041), tumor staging (P = 0.023) and shorter survival (P = 0.035) of HCC patients.	Yes	Ectopic expression of LINC01554 inhibited HCC cell growth, colony formation in soft agar, foci formation, and tumor formation in nude mice. 	30809309
LINC01550	LncRNA	Homo sapiens	Melanoma	melanoma tissues	Expression(lower expressed)	qRT-PCR//MTT//Cell Cycle Assay//Transwell Assay	 We found that lncRNA LINC01550 was significantly down-regulated in the melanoma tissues as compared to the normal tissues.	The low expression of LINC01550 was tightly associated with shorter overall survival and disease-free survival of patients with melanoma.	Yes	 LINC01550 expression is negatively associated with tumor cell proliferation and invasion abilities in melanoma as evidenced by the single-cell RNA sequencing (scRNA-seq) databases. Up-regulation of LINC01550 significantly inhibited proliferation and invasion abilities, as well as induced cell apoptosis and G1 and S phase arrest of the melanoma cells. 	33609219
LINC01546	LncRNA	Homo sapiens	Stomach Neoplasms	GCs 	Interaction(PKM2 )	RNA Pull-Down//Co-IP//CCK8//qRT-PCR//RIP//FISH//Transwell Assay	 Long non-coding RNA (lncRNA) VAL is significantly upregulated in GCs and indicates poor prognosis. Mechanistically, VAL strengthens the enzymatic activity of PKM2 and aerobic glycolysis of GC cells through directly binding with PKM2 to abrogate the PKM2-Parkin interaction, and to suppress Parkin-induced polyubiquitination of PKM2. 	 Long non-coding RNA (lncRNA) VAL is significantly upregulated in GCs and indicates poor prognosis. 	Yes	 Functional assays showed that VAL promotes GC malignant progression. 	36229913
LINC01537	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(RIPK4/TRIM25/RIPK4 )	RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay	LINC01537 was significantly overexpressed in GC tissues and associated with a poor prognosis. Mechanistically, LINC01537 stabilizes RIPK4 by reducing the binding of RIPK4 to TRIM25 and reducing its ubiquitination degradation, thereby promoting the expression of the NF-κB signaling pathway. According to our findings, the LINC01537-RIPK4-NF-κB axis promoted GC metastasis and tumorigenesis.	LINC01537 was significantly overexpressed in GC tissues and associated with a poor prognosis. 	Yes	Functional experimental results revealed that LINC01537 promoted the proliferation, invasion, and migration of GC cells.  The animal experiments revealed that LINC01537 promoted tumorigenesis and metastasis in vivo.	36358656
LINC01535	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-761)	qRT-PCR//Luciferase Report Assay//RIP	LINC01535 expression was observed to be upregulated in CRC tissues and cell lines. A luciferase reporter assay demonstrated that LINC01535 regulated miR-761 directly and RNA-binding protein immunoprecipitation further confirmed that the suppression of LINC01535 by miR-761 was via an RNA-induced silencing complex. 		Yes	A functional study suggested that LINC01535 silencing inhibited CRC cell proliferation and invasion but enhanced cisplatin sensitivity of CRC cells, while co-transfection with a miR-761 inhibitor reversed these biological effects. 	33986850
LINC01436	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[targeting miR-30a-3p ]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Microarray//ChIP	Here, we identified a novel up-regulated lncRNA, LINC01436 (RefSeq: NR_110419.1), in non-small cell lung cancer (NSCLC). Mechanistically, LINC01436 exerted biological functions by acting as a microRNA (miR)-30a-3p sponge to regulate the expression of its target gene EPAS1. Our findings characterize LINC01436 as a new hypoxia-sensitive lncRNA with oncogenic function in NSCLC, suggesting that LINC01436 may be a potential biomarker for prognosis and a potential target for treatment.	High expression of LINC01436 was significantly associated with poor overall survival.	Yes	Gain- and loss-of-function studies revealed that LINC01436 acted as a proto-oncogene by promoting lung cancer cell growth, migration and invasion in vitro. Xenograft tumor assays in nude mice confirmed that LINC01436 promoted tumor growth and metastasis in vivo.	30614188
LINC01433	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	interaction[sponging miR-1301]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	Linc01433 was abnormally up-regulated in ESCC tissues and cells.  Linc01433 participated in ESCC progression by regulating miR-1301 and it could function as a novel biomarker in ESCC diagnosis and treatment.	 High level of linc01433 was positively correlated with tumor size and lymph node metastasis in ESCC patients.	Yes	 Up-regulation of linc01433 promoted cell proliferation and migration. 	32432741
LINC00941	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(TGF-β/SMAD2/3 axis)	RNA Pull-Down//Western Blot//ISH//Co-IP//RIP//qRT-PCR//IP//IHC	 LINC00941 was shown to be upregulated in CRC, and upregulated LINC00941 was associated with poor prognosis. Our data reveal the essential role of LINC00941 in metastatic CRC via activation of the TGF-β/SMAD2/3 axis, which provides new insight into the mechanism of metastatic CRC and a novel potential therapeutic target for advanced CRC.	LINC00941 was shown to be upregulated in CRC, and upregulated LINC00941 was associated with poor prognosis.	Yes	Functionally, LINC00941 promoted migratory and invasive capacities and accelerated lung metastasis in nude mice.	32737443
LINC01348	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(SF3B3/EZH2/JNK/c-Jun/Snail )	qRT-PCR	 In this study, we identified a novel lncRNA, LINC01348, which was significantly downregulated in HCC and correlated with survival functions in HCC patients. Our data collectively highlight those novel regulatory associations involving LINC01348/SF3B3/EZH2/JNK/c-Jun/Snail are an important determinant of metastasis in HCC cells and support the potential utility of targeting LINC01348 as a therapeutic strategy for HCC.	 In this study, we identified a novel lncRNA, LINC01348, which was significantly downregulated in HCC and correlated with survival functions in HCC patients.	Yes	Ectopic expression of LINC01348 induced marked inhibition of cell growth, and metastasis in vitro and in vivo.	34140643
LINC01320	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell strains	Interaction( miR-324-3p)	Transfection//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	We conclude that LINC01320 is highly expressed in PC tissues and cell strains.In addition, LINC01320 is expressed by miR-324-3p, which is also supported by in vivo experiments.	LINC01320 high expression was bound up with a poor prognosis. 	Yes	LINC01320 gene knockout inhibited the growth, migration, and invasiveness of PC cells. 	34976325
LINC01315	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues	Interaction(microRNA-876-5p/GRK5)	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	A significant upregulation of LINC01315 was observed in TNBC, which was associated with disease development and severity of patients.  Additionally, miR-876-5p was demonstrated to be a target of LINC01315 and regulate the expression of GRK5, through which LINC01315 modulated the progression of TNBC. 	 The upregulation of LINC01315 could be a symptom of the poor prognosis of patients. 	Yes	The knockdown of LINC01315 suppressed the main cellular processes of TNBC progression. 	35412954
LINC01315	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC and ALDH+ cells	Interaction(miR-484/DLK1 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	 LINC01315 was high-expressed in CRC and ALDH+ cells. 		Yes	 LINC01315 silencing suppressed the migration, invasion, and sphere formation of CRC cells and tumor growth, and downregulated expressions of CSC molecules (ALDH, cluster of difference 44 (CD44), Prominin, and sex determining region Y-box 2 (SOX2)), Zinc Finger E-Box Binding Homeobox 1 (ZEB1) and Vimentin but upregulated E-Cadherin expression. 	35156543
LINC01315	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells 	interaction[binding to miR-211]	Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay	LINC01315 and DLG3 were determined to be poorly expressed while microRNA-211 (miR-211) was highly expressed in OSCC tissues and cells using RT-qPCR and western blot analysis. These findings suggest that LINC01315 elevates DLG3 expression by competitively binding to miR-211, thereby suppressing OSCC progression.		Yes	Upon altering the expression of LINC01315, and/or miR-211 in OSCC cells with shRNA, mimic, or an inhibitor, we assessed their effects on OSCC cell proliferation, migration, invasion, and apoptosis. LINC01315 knockdown enhanced OSCC cell proliferation, migration and invasion, but dampened their apoptosis, all of which could be reversed by miR-211 inhibition.	33117688
LINC01311	LncRNA	Homo sapiens	Thyroid Neoplasms	 TC cells and tissues	Interaction(miR-146b-5p/IMPA2 axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	 The TC cells and tissues exhibited a downregulation of LINC01311 and IMPA2 and an upregulation of miR-146b-5p.  The luciferase reporter and RIP assays verified that miR-146b-5p recognizes LINC01311 and IMPA2 3'UTR by base pairing. 		Yes	 LINC01311 overexpression retarded TC cell growth in vitro as well as in vivo. 	36423383
LINC01311	LncRNA	Homo sapiens	Alzheimer Disease	SH-SY5Y cells	Interaction( hsa-miR-146a-5p)	qRT-PCR//Luciferase Report Assay	 LINC01311 was downregulated whereas hsa-miR-146a-5p upregulated in AB1-42 treated SH-SY5Y cells.  Our work demonstrated that the epigenetic axis of LINC01311/hsa-miR-146a-5p was involved in the functional regulation of human-lineage neurons in a cellular model of AD, thus suggesting a clinical potential of exploring epigenetic network for treating AD patients.		Yes	 LINC01311 upregulation and hsa-miR-146a-5p downregulation protected AB1-42-induced apoptosis, proliferation slowdown, autophagy, and APP accumulations in SH-SY5Y cells. Hsa-miR-146a-5p overexpression reversed the protection of LINC01311 on AB1-42-induced neural injuries.	33830627
LINC01305	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[miR-129-5p/Sox4 axis]	RNA Pull-Down//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of LINC01305 was evidently elevated in CC tissues and cell lines than that in controls and associated with clinicopathological features. LINC01305 acts as a competitive endogenous RNA (ceRNA) and regulates Sox4 via sponging miR-129-5p, contributing to the diagnosis and treatment of CC.	The expression of LINC01305 was evidently elevated in CC tissues and cell lines than that in controls and associated with clinicopathological features.	Yes	Downregulating LINC01305 suppressed malignant phenotypes (proliferation, migration, invasion) of Hela and SiHa cells.	33312390
LINC01305	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tumor tissues	Regulation(KHSRP )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Tunel//Flow Cytometry//qRT-PCR//FISH//RIP//IHC	The results showed that LINC01305 was increased in CC tumor tissues and was correlated with a lower survival rate.  Moreover, the effect of LINC01305 on CC was mediated through interacting with the RNA-binding protein, KHSRP. Furthermore, LINC01305 was mainly distributed in exosomes and was transferred to recipient cells to enhance CC progression.	The overexpression and knockdown of LINC01305 enhanced and inhibited the progression of CC, respectively. 	Yes	The overexpression and knockdown of LINC01305 enhanced and inhibited the progression of CC, respectively. Additionally, the upregulation of LINC01305 promoted tumor growth in xenograft mice.	33638945
LINC01303	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[sponging miR-101-3p]	CCK8	In our study, we found that the expression of LINC01303 was significantly higher in GC tissues than in adjacent tissues by real-time quantitative PCR. After the bioinformatics analysis, we found that LINC01303 can be used as a miR-101-3p sponge to competitively adsorb miR-101-3p with EZH2. Therefore, our results indicate that LINC01303 promotes the expression of EZH2 by inhibiting miR-101-3p activity and promotes GC progression. 		Yes	We can significantly inhibit the malignant proliferation, migration and invasion of GC cells by silencing LINC01303 expression. In addition, LINC01303 knockdown can also inhibit GC growth in vivo. 	31497936
LINC01303	LncRNA	Homo sapiens	laryngeal carcinoma	LSCC tissues 	Interaction(miR-200c/TIMP2 axis)	Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//ChIP	LINC01303 expression in LSCC tissues was notably higher than that in adjacent normal tissues. Mechanically, LINC01303 acted as carcinogenic lncRNA in LSCC by regulating miR-200c/TIMP2 axis.	High LINC01303 expression was bound up with lymphatic metastasis and advanced clinical stage. 	Yes	 In addition, inhibition of LINC01303 by siRNA could evidently block LSCC cell proliferation, induce apoptosis, and inhibit invasion and migration. 	33841686
LINC01303	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues & cells	Interaction(miR-429/ZEB1/EMT Axis)	In Vivo Experiment//Transfection//FISH//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	"LINC01303 expression was higher in OSCC tissues compared with adjacent nontumor tissues. LINC01303 was found to be localized in the cytoplasm of OSCC cells. Knockdown of LINC01303 inhibited OSCC cell proliferation and invasion, whereas increasing the expression of LINC01303 showed the opposite effects. Furthermore, LINC01303 served as a miR-429 ""sponge"" and positively regulated ZEB1 expression. Moreover, LINC01303 promoted OSCC through miR-429/ZEB1 axis both in vivo and in vitro."		Yes	Knockdown of LINC01303 inhibited OSCC cell proliferation and invasion, whereas increasing the expression of LINC01303 showed the opposite effects. 	34912458
LINC01287	LncRNA	Homo sapiens	Breast Neoplasms	BC cells and tissues	Interaction(miR-98/IGF1R )	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 LINC01287 expression markedly increased in BC cell lines. Subsequent studies identified LINC01287 as a downstream target of miR-98.In addition, LINC01287 knockdown and miR-98 overexpression significantly stagnated progression of BC cells. LINC01287 knockdown also downregulated IGF1R levels. Moreover, LINC01287 knockdown notably downregulated the phosphorylation of MEK1/2 and ERK1/2. Our findings showed that LINC01287 was overexpressed in BC cells and tissues.		Yes	The in vivo assay verified that LINC01287 can regulate tumorigenesis of BC. 	35695608
LINC01278	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-134-5p/KDM2A axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 LINC01278 was upregulated in CRC tissues and cell lines, and knockdown of LINC01278 suppressed CRC cell progression.  Our study demonstrated that LINC01278 upregulated KDM2A to promote CRC progression by interacting with miR-143, suggesting that LINC01278 might be a new therapeutic target of CRC.		Yes	 LINC01278 was upregulated in CRC tissues and cell lines, and knockdown of LINC01278 suppressed CRC cell progression. 	33155208
LINC01278	LncRNA	Homo sapiens	Osteosarcoma	 tumor tissues 	regulation[miR-133a-3p/PTHR1 signaling]	qRT-PCR	Then, we found that the expression of LINC01278 tested by quantitative reverse-transcription polymerase chain reaction was enhanced in tumor tissues compared with the para-carcinoma tissues and related to clinical stage, distant metastasis in osteosarcoma. Our findings clarified that the carcinogenic effect of LINC01278 in osteosarcoma was mediated through miR-133a-3p/PTHR1 signaling, creating a novel insight into good targets for the therapy and prognosis of osteosarcoma.	Then, we found that the expression of LINC01278 tested by quantitative reverse-transcription polymerase chain reaction was enhanced in tumor tissues compared with the para-carcinoma tissues and related to clinical stage, distant metastasis in osteosarcoma. 	Yes	 Moreover, LINC01278 promoted proliferation and restrained apoptosis in osteosarcoma cells.	31994731
LINC01278	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and serum	Interaction(miR-134-5p/KRAS Axis)	qRT-PCR//RNA Pull-Down	qRT-PCR showed that LINC01278 increased in OS tissues and serum, indicating poor prognosis. In addition, LINC01278 was also of high value for OS diagnosis. Functional experiments showed that LINC01278 inhibited KRAS-mediated OS cell proliferation and metastasis through miR-134-5p. Finally, the results of an in vivo animal model indicated that LINC01278 promoted OS growth.	qRT-PCR showed that LINC01278 increased in OS tissues and serum, indicating poor prognosis. 	Yes	Functional experiments showed that LINC01278 inhibited KRAS-mediated OS cell proliferation and metastasis through miR-134-5p. Finally, the results of an in vivo animal model indicated that LINC01278 promoted OS growth.	33531816
LINC01270	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-326/EFNA3 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Our findings indicated that LINC01270 expression was significantly up-regulated in GC tissues and cell lines. Functional experiments identified that lncRNA LINC01270 could positively regulate EFNA3 expression by serving as a competing endogenous RNA (ceRNA) for miR-326. Through rescue assays, inhibition of GC progression caused by LINC01270 suppression was found to be reversed by the application of miR-326 inhibitor or EFNA3 overexpression. 		Yes	Additionally, LINC01270 knockdown attenuated GC progression through inhibiting cell proliferation, migration, and invasion. 	35345980
LINC01270	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC tissues and cells	Regulation（GSTP1methylation）	qRT-PCR//MTT	 LINC01270 was up-regulated and GSTP1 was down-regulated in EC tissues and cells. We found that LINC01270 recruited the DNA methyltransferases DNMT1, DNMT3A and DNMT3B initiating GSTP1 promoter methylation, thereby leading to the proliferation, migration, invasion and drug resistance of EC cells. 		Yes	Silencing of LINC01270 inhibited migration and invasion, and enhanced the sensitivity of 5-FU in EC cells. 	33199829
LINC01270	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues 	Expression[highly expressed]	qRT-PCR	 Among these, two lincRNAs (LINC01270 and LINC00449) were significantly associated with both worse overall survival and DFS and were expressed at significantly higher levels in tumor tissues compared with adjacent normal breast tissues (log2[Fold Change] > 0.5 and FDR < 0.05). 		Yes	We further evaluated the potential functions of LINC01270 and LINC00449 using in vitro functional experiments and found that siRNA-mediated knockdown of LINC01270 and LINC00449 expression significantly decreased cell viability, colony formation and cell migration ability in TNBC cells (P < 0.05).	33247368
LINC01270	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tumor tissues and cell lines	Interaction(miR-326/PI3K/AKT pathway)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay	The overexpression of LINC01270 was then verified in LUAD tumor tissues and cell lines by qRT-PCR.  Moreover, LINC01270 was found inhibiting miR-326 and thereby overexpressing the abundance of LARP1 to promote LUAD development via PI3K/AKT pathway. 		Yes	 LINC01270 knockdown resulted in impaired cell proliferative and invasive ability via CCK-8 assay, EdU assay, colony formation assay, transwell assay, while aberrant upregulation of LINC01270 led to enhanced cell growth and invasion.It was also proved that LINC01270 knockdown could suppress LUAD tumor growth in vivo. 	36694453
LINC01320	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	Interaction(miR495-5p/RAB19 axis)	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LINC01320 was highly expressed in gastric cancer tissues and cells. Moreover, miR-495-5p was predicted and demonstrated to target LINC01320 and RAB19. 		Yes	 LINC01320 overexpression promoted the proliferation, migration, and invasion of gastric cancer cells, while LINC01320 knockdown exerted the opposite effects.	34288797
LINC01354	LncRNA	Homo sapiens	Osteosarcoma	OS tissues, serum and cells	regulation[Integrin β1]	qRT-PCR//Western Blot//Transwell Assay	LINC01354 was overexpressed in OS tissues, serum and cells.LINC01354 promote OS cell EMT and invasion through up-regulating integrin β1.		Yes	LINC01354 overexpression promoted OS cells invasion, EMT and integrin β1 expression, while knockdown of LINC01354 inhibited OS cell invasion, epithelial-mesenchymal transition (EMT) and integrin β1 expression. 	32111497
LINC01426	LncRNA	Homo sapiens	Glioma	glioma cells	Interaction(miR-661/Mdm2 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//IHC//Bioinformatics Analysis	LINC01426, which was high-expressed in glioma and was related to poor prognosis, could be used as a diagnostic marker for glioma. LINC01426 targeted and inversely correlated with miR-661, which was low-expressed in glioma. MiR-661 inhibitor evidently overturned the effect of siLINC01426 on biological functions, proliferation, and apoptosis-related proteins of glioma cells. Mdm2 bound to miR-661. Moreover, siMdm2 reversed the effects of miR-661 inhibitor on the biological characteristics and Mdm2/p53/p21 expression of glioma cells.	LINC01426, which was high-expressed in glioma and was related to poor prognosis, could be used as a diagnostic marker for glioma.	Yes	 SiLINC01426 inhibited the malignant phenotype of glioma cells in vitro and attenuated tumor growth and PCNA expression in vivo, while the effects of LINC01426 were the opposite. 	35772605
LINC01354	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//RNA Pull-Down//RIP//Western Blot	The upregulation of LINC01354 in CRC and its prognostic significance were identified by TCGA database and confirmed in CRC tissues. Our investigations proposed novel regulatory axis of LINC01354/hnRNP-D/Wnt/β-catenin, which might be in favor of exploring novel therapeutic regimens for the clinical treatment of CRC.		Yes	 Functionally, forced expression of LINC01354 promoted, while knockdown of LINC01354 inhibited cell proliferation, migration and EMT phenotype formation of CRC cells. 	30987669
LINC01426	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cell lines 	regulation[miR-345-3p,VAMP8]	CCK8//qRT-PCR//Luciferase Report Assay//RIP	 LINC01426 is up-regulated in malignant GBM tissues and cell lines and it is capable to promote GBM cell proliferation and growth. Mechanistically, LINC01426 serves as a molecular sponge to sequester the miR345-3p and thus enhancing the level of VAMP8, an oncogenic coding gene, to promote GBM progression.		Yes	LINC01426 is up-regulated in malignant GBM tissues and cell lines and it is capable to promote GBM cell proliferation and growth. 	32699526
LINC01426	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	interaction[hsa-miR-30b-3p]	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//FISH//MTT//Luciferase Report Assay//Transwell Assay	We note that LINC01426 expression was markedly upregulated in LUAD tissues, and that functional assays verified that LINC01426 knockdown markedly inhibited cell proliferation, migration, and invasion in vitro. Our study also found that LINC01426 bound to hsa-miR-30b-3p as a competitive endogenous RNA in LUAD.	 Moreover, LINC01426 affected LUAD wound healing by interacting and combining with AZGP1, and LINC01426 expression was significantly associated with tumor-node-metastasis (TNM) staging and prognosis in patients with LUAD.	Yes	We note that LINC01426 expression was markedly upregulated in LUAD tissues, and that functional assays verified that LINC01426 knockdown markedly inhibited cell proliferation, migration, and invasion in vitro. Xenografts derived from A549 cells knocked down of LINC01426 had evidently lower tumor weights and smaller tumor volumes. 	32953928
LINC01426	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues 	Regulation(hedgehog pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Co-IP//Tunel//Flow Cytometry//qRT-PCR//FISH//RIP//Colony Formation Assay//EdU Staining//IF	We applied bioinformatics analysis to find the expression of LINC01426 was upregulated in LUAD tissue. Functionally, silencing of LINC01426 obviously suppressed the proliferation, migration, epithelial-mesenchymal transition (EMT), and stemness of LUAD cells. Then, we observed that LINC01426 functioned through the hedgehog pathway in LUAD. The effect of LINC01426 knockdown could be fully reversed by adding hedgehog pathway activator SAG. In addition, we proved that LINC01426 could not affect SHH transcription and its mRNA level. Pull-down sliver staining and RIP assay revealed that LINC01426 could interact with USP22. Ubiquitination assays manifested that LINC01426 and USP22 modulated SHH ubiquitination levels. Rescue assays verified that SHH overexpression rescued the cell growth, migration, and stemness suppressed by LINC01426 silencing. In conclusion, LINC01426 promotes LUAD progression by recruiting USP22 to stabilize SHH protein and thus activate the hedgehog pathway.		Yes	Pull-down sliver staining and RIP assay revealed that LINC01426 could interact with USP22. Ubiquitination assays manifested that LINC01426 and USP22 modulated SHH ubiquitination levels. Rescue assays verified that SHH overexpression rescued the cell growth, migration, and stemness suppressed by LINC01426 silencing.	33568633
LINC01426	LncRNA	Homo sapiens	lung non-small cell carcinoma	NSCLC tissues and cells	Interaction(miR-143-3p/USP28)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Our results confirmed that LINC01426 and USP28 expression were increased, while miR-143-3p expression was decreased in NSCLC tissues and cells. Additionally, LINC01426 regulated USP28 expression by sponging miR-143-3p. USP28 overexpression partly overturned the inhibitory effect of miR-143-3p on NSCLC progression. 		Yes	 Further functional experiments demonstrated that LINC01426 inhibition markedly impaired cell proliferation, migration, invasion, autophagy, and glycolysis while induced apoptosis in NSCLC cells, and LINC01426 derived malignant behaviors of NSCLC cells by sponging miR-143-3p. 	35639219
LINC01419	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		regulation[ EZH2-regulated RECK]	RNA-seq	Interaction between LINC01419 and FUS stabilized EZH2 mRNA thereby enhancing EZH2 expression.		Yes	In vitro study revealed that LINC01419 promotes growth and migration of HCC cells.	32522890
LINC01419	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(ZIC1/PI3K/Akt signaling pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Transwell Assay	 According to the results, LINC01419 was highly expressed in HCC tissues and cells, while ZIC1 was poorly expressed.LINC01419 targeted and downregulated ZIC1 expression.Furthermore, LINC01419 increased the methylation of ZIC1 promoter and repressed ZIC1 expression. PI3K/Akt signaling pathway was activated by LINC01419 overexpression and ZIC1 knockdown, under which conditions, the HCC cell self-renewal and proliferation were promoted while cell apoptosis was attenuated, accompanied by accelerated formation and metastasis of xenografted tumors in mice.		Yes	PI3K/Akt signaling pathway was activated by LINC01419 overexpression and ZIC1 knockdown, under which conditions, the HCC cell self-renewal and proliferation were promoted while cell apoptosis was attenuated, accompanied by accelerated formation and metastasis of xenografted tumors in mice.	33772101
LINC01419	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-519a-3p/PDRG1 axis ]	RNA Pull-Down//Tunel//qRT-PCR//Transwell Assay//EdU Staining//IF	LINC01419 expression was elevated in OS tissues and cells.LINC01419 mediates malignant phenotypes in OS by targeting miR-519a-3p/PDRG1 axis.		Yes	Functionally, LINC01419 accelerated OS cell proliferation, motility and EMT. In vivo assay showed that silencing LINC01419 hindered the growth of OS tumors.	32390762
LINC01410	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues 	interaction[miR-3128]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In the present study, LINC01410 was identified to be highly expressed in CC tissues compared to adjacent normal tissues. In conclusion, the present study demonstrated that LINC01410 functions as an oncogene in CC, at least in part by directly inhibiting miR-3128.	It was indicated that high expression of LINC01410 in CC tissues was associated with poor prognosis.	Yes	Further functional study suggested that LINC01410 knockdown significantly reduced the proliferation and invasive capacity of HT-29 and SW620 cells, and inhibited the cell cycle. 	30546401
LINC01410	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(miR-497-5p/HMGA2 axis)	qRT-PCR//Luciferase Report Assay	LINC01410 and HMGA2 were high, and miR-497-5p showed low expression in OS tissues and cells.  We have demonstrated that LINC01410 promoted OS development partly by miR-497-5p/HMGA2 signal transduction pathway and this provides a reference for studying the mechanism of LINC01410 in OS.		Yes	Cell function assay demonstrated that LINC01410 or HMGA2 knockdown or miR-497-5p overexpression obviously restrained OS proliferation, invasion, and migration. Oppositely, inhibiting miR-497-5p had the opposite effects. 	34605103
LINC01410	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(miR-122-5p/NDRG3 axis)	CCK8//qRT-PCR	LINC01410 was overexpressed in OS tissues. Our studies also showed that LINC01410 binds to miR-122-5p, and miR-122-5p binds to NDRG3. 		Yes	 Furthermore, it was confirmed that LINC01410 facilitated OS cell proliferation and migration. 	33583123
LINC01410	LncRNA	Homo sapiens	Glioma	 glioma cells	Interaction( miR-506-3p/NOTCH2 )	RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//ChIP	Our data supported that LINC01410 was up-regulated in glioma cells.  Bioinformatics predictions and the integrated experiments identified that MYC activated LINC01410 transcription and LINC01410 promoted the levels of NOTCH2 through sponging miR-506-3p and further motivated Notch signaling pathway. 		Yes	 Rescue assays validated that LINC01410 exerted its influential functions on glioma cell proliferation and apoptosis via enhancing NOTCH2 expression.	33712887
LINC01410	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	Interaction[regulating the miR-497-5p and IFITM3 gene expression]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The expression of LINC01410 in the pancreatic cancer tissues was significantly higher than that in the adjacent tissues [(3.46±0.32) vs (0.65±0.08), P<0.01]. Down-regulation of LINC01410 expression inhibits the proliferation and migration of pancreatic cancer BxPC-3 cells, and its mechanism may be closely related to regulating the miR-497-5p and IFITM3 gene expression.		Yes	After knock-down of the LINC01410 expression in the pancreatic cancer cell line BxPC-3, the cell proliferation was significantly inhibited (P<0.05), and the cell migration ability was decreased (P<0.05). 	31137129
LINC01410	LncRNA	Homo sapiens	Gallbladder Neoplasms	GBC tissues 	Interaction(STAT5 )	In Vivo Experiment//RNA Pull-Down//Western Blot//ISH//Transfection//Wound Healing Assay//qRT-PCR//RIP//migration assay//Cell Proliferation Assay	LINC01410 was significantly upregulated in the GBC tissues compared to adjacent non-tumor tissues. From RNA pull-down and RIP assay, we identified that STAT5 was a critical downstream target of LINC01410.	 High LINC01410 expression was significantly associated with poor prognosis of GBC patients.	Yes	Overexpression of LINC01410 promoted GBC cell proliferation, migration, and invasion in vitro and GBC progression in vivo, whereas LINC01410 downregulation rescued these effects in vitro. 	34322379
LINC01410	LncRNA	Homo sapiens	Cholangiocarcinoma	 CCA tissues and CCA cell	regulation[miR-124-3p/SMAD5 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The high expression of LINC01410 was proved in CCA tissues and CCA cell lines. LINC01410 facilitates cell proliferation, migration and invasion through miR-124-3p/SMAD5 axis.	 Also, CCA patients with high LINC01410 level presented poor prognosis.	Yes	LINC01410 deficiency impeded cell proliferation, migration and invasion in HuCCT1 and RBE cell lines.	31951299
LINC01410	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	Regulation(miR-545-3p/HK2 Axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	LINC01410 and HK2 were highly expressed while miR-545-3p was lowly expressed in NB tissues and cells. LINC01410 knockdown inhibited tumorigenesis by repressing cell proliferation and invasion, and increased the radiosensitivity via inhibiting colony formation rates and glycolysis. LINC01410 knockdown also suppressed tumor growth in vivo. Moreover, miR-545-3p could bind to LINC01410 and its downregulation reversed the effects of LINC01410 knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-545-3p and its overexpression attenuated the effects of miR-545-3p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, LINC01410 functioned as a molecular sponge of miR-545-3p to regulate HK2 expression.		Yes	LINC01410 knockdown inhibited tumorigenesis by repressing cell proliferation and invasion, and increased the radiosensitivity via inhibiting colony formation rates and glycolysis. LINC01410 knockdown also suppressed tumor growth in vivo.	34040388
LINC01391	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-12116/CMTM2 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Here, we report that LINC01391 was low expressed in GC tissues and cell lines.  LINC01391 restrained aerobic glycolysis and tumorigenesis of GC via targeting miR-12116/CMTM2 axis, which provides new insights into mechanism of GC progression.		Yes	 LINC01391 overexpression hampered GC cell proliferation, migration, invasion and aerobic glycolysis, while LINC01391 knockdown demonstrated the opposite effects.	33033510
LINC01385	LncRNA	Homo sapiens	Osteoarthritis	OA tissues and IL-1β-induced HC-a	Interaction(microRNA-140-3p/TLR4 axis)	qRT-PCR//MTT//Co-IP//Western Blot	LINC01385 mRNA expression level was increased in OA tissues and IL-1β-induced HC-a.In addition, it was confirmed that LINC01385 targeted miR-140-3p, while TLR4 was a target gene of miR-140-3p. Negative correlations between LINC01385 and miR-140-3p, and between miR-140-3p and TLR4 were observed in OA tissues. 		Yes	LINC01385 knockdown and miR-140-3p mimics reduced the concentration of inflammatory factors in IL-1β-induced HC-a and promoted cell survival. 	34539840
LINC01385	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissue	regulation[miR-140-3p/Twist1 signaling pathway]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Our data showed that LINC01385 expression was significantly increased NPC and correlated with advanced clinical features and poor prognosis.Thus, we illustrated that LINC01385 aggravated the progression of NPC by sponging miR-140-3p and upregulating Twist1 expression, which implied LINC01385 might serve as a new potential therapeutic target for NPC treatment.	Our data showed that LINC01385 expression was significantly increased NPC and correlated with advanced clinical features and poor prognosis.	Yes	 Function assays showed that knockdown of LINC01385 expression reduced the proliferation and invasion abilities of NPC cells in vitro. 	32264733
LINC01355	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction[repression of CCND1]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Colony Formation Assay//ChIP	 LINC01355 were downregulated in breast cancer cells relative to non-malignant breast epithelial cells.LINC01355 acts as a tumor suppressor in breast cancer, which is ascribed to enhancement of FOXO3-mediated transcriptional repression of CCND1. 		Yes	 Overexpression of LINC01355 significantly inhibited proliferation, colony formation, and tumorigenesis of breast cancer cells. 	31243265
LINC01608	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell line	Regulation(EGFR/ERK axis)	ISH//qRT-PCR//RIP//Luciferase Report Assay//IHC	LINC01608 was overexpressed in HCC tissues, and high LINC01608 expression predicted poor overall survival (OS) and disease-free survival (DFS) in HCC patients. Furthermore, we demonstrated that LINC01608 could sponge to miR-875-5p and activate the EGFR/ERK pathway. Moreover, we identified transcriptional factor YY1 could bind to the promoter of LINC01608 and induce its transcription.	LINC01608 was overexpressed in HCC tissues, and high LINC01608 expression predicted poor overall survival (OS) and disease-free survival (DFS) in HCC patients. 	Yes	LINC01608 could promote HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and in vivo.	36385489
LINC01612	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-494/ATF3/p53 axis)	qRT-PCR	 In this study, we discovered that Linc01612 is significantly down-regulated in HCC tissues than in non-tumor tissues and correlated with poor prognosis. Mechanistically, in p53-expressing hepatoma cells, Linc01612 acts as a competitive endogenous RNA and promotes the expression of activation transcription factor 3 (ATF3) by sponging microRNA-494 (miR-494), which in turn inhibits MDM2-mediated ubiquitination of p53 and activates the p53 pathway. Furthermore, in p53-null hepatoma cells, Linc01612 exerts its biological functions by physically interacting with Y-box binding protein 1 protein (YBX1) and promoting the ubiquitin-mediated degradation of YBX1. Interestingly, the Linc01612-YBX1 signaling pathway is also present in p53-expressing hepatoma cells.	 In this study, we discovered that Linc01612 is significantly down-regulated in HCC tissues than in non-tumor tissues and correlated with poor prognosis. 	Yes	Linc01612 mainly localizes in the cytoplasm and functions as a tumor suppressor by repressing the growth and metastasis of hepatoma cells in vitro and in vivo.	35541917
LINC01614	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cells	Interaction(ANXA2 and p65 /NF-κB)	qRT-PCR//RNA-seq//Western Blot//Microarray	A CAF-specific long noncoding RNA, LINC01614, packaged by CAF-derived exosomes, mediates the enhancement of glutamine uptake in LUAD cells. Mechanistically, LINC01614 directly interacts with ANXA2 and p65 to facilitate the activation of NF-κB, which leads to the upregulation of the glutamine transporters SLC38A2 and SLC7A5 and eventually enhances the glutamine influx of cancer cells. 	Clinically, LINC01614 expression in CAFs is associated with the glutamine influx and poor prognosis of patients with LUAD.	Yes	Reciprocally, tumor-derived proinflammatory cytokines upregulate LINC01614 in CAFs, constituting a feedforward loop between CAFs and cancer cells. Blocking exosome-transmitted LINC01614 inhibits glutamine addiction and LUAD growth in vivo.	36209111
LINC02446	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues 	Interaction(EIF3G/mTOR )	qRT-PCR//RNA Pull-Down//RIP	 In the present study, we used the TCGA and GEO databases and identified LINC02446 as associated with prognosis and differentially expressed in bladder cancer tissues and para-cancer tissues. Additionally, we found that LINC02446 could bind to the EIF3G protein and regulate the protein stability of EIF3G and then inhibit the mTOR signalling pathway.		Yes	Then, we found that LINC02446 could affect the proliferation, migration and invasion of BC cells. 	33526846
LINC02418	LncRNA	Homo sapiens	Colonic Neoplasms	CRC tissues	regulation[miR-34b-5p/BCL2 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418/miR-34b-5p/BCL2 axis in CRC.	 LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. 	Yes	 LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells.LINC02418 reduced cell proliferation, while transfection of miR-34b-5p inhibitor or BCL2 into LINC02418-silenced CRC cells significantly promoted CRC cells growth.	32973404
LINC02418	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LAD specimens and cells	regulation[miR-4677-3p/KNL1 signaling]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	High expression of LINC02418 was observed in LAD specimens and cells.LINC02418 contributes to the malignancy in LAD via miR-4677-3p/KNL1 signaling, providing a probable therapeutic direction for LAD.		Yes	Downregulation of LINC02418 obstructed the proliferation and motility of LAD cells.	32795273
LINC02381	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues 	regulation[Wnt Signaling Pathway]	qRT-PCR//Luciferase Report Assay//Microarray	 Looking for the potential molecular regulators of gastric cancer incidence and progression, LINC02381 was identified as a downregulated lncRNA in gastric cancer tissues by analysis of available microarray and RNA-seq data and RT-qPCR confirmed this differential expression.Furthermore, we found that increased expression of LINC02381 attenuates Wnt pathway activity. 		Yes	 Also, functional analysis indicates that LINC02381 arrests cell cycle, increases apoptosis and caspase activity, and reduces cell survival and proliferation rate of the human gastric cancer cell lines AGS and MKN45. 	33194632
LINC02381	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[PI3K-Akt signaling pathway]	qRT-PCR	Consistently, RT-qPCR results showed that LINC02381 was down regulated in CRC tissues and also in different cancerous cell lines. Altogether, the result of this study suggests that LINC02381 might have suppressive effects on human colorectal cancer tumorigenesis partly by regulating PI3K signaling pathway.		Yes	 Then, the functional changes of the cells in response to LINC02381 alteration were assessed and the data indicated that LINC02381 up-regulation suppressed cell viability and proliferation while increasing the apoptosis in CRC-originated cell lines.	32092325
LINC02381	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma specimens and cells	Interaction(miR-503-5p/CDCA4 axis)	qRT-PCR//RIP//ChIP	We observed that the expression of LINC02381 and cell division cycle-associated protein 4 (CDCA4) were distinctly increased in osteosarcoma specimens and cells, while miR-503-5p expression was decreased. Additionally, ETS transcription factor ELK1 (ELK1) could bind directly to the LINC02381 promoter region and activate its transcription. What's more, LINC02381 could down-regulate CDCA4 via sponging miR-503-5p, and there existed a negative correlation between LINC02381 expression and miR-503-5p expression in 92 osteosarcoma samples. Rescue experiments proved the carcinogenic role of LINC02381/miR-503-5p/CDCA4 axis in osteosarcoma progression. 	Clinical assays revealed that high LINC02381 was associated with advanced clinical progress and poor clinical outcome. 	Yes	Functionally, knockdown of LINC02381 suppressed the proliferation, migration and invasion of osteosarcoma cells. 	33640603
LINC02381	LncRNA	Homo sapiens	Glioma	 glioma cells	Interaction(CEBPβ/CBX5 )	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	By RT-qPCR, we confirmed LINC02381 upregulation in glioma cells. To conclude, LINC02381 could facilitate CBX5 transcription via interaction with CEBPβ, thus exerting its oncogenic role in glioma cells, which could contribute to better understanding of glioma.		Yes	Functional experiments demonstrated that LINC02381 knockdown repressed glioma cell proliferation and induced apoptosis. 	34274429
LINC02362	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(miR-516b-5p/ SOSC2 axis)	qRT-PCR//Western Blot	 Here, we found that a long non-coding RNA (lncRNA) named LINC02362, whose biological effects have yet been unveiled in cancers, was associated with a better prognosis in patients with HCC.  Moreover, miR-516b-5p was enriched as a target of LINC02362, which functioned as a sponge to regulate the endogenous levels of miR-516b-5p. Furthermore, we confirmed that SOSC2 served as a downstream target gene which was negatively controlled by miR-516b-5p. Importantly, a series of rescue experiments indicated that the tumor-suppressive effects of LINC02362 were achieved through the modulation of the miR-516b-5p/SOSC2 axis. 	 Here, we found that a long non-coding RNA (lncRNA) named LINC02362, whose biological effects have yet been unveiled in cancers, was associated with a better prognosis in patients with HCC. 	Yes	Gain-of-function analyses showed that LINC02362 inhibited the survival, migration, invasion and epithelial-to-mesenchymal transition (EMT) of HCC cells. 	34990401
LINC02323	LncRNA	Homo sapiens	Ovarian Neoplasms	blood	regulation[TGF-β receptor 1,miR-1343-3p]	qRT-PCR//MTT//Western Blot//Microarray	  In patients with ovarian cancer, lncRNA LINC02323 expression was up-regulated and miR-1343-3p expression was down-regulated. Our findings show that Novel long noncoding RNA LINC02323 promotes cell growth of ovarian cancer via TGF-β receptor 1 by miR-1343-3p.		Yes	Over-expression of lncRNA LINC02323 promoted cell growth and reduced LDH activity levels in vitro model by suppression of miR-1343-3p expression. 	33247856
LINC02321	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissue	Regulation(VEGFA )	CCK8//qRT-PCR	 The Cancer Genome Atlas prediction and RT?qPCR experimental results demonstrated that only LINC02321 was highly expressed in bladder cancer tissue and promoted the proliferation, invasion, migration and cisplatin resistance of the malignancy. 		Yes	 The Cancer Genome Atlas prediction and RT?qPCR experimental results demonstrated that only LINC02321 was highly expressed in bladder cancer tissue and promoted the proliferation, invasion, migration and cisplatin resistance of the malignancy. 	36579659
LINC02273	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[LINC02273-hnRNPL-AGR2 axis ]	RNA Pull-Down//ChIP//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//Transwell Assay	We identified a novel long noncoding RNA LINC02273, whose expression was significantly elevated in metastatic lesions compared to the primary tumors, by genetic screen of matched tumor samples.Mechanistically, hnRNPL-LINC02273 formed a complex which activated AGR2 transcription and promoted cancer metastasis. The recruitment of hnRNPL-LINC02273 complex to AGR2 promoter region epigenetically upregulated AGR2 by augmenting local H3K4me3 and H3K27ac levels.		Yes	Increased LINC02273 promoted breast cancer metastasis in vitro and in vivo. 	31856843
LINC02273	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Regulation( β-catenin)	qRT-PCR	Here, we showed the expression pattern and biological function of a recently identified lncRNA, LINC02273, in HCC. LINC02273 played a critical role in HCC progression via stabilizing β-catenin. 		Yes	Knockdown of LINC02237 remarkably inhibited the proliferation, stemness, migration, and invasion abilities, whereas it increased the apoptosis of HCC cells.	35132378
LINC02257	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC specimens and cell lines	Expression(highly expressed)	CCK8//qRT-PCR	We found that the expression of LINC02257 exhibited variable patterns of upregulation or downregulation in the various forms of cancer. In CRC, LINC02257 expression was distinctly increased in CRC specimens compared with normal specimens. The results of ROC curves revealed that the AUC was 0.886 (0.862 to 0.909, 95% CI, p < 0.001) in a comparison between CRC specimens and matched normal specimens. Survival studies revealed that high LINC02257 expression was associated with shorter overall survival and disease specific survival.  More importantly, multivariate assays confirmed that high expression of LINC02257 was an independent prognostic factor for CRC patients. The results of RT-PCR indicated that LINC02257 expression was distinctly overexpressed in both CRC specimens and cell lines. 	In CRC, LINC02257 expression was distinctly increased in CRC specimens compared with normal specimens. The results of ROC curves revealed that the AUC was 0.886 (0.862 to 0.909, 95% CI, p < 0.001) in a comparison between CRC specimens and matched normal specimens. Survival studies revealed that high LINC02257 expression was associated with shorter overall survival and disease specific survival. 	Yes	 The results of RT-PCR indicated that LINC02257 expression was distinctly overexpressed in both CRC specimens and cell lines. 	36124032
LINC02253	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell	Regulation(KRT18/MAPK/ERK pathwa)	Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	Here, we identified a novel oncogene, lncRNA LINC02253, in GC. LINC02253 expression was found to be significantly increased in GC. And LINC02253 expression was closely correlated with tumor size, lymph node metastasis and TNM stage of GC. Besides, GC patients with higher LINC02253 expression had worse 5-year overall survival. Additionally, LINC02253 promoted GC cell growth, migration and invasion both in vitro and in vivo. Mechanistically, we determined that LINC02253 increased KRT18 expression through enhancing the stability of KRT18 mRNA. Furthermore, LINC02253 increased m6A modification of KRT18 mRNA to stabilize KRT18 mRNA by recruiting m6A writer METTL3. And, rescue experiments revealed that KRT18 mediated the effects of LINC02253 on growth, migration and invasion of GC cells through activating MAPK/ERK signaling pathway. In conclusion, we demonstrates that oncogenic lncRNA LINC02253 positively regulates GC growth and metastasis via increasing METTL3-mediated mRNA stability of KRT18, extending the understanding of GC pathogenesis regulated by lncRNAs.	LINC02253 expression was found to be significantly increased in GC. And LINC02253 expression was closely correlated with tumor size, lymph node metastasis and TNM stage of GC. Besides, GC patients with higher LINC02253 expression had worse 5-year overall survival.	Yes	Mechanistically, we determined that LINC02253 increased KRT18 expression through enhancing the stability of KRT18 mRNA. And, rescue experiments revealed that KRT18 mediated the effects of LINC02253 on growth, migration and invasion of GC cells through activating MAPK/ERK signaling pathway.	35136989
LINC02200	LncRNA	Homo sapiens	Sinonasal Squamous Cell Carcinoma	 SNSCC tissue	Interaction(NF-κB)	ChIP//Western Blot//Wound Healing Assay//CCK8//RIP//Transwell Assay	The expression of RP11-159K7.2 in SNSCC tissue was significantly higher than that in adjacent tissues. RP11-159K7.2 directly bound to nuclear factor-κB (NF-κB) in SNSCC cells, and the regulation of RP11-159K7.2 on the proliferation and invasion of SNSCC cells depended on NF-κB.	After the down-regulation of RP11-159K7.2, the proliferation, migration and invasion ability of SNSCC cells decreased significantly, and the growth of SNSCC xenograft was significantly inhibited. 	Yes	RP11-159K7.2 expression was closely related with T grade, nodal metastasis and differentiation of SNSCC (χ2 value was 4.697, 4.235 and 10.753, respectively, all P<0.05). The five-year survival rate of RP11-159K7.2 high expression patients was significantly lower than that of RP11-159K7.2 low expression ones (P=0.013 7). 	34256488
LINC02154	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Regulation(SPC24/PI3K/AKT )	qRT-PCR	 We identified a new lncRNA, Linc02154, that is highly expressed in HCC cells and tissues of patients with a poor overall survival. Using a dual luciferase reporter assay we found that Linc02154 can enhance SPC24 promoter (-500 bp ~ -1000 region) activity. Exogenous over-expression of Linc02154 led to up-regulation of SPC24 by activating PI3K/AKT and its downstream signals, including cell cycle progression and EMT-associated gene expression.	 We identified a new lncRNA, Linc02154, that is highly expressed in HCC cells and tissues of patients with a poor overall survival.	Yes	 Functional experiments revealed that exogenous Linc02154 expression in MHCC-97H and SK-Hep1 cells promoted their proliferation, migration and invasion in vitro and their tumorigenesis in vivo. 	35543858
LINC02145	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	regulation[miRNA-140/MMP9 axis]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	FLJ33360 was upregulated in HCC tissues relative to paracancerous ones. It accelerates the metastasis of HCC through targeting miRNA-140/MMP9 axis.		Yes	After knockdown of FLJ33360, migratory and invasive capacities in Bel-7402 and HepG2 cells were attenuated. 	32194906
LINC02042	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cell lines, tissues and plasma	regulation[c-Myc,YBX1 ]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay//ChIP	 Linc02042 was found to be markedly upregulated in ESCC cell lines, tissues and plasma, and was closely correlated with malignant clinical features. Mechanistically, linc02042 acted as a scaffold for YBX-1 binding to the 3'-UTR of c-Myc mRNA, leading to enhanced c-Myc mRNA stability, thereby facilitating ESCC growth and metastasis. 		Yes	Knockdown of linc02042 significantly inhibited ESCC cell viability and invasion in vitro as well as tumor growth and lung metastasis in vivo, whereas overexpression of linc02042 resulted in the opposite results.	32161513
LINC02041	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	regulation[Notch pathway]	qRT-PCR//Western Blot	RP11-567G11.1 expression was significantly up-regulated in RCC tissues and cells. RP11-567G11.1 accelerates the proliferative and invasive abilities of RCC through activating the Notch pathway. 	Meanwhile, RP11-567G11.1 was highly expressed in RCC patients with advanced stage. 	Yes	Knockdown of RP11-567G11.1 significantly attenuated proliferative and invasive abilities of 786-O and 769-P cells. 	32432737
LINC02418	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC  tissues,cell lines	Interaction[miR-4677-3p/SEC61G]	CCK8//qRT-PCR//Transwell Assay	 LINC02418 was found as upregulated expression in both NSCLC tissues and cells.  Mechanistically, we showed LINC02418 could interact with microRNA-4677-3p (miR-4677-3p) to regulate Sec61 gamma subunit (SEC61G) expression.		Yes	 Functional assays showed that LINC02418 knockdown suppressed NSCLC cell proliferation and invasion but promoted cell apoptosis, while the overexpression of LINC02418 exerts opposite effects. 	31841189
LINC02465	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[PI3K/AKT pathway ]	IHC//Western Blot//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	As shown in Fig. 1B, LINC02465 exhibits markedly high expression in tumor tissues compared with adjacent nontumor tissues. We also discovered that LINC02465 level is remarkably increased in four GC cell lines (SGC7901, MGC-803, AGS, and BGC-823) in comparison with normal gastric cell line GES-1 (Fig. 1E). Taken together, LINC02465 is an oncogenic lncRNA that facilitates the tumorigenesis and progression of GC via PI3K/AKT pathway, demonstrating a novel effective therapeutic target and prognostic biomarker for GC patients.	Here we discover LINC02465, a novel recognized lncRNA, is upregulated and correlated with tumor size, tumor stage, lymph node metastasis, and differentiation in gastric cancer. In addition, we found that high LINC02465 level in GC patients is closely related to poor prognosis.	Yes	 Moreover, our findings reveal that LINC02465 silence suppresses cell proliferation and migration, invasion, and epithelial-mesenchymal transition in vitro. Conversely, LINC02465 overexpression displays a completely opposite way. 	30632400
LINC01614	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Interaction( GSK‑3β and AXIN1/ WNT/β‑catenin signaling pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//Colony Formation Assay//EdU Staining//Transwell Assay	 linc01614 was notably upregulated in PC tissues and cell lines and was associated with the poor disease-free survival of patients with PC according to the analysis of The Cancer Genome Atlas?derived datasets.  Mechanistically, linc01614 overexpression stabilized the level of β‑catenin protein to hyperactivate the WNT/β‑catenin signaling pathway in PC cells. Further analyses revealed that linc01614 bound to GSK‑3β and perturbed the interaction between GSK‑3β and AXIN1, thereby preventing the formation of the β‑catenin degradation complex and reducing the degradation of β‑catenin. 	 linc01614 was notably upregulated in PC tissues and cell lines and was associated with the poor disease-free survival of patients with PC according to the analysis of The Cancer Genome Atlas?derived datasets. 	Yes	 Functionally, linc01614 knockdown suppressed PC cell proliferation, migration and invasion in vitro, and inhibited tumor proliferation in vitro and in vivo. 	35929518
LINC02470	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	Interaction( LINC02470-miR-143-3p-SMAD3 ceRNA axis)	qRT-PCR//Western Blot	After screening the intersection of bioinformatic pipelines, LINC02470 was identified as the most upregulated lncRNA during bladder cancer initiation and progression.  On a molecular level, miR-143-3p directly targets and reduces both LINC02470 and SMAD3 RNA expression. Therefore, the LINC02470-miR-143-3p-SMAD3 ceRNA axis rescues SMAD3 translation upon LINC02470 sponging miR-143-3p, and SMAD3 consequently activates the TGF-β-induced EMT process.		Yes	Both in vitro and in vivo biological effects indicated that LINC02470 promotes bladder cancer cell viability, migration, invasion, and tumorigenicity.	35205713
LINC02908	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-661/HDAC11 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found C9orf139 was highly expressed in ESCC and knock down the expression of C9orf139 significantly suppressed cell proliferation, promoted apoptosis, and inhibited migration and invasion. C9orf139 was able to negatively regulate miR-661 expression. At the same time, HDAC11 expression was negatively regulated by miR-661. The C9orf139/miR-661/HDAC11 axis was further involved in regulating the expression of the NF-κB signaling pathway.		Yes	We found C9orf139 was highly expressed in ESCC and knock down the expression of C9orf139 significantly suppressed cell proliferation, promoted apoptosis, and inhibited migration and invasion. 	35917643
LINC02893	LncRNA	Homo sapiens	Osteosarcoma	 cell lines	regulation[TP53INP1]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IP//Colony Formation Assay	The current study showed that long non-coding RNA NR_027471 was downregulated in osteosarcoma cells.These results suggested that overexpression of NR_027471 upregulated TP53INP1 by sponging to miR-8055, leading to suppression of osteosarcoma cell proliferation and progression.		Yes	In vitro and in vivo studies indicated that upregulation of NR_027471 impeded the viability, proliferation, and invasion of osteosarcoma, as well as induced cell cycle arrest at G1.	33117693
LINC02883	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Expression[highly expressed]	qRT-PCR	We confirmed that KMU15 was expressed higher in bladder cancer tissues than paired control tissues. 	Moreover, the expression of KMU15 was significantly positively correlated with the grade, stage, metastasis, and recurrence of bladder cancer and was significantly negatively correlated with the prognosis. 	Yes	In addition, KMU15 knockdown could significantly inhibit bladder cell proliferation, adhesion, migration, and chemoresistance and promoted apoptosis. Knockdown of KMU15 inhibited the growth of xenografts in nude mice and significantly prolonged the survival of tumor-bearing mice under cisplatin.	31850704
LINC02882	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue and cell lines	regulation[miR-339-HNRNPA1 interaction network]	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay	Here we identified a novel lncRNA RP11-81H3.2 that was highly expressed in the GC tissue and cell lines.Mechanistically, we demonstrated that RP11-81H3.2 directly interacted with miR-339 while miR-339 regulated the HNRNPA1 expression by targeting HRRNPA1 3'-UTR. RP11-81H3.2-miR-339-HNRNPA1 interaction network regulated the GC cell proliferation, migration, and invasion.		Yes	 RP11-81H3.2 knockdown significantly inhibited the proliferation, migration, and invasion of GC cells. Moreover, our results confirmed that RP11-81H3.2 knockdown suppressed the tumor growth of GC in a xenograft model in vivo. 	32052594
LINC02875	LncRNA	Homo sapiens	Glioma	 glioma cells	Epigenetics [methylation ]	Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	Furthermore, we identified two lncRNAs termed PCBP1-AS1 and LINC02875 that may be involved in the malignant progression of glioma cells by using the TCGA database.		Yes	 Loss-of-function assays confirmed that knockdown of PCBP1-AS1 and LINC02876 inhibited the proliferation, migration, and invasion of glioma cells.	33828990
LINC02870	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and cells	Interaction(EIF4G1)	qRT-PCR	Upregulated expressions of LINC02870 were also found in our HCC samples compared to the para-tumor samples.  Intriguingly, the most promising binding protein of LINC02870 was predicted and confirmed to be eukaryotic translation initiation factor 4 gamma 1 (EIF4G1), an important component of the eukaryotic translation initiation factor 4F complex that initiates cap-dependent translation. Further investigation showed that LINC02870 increased the translation of SNAIL to induce malignant phenotypes in HCC cells. 	Additionally, HCC patients with higher expression levels of LINC02870 and EIF4G1 had shorter survival times than those with lower expression levels. 	Yes	Moreover, overexpression of LINC02870 promoted the growth, migration, and invasion of HCC cells. 	36583796
LINC02835	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[Binding p120-Catenin]	RNA Pull-Down//Northern Blot//Western Blot//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	Mechanistically, lncMER52A stabilized p120-catenin and triggered the activation of Rho GTPase downstream of p120-catenin. Furthermore, we found that chromatin accessibility was crucial for the expression of lncMER52A. In addition, YY1 transcription factor bound to the cryptic MER52A LTR promoter and drove lncMER52A transcription in HCC. In conclusion, we identified an LTR-activated lncMER52A, which promoted the progression of HCC cells via stabilizing p120-catenin and activating p120-ctn/Rac1/Cdc42 axis. LncMER52A could serve as biomarker and therapeutic target for patients with HCC. SIGNIFICANCE: A novel long noncoding RNA lncMER52 modulates cell migration and invasion via posttranslational control of p120-catenin protein stability.	HCC patients with higher lncMER52A had advanced TNM stage, less differentiated tumors, and shorter overall survival. 	Yes	LncMER52A promoted invasion and metastasis of HCC cells in vitro and in vivo.	31874857
LINC02747	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	regulation[ LINC02747/miR-608/TFE3 pathway]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	We found that lncRNA LINC02747 was highly expressed in ccRCC (P < 0.001) and was closely related to high TNM stage (P = 0.006) and histological grade (P = 0.004) and poor prognosis of patients (P < 0.001). The LINC02747/miR-608/TFE3 pathway may become a new therapeutic target for ccRCC.	We found that lncRNA LINC02747 was highly expressed in ccRCC (P < 0.001) and was closely related to high TNM stage (P = 0.006) and histological grade (P = 0.004) and poor prognosis of patients (P < 0.001).	Yes	In vivo and in vitro experiments confirmed that LINC02747 could promote the proliferation of ccRCC cells. 	33425728
LINC02605	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-29c)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The result of dual-luciferase reporter assay represented a direct interaction of RP11-79H23.3 with miR-29c, which suppressed miR-29c expression that showed inversely correlation in NSCLC. Moreover, RP11-79H23.3 siRNA facilitated the progression of NSCLC partially via regulating the expression of miR-29c and the activation of Wnt/β-catenin signaling pathway. 		Yes	 RP11-79H23.3 downregulation facilitated cell proliferation, migration, and invasion of NSCLC.	35972581
LINC02605	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC tissues and cells	interaction[PTEN,hsa-miR-107 ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	We found that lncRNA RP11-79H23.3 and phosphatase and tensin homolog (PTEN) were significantly downregulated in BC tissues and cells.Mechanistically, we identified that RP11-79H23.3 could directly bind to miR-107 and abolish the suppressive effect on target gene PTEN, which leads to inactivation of the PI3K/Akt signaling pathway.	 Meanwhile, RP11-79H23.3 expression was negatively correlated with clinical stage in BC.	Yes	Functionally, we found that overexpression of RP11-79H23.3 could suppress cell proliferation, migration, and cell cycle progression, rearrange the cytoskeleton, and induce apoptosis in vitro. Moreover, upregulation of RP11-79H23.3 inhibited the angiogenesis, tumorigenesis, and lung metastasis in vivo, whereas RP11-79H23.3 knockdown exerted a contrary role. 	30149689
LINC02587	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells lines	Interaction(miR-143-3p/VDAC1 pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//Invasion Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	In the paper, we reported that MEOX2-AS1 levels were distinctly upregulated in CC cells and tissues, and higher MEOX2-AS1 expressions indicated a poor clinical outcome. Besides, STAT1 could activate transcriptions of MEOX2-AS1 by binding directly to its promoter region. The silence of MEOX2-AS1 suppressed the metastatic and proliferative ability of CC cells, as revealed by functional assays. Mechanistically, MEOX2-AS1 sponged miR-143-3p to regulate VDAC1 expressions. Furthermore, miR-143-3p inhibitor reversed the anti-proliferation and anti-metastasis effect of MEOX2-AS1 knockdown. 		Yes	Loss-of-function experiments were performed for the assays of proliferation, migration, and invasion of CC cells after various treatments.	34224325
LINC02580	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	interaction[targeting SRSF1]	RNA Pull-Down//ChIP//Western Blot//qRT-PCR//FISH//RIP//Transwell Assay	LINC02580 was highly downregulated in HCC cohorts and was identified as a tumor suppressor.  With respect to the underlying mechanism, we found that LINC02580 modulates the epithelial-mesenchymal transition (EMT) associated pathway in HCC cells by specifically binding to serine and arginine-rich splicing factor 1 (SRSF1).	Low LINC02580 expression in patients with HCC was correlated with poor prognosis.	Yes	Functional assays indicated that LINC02580-deficient cells show enhanced colony formation, migration, and invasion in vitro and promote subcutaneous tumor formation and distant lung metastasis in vivo.	33168192
LINC02544	LncRNA	Homo sapiens	lung squamous cell carcinoma	LUSC tissues and cell line	Interaction(miR-138-5p)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Linc02544 was overexpressed in LUSC tissues from positive lymph node metastasis-positive and TNM high-stage patients.Expression of MMP-2, MMP-9, and vimentin was decreased while E-cadherin was increased in si-linc02544 cells compared with that in untreated cells. Mechanistically, we identified that linc02544 acted as a sponge of miR-138-5p, which expression had a negative correlation. E2F3 was a potential target of miR-138-5p.	Linc02544 was overexpressed in LUSC tissues from positive lymph node metastasis-positive and TNM high-stage patients.Low linc02544 expression was associated with a longer survival rate.	Yes	Downregulation of linc02544 by si-linc02544 restrained cell growth capacities, migration, and invasion abilities.	35635595
LINC02535	LncRNA	Homo sapiens	Stomach Neoplasms	PDGC tissues	Expression [highly expressed]	Bioinformatics Analysis//Wound Healing Assay//Migration Assay//CCK8//RNA-seq//Cell Apoptosis Assay//Invasion Assay	LINC02535 expression was upregulated in PDGC and contributed to cell proliferation, migration, invasion and wound healing, whereas its inhibition in PDGC facilitated cell apoptosis.		Yes	LINC02535 expression was upregulated in PDGC and contributed to cell proliferation, migration, invasion and wound healing, whereas its inhibition in PDGC facilitated cell apoptosis.	34125981
LINC02535	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues and cells	Interaction(miR-30a-5p/GALNT3 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that LINC02535 was increased in LUAD tissues and cells, and LINC02535 was correlated with the poor prognosis of LUAD patients. miR-30a-5p acts as a tumor suppressor in LUAD by targeting GALNT3.  LINC02535 acts as a competing endogenous RNA (ceRNA) to interact with miR-30a-5p, thereby upregulating the expression of GALNT3, enhancing the function of MUC1, and activating the NF-κB signaling pathway, promoting the malignant progression of LUAD cells.		Yes	 We also demonstrated that LINC02535 might function as the sponge of miR-30a-5p to up-regulate GALNT3, and consequently promote the proliferation and metastasis of LUAD. 	35852407
LINC02532	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The qRT-PCR assay demonstrated that the LINC02532 expression level was significantly upregulated in the GC cell lines and 52 paired tissues.	Kaplan-Meier survival analysis based on The Cancer Genome Atlas data showed that patients with higher LINC02532 expression had poorer prognosis than those with lower LINC02532 expression. The correlation analysis between expression and clinicopathological features revealed that high expression of LINC02532 was associated with a high TNM stage (P = 0.008) and poor differentiation grade (P = 0.023). 	Yes	 Functional experiments showed that LINC02532 promoted GC cell proliferation, migration, and invasion.	30788037
LINC02499	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression[lower expressed]	qRT-PCR	 LINC02499 expression was remarkably decreased in HCC tissues compared to adjacent non-tumor tissues based on TCGA (P < 0.001) and GEO databases (P < 0.001) and our HCC cohort (P < 0.001).	Decreased LINC02499 was also significantly associated with poorer overall survival in both the TCGA database (P = 0.009) and our HCC cohort (P = 0.002). Furthermore, the receiver operating characteristic analysis indicated that LINC02499 showed a good performance in HCC diagnosis (area under the curve = 0.879, P < 0.001), and both sensitivity and specificity were 83.8%.	Yes	In addition, up- and downregulated LINC02499 significantly impacted proliferation, migration, and invasion abilities of HCC cells in vitro.	32039538
LINC02475	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Expression(highly expressed)	qRT-PCR	 LINC02475 expression was elevated in HCC, performed well in the diagnosis, and independently predicts poor overall survival (hazard ratio = 1.389, 95% confidence interval = 1.047-1.843, p = 0.023), as well as progression-free survival (hazard ratio = 1.396, 95% confidence interval = 1.016-1.917, p = 0.040) of HCC patients.	 LINC02475 expression was elevated in HCC, performed well in the diagnosis, and independently predicts poor overall survival (hazard ratio = 1.389, 95% confidence interval = 1.047-1.843, p = 0.023), as well as progression-free survival (hazard ratio = 1.396, 95% confidence interval = 1.016-1.917, p = 0.040) of HCC patients.	Yes	Moreover, LINC02475 enhanced the tumorigenic pathways necessary for cell stemness, DNA replication required for cell proliferation, epithelial-mesenchymal transition involved in metastasis, and DNA damage repair pathways that drove cell radioresistance and cisplatin resistance, thus promoting HCC progression. 	36118852
LINC02474	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(GZMB)	In Vivo Experiment//Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//FISH//RNA-seq//Invasion Assay	The expression of LINC02474 was significantly up-regulated in CRC tissues. Besides, down-regulation of LINC02474 promoted the expression of GZMB, and interference of GZMB could increase the metastatic abilities of CRC cells while reducing apoptosis. 		Yes	Moreover, depletion of LINC02474 damaged the metastatic abilities of CRC cells in vivo and in vitro while boosting apoptosis. Besides, up-regulation of LINC02474 could promote migration and invasion, while apoptosis was inhibited in CRC cells. 	33898319
LINC02041	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	Expression[Expression[Expression[highly expressed]-expression]-expression]	CCK8//qPCR//Western Blot	The results illustrated that RP11-567G11.1 was significantly Expression[Expression[up-expression]-expression]-regulated in poorly differentiated pancreatic cancer tissues as compared to its expression in non-tumor tissues.		Yes	 Additionally, depletion of RP11-567G11.1 in pancreatic cancer cells inhibited proliferation and cell cycle progression, induced apoptosis, sExpression[Expression[up-expression]-expression]pressed the stem cell-like phenotype, and increased sensitivity to gemcitabine. 	30802827
LINC02023	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue	Interaction[PTEN ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//IHC	 This study aims to show that long noncoding RNA (lncRNA) Linc02023 aberrant downregulation in colorectal cancer correlates positively with the expression of PTEN and CDKN2B but negatively with the tumor size in patients and xenografted mouse models. Mechanistically, Linc02023 specifically binds to PTEN and blocks its interaction with and ubiquitination by WWP2, stabilizing it and suppressing its downstream expression. In conclusion, this study demonstrates that lncRNA Linc02023 may serve as a novel therapeutic target by restoring the PTEN tumor suppressor activity.		Yes	CDKN2B but negatively with the tumor size in patients and xenografted mouse models. The gain- and loss-of-function investigation reveals that Linc02023 suppresses the proliferation of colorectal cancer cells in vitro and in vivo with apoptosis promotion and cell cycle rearrangement.	30849479
LINC01980	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction[GADD45A  ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Microarray	In this study, we identified a novel lncRNA LINC01980, located in both the cytoplasm and nucleus, which was significantly upregulated in esophageal squamous cell carcinoma (ESCC) tissues through microarray profiling.  Further experiments demonstrated that GADD45A promoted ESCC cell growth, indicating that GADD45A may be a downstream target of LINC01980.	Further analysis revealed that LINC01980 overexpression was positively correlated with deeper invasion of cancer, positive lymph node metastasis, and advanced TNM stage. 	Yes	In vitro and in vivo experiments demonstrated that LINC01980 promoted ESCC growth.	30935686
LINC01980	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	esophageal cancer cells and ESCC tissues	regulation[miR-190a-5p/MYO5A pathway]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	The high expression of LINC01980 was detected in ESCC tissues and cells, and predicted poor prognosis.Therefore, these findings suggest that LINC01980 may act as an oncogenic lncRNA in ESCC and LINC01980/miR-190a-5p/MYO5A pathway contributes to the development of ESCC.	The high expression of LINC01980 was detected in ESCC tissues and cells, and predicted poor prognosis.	Yes	 LINC01980 promoted the cell proliferation, migration, invasion ability and epithelial-mesenchymal transition (EMT) progress in ESCC cells.	32325088
LINC01711	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	The tumor tissues and paired normal adjacent tissues	Interaction(miR-326/FSCN1 axis)	qRT-PCR//RIP//Western Blot	In this study, we detected high expression of lncRNA LINC01711 in ESCC tissues and was associated with poor prognosis. Linc01711 was identified as a competitive endogenous RNA that suppressed miR-326, and up-regulated the expression of fascin actin-bundling protein 1 (FSCN1). 	In this study, we detected high expression of lncRNA LINC01711 in ESCC tissues and was associated with poor prognosis. 	Yes	Silencing LINC01711 can inhibit the proliferation, migration, invasion, and growth of ESCC cell lines, and induce apoptosis.	34370713
LINC01711	LncRNA	Homo sapiens	Glioblastoma	glioma cells,  GBM tissues	Interaction( miR-34a/ZEB1)	qRT-PCR//ChIP//Western Blot	 We show that LINC01711 expression is significantly upregulated in GBM tissues and is associated with poor overall survival of GBM patients. In addition, LINC01711 depletion sensitizes glioma cells to Temozolomide (TMZ) induced apoptosis by inhibiting ZEB1 expression. LINC01711 functions as a competing endogenous RNA for miR-34a and promotes ZEB1 expression to regulate invasion. 	 We show that LINC01711 expression is significantly upregulated in GBM tissues and is associated with poor overall survival of GBM patients.	Yes	Loss-of-function studies illustrate that LINC01711 promotes proliferation, migration, and invasion in GBM. 	36341927
LINC01705	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	interaction[binding to miR-186-5p]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Our findings revealed high LINC01705 expression in breast cancer tissues relative to adjacent non-cancerous tissues (n = 40, P < 0.001). In conclusion, our results suggest that LINC01705 is implicated in the progression of breast cancer via competitively binding to miR-186-5p as a competing endogenous RNA (ceRNA), thereby regulating TPR expression.		Yes	Overexpression of LINC01705 notably enhanced cell migration and proliferation in breast cancer.	32849791
LINC01705	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cell lines	regulation[miR-4722-3p/P2RY8 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our results demonstrated that the expression of RP11?400N13.3 was significantly upregulated in both colorectal cancer tissues and cell lines as compared to normal adjacent tissues and normal colonic epithelial cells by RT?qPCR, respectively. In conclusion, our results revealed that RP11‑400N13.3 promoted colorectal cancer progression via modulating the miR‑4722‑3p/P2RY8 axis, thus suggesting RP11‑400N13.3 as a potential therapeutic target for the treatment of colorectal cancer.	Upregulation of RP11?400N13.3 was found to be correlated with a poor overall survival rate. 	Yes	 Functional studies revealed that RP11?400N13.3 facilitated the proliferation, migration, invasion and tumor growth of colorectal cancer cells while inhibiting the apoptosis of cancer cells in vitro and in vivo.	32901883
LINC01679	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa cells	Interaction(miR-3150a-3p/SLC17A9 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay	 LINC01679 regulated miR-3150a-3p level by sponging it. Importantly, miR-3150a-3p overexpression was related to the increased proliferation and decreased apoptosis of PCa cells. Rescue assays suggested that miR-3150a-3p mimics rescued the repression on PCa progression mediated by LINC01679 upregulation, but SLC17A9 downregulation reversed the miR-3150a-3p inhibitor-mediated repression on PC progression. 		Yes	 According to our results, LINC01679 depletion promoted cell proliferation, metastasis, tumor growth, and inhibited cell apoptosis in vivo and in vitro, which was also associated with poor survival. 	34900992
LINC01638	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues and cells	interaction[c-Myc]	Western Blot//ISH//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//IHC//Invasion Assay//ChIP	Here, we demonstrated that LINC01638 is highly expressed in TNBC tissues and cells. Mechanistically, LINC01638 interacts with c-Myc to prevent SPOP-mediated c-Myc ubiquitination and degradation. 	LINC01638 overexpression predicts a poor outcome of breast cancer patients. 	Yes	 LINC01638 knockdown suppresses tumor proliferation and metastasis both in vitro and in vivo.	30002443
LINC01638	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells and tissues	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	Linc01638 was found to be remarkably overexpressed in HER2-positive breast cancer cells and tissues.Suppression of linc01638 enhanced cell apoptosis, as well as inhibited the growth and invasiveness of HER2-positive breast cancer cells in vitro and tumor progression and metastasis in vivo. 		Yes	Suppression of linc01638 enhanced cell apoptosis, as well as inhibited the growth and invasiveness of HER2-positive breast cancer cells in vitro and tumor progression and metastasis in vivo. 	29992881
LINC01638	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression[Expression[Expression[highly expressed]-expression]-expression]	CCK8//qRT-PCR	 LINC01638 lncRNA and glucose transporter 1 (GLUT1) were Expression[Expression[up-expression]-expression]regulated in tumor tissues compared with adjacent healthy tissues of patients with HCC.		Yes	Overexpression of LINC01638 lncRNA and GLUT1 promoted glucose Expression[Expression[up-expression]-expression]take, while LINC01638 lncRNA and GLUT1-knockExpression[down-expression] led to inhibited glucose Expression[Expression[up-expression]-expression]take of cells of HCC cell lines.Overexpression of LINC01638 lncRNA mediated the Expression[Expression[up-expression]-expression]regulation of GLUT1 expression and accelerated cell proliferation.	31516592
LINC01638	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	Regulation[TGF‑β signaling]	qRT-PCR//ELISA	 In the present study, LINC01638 was significantly upregulated in tumor tissues compared with adjacent healthy tissues in the majority of patients with PDAC.		Yes	 LINC01638 overexpression promoted, while shRNA silencing inhibited, migration and invasion of cell of a PDAC cell line.	31702018
LINC01638	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	thyroid gland epithelial cell line 	Regulation(Axin2 / Wnt/β-catenin signaling pathway)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//cell invasion assay//Colony Formation Assay//IF	We found that LINC01638 was upregulated in PTC cells compared with normal thyroid gland epithelial cell line Nthy-ori3-1.  ELK1 could act as a transcription factor of LINC01638 and induce LINC01638 expression. LINC01638 silencing inhibited cell proliferation, migration and invasion, and obstructed the progress of TPC-1 cell cycle. LINC0163 silencing activated Axin2 while suppressing the expressions of β-catenin, Cyclin-D1 and c-MYC. Rescue experiment utilizing the transfection of Axin2 overexpression plasmid weakened LINC01638 overexpression-enhanced TPC-1 cell proliferation, metastasis, cell cycle progress and Wnt/β-catenin pathway. 		Yes	LINC01638 silencing inhibited cell proliferation, migration and invasion, and obstructed the progress of TPC-1 cell cycle. LINC0163 silencing activated Axin2 while suppressing the expressions of β-catenin, Cyclin-D1 and c-MYC. Rescue experiment utilizing the transfection of Axin2 overexpression plasmid weakened LINC01638 overexpression-enhanced TPC-1 cell proliferation, metastasis, cell cycle progress and Wnt/β-catenin pathway. 	34281460
LINC01638	LncRNA	Homo sapiens	laryngeal squamous cell carcinoma	LSCC tissues	Interaction(miR-523-5p/BATF3 axis)	In Vivo Experiment//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	In the present study, we found that LINC01638 was highly expressed in LSCC tissues. In terms of mechanism, LINC01638 was found to sponge miR-523-5p and promote BATF3 expression. In summary, our results demonstrated that LINC01638/miR-523-5p/BATF3 axis plays a crucial function in initiating LSCC development and may be a potential target for tumor therapy.	And LINC01638 expression was positively correlated with clinical stage and lymph node metastasis. Patients with LINC01638 high expression displayed a low survival rate. 	Yes	 Results from CCK8, colony formation, and transwell assays showed that LINC01638 knockdown suppressed the proliferation, migration and invasion of LSCC cells in vitro. Animal experiments indicated that LINC01638 silencing attenuated tumor growth in vivo. 	33714208
LINC01635	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer and in non-small cell lung carcinoma (NSCLC) cell lines	Interaction(miR-455-5p)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Next, it was confirmed that LINC01635 was upregulated significantly in samples from patients with lung cancer and in non-small cell lung carcinoma (NSCLC) cell lines.  Furthermore, it was found that LINC01635 could bind to microRNA (miRNA or miR)-455-5p and regulate the expression of a series of miR-455-5p-targeting tumor-related genes. Knockdown of miR-455-5p partially rescued the progression of lung cancer cells that was suppressed by LINC01635 silencing.		Yes	 Silencing LINC01635 suppressed the proliferation and metastasis of NSCLC cells in vitro and in vivo. 	36420078
LINC01617	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer and adjacent tissues	Regulation[AKT pathway]	qRT-PCR	We found that LINC01617 was overexpressed in esophageal cancer, and its expression was associated with poor prognosis of esophageal cancer. The Akt pathway may be involved in the regulation of cell activity in esophageal cancer.	We found that LINC01617 was overexpressed in esophageal cancer, and its expression was associated with poor prognosis of esophageal cancer.	Yes	 In vitro experiments confirmed that knockout of LINC01617 significantly inhibited the proliferation, migration and invasion of esophageal cancer cells. Moreover, knockout of LNC01617 can inhibit the growth of esophageal cancer in nude mice.	30120975
LINC01615	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissues	Interaction(miR-3653-3p/ZEB2 )	qRT-PCR//Western Blot	TCGA suggested that LINC01615 was high-expressed in colon cancer, as verified in clinical and cell samples, and patients with LINC01615 overexpression suffered from a poor prognosis. LINC01615, which was targeted by miR-3653-3p, partially offset the inhibitory effect of miR-3653-3p on colon cancer cells. The downstream target gene ZEB2 of miR-3653-3p was high-expressed in colon cancer. MiR-3653-3p was negatively correlated with LINC01615 or ZEB2, while LINC01615 was positively correlated with ZEB2. 	.TCGA suggested that LINC01615 was high-expressed in colon cancer, as verified in clinical and cell samples, and patients with LINC01615 overexpression suffered from a poor prognosis. 	Yes	Silent LINC01615 blocked the malignant development of colon cancer cells through regulating related genes expressions, while overexpressed LINC01615 had the opposite effect. 	34965191
LINC01615	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 502 HNSCC tissues and 44 normal tissues	Expression(highly expressed)	Migration Assay//MTT//Invasion Assay//Transwell Assay	Clinical correlation analysis revealed that the LINC01615 increased with increasing the T stage, N stage, pathology grade, and clinical stage. 	Clinical correlation analysis revealed that the LINC01615 increased with increasing the T stage, N stage, pathology grade, and clinical stage. 	Yes	Functionally, silencing of LINC01615 suppresses cell proliferation, invasion, and migration in HEP-2 and TU212 cells.	35794984
LINC01614	LncRNA	Homo sapiens	Stomach Neoplasms	GC cases  and GC cell lines	Regulation	Other	 In contrast, the lncRNA-based subtype 1 (L1) has the best survival outcome, while LINC01614 expression further segregated a subgroup of L1 cases with worse survival and increased chance of developing distal metastasis. 		Yes	We demonstrated that LINC01614 over-expression is an independent prognostic factor in L1 and network-based functional prediction implicated its relevance to cell migration. Over-expression and CRISPR-Cas9-guided knockout experiments further validated the functions of LINC01614 in promoting GC cell growth and migration. 	33742127
LINC01614	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Expression(highly expressed)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RNA-seq//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	 LINC01614 expression was identified and found to be upregulated in GC tissues and cells. 		Yes	 The study findings revealed that LINC01614 promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Knockdown of LINC01614 arrested cell cycle distribution at the G2/M phase.Further, LINC01614 also promoted tumor growth in vivo.	34691143
LINC01614	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 Chinese population	Mutation(rs16854802, rs3113503 )	CCK8//qRT-PCR	 In this study, we found that rs16854802 A > G (odds ratio [OR] = 1.42, 95% confidence interval [CI]: 1.22-1.77, p < 0.001) and rs3113503 G > C (OR = 1.38, 95% CI: 1.15-1.64, p < 0.001) in LINC01614 increased the risk of HNSCC in the Chinese population.  Functional bioinformatic analysis and luciferase reporter assay revealed that rs3113503 G > C variant disrupted the binding of miRNA-616-3p to LINC01614, which resulted in the increased expression of LINC01614. Mechanistically, allele C of rs3113503 in LINC01614 was more effective than allele G in activating the PI3K/AKT signaling pathway. Moreover, the reduced expression of LINC01614 also inhibited the activation of the PI3K/AKT signaling pathway.	 Further analysis of the TCGA database demonstrated that the upregulated LINC01614 in HNSCC cancer tissues was associated with poor prognostic in HNSCC patients. 	Yes	 In vitro experiments showed that knockdown of LINC01614 inhibited the proliferation, invasion, and migration ability of HNSCC cells. 	35687049
LINC01614	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC cell	Regulation	qRT-PCR//Transwell Assay	And we found that only LINC01614 was concerned with a candidate prognostic signature in EC.  		Yes	The results of CCK8 and Transwell assays showed that suppression of LINC01614 inhibited EC cell proliferation and migration.	35116503
LINC01748	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR‑520a‑5p/HMGA1 pathway )	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	Data from The Cancer Genome Atlas dataset and patients recruited into the present study showed that LINC01748 was overexpressed in NSCLC. Mechanistically, LINC01748 could act as a competing endogenous (ce)RNA to sponge microRNA(miR)‑520a‑5p, to increase the expression level of the target gene, high mobility group AT‑hook 1 (HMGA1) in the NSCLC cell lines. Furthermore, rescue experiments illustrated that the functions exerted by LINC01748 knockdown were negated by miR‑520a‑5p inhibition or HMGA1 overexpression. 	Patients with high LINC01748 mRNA expression level had shorter overall survival rate compared with that in patients with low LINC01748 mRNA expression level. 	Yes	Then, knockdown of LINC01748 mRNA expression level reduced cell proliferation, migration and invasion, but increased cell apoptosis in vitro. Knockdown of LINC01748 also reduced tumor growth in vivo. 	34970695
LINC01783	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC cells (SCC1, Cal27, UM1 and SCC4) and 22 TSCC cases	Interaction(miR-199b-5p )	Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay	In this research, we indicated that LINC01783 was up-regulated in TSCC cells (SCC1, Cal27, UM1 and SCC4) when compared to NHOK cell.RT-qPCR analysis indicated that LINC01783 was overexpressed in 22 TSCC cases (73.3%, 22/30) compared with no-tumour specimens.LINC01783 level was up-regulated in TSCC specimens when compared to no-tumour specimens.Overexpression of LINC01783 sponged miR-199b-5p in TSCC cell and elevated expression of LINC01783 inhibited miR-199b-5p expression. Moreover, we illustrated that miR-199b-5p was down-regulated in TSCC cells and specimen and LINC01783 level was up-regulated in TSCC specimens when compared to no-tumour specimens. 		Yes	Ectopic expression of LINC01783 promoted TSCC cell cycle and growth and EMT progression in both TSCC cell SCC1 and Cal27.	34363308
LINC01783	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines	Regulation(Notch pathway and sponging miR-432-5p)	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth.		Yes	Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown.	33902591
LINC01857	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-2052/CENPQ axis)	qRT-PCR	The results showed that LINC01857 and CENPQ were highly expressed in BC tissues and cells, while miR-2052 was contrarily expressed.  In vitro study showed that low expression of linc01857 could inhibit the migration ability and vascularization of BC cells, and mir-2052 inhibitor partially restored the effect of si-LINC01857 on the migration ability and vascularization of BC cells. Likewise, inhibition of CENPQ can partially rescue the effects of miR-2052 inhibitor on the migration ability and vascularization of BC cells. In vivo studies showed that down-regulation of LINC01857 notably suppressed tumor growth and angiogenesis in nude mice. The miR-2052 inhibitor partially restored the effects of si-LINC01857. 		Yes	 In vitro study showed that low expression of linc01857 could inhibit the migration ability and vascularization of BC cells, and mir-2052 inhibitor partially restored the effect of si-LINC01857 on the migration ability and vascularization of BC cells. Likewise, inhibition of CENPQ can partially rescue the effects of miR-2052 inhibitor on the migration ability and vascularization of BC cells. In vivo studies showed that down-regulation of LINC01857 notably suppressed tumor growth and angiogenesis in nude mice. The miR-2052 inhibitor partially restored the effects of si-LINC01857. 	36046633
LINC01977	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction( TGF-β/SMAD3)	IHC//Western Blot//ISH//qPCR//FISH//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining//IF	We found that LINC01977, a cancer-testis lncRNA, was hijacked by SE, which promoted proliferation and invasion both in vitro and in vivo.LINC01977 interacted with SMAD3 to induce its nuclear transport, which facilitated the interaction between SMAD3 and CBP/P300, thereby regulating the downstream target gene ZEB1. Additionally, SMAD3 up-regulated LINC09177 transcription by simultaneously binding the promoter and SE, which was induced by the infiltration of M2-like tumor-associated macrophages (TAM2), subsequently activating the TGF-β/SMAD3 pathway. Moreover, LINC01977 expression was positively correlated with TAM2 infiltration and SMAD3 expression, especially in early-stage LUAD. Higher chromatin accessibility in the SE region of LINC01977 was observed with high expression of TGF-β. 	Early-stage LUAD patients with high LIN01977 expression had a shorter disease-free survival.	Yes	We found that LINC01977, a cancer-testis lncRNA, was hijacked by SE, which promoted proliferation and invasion both in vitro and in vivo.	35982471
LINC01969	LncRNA	Homo sapiens	Ovarian Neoplasms	Ovarian Cancer tissues	interaction[LINC01969/miR-144-5p/LARP1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	The results of the current study showed that LINC01969 was dramatically upregulated in OC, and patients with lower LINC01969 expression levels tended to have better overall survival. In conclusion, the LINC01969/miR-144-5p/LARP1 axis is a newly identified regulatory signaling pathway involved in OC progression.	The results of the current study showed that LINC01969 was dramatically upregulated in OC, and patients with lower LINC01969 expression levels tended to have better overall survival. 	Yes	Further experiments demonstrated that LINC01969 promoted the migration, invasion, and proliferation of OC cells in vitro and sped up tumor growth in vivo. 	33614632
LINC01963	LncRNA	Homo sapiens	Pancreatic Carcinoma	pancreatic carcinoma tissues and cell lines	interaction[miR-641/TMEFF2]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 lncRNA LINC01963 was confirmed to be lower expressed in pancreatic carcinoma tissues and cell lines.Long non-coding RNA LINC01963 inhibits progression of pancreatic carcinoma by targeting miR-641/TMEFF2.		Yes	By up-regulating the expression of lncRNA LINC01963 in pancreatic carcinoma cell lines, colony number, cell cycle, proliferation and invasion were inhibited, while apoptosis was improved.	32559621
LINC01939	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[ as a ceRNA for miR-17-5p to regulate EGR2 expression]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that LINC01939 expression was significantly downregulated in GC tissues and cell lines. Taken together, these results suggested that LINC01939 repressed GC invasion and migration by functioning as a ceRNA for miR-17-5p to regulate EGR2 expression. Our findings provided a novel prognostic marker and therapeutic target for GC patients	Low expression of LINC01939 was correlated with tumor metastasis and shorter survival in GC patients. 	Yes	Functionally, LINC01939 overexpression remarkably inhibited the invasion and migration of GC cells in vitro and in vivo.	30683847
LINC01939	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC tissues and cell lines	regulation[ down-regulation of miR-154]	qRT-PCR//Wound Healing Assay//Western Blot	LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis.Up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.		Yes	 LINC01939 overexpression impeded proliferation and migration, and induced apoptosis.	32138544
LINC01929	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue samples and cell lines	Interaction(miR-137-3p/FOXC1 Axis)	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our findings demonstrated that LINC01929 was highly expressed in OSCC tissue samples and cell lines, whereas miR-137-3p expression was downregulated. Mechanistically, LINC01929 acted as a sponge for miR-137-3p to elevate FOXC1 expression, which is the target of miR-137-3p. In addition, downregulated miR-137-3p expression rescued the suppressive behaviors of LINC01929 knockdown on the biological behaviors of OSCC cells. Taken together, LINC01929 functioned as a tumor-promoting lncRNA via the miR-137-3p/FOXC1 axis in OSCC, suggesting novel targets for OSCC therapy.		Yes	LINC01929 acted as a carcinogenic lncRNA with accelerated OSCC cell proliferation, migration and invasion, and suppression of apoptosis. We further indicated that LINC01929 facilitated tumor growth in xenograft mouse models.	33968763
LINC01857	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Regulation[regulates CREB1 ]	qRT-PCR	In this study, we found that LINC01857 was highly expressed in breast cancer tissues and cells (p < 0.05).  Taken together, our findings demonstrated that LINC01857 promoted breast cancer development by promoting H3K27Ac and CREB1 transcription via enhancing CREBBP enrichment in the CREB1 promoter region.	High LINC01857 expression predicted poor prognosis in breast cancer patients.	Yes	Functionally, LINC01857 silencing impaired proliferation and enhanced apoptosis of breast cancer cells ( p < 0.05).Decreased LINC01857 inhibited breast cancer cells migration and invasion ability ( p < 0.05).	30628071
LINC01857	LncRNA	Homo sapiens	pancreatic adenocarcinoma	PDAC tissues and cells	Interaction( miR-19a-3p/SMOC2)	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	 LINC01857 levels were significantly elevated in PDAC. MiR-19a-3p was a downstream target of LINC01857, and miR-19a-3p levels were significantly decreased in PDAC cells. In addition, SMOC2 expression had a negative correlation with that of miR-19a-3p, and SMOC2 was a downstream target of miR-19a-3p. Furthermore, SMOC2 upregulation partially abolished the inhibitive influence of LINC01857 downregulation on cell proliferation, migration, invasion, and the EMT process.		Yes	Knockdown of LINC01857 significantly restrained the proliferation, migration, invasion, and Epithelial-Mesenchymal Transition (EMT) process of PDAC cells. 	35662010
LINC01787	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines(MDA-MB-231,MCF-7)	Interaction[Disrupting miR-125b ]	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay	LINC01787 is up-regulated in breast cancer tissues and is associated with advanced stages and poor survival.In conclusion, our findings identified a novel up-regulated and oncogenic lncRNA LINC01787 in breast cancer, which binds pre-miR-125b and represses mature miR-125b generation.	LINC01787 is up-regulated in breast cancer tissues and is associated with advanced stages and poor survival.	Yes	Functional assays showed that LINC01787 promotes breast cancer cell proliferation and migration and breast cancer xenograft growth in vivo, which is abolished by the mutation of pre-miR-125b binding sites on LINC01787 or overexpression of miR-125b.	31750242
LINC01857	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[miR-1281/TRIM65 axis]	CCK8//qPCR//Luciferase Report Assay//Transwell Assay	In the present research, LINC01857 levels were found to be upregulated in glioma.  Collectively, this study first demonstrated that a novel LINC01857/miR-1281/TRIM65 signaling regulates glioma progression.	 In addition, LINC01857 expression is negatively correlated with survival rate in glioma patients. 	Yes	Functional investigation revealed that LINC01857 downregulation impaired glioma proliferation and invasiveness. Furthermore, LINC01857 knockdown led to repressed growth of glioma in vivo. 	31049960
LINC01857	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cells	Regulation(PI3K/mTOR pathway and EMT process&miR-141-3p/MAP4K4 axis)	qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis			Yes	Bioinformatics analysis and luciferase reporter assay confirmed that LINC01857 may serve as a sponge for miR-141-3p and miR-141-3p may target MAP4K4. Mechanically, the regulatory action of miR-141-3p/MAP4K4 on DLBCL cellular behaviors was regulated by LINC01857.	33311569
LINC01852-201	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	We found that expression of Wnt2b, β-catenin, cyclinD1, N-cadherin, vimentin, and snail was increased in GC tissues, while expression of ENST00000434223 and E-cadherin was decreased.		Yes	Furthermore, the rate of apoptosis was decreased and cell proliferation, invasion and migration were increased in response to downregulation of ENST00000434223. By contrast, upregulation of ENST00000434223 exhibited the opposite effects in MKN-45 cells.	30138664
LINC01852-201	LncRNA	Homo sapiens	Kidney Neoplasms	renal cancer tissues and para-cancerous tissues ,cell lines(786-O,ACHN)	Regulation[Wnt/hygro-catenin signaling pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	"The results indicated that 
ENST00000434223 was lowly expressed in renal 
carcinoma tissue (Figure 1A) when compared 
with paired para-cancerous tissues. In addition, 
the expression level of ENST00000434223 786-o 
and ACHN cells was notably lower than that of 
proximal tubule epithelial cell line hk-2 .At the same time, interference or overexpression of ENST00000434223 could affect the expression level of proteins related to the Wnt/β-catenin signal pathway."	 	Yes	In addition, down-regulating ENST00000434223 could enhance the viability, metastasis and invasiveness of renal cancer cells. However, overexpressing ENST00000434223 remarkably weakened the above cell functions. 	31486486
LINC01833	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	cells 	Interaction(miR-129-5p/PROM2 axis)	qRT-PCR//RIP	RP11-89 promoted cell proliferation, migration and tumorigenesis and inhibited cell cycle arrest via the miR-129-5p/PROM2 axis. 		Yes	RP11-89 promoted cell proliferation, migration and tumorigenesis and inhibited cell cycle arrest via the miR-129-5p/PROM2 axis. 	34728613
LINC01833	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissue	regulation[MiR-519e-3p/S100A4 Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	qRT-PCR assay further revealed significantly higher expression of linc01833 in LUAD tissue than the adjacent normal tissue (Figure 1C).Rescue assay demonstrated that linc01833 acted on the miR-519e-3p/S100A4 axis.		Yes	Linc01833 OE can significantly improve proliferation as well as invasion ability of LC cells and promote the EMT process.	33173348
LINC01819	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(KLF5)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//qRT-PCR//FISH//ChIP-seq//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining	Here, we demonstrate that lncRNA KPRT4 promotes BLBC cell proliferation in vitro and in vivo. Mechanistically, KLF5 directly binds to the promoter of KPRT4 to promote KPRT4 transcription. Reciprocally, KPRT4 recruits the YB-1 transcription factor to the KLF5 promoter by interacting with YB-1 at its 5' domain and forming an RNA-DNA-DNA triplex structure at its 3' domain, resulting in enhanced transcription of KLF5 and ultimately establishing a feedforward circuit to promote cell proliferation. Moreover, the antisense oligonucleotide (ASO)-based therapy targeting KPRT4 substantially attenuated tumor growth in vivo. Clinically, the expression levels of YB-1, KLF5 and KPRT4 are positively correlated in clinical breast specimens.		Yes	Here, we demonstrate that lncRNA KPRT4 promotes BLBC cell proliferation in vitro and in vivo. Mechanistically, KLF5 directly binds to the promoter of KPRT4 to promote KPRT4 transcription. Reciprocally, KPRT4 recruits the YB-1 transcription factor to the KLF5 promoter by interacting with YB-1 at its 5' domain and forming an RNA-DNA-DNA triplex structure at its 3' domain, resulting in enhanced transcription of KLF5 and ultimately establishing a feedforward circuit to promote cell proliferation. Moreover, the antisense oligonucleotide (ASO)-based therapy targeting KPRT4 substantially attenuated tumor growth in vivo. Clinically, the expression levels of YB-1, KLF5 and KPRT4 are positively correlated in clinical breast specimens.	35259457
LINC01793	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 cancer tissues and cell lines 	Expression(highly expressed)	qRT-PCR//MTT//Transwell Assay	 LINC01793 level was upregulated in cancer tissues and cell lines of OSCC, and its expression was increased in cancer tissues from patients with lymph node metastasis. 	Moreover, high LINC01793 level was positively correlated with T category, TNM stage, lymph node metastasis, and local recurrence. 	Yes	 Functionally, cell proliferation, invasion and migration of SCC9 and Cal27 cells were decreased after knockdown of LINC01793. Consistently, silence of LINC01793 induced G0/G1 cell cycle arrest in OSCC cells.	33713982
LINC01260	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		regulation[miR-562/CYLD/NF-κB Pathway]	Western Blot//CCK8//qRT-PCR//ELISA//Colony Formation Assay//Transwell Assay	 In NSCLC tissues and cell lines, LINC01260 expression was downregulated, which corresponded to a lower survival rate of patients with NSCLC.	 In NSCLC tissues and cell lines, LINC01260 expression was downregulated, which corresponded to a lower survival rate of patients with NSCLC.	Yes	Knockdown of LINC01260 accelerated the proliferation, colony formation, and migration of NSCLC cells.	33116647
LINC01260	LncRNA	Homo sapiens	Non-alcoholic Fatty Liver Disease	 OA group,  LO2 cells	Interaction(RXRB )	qRT-PCR//Oil Red O Staining//Transfection//RNA-seq	Fluorescence quantitative PCR showed that the expression of LINC01260 in the OA group was downregulated by 0.35 ± 0.07-fold (P < 0.05).  The formation of lipid droplets in LO2 cells of the LINC01260 GOF group decreased significantly (P < 0.05).		Yes	Overexpression of LINC01260 significantly induced RXRB transcription (P < 0.05) and translation, and RXRB silence attenuated the lipids decrease induced by LINC01260 overexpression.	35016686
LINC01255	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow cells of AML patients	Interaction(BMI1/MCP-1/ p53-p21 )	qRT-PCR//Western Blot	LncRNA LINC01255 is highly expressed in bone marrow cells of AML patients, CD34+ cells of MDS-AML patients and AML cell lines and the higher expression of LINC01255 is associated with poor survival rate of AML patients. LINC01255 can interact with BMI1 and repress the transcription of MCP-1 to active p53-p21 pathway, thus inhibiting the senescence of human mesenchymal stromal and proliferation of acute myeloid leukemia cell.	LncRNA LINC01255 is highly expressed in bone marrow cells of AML patients, CD34+ cells of MDS-AML patients and AML cell lines and the higher expression of LINC01255 is associated with poor survival rate of AML patients. 	Yes	LINC01255 can interact with BMI1 and repress the transcription of MCP-1 to active p53-p21 pathway, thus inhibiting the senescence of human mesenchymal stromal and proliferation of acute myeloid leukemia cell.	33405050
LINC01023	LncRNA	Homo sapiens	Hepatoblastoma	hepatoblastoma tissue and cell lines	Interaction(miR-378a-5p/WNT3 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay	LINC01023 was significantly upregulated in hepatoblastoma tissue and cell lines rather than in adjacent normal hepatic tissue and QSG7701 cell lines. To the best of our knowledge, this study is the first study demonstrating the role of LINC01023 in hepatoblastoma tumorigenesis through the LINC01023/miR-378a-5p/Wnt3 axis. 		Yes	LINC01023 silencing attenuated cell proliferation, colony formation and increased cell apoptosis. Conversely, LINC01023 upregulation results in significant increase in cell proliferation, and colony formation activities however, a significant reduction in apoptosis activity was reported. Interaction between the LINC01023 and WNT3 was confirmed by dual luciferase assay. Xenograft animal tumorgenicity test confirmed the in-vivo tumorigenesis potential of LINC01203. 	36576714
LINC01018	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-182-5p)	Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	LINC01018 was significantly down-regulated in glioma tissues and cell lines. LINC01018 directly target to miR-182-5p. Forced up-regulation of miR-182-5p reversed the inhibitory effects on proliferative and metastatic abilities of glioma cells with LINC01018 overexpression. Lastly, the bioinformatics analyses revealed that LINC01018/miR-182-5p axis mediated a cluster of downstream genes (ADRA2C, RAB6B, RAB27B, RAPGEF5, STEAP2, TAGLN3, and UNC13C), which were potential key factors in the development of glioma.		Yes	Overexpression of LINC01018 dramatically inhibited cell proliferation, migration, and invasion and reverse EMT process in glioma. 	36094613
LINC01018	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(LncRNA LINC01018/miR-942-5p/KNG1 axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	MiR-942-5p targeted KNG1, and LINC01018 sponged miR-942-5p. The high survival rate of patients was related to low miR-942-5p level. MiR-942-5p was highly expressed, whereas KNG1 was lowly expressed in glioma. MiR-942-5p was negatively correlated with KNG1. The levels of miR-942-5p and KNG1 were decreased by LINC01018 knockdown, and LINC01018 expression was suppressed by miR-942-5p mimic. MiR-942-5p inhibitor, KNG1, and LINC01018 had the opposite effect to miR-942-5p mimic.		Yes	 Silent LINC01018 or KNG1 and miR-942-5p mimic enhanced the migration, invasion, and proliferation of glioma cells, and regulated the expressions of metastasis-related and proliferation-related genes. LINC01018 knockdown and miR-942-5p mimic promoted glioma tumor growth in mice.	36550594
LINC01013	LncRNA	Homo sapiens	Cardiovascular Diseases	endothelial cells	Regulation(RAD22/VEGFA)	qRT-PCR//Wound Healing Assay//RNA Pull-Down//Western Blot	 In our study we show that long non-coding RNA Aerrie (linc01013) contributes to the DNA signaling and repair mechanism.  Aerrie associates with YBX1 and together they act as important factors in DNA damage signaling and repair. 		Yes	Silencing of Aerrie in endothelial cells impairs angiogenesis, migration, and barrier function.	33505972
LINC01004	LncRNA	Homo sapiens	Pituitary Neoplasms	PA cells	Interaction(miR-323a-3p/136-5p/RCN2 axis)	In Vivo Experiment//RNA Pull-Down//IHC//Transfection//CCK8//qRT-PCR//Flow Cytometry//FISH//Luciferase Report Assay//Colony Formation Assay	 In this study, we discovered that long intergenic non-protein coding RNA 1004 (LINC01004) was aberrantly up-regulated in PA cells. By using bioinformatics tools and a series of mechanism assays, LINC01004 was identified to sponge miR-323a-3p/miR-136-5p to enhance the expression of RCN2 in PA. 		Yes	Functional assays manifested that LINC01004 promoted malignant behaviors of PA cells in vitro and growth of PA in vivo. 	35490653
LINC01003	LncRNA	Homo sapiens	Multiple Myeloma	 peripheral blood samples of MM patients	Interaction(miR-33a-5p/PIM1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//MTT//Luciferase Report Assay//ELISA	Low expression of LINC01003 was observed in MM cell lines and peripheral blood samples of MM patients.  We then identified miR-33a-5p as a downstream target of LINC01003, and confirmed that PIM1 was a direct target gene of miR-33a-5p. Both high expression of miR-33a-5p and low expression of PIM1 reversed the suppressive effects of LINC01003 overexpression on cell adhesion and viability, and the promoting effect on apoptosis in MM cells.		Yes	Both LINC01003 up-regulation and miR-33a-5p down-regulation repressed cell viability and adhesion, and promoted apoptosis of MM cells. Moreover, LINC01003 suppressed the growth of xenograft tumor in mice. 	33865032
LINC00997	LncRNA	Homo sapiens	Colorectal Neoplasms	MCRC tissues	Interaction(miR-512-3p)	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	 Results revealed that LINC00997 was frequently overexpressed in MCRC tissues, which was positively related to the tumor metastasis and stage. Luciferase reporter assay confirmed that LINC00997 could target miR-512-3p. In conclusion, LINC00997 regulated the metastasis of CRC by targeting miR-512-3p, providing some insights into the regulatory mechanism of CRC.	 Results revealed that LINC00997 was frequently overexpressed in MCRC tissues, which was positively related to the tumor metastasis and stage.	Yes	Additionally, LINC00997 was significantly elevated in CRC cells and LINC00997 silencing inhibited the invasion, migration and EMT of CRC cells, which was restored by miR-512-3p inhibitor. 	33570445
LINC00997	LncRNA	Homo sapiens	Carcinoma, Renal Cell	KIRC tissues	Regulation[LINC00997-STAT3-S100A11 axis]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Western Blot	 In 18 cases of KIRC, we found that LINC00997 expression was greater in cancer tissues and metastases than in normal tissues.Consequently, the LINC00997-STAT3-S100A11 axis may promote the development of KIRC, and LINC00997 may represent a potential prognostic biomarker and therapeutic target for KIRC patients.	These results revealed that S100A11 is positively associated with LINC00997 in KIRC, which is positively correlated with metastasis-associated molecules VIM, MMP2 and MMP7. 	Yes	Our in vitro wound healing assay and Transwell tests demonstrated that interfering with either LINC00997 or S100A11 expression reduced migration of 786-O cells by inhibiting VIM, MMP2 and MMP7 expression.	31442606
LINC00996	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Regulation(JAK-STAT3)	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	Compared with adjacent normal lung tissues, Linc00996 was significantly downregulated in LUAD, and its expression was negatively correlated with T stage, N stage, and pathological stage.  Via GSEA and ssGSEA, we observed that Linc00996 might be connected with immune infiltration in LUAD, and Linc00996 might inhibit tumorigenesis and metastasis by regulating antigen processing and presentation, JAK-STAT3, and cell adhesion molecular signaling pathways.	Compared with adjacent normal lung tissues, Linc00996 was significantly downregulated in LUAD, and its expression was negatively correlated with T stage, N stage, and pathological stage. 	Yes	 An in vitro study suggested that enhanced Linc00996 expression could inhibit cell proliferation, clonal formation, migration, and invasion in LUAD cell lines. 	36118847
LINC00994	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[regulating miR-765-3p]	qRT-PCR//Luciferase Report Assay	Compared to adjacent samples, the LINC00994 expression was increased in GC tissues by qRT-PCR assay. LINC00994 induced GC cell invasion and growth via modulating miR-765-3p.		Yes	Furthermore, Elevated expression of LINC00994 induced GC cell invasion, proliferation and cycle. 	31737214
LINC00994	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	Regulation[miR-765-3p/RUNX2 axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Microarray//Transwell Assay	Our microarray results first indicated long intergenic non-protein coding RNA 994 (LINC00994) as an upregulated long non-coding RNA (lncRNA) and miR-765-3p as a downregulated microRNA (miRNA) in pancreatic cancer tissues (Fold change ≥ 2 and P < 0.05; three paired samples).Furthermore, the expression of LINC00994 was negatively correlated with that of miR-765-3p in 10 pancreatic cancer specimens. Runt-related transcription factor 2 (RUNX2), a molecule that contributes to the aggressive behaviors of pancreatic cancer, was herein verified as a novel target for miR-765-3p. Like LINC00994, its expression was elevated in pancreatic cancers. Silencing of LINC00994 and RUNX2 reduced each other's expression in both Panc-1 and AsPC-1 cells. RUNX2 3'UTR and LINC00994 competed to bind miR-765-3p. Additionally, LINC00994-silenced cells regained their aggressive behaviors when miR-765-3p was antagonized, which was accompanied with RUNX2 re-expression.		Yes	We found that LINC00994 silencing inhibited the growth, migration and invasion, and promoted the G1 cell cycle arrest and apoptosis in Panc-1 and AsPC-1 cells.	30739523
LINC00993	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and paired peritumor tissue	Expression[lower expressed]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Transwell Assay	Subgroup analysis showed that LINC00993 was downregulated in breast cancer tissues when compared to its paired peritumor tissues in TNBC group	 	Yes	LINC00993 located mainly in the nucleus. LINC00993 suppressed TNBC growth both in vitro and in vivo. 	31921620
LINC00993	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues,cell lines	Expression[lower expressed]	CCK8//qPCR//Western Blot	LncRNA TCONS_l2_00002973 expression was lower in tumor tissue compared to paired adjacent tissue (p<0.001). Further in vitro experiments disclosed that lncRNA TCONS_l2_00002973 expression was reduced in various breast cancer cell lines compared to normal breast cell line	LncRNA TCONS_l2_00002973 expression was lower in tumor tissue compared to paired adjacent tissue (p<0.001), and its low expression was associated with increased T stage (p=0.002), raised N stage (p=0.003) and advanced TNM stage (p=0.005) in TNBC patients. Poor OS was found in lncRNA TCONS_l2_00002973 low expression groExpression[Expression[up-expression]-expression] compared to lncRNA TCONS_l2_00002973 high expression groExpression[Expression[up-expression]-expression] (p=0.006).	Yes	lncRNA TCONS_l2_00002973 repressed cell proliferation and enhanced cells apoptosis in MDA-MB-231 cells.	31128002
LINC00992	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-361-5p/Twist1 )	qRT-PCR	RT-qPCR revealed that LINC00992 was highly expressed in HCC tissues and cells. Our result showed that the expression of miR-361-5p was lower in the LINC00992 (+) group than in the LINC00992 (-) group. CCK-8 and Transwell showed that LINC00992 promoted HCC cell proliferation, migration, and invasion, whereas dual-luciferase reporter assay and RNA pull-down assay showed that LINC00992 combined with miR-361-5p to act as a miRNA decoy in HCC. RT-qPCR and Western blotting confirmed that LINC00992 upregulated the expression of the Twist1 gene in HCC cells by downregulating expression of miR-361-5p. CCK-8 and Transwell assays confirmed that LINC00992 promoted the proliferation, metastasis, and invasiveness of HCC cells by downregulating miR-361-5p levels and consequently upregulating Twist1 expression, implying that these three elements may be promising targets for HCC therapy.		Yes	CCK-8 and Transwell showed that LINC00992 promoted HCC cell proliferation, migration, and invasion, whereas dual-luciferase reporter assay and RNA pull-down assay showed that LINC00992 combined with miR-361-5p to act as a miRNA decoy in HCC. RT-qPCR and Western blotting confirmed that LINC00992 upregulated the expression of the Twist1 gene in HCC cells by downregulating expression of miR-361-5p. CCK-8 and Transwell assays confirmed that LINC00992 promoted the proliferation, metastasis, and invasiveness of HCC cells by downregulating miR-361-5p levels and consequently upregulating Twist1 expression, implying that these three elements may be promising targets for HCC therapy.	36084427
LINC00987	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	Interaction(miR-376a-5p/FNBP1 )	qRT-PCR//Western Blot	 LINC00987 was found to be upregulated in osteosarcoma cells. In conclusions, this study suggests LINC00987 silencing inhibits osteosarcoma cell proliferation, migration, and invasion by sponging miR-376a-5p to regulate FNBP1 expression.		Yes	LINC00987 silencing suppressed proliferation, migration, and invasion of osteosarcoma cells. 	35201476
LINC00987	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive	COPD tissues	regulation[Let-7b-5p/SIRT1 Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ELISA	LINC00987 expression was strikingly downregulated and let-7b-5p expression was obviously upregulated in COPD tissues and LPS-induced BEAS-2B cells compared with control groups.LINC00987 ameliorated COPD through modulating LPS-induced cell apoptosis, oxidative stress, inflammation and autophagy via sponging let-7b-5p to associate with SIRT1.		Yes	LINC00987 overexpression promoted BEAS-2B cells against LPS-mediated viability, apoptosis, oxidative stress, inflammation and autophagy, whereas these effects were attenuated by let-7b-5p mimic or SIRT1 knockdown.	33311978
LINC00976	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Interaction[linc00976/miR-137/OTUD7B/EGFR axis]	IP//Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 linc00976 expression was overexpressed in PC tissues and cell lines and was positively associated with poorer survival in patients with PC. Ultimately, OTUD7B mediates EGFR and MAPK signaling pathway, suggesting that linc00976/miR-137/OTUD7B/EGFR axis may act as a potential biomarker and therapeutic target for PC.	 linc00976 expression was overexpressed in PC tissues and cell lines and was positively associated with poorer survival in patients with PC. 	Yes	Function studies revealed that linc00976 knockdown significantly suppressed cell proliferation, migration and invasion in vivo and in vitro, whereas its overexpression reversed these effects. 	31747939
LINC00976	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissue samples and cell lines	Interaction(miR-3202/GPX4 axis)	RNA Pull-Down//Western Blot//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//EdU Staining	Compared with normal controls, linc00976 was dramatically upregulated in CCA tissue samples and cell lines. Mechanistically, linc00976 competitively interacted with miR-3202 to upregulate GPX4 expression, thus contributing to the malignant biological behavior of CCA cells. Moreover, we demonstrated that JUND specifically interacts with the linc00976 promoter and activates linc00976 transcription. Accordingly, JUND promotes linc00976 transcription, and linc00976 plays a crucial role in accelerating CCA tumorigenesis and metastasis and inhibiting ferroptosis by modulating the miR-3202/GPX4 axis. 	 Patients with CCA exhibiting high linc00976 expression had a highly advanced clinical stage, substantial lymph node metastasis, and poor overall survival. 	Yes	Knockdown of linc00976 significantly repressed proliferation and metastasis and promoted ferroptosis of CCA cells both in vitro and in vivo, whereas linc00976 overexpression exerted the opposite effect. 	36400758
LINC00974	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues	Interaction[upregulates CDK6]	CCK8//qRT-PCR//Cell Cycle Assay//Western Blot	 The authors observed in this study that LINC00974 was upregulated in gastric cancer (GC) and positively correlated with CDK6.In GC tissues, LINC00974 and CDK6 were positively correlated. In GC cells, LINC00974 overexpression led to upregulated, whereas LINC00974 siRNA silencing led to downregulated CDK6.	Survival analysis showed that high levels of LINC00974 and CDK6 predicted poor survival. 	Yes	 Analysis of cell cycle progression and proliferation showed that LINC00974 and CDK6 overexpression promoted and siRNA silencing inhibited G1-S transition and cell proliferation.	31596614
LINC00974	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Interaction[downregulate miR-122]	qRT-PCR//Transwell Assay//Western Blot	The authors found that LINC00974 was upregulated in oral squamous cell carcinoma (OSCC) and predicted poor survival.Therefore, LINC00974 can downregulate miR-122 to upregulate RhoA in OSCC, thereby promoting cell invasion and migration.	The authors found that LINC00974 was upregulated in oral squamous cell carcinoma (OSCC) and predicted poor survival.	Yes	 In invasion and migration assay, miR-122 overexpression resulted in reduced, whereas LINC00974 and RhoA overexpression resulted in increased rate of cancer cell migration and invasion. 	31702382
LINC01018	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML tissues	Interaction(miR-499a-5p/PDCD4 )	qRT-PCR//Luciferase Report Assay	LINC01018 and PDCD4 were downregulated in AML, while miR-499a-5p was upregulated. LINC01018 acted as a sponge of miR-499a-5p, and PDCD4 was demonstrated to be targeted by miR-499a-5p. Knockdown of miR-499a-5p suppressed AML cell proliferation and promoted AML cell apoptosis, but silencing PDCD4 abolished this effect. LINC01018 inhibited AML cell growth by modulating PDCD4 through suppression of miR-499a-5p, providing a feasible theoretical basis for the treatment of AML.		Yes	 LINC01018-overexpression suppressed AML cell proliferation and induced AML cell apoptosis, while miR-499a-5p transfection reversed these effects.	34079594
LINC01048	LncRNA	Homo sapiens	Skin Neoplasms	CSCC tissues	Interaction[binding to TAF15  ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//EdU Staining//ChIP	 Obviously, LINC01048 was expressed higher in the CSCC tissues and recurrence tissues compared with that in adjacent normal tissues and non-recurrence tissues.In conclusion, USF1-induced upregulation of LINC01048 promoted CSCC by interacting with TAF15 to upregulate YAP1.	Furthermore, Kaplan-Meier analysis revealed the negative correlation between LINC01048 expression and the overall survival and disease-free survival of CSCC patients. 	Yes	Subsequently, functional assays were conducted to prove the inhibitory effect of silenced LINC01048 on the proliferation and apoptosis of CSCC cells.	30931936
LINC01106	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	Interaction(miR-34a-5p/MYCN Axis)	In Vivo Experiment//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	LncRNA LINC01106 and MYCN expression were boosted and miR-34a-5p expression was reduced in GC cells and tissues compared to their controls.		Yes	 Functionally, decreased lncRNA LINC01106 or increased miR-34a-5p restrained GC cells in viability, invasion, and migration in vitro. LINC01106 down-regulation suppressed tumor growth of mice in vivo. In terms of mechanism, lncRNA LINC01106 directly targeted miR-34a-5p and was inversely correlated with miR-34a-5p. 	34550549
LINC01050	LncRNA	Homo sapiens	Stomach Neoplasms	 gastric cancer tissues	Interaction(miR-7161-3p to regulate SPZ1 expression)	RNA Pull-Down//Northern Blot//Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//Invasion Assay//ChIP	LINC01050 was significantly up-regulated in gastric cancer, and its high expression was positively correlated with a poor prognosis.  Moreover, mechanistic investigations revealed that LINC01050 functions as a molecular sponge to absorb cytosolic miR-7161-3p, which reduces the miR-7161-3p-mediated translational repression of SPZ1, thus contributing to gastric cancer progression.	LINC01050 was significantly up-regulated in gastric cancer, and its high expression was positively correlated with a poor prognosis. 	Yes	Furthermore, overexpression of LINC01050 was confirmed to promote gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition in vitro and tumor growth in vivo. At the same time, its knockdown inhibited gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition in vitro along with tumor growth and metastasis in vivo.	34749766
LINC01094	LncRNA	Homo sapiens	Glioma	glioma patient tissues 	Interaction(miR-224-5p/CHSY1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//FISH//RIP//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Significantly, we revealed that the expression levels of LINC01094 were elevated in the glioma patient tissues compared to adjacent normal tissues. The LINC01094 expression was enhanced in the glioma cell lines.  Thus, we conclude that lncRNA LINC01094 promotes glioma progression by modulating miR-224-5p/CHSY1 axis.		Yes	 The depletion of LINC01094 inhibited cell viability and colony formation in the glioma cells. Meanwhile, the migration and invasion of glioma cells were impaired by the depletion of LINC01094. 	34716872
LINC01094	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC cells and clinical tissues	regulation[Upregulating SLC2A3 via MicroRNA-184]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//RIP//Flow Cytometry//Transwell Assay	In ccRCC cells and clinical tissues, LINC01094 and SLC2A3 were highly expressed while miR-184 was lowly expressed. Taken together, silencing LINC01094 inhibited SLC2A3 expression by up-regulating miR-184, thereby inhibiting the development of ccRCC.		Yes	Silencing LINC01094, up-regulating miR-184, or reducing SLC2A3 inhibited the growth, migration, and invasion of ccRCC cells. Tumor growth was suppressed by silenced LINC01215 via reducing the expression of SLC2A3 via miR-184.	33173535
LINC01093	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[LINC01093-IGF2BP1-GLI1 axis]	FISH//RNA Pull-Down//RIP	We report a novel, liver-specific lncRNA LINC01093 that shows significant downregulation in HCC tissues.The liver-enriched lncRNA LINC01093 is a promising prognostic indicator for HCC patients, and the newly identified LINC01093-IGF2BP1-GLI1 axis shows potential for therapeutic targets in HCC.	 LINC01093 expression is inversely correlated with cancer embolus and HCC TNM stage and as a prognostic predictor for HCC patients.	Yes	 LINC01093 overexpression significantly suppresses HCC cell proliferation and metastasis in vitro and in vivo. Conversely, its knockdown promotes HCC progression.	30790682
LINC01089	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-27a-3p/TET1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	 LINC01089 down-regulation was observed in GC tissues and cell lines. LINC01089 impedes the proliferation, migration, and invasion of GC cells by adsorbing miR-27a-3p and up-regulating the expression of TET1.	 Low expression level of LINC01089 in GC tissues was markedly linked to larger tumor size, higher T stage, as well as lymphatic metastasis of the patients. 	Yes	Functional experiments implied that LINC01089 overexpression impeded the proliferation, migration, as well as invasion of GC cells, whereas LINC01089 knockdown promoted the above malignant phenotypes. 	33088215
LINC01089	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	interaction[binds to miR-145-5p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	High LINC01089 expression was observed in GC cells.  LINC01089 competitively binds to miR-145-5p to mediate SOX9 expression.		Yes	LINC01089 overexpression notably expedited cell migration, proliferation, and invasion. 	32982308
LINC01089	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	interaction[sponging miR-3187-3p]	qRT-PCR//Transwell Assay	LINC01089 expression was significantly reduced in NSCLC tissues and cells. LINC01089 attenuates tumor proliferation, migration, and invasion by sponging miR-3187-3p in NSCLC.		Yes	Gain-of-function studies further demonstrated that LINC01089 overexpression inhibited proliferation, migration, and invasion of lung cancer cell lines, A549 and SK-MES-1.	33269007
LINC01089	LncRNA	Homo sapiens	Lung Neoplasms	  lung cancer tissues	Interaction(miR-301b-3p/HPDG axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	Our data revealed that LINC01089, directly suppressed by YY1, inhibited lung cancer progression by targeting the miR-301b-3p/HPGD axis. LINC01089, directly suppressed by YY1, functioned as a competing endogenous RNA against miR-301b-3p to increase HPGD expression.	 Graphical abstract 1. LINC01089 expression was downregulated in lung cancer tisuues and cell lines, and low LINC01089 levels predicted a poor clinical outcome.	Yes	 LINC01089 knockdown enhanced proliferation, invasion, and migration of H1299 and A549 cells in vitro and promoted lung cancer cell tumorigenesis and metastasis in vivo. 	34561789
LINC01089	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue and cell lines.	Expression(lower expressed)	qRT-PCR	LIMT expression was significantly lower in HCC than in normal liver tissue. 		Yes	 Functionally, overexpression of LIMT repressed the proliferation, invasion, and EMT of HCC cells, while LIMT knockdown increased proliferation, invasion, and EMT of HCC cells in vitro.Furthermore, LIMT overexpression suppressed HCC growth and metastasis while silencing of LIMT had an opposite effect in vivo.	35526240
LINC01089	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	Regulation(Hippo pathway )	qRT-PCR	LINC01089 was down-regulated in osteosarcoma cells and overexpressing LINC01089 was validated to restrain cell growth in vitro and tumor growth in vivo. Additionally, silencing LINC01089 could exacerbate cell malignant behaviors. Correlation of LINC01089 and Hippo pathway was proved. Overexpressing LINC01089 could activate Hippo pathway to exert antitumor effects.		Yes	LINC01089 was down-regulated in osteosarcoma cells and overexpressing LINC01089 was validated to restrain cell growth in vitro and tumor growth in vivo. 	36399257
LINC01089	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells and tissues	regulation[inhibiting miR-27a-3p and increasing BTG2]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	The expression of LINC01089 in CC was markedly down-regulated.  LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to up-regulate BTG2 expression.	The low expression of LINC01089 in CC was closely associated with a larger tumor size and positive lymph node metastasis. 	Yes	Moreover, overexpression of LINC01089 impeded the proliferation and metastasis of CC cells, whereas knockdown of LINC01089 had the opposite biological functions.	33025678
LINC01089	LncRNA	Homo sapiens	Thyroid Neoplasms	 thyroid cancer tissues and cells	Interaction(miR-27b-3p/FBLN5)	Western Blot//Bioinformatics Analysis//Transfection//qRT-PCR//Luciferase Report Assay//Invasion Assay	Here, The Cancer Genome Atlas (TCGA) database showed that LINC01089 expression is remarkably reduced in thyroid cancer tissues.  In conclusion, LINC01089 plays a tumor-suppressive role by binding miR-27b-3p to increase FBLN5 expression, confirming that LINC01089 has tremendous potential to become a therapeutic target for thyroid cancer treatment.	 Lower LINC01089 expression was correlated with higher tumor stage and regional lymph node metastasis.	Yes	Furthermore, LINC01089 overexpression effectively blocked thyroid cancer cell proliferation, migration, and invasion. 	36306007
LINC01089	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD	Interaction(miR-543/ Bcl-2, Bax and Cleaved caspase-3)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	LINC01089 improved overall survival of LUAD patients and was low-expressed in LUAD. MiR-543 was determined as a target gene of LINC01089, and was high-expressed in LUAD tissues. Upregulating miR-543 expression induced the opposite effects to LINC01089 upregulation on these cellular biological behaviors and the expressions of Bcl-2, Bax and Cleaved caspase-3. 		Yes	Upregulating LINC01089 expression reduced LUAD cell viability, inhibited colony formation, enhanced apoptosis, accompanied by downregulated Bcl-2 and miR-543 and upregulated Bax and Cleaved caspase-3. 	33892399
LINC01088	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction(miR-95/LATS2)	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 LINC01088 and LATS2 mRNA expression decreased, and miR-95 increased in gastric cancer tissues.  LINC01088 has an excellent positive correlation with LATS2 mRNA, which may be a ceRNA pair; LINC01088 has binding sites with miR-95. 		Yes	 Gene interference tests on gastric cancer cell lines revealed that LINC01088 could prevent gastric cancer cells from proliferating, invading, and migrating. The function of LINC01088 is achieved by regulating the miR-95/LATS2 pathway through the ceRNA mechanism.	35728587
LINC01088	LncRNA	Homo sapiens	Glioma	glioma cell 	Interaction(SNRPA )	RNA Pull-Down//Transfection//qRT-PCR//RIP//Transwell Assay	Mechanistically, we verified LINC01088 physically interacted with small nuclear ribonucleoprotein polypeptide A (SNRPA) and regulated the expression of SNRPA at the transcription level. Phenotypic analysis ascertained that LINC01088 substantively aggravated glioma cell progression in an SNRPA-dependent manner, and SNRPA played a pivotal part in the tumor-promoting properties of LINC01088. 		Yes	Functionally, LINC01088 silencing degraded cell proliferation, invasion in glioma, while LINC01088 overexpression elicited opposite results. 	35392763
LINC01088	LncRNA	Mus musculus	Colorectal Neoplasms	colorectal cancer tissues and CRC cell lines	Regulation(microRNAs/G3BP1/PD-L1 axis)	CCK8//qRT-PCR//RIP	We found that LINC01088 was significantly upregulated in colorectal cancer tissues and CRC cell lines compared to adjacent normal tissues and colonic epithelial cells. High LINC01088 levels were correlated with adverse outcomes in patients with CRC. LINC01088 was mainly located in the cytoplasm. LINC01088 knockdown suppressed the proliferation, migration, invasion, and immune escape of colorectal cancer cells. Mechanistically, LINC01088 bound directly to miR-548b-5p and miR-548c-5p that were significantly upregulated Ras GTPase-activating protein-binding proteins 1 (G3BP1) and programmed death ligand 1 (PD-L1) expression, altering CRC cell phenotypes. In mouse xenograft models, LINC01088 knockdown restrained CRC tumor growth and lung metastasis. Furthermore, G3BP1 overexpression reversed LINC01088-knockdown-mediated inhibitory effects on tumor growth. Notably, LINC01088 knockdown downregulated PD-L1 expression, while G3BP1 overexpression restored PD-L1 expression in xenograft tumors. Besides, LINC01088 knockdown repressed CRC organoid growth ex vivo.	High LINC01088 levels were correlated with adverse outcomes in patients with CRC.	Yes	LINC01088 knockdown suppressed the proliferation, migration, invasion, and immune escape of colorectal cancer cells. Mechanistically, LINC01088 bound directly to miR-548b-5p and miR-548c-5p that were significantly upregulated Ras GTPase-activating protein-binding proteins 1 (G3BP1) and programmed death ligand 1 (PD-L1) expression, altering CRC cell phenotypes. In mouse xenograft models, LINC01088 knockdown restrained CRC tumor growth and lung metastasis. Furthermore, G3BP1 overexpression reversed LINC01088-knockdown-mediated inhibitory effects on tumor growth. Notably, LINC01088 knockdown downregulated PD-L1 expression, while G3BP1 overexpression restored PD-L1 expression in xenograft tumors. Besides, LINC01088 knockdown repressed CRC organoid growth ex vivo.	35357586
LINC01087	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues	regulation[miR-335-5p/Rock1]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	 The qRT-PCR assay revealed that the LINC01087 expression in BC tissues was higher than that in corresponding tumor-adjacent tissues, and survival analysis revealed an unfavorable prognosis of patients with high expression of LINC01087. Furthermore, LINC01087 can act as a miR-335-5p sponge to affect the expression of ROCK1 and affect the invasion and migration of BCCs.	 The qRT-PCR assay revealed that the LINC01087 expression in BC tissues was higher than that in corresponding tumor-adjacent tissues, and survival analysis revealed an unfavorable prognosis of patients with high expression of LINC01087.	Yes	Down-regulation of LINC01087 could slow down the proliferation, invasion, and migration of BCCs and accelerate apoptosis of them in vitro. 	33061456
LINC01082	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Transwell Assay	 The results revealed that LINC01082 was significantly decreased in tissues and cell lines of colon cancer.		Yes	Overexpressed LINC01082 significantly suppressed the proliferation ability of colon cancer cells. The migration and invasion of colon cancer cells were also suppressed after LINC01082 overexpression.	31432387
LINC01061	LncRNA	Homo sapiens	Cholangiocarcinoma	cell lines	Interaction[sponges miR-612]	qPCR//CCK8//RIP//FISH//Luciferase Report Assay//Transwell Assay	Firstly, it was observed that LINC01061 expression was heightened in CCA cell lines, whose knockdown suppressed cell proliferation, induced cell apoptosis and restrained cell migration.To sum up, our present exploration demonstrated that LINC01061 sponges miR-612 so as to upregulate SEMA4D expression for the progression of CCA, suggesting an optional promising and effective target for the therapy of patients with CCA.		Yes	Firstly, it was observed that LINC01061 expression was heightened in CCA cell lines, whose knockdown suppressed cell proliferation, induced cell apoptosis and restrained cell migration.	30967271
LINC00974	LncRNA	Homo sapiens	Oral Submucous Fibrosis	OSF tissues	Regulation[TGF-β/Smad signaling]	qRT-PCR//Wound Healing Assay	We found that the expression of LINC00974 in OSF tissues or myofibroblasts was aberrantly upregulated, and there was a positive correlation between LINC00974 and myofibroblast markers.  Altogether, these findings suggested that arecoline-increased myofibroblast transdifferentiation was via LINC00974-mediated activation of TGF-β signaling.		Yes	Our results showed that inhibition of LINC00974 suppressed the myofibroblast activities, while overexpression of LINC00974 increased the activation.	30447113
LINC00968	LncRNA	Homo sapiens	Coronary Artery Disease	CAD tissues	Regulation[regulating miR-9-3p ]	qRT-PCR	 We showed that the LINC00968 expression level was upregulated in the CAD tissues compared with normal arterial tissues.Finally, we showed that ectopic expression of LINC00968 promoted endothelial cell proliferation and migration partly through regulating miR-9-3p expression. These results suggested that LINC00968 plays a crucial role in the progression of the CAD.		Yes	Ectopic expression of LINC00968 regulated the proliferation and migration of endothelial cell.	30485507
LINC00963	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	interaction[ binding to miR-612]	qRT-PCR//Transwell Assay	LINC00963 expression was higher in GC tissues than in adjacent normal tissues.  LINC00963 promoted the progression of GC by competitively binding to miR-612 to regulate the expression of CDC5L and mediated DC-related anti-tumor immune response. Thus, targeting LINC00963 may be a promising therapeutic strategy for GC.		Yes	Upregulation of LINC00963 was related to the poor prognosis of patients with GC. Knockdown of LINC00963 inhibited the proliferation, invasion, and metastasis but promoted the apoptosis of GC cells. Furthermore, silencing of LINC00963 in GC cells significantly suppressed the tumor growth of GC. 	33376349
LINC00958	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue and cell lines	Regulation[LINC00958/miR-185-5p/YWHAZ regulatory axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 LINC00958 expression was remarkably up-regulated in the OSCC tissue and cell lines.Taken together, the findings in this research reveal the modulation of LINC00958 for the OSCC tumorigenesis through the miR-185-5p/YWHAZ axis, which might be useful for the mechanical investigation associated with OSCC therapeutic target.	Clinical investigation showed that LINC00958 overexpression was associated with poor prognosis, acting as an independent prognostic factor for OSCC.	Yes	Loss- and gain-of-function assays indicated that LINC00958 promoted the proliferation, invasion and reduced the apoptosis of OSCC cells in vitro. In vivo, knockdown of LINC00958 repressed the tumor growth. 	31442551
LINC00958	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells 	Interaction( miR-4306/AIM2/SIRT/p53 )	CCK8//qRT-PCR//RIP	 We found that LINC00958 showed upregulation in OSCC cells compared to normal oral epithelial cells.		Yes	 LINC00958 silencing significantly suppressed OSCC cell proliferation, induced cell death and reduced autophagy. 	34384029
LINC00958	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Interaction(miR-4306/CEMIP axis)	qRT-PCR//Luciferase Report Assay	 LINC00958 expression levels significantly increased in osteosarcoma tissues while miR-4306 expression levels significantly decreased, and the expression of these two genes was negatively correlated. Subcellular fractionation analysis and RNA FISH assay demonstrated that LINC00958 was mainly localized in the cytoplasm. Dual-luciferase reporter gene assay verified that LINC00958 competitively bound miR-4306 and repressed its expression. Silencing of LINC00958 inhibited proliferation, cell cycle, metastasis, and invasion of osteosarcoma cells while inducing cellular apoptosis. The introduction of miR-4306 inhibitors reversed the tumor-suppressing effect of silencing LINC00958. miR-4306 binds to CEMIP and suppressed its expression. Xenograft tumor experiments and tumor metastasis assays in nude mice demonstrated that silencing LINC00958 inhibited osteosarcoma cells' growth and metastasis while inhibiting miR-4306 reversed this effect. Kaplan-Meier analysis showed that high expression of LINC00958 was significantly associated with poor prognosis of osteosarcoma patients.	Kaplan-Meier analysis showed that high expression of LINC00958 was significantly associated with poor prognosis of osteosarcoma patients.	Yes	Dual-luciferase reporter gene assay verified that LINC00958 competitively bound miR-4306 and repressed its expression. Silencing of LINC00958 inhibited proliferation, cell cycle, metastasis, and invasion of osteosarcoma cells while inducing cellular apoptosis. The introduction of miR-4306 inhibitors reversed the tumor-suppressing effect of silencing LINC00958.	33928604
LINC00958	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissue	Regulation[LINC00958-miR-625-NUAK1 pathway ]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	LINC00958 was found to be upregulated in NPC tissue specimens and cell lines.  The LINC00958-miR-625-NUAK1 pathway might be a target for anticancer therapy in patients with NPC.	The LINC00958 overexpression significantly correlated with tumor size, lymph node status, TNM stage, and worse overall survival among NPC patients.	Yes	Downregulation of LINC00958 suppressed NPC cell proliferation, migration, and invasion and induced apoptosis in vitro. Additionally, the LINC00958 knockdown impaired tumor growth in vivo. 	31819474
LINC00958	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 tissue samples of LAD	regulation[miR-625-5p/CPSF7 axis]	RNA Pull-Down//Western Blot//Tunel//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 LINC00958 was found notably overexpressed in LAD, which was associated with the stimulation of its promoter activity induced by SP1. LINC00958 might drive LAD progression via mediating miR-625-5p/CPSF7 axis, indicating the potential of targeting LINC00958 for the treatment of LAD.		Yes	 LINC00958 depletion dramatically inhibited LAD cell proliferation, migration and invasion capacities by acting as a miR-625-5p sponge. 	31997940
LINC00958	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues, lung cancer cells	Expression(highly expressed)	RNA Pull-Down//CCK8//qRT-PCR//FISH//RNA-seq//Luciferase Report Assay//IHC//Bioinformatics Analysis	The expression of LINC00958 in LUAD tissues was significantly upregulated when compared with that in adjacent tissues and could independently predict poor survival of patients with LUAD. LINC00958 localized to the nucleus, regulated oncogenes and metabolism-related and immune response-related genes, and interacted with histones. The targets of LINC00958 were TRPV3, STAP2, and EDN2 promoters with motifs of HOXA1, NANOG, FOSL2, JUN, and ATF4. Moreover, HOXA1 overexpression mitigated the LINC00958 knockdown-induced oncogenic phenotype. MYC/MAX motif, which was detected at the cis-element of LINC00958, trans-activated the LINC00958 promoter.	The expression of LINC00958 in LUAD tissues was significantly upregulated when compared with that in adjacent tissues and could independently predict poor survival of patients with LUAD.	Yes	LINC00958 knockdown significantly inhibited the growth and metastasis of lung cancer cells in vitro and in vivo. 	35223488
LINC00958	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Interaction(miR-145-3p/TCF4 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	LINC00958 was remarkably upmodulated in EC. LINC00958 was validated to decoy miR-145-3p and repressed its expression, and TCF4 was uncovered to be a target gene of miR-145-3p and negatively modulated by miR-145-3p. 	Moreover, its overexpression was strongly linked to unfavorable overall survival of the patients. 	Yes	Functional experiments confirmed that in vitro knockdown of LINC00958 suppressed EC cell proliferation and metastasis. 	33885186
LINC00958	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Interaction(LINC00958/miR-627 signal axis)	cell invasion assay//Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	 Long noncoding RNA ENST00000504230 (LncRNA ENST00000504230, known as LINC00958) was overexpressed in many cancers and associated with cancer development. LINC00958 was up-regulated in PTC tissues and cells, while the expression of miR-627 was lowly expressed.  TRIM44 was confirmed as a target of miR-627. Overexpression of miR-627 in PTC inhibited the proliferation, migration, and invasion by down-regulating the expression of TRIM44. 		Yes	Knockdown of LINC00958 inhibited the proliferation, migration, and invasion by elevating miR-627 expression in PTC cells. T	35199939
LINC00944	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 renal cell carcinoma (RCC) tissues and cell lines	Expression [highly expressed]	qRT-PCR	 In our study, we identified the expression of lncRNA LINC00944 is significantly elevated in renal cell carcinoma (RCC) tissues and cell lines and high LINC00944 expression is significantly correlated with the tumor stage and prognosis of RCC. 	high LINC00944 expression is significantly correlated with the tumor stage and prognosis of RCC. 	Yes	The knockdown of LINC00944 by CRISPR/dCas9-KRAB in higher expressing 786-O and 769-P RCC cells could significantly decrease proliferation and migration and also promote phosphorylation of Akt compared with the control group. 	34291088
LINC00943	LncRNA	Mus musculus	Parkinson Disease	 SK-N-SH cell, brain tissues	Interaction(miR-338-3p/SP1 axis)	qRT-PCR//Western Blot	Our data showed that LINC00943 was highly expressed in the brain tissues of MPTP-treated mice and MPP+-induced SK-N-SH cells.  In terms of mechanism, we pointed out that LINC00943 could sponge miR-338-3p, and miR-338-3p could target SP1. The negative regulation of si-LINC00943 on MPP+-induced SK-N-SH cell injury could be reversed by miR-338-3p inhibitor. Moreover, miR-338-3p had a protective effect on SK-N-SH cells from MPP+-induced injury, which could be reversed by SP1 overexpression. Additionally, we confirmed that LINC00943 positively regulated SP1 via sponging miR-338-3p.		Yes	Knockdown of LINC00943 could promote the proliferation, while inhibit the apoptosis and inflammation of MPP+-induced SK-N-SH cells to alleviate cell injury.	35123924
LINC00942	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues	Interaction(miR-5006-5p/FZD1)	Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	 We discovered that LINC00942 was up-regulated in LUAD tissues compared with adjacent tissues.  Mechanically, LINC00942 exerted its effects via enhancing Wnt signaling. LINC00942 functioned as competing endogenous RNA (ceRNA) by binding to miR-5006-5p, upregulating the expression of FZD1, which was a direct target of miR-5006-5p.	 Besides, we found the increased LINC00942 expression was associated with poor survival.	Yes	 In addition, silencing of LINC00942 suppressed the proliferation, migration, invasion and facilitated the apoptosis of A549 and H1299 cells. Moreover, silencing of LINC00942 repressed the expression of PCNA, Bcl-2, and enhanced Bax expression in A549 and H1299 cells. 	34253104
LINC00941	LncRNA	Homo sapiens	Stomach Neoplasms		Regulated[up-regulated]	Western Blot//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	Our findings confirmed that LINC00941 plays an important oncogenic function in GC and may serve as a potential biomarker for diagnosis and prognosis of GC.		Yes	To validate our findings, we utilized the loss-of-function analysis to reveal the biological function of LINC00941 in GC cells. Loss-of-function analysis revealed that silence of LINC00941 inhibits GC cells proliferation, migration, and invasion in vitro and modulates tumor growth in vivo.	30723491
LINC00941	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cells	Interaction(miR-205-5p/MYC axis)	CCK8//qRT-PCR//RIP//Western Blot	LINC00941 expression level was elevated in colon cancer tissues and cells. In addition, LINC00941 regulated the expression of MYC by sponging miR-205-5p as a competitive endogenous RNA, and miR-205-5p knockdown reversed the tumor inhibition of LINC00941 knockdown on colon cancer cells. 		Yes	 LINC00941 overexpression accelerated proliferation, migration, and invasion of colon cancer cells, while the LINC00941 knockdown showed the opposite results. Xenograft model assay confirmed that LINC00941 silencing could inhibit colon cancer cell growth and metastasis.	33654409
LINC00941	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 cell lines and tumour tissues	regulation[WNT/β-catenin signaling pathway]	qRT-PCR//Northern Blot//Luciferase Report Assay//Colony Formation Assay	Thus, LINC00941/CAPRIN2/ WNT/β-catenin signaling pathway provides new therapeutic targets for OSCC treatment.		Yes	Functional assays suggest that both LINC00941 and CAPRIN2 play pivotal roles in promoting OSCC cell proliferation and colony formation. In vivo assay further confirmed the role of LINC00941 in promoting OSCC cell tumour formation.	32691935
LINC00941	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(hnRNPK)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In this study, we report a never identified before lncRNA, LINC00941, which was highly expressed in OSCC tissues and cells. In silico analyses revealed heterogeneous nuclear ribonucleoprotein K (hnRNPK) to be a strong positive regulator of LINC00941 activity. Experimental verification of this association revealed a direct interaction of LINC00941 and hnRNPK to induce cell growth and invasion by activating EMT in OSCC cells. 		Yes	 Expression of LINC00941 promoted cell proliferation, migration, invasion, and metastasis of OSCC cells In Vitro by inducing epithelial-mesenchymal transition (EMT) and activating the Wnt/β-catenin signaling cascade. 	35037538
LINC00941	LncRNA	Homo sapiens	Glioma	 all glioma subtypes	Expression(highly expressed)	Western Blot//CCK8//qRT-PCR//Cell Apoptosis Assay//Invasion Assay//Transwell Assay	Here, we reported that lncRNA-LINC00941 was highly expressed in all glioma subtypes.		Yes	 Overexpression of lncRNA-LINC00941 in U87 cells promoted cellular proliferation and invasiveness, and suppressed apoptosis.	36375627
LINC00941	LncRNA	Homo sapiens	Pancreatic Neoplasms	PDAC patients	Interaction(MST1/PP2A)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//ISH//qRT-PCR//RIP//Colony Formation Assay//IF	By analyzing a long noncoding RNA (lncRNA) dataset, we found that increased LINC00941 expression led to poor outcomes in PDAC patients. Mechanistically, LINC00941 was found to interact with mammalian STE20-like protein kinase 1 (MST1), which facilitated the protein phosphatase 2A (PP2A)-mediated dephosphorylation of MST1, resulting in Hippo pathway activation and consequently, enhanced glycolysis in PDAC. 	By analyzing a long noncoding RNA (lncRNA) dataset, we found that increased LINC00941 expression led to poor outcomes in PDAC patients. 	Yes	Furthermore, in vitro and in vivo experiments revealed that LINC00941 promoted PDAC cancer cell growth by enhancing aerobic glycolysis. 	34513310
LINC00941	LncRNA	Homo sapiens	Pancreatic Neoplasms	 PC tissues 	Interaction(ANXA2/NEDD4L)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//Co-IP//Migration Assay//qRT-PCR//RIP//Cell Proliferation Assay//Invasion Assay//IF	 By using PCR analysis, we found that LINC00941 was overexpressed in PC tissues and was higher in patients with liver metastasis than in patients without liver metastasis. Mechanically, LINC00941 functioned as a decoy to bind to ANXA2 and suppressed its degradation by enclosing the domain that binds to NEDD4L. Eventually, LINC00941 upregulated ANXA2 and activated FAK/AKT signaling, increasing PC cell proliferation and metastasis. 	In addition, high LINC00941 expression was associated with a poor prognosis. 	Yes	The results suggested that LINC00941 overexpression promoted PC proliferation and metastasis. 	35977942
LINC00958	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation(NUDT19/mTORC1/P70S6K signalling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP	The LINC00958 was up-regulated in HCC tissues and cell lines. The analysis of TCGA and StarBase showed that NUDT19 was a direct target of LINC00958 and was positively regulated by LINC00958. Besides, NUDT19 activated mTORC1/P70S6K signalling pathway. 		Yes	LINC00958 silencing inhibited cell proliferation, migration, and EMT process of HCC.	33979257
LINC00958	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Expression[highly expressed]	qRT-PCR//Luciferase Report Assay//RIP//FISH	 We identified a lipogenesis-related lncRNA, LINC00958, whose expression was upregulated in HCC cell lines and tissues.	High LINC00958 level independently predicted poor overall survival.	Yes	Functional assays showed that LINC00958 aggravated HCC malignant phenotypes in vitro and in vivo.	31915027
LINC00958	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cell lines	Regulation(Wnt/ β-Catenin Signaling)	qRT-PCR//Luciferase Report Assay	Higher levels of LINC00958 were observed in EOC tissues and cell lines.Our data also revealed that high LINC00958 expression was partly induced by STAT1. Mechanistic investigation showed that the inhibitory effect of LINC00958 knockdown on EOC cells was mediated by the Wnt/β-catenin signaling.		Yes	Functionally, knockdown of LINC00958 suppressed the proliferation, migration, and invasion of EOC cells. 	34790276
LINC00963	LncRNA	Homo sapiens	Prostatic Neoplasms	 CRPC tissues	regulation[ miR-542-3p,NOP2]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//RNA-seq//Transwell Assay	Recent studies have revealed that non-coding RNAs in PCa can enhance metastasis and progression, while the mechanisms are still unclear. In this study, we reported that the long noncoding RNA-LINC00963 was increased in CRPC tissues and promoted migration of PCa cells in vitro and their metastasis in vivo. Taken together, our results show that LINC00963 acts as an inducer of PCa metastasis by binding miR-542-3p, thereby promoting NOP2.		Yes	Recent studies have revealed that non-coding RNAs in PCa can enhance metastasis and progression, while the mechanisms are still unclear. In this study, we reported that the long noncoding RNA-LINC00963 was increased in CRPC tissues and promoted migration of PCa cells in vitro and their metastasis in vivo.	32554858
LINC00963	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells	Interaction(miR-34c/LINC00963 target)	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	The long non-coding RNA LINC00963 was found to have a significantly high expression level in breast cancer while it can be down-regulated by corylin. MiR-34c was increased by corylin treatment depending on p53, and it was firstly identified that the LINC00963 was a direct target of miR-34c. Corylin was verified here that it prohibited MCF-7 migration and invasion depending on miR-34c/LINC00963 target. In conclusion, corylin suppresses metastasis of breast cancer cells via increasing miR-34c expression, which was dependent on p53. LINC00963 was a direct target of miR-34c and the target axis was necessary for corylin function.		Yes	In addition, both wound-healing assay and transwell assay showed that LINC00963 induced breast cancer cells metastasis. 	33550958
LINC00963	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR‑1281 and TRIM65)	CCK8//qRT-PCR//Western Blot	LINC00963 was highly expressed in CRC tissues and cells, while miR?1281 was downregulated. Mechanistically, LINC00963 sponged miR‑1281 and repressed its expression in CRC cells, resulting in the upregulation of TRIM65. LINC00963 positively regulates TRIM65 in CRC progression by repressing miR‑1281 expression, showing potential as a therapeutic target for treating CRC.		Yes	 Functionally, LINC00963 facilitated the proliferation, colony formation, migration and invasion of CRC cells, and increased the expression levels of Ki67, matrix metalloproteinase (MMP)2 and MMP9, while miR?1281 had the opposite biological functions. 	34498706
LINC00963	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(miR‑10b/FGF13 axis)	qRT-PCR//Wound Healing Assay//Western Blot	Firstly, the LINC00963 expression was detected using reverse transcription‑quantitative PCR and the results demonstrated that LINC00963 expression levels were significantly increased in CRC tissues and cell lines compared with healthy tissues and HpoEpiC cells, respectively. Collectively, the results of the present study suggested a potential role of the LINC00963/miR-10b/FGF13 axis in the tumorigenesis and progression of CRC, indicating a novel lncRNA-based diagnostic or therapeutic target for CRC.	Online database analysis indicated that high levels of LINC00963 were associated with low survival rates. 	Yes	The results of functional experiments, such as CCK‑8 assay, colony formation assay, wound healing assay and Transwell invasion assay, indicated that LINC00963 knockdown significantly inhibited CRC cell proliferation, colony formation, migration and invasion compared with the small interfering RNA (si)‑negative control (NC) group. 	33495804
LINC00963	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Regulation [PI3K/AKT pathway]	qRT-PCR	 The expression level of LINC00963 in HCC tissues was remarkably higher than that in paracancerous tissues, indicating a potential diagnostic significance of LINC00963.  Furthermore, the PI3K/AKT expression was increased after overexpression of LINC00963, while AKT siRNA effectively reversed the prolonged G0/G1 phase caused by LINC00963 overexpression.	 The expression level of LINC00963 in HCC tissues was remarkably higher than that in paracancerous tissues, indicating a potential diagnostic significance of LINC00963.  The progression-free -with the tumor size and TNM stage, but not with age, gender, histological type and lymph node metastasis.	Yes	Overexpression of LINC00963 significantly enhanced the proliferation ability of HepG2 and HCC cells and prolonged their G0/G1 phase.	29630107
LINC00963	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-378g / CHI3L1 Axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//EdU Staining//Transwell Assay	 In our study, the GSE119054 microarray was analyzed, and LINC00963 showed a significant higher level in ovarian cancer tissues compared with controls.In addition, results show that LINC00963 is a cytoplasmic lncRNA that shares the miRNA response elements (MREs) of miR-378g with CHI3L1, which is confirmed by a luciferase reporter assay and AGO2-dependent RNA immunoprecipitation (RIP).	It was discovered that LINC00963 displayed a close relationship with unfavorable prognosis, and it was prominently raised in OC tissues of patients with lymph node metastasis. 	Yes	What's more, LINC00963 downregulation in OC cells inhibited cell migration and invasion and inverted EMT triggered by TGF-β1. LINC00963 downregulation also inhibited tumorigenesis in nude mice. 	32021459
LINC00963	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Regulation[miR-204-3p/FN1 axis]	Western Blot//Wound Healing Assay//CCK8//Luciferase Report Assay//PCR//Transwell Assay	 LINC00963 was verified to be highly expressed in OS samples and cells. The luciferase reporter assay showed that LINC00963 can suppress miR-204-3p by directly binding miR-204-3p. Rescue experiment results indicated that function of LINC00963 in osteosarcoma was miR-204-3p dependant. Besides, we initially explored Fibronectin-1 (FN1) as the target of LINC00963/miR-204-3p axis in osteosarcoma. 		Yes	Furthermore, LINC00963 overexpression was found to promote proliferation, migration, and invasion in vitro. 	30975024
LINC00963	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCC tissues	regulation[miR-214-5p/RAB14 axis]	qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 LINC00963 expression was significantly increased in ESCC tissues and correlated with advanced TNM stage, metastasis, and poor prognosis. LINC00963 might promote ESCC cells proliferation and invasion via regulating the miR-214-5p/RAB14 axis and it might serve as a therapeutic target for ESCC treatment.	 LINC00963 expression was significantly increased in ESCC tissues and correlated with advanced TNM stage, metastasis, and poor prognosis.	Yes	The knockdown of LINC00963 expression reduced ESCC cells proliferation, invasion in vitro, and reduced tumor growth in vivo. 	31957829
LINC00963	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	regulation[miR-506/BCAT1 Axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	We found that LINC00963 was upregulated in glioma cells and tissues and associated with the poor prognosis of patients with glioma.Our data revealed that LINC00963 confers oncogenic function in the progression of glioma and that the LINC00963/miR-506/BCAT1 axis may be a novel mechanism and therapeutic strategy for this disease.		Yes	Ectopic expression of LINC00963 promoted cell proliferation, cell cycle progression, migration, and invasion in vitro and tumorigenesis in vivo.	32273770
LINC00963	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-124-3p/FZD4 pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, LINC00963 was significantly upregulated in CRC tissues and cells.Our study demonstrated that LINC00963/miR-124-3p/FZD4 played a curial role in cell proliferation and migration in CRC.		Yes	Functionally, LINC00963 knockdown inhibited cell progression in CRC.	32744689
LINC00958	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cell lines	Interaction(miR-3064-5p/LEMD1/PI3K/AKT pathway)	BrdU//qRT-PCR//RIP//Western Blot	LINC00958 and LEMD1 were found to have increased, while the expression of miR-3064-5p was decreased in colorectal cancer tissues and cell lines. Notably, LINC00958 inhibited miR-3064-5p and promoted LEMD1; the miR-3064-5p inhibitor abrogated the effect of LINC00958 silencing in colorectal cancer cells. Additionally, LEMD1 knockdown inhibited the activation of PI3K/AKT signaling. 		Yes	Silencing of LINC00958 hampered cell viability, proliferation, migration, and invasion, while enhancing the apoptosis in colorectal cancer cells. 	34672237
LINC00963	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	 SUDHL4 cell line 	Interaction(miR-320a/XBP1)	In Vivo Experiment//Western Blot//qPCR//CCK8//Flow Cytometry//Luciferase Report Assay//IHC//IF	Following LINC00963 overexpression in vitro, SUDHL4 cell line showed a marked increase in the level of UPR-related GRP78, p-IRE1 and spliced XBP-1/XBP-1(s), apoptosis-related Bax and cleaved caspase 3, as well as autophagy-related Beclin1 and LC3II, whereas miR-320a mimic greatly diminished the effects of LINC00963 overexpression. Moreover, LINC00963 targeted miR-320a while miR-320a bound to the 3'UTR of XBP1.		Yes	 It was also found that LINC00963 overexpression resulted in significantly delayed tumor growth in a xenograft model of DLBCL.	34112145
LINC00963	LncRNA	Homo sapiens	Pulmonary Arterial Hypertension	PASMCs and PAH mouse model	Interaction(microRNA-328-3p/profilin 1 axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//H&E Staining//Transwell Assay	In hypoxia-induced PASMCs and PAH mouse model, high expression levels of LINC00963 and PFN1, and low expression of miR-328-3p, were determined.  The inhibitory effects of LINC00963 silencing on cell viability, migration, and the levels of VEGF, FGF-2, and HIF-α were partly eliminated by miR-328-3p inhibitor or increasing the expression of PFN1. Hypoxia treatment increased the levels of RVSP, mPAP, and RV/(LV+S), as well as the thickness of pulmonary artery wall.		Yes	The viability, migration of hypoxia-induced PASMCs, the expression of VEGF, FGF-2, and HIF-α were significantly repressed by transfection of si-LINC00963 or miR-328-3p mimics. 	35349725
LINC00960	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	Interaction(miR-107/SALL4 )	qRT-PCR//Western Blot	 Further investigation revealed that LINC00960 could regulate SALL4 by sponging miR-107 to promote the progression of OS. 		Yes	 In vitro study showed that silencing LINC00960 inhibited proliferation, migration and invasion of 143B and MG63. In vivo study demonstrated that knockdown of LINC00960 repressed tumor growth. 	35033873
LINC00960	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LADC tumor tissues and cell lines	Interaction(miR-124a/SphK1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//ELISA//Colony Formation Assay//Transwell Assay	We observed that LINC00960 was overexpressed in LADC tumor tissues and cell lines.Moreover, LINC00960 sponged miR-124a to inhibit the SphK1/S1P pathway in LADC cells. The luciferase reporter assay results demonstrated an interaction between miR-124a and LINC00960 or SphK1. This interaction was confirmed using the RNA pull-down assay. In addition, miR-124a downregulation or SphK1 upregulation reversed the inhibitory effects of LINC00960 knockdown on cellular functions of LADC cells, suggesting that LINC00960 may be a potential therapeutic biomarker for LADC via the miR-124a/SphK1 axis. 		Yes	LINC00960 knockdown suppressed the proliferation, migration, and invasion of LADC cells.  LINC00960 knockdown markedly reduced the rate of tumor growth. 	34738865
LINC00958	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue and cell	Regulation(GLUT1 )	In Vivo Experiment//qRT-PCR//MeRIP-seq//Western Blot	Here, our team discovered that lncRNA LINC00958 expression up-regulated in GC tissue and cells. Mechanistically, methylated RNA immunoprecipitation sequencing (MeRIP-Seq) found that there were m6 A-modificated sites in LINC00958, and moreover m6 A methyltransferase KIAA1429 catalyzed the m6 A modification on LINC00958 loci. Moreover, LINC00958 interacted with GLUT1 mRNA via the m6 A-dependent manner to enhance GLUT1 mRNA transcript stability, thereby positively regulating the aerobic glycolysis of GC.	Clinically, high-expression of LINC00958 was clinically correlated to lower survival of GC patients. 	Yes	Functionally, in vitro assays demonstrated that LINC00958 promoted the GC cells' aerobic glycolysis.	34409730
LINC00958	LncRNA	Homo sapiens	Breast Neoplasms	BC tissue and cells	Interaction(miR-378a-3p/YY1 axis)	CCK8//qRT-PCR//Flow Cytometry	we also detected the levels of LINC00958 in BC cell lines and found that LINC00958 was markedly upregulated compared to that in normal cells 	the lncRNA LINC00958 indicated an unfavorable prognosis for patients with BC.	Yes	Functional assays found that LINC00958 upregulation regulated the proliferation and apoptosis of BC cells.	33531456
LINC00958	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Regulation[JNK/c-JUN Signaling]	Western Blot//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	First of all, the online databases suggested that LINC00958 was slightly expressed in human normal lung tissues but upregulated in LUSC tissues.By and large, our work illustrated that LINC00958 facilitates tumorigenesis in NSCLC by activating the JNK/c-JUN signaling pathway, indicating a new road for diagnosis and treatment of both LUAD and LUSC.		Yes	In addition, we elucidated that knockdown of LINC00958 led to impaired proliferation, induced apoptosis, and hampered migration in LUAD cells.	31855084
LINC00958	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(MiR-204-3p/KIF2A Axis)	qRT-PCR//Luciferase Report Assay//IHC//Western Blot	We found that LINC00958 was up-regulated in NSCLC tissues and cell lines. Besides, miR-204-3p was identified as a target of LINC00958 and miR-204-3p inhibitor could reverse the inhibitory effect of LINC00958 knockdown on proliferation and migration of NSCLC cells. We also validated that KIF2A, a direct target of miR-204-3p, was responsible for the biological role of LINC00958. KIF2A antagonized the effect of miR-204-3p on NSCLC cell proliferation and migration and was regulated by LINC00958/miR-204-3p. 		Yes	 Down-regulation of LINC00958 inhibited cell proliferation and migration in vitro and suppressed tumor growth in vivo.	34269081
LINC01106	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues and cells	regulation[miR-449a/MET Axis]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	 LncRNA LINC01106 expression was highly up-regulated in EC tissues and cells.Silencing of LINC01106 inhibits the occurrence and development of EC via regulating the miR-449a/MET axis. 		Yes	The proliferation, migration and invasion of EC cells in vitro were inhibited by the transfection of sh-LINC01106. The growth of tumor xenograft was suppressed by injection of sh-LINC01106. 	33061446
LINC01111	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues,blood	Regulation[LINC01111/miR-3924/DUSP1 axis ]	Western Blot//Wound Healing Assay//Invasion Assay//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Colony Formation Assay//EdU Staining//IF	Here, we report a novel lncRNA, LINC01111, that is clearly downregulated in PC tissues and plasma of PC patients and acts as a tumor suppressor. Overall, these data reveal that LINC01111 is a potential diagnostic biomarker for PC patients, and the newly identified LINC01111/miR-3924/DUSP1 axis can modulate PC initiation and development.	We found that the LINC01111 level was negatively correlated with the TNM stage but positively correlated with the survival of PC patients. 	Yes	The overexpression of LINC01111 significantly inhibited cell proliferation, the cell cycle, and cell invasion and migration in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, the knockdown of LINC01111 enhanced cell proliferation, the cell cycle, and cell invasion and migration in vitro, as well as tumorigenesis and metastasis in vivo.	31767833
LINC01243	LncRNA	Homo sapiens	Endometrial Neoplasms		regulation[up-regulation]	Flow Cytometry//qRT-PCR//Transwell Assay	We first confirmed the partial knockdown of both LINC01133 and LINC01243 expression in Ishikawa and HEC-1-A cells using RT-qPCR. Following confirmation of lncRNA knockdown, we assessed the effect of knockdown on EC malignancy. 		Yes	 Furthermore, Transwell and scratch invasion assays revealed decreased migration and invasion of the two EC cell lines, respectively.	32929617
LINC01224	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells	Interaction(miR-193a-5p/NUP210 Axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In this study, LINC01224 was highly expressed in TNBC cells.Additionally, LINC01224 stabilized NUP210 mRNA through interaction with miR-193a-5p, thereby aggravating the malignant phenotypes of TNBC. 		Yes	Moreover, LINC01224 downregulation inhibited TNBC cell proliferation, migration, and invasion, and promoted cell apoptosis. 	36127622
LINC01215	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	GEO(10 normal samples and 53 ovarian cancer samples)	Expression [highly expressed]	CCK8//qRT-PCR//RNA Pull-Down	LINC01215 was identified as an upregulated long noncoding RNA (lncRNA) in EOC		Yes	Overexpressing LINC01215 contributed to downregulated levels of RUNX3, as demonstrated by the recruitment of methylation-related proteins. Silencing of LINC01215 elevated the expression of RUNX3, thus suppressing cell proliferation, migration, invasion and EMT and decreasing the expressions of MMP-2, MMP-9 and Vimentin, but increased the expression of E-cadherin. 	34052627
LINC01198	LncRNA	Homo sapiens	Glioma	cell lines	regulation[PI3K/AKT pathway]	RNA Pull-Down//IHC//Western Blot//Co-IP//Tunel//qRT-PCR//FISH//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//ChIP	 In our study, LINC01198 was proved to be up-regulated in glioma cell lines, and silenced LINC01198 curbed glioma cell proliferation and accelerated cell apoptosis. Jointly, LINC01198 activates PI3 K/AKT signalling to exert oncogenic function in gliomagenesis by regulating PIK3CA and PTEN, which highlights a new approach for glioma treatment.		Yes	 In our study, LINC01198 was proved to be up-regulated in glioma cell lines, and silenced LINC01198 curbed glioma cell proliferation and accelerated cell apoptosis.	32378450
LINC01197	LncRNA	Mus musculus	Arthritis, Rheumatoid	 synovial tissues	regulation[microRNA-150/THBS2 axis]	qRT-PCR	LINC01197 was poorly expressed in the synovial tissues in the RA model mice.The current study suggested that LINC01197 sponged miR-150 to promote THBS2 expression, leading to TLR4/NF-κB inactivation, and ameliorated RA inflammation. These findings may offer new insights into RA treatment.		Yes	Overexpression of LINC01197 reduced RA severity in mice and inhibited proliferation and inflammatory responses as well as promoted apoptosis in RA-FLS. 	32540401
LINC01194	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and NSCLC lines	regulation[LINC01194/miR-486-5p Axis]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	LncRNA LINC01194 was highly expressed in NSCLC tissues and NSCLC lines (A549, H1299, H460 cells, H1975), and lncRNA LINC01194 significantly promoted cell proliferation and migration of NSCLC cells.LncRNA LINC01194 promoted the progression of NSCLC by modulating the miR-486-5p/CDK4 axis.		Yes	LncRNA LINC01194 was highly expressed in NSCLC tissues and NSCLC lines (A549, H1299, H460 cells, H1975), and lncRNA LINC01194 significantly promoted cell proliferation and migration of NSCLC cells.	32346298
LINC01194	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Expression[highly expressed]	Western Blot//Migration Assay//CCK8//qRT-PCR//Cell Cycle Assay//Invasion Assay	Using RT-PCR, we found that Linc01194 is highly expressed in HCT116 cells. 	In the survival analysis, we found that Linc01194 is correlated with poor survival of colon cancer patients. 	Yes	 In addition, by suppressing the expression of Linc01194 in colon cancer cell lines, cell proliferation and migration were inhibited. 	30962722
LINC01194	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and in clinical samples	Interaction(miR-655-3p/SMAD )	Western Blot//CCK8//qRT-PCR//Cell Apoptosis Assay//Transwell Assay	 LINC01194 was overexpressed in HCC cells and in clinical samples.  We also confirmed that miR-655-3p could bind to LINC01194, and miR-655-3p was downregulated in HCC. The upregulation of miR-655-3p suppressed HCC cell invasion and migration, and enhanced the number of apoptotic cells. SMAD5, which was overexpressed in HCC cell lines, was directly targeted by miR-655-3p. 		Yes	ILINC01194 silencing suppressed proliferation and migration; however, it promoted apoptosis in HCC cell lines. 	34978464
LINC01194	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	regulation[miR-641/SETD7 axis]	Western Blot//Tunel//Flow Cytometry//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 LINC01194 was significantly upregulated in LUAD tissues and cell lines. LINC01194 promotes the progression of LUAD by enhancing miR-641-targeted SETD7. The LINC01194/miR-641/SETD7 axis might provide new molecular targets for treating LUAD.		Yes	Knockdown of LINC01194 resulted in decreased cell proliferation, migration and invasion, and increased apoptosis. 	33372601
LINC01194	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC  tissue 	regulation[miR-655,SOX18 ]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	We found that the expression levels of LINC01194 were highly expressed in LSCC, which was negatively correlated with the clinical outcome of LSCC patients. Furthermore, we elucidated that LINC01194 promoted SOX18 expression in LSCC cells via functioning as a molecular sponge for miR-655.	We found that the expression levels of LINC01194 were highly expressed in LSCC, which was negatively correlated with the clinical outcome of LSCC patients.	Yes	 Functional assays indicated that LINC01194 knockdown distinctly inhibited LSCC cells proliferation, induced apoptosis, and also attenuated LSCC cells migration and invasion in vitro.	32703403
LINC01189	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCV-infected HCC tumors and cell lines	Interaction(Hsa-miR-155-5p )	Cell Proliferation Assay//qRT-PCR//Luciferase Report Assay	LINC01189 is downregulated in HCV-infected HCC tumors and cell lines.Hsa-miR-155-5p was confirmed to be a ceRNA target of LINC01189 in HCC. Upregulating hsa-miR-155-5p reversed the LINC01189-mediated inhibition on HCC proliferation and 5-FU chemoresistance.		Yes	LINC01189 overexpression inhibited HCC cancer cell proliferation and 5-FU chemoresistance.	33059056
LINC01186	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and an NPC cell line	Expression[lower expressed]	Wound Healing Assay//CCK8//qRT-PCR//Cell Apoptosis Assay//Transwell Assay	 In the present study, the expression of lncRNA ZNF674-1 in NPC tissues and an NPC cell line was analyzed and was revealed to be downregulated compared with normal tissues and cells. 		Yes	When the expression of lncRNA ZNF674-1 was reduced in NPC cells, the proliferation, migration and invasion of these cells was promoted, whereas the apoptosis of these cells was decreased. On the contrary, when overexpressed, the expression of lncRNA ZNF674-1 inhibited the proliferation, invasion and migration of cells, but promoted cell apoptosis.	29805695
LINC01160	LncRNA	Homo sapiens	Nasopharyngeal carcinoma		regulation[STAT1 ]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	LINC01160 is upregulated in NPC and can promote a malignant cell phenotype.		Yes	STAT1 is a transcription factor of LINC01160 and can promote a malignant cell phenotype through upregulating LINC01160 expression.	33263259
LINC01152	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[IL-23]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay	In this study we found that the expression of LINC01152 was significantly increased in HBV positive HCC tissues and cells and was induced by HBx in vitro.Mechanistically, HBx could increase the transcription of LINC01152. Elevated LINC01152 binds to the promoter region of IL-23, promoting its transcriptional activity and upregulating the levels of Stat3 and p-Stat3. Our findings suggest that LINC01152 plays an important role in HBV-related hepatocellular carcinoma development and may serve as a therapeutic marker for hepatocellular carcinoma.		Yes	The overexpression of LINC01152 could increases HCC cell proliferation and promotes tumor formation in nude mice	31054511
LINC01140	LncRNA	Homo sapiens	Lung Neoplasms	LC and paracancerous tissues	Regulation	In Vivo Experiment	We found that LINC01140 was highly expressed in human LC tissues and cell lines. High LINC01140 levels were associated with poor survival in patients with LC. LINC01140 upregulation promoted the proliferation, migration, and invasion of LC cells through direct interaction with miR-33a-5p and miR-33b-5p, thereby contributing to c-Myc expression and also inhibited cisplatin-induced cell apoptosis.		Yes	In subcutaneous tumor xenograft mice, LINC01140 knockdown markedly reduced tumor growth and lung metastasis.	34446576
LINC01140	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	MIBC tissues	regulation[LINC01140/miR-140-5p/FGF9 axis]	Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//H&E Staining//ELISA//Transwell Assay//IF	The long noncoding RNA (lncRNA) LINC01140 was positively correlated with FGF9 and was significantly upregulated in MIBC tissues. In conclusion, LINC01140, miR-140-5p, and FGF9 form a lncRNA-miRNA-mRNA axis that modulates the bladder cancer phenotype, affects macrophage M2 polarization through the tumor microenvironment, and in turn affects bladder cancer cell aggressiveness.		Yes	LINC01140 knockdown inhibited the viability, migratory capacity and invasive capacity of T24 cells; culture in si-LINC01140-CM also inhibited macrophage M2 polarization, while promoting M1 polarization. 	33234721
LINC01140	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction(miR-139-5p/HOXA9 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	LINC01140 was overexpressed in osteosarcoma and knocking down LINC01140 restrained the proliferation and invasion of osteosarcoma cells and EMT. In Saos2 and MG63 cells, LINC01140 sponged miR-139-5p, and a miR-139-5p inhibitor overturned the suppression of LINC01140 knockdown on the proliferation and migration of osteosarcoma cells. Moreover, miR-139-5p depressed the invasion, proliferation, and EMT of osteosarcoma cells via targeting HOXA9.		Yes	LINC01140 was overexpressed in osteosarcoma and knocking down LINC01140 restrained the proliferation and invasion of osteosarcoma cells and EMT.	35800618
LINC01140	LncRNA	Homo sapiens	Glioma	Glioma Cells	regulation[miR-199a-3p/ZHX1 Axis]	CCK8//qRT-PCR//Western Blot	 The expressions of LINC01140 were promoted in glioma. LINC01140 could promote glioma developments by modulating the miR-199a-3p/ZHX1 axis.		Yes	 Silencing LINC01140 could inhibit glioma cell viabilities, migration, and invasion.	32184618
LINC01139	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC specimens and cell lines	regulation[MYBL2,miR-30]	qRT-PCR	We found that LINC01139 was over-expressed in HCC specimens and cell lines, and its upregulation was observed to be associated with advanced TNM stage, lymph node metastasis and poor clinical prognosis of HCC patients. Overall, LINC01139 may exhibit an oncogenic function in HCC via acting as a sponge for miR-30 to upregulate MYBL2, and may serve as a potential therapeutic target and a prognostic biomarker for HCC patients.	We found that LINC01139 was over-expressed in HCC specimens and cell lines, and its upregulation was observed to be associated with advanced TNM stage, lymph node metastasis and poor clinical prognosis of HCC patients. Multivariate analyses confirmed that LINC01139 expression was an independent poor prognostic factor for HCC patients. 	Yes	Functionally, the knockdown of LINC01139 suppressed cell proliferation, clone formation and metastasis of HCC cells.	32115147
LINC01139	LncRNA	Homo sapiens	pancreatic adenocarcinoma	blood	Interaction[ROCK1 ]	Western Blot//CCK8//qRT-PCR//ELISA//Transwell Assay	In the present study, it was determined that the plasma levels of LINK-A lncRNA and Rho-associated protein kinase 1 (ROCK1) were significantly increased in patients with pancreatic adenocarcinoma compared with those in healthy controls. Overexpression of LINK-A lncRNA led to upregulation of ROCK1 expression, while overexpression of ROCK1 had no significant effect on LINK-A lncRNA expression. It may therefore be concluded that LINK-A lncRNA may have a role in pancreatic adenocarcinoma, at least in part, by promoting ROCK1 expression.		Yes	 Silencing of LINK-A led to inhibition of pancreatic adenocarcinoma cell proliferation, migration and invasion. Simultaneous overexpression of ROCK1 attenuated the inhibitory effect of LINK-A silencing on cancer cell proliferation, migration and invasion.	32104251
LINC01139	LncRNA	Homo sapiens	Osteosarcoma	blood	Interaction[Expression[highly expressed]regulating HIF1α]	qRT-PCR//Transwell Assay//Western Blot	The results demonstrated that plasma levels of LINK-A lncRNA were significantly higher in patients with metastatic osteosarcoma (MO) compared with healthy controls and patients with non-metastatic osteosarcoma (NMO). Expression[up-expression]regulated expression of hypoxia-inducible factor 1α (HIF1α) was observed in cancer cells following LINK-A lncRNA overexpression. Exogenous HIF1α treatment did not significantly affect the expression of LINK-A lncRNA in cancer cells, whereas treatment with an HIF1α inhibitor significantly attenuated the effects of LINK-A lncRNA overexpression on cancer cell migration and invasion.		Yes	LINK-A lncRNA overexpression significantly promoted cancer cell migration and invasion in osteosarcoma cell lines MG-63 and U20S.	31186711
LINC01224	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-2467)	RNA Pull-Down//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//cell invasion assay//Colony Formation Assay	Presently, LINNC01224 expression was elevated and miR-2467 expression was down-regulated in NSCLC, compared with standard control.  Then we described the reciprocal correlation between LINC01224 and miR 2467. Afterward, the dual-luciferase reporter assay, RIP assay and RNA pull-down assay validated the base-pair interaction between LINC01224 and miR-2467. 		Yes	Moreover, our findings demonstrated that the silence of LINC01224 inhibited cell proliferation and invasion in NSCLC and enhanced cisplatin (CDDP) sensitivity in vitro. Besides, rescue assays verified that miR-2467 inhibitor could reverse the effects on cell biological activities and CDDP resistance caused by knockdown of LINC01224. Finally, in vivo experiments implicated that knockdown of LINC01224 could inhibit NSCLC tumor growth. 	34403779
LINC01224	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tumor tissue and cell lines	Interaction(miR‑485‑5p/AKT3 )	qRT-PCR//RNA Pull-Down//Western Blot	LINC01224 expression was significantly upregulated in both EC tumor tissue and cell lines. LINC01224 directly bound to and downregulated miR‑485‑5p to elevate the expression levels of AKT3, thereby promoting EC progression. The present data demonstrated the expression levels, clinical relevance and functional mechanism of LINC01224 in EC. LINC01224 promoted EC development via sponging miR‑485‑5p to elevate AKT3 expression levels; this may provide a promising therapeutic target pathway for EC treatment.	 The upregulation of LINC01224 was negatively associated with survival of patients with EC. 	Yes	Functionally, LINC01224 promoted proliferation and inhibited apoptosis of EC cells;  LINC01224 depletion in EC cells hindered tumor growth in a xenograft model.	34278482
LINC01116	LncRNA	Rattus norvegicus	Glioma	glioma tissues	Interaction(microRNA‑744‑5p‑MDM2‑p53 axis)	In Vivo Experiment//Western Blot//Tunel//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	LINC01116 was found to be highly expressed in glioma tissues, which was associated with a malignant phenotype. LINC01116 promoted the proliferation and invasiveness of glioma cells, and inhibited the p53 pathway by preserving the expression of MDM2 mRNA via miR‑744‑5p sponging. Furthermore, a low degree of miR‑744‑5p expression was observed in glioma tissues, which was negatively associated with the expression of LINC01116. Overexpression of miR‑744‑5p inhibited the proliferation and invasiveness of glioma cells, which was rescued by LINC01116. Finally, LINC01116 knockdown inhibited tumor growth in nude mice. In conclusion, LINC01116 is aberrantly expressed and promotes the progression of glioma by regulating the miR‑744‑5p‑MDM2‑p53 pathway. In future, targeting LINC01116 may therefore be a potential therapeutic approach for patients with glioma.		Yes	Furthermore, a low degree of miR‑744‑5p expression was observed in glioma tissues, which was negatively associated with the expression of LINC01116. Overexpression of miR‑744‑5p inhibited the proliferation and invasiveness of glioma cells, which was rescued by LINC01116. Finally, LINC01116 knockdown inhibited tumor growth in nude mice.	33760190
LINC01224	LncRNA	Homo sapiens	Colonic Neoplasms	CC tumor tissues and CC cell lines	Interaction(miR-485-5p/MCL1)	qRT-PCR//Western Blot	LINC01224 was highly expressed in CC tumor tissues and CC cell lines, and its expression was associated with the overall survival of CC patients. LINC01224 was verified to sponge miR-485-5p and consequently targeted MCL1. MiR-485-5p inhibitor or MCL1 overexpression (MCL1 OE) markedly restored the repressive effect of the si-LINC01224 pool on MCL1 expression level, as well as proliferation, migration, and invasion of HT29 and SW480 cells.	LINC01224 was highly expressed in CC tumor tissues and CC cell lines, and its expression was associated with the overall survival of CC patients. 	Yes	 The LINC01224-siRNAs (si-LINC01224) markedly suppressed the level of LINC01224 in CC cell lines (HT29 and SW480 cells) and consequently significantly suppressed the proliferation, migration, and invasion of the HT29 and SW480 cells.	34675675
LINC01235	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	Expression(highly expressed)	Western Blot//Invasion Assay//qRT-PCR//Bioinformatics Analysis//Transwell Assay	The qRT-PCR assay confirmed that LINC01235 is significantly over-expressed in GC cells and tissues. 	Additionally, the overall survival analysis showed that patients with a higher LINC01235 expression had a poorer prognosis than those with a lower LINC01235 expression. Univariate Cox regression analysis indicated that high LINC01235 expression is positively correlated with poor prognosis. 	Yes	Invitro assays suggested that LINC01235 knockdown suppresses GC cell migration and invasion. GSEA revealed that high LINC01235 expression is strongly enriched in the EMT pathway. Western blotting results revealed that LINC01235 silencing decreases the expression of EMT-induced proteins. 	33771634
LINC01234	LncRNA	Homo sapiens	Breast Neoplasms	 BC tissues, BC cell 	Interaction(miR-525-5p/CSDE1 )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay	We screened out LINC01234, found to be significantly increased in BC tissues, associated with a poor prognosis, and positively correlated with tumor size of BC. Dual-luciferase reporter®, RNA pull-down, and RNA immunoprecipitation assays confirmed that LINC01234 and CSDE1 directly interacted with miR-525-5p. Upregulation of miR-525-5p and suppression of CSDE1 inhibited BC cell growth and induced cell apoptosis.	We screened out LINC01234, found to be significantly increased in BC tissues, associated with a poor prognosis, and positively correlated with tumor size of BC. 	Yes	 Knockdown of LINC01234 suppressed BC cell growth and facilitated apoptosis. 	35923244
LINC01234	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung tissue	interaction[HNRNPA2B1,miR-106b]	qRT-PCR//RNA Pull-Down	LINC01234 was overexpressed in NSCLC compared with normal lung tissue and correlated positively with poor prognosis. We identified numerous lncRNAs with dysregulated expression in NSCLC and demonstrated a novel oncogenic axis involving LINC01234, HNRNPA2B1, miR-106b-5p, CRY2, and c-Myc. Components of this axis may be potential novel targets for NSCLC.	LINC01234 was overexpressed in NSCLC compared with normal lung tissue and correlated positively with poor prognosis. 	Yes	 Downregulation of LINC01234 impaired cell proliferation in vitro and tumor growth in vivo.	32246902
LINC01234	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	Interaction(LINC01234/miR-433-3p/GRB2 )	CCK8//Colony Formation Assay//EdU Staining	 LINC01234 was abundantly expressed in NSCLC cells.  LINC01234 competitively bound to miR-433-3p and miR-433-3p directly targeted GRB2. miR-433-3p knockdown or GRB2 overexpression counteracted the repressive effect of LINC01234 silencing on NSCLC cell malignant proliferation.		Yes	 LINC01234 silencing reduced NSCLC cell proliferation while LINC01234 overexpression enhanced cell proliferation.	35747966
LINC01234	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer cell lines and tissues	regulation[miR-1284/TRAF6 axis]	qRT-PCR	First, we found that LINC01234, localized in the cytoplasm, was increased in both colorectal cancer cell lines and tissues.Collectively, this study clarified the biological significance of LINC01234/miR-1284/TRAF6 axis in colorectal cancer progression, providing insights into LINC01234 as novel potential therapeutic target for colorectal cancer therapeutic from bench to clinic.		Yes	Subsequent functional assays suggested LINC01234 knockdown suppressed cell proliferation, migration, and invasion of colorectal cancer cells, while blocked cell cycle and induced cell apoptosis. 	31904146
LINC01234	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and CRC cell lines	regulation[KLF6 ]	qRT-PCR	LINC01234 expression was significantly upregulated in CRC tissues and CRC cell lines than in non-tumor tissues and normal epithelial cells, respectively.  LINC01234 could be a prognostic biomarker in CRC patients. Upregulation of LINC01234 in CRC promotes tumor development through negative regulation of KLF6.	LINC01234 was associated with high tumor stage, larger tumor size, and metastasis. 	Yes	 Cell proliferation was inhibited by LINC01234 knockdown, whereas apoptosis was enhanced.	31650732
LINC01234	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(ASS1/p53)	qRT-PCR	Clinically, LINC01234 was highly expressed in HCC, and a high LINC01234 expression level was correlated with a poor prognosis of patients with HCC. Mechanistically, LINC01234 downregulated the expression of ASS1, leading to am increased aspartate level and activation of the mammalian target of rapamycin pathway. LINC01234 bound to the promoter of ASS1 and inhibited transcriptional activation of ASS1 by transcriptional factors, including p53. 	Clinically, LINC01234 was highly expressed in HCC, and a high LINC01234 expression level was correlated with a poor prognosis of patients with HCC. 	Yes	 LINC01234 promoted cell proliferation, migration, and drug resistance by orchestrating aspartate metabolic reprogramming in HCC cells. Finally, inhibiting LINC01234 dramatically impaired tumor growth in nude mice and sensitized HCC cells to sorafenib. 	35192933
LINC01234	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cells	Interaction(microRNA-27b-5p)	qRT-PCR//Bioinformatics Analysis//Western Blot	 Up-regulated LINC01234 exhibited in OC tissues and cells. LINC01234 could restore SIRT5 expression by binding to miR-27b-5p. Down-regulated miR-27b-5p reversed the effect of silenced LINC01234 on OCSCs development and tumorigenesis in vivo.		Yes	 Down-regulated LINC01234 or elevated miR-27b-5p suppressed OCSCs progression and tumorigenesis in vivo. 	35230909
LINC01234	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer cells	Expression[highly expressed]	qRT-PCR	Expression of lncRNA LINC01234 was found to be markedly upregulated in the CEC2 cell line. 		Yes	After this, the LINC01234 knockdown effects on cell proliferation, migration, invasion, and apoptosis were evaluated by cell proliferation assay, wound healing assay, invasion assay, and flow cytometric analysis in vitro.	30519325
LINC01234	LncRNA	Homo sapiens	Multiple Myeloma	Multiple myeloma tissues	Regulation[miR-124-3p/GRB2 axis]	RNA Pull-Down//Western Blot//ISH//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//EdU Staining	Our results indicated that LINC01234 was over-expressed in tumor tissues of MM patients.In this study, a novel established regulatory manner of LINC01234/miR-124-3p/GRB2 axis was systematically studied, which may hold promise as a promising target for MM treatment.		Yes	Our results indicated that LINC01234 was over-expressed in tumor tissues of MM patients, and LINC01234 down-regulation remarkably inhibited cell proliferation, cycle progression and promoted cell apoptosis in MM cells.	31737211
LINC01234	LncRNA	Homo sapiens	Pancreatic Neoplasms	 pancreatic cancer cells and tissues	Interaction(miR-513a-3p/H6PD )	Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	 LINC01234 and H6PD levels were elevated while miR-513a-3p level was reduced in pancreatic cancer cells and tissues.MiR-513a-3p depletion or H6PD elevation could abrogate the inhibitory effects of LINC01234 silencing on pancreatic cancer cells. LINC01234 sponged miR-513a-3p that targeted H6PD.		Yes	 LINC01234 deficiency hindered the malignant biological activities of pancreatic cancer cells.	36343541
LINC01234	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Interaction[regulating OTUB1 ]	qRT-PCR	In this study, we first found that LINC01234 expressions were distinctly upregulated in both NSCLC samples and cell lines using RT-PCR.Mechanistic investigations revealed LINC01234 promotes the progression of NSCLC cells by the modulation of miR-140 to positively regulate OTUB1 expression.	The results form clinical investigations indicated that high LINC01234 expressions were associated with positively lymph node metastasis and advanced tumor-metastasis-node (TMN) stage. Kaplan-Meier assays indicated that patients with NSCLC having high LINC01234 expressions tend to have unfavorable clinical prognosis. Using multivariate assays, it was confirmed that LINC01234 was an independent prognostic factor for patients with NSCLC. 	Yes	In vitro assays showed that inhibition of LINC01234 suppressed NSCLC cell proliferation, cell colony formation and metastasis, and greatly promoted apoptosis.	31106421
LINC01234	LncRNA	Homo sapiens	Carcinoma, Renal Cell		regulation[ HIF-2α]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Together, these datas showed that LINC01234 was likely to regulate the progression of ccRCC by HIF-2α pathways, and LINC01234 was both a promising prognostic biomarker and a potential therapeutic target for ccRCC.		Yes	LINC01234 knockdown impaired cell proliferation, migration and invasion in vitro as compared to negative control.	33088626
LINC01234	LncRNA	Homo sapiens	Melanoma	melanoma cells	Interaction(miR-625-5p/PKM2 axis)	qRT-PCR	Functional analysis of two SFPQ-enriched lncRNA, LINC00511 and LINC01234, demonstrated that these genes independently contribute to the melanoma phenotype and a more detailed analysis of LINC00511 indicated that this occurs in part via modulation of the miR-625-5p/PKM2 axis.		Yes	Functional analysis of two SFPQ-enriched lncRNA, LINC00511 and LINC01234, demonstrated that these genes independently contribute to the melanoma phenotype and a more detailed analysis of LINC00511 indicated that this occurs in part via modulation of the miR-625-5p/PKM2 axis.	34218270
LINC01232	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	Interaction(miR-506-5p/PAK1 Axis)	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 LINC01232 was overexpressed in gastric cancer tissues and cells, and mainly located in nucleus.  MiR-506-5p was downregulated in gastric cancer tissues and cells. LINC01232 sponged miR-506-5p to accelerate migration and EMT. PAK1 was certified to be a target of miR-506-5p, inhibition of PAK1 could interrupt LINC01232 overexpression-induced migration of gastric cancer cells.		Yes	 The inhibition of LINC01232 could suppress migration, invasion and EMT of gastric cancer cells. 	35592108
LINC01232	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC cell lines 	Interaction(miR-370-5p/PIM3 axis)	qRT-PCR//FISH	In the current study, we detected LINC01232 expression utilizing quantitative real-time polymerase chain reaction (RT-qPCR) and discovered that LINC01232 was overexpressed in BC cell lines versus normal cell line. Next, miR-370-5p was proved to bind with LINC01232 by RNA pull down, RNA-binding protein immunoprecipitation (RIP) and luciferase reporter assays. Furthermore, PIM3 expression was negatively modulated by miR-370-5p and markedly increased in BC cell lines. Moreover, PIM3 silence repressed proliferation, migration and invasion but triggered apoptosis of BC cells. The rescue assays validated that upregulation of PIM3 recovered the effects of LINC01232 silence on the growth of BC cells. 		Yes	Functionally, LINC01232 deficiency suppressed cell proliferation, migration and invasion. 	35338769
LINC01232	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	Interaction(IGF2BP2/TGFBR1)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//ChIP	 RT-qPCR results revealed that LINC01232 expression was high in NSCLC cells.Luciferase reporter assay and ChIP assay validated that forkhead box P3 (FOXP3) could bind to LINC01232 promoter and activate LINC01232 transcription. Further, LINC01232 was certified to activate TGF-β signaling pathway through regulating transforming growth factor beta receptor 1 (TGFBR1). After RIP and RNA pull down assays, insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) was proven as the RNA-binding protein (RBP) for LINC01232. LINC01232 promoted TGFBR1 mRNA stability via recruiting IGF2BP2. Subsequently, LINC01232 was verified to accelerate NSCLC cell stemness and induce macrophage M2 polarization via upregulating TGFBR1. 		Yes	Flow cytometry and sphere formation assays indicated that LINC01232 significantly promoted NSCLC cell stemness.	35026283
LINC01224	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-2467 )	CCK8//qRT-PCR	LINC01224 expression was observed to be up-regulated in CRC tissues and cell lines. Functional studies suggested that LINC01224 silence inhibited CRC cells proliferation and invasion of CRC cells, while co-transfection with a miR-2467 inhibitor reversed these biological effects. 		Yes	Functional studies suggested that LINC01224 silence inhibited CRC cells proliferation and invasion of CRC cells, while co-transfection with a miR-2467 inhibitor reversed these biological effects. 	33542656
LINC01224	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue samples and cell lines	Interaction(miR-485-5p/MYO6 axis)	qRT-PCR//Transwell Assay//RIP//ChIP	 LINC01224 abundance was elevated in CRC tissue samples and cell lines. MiR-485-5p was sponged by LINC01224, and miR-485-5p downregulation relieved the influence of LINC01224 interference on CRC progression. MYO6 was targeted via miR-485-5p and regulated via LINC01224/miR-485-5p axis. MiR-485-5p overexpression suppressed CRC cell proliferation, migration, and invasion and facilitated apoptosis. MYO6 upregulation mitigated the role of miR-485-5p. 	 Elevated LINC01224 might indicate the lower 5-year overall survival in 52 CRC patients. 	Yes	LINC01224 was upregulated via the transcription factor YY1. LINC01224 knockdown restrained CRC cell proliferation, migration, and invasion and increased apoptosis. LINC01224 knockdown decreased xenograft tumor growth.	34535152
LINC01139	LncRNA	Homo sapiens	Osteosarcoma	 patients with osteosarcoma	regulation[TGF-β1]	Flow Cytometry//qRT-PCR//ELISA//Transwell Assay	 LINK-A lncRNA and TGF-β1 were upregulated in patients with osteosarcoma compared with healthy controls.  These data indicated that LINK-A lncRNA is upregulated in osteosarcoma and may regulate migration, invasion and stemness of osteosarcoma cells through TGF-β1.		Yes	 LINK-A lncRNA shRNA silencing inhibited, whereas TGF-β1 treatment promoted cell migration, invasion and stemness.	32218837
LINC01139	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian tissues	Interaction[HIF1α]	qRT-PCR	As shown in Figure 1, compared with the control groExpression[Expression[up-expression]-expression], LINK-A was significantly higher in patients with the 3 types of metastatic ovarian carcinoma (p<0.05), while no significant difference in LINK-A expression was found between non-metastatic ovarian carcinoma and healthy controls (p>0.05). In addition, LINK-A overexpression also significantly promoted migration (p<0.05, Figure 4B) and invasion (p<0.05, Figure 4C) of cancer cells. We found that LINK-A was significantly higher in ovarian carcinoma patients than in healthy controls in ovarian biopsies and in serum. LINK-A expression effectively distinguished patients with metastatic ovarian carcinoma from healthy controls. LINK-A overexpression promoted cancer cell migration and invasion, and also Expression[Expression[up-expression]-expression]regulated the expression of HIF1alpha.	 As shown in Figure 1, compared with the control groExpression[Expression[up-expression]-expression], LINK-A was significantly higher in patients with the 3 types of metastatic ovarian carcinoma (p<0.05), while no significant difference in LINK-A expression was found between non-metastatic ovarian carcinoma and healthy controls (p>0.05). These data suggest that Expression[Expression[up-expression]-expression]regulation of LINK-A in ovarian tissues participates in the distant metastasis of ovarian carcinoma.	Yes	As shown in Figure 1, compared with the control groExpression[Expression[up-expression]-expression], LINK-A was significantly higher in patients with the 3 types of metastatic ovarian carcinoma (p<0.05), while no significant difference in LINK-A expression was found between non-metastatic ovarian carcinoma and healthy controls (p>0.05). In addition, LINK-A overexpression also significantly promoted migration (p<0.05, Figure 4B) and invasion (p<0.05, Figure 4C) of cancer cells. 	30912527
LINC01139	LncRNA	Homo sapiens	Diabetic Nephropathies	diabetic nephropathy tissues	Interaction[HIF1α]	qRT-PCR//ELISA//Western Blot	 The results revealed that LINK-A lncRNA and HIF1α were downregulated in patients with diabetic nephropathy, as well as in diabetic patients without complications.  LINK-A lncRNA overexpression also promoted HIF1α expression in mouse podocyte cells, while HIF1α overexpression did not significantly affect LINK-A lncRNA expression.		Yes	LINK-A lncRNA and HIF1α overexpression inhibited the apoptosis of mouse podocyte cells under a high glucose treatment.	31258644
LINC01139	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Regulation	Transfection//Wound Healing Assay//qPCR//MTT//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	LINK-A down-regulation significantly reduced cell viability, colony-forming ability and cell migration, as measured by MTT, colony formation and invasion assays. Finally, cell cycle analysis and Annexin-V/7AAD staining indicated that apoptosis was influenced by LINK-A silencing.		Yes	LINK-A down-regulation significantly reduced cell viability, colony-forming ability and cell migration, as measured by MTT, colony formation and invasion assays. Finally, cell cycle analysis and Annexin-V/7AAD staining indicated that apoptosis was influenced by LINK-A silencing.	33602983
LINC01128	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Interaction(miR-27b-3p)	qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC01128 was up-regulated in glioma tissues and cells. Silencing LINC01128 targeting miR-27b-3p inhibited the proliferation, migration, and invasion activity of glioma cells. Moreover, there was a negative correlation between LINC01128 and miR-27b-3p.		Yes	Silencing LINC01128 targeting miR-27b-3p inhibited the proliferation, migration, and invasion activity of glioma cells. Moreover, there was a negative correlation between LINC01128 and miR-27b-3p.	36382487
LINC01127	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Interaction[ERK and AKT]	Flow Cytometry//qRT-PCR//Western Blot	LINC01127 expression in ovarian cancer tissues was significantly higher than that in normal ovary tissues. LINC01127 may be involved in the development of ovarian cancer by accelerating cell cycle progression through promoting the phosphorylation of ERK and AKT.	The expression level of LINC01127 was negatively correlated with the prognosis of patients with ovarian cancer. 	Yes	Tumorigenicity assay in nude mice showed that low expression of LINC01127 inhibited the growth of ovarian tumors. 	30787997
LINC01123	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[miR-199a-5p/c-Myc axis]	qRT-PCR//RNA-seq//RIP//ChIP	 Three hundred sixty-four differentially expressed genes were identified in RNA-seq assay, and LINC01123 was one of the most overexpressed lncRNAs. Further validation in expanded NSCLC cohorts confirmed that LINC01123 was upregulated in 92 paired NSCLC tissues and associated with poor survival. Meanwhile, LINC01123 increased c-Myc mRNA expression by sponging miR-199a-5p. In addition, rescue experiments showed that LINC01123 functioned as an oncogene depending on miR-199a-5p and c-Myc.	 Further validation in expanded NSCLC cohorts confirmed that LINC01123 was upregulated in 92 paired NSCLC tissues and associated with poor survival.	Yes	Functional assays showed that LINC01123 promoted NSCLC cell proliferation and aerobic glycolysis. 	31488218
LINC01123	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	regulation[miR-625-5p/LASP1 Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results show that LINC01123 expression is abnormally elevated in CRC tissues and cell lines.The data indicate that high LINC01123 exerts its oncogenic roles by regulating the miR-625-5p/LASP1 axis in CRC progression.	High LINC01123 expression closely correlates with poor prognosis, advanced TNM stage, and lymph-node metastasis. 	Yes	 The authors also show that knockdown of LINC01123 inhibits proliferation and invasion in CRC cells. 	32423238
LINC01123	LncRNA	Homo sapiens	Colorectal Neoplasms	 colorectal cancer tumor tissues and cells	Interaction(SRSF7)	qRT-PCR//Wound Healing Assay//RNA Pull-Down//Western Blot	 LINC01123 was up-regulated in colorectal cancer tumor tissues. The proliferation, invasion and migration ability of colorectal cancer cells were decreased significantly after LINC01123 knockdown, and it may inhibit its expression by interacted with SRSF7, thereby promoting colorectal cancer progression.		Yes	The proliferation, invasion and migration ability of colorectal cancer cells were decreased significantly after LINC01123 knockdown, and it may inhibit its expression by interacted with SRSF7, thereby promoting colorectal cancer progression.	35325644
LINC01123	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-34a-5p/TUFT1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 Here, we found that the expression of LINC01123 was clearly upregulated in HCC tissues compared to nontumor tissues.  In conclusion, LINC01123 was overexpressed in HCC and accelerated cancer cell proliferation and invasion by regulating the miR-34a-5p/TUFT1 axis.		Yes	 Next, we demonstrated that LINC01123 knockdown suppressed the proliferation, migration and invasion of HCC cells in vitro. Depletion of LINC01123 inhibited HCC xenograft growth in vivo. 	32760198
LINC01123	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tumor tissues	Interaction(miR-34a-5p)	qRT-PCR//Luciferase Report Assay	The analysis results showed that LINC01123 was overexpressed in OSCC tumor tissues; also, the prognosis of patients with OSCC with high LINC01123 expression levels was poor. MiR-34a-5p was a target of LINC01123, and its inhibitor could reverse the effect of silenced LINC01123 on the progression of OSCC.	The analysis results showed that LINC01123 was overexpressed in OSCC tumor tissues; also, the prognosis of patients with OSCC with high LINC01123 expression levels was poor. 	Yes	 The knockdown of LINC01123 inhibited the proliferation, migration, and invasion of OCSS cells. 	34511356
LINC01123	LncRNA	Homo sapiens	Osteosarcoma	OS cell lines 	Interaction(miR-516b-5p/Gli1 axis)	qRT-PCR//RIP	In this study, the expression of LINC01123 was significantly upregulated in OS cell lines than in a human osteoblast cell line. Mechanistically, LINC01123 acted as a competing endogenous RNA by sponging miR-516b-5p, thus, increasing Gli1 expression by directly targeting its 3'UTR. 		Yes	Furthermore, in vitro and in vivo experiments confirmed that knockdown of LINC01123 suppressed cell progression. 	33837611
LINC01123	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Interaction(miR-214-3p/B7-H3)	Western Blot//Wound Healing Assay//Invasion Assay//Migration Assay//CCK8//FISH//qRT-PCR//Flow Cytometry//ELISA//Bioinformatics Analysis	Our results indicated that LINC01123 and B7-H3 were highly expressed in HNSCC and are associated with poor prognosis in patients. Notably, overexpression of LINC01123 or B7-H3 or downregulation of miR-214-3p inhibited the function of CD8+T cells and promoted the progression of HNSCC. Therefore, LINC01123 acts as a miR-214-3p sponge to inhibit the activation of CD8+T cells and promote the progression of HNSCC by upregulating B7-H3.	Our results indicated that LINC01123 and B7-H3 were highly expressed in HNSCC and are associated with poor prognosis in patients. 	Yes	Notably, overexpression of LINC01123 or B7-H3 or downregulation of miR-214-3p inhibited the function of CD8+T cells and promoted the progression of HNSCC. 	35115487
LINC01116	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Expression[highly expressed]	qRT-PCR//Transwell Assay	LINC01116 and lncRNA CASC11 were both upregulated in cancer tissues compared to cancer-adjacent tissues.	 Expression levels of LINC01116 and CASC11 were increased with the increase in clinical stages. 	Yes	Overexpression of LINC01116 and CASC11 led to promoted invasion and migration of gastric cancer cells.	31632064
LINC01116	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	interaction[miR-9-5p/STMN1]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	LINC01116 was expressed higher in CRC tissues and cells. 	Patients with higher expression of LINC01116 had worse prognosis. 	Yes	Knockdown of LINC01116 suppressed development of CRC cell. 	33116633
LINC01116	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	cell lines	regulation[regulates ELK3 and HOXD8 ]	RNA Pull-Down//ChIP//Western Blot//Colony Formation Assay//Flow Cytometry//qRT-PCR//FISH//IF//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	In our study, we detected that the expression of LINC01116 was boosted in BCa cells.  In conclusion, HOXD8-enhanced LINC01116 contributes to the progression of BCa via targeting ELK3 and HOXD8, which might provide new targets for treating patients with BCa.		Yes	Moreover, the results of a series of functional assays showed that LINC01116 knockdown suppressed the proliferation, migration, and invasion of BCa cells.	33311496
LINC01116	LncRNA	Homo sapiens	Glioma	 glioma tissue,cell lines	Interaction[targeted by miR-31]	qRT-PCR//Luciferase Report Assay//Transwell Assay	Linc01116 is highly expressed in glioma tissue and cells, along with low expression of miR-31, and there was a negative correlation between the expression of linc01116 and miR-31 in glioma tissue. The luciferase gene reporter system had confirmed that linc01116 targeted miR-31 and miR-31 targeted radixin in U251 cells. Moreover, radixin was downregulated and decreased E-cadherin protein expression, but increased MMP-9 and vimentin protein expression in U251 cells.	In addition, the expression of linc01116 in glioma patients with metastasis was significantly higher than that in patients without metastasis, while miR-31 was significantly lower.	Yes	In vitro and in vivo studies shown that linc01116 promoted invasion and migration of glioma cells.	31933922
LINC01116	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction(miR-744-5p/ TGF-β1)	In Vivo Experiment//cell invasion assay//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	GEO database and clinical research revealed that the expression level of LINC01116 in glioma increased, and the elevation of LINC01116 was closely related to the adverse prognosis of clinical patients. Western blot analysis and qRT-PCR analysis showed that LINC01116 regulated TGF-β1 by mediating miR-744-5p. 		Yes	 Functional experiments showed that the inhibition of LINC01116 could up-regulate miR-744-5p-mediated proliferation and metastasis of glioma cells. Finally, the analysis of animal models in vivo showed that LINC01116 could regulate the tumor growth of glioma.	34150180
LINC01116	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Cell Apoptosis Assay//Cell Cycle Assay//EdU Staining//Transwell Assay	 In this work, we found that LINC01116 was overexpressed in LUAD tissues and cell lines and that increased expression was significantly associated with worse prognoses in patients with LUAD. 	 In this work, we found that LINC01116 was overexpressed in LUAD tissues and cell lines and that increased expression was significantly associated with worse prognoses in patients with LUAD. 	Yes	 Downregulation of LINC01116 significantly inhibited cell proliferation and migration, promoted cell apoptosis, and prevented cell progression from G1 to S phase. 	32913506
LINC01116	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LAD tissues and cells	Interaction(miR-744-5p/CDCA4 axis)	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	LINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1. MiR-744-5p could bind to LINC01116. MiR-744-5p inhibitor reversed the inhibitory effects of silencing LINC01116 on LAD malignant behaviors. In addition, cell division cycle-associated protein 4 (CDCA4) shared binding sites with miR-744-5p.		Yes	LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells. 	34090440
LINC01116	LncRNA	Homo sapiens	Prostatic Neoplasms	Human prostate cancer cell lines (DU145, PC3, LNCAP, 22RV1, VCaP) and human prostate epithelial cell line (RWPE-1)	Interaction(miR-744-5p/UBE2L3 axis)	RNA Pull-Down//Western Blot//FISH//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//IF	LINC01116 was found to be highly expressed in prostate cancer cells. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. 		Yes	Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. 	33726770
LINC01116	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	SCLC tissues	Interaction(miR-93-5p/STAT3)	Transfection//qPCR//Transwell Assay//Western Blot	LINC01116 was highly expressed in SCLC and predicted poor survival. In SCLC tissues, the expression of LINC01116 was positively correlated with STAT3. Bioinformatics analysis revealed that miR-93-5p may target LINC01116. 	LINC01116 was highly expressed in SCLC and predicted poor survival. 	Yes	Overexpression of LINC01116 increased STAT3 but did not affect the expression of miR-93-5p. Transwell assay showed that LINC01116 and STAT3 increased cell invasion and migration rates. MiR-93-5p played an suppressed cell behaviors and suppressed the role of LINC01116.	33535997
LINC01128	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[Wnt/β-catenin signalling pathway]	Northern Blot//Western Blot//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay	GEO data sets analysis revealed that the expression of LINC01128 was increased in OS.  In summary, this study demonstrates that LINC01128 facilitates OS by functioning as a sponge of miR-299-3p, thus promoting MMP2 expression and activating the Wnt/β-catenin signalling pathway.		Yes	 Functional studies revealed that LINC01128 knockdown reduced the proliferation, migration and invasion of OS cells both in vitro and in vivo.	33108067
LINC01132	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC specimens	Interaction(microRNA‑431‑5p/SOX9 axis)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Herein, LINC01132 was overexpressed in EOC and was significantly associated with poor patient prognosis. Generally, LINC01132 exhibited oncogenic activities in EOC cells by regulating the outcome of the miR‑431‑5p/SOX9 axis, providing an effective target for EOC diagnosis, therapy and prognosis evaluation.	Herein, LINC01132 was overexpressed in EOC and was significantly associated with poor patient prognosis. 	Yes	Functionally, cell experiments revealed that LINC01132 depletion produced cancer?suppressive effects in EOC cells and regulated cell proliferation, migration, invasion and apoptosis in vitro. Additionally, the loss of LINC01132 attenuated tumour growth in vivo.	34132375
LINC01133	LncRNA	Homo sapiens	Endometriosis	ectopic endometriotic lesions	Expression(highly expressed)	Western Blot//Flow Cytometry//qRT-PCR//RNA-seq//Cell Proliferation Assay//Cell Cycle Assay//IF	We found that LINC01133 is upregulated in ectopic endometriotic lesions. 		Yes	 Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells.	34445100
LINC01133	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Regulation[ PI3K/AKT pathway]	qRT-PCR	We observed that LINC01133 was significantly increased in HCC cells including HepG2, Hep3B, MHCC-97L, SK-Hep-1, and MHCC-97H cells compared with the normal human liver cell line HL-7702.Taken these together, we revealed that LINC01133 contributed to HCC progression by activating the PI3K/AKT pathway.		Yes	 Knockdown of LINC01133 was able to inhibit HCC cell proliferation, cell colony formation, cell apoptosis, and blocked cell cycle arrest in the G1 phase. For another, downregulation of LINC01133 repressed HCC cell migration and invasion.	30548306
LINC01139	LncRNA	Homo sapiens	Lymphoma, Mantle-Cell	blood	Expression[highly expressed]	Cell Proliferation Assay//qRT-PCR//ELISA//Western Blot	We found that, compared with healthy controls, plasma levels of LINK-A lncRNA and survivin were significantly increased in patients with mantle cell lymphoma.		Yes	LINK-A lncRNA overexpression promoted cell proliferation, inhibited cell apoptosis, and upregulated survivin expression, while LINK-A lncRNA knockdown had the opposite effect.	30636001
LINC01138	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 A549 and H460 cells	Regulation	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 A series of in vitro experiments demonstrated that knockdown of LINC01138 dampened variability, proliferation, and motility of A549 and H460 cells. 		Yes	 A series of in vitro experiments demonstrated that knockdown of LINC01138 dampened variability, proliferation, and motility of A549 and H460 cells. 	36060239
LINC01134	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	regulation[AKT1S1 and NF-κB Signaling]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, via analyzing The Cancer Genome Atlas Liver Hepatocellular Carcinoma dataset, we identified a novel lncRNA LINC01134, which is highly expressed in HCC tissues and correlated with microvascular invasion, macrovascular invasion, recurrence, and poor overall survival of HCC patients.Taken together, these findings recognized LINC01134 as a novel oncogenic lncRNA, which indicates vascular invasion, recurrence, and poor overall survival of HCC patients. LINC01134 promotes HCC metastasis via activating AKT1S1 expression and subsequently activating NF-κB signaling. 	In this study, via analyzing The Cancer Genome Atlas Liver Hepatocellular Carcinoma dataset, we identified a novel lncRNA LINC01134, which is highly expressed in HCC tissues and correlated with microvascular invasion, macrovascular invasion, recurrence, and poor overall survival of HCC patients.	Yes	 Functional experiments revealed that ectopic expression of LINC01134 promotes HCC cell migration and invasion in vitro and HCC liver metastasis and lung metastasis in vivo. Knockdown of LINC01134 represses HCC cell migration and invasion in vitro and HCC liver metastasis and lung metastasis in vivo.	32656205
LINC01134	LncRNA	Homo sapiens	Liver Neoplasms	cell lines	Regulation(p53 )	RNA Pull-Down//Transfection//Wound Healing Assay//qRT-PCR//RNA-seq//Cell Proliferation Assay//Invasion Assay//Transwell Assay	Based on the intersection of our own RNA-seq, TCGA RNA-seq, and TCGA survival analysis data, TLNC1 was identified as a potential tumorigenic lncRNA of liver cancer.  TLNC1 exerted its tumorigenic function through interaction with TPR and inducing the TPR-mediated transportation of p53 from nucleus to cytoplasm, thus repressing the transcription of p53 target genes and finally contributing to the progression of liver cancer.		Yes	TLNC1 significantly enhanced the growth and metastasis of hepatoma cells both in vitro and in vivo. 	35477447
LINC01133	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction(miR-145-5p/YES1)	RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In the present study, we found that linc01133 was significantly upregulated in gastric cancer tissues compared to non-tumorous gastric tissues.  The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to upregulate the expression of YES1, which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 upregulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. 	 Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. 	Yes	 In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. 	35017464
LINC01133	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[regulating SOX4 expression through EZH2]	ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Transwell Assay	 In this study, we found that the LINC01133 expression was significantly down-regulated in breast cancer samples and was associated with progression and poor prognosis of breast cancer.Mechanistic investigations revealed that LINC01133 repressed SOX4 expression by recruiting EZH2 to SOX4 promoter. Moreover, rescue experiments further confirmed that LINC01133 functional acted as an anti-oncogene, at least partly, via repressing SOX4 in breast cancer. Taken together, these findings imply that LINC01133 could serve as a novel prognostic biomarker and potential therapeutic target for breast cancer.		Yes	Further experiments demonstrated that overexpression of LINC01133 inhibited invasion and metastasis in breast cancer both in vitro and in vivo.	31557401
LINC01133	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cell lines	regulation[miR-495-3p/TPD52 axis]	Western Blot//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	We found that LINC01133 was upregulated in EOC tissues and cell lines.  Generally, our study showed that LINC01133 interacted with miR-495-3p to promote metastasis in EOC by regulating TPD52. 		Yes	Functional experiments demonstrated that LINC01133 could facilitate cancer cell migration and invasion in vitro and tumor metastasis in vivo.	33036757
LINC01133	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues,cell lines	regulation[miR-30b-5p/Rab3D Axis]	qRT-PCR	The results showed that LINC01133 was highly expressed in RCC tissue specimens and cell lines.Taken together, these findings indicated that LINC01133 might be an oncogene in RCC through regulation of the miR-30b-5p/Rab3D axis. 		Yes	Downregulation of LINC01133 significantly inhibited the proliferation, migration, and invasion of RCC cells.  In vivo study showed that LINC01133 knockdown suppressed tumor growth in the nude mice. 	33054325
LINC01133	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 49 patients with HCC(WGS)	Interaction(miR-199a-5p/SNAI1)	qRT-PCR//Luciferase Report Assay//Western Blot	 Genomic copy numbers of LINC01133 were increased in HCC, which were positively related with the elevated expression of LINC01133.  LINC01133 sponged miR-199a-5p, resulting in enhanced expression of SNAI1, which induced epithelial-to-mesenchymal transition (EMT) in HCC cells. In addition, LINC01133 interacted with Annexin A2 (ANXA2) to activate the ANXA2/STAT3 signaling pathway.	 Increased copy number of LINC01133 predicted the poor prognosis in HCC patients.	Yes	LINC01133 overexpression in HCC cells promoted proliferation and aggressive phenotypes in vitro, and facilitated tumor growth and lung metastasis in vivo, whereas LINC01133 knockdown had the opposite effects. 	34047479
LINC01133	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cell lines	Interaction[binding to YBX1]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Colony Formation Assay//Transwell Assay	 In this work, we demonstrated that LINC01133 was significantly downregulated in NPC tissues and cell lines. Besides, Fluorescence in situ hybridization (FISH) assay was performed to determine the localization of LINC01133 and LINC01133 was observed mainly distributed in the nucleus. Importantly, RNA pull-down and RIP assays showed that LINC01133 directly combined with YBX1, and YBX1 can partly reverse the repression of NPC cell proliferation, migration, and invasion caused by LINC01133. Collectively, our exploration indicate that LINC01133 inhibits the malignant-biological behavior of NPC cells by binding to YBX1, thereby suggesting a novel biomarker for the NPC prognosis and treatment.		Yes	 Loss and gain of function experiments provided evidence that LINC01133 inhibited NPC cell proliferation, invasion and migration both in vitro and in vivo.	31106003
LINC01133	LncRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer tissue and cell	Interaction[LRRK2]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The findings revealed a poor expression of LINC01133 in ovarian cancer tissue and cell, which was predominantly expressed in the cytoplasm.  In conclusion, because of its role as an miR-205 sponge, LINC01133 repressed the development of ovarian cancer by up-regulating LRRK2.		Yes	LINC01133 repressed cell proliferation, invasion, migration, and tumorigenic ability.	31640854
LINC01133	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	exosomes of SV-HUC-1 and low in that of BC cells	Expression [highly expressed]	qRT-PCR//Western Blot//Transwell Assay	 We discovered that LINC01133 expression was high in exosomes of SV-HUC-1 and low in that of BC cells. Additionally, exosomes restrained cell viability, proliferation, migration, and invasion. Similarly, LINC01133 exerted the same function on BC cells. In addition, the Wnt signaling pathway could be inactivated by LINC01133.  In addition, the Wnt signaling pathway could be inactivated by LINC01133. 		Yes	Additionally, exosomes restrained cell viability, proliferation, migration, and invasion. Similarly, LINC01133 exerted the same function on BC cells. 	33728699
LINC01133	LncRNA	Homo sapiens	Endometrial Neoplasms		regulation[up-regulation]	Flow Cytometry//qRT-PCR//Transwell Assay	We first confirmed the partial knockdown of both LINC01133 and LINC01243 expression in Ishikawa and HEC-1-A cells using RT-qPCR. Following confirmation of lncRNA knockdown, we assessed the effect of knockdown on EC malignancy. 		Yes	 Furthermore, Transwell and scratch invasion assays revealed decreased migration and invasion of the two EC cell lines, respectively.	32929617
LINC01133	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma		Interaction(AXIN2/Wnt/β-catenin pathway )	qRT-PCR//ChIP	 We analyzed the expression of LINC01133 in PDAC and found that exosomal LINC01133 expression was high and positively correlated with higher TNM stage and poor overall survival rate of PDAC patients.  We subsequently evaluated the effect of LINC01133 on the Wnt/β-catenin pathway and confirmed that LINC01133 can interact with Enhancer Of Zeste Homolog 2 (EZH2) and then promote H3K27 trimethylation. This can further silence AXIN2 and suppress GSK3 activity, ultimately activating β-catenin. 	 We analyzed the expression of LINC01133 in PDAC and found that exosomal LINC01133 expression was high and positively correlated with higher TNM stage and poor overall survival rate of PDAC patients. 	Yes	We also observed that LINC01133 promoted the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of pancreatic cancer cells.	33824474
LINC01133	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cell lines	Interaction[LINCO1133/miR-4784 ]	Migration Assay//CCK8//qRT-PCR//EdU Staining//Transwell Assay	 LINC01133 expression profile was validated by digging The Cancer Genome Atlas (TCGA) database and qRT-PCR analysis. Mechanically, LINC01133 functioning as a ceRNA targeted miR-4784 to augment AHDC1 expression. Finally, LINCO1133/miR-4784 aggravated the malignant growth and aggressiveness and EMT of cervical cancer in an AHDC1-dependant way.		Yes	Apoptotic rate of cervical cancer cells was promoted after silencing LINCO1133.	31390932
LINC01133	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissue	regulation[miR-30a-5p/FOXD1]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	We observed that LINC01133 expression in CC clinical samples was significantly increased, with high expression associated with higher T stage and negative HPV infection of the patients. LINC01133 was a sponge of tumor suppressor miR-30a-5p, and it enhanced the expression of FOXD1 indirectly and functioned as an oncogenic lncRNA in CC.	We observed that LINC01133 expression in CC clinical samples was significantly increased, with high expression associated with higher T stage and negative HPV infection of the patients. 	Yes	Its overexpression remarkably accelerated proliferation and metastasis of CC cells, with reduced apoptosis. 	33078907
LINC01133	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Regulation(LINC01133-PROTOR1/PRR5 pathway)	RNA Pull-Down//Western Blot//qRT-PCR//FISH//RIP//RNA-seq//IHC	We found that LINC01133 exerted protumorigenic roles in TNBC and that it governed a previously undescribed mTOR Complex 2 (mTORC2)-dependent pathway that activated AKT in a PI3K-independent manner. Mechanistically, LINC01133 induced the expression of the mTORC2 component PROTOR1/PRR5 by competitively coupling away its negative messenger RNA (mRNA) regulator, the heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1). PROTOR1/PRR5 in turn was sufficient and necessary for LINC01133-triggered functions, casting previously unappreciated roles for this Rictor-binding protein in cellular signaling and growth. 	 Notably, LINC01133 antagonism undermined cellular growth, and we show that the LINC01133-PROTOR1/PRR5 pathway was tightly associated with TNBC poor patient survival. 	Yes	 Notably, LINC01133 antagonism undermined cellular growth, and we show that the LINC01133-PROTOR1/PRR5 pathway was tightly associated with TNBC poor patient survival. 	36269860
ELFN1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-1250)	colony Formation Assay//In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//Cell Viability Assay//Invasion Assay//Transwell Assay	First, we found that ELFN1-AS1 was highly abundant in the human CRC tissues and cell lines. 		Yes	Silence of ELFN1-AS1 expression reduced cell proliferation, colony formation, migration and invasion, while inducing apoptosis in vitro; moreover, knockdown of ELFN1-AS1 decreased the size and weight of tumor in vivo.Luciferase reporter assay revealed that ELFN1-AS1 interacted with miR-1205 and suppressed its expression. 	34337713
ELFN1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	Colon Cancer tissues and cell lines	regulation[miR-191-5p/SATB1 axis]	CCK8//qRT-PCR//EdU Staining	 Results uncovered that ELFN1-AS1 expression was prominently raised in colon cancer cells and tissues.To sum up, ELFN1-AS1 drives colon cancer cells to proliferate and invade through adjusting the miR-191-5p/SATB1 axis. 		Yes	ELFN1-AS1 decrement restrained cells to grow through interfering with distribution of cell cycle and promoting apoptosis.	33634016
MANCR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC cells and tissues	Expression(highly expressed)	Wound Healing Assay//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	 In addition, we revealed that MANCR was highly expressed in ccRCC cells and tissues and downregulation of MANCR inhibited cell proliferation and migration. In contrast, apoptosis of 786-O and SN12C cells was promoted with MANCR suppression.		Yes	 In addition, we revealed that MANCR was highly expressed in ccRCC cells and tissues and downregulation of MANCR inhibited cell proliferation and migration. In contrast, apoptosis of 786-O and SN12C cells was promoted with MANCR suppression.	36217399
hsa_circ_0001093	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	Interaction(miR-579-3p/glutaminase axis)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	Here, we found that circ_0001093 expression was up-regulated in ESCC tissues and cell lines. Mechanistically, circ_0001093 acted as a competing endogenous RNA (ceRNA) by sponging miR-579-3p, thereby increasing GLS expression. Furthermore, the inhibitory effects of circ_0001093 knockdown on the invasion, migration and glutamine metabolism were partly rescued by miR-579-3p inhibition or GLS over-expression in ESCC cells. Additionally, miR-579-3p expression was down-regulated in ESCC tissues, while GLS expression was up-regulated. 	 Increased circ_0001093 expression predicted an unfavourable prognosis, and was associated with the lymph node metastasis, TNM staging and tumor size in ESCC tissues. 	Yes	Circ_0001093 knockdown suppressed cell proliferation, invasion, migration and glutamine metabolism of ESCC cells, while circ_0001093 over-expression showed the opposite effects. 	35322289
hsa_circ_0005231	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC plasma, tissues and cells	Interaction(miR-383-5p/KIAA0101)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	Circ_0005231 was upregulated in ESCC plasma, tissues and cells.  Circ_0005231 acted as a sponge of miR-383-5p, and circ_0005231 regulated ESCC cellular behavior by sponging miR-383-5p. Moreover, miR-383-5p directly targeted KIAA0101, and circ_0005231 positively regulated KIAA0101 expression by sponging miR-383-5p. Furthermore, circ_0005231 knockdown suppressed the malignant behavior of ESCC cells by downregulating KIAA0101.		Yes	Cell proliferation, migration and invasion were significantly restrained by knockdown of circ_0005231 in ESCC cells. Importantly, knockdown of circ_0005231 blocked xenograft tumor growth in vivo.	35524161
hsa_circ_0007624	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell line	Interaction(miR-224-5p/CPEB3/EGFR/PI3K/AKT signaling)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Here, we found that circ_0007624 was significantly underexpressed in ESCC tissues, and low expression of circ_0007624 was indicative of a poor prognosis. Mechanistically, circ_0007624 could serve as a competing endogenous RNA (ceRNA) by sponging miR-224-5p to antagonize its inhibitory effect on the target cytoplasmic polyadenylation element binding protein 3 (CPEB3). Rescue experiments showed that the anti-cancer properity role of circ_0007624 in ESCC is partly reversed by the restoration of miR-224-5p or down-regulation of CPEB3. Furthermore, EGFR/PI3K/AKT pathway was involved in the regulation of circ_0007624/miR-224-5p/CPEB3 axis in ESCC. 	Here, we found that circ_0007624 was significantly underexpressed in ESCC tissues, and low expression of circ_0007624 was indicative of a poor prognosis. 	Yes	Overexpressing circ_0007624 or silencing miR-224-5p suppressed cell proliferation, metastasis, epithelial-mesenchymal transition (EMT), and promoted apoptosis in vitro. Also, circ_0007624 up-regulation slowed ESCC tumor growth in vivo.	35998761
hsa_circ_0008726	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	Interaction(miR-206/HOXA13 pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Expression of circ_0008726 was up-regulated in ESCC tissues and cells. Circ_0008726 acted as a sponge for miR-206, and HOXA13 was a target of miR-206. The suppressive effects of circ_0008726 knockdown on cell proliferation, invasion, and angiogenesis were abated by miR-206 down-regulation. Meanwhile, overexpression of HOXA13 partially reversed the suppressive effects of miR-206 enrichment on ESCC cell malignant behaviors. Knockdown of circ_0008726 inhibited ESCC tumor growth in vivo.		Yes	 Knockdown of circ_0008726 repressed proliferation, invasion, angiogenesis, and promoted apoptosis of ESCC cells.	36190650
circRUNX1	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-449b-5p/FOXP3 axis)	In Vivo Experiment//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	CircRUNX1 was found to be significantly up-regulated in ESCC tissues and associated with TNM stage and differentiation grade.CircRUNX1 enhanced FOXP3 expression by competitively sponging miR-449b-5p. Notably, both miR-449b-5p mimics and FOXP3 knockdown restored the effects of circRUNX1 overexpression on cell proliferation and metastasis. Furthermore, IGF2BP2 binding to circRUNX1 prevented its degradation.		Yes	 Functionally, circRUNX1 promoted ESCC cell proliferation and metastasis in vitro and in vivo. 	36522683
circCYP24A1	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(PKM2/ NF-κB pathway)	Wound Healing Assay//CCK8//qRT-PCR//FISH//Colony Formation Assay//Invasion Assay//Transwell Assay	 In this study, we identified circCYP24A1 in ESCC tissues by RNA sequencing, which is up-regulated in 114 cases of ESCC tissues and acts as a novel prognosis-related factor. Mechanistically, chemokine (C-Cmotif) ligand 5 (CCL5) is functional downstream mediator for circCYP24A1, which is screened by mRNA microarray. Moreover, circCYP24A1 physically interacts with M2 isoform of pyruvate kinase (PKM2). Rescue experiments showed that PKM2 knockdown partly reverses the promotional effects of circCYP24A1. It was revealed that circCYP24A1 increases secretion of CCL5 through the mechanism mainly by interacting with PKM2, an activator of NF-κB pathway, and thereby accelerate malignant progression of ESCC.		Yes	Moreover, circCYP24A1 promoted the ability of proliferation, migration, invasion and clone formation in vitro, as well as tumor growth in vivo. 	36514094
circHIPK3	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(microRNA-124/AKT3)	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The results showed that the expression of circHIPK3 was considerably higher in tumor tissues from ESCC patients than that of adjacent tissues, which was associated with a poor prognosis. Mechanistically, we discovered that circHIPK3 behaved like a sponge, absorbing microRNA-124 (miR-124) and promoting serine/threonine kinase 3 (AKT3) expression. Our findings indicate that circHIPK3 acts as an oncogene in ESCC and that the circHIPK3-AKT3 axis may be a therapeutic target for patients with ESCC.	The results showed that the expression of circHIPK3 was considerably higher in tumor tissues from ESCC patients than that of adjacent tissues, which was associated with a poor prognosis.	Yes	Additionally, silencing of circHIPK3 expression retarded esophageal cancer cell proliferation, migration and epithelial-mesenchymal transition (EMT) in vitro, as well as the growth in vivo. 	35443871
hsa_circ_0001741	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-491-5p/NOTCH3 )	RNA Pull-Down//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//Transwell Assay	We found that hsa_circ_0001741 was upregulated in ESCC tissues and was positively related to lymphatic metastasis, higher TNM stage, and poor prognosis. Mechanistically, analysis of the relationship between hsa_circ_0001741 and tumor suppressor miR-491-5p revealed that hsa_circ_0001741 functioned as a miR-491-5p sponge. Specifically, hsa_circ_0001741 bound to miR-491-5p to prevent the microRNA from binding to the 3'-UTR of NOTCH3 mRNA and suppressing NOTCH3 expression. Moreover, the ablation of hsa_circ_0001741 significantly inhibited the tumorigenicity in vivo. 	We found that hsa_circ_0001741 was upregulated in ESCC tissues and was positively related to lymphatic metastasis, higher TNM stage, and poor prognosis.	Yes	 Functionally, hsa_circ_0001741 promoted ESCC cell stemness, invasion, and migration in vitro. 	35693080
hsa_circ_0046264	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues	interaction[hsa-miR-1245]	Flow Cytometry//qRT-PCR//MTT//Western Blot	Hsa_circ_0046264 and BRCA2 were down-regulated in lung cancer tissues while miR-1245 was up-regulated. Overexpression of hsa_circ_0046264 could up-regulate BRCA2 expression through down-regulating of miR-1245.		Yes	 Hsa_circ_0046264 inhibited the tumor growth in vivo.	29891014
hsa_circ_0007059	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissuesand the adjacent non-tumor tissues	 Interaction[inhibiting microRNA-378]	CCK8//qRT-PCR//Western Blot	Results in Fig. 1A revealed that hsa_circ_0007059 expression was clearly repressed in lung cancer tissue as contrasted to that in the adjacent tissues (P < 0.001). The investigations manifested that hsa_circ_0007059 abated cell proliferation and EMT process in lung cancer cells via inactivation of Wnt/β-catenin and ERK1/2 pathways via suppressing miR-378.	 	Yes	Overexpressed hsa_circ_0007059 evidently restrained cell proliferation, elevated p53 and repressed CyclinD1 expression, meanwhile triggered apoptosis and enhanced Bax and Cleaved-Caspase-3 expression. 	31351967
circHIPK3	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cells	regulation[AKT/mTOR signaling pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	CircHIPK3 was upregulated, while miR-381-3p was downregulated in lung cancer tissues and cells. In conclusion, the silencing of circHIPK3 inhibited lung cancer progression, at least in part, by sponging miR-381-3p and inactivating the AKT/mTOR signaling pathway.		Yes	And circHIPK3 deficiency inhibited lung cancer progression by lowering cell proliferation, migration, glycolysis, and promoting apoptosis of lung cancer cells in vitro.	33817257
circCCS	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues 	regulation[miR-383/E2F7 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-CCS was upregulated in lung cancer and could predict poor prognosis.Circ-CCS was shown to facilitate lung cancer progression via the miR-383/E2F7 axis, exhibiting the pivotal value of circ-CCS in diagnosis and treatment of lung cancer.	Circ-CCS was upregulated in lung cancer and could predict poor prognosis.	Yes	Downregulation of circ-CCS inhibited lung cancer cell growth and metastasis while promoted apoptosis in vitro, and suppressed tumorigenesis of lung cancer in vivo.	33359669
circPRKCI	CircRNA	Homo sapiens	Lung Neoplasms	LCa tumor tissues and cell lines	regulation[microRNA-150-5p/MECP2 axis]	CCK8//qRT-PCR//Transwell Assay	Circ-PRKCI level was remarkably elevated in LCa tumor tissues and cell lines.Our study shows for the first time that circ-PRKCI modulates the progression of LCa through microRNA-150-5p/MECP2 axis.	At the same time, highly expressed circ-PRKCI was correlated with the poor prognosis of LCa patients. 	Yes	In vitro cell experiments revealed that inhibition of circ-PRKCI in LCa cell lines remarkably inhibited cell invasiveness and proliferation.	33155212
hsa_circ_0001421	CircRNA	Homo sapiens	Lung Neoplasms	LC tissues and cells	regulation[miR-4677-3p/CDCA3]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Circ_0001421 was increased in LC tissues and cells,Circ_0001421 promoted cell proliferation, migration, invasion and glycolysis in LC by regulating the miR-4677-3p/CDCA3 axis, which providing a new mechanism for LC tumor progression.		Yes	Circ_0001421 was increased in LC tissues and cells, and knockdown of circ_0001421 repressed cell proliferation, migration, invasion and glycolysis in vitro.Meanwhile, circ_0001421 knockdown inhibited LC tumor growth in vivo. 	33109222
hsa_circ_0046264	CircRNA	Homo sapiens	Lung Neoplasms	NSCLC tissues	Expression[highly expressed]	Wound Healing Assay//CCK8//qRT-PCR//Microarray//Transwell Assay	It was shown in the results of gene microarray assay that hsa_circ_0046264 was the most prominently upregulated gene, and RT-qPCR assay further proved that hsa_circ_0046264 expression was upregulated remarkably in the tissues of tumor patients.	Clinical analysis indicated that the expression level of hsa_circ_0046264 was notably associated with the patient's age, tumor size, tumor-node-metastasis (TNM) stage, and lymph node metastasis (p<0.01). In addition, Kaplan-Meier statistical analysis manifested that the patients in hsa_circ_0046264 low-expression group had a markedly longer survival than those in hsa_circ_0046264 high-expression group.	Yes	 According to the results of wound-healing assay, the migratory ability of A549 cells was distinctly strengthened in hsa_circ_0046264 overexpression group compared with that in the control group (p<0.05). Moreover, the transwell assay results pointed out that the invasive ability of A549 cell lines at 48 h after overexpression of hsa_circ_0046264 was evidently stronger than that in control group (p<0.05). Under the stimulation of different doses of cisplatin, hsa_circ_0046264 overexpression group had a clearly raised survival rate of A549 cells in comparison with control group, and the differences in data were statistically significant (p<0.01).	33015793
hsa_circ_010763	CircRNA	Homo sapiens	Lung Neoplasms	NSCLC tissues and cells	regulation[miR-715,c-Myc]	CCK8//qRT-PCR//Luciferase Report Assay	We found that both circRNA_010763 and c-Myc were upregulated in human NSCLC tissues and cells.  In this study, we found that circRNA_010763 was highly expressed in human NSCLC tissues, which could promote tumor proliferation, migration and invasion through serving as a molecular sponge by modulating the inhibitory effect of miR-715 on oncogene c-Myc.		Yes	qRT-PCR and CCK-8 assay showed that circRNA_010763 expression is associated with the proliferation of NSCLC cells. Transwell assay showed that circRNA_010763 regulated the migration ability of NSCLC cells. 	32706069
circFOXP1	CircRNA	Homo sapiens	Lung Neoplasms	 LUAD tissues and LUAD cell lines	regulation[miR-185-5p/Wnt1 signaling pathway]	Tunel//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	The circFOXP1 expression was increased in LUAD patients and LUAD cell lines. These data suggested that circFOXP1 promoted cell proliferation and repressed cell apoptosis in LUAD by regulating miR-185-5p/WNT1 signaling pathway.		Yes	The downregulation of circFOXP1 significantly repressed LUAD cell proliferation and promoted cell apoptosis. 	32633368
circABCB10	CircRNA	Homo sapiens	Lung Neoplasms	 LCa tissues and cell lines	regulation[microRNA-217 expression]	CCK8//qRT-PCR//Luciferase Report Assay	CircABCB10 showed abnormally high expression in LCa tissues and cell lines and was related to the poor prognosis of patients.Finally, cell functional experiments showed that microRNA-217 is a key downstream gene that mediates the regulation of circABCB10 on LCa cell function.	CircABCB10 showed abnormally high expression in LCa tissues and cell lines and was related to the poor prognosis of patients.	Yes	In vitro cell experiments demonstrated that knocking down circABCB10 remarkably suppressed the proliferation and migration ability of LCa cells.	32572881
circPOLA2	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	regulation[miR-326/GNB1 axis]	qRT-PCR	 Circ_POLA2 was highly expressed in lung cancer tissues and predicted a poor prognosis in lung cancer patients.In conclusion, circ_POLA2 promotes lung cancer cell stemness and progression via regulating the miR-326/GNB1 axis, which might serve as a novel therapeutic target for lung cancer patients.		Yes	Knockdown of circ_POLA2 inhibited the stemness of lung cancer cells, which is evident by the decreased sphere-formation ability, ALDH1 activity, and stemness marker expression, but had no effects on cell viability. 	32511866
circZFR	CircRNA	Homo sapiens	Lung Neoplasms	LC tumors	regulation[circZFR/CCND1 signaling]	ISH//qRT-PCR	CircRNA circZFR was highly expressed in LC tumors. The possible mechanism was to regulating expression of CCND1, indicating the circZFR/CCND1 signaling might be a promising therapeutic target for LC treatment.		Yes	CircZFR depletion substantially decreased tumor growth compared to WT control cells. CircZFR overexpression was dramatically increased cell growth in LC cell lines. Consequently, circZFR overexpression substantially promoted tumor propagation. 	35117697
circLPAR3	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-873-5p/LDHA axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//Colony Formation Assay//EdU Staining//Transwell Assay	 CircLPAR3 is a stable circRNA and was increased in ESCC tissues and cells. Mechanistically, circLPAR3 served as a sponge for miR-873-5p, which targeted LDHA. Moreover, circLPAR3 could regulate LDHA expression by sponging miR-873-5p. Thereafter, rescue experiments suggested that miR-873-5p inhibition reversed the anticancer effects of circLPAR3 silencing on ESCC cells. Furthermore, miR-873-5p overexpression restrained ESCC cell Warburg effect and oncogenic phenotypes, which were abolished by LDHA up-regulation.		Yes	circLPAR3 knockdown suppressed ESCC cell Warburg effect, proliferation, metastasis, and induced apoptosis in vitro, and impeded xenograft tumor growth and Warburg effect in ESCC mice models.	36484173
hsa_circ_0000277	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC cells and tissues	Interaction(miR-873-5p/SOX4 axis )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 Hsa_circ_0000277 expression was increased in ESCC cells and tissues, and it had important clinical significance. Hsa_circ_0000277 acted as a microRNA-873-5p (miR-873-5p) sponge and Sry-related high-mobility group box 4 (SOX4) was validated as a target of miR-873-5p. Moreover, hsa_circ_0000277/miR-873-5p axis and miR-873-5p/SOX4 axis regulated ESCC cell progression and DDP resistance. Hsa_circ_0000277/miR-873-5p axis activated SOX4/Wnt/β-catenin signaling pathway. Hsa_circ_0000277 facilitated tumorigenesis and DDP resistance by miR-873-5p/SOX4 axis in vivo.		Yes	Downregulation of hsa_circ_0000277 repressed ESCC cell proliferation, colony formation, cell cycle, and DDP resistance.	35241028
hsa_circ_0030998	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues 	Interaction(miR-558)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In a previous study, hsa_circ_0030998 was identified as a circRNA downregulated in lung cancer, but its potential implications and mechanisms in lung cancer were not addressed. Here, we showed that overexpressing circ_0030998 decreased proliferation, migration, and invasion of lung cancer cells, while also dampening resistance to Taxol, a classical antitumor drug. 	 A high circ_0030998 expression was correlated with a high survival rate in lung cancer patients. 	Yes	 Here, we showed that overexpressing circ_0030998 decreased proliferation, migration, and invasion of lung cancer cells, while also dampening resistance to Taxol, a classical antitumor drug. Depleting circ_0030998 reversed these phenotypic effects. 	33190405
hsa_circ_0003823	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-607/CRISP3 Axis)	CCK8//qRT-PCR//Western Blot	Our results revealed that hsa_circ_0003823 was highly expressed in ESCC and associated with poor prognosis.In the section of mechanism experiments, hsa_circ_0003823 regulated CRISP3 by targeting microRNA-607 (miR-607) to promote progression of ESCC. 		Yes	Further results indicated that hsa_circ_0003823 promoted proliferation and metastasis ability of ESCC. 	36263172
circIMMP2L	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC patients and LNM patients	Expression [highly expressed]	qRT-PCR//RIP	 CircIMMP2L, commonly upregulated in tumor and plasma from advanced-stage ESCC patients and LNM patients, predicts poorer patient survival. CircIMMP2L was also found to be a significant indicator for LNM, even in the T1 stage of ESCC. Mechanistically, cytoplasmic circIMMP2L interacted with CtBP1 and facilitated the nuclear retention of CtBP1 in a CtBP2-independent manner.	 CircIMMP2L, commonly upregulated in tumor and plasma from advanced-stage ESCC patients and LNM patients, predicts poorer patient survival. 	Yes	CircIMMP2L depletion suppressed the malignant progression of ESCC both in vitro and in vivo. 	34586741
circRIMS	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Interaction(miR-613)	qRT-PCR//Western Blot//Luciferase Report Assay//FISH	We found that CircRIMS was overexpressed in ESCC and predicted poor survival. In addition, miR-613 was under expressed in ESCC and inversely correlated with CircRIMS. In ESCC cells, CircRIMS overexpression decreased the expression of miR-613 and increased the methylation of miR-613 gene.	We found that CircRIMS was overexpressed in ESCC and predicted poor survival. 	Yes	Cell proliferation assay showed that CircRIMS overexpression reduced the inhibitory effects of miR-613 overexpression on cell proliferation. Animal experience finally illustrated that CircRNA CircRIMS downregulated miR-613 through methylation to promote tumor growth.	34135635
hsa_circ_0014715	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	esophageal squamous cell carcinoma tissues and cell lines	Expression(highly expressed)	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	We found that circ_0014715 was highly expressed in esophageal squamous cell carcinoma tissues and cell lines.	The correlation analysis of clinicopathological features and gene expression revealed that high expression of circ_0014715 was related to nerve invasion, vascular invasion, more advanced tumor-node-metastasis (TNM) stage and poor differentiation grade. 	Yes	Experiments with cultured cells showed that knockdown of circ_0014715 significantly restrained cell proliferation, migration, invasion, wound healing and accelerated cell apoptosis. And cell cycle arrest at G2 phase was observed via flow cytometry. Overexpression of circ_0014715 caused the opposite effects. 	34163248
hsa_circ_2646	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction(miR-124/PLP2 signaling pathway)	CCK8//qRT-PCR//Western Blot	We found that CircRNA_2646 was up-regulated in ESCC, negatively correlated with the expression of miR-124 and positively associated with TNM stage and lymph node metastasis of ESCC.  Luciferase reporter assay showed that CircRNA_2646 interacted with miR-124 in ESCC Eca109 and TE-1 cells. Furthermore, it was found that the oncogene Proteolipid Protein 2 (PLP2) was the target gene of miR-124. In Eca109 and TE-1 cells, restoration of miR-124 decreased the level of PLP2 and inhibited PLP2-induced cell proliferation, migration, invasion, and EMT, but enhanced cell apoptosis.	We found that CircRNA_2646 was up-regulated in ESCC, negatively correlated with the expression of miR-124 and positively associated with TNM stage and lymph node metastasis of ESCC. 	Yes	Moreover, ectopical overexpression of CircRNA_2646 accelerated cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT), but restoration of miR-124 abrogated these functions and promoted Bcl-2-dependent cell apoptosis.The in vivo study confirmed that CircRNA_2646 promoted ESCC development by repressing miR-124 and activating PLP2. 	33976115
hsa_circ_0087378	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 patients with ESCC	Interaction(miR-140-3p/E2F3 Axis)	CCK8//qRT-PCR//RIP//Western Blot	 We demonstrated that upregulated circ_0087378 expression was positively associated with tumor size, histological grade, tumor stage, the presence of metastasis, and worse survival in patients with ESCC. Mechanistically, we showed that circ_0087378 could directly bind to miR-miR-140-3p and relieve the suppression for target E2F3, which accelerated cell proliferation, migration, and invasion. Correlation analysis in ESCC specimens supported the involvement of the circ_0087378/miR-140-3p/E2F3 axis in ESCC progression.	We demonstrated that upregulated circ_0087378 expression was positively associated with tumor size, histological grade, tumor stage, the presence of metastasis, and worse survival in patients with ESCC. 	Yes	Our results further revealed that knockdown of circ_0087378 suppressed the proliferation, migration, and invasion of ESCC cells and reduced tumor growth in vivo. 	33680929
circNRIP1	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	Interaction(miR-595/SEMA4D axis and PI3K/AKT pathway)	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Expression of circ_NRIP1 was upregulated in ESCC tissues and cells.  The suppressive role of circ_NRIP1 knockdown in cell growth, migration and invasion in vitro was abated by blocking miR-595; meanwhile, miR-595 overexpression elicited similar anti-tumor role in KYSE30 and KYSE450 cells, which was abrogated by restoring SEMA4D. Notably, circ_NRIP1 was a sponge for miR-595, and SEMA4D was a target of miR-595. Besides, PI3K/AKT signal was inhibited by circ_NRIP1 knockdown and/or miR-595 overexpression via indirectly or directly regulating SEMA4D.		Yes	Knockdown of circ_NRIP1 could enhance apoptosis rate and E-cadherin expression, but suppress colony formation, cell viability, migration, invasion, and snail expression in KYSE30 and KYSE450 cells, as well as retarded tumor growth in mice. 	33957921
circDOCK5	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Interaction(miR-627-3p/TGFB2 signaling)	CCK8//qRT-PCR	"Tissue microarray analysis identified circ-DOCK5 to be downregulated in ESCC tissues, and its downregulation correlated with poor prognosis. circ-DOCK5 increased the stability of miR-627-3p by functioning as a ""reservoir"" for miR-627-3p to partially reverse the ZEB1-enhanced migration and invasion in ESCC. MiR-627-3p inhibited the expression of TGFB2 and the secretion of TGF-β, which further resulted in downregulation of ZEB1 and suppression of TGF-β-induced EMT. In vivo experiments showed that ZEB1 promoted metastasis in ESCC by regulating expression of circ-DOCK5. Therefore, the present study revealed that ZEB1-mediated downregulation of circ-DOCK5 facilitates metastasis in ESCC by forming a positive feedback loop with TGF-β by altering the miR-627-3p/TGFB2 signaling."	Tissue microarray analysis identified circ-DOCK5 to be downregulated in ESCC tissues, and its downregulation correlated with poor prognosis. 	Yes	In vivo experiments showed that ZEB1 promoted metastasis in ESCC by regulating expression of circ-DOCK5. Therefore, the present study revealed that ZEB1-mediated downregulation of circ-DOCK5 facilitates metastasis in ESCC by forming a positive feedback loop with TGF-β by altering the miR-627-3p/TGFB2 signaling.	34216686
hsa_circ_0006948	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(microRNA-3612/LASP1 Axis)	CCK8//qRT-PCR	Circ_0006948 and LASP1 were increased, and miR-3612 was decreased in ESCC tissues and cells. Mechanically, circ_0006948 could act as a sponge of miR-3612 to regulate LASP1 expression. In addition, circ_0006948 silencing inhibited ESCC tumor growth in vivo.		Yes	Furthermore, circ_0006948 knockdown could suppress cell viability, colony number, migration, invasion, glycolysis, and boost apoptosis in ESCC cells.	34024023
hsa_circ_0000700	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC cell lines	Interaction(miR-1229)	CCK8//qRT-PCR//Western Blot	circ_0000700 expression was significantly upregulated in ESCC cell lines. Mechanistically, circ_0000700 was identified as a sponge of miR-1229 and could activate PRRG4, REEP5, and PSMB5 indirectly to promote ESCC progression.		Yes	 In vitro, the proliferative and migratory capacities of ECA-109 and TE-1 cells were inhibited by knocking down circ_0000700 expression.	33854621
circDUSP16	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues, cells,	Interaction(miR-497-5p/TKTL1 Axis)	CCK8//qRT-PCR	 CircDUSP16 level was elevated in ESCC tissues, cells, and hypoxia-stimulated ESCC cells.CircDUSP16 knockdown suppressed hypoxia-induced ESCC cell growth, invasion, and glycolysis by regulating TKTL1 expression through sponging miR-497-5p.		Yes	Knockdown of circDUSP16 suppressed hypoxia-induced ESCC cell viability, colony formation, migration, invasion, and glycolysis. 	33326930
hsa_circ_0001821	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells	Interaction(RUNX3/circ_0001821/NF-κB)	Other	Based on the collected data, circ_0001821 was highly expressed in ESCC cells.  With regard to its mechanism, RUNX3 promoted PVT1 transcription, further upregulating circ_0001821. Moreover, circ_0001821 sponged miR-423-5p to upregulate BTRC, thus promoting IKBA ubiquitination, and circ_0001821 decreased IKBA expression to activate NF-κB signaling pathway. 		Yes	Circ_0001821 knockdown retarded ESCC cell proliferation and tumor growth, while promoting G2-M cell cycle arrest. 	35913453
circATIC	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction( miR-326/ID1 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-ATIC was found to be upregulated in ESCC tissues and cells.  Furthermore, we found that circ-ATIC could sponge miR-326, and miR-326 could target ID1. The rescue experiments revealed that miR-326 inhibitor could reverse the negative regulation of circ-ATIC silencing on ESCC progression, and ID1 overexpression also inverted the inhibitory effect of miR-326 on ESCC progression. In addition, we confirmed that the expression of ID1 was positively regulated by circ-ATIC. 		Yes	Silenced circ-ATIC suppressed the proliferation, migration, invasion, promoted the apoptosis and oxidative stress of ESCC cells. The tumor growth of ESCC also was inhibited by circ-ATIC knockdown. 	35064360
circARAP2	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	Interaction(miR-761/FOXM1 axis)	CCK8//qRT-PCR	 The result of the expression profile analyses regarding human circRNAs in ESCC demonstrated that circ-ARAP2 was up-regulated significantly in both ESCC tissues and cell lines.  The data also suggested that miR-761 and FOXM1 were circ-ARAP2 downstream targets which were confirmed through luciferase reporter analysis. 		Yes	 Downregulation circ-ARAP2 suppressed ESCC proliferation, tumor growth and metastasis in both in vivo and in vitro.  Overexpression of FOXM1 or inhibiting miR-761 restored ESCC cell proliferation and invasion ability after silencing circ-ARAP2. The study also found that circ-ARAP2 influenced the endothelial-mesenchymal transition (EMT) and cancer stem cells differently by regulating miR-761/FOXM1.	35842667
circAGFG1	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	Interaction(miR-497-5p/SLC1A5 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 Circ-AGFG1 expression was upregulated in ESCC tissues and cell lines.  Circ-AGFG1 acted as a sponge for miR-497-5p, and miR-497-5p interacted with the 3' untranslated region (3'UTR) of SLC1A5. miR-497-5p silencing largely abolished circ-AGFG1 silencing-induced effects in ESCC cells. miR-497-5p overexpression-mediated influences in ESCC cells were largely reversed by the addition of SLC1A5 expressing plasmid. Circ-AGFG1 could upregulate SLC1A5 expression by sponging miR-497-5p. 		Yes	 Circ-AGFG1 silencing suppressed the proliferation, migration, invasion and glutaminolysis and triggered the apoptosis of ESCC cells. Circ-AGFG1 knockdown significantly slowed down tumor growth in vivo .	36206112
circADAMTS6	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(AGR2/Hippo)	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//FISH//Colony Formation Assay//Transwell Assay	 We assessed circADAMTS6 expression in ESCC tissues and cells, and the relationship between circADAMTS6 expression and overall survival of ESCC patients.  Induced AGR2 expression was able to rescue the loss of function induced by si-circADAMTS6 in KYSE150 cell. CircADAMTS6 may acts as oncogene by activating AGR2 and the Hippo signaling pathway coactivator YAP in ESCC.	Results found that up-regulation of circADAMTS6 was associated with poor overall survival and may acted as an independent risk factor for ESCC prognosis.	Yes	Knockdown of circADAMTS6 significantly inhibited the proliferation, migration and invasion of ESCC cells and growth of xenograft tumors in vivo. 	35962061
circFAM120B	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cancer tissues and patient plasma	Interaction(miR-661/PPM1L axis and the PKR/p38 MAPK/EMT pathway)	RNA Pull-Down//Western Blot//Invasion Assay//Co-IP//Migration Assay//CCK8//qRT-PCR//FISH//RIP//RNA-seq//Luciferase Report Assay//Colony Formation Assay//EdU Staining	 We observed that circFAM120B (hsa_circ_0001666) was frequently downregulated in cancer tissues and patient plasma, and its expression level was related to overall survival in ESCC patients.Mechanistically, circFAM120B was predominantly located in the cytoplasm, guarantying its sponging for miR-661 to restore the expression of PPM1L, a tumor suppressor. 	 We observed that circFAM120B (hsa_circ_0001666) was frequently downregulated in cancer tissues and patient plasma, and its expression level was related to overall survival in ESCC patients.	Yes	Overexpression of circFAM120B inhibited the proliferation, metastasis, and invasion of ESCC while silencing it enhanced malignant phenotypes. 	35436983
circPUM1	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cell lines	Interaction(esophageal squamous cell carcinoma)	CCK8//qRT-PCR//RNA Pull-Down	The expression level of circPUM1 is positively correlated with HIF1α accumulation under CoCl2-induced intracellular hypoxic-like condition in esophageal squamous cell carcinoma (ESCC) cell lines. Importantly, circPUM1 acts as a scaffold for the interaction between UQCRC1 and UQCRC2 in ESCC cell lines. 		Yes	Knock-down of circPUM1 would result in lower intracellular oxygen concentration, downregulated oxidative phosphorylation, decrease of mitochondrial membrane potential, increase of ROS generation and shrinking of mitochondria, respectively. CircPUM1 depletion induces dysfunction of the mitochondrial complex III and the cleavage of caspase3 spontaneously. Interestingly, disruption of circPUM1 led to pyroptosis that initiates the cell death of ESCC cell lines. 	35153295
hsa_circ_0003340	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-940/PRKAA1 axis)	CCK8//qRT-PCR//Western Blot	Upregulated circ_0003340 and PRKAA1, and downregulated miR-940 levels were detected in ESCC.Circ_0003340 acted as a ceRNA for miR-940 in regulating ESCC progression and miR-940 was proved to target PRKAA1 to arrest ESCC progression in vitro. 		Yes	Meanwhile, ESCC progression was apparently restrained by circ_0003340 knockdown in vitro.Finally, in vivo experiments established that silencing of circ_0003340 slowed tumor growth in vivo.	35297212
hsa_circ_0023984	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC patients and cells	Interaction(miR-134-5p/cystatin-s axis)	CCK8//qRT-PCR//Western Blot	We found that ESCC patients with high circ_0023984 expression was associated with a poor prognosis. Circ_0023984 interacted with miR-134-5p and inhibited its activity, which promoted the expression of CST4 (Cystatin-S). Circ_0023984 also regulated tumorigenesis in a CST4-dependent manner. Together, our study indicates that the oncogenic role of Circ_0023984 is mediated by miR-134-5p/CST4 Axis in ESCC, which could serve as potential targets for future therapeutic strategies.	We found that ESCC patients with high circ_0023984 expression was associated with a poor prognosis. 	Yes	The knockdown of circ_0023984 suppressed cell growth, invasion, and migration in ESCC cells. 	35440286
hsa_circ_0012673	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	regulation[miR-320a/LIMK18521 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Circ_0012673 was overexpressed in lung cancer tissues and cell lines.Circ_0012673 was a tumor-promoter in lung cancer via acting as competing endogenous RNA to regulate LIMK1 expression by binding miR-320a.		Yes	Loss-of-functional experiment confirmed that knockdown of circ_0012673 constrained proliferation, motility and Epithelial-Mesenchymal Transition (EMT), but induced apoptosis by targeting miR-320a. 	32141553
circZNF609	CircRNA	Homo sapiens	Lung Neoplasms	cell lines	Interaction(miR-142-3p)	In Vivo Experiment//Migration Assay//CCK8//FISH//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	In current work, it was discovered that circZNF609 functioned as an onco-circRNA, which exhibited high expression as well as facilitated the proliferation and migration in LC cells. Next, we discovered that FUS RNA-binding 		Yes	circZNF609 is oncogenic and regulates proliferation, migration, and apoptosis in LC cells. (	33459380
circErbin	CircRNA	Homo sapiens	Colorectal Neoplasms	cell line	regulation[miR-125a-5p-5p/miR-138-5p/4EBP-1 axis]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Circ-Erbin was highly expressed in the CRC cells and Circ-Erbin overexpression facilitated the proliferation, migration and metastasis of CRC in vitro and in vivo.Our findings uncover a key mechanism for circ-Erbin mediated HIF-1α activation by miR-125a-5p-5p/miR-138-5p/4EBP-1 axis and circ-ERBIN is a potential target for CRC treatment.		Yes	Circ-Erbin was highly expressed in the CRC cells and Circ-Erbin overexpression facilitated the proliferation, migration and metastasis of CRC in vitro and in vivo.	33225938
circITGA7	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[ITGA7]	qRT-PCR	 In this study, we demonstrated that a novel circRNA (circITGA7) and its linear host gene ITGA7 are both significantly downregulated in colorectal cancer (CRC) tissues and cell lines. Mechanistically, by using RNA-sequencing and KEGG enrichment analysis, we found that circITGA7 is a negative regulator of the Ras signalling pathway, and that ITGA7 is associated with cytokine-related signalling pathways.		Yes	 Functional assays demonstrated that ectopic circITGA7 expression suppressed the growth and metastasis of CRC cells in vitro and in vivo. Knockdown of circITGA7 or ITGA7 promoted the proliferation and migration of CRC cells in vitro, and enhanced CRC growth in vivo.	29943828
hsa_circ_0009361	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues,cell lines 	Interaction[hsa_circ_0009361/miR-582/APC2]	qRT-PCR//RIP//FISH	n the present study, hsa_circ_0009361 was significantly Expression[down-expression]-regulated in CRC tissues and cells.Hsa_circ_0009361 was identified as the sponge of miR-582 by fluorescence in situ hybridization (FISH), RNA immunoprecipitation (RIP), and luciferase reporter assays.Overexpression of hsa_circ_0009361 Expression[Expression[up-expression]-expression]-regulated the expression of adenomatous polyposis coli 2 (APC2) and inhibited the activity of the Wnt/β-catenin pathway by competitively combining with miR-582. Exogenous miR-582 and APC2 interventions could reverse the multiple biological functions mediated by hsa_circ_0009361 in CRC cells. In vivo experiments also confirmed that hsa_circ_0009361 inhibited the growth and metastasis of CRC. Hsa_circ_0009361 acted as a tumor sExpression[Expression[up-expression]-expression]pressive sponge of miR-582, which could Expression[Expression[up-expression]-expression]-regulate the expression of APC2, inhibit the Wnt/β-catenin signaling, and sExpression[Expression[up-expression]-expression]press the growth and metastasis of CRC.		Yes	Low expression level of hsa_circ_0009361 promoted the proliferation, epithelial-mesenchymal transition (EMT), migration, and invasion of CRC cells.	31109967
hsa_circ_0026344	CircRNA	Homo sapiens	Colorectal Neoplasms	 cell lines (SW480 and Caco-2) 	Interaction[ miR-183]	qRT-PCR//Western Blot//Transwell Assay	CCL20 and CXCL8 synergized to facilitate the proliferation, migration and invasion of CRC cells. At the meantime, E-cadherin was downregulated, whereas N-cadherin, Vimentin and Snail were up-regulated by CCL20 and CXCL8 co-stimulation, which was accompanied by the mobilization of PI3K/AKT/ERK signalling. More interestingly, the expression of circ_0026344 was down-regulated by CCL20 and CXCL8 co-stimulation. Silence of circ_0026344 increased the migratory and invasive capacities of CRC cells and increased EMT process as well. Overexpression of circ_0026344 led to a contrary impact. miR-183 was negatively regulated by circ_0026344, and the inhibitory effects of circ_0026344 overexpression on Wnt/β-catenin pathway were reversed when miR-183 was overexpressed. 		Yes	Silence of circ_0026344 increased the migratory and invasive capacities of CRC cells and increased EMT process as well. Overexpression of circ_0026344 led to a contrary impact. 	31608699
circFMN2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[miR-1182/hTERT signaling pathways]	qRT-PCR//Luciferase Report Assay	 circFMN2 was found to be significantly up-regulated in CRC tissues and cell lines. Bioinformatics analysis predicted that there is a circFMN2/miR-1182/hTERT axis in CRC progression. Dual-luciferase reporter system validated the direct interaction of circFMN2, miR-1182, hTERT. Western blot verified that inhibition of circFMN2 decreased hTERT expression. Importantly, we demonstrated that circFMN2 was up-regulated in serum exosomes from CRC patients.		Yes	Moreover, knockdown of circFMN2 significantly inhibited cell proliferation and migration in vitro. 	31738400
circVAPA	CircRNA	Homo sapiens	Colorectal Neoplasms	blood	Interaction[sponging miR-101]	qRT-PCR//Luciferase Report Assay//RNA-seq	Using quantitative real-time polymerase chain reaction (qRT-PCR), circVAPA was found to be up-regulated in CRC patients' tissues and plasma.  Luciferase reporter assay confirmed a direct interaction between circVAPA and miR-101. Furthermore, circVAPA had no effect on the expression level of miR-101, and miR-101 over-expression had the similar tumor-suppressing effects as circVAPA silencing. The tumor-promoting effect of circVAPA over-expression could be reversed by the up-regulation of miR-101. 		Yes	Gain-of-function and loss-of-function studies in CRC cell lines indicated that circVAPA could promote CRC cell proliferation, migration, invasion, and inhibit apoptosis.	30797148
hsa_circ_0136666	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[miR-136/SH2B1 axis]	qRT-PCR	In the present study, through circRNA high-throughput sequencing and quantitative real-time polymerase chain reaction, we identified that hsa_circ_0136666 was significantly overexpressed in CRC tissues and cell lines.Mechanistically, we revealed that hsa_circ_0136666 could increase SH2B1 expression via competitively binding miR-136 in CRC cells. In addition, SH2B1 overexpression could reverse the effects of hsa_circ_0136666 inhibition on CRC cell progression. In conclusion, our data suggested that hsa_circ_0136666 could promote CRC cell progression via the miR-136/SH2B1 axis, elucidating a novel approach to improve the effectiveness of CRC treatment.	 High hsa_circ_0136666 expression was associated with poor overall survival of patients with CRC. 	Yes	In vitro function assays showed that hsa_circ_0136666 inhibition suppressed CRC cell proliferation, migration, invasion, and arrested CRC cells in the G0/G1 phase. Furthermore, we showed that hsa_circ_0136666 inhibition reduced CRC cell growth in vivo.	30370521
circCAMSAP1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue	Regulation[ miR-328-5p/E2F1 Axis]	Western Blot//FISH//RIP//RNA-seq//IHC	In this study, we determined the circRNA expression profile by next-generation RNA sequencing from eight CRC and paired non-cancerous matched tissues. circCAMSAP1 (originating from exon 2 to exon 3 of the CAMSAP1 gene, hsa_circ_0001900) was significantly upregulated in CRC tissues.Mechanism study of upstream biogenesis of circCAMSAP1 indicated that circCAMSAP1 cyclization in CRC was mediated by splicing factor epithelial-splicing regulatory protein 1. Moreover, circCAMSAP1 acted as a sponge for miR-328-5p and abrogated its suppression on transcription factor E2F1. Taken together, our data indicated an essential role of the circCAMSAP1/miR-328-5p/E2F1 axis in the progression of CRC, which implied that circCAMSAP1 could serve as a diagnostic and prognostic biomarker as well as a potential therapeutic target for CRC.	 Increased circCAMSAP1 expression was significantly correlated with advanced tumor/node/metastasis (TNM) stage and shortened overall survival. 	Yes	Functionally, circCAMSAP1 promoted the malignant behavior of CRC. 	31951832
hsa_circ_0079993	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal tissue	Regulation[miRNA-203a-3p.1/CREB1 axis]	CCK8//qRT-PCR//Colony Formation Assay	In CRC tissue POLR2J4 expression was reduced, and circ_0079993 expression was increased compared with normal tissue. Also, circ_0079993 was predicted to sponge multiple miRNAs, miR-203a-3p.1 was verified as a target of circ_0079993, and circ_0079993 indirectly regulated mRNA expression of the CREB1 gene by sponging miR-203a-3p.1 in CRC cells. The use of anti-miR-203a-3p.1 reversed the inhibitory effects of circ_0079993 knockdown on CRC cell proliferation. CONCLUSIONS The findings supported that hsa_circ_0079993 acts as an oncogene in CRC through the miRNA-203a-3p.1/CREB1 axis.		Yes	Knockdown of circ_0079993 significantly inhibited the proliferation of CRC cells in vitro. 	31515467
hsa_circ_0002138	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[lower expressed]	qRT-PCR	In this study, we investigated the expression level of circ_0002138 in 35 paired CRC tissues by quantitative real-time polymerase chain reaction (qRT-PCR) and found that circ_0002138 was stably down-regulated in CRC tissues compared to paired adjacent normal tissues (P < 0.001). 		Yes	Additionally, functional analysis demonstrated that circ_0002138 significantly inhibited CRC cell proliferation in vitro.	30841415
circITGA7	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Interaction[sponging miR-3187-3p and increasing ASXL1]	Western Blot//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay	CircRNA sequencing analysis suggested that compared to that in adjacent normal control tissue, the expression of circ-ITGA7, a novel circRNA, is decreased significantly in CRC.		Yes	Gain-of-function studies further demonstrated that circ-ITGA7 suppressed proliferation of CRC cells.	31372051
circNSD2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[circ-NSD2/miR-199b-5p/DDR1/JAG1 axis]	qRT-PCR	Circ-NSD2 expression was elevated in CRC tissues and was markedly increased in advanced stages or metastatic tumours of CRC patients. Taken together, our findings highlight a novel oncogenic function of circ-NSD2 and uncover a key mechanism for the circ-NSD2/miR-199b-5p/DDR1/JAG1 axis in CRC metastasis, which may serve as a prognostic factor and therapeutic target for antimetastatic therapy in CRC patients.		Yes	Gain-of-function and loss-of-function experiments demonstrated that circ-NSD2 promoted migration and metastasis of CRC in vitro and in vivo.	30666650
hsa_circ_0005075	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[Wnt/β-catenin pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 We observed that circ_0005075 expression was significantly up-regulated in both CRC tissues and cell lines.Further mechanistic investigation showed that circ_0005075 displayed its tumor-promotive roles through activating Wnt/β-catenin pathway.		Yes	Cellular studies indicated that circ_0005075 can enhance the proliferation, migration, and invasion capacities of CRC cells, thereby promoting tumor progression.	31081084
hsa_circ_0021977	CircRNA	Homo sapiens	Colorectal Neoplasms	blood	Regulation[circ_0021977/miR-10b-5p/P21 and P53 regulatory axis ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Colony Formation Assay//Transwell Assay	" The results showed that the
patients with CRC had lower circ_0021977 expression.The results showed that the circ_0021977/miR-10b-5p/p21&p53 regulatory axis suppresses proliferation, migration, and invasion by CRC cells. "	 Low circ_0021977 expression in patients with CRC is associated with higher tug-lymph node metastasis (TNM) stage and poorer prognosis compared with patients with high circ_0021977 expression.	Yes	" The
above experimental results show that circ_0021977 can inhibit the
proliferation and metastasis of CRC cells in vitro.The above experimental results suggest that
circ_0021977 can inhibit the proliferation of CRC cells in vivo."	31595500
hsa_circ_101555	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[miR-597-5p]	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//Cell Cycle Assay//EdU Staining//IF	In this study, we evaluated the expression profile of circRNAs in 10 CRC tissues and their corresponding normal-appearing tissues (NATs) by microarray, and identified that hsa_circ_101555 (circ101555) was significantly up-regulated in tumor tissues and closely related to the prognosis of CRC patients. aken together, our results proved that circ101555 might function as a competing endogenous RNA of miR-597-5p to up-regulate CDK6 and RPA3 expression in CRC. 	In this study, we evaluated the expression profile of circRNAs in 10 CRC tissues and their corresponding normal-appearing tissues (NATs) by microarray, and identified that hsa_circ_101555 (circ101555) was significantly up-regulated in tumor tissues and closely related to the prognosis of CRC patients. 	Yes	The results in vitro and in vivo showed that silencing circ101555 expression significantly suppressed cell proliferation, induced apoptosis and impaired the DNA repair capacity of CRC cells, while rescue experiments suggested that down-expression of miR-597-5p could significantly attenuate the biological effects of circ101555 knockdown on CRC cells. 	31300733
hsa_circ_0053277	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction[sponging miR-2467-3p ]	qRT-PCR	 In this study, our results showed that the expression of hsa_circ_0053277 was markedly upregulated in CRC tissues and cells. To sum up, hsa_circ_0053277 facilitated the development of CRC by sponging miR-2467-3p to upregulate MMP14 expression.		Yes	Knockdown of hsa_circ_0053277 inhibited cell proliferation, migration, and epithelial-mesenchymal transition (EMT) process in CRC.	31549406
hsa_circ_0104631	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Regulation[PTEN/Akt/mTOR signaling pathway ]	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	QRT-PCR results showed that Circ-0104631 was highly expressed in tissues of patients with CRC when compared with that of normal control tissues.Circ-0104631 was highly expressed in CRC tissues. Furthermore, knockdown of Circ-0104631 could inhibit the growth and metastasis of CRC cells by regulating PTEN/Akt/mTOR signaling pathway.		Yes	In vitro experiment demonstrated that inhibition of Circ-0104631 in SW480 and LoVo cells could markedly decrease cell growth and metastasis abilities.	31210299
hsa_circ_000166	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[miR-326/LASP1 Axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	Then, we confirmed an upregulation of hsa_circRNA_000166 in CRC tissues and cell lines and observed that higher expression of hsa_circRNA_000166 was associated with poor 5-year survival rate of patients with CRC.Taken together, our results indicated that downregulation of hsa_circRNA_000166 inhibited the cell growth and facilitated apoptosis during CRC development by sponging the miR-326/LASP1 pathway.	Then, we confirmed an upregulation of hsa_circRNA_000166 in CRC tissues and cell lines and observed that higher expression of hsa_circRNA_000166 was associated with poor 5-year survival rate of patients with CRC.	Yes	Next, we investigated the function of hsa_circRNA_000166 during CRC progression by knocking down its expression. Cell growth and apoptosis assay revealed that hsa_circRNA_000166 regulated the cell growth and apoptosis in CRC cell lines. 	33376485
circGLG1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	interaction[circ_GLG1-miR-622-KRAS axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_GLG1 expression was significantly higher in CRC tissues than in adjacent normal tissues. Our study revealed the role of the circ_GLG1-miR-622-KRAS axis in CRC.		Yes	 Knocking down circ_GLG1 in DLD1 cells inhibited tumor cell viability, proliferation, invasion, and migration, and these effects were reversed by co-transfecting an miR-622 inhibitor.	33335404
hsa_circ_0000392	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-193a-5p/PIK3R3/AKT axis]	qRT-PCR//RNA Pull-Down	CircRNA_0000392 was significantly upregulated in CRC compared with normal adjacent tissues and cell lines.  CircRNA_0000392 functions as an oncogene through the miR-193a-5p/PIK3R3/Akt axis in CRC cells, suggesting that circRNA_0000392 is a potential therapeutic target for the treatment of colorectal cancer and a predictive marker for CRC patients.	The expression level of circRNA_0000392 was positively correlated with the malignant progression of CRC. 	Yes	Functional studies revealed that reducing the expression of circRNA_0000392 could inhibit the proliferation and invasion of CRC both in vitro and in vivo.	33317596
hsa_circ_100876	CircRNA	Homo sapiens	Colorectal Neoplasms	 Cc tissues and cell lines	Expression[highly expressed]	qRT-PCR	The results of this study manifested that circRNA-100876 was abnormally overexpressed in Cc tissues and cell lines, and the high expression of circRNA-100876 was clearly associated with the Clinical stage, T classification and Lymph node metastasis of Cc patients.	The results of this study manifested that circRNA-100876 was abnormally overexpressed in Cc tissues and cell lines, and the high expression of circRNA-100876 was clearly associated with the Clinical stage, T classification and Lymph node metastasis of Cc patients.	Yes	In addition, it was demonstrated that the inhibition of circRNA-100876 reduced the invasion ability of Cc cells.	33275225
circZNF609	CircRNA	Homo sapiens	Colorectal Neoplasms	Colorectal Cancer Tissue	Expression[Expression[lower expressed]-expression]	qPCR//Western Blot	CircZNF609 was significantly Expression[down-expression]-regulated in colorectal cancer tissues compared with adjacent normal tissues and in the serum of patients with colorectal cancer compared with healthy controls, verified by receiver operating characteristic (ROC) curve analysis.  Expression of circZNF609 induced apoptosis and Expression[Expression[up-expression]-expression]regulated expression of the pro-apoptotic protein, Bax, Expression[down-expression]-regulated the expression of the anti-apoptotic protein, Bcl-2, and Expression[Expression[up-expression]-expression]regulated p53.		Yes	There was low expression of circZNF609 in HCT116 cells, and overexpression inhibited cell proliferation but had no effect on PCNA and c-Myc protein expression.	31401644
hsa_circ_100290	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Regulation[circRNA_100290/miR-516b/FZD4/Wnt/β-catenin ]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	Here, our report showed that circRNA_100290 level was significantly increased in CRC tissues and cell lines. 	Besides, circRNA_100290 expression was positively correlated with tumor metastasis while inversely correlated with prognosis.	Yes	Silencing circRNA_100290 markedly reduced cell proliferation rate, inhibited migration and invasion abilities, but promoted apoptosis in vitro. 	30173892
circCPA4	CircRNA	Homo sapiens	Lung Neoplasms	 tissues and cells	Interaction(miR-214-3p/TGIF2 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	We determined that CircCPA4 and TGIF2 were increased, and miR-214-3p was decreased in lung cancer tissues and cells.		Yes	 Functionally, circCPA4 knockdown could suppress colony formation, migration, invasion, cell cycle progression, and expedite apoptosis of lung cancer cells in vitro. Mechanically, circCPA4 could regulate TGIF2 expression by sponging miR-214-3p. In addition, circCPA4 deficiency inhibited the tumor growth in lung cancer in the mouse model.	34741437
hsa_circ_0010235	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cells	Interaction(miR-636/PDL1 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Circ_0010235 was overexpressed in lung cancer. MiR-636 was a target of circ_0010235, and miR-636 inhibition reversed the effects of circ_0010235 knockdown in lung cancer cells. PDL1 was a direct target of miR-636, and miR-636 suppressed the proliferation and invasion and increased apoptosis and antitumor immunity in lung cancer cells by downregulating PDL1. Moreover, circ_0010235 positively regulated PDL1 expression by sponging miR-636.		Yes	Circ_0010235 knockdown inhibited proliferation, invasion and immune escape and promoted apoptosis of lung cancer cells. Additionally, circ_0010235 knockdown hampered tumorigenesis in vivo.	35167195
hsa_circ_0043256	CircRNA	Homo sapiens	Lung Neoplasms	GEO(1016 lung cancer samples and 129 matched normal samples)	Expression [lower expressed]	Cell Cycle Assay//IHC//EdU Staining//qRT-PCR	A total of three downregulated circRNAs (hsa_circ_0043256, hsa_circ_0029426, and hsa_circ_0049271) were obtained using a Venn diagram of three datasheets.		Yes	In addition, functional experiment results indicated that hsa_circ_0043256 could inhibit cell proliferation and cell-cycle progression of NSCLC cells in vitro. 	34806315
hsa_circ_0044516	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cells	Interaction(miR-136/MAT2A )	RNA Pull-Down//Western Blot//Bioinformatics Analysis//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Invasion Assay//Transwell Assay	Recently, we observed that circ_0044516 expression levels were obviously elevated in lung cancer tissues and cells.  Moreover, in vivo xenograft experiments showed that circ_0044516 downregulation reduced tumor growth. Mechanistically, in lung cancer and using bioinformatics, we demonstrated that circ_0044516 sponges miR-136 targeting MAT2A. 		Yes	We observed that knockdown of circ_0044516 dramatically repressed cell proliferation, increased cell apoptosis, and repressed the cell cycle.Moreover, A549 and SPCA1 cell migration and invasion abilities were greatly repressed by circ_0044516 siRNA.  Moreover, in vivo xenograft experiments showed that circ_0044516 downregulation reduced tumor growth. Mechanistically, in lung cancer and using bioinformatics, we demonstrated that circ_0044516 sponges miR-136 targeting MAT2A. 	34258296
hsa_circ_0001320	CircRNA	Homo sapiens	Lung Neoplasms	Sixty pairs of human lung adenocarcinoma or lung squamous cell carcinoma tissues and normal adjacent tissues	Interaction(miR-558)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Further study found that circ0001320 was down-regulated in lung cancer cells, localized in the cytoplasm, and had multiple miR-558 binding sites. MiR-558 was up-regulated in lung cancer cells, and bound the downstream target genes TNFAIP1 and TPM1 to inhibit their expression.		Yes	After transfection with circ0001320 overexpression vector, miR-558 up-regulation or down-regulation of TNFAIP1, or TPM1 expression significantly reversed the inhibition of cell growth and invasion by circ0001320. 	33128699
circMETTL15	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cells	Interaction(miR-1299/PDL1 axis)	In Vivo Experiment//Western Blot//Tunel//Flow Cytometry//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	Circ-METTL15 was upregulated in lung cancer tissues and cells. Circ-METTL15 was a sponge of miR-1299, and it could exert regulatory function in lung cancer via miR-1299. Furthermore, PDL1 was a functional target of miR-1299, and miR-1299 inhibited lung cancer cell development via decreasing PDL1 expression. 		Yes	Circ-METTL15 silencing suppressed cell proliferation, colony formation, invasion, immune escape and promoted cell apoptosis in lung cancer cells. 	34796777
hsa_circ_103820	CircRNA	Homo sapiens	Lung Neoplasms	GEO	Interaction(miR-200b-3p to release LATS2 and SOCS6)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Western Blot	In the present study, we identified a novel circular RNA, hsa_circ_103820, based on Gene Expression Omnibus (GEO) data. Regarding the mechanism, we revealed that miR-200b-3p was a direct target of hsa_circ_103820 and that LATS2 and SOCS6 were the downstream target genes of miR-200b-3p. Therefore, we identified a novel potential tumor suppressive function of hsa_circ_103820 in lung cancer.		Yes	Functionally, overexpression of hsa_circ_103820 showed significant inhibitory effects on the proliferation, migration and invasion of lung cancer cells, and knockdown of hsa_circ_103820 played promoting roles.	33589592
hsa_circ_0001073	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer cells	Interaction(miR-626/LIFR axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	Results showed that circ_0001073 abundance was down-regulated in lung cancer cells.miR-626 was targeted via circ_0001073, and circ_0001073 inhibited lung cancer progression via reducing miR-626 expression. LIFR was targeted via miR-626, and miR-626 knockdown constrained cell viability and invasion and facilitated apoptosis in lung cancer cells via up-regulating LIFR.		Yes	circ_0001073 constrained cell viability and invasion and facilitated apoptosis in lung cancer cells.	33475233
circCD151	CircRNA	Homo sapiens	Lung Neoplasms	human lung epithelial cells	Interaction(miR‑30d‑5p/GLI2)	CCK8//qRT-PCR//Transwell Assay	The relative expression level of circCD151 in A549 and NCI?H292 cells was significantly higher compared with that in human lung epithelial cells.  Double luciferase reporter assay confirmed the ceRNA regulatory mechanism of circCD151/miR‑30d‑5p/GLI2. 		Yes	In A549 and NCI‑H292 cells, silencing circCD151 decreased cell activity and clonal formation ability and invasion ability was also significantly decreased. circCD151 was upregulated in A549 and NCI‑H292 cells and the activity and clonal formation ability of A549 and NCI‑H292 cells were significantly increased and the invasion ability was also significantly increased.	34368867
circPTCH1	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines 	Interaction(miR-34c-5p/MYCN axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Our research demonstrated that the expression of circPTCH1 was upregulated in lung cancer tissues and cell lines and increased in metastatic tissues compared to that of non-metastatic tissues.circPTCH1 sponging miR-34c-5p to target MYCN was revealed by dual-luciferase reporter and a RIP assay. In addition, the expression level of miR-34c-5p was reduced in lung cancer tumor tissues, and MYCN was significantly increased in lung cancer tumor tissues.Further, cytological studies found that circPTCH1 reduced lung cancer cells' migration and invasion by targeting MYCN via miR-34c-5p.		Yes	Further, cytological studies found that circPTCH1 reduced lung cancer cells' migration and invasion by targeting MYCN via miR-34c-5p.	34531664
hsa_circ_0048856	CircRNA	Homo sapiens	Lung Neoplasms	NSCLC serum and cell lines	Interaction(miR-1287-5p)	qRT-PCR//Western Blot//Transwell Assay	Exosomes circ_0048856 was enhanced in NSCLC serum and cell lines (P < 0.001). MiR-1287-5p could be effaced by circ_0048856. MiR-1287-5p reversed the biological behavior changes of NSCLC cells which induced by circ_0048856. 	Exosome derived circ_0048856 had high diagnostic value for NSCLC.	Yes	Exosome circ_0048856 facilitated proliferation, migration and invasion, inhibited apoptosis of NSCLC cells. In vivo, exosomal circ_0048856 could significantly promote tumor growth (P < 0.001).	35228162
circERBB2	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cells	Interaction(miR-7-5p/FOXM1 axis)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	 Circ-ERBB2 and FOXM1 were upregulated, while miR-7-5p was decreased in lung cancer tissues and cells.Additionally, miR-7-5p directly interacted with circ-ERBB2 and FOXM1. Also, propofol played an antitumor role in lung cancer via modulating miR-7-5p or FOXM1. 		Yes	Propofol suppressed lung cancer cell progression by regulating circ-ERBB2.Moreover, circ-ERBB2 knockdown enhanced the suppressive effect of propofol on tumor growth in vivo.	33506582
circGRHPR	CircRNA	Homo sapiens	Lung Neoplasms	NSCLC cell lines	Interaction(RNA-binding protein PCBP2)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Invasion Assay//IF	 In this study, circ_GRHPR expression was found to be significantly upregulated in the serum of five patients with non-small cell lung cancer (NSCLC), compared to that in healthy controls. It is expressed at high levels in NSCLC cell lines, as revealed by qRT-PCR analysis. Functionally, we demonstrated that circ_GRHPR promotes NSCLC proliferation and invasion in vitro and in vivo by cell proliferation, transwell, cell cycle, and tumour-forming assays.Mechanistically, RNA pull-down and RNA immunoprecipitation assays showed that circ_GRHPR interacts with the RNA-binding protein poly(rC)-binding protein 2 (PCBP2) and regulates its subcellular localisation by forming the circ_GRHPR/PCBP2 complex, localizing PCBP2 mainly in the cytoplasm and reducing the proportion found in the nucleus.		Yes	 Functionally, we demonstrated that circ_GRHPR promotes NSCLC proliferation and invasion in vitro and in vivo by cell proliferation, transwell, cell cycle, and tumour-forming assays.	33987874
circFAT3	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	Interaction(circ-FAT3/miR-136-5p/HuR)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//IHC//Transwell Assay	In the present study, we found an onctogenic circRNA in lung cancer, FAT atypical cadherin 3 (FAT3) circRNA (circ-FAT3) was remarkably upregulated in lung cancer in comparison to paired normal tissues.Overall, our data reveal the previously uncharacterized regulatory loop of circ-FAT3/miR-136-5p/HuR in lung cancer and provide novel evidence for the importance of circRNA as a ceRNA in tumorigenesis.	 High circ-FAT3 was closely linked to larger tumour size, lymph node metastasis, later clinical stage, as well as dismal outcome. 	Yes	Stable knockdown of circ-FAT3 inhibited cell proliferation and metastasis both in vitro and in vivo. 	34647573
circEIF3I	CircRNA	Homo sapiens	Lung Neoplasms	LC tumor tissues and cells	Interaction(miR-1253/NOVA2/Wnt/β-catenin )	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 Circ-EIF3I was upregulated in LC tumor tissues and cells. Circ-EIF3I might function as an oncogene in LC, which promoted LC progression by the miR-1253/NOVA2/Wnt/β-catenin network.		Yes	Silenced circ-EIF3I could suppress the proliferation, migration, invasion, and enhance the apoptosis of LC cells in vitro, as well as reduce LC tumor growth in vivo. 	36193788
circSATB2	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer cells	Interaction(miR-330-5p/PEAK1 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	CircSATB2 interacted with microRNA-330-5p (miR-330-5p) and miR-330-5p targeted pseudopodium enriched atypical kinase 1 (PEAK1). In addition, circSATB2 affected the PEAK1 level via sponging miR-330-5p in lung cancer cells.All results suggested that exosomal transfer of circSATB2 contributed to the malignant development of lung cancer by acting as a sponge of miR-330-5p to upregulate PEAK1.		Yes	Exosomes enhanced cell proliferation, invasion, and migration by carrying circSATB2. Exosomal circSATB2 abrogated the inhibitory effect of short hairpin (sh)-circSATB2 on lung cancer progression. Moreover, circSATB2 promoted tumor growth in vivo via exosomes.	36148757
hsa_circ_0006692	CircRNA	Homo sapiens	Lung Neoplasms	 NSCLC specimens and cells	Interaction(miR-205-5p/CDK19 Axis)	Western Blot//Wound Healing Assay//CCK8//Invasion Assay//Transwell Assay	Hsa_circ_0006692 was over-expressed in 60 cases of NSCLC specimens and cells, which was positively correlated with TNM stage, tumor size, and invasion of the lung basal layer. The results of the dual-luciferase reporter assay, RNA immunoprecipitation, and pull-down assays indicated that hsa_circ_0006692 sponged miR-205-5p, which targeted CDK19 and facilitated the malignant behaviors of lung cancer cells.		Yes	 The results of the in vitro and in vivo studies revealed that the over-expression of hsa_circ_0006692 facilitated NSCLC cell growth, migration, and invasion, cell cycle arrest at the S phase, and the activation of BCL-2, CCND1, and PCNA. 	35627232
circTFF1	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer cell lines 	Interaction( miR-29c-3p/DNMT3A Axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	CircTFF1 was found to be upregulated in lung cancer cell lines used in this study. Additionally, BCL6B exerted suppressive impacts on lung cancer cell line malignant behavior. Moreover, circTFF1 acted as the miR-29c-3p sponge to upregulate DNMT3A, which facilitated the methylation of BCL6B. In all, circTFF1 promoted proliferation, migration and invasion of lung cancer cell lines by facilitating methylation of BCL6B promoter via miR-29c-3p/DNMT3A axis.		Yes	Functional experiments revealed circTFF1 facilitated cell proliferation, migration and invasion. 	36376550
circTAB2	CircRNA	Homo sapiens	Lung Neoplasms	cancer tissues and cells	Interaction(miR-3142/GLIS2)	Western Blot//Migration Assay//Flow Cytometry//Invasion Assay//Transwell Assay	CircTAB2 exhibited low expression in cancer tissues. Functional studies revealed that circTAB2 acted as a miRNA sponge, directly interacted with miR-3142 and consequently regulated GLIS2 /AKT. 		Yes	Gain and loss-of-function assays indicated that circTAB2 could inhibit cell proliferation, migration and invasion. 	36574090
circSAR1A	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer samples and cells	Interaction(miR-21-5p/TXNIP axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 circ_SAR1A and TXNIP were down-regulated while miR-21-5p was up-regulated in lung cancer samples and cells.  circ_SAR1A was located predominantly in the cytoplasm; it inhibited lung cancer growth in vitro and in vivo by sponging to miR-21-5p. miR-21-5p silencing suppressed lung cancer malignancy by targeting TXNIP.		Yes	 circ_SAR1A was located predominantly in the cytoplasm; it inhibited lung cancer growth in vitro and in vivo by sponging to miR-21-5p. miR-21-5p silencing suppressed lung cancer malignancy by targeting TXNIP.	35334496
hsa_circ_141539	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and adjacent non-cancer tissues (50 pairs) and cell lines	Interaction(miR-4469)	qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	The results revealed that circRNA_141539 was significantly up-regulated in patients with ESCC.  The dual-luciferase reporter assay identified that circRNA_141539 directly binds to miR-4469 and also revealed that cyclin-dependent kinase-3 (CDK3) was negatively regulated by miR-4469. 	Furthermore, high circRNA_141539 expressions were significantly associated with TNM stage, differentiation and poor prognosis, revealing high diagnostic value (P<0.05).	Yes	Furthermore, circRNA_141539 overexpression promoted cell proliferation and invasion, while circRNA_141539 silencing inhibited cell proliferation and invasion (P<0.05).	33504681
circLARP4	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cell lines	regulation[PTEN/PI3K/AKT Pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	CircLARP4 expression was observably downregulated in ESCC cell lines, and overexpressed circLARP4 restrained cell proliferation and migration whereas boosted cell apoptosis in ESCC.CircLARP4 sponges miR-1323 and hampers tumorigenesis of ESCC through modulating PTEN/PI3K/AKT pathway.		Yes	CircLARP4 expression was observably downregulated in ESCC cell lines, and overexpressed circLARP4 restrained cell proliferation and migration whereas boosted cell apoptosis in ESCC.	31897898
circUBAP2	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tumour tissues	regulation[microRNA-422a/Rab10 axis]	qRT-PCR	In the present study, circUBAP2 expression was found to be upregulated in ESCC tumour tissues.These findings suggested that circUBAP2 acted as oncogene through regulating the miR-422a/Rab10 axis in ESCC.		Yes	 Knockdown of circUBAP2 through infection with lentiviral vector encoding shRNA targeting circUBAP2 (sh-circUBAP2) inhibited the proliferation, migration and invasion of ESCC cells. In addition, circUBAP2 significantly promoted the proliferation, migration and invasion of ESCC cells. In vivo xenograft assay demonstrated that circUBAP2 downregulation suppressed the tumour growth of ESCC. 	32012318
circPLCD1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	4 paired NSCLC and normal tissues	Interaction(miR-375/miR-1179/PTEN )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//ChIP	 Here, by performing circRNA high throughput sequencing in 4 paired NSCLC and normal tissues, we found a NSCLC-associated circRNA, circ-PLCD1, which was evidently downregulated in NSCLC tissues and cell lines.Mechanistically, circ-PLCD1 acted as a competitive endogenous RNA (ceRNA) to sponge miR-375 and miR-1179 and elevate PTEN, a well-known inhibitor of oncogenic PI3K/AKT signaling, thereby repressing NSCLC tumorigenesis.		Yes	Circ-PLCD1 was transcriptionally activated by tumor-inhibiting protein p53, and exogenous expression of circ-PLCD1 inhibited NSCLC cell proliferation, invasion and induced apoptosis. 	35301686
circSEC61A1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC patients	Interaction(miR-513a-5p/PEX5 )	qRT-PCR//Transwell Assay	Our data demonstrated that circSEC61A1 was upregulated in NSCLC patients, showing an association with poorer survival outcomes. Furthermore, circSEC61A1 could regulate PEX5 expression through competitive absorption of miR-513a-5p. 	Our data demonstrated that circSEC61A1 was upregulated in NSCLC patients, showing an association with poorer survival outcomes. 	Yes	In cell experiments, circSEC61A1 overexpression promoted NSCLC malignant phenotypes, glycolysis, EMT, and Wnt/β-catenin pathway activation, whereas circSEC61A1 underexpression did the opposite. Knockdown of circSEC61A1 limited tumor growth and metastasis.	36567627
hsa_circ_0008717	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(microRNA-1287-5p/P21-activated kinase 2 (PAK2) axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_0008717 was highly expressed in NSCLC. Circ_0008717 sponged miR-1287-5p to elevate PAK2, a downstream target of miR-1287-5p. Silencing of miR-1287-5p blocked the antitumor effects of circ_0008717 knockdown in NSCLC cells. Besides, miR-1287-5p repressed cell oncogenic behaviors in NSCLC by targeting PAK2.		Yes	 Functionally, circ_0008717 deficiency suppressed cell malignant phenotypes in NSCLC in vitro and in nude mice. 	35333693
hsa_circ_0003288	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissues and cell lines	Interaction(miR-145)	In Vivo Experiment	We verified that hsa_circ_0003288 expression was upregulated in lung cancer tissues and cell lines. Mechanistically, hsa_circ_0003288 negatively regulated miR-145 to exert the oncogenic role in lung cancer. Overexpression of miR-145 decreased cell proliferation, induced apoptosis, and suppressed migration and invasion in lung cancer.		Yes	Overexpression of hsa_circ_0003288 dramatically promoted lung cancer cell proliferation, colony formation, inhibited apoptosis, and increased cell migration and invasion in vitro. Xenograft experiments showed that hsa_circ_0003288 overexpression accelerated tumor growth in vivo.	35001875
hsa_circ_001678	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 non-small cell lung cancer (NSCLC) tissues and cells	Interaction(miRNA-326/ZEB1 axis )	In Vivo Experiment//RNA Pull-Down//qRT-PCR//Luciferase Report Assay//Transwell Assay	High-throughput circular RNA (circRNA) sequencing identified circRNA_001678 (circ_001678) as an upregulated circRNA in non-small cell lung cancer (NSCLC) tissues. Furthermore, circ_001678 could sponge miR-326 to up-regulate ZEB1. On the other hand, the tumor-promoting effects of circ_001678 could be inhibited by anti-PD-L1/PD-1 treatment. Mechanistically, circ_001678 led to the activation of the PD-1/PD-L1 pathway to promote CD8+ T cell apoptosis, thereby inducing NSCLC cell immune escape via regulation of the miR-326/ZEB1 axis. 		Yes	 Accordingly, we uncovered that circ_001678 over-expression augmented NSCLC progression in vitro and enhanced tumorigenicity ability in vivo. The interaction between circ_001678 and miR-326 predicted online was verified by means of luciferase and RNA pull-down assays.	35848890
hsa_circ_0004396	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-615-5p/PAK1 axis)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay	 Hsa_circ_0004396 and PAK1 levels were upregulated, while miR-615-5p was declined in NSCLC.  Hsa_circ_0004396 functions as a molecular sponge of miR-615-5p to regulate PAK1 expression. Moreover, hsa_circ_0004396 knockdown inhibited NSCLC tumor growth in vivo.		Yes	 Hsa_circ_0004396 silencing inhibited NSCLC cell malignant behavior and induced radiosensitivity. Moreover, hsa_circ_0004396 knockdown inhibited NSCLC tumor growth in vivo.	35500159
hsa_circ_0000808	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cancer cells	Interaction(miR-1827/SLC1A5 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 Circ_0000808 expression was upregulated in NSCLC tissues and cancer cells, and its silencing inhibited NSCLC cell proliferation, migration, and invasion and led to apoptosis. Further results confirmed that circ_0000808 interacted with miR-1827 to positively regulate SLC1A5. 		Yes	 Circ_0000808 expression was upregulated in NSCLC tissues and cancer cells, and its silencing inhibited NSCLC cell proliferation, migration, and invasion and led to apoptosis. 	36192755
circEHD2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tisssues	Interaction( miR-3186-3p/FOXK1 )	qRT-PCR//Colony Formation Assay//Western Blot	 The results clarified in NSCLC elevated expression of circEHD2 and declined expression of microRNA (miR)-3186-3p. All in all, circEHD2 accelerates the proliferation and glycolysis of NSCLC, but refrains autophagy and apoptosis via strengthening FOXK1 via the adsorption of miR-3186-3p, which is supposed to be a latent molecular target for NSCLC therapy later.		Yes	Repressive circEHD2 or enhancive miR-3186-3p facilitated cell apoptosis rate and autophagy substrates LC3BII and Beclin-1, but curbed the colony-formation and DNA replication ability of NSCLC, glucose consumption, lactic acid production, glycolytic rate-limiting enzyme HK-2 and glutamine hydrolase GLS1 and P62, while overexpressed circEHD2 was adverse.	35220908
circDLG1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-630/CENPF axis)	qRT-PCR//Transwell Assay//Western Blot	CircDLG1 and CENPF were highly expressed in NSCLC, while miR-630 was downregulated.Mechanistically, circDLG1 deficiency modulated NSCLC cell malignant development through interacting with miR-630. Furthermore, CENPF was targeted by miR-630, and circDLG1 could positively control CENPF expression through acting as an miR-630 sponge.		Yes	CircDLG1 silencing repressed proliferation, migration, and invasion, and expedited apoptosis of NSCLC cells in vitro. 	35748916
hsa_circ_0000514	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-330-5p and HMGA2)	Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Circ_0000514 expression was up-regulated in NSCLC tissues. Circ_0000514 was identified as a molecular sponge to decoy miR-330-5p, and HMGA2 was proven to be a target gene of miR-330-5p. Moreover, circ_0000514 positively regulated HMGA2 expression, and its biological effect was dependent on miR-330-5p/HMGA2 axis.		Yes	 Circ_0000514 significantly facilitated the growth, cell cycle progression, metastatic potential, and repressed the apoptosis of NSCLC cells.	35552087
circTADA2A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,  A549 and H1299 cells	Interaction(miR-450b-3p/HMGN5 )	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Western Blot	 CircTADA2A expression was significantly upregulated and correlated with poor overall survival of NSCLC patients. circTADA2A functioned as a competing endogenous RNA to sponge miR-450b-3p to promote the expression of HMGN5 mRNA and protein. Furthermore, a positive relationship between circTADA2A and HMGN5 existed in NSCLC tissues. There were negative relationships between circTADA2A and miR-450b-3p as well as miR-450b-3p and HMGN5 in NSCLC tissues.	 CircTADA2A expression was significantly upregulated and correlated with poor overall survival of NSCLC patients. 	Yes	Functionally, circTADA2A inhibition successfully suppressed the proliferation, invasion, and migration of A549 and H1299 cells. 	35261900
circHSP90A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	Regulation(STAT3/PD-1/PD-L1 )	Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay	Results depicted that circ-HSP90A was cyclization from its host gene heat shock protein 90 alpha (HSP90A) and was up-regulated in NSCLC cells. Mechanistically, circ-HSP90A recruited ubiquitin specific peptidase 30 (USP30) to stabilize HSP90A and then stimulated the signal transducer and activator of transcription 3 (STAT3) signaling. Meanwhile, circ-HSP90A sponged miR-424-5p to programmed cell death ligand 1 (PD-L1).		Yes	 Circ-HSP90A depletion retarded proliferation, migration, invasion, and immune evasion. 	35750765
hsa_circ_0075048	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-1225-5p/HMGB2)	qRT-PCR//Western Blot//Transwell Assay	Circ_0075048 was increased in NSCLC tissues and cells. Downregulation of miR-1225-5p recuperated the effects of circ_0075048 knockdown on NSCLC progression. The effects of miR-1225-5p on cell proliferation, apoptosis, migration, invasion and sphere formation were attenuated by HMGB2 overexpression.		Yes	NSCLC cell proliferation, migration, invasion and sphere formation ability were decreased by circ_0075048 knockdown, and cell apoptosis was induced. 	36416408
circFARSA	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-15a-5p/B7H3 )	CCK8//qRT-PCR//FISH//RIP//Transwell Assay	 The present study demonstrated that circFARSA was upregulated in NSCLC tissues and cell lines, and its expression was positively correlated with poor prognosis of patients with NSCLC.Mechanistically, circFARSA facilitated the malignant phenotype of NSCLC cells by enhancing B7H3 expression through sponging miR-15a-5p.		Yes	 Further experiments revealed that circFARSA knockdown inhibited cell proliferation, migration, and invasion in vitro experiments, but overexpression of circFARSA exhibited opposite results. 	35920698
circATXN7	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-7-5p/PFN2)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	 CircATXN7 and PFN2 were highly expressed in NSCLC, whereas miR-7-5p expression had the opposite trend.CircATXN7 served as a miR-7-5p sponge, and circATXN7 regulated malignant behaviors of NSCLC cells through sponging miR-7-5p. PFN2 acted as a miR-7-5p target. PFN2 silencing overturned the promoting effect of miR-7-5p inhibitor on NSCLC cell malignancy, while PFN2 overexpression reversed the inhibitory impact of miR-7-5p mimic on NSCLC cell malignancy.		Yes	CircATXN7 overexpression constrained apoptosis and promoted proliferation, metastasis, invasion, and epithelial-mesenchymal transition of NSCLC cells, but circATXN7 silencing played the opposing influence and repressed xenograft tumor growth in vivo. 	35445786
circMIIP	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-766-5p/FAM83A )	Wound Healing Assay//CCK8//qRT-PCR//IHC//Bioinformatics Analysis//Transwell Assay	CircMIIP was highly expressed in NSCLC tissues and cell lines. CircMIIP acted as a molecular sponge for miR-766-5p, and circMIIP silencing-mediated anti-tumor effects were largely overturned by the knockdown of miR-766-5p in NSCLC cells. miR-766-5p interacted with the 3' untranslated region (3'UTR) of FAM83A, and FAM83A overexpression largely reversed miR-766-5p accumulation-induced anti-tumor effects in NSCLC cells. CircMIIP competitively bound to miR-766-5p to elevate the expression of FAM83A in NSCLC cells. 		Yes	CircMIIP knockdown restrained the proliferation, migration and invasion and induced the apoptosis of NSCLC cells. CircMIIP knockdown significantly restrained xenograft tumor growth in vivo.	35013754
circBIRC6	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-217/APPBP2 )	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	CircBIRC6 was overexpressed in NSCLC tissues and cells. Mechanically, circBIRC6 functioned as miR-217 sponge to promote APPBP2 expression in NSCLC cells. MiR-217 inhibition rescued circBIRC6 knockdown-mediated effects on NSCLC cell colony formation, metastasis, and apoptosis. Overexpression of miR-217 inhibited the malignant phenotypes of NSCLC cells, while the effects were abrogated by elevating APPBP2.		Yes	Knockdown of circBIRC6 repressed the colony formation and metastasis and facilitated apoptosis of NSCLC cells in vitro and restrained tumorigenesis in vivo. 	35191420
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC samples and cells	Interaction(miR-193a-3p/IRF4)	qRT-PCR//RNA Pull-Down//Western Blot	We observed an overt elevation in circ_0020123 expression in NSCLC samples and cells, and NSCLC patients with high circ_0020123 expression had a poor prognosis. Circ_0020123 could absorb miR-193a-3p to regulate IRF4 expression. miR-193a-3p silencing overturned circ_0020123 knockdown-mediated impacts on NSCLC cell malignancy, autophagy, and glycolysis. And IRF4 overexpression reversed miR-193a-3p mimic-mediated effects on NSCLC cell malignancy, autophagy, and glycolysis. Circ_0020123 promoted glycolysis and tumor growth by upregulating IRF4 through sequestering miR-193a-3p in NSCLC, offering a novel mechanism by which circ_0020123 is responsible for the malignancy, autophagy, and glycolysis of NSCLC cells.	We observed an overt elevation in circ_0020123 expression in NSCLC samples and cells, and NSCLC patients with high circ_0020123 expression had a poor prognosis. 	Yes	Circ_0020123 knockdown constrained xenograft tumor growth in vivo and curbed cell proliferation, migration, and glycolysis, and accelerated cell apoptosis and autophagy in NSCLC cells in vitro.	35225648
hsa_circ_0018189	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells and samples	Interaction(miR-656-3p/xCT)	qRT-PCR//Luciferase Report Assay//Western Blot	Hsa_circ_0018189 abundance was overexpressed in NSCLC cells and samples.  Hsa_circ_0018189 could up-regulate xCT by sponging miR-656-3p. And miR-656-3p downregulation or xCT overexpression partly overturned hsa_circ_0018189 knockdown or miR-656-3p mimic-mediated repression of NSCLC cell malignancy.		Yes	 Deficiency of hsa_circ_0018189 lowered NSCLC cell proliferative, migrating, invading, and glutamine metabolism capacities, and hsa_circ_0018189 silencing inhibited the growth of tumors in vivo.	36164726
hsa_circ_0016760	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-4295/E2F3 axis,)	qRT-PCR//Luciferase Report Assay//Western Blot	Circ_0016760 and E2F3 expression levels were upregulated in NSCLC tissues and cells, while miR-4295 was downregulated.  Circ_0016760 could bind to miR-4295, and negatively modulate its expression in NSCLC cells. Besides, miR-4295 directly targeted E2F3 and inversely regulated E2F3 expression. 		Yes	More importantly, Circ_0016760 facilitated proliferation and glycolysis of NSCLC cells by increasing E2F3 by sponging miR-4295 as well as promoted the tumor growth in vivo. 	33232618
hsa_circ_0000317	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction( miR-494-3p/PTEN/PI3K/AKT pathway)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//FISH//MTT//Luciferase Report Assay	 Circ_0000317 expression level was reduced in NSCLC tissues and cell lines. In addition, circ_0000317, was identified as a competitive endogenous RNA, which could sponge miR-494-3p to increase PTEN expression and activate PI3K/AKT pathway.	Circ_0000317 expression in NSCLC patients was associated with TNM stage and lymphatic metastasis. 	Yes	Circ_0000317 overexpression restrained the proliferation, migration, and invasion of NSCLC cells, but co-transfection of miR-494-3p mimics partially reversed this effect. 	35917658
hsa_circ_0070659	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues and cells	Interaction(miR-377/RAB3C axis)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our experimental results showed that circ_0070659 levels were largely increased in tumor tissues and cells. Our study revealed a novel signaling pathway that circ_0070659/miR-377/RAB3C axis regulates tumor progression, and it may become a new therapeutic target for NSCLC.		Yes	Biologically, knockdown of circ_0070659 obviously inhibited proliferation, migration, and invasion of NSCLC cells.	36694911
circCNOT6L	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues/cells	regulation[miR-384/FN1 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	CircCNOT6L and FN1 levels were upregulated, and miR-384 level was downregulated in ESCC tissues/cells. Our results demonstrated that circCNOT6L positively regulated the development of ESCC cells via modulating miR-384/FN1 axis. 		Yes	CircCNOT6L knockdown attenuated ESCC cell proliferation and iron metabolism disorder, as well as accelerated apoptosis. 	32329843
circZCCHC6	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC serum, tissues, and cells	Interaction(miR-433-3p/LPCAT1)	RNA Pull-Down//Northern Blot//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	CircZCCHC6 was highly expressed in NSCLC serum, tissues, and cells. The mechanical analysis suggested that circZCCHC6 acted as a sponge of miR-433-3p to regulate LPCAT1 expression.CircZCCHC6 inhibited the progression of NSCLC cells partly by regulating the miR-433-3p/LPCAT1 axis, implying a promising therapeutic target for the NSCLC treatment.		Yes	Moreover, circZCCHC6 knockdown could repress cell viability, cell cycle progression, migration, invasion, and EMT in NSCLC cells in vitro. . CircZCCHC6 silencing hindered cell growth and EMT of NSCLC in vivo.	35089454
hsa_circ_0010235	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-433-3p/TIPRL axis)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	Hsa_circ_0010235 and TIPRL were highly expressed in NSCLC tissues and cells, while miR-433-3p was downregulated. Hsa_circ_0010235 sponged miR-433-3p to upregulate TIPRL expression, so as to affect NSCLC development. Hsa_circ_0010235 knockdown also blocked tumor growth in vivo.		Yes	 Depletion of hsa_circ_0010235 or gain of miR-433-3p repressed proliferation and autophagy but promoted apoptosis in NSCLC cells.	33494763
hsa_circ_0015278	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(microRNA 1278/SOCS6 gene axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//IHC//Transwell Assay	Circ_0015278 was downregulated in NSCLC tissues and cells, and its reduced expression indicated poor prognosis. Mechanically, circ_0015278 acted as an miR-1278 sponge to reduce its quantity, and miR-1278 targeted SOCS6 to inhibit its expression in NSCLC cells. Circ_0015278 promoted SOCS6 expression by sponging miR-1,278 in NSCLC cells. Overexpression of circ_0015278 attenuated the malignant phenotypes of NSCLC through sponging miR-1278 and consequently promoting SOCS6 expression.	Circ_0015278 was downregulated in NSCLC tissues and cells, and its reduced expression indicated poor prognosis. 	Yes	Overexpression of circ_0015278 restrained the proliferation, colony formation, invasion, and epithelial-mesenchymal transition (EMT) of NSCLC cells and induced NSCLC cell apoptosis. Moreover, overexpression of circ_0015278 inhibited the growth of NSCLC in vivo.	34532392
circPUM1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines.	Interaction(miR-590-5p/METTL3 axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay	CircPUM1 was highly expressed in NSCLC tissues and cell lines.Moreover, circPUM1 directly bound to miR-590-5p, and miR-590-5p inhibitor reversed the inhibitory effects of circPUM1 knockdown on NSCLC carcinogenesis. Additionally, miR-590-5p suppressed NSCLC progression by directly targeting and regulating METTL3. 		Yes	 CircPUM1 knockdown suppressed cell proliferation, cell cycle and glycolysis in vitro. In addition, it was also proved circPUM1 silencing impeded tumor growth and glycolysis in the murine xenograft model by regulating miR-590-5p/METTL3 axis. 	34097560
circUBAP2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Clinical samples and NSCLC cell lines 	Interaction(miR3182-KLF4 )	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	circUBAP2 exhibited significantly elevated average level in our clinical samples of NSCLC, compared with normal tissues.Further experiments indicated that circUBAP2 promoted malignant biological behavior of NSCLC tumor cells by targeting KLF4 through modulating miR-3182 expression.	CircUBAP2 level was positively correlated with disease stage and metastatic status. 	Yes	circUBAP2 significantly enhanced the migration, proliferation and chemo-resistance of NSCLC cell lines.	33882454
circMMP11	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-143 )	CCK8//qRT-PCR	We found that circMMP11 was overexpressed in NSCLC and predicted patients' poor survival.Moreover, a close correlation between circMMP11 and miR143 was observed. In NSCLC cells, circMMP11 overexpression reduced miR-143 expression and increased miR-143 methylation.	We found that circMMP11 was overexpressed in NSCLC and predicted patients' poor survival.	Yes	 CCK-8 assay analysis showed that miR-143 reversed the enhancing effects of circMMP11 overexpression on cell proliferation.	34749774
hsa_circ_0006988	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-491-5p/MAP3K3 axis)	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//IHC	Circ_0006988 abundance was increased in NSCLC tissues and cells.  Circ_0006988 sponged miR-491-5p, which directly targeted MAP3K3. MiR-491-5p overexpression repressed NSCLC cell malignant behaviors. 		Yes	Circ_0006988 silencing restrained NSCLC cell proliferation, migration, invasion and angiogenesis, and induced apoptosis. MiR-491-5p downregulation or MAP3K3 overexpression reversed the effect of circ_0006988 silencing on NSCLC cell progression. In addition, circ_0006988 knockdown reduced xenograft tumor growth. 	34189997
hsa_circ_0001947	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(MiR-661/DOK7 Axis )	CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	Circ_0001947 was low-expressed in NSCLC tissues and cells. MiR-661 was a target gene of circ_0001947 that participated in the regulation of circ_0001947 on cell biological behaviors. Furthermore, DOK7, the target gene of miR-661, partly participated in the regulation of miR-661 on cell viability.		Yes	Circ_0001947 knockdown intensified cell viability and proliferation, induced cell cycle arrest at S phase, suppressed apoptosis and evidently enhanced miR-510, miR-587, miR-661 and miR-942 levels, while circ_0001947 overexpression did the opposite. 	34528912
circZNF124	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-498/YES1 axis)	qRT-PCR//Western Blot//Transwell Assay	 As results, we found that the expression of circ-ZNF124 was elevated in NSCLC tissues and cells. In conclusion, these findings supported that circ-ZNF124 regulated the expression of YES1 by acting as a sponge of miR-498, thus restraining NSCLC development by inactivating the Wnt/β-catenin signaling pathway, which provided a novel strategy to treat NSCLC.		Yes	 Functionally, circ-ZNF124 downregulation inhibited NSCLC cell proliferation and invasion but induced apoptosis and cycle arrest in vitro, and blocked tumor growth in vivo by animal experiments. 	33186139
hsa_circ_0074027	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(microRNA-362-3p/clathrin heavy chain axis)	Transwell Assay//qRT-PCR//Colony Formation Assay//Western Blot	We found that The enrichment of circ_0074027 and CLTC protein was elevated, and a significant reduction in the expression of miR-362-3p was observed in NSCLC tissues and cells relative to adjacent normal tissues and human bronchial epithelial cells 16HBE.Circ_0074027/miR-362-3p/CLTC axis was first found to regulate the malignance of NSCLC cells. 		Yes	Circ_0074027 and CLTC could accelerate the colony formation and metastasis and suppress the apoptosis of NSCLC cells.Circ_0074027 acted as an oncogene to promote the growth of NSCLC tumors in vivo. 	32932275
hsa_circ_0001806	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-1182/NOVA2 Axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Circ_0001806 expression in NSCLC tissues and cell lines was substantially augmented, while miR-1182 expression was markedly decreased. Circ_0001806 indirectly enhanced NOVA2 expression by specifically down-modulating miR-1182.		Yes	Circ_0001806 facilitated the multiplication, migration and invasion of H1650 and HCC827 cells, while miR-1182 exerted the opposite effect.	33854376
hsa_circ_0000517	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-326/miR-330-5p)	qRT-PCR//Western Blot//RNA Pull-Down//Transwell Assay	Circ_0000517 was shown to be up-regulated in NSCLC tissues and cell lines. Mechanistically, circ_0000517 was demonstrated to up-regulate MMP2 expression via decoying miR-326 and miR-330-5p to facilitate the malignant biological behaviors of NSCLC cells.	 The up-regulation of circ_0000517 is closely associated with advanced clinical stage of cancer, lymph node metastasis, and poor prognosis in NSCLC patients. 	Yes	 Circ_0000517 knockdown impeded the proliferation, migration, and invasion of NSCLC cells and enhanced their apoptosis. 	34837683
hsa_circ_0060937	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-195-5p/HMGB3 pathway)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Transwell Assay	.Circ_0060937 and HMGB3 levels were elevated, whereas miR-195-5p level was dropped in NSCLC. Knockdown of circ_0060937 restrained NSCLC development via absorbing miR-195-5p. Circ_0060937 silencing inhibited NSCLC progression by mediating HMGB3. 		Yes	Circ_0060937 down-regulation restrainedNSCLC cell proliferation, migration, invasion and glycolysis, and triggered apoptosis.Besides, circ_0060937 depletion suppressed tumor growth in vivo.	34470585
circVAPA	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tissues and cell lines of NSCLC	Interaction(miR-876-5p/WNT5A axis)	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Our findings demonstrated high expression of circVAPA in tissues and cell lines of NSCLC.Mechanistically, circVAPA acted as a competing endogenous RNA to up-regulate WNT5A by sponging miR-876-5p. Moreover, circVAPA activated Wnt/β-catenin signaling by up-regulation of WNT5A. 		Yes	Knockdown of circVAPA had a suppressive effect on cell proliferation, migration, invasion and stemness, and also inhibited tumor growth in vivo	33619796
circPGC	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-532-3p/FOXR2 network.)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results showed that circ-PGC and FOXR2 were upregulated in NSCLC tissues and cells. In conclusion, circ-PGC positively regulated FOXR2 expression by competitively binding to miR-532-3p, thereby promoting the development of NSCLC, and the Wnt/β-catenin signaling pathway might be activated by the circ-PGC/miR-532-3p/FOXR2 network.miR-532-3p/FOXR2 network.		Yes	Circ-PGC knockdown or FOXR2 knockdown inhibited NSCLC cell viability, colony formation, cell migration, invasion and glycolysis metabolism, and FOXR2 overexpression rescued these inhibitory effects caused by circ-PGC knockdown.	34494941
hsa_circ_0000376	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-488-3p/BRD4 axis and the PI3K/PKB signaling pathway)	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0000376 was highly expressed in NSCLC tissues and cells. Circ_0000376 downregulation inhibited NSCLC cell proliferation, invasion and migration, promoted cell apoptosis and cell cycle arrest and slowed tumor growth in vivo. Circ_0000376 competitively bound to miR-488-3p to regulate the expression of BRD4. Rescue experiments showed that miR-488-3p deficiency reversed the effects of circ_0000376 downregulation, and miR-488-3p restoration-suppressed cell proliferation, migration and invasion were recovered by BRD4 overexpression. Moreover, circ_0000376 downregulation weakened the levels of phosphorylated PI3K and PKB, thus reducing the activity of the PI3K/PKB pathway.		Yes	Rescue experiments showed that miR-488-3p deficiency reversed the effects of circ_0000376 downregulation, and miR-488-3p restoration-suppressed cell proliferation, migration and invasion were recovered by BRD4 overexpression.	34730838
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-384/TRIM44 Axis)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Western Blot	Levels of circ_0020123 and TRIM44 were enhanced, and the miR-384 level was attenuated in NSCLC tissues and cells.Besides, circ_0020123 interacted with miR-384, and miR-384 targeted TRIM44. Circ_0020123 regulated cell progression by regulating miR-384 and subsequently mediated TRIM44 expression.		Yes	Circ_0020123 depletion attenuated the abilities of NSCLC cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT), and induced apoptosis. Besides, circ_0020123 depletion repressed tumor growth in vivo.	33442296
hsa_circ_0102231	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	Interaction(miR-145/RBBP4 axis )	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Western Blot	We found that hsa_circ_0102231 level was higher in NSCLC cells. hsa_circ_0102231 is mainly localized to the cytoplasm.hsa_circ_0102231 promotes NSCLC cell proliferation and invasion by sponge for miR-145.miR-145 significantly decreases the RBBP4 promoter activity, and its mRNA and protein levels. RBBP4 is an oncogene to promote proliferation and invasion ability.		Yes	hsa_circ_0102231 promotes NSCLC cell proliferation and invasion by sponge for miR-145.	33084863
circRHOT1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer cell lines and clinical tumor tissues	Regulation(KAT5/c-MYC)	Western Blot//qRT-PCR//FISH//RIP//MTT//ChIP	We found that circRHOT1 were elevated in the clinical tumor tissues relative to that in the peritumor tissues from NSCLC patients.circRHOT1 was up-regulated in human lung cancer cell lines compared with normal human lung epithelial cell line.. In summary, we concluded that circRHOT1 contributed to pathogenesis of NSCLC by epigenetically enhancing c-MYC expression through recruiting KAT5. 		Yes	 MTT assays revealed that the silencing of circRHOT1 by siRNA suppressed cell viabilities of NSCLC cells. Colony formation and Edu assays confirmed that circRHOT1 knockdown attenuated NSCLC cell proliferation in vitro. 	34406978
circSCAP	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer tissues	Interaction(SF3A3/MDM4-S/p53 )	RNA Pull-Down//Wound Healing Assay//qRT-PCR//RIP//FISH//IP//Transwell Assay	We screened the expression profiles of human circRNAs in lung cancer tissues and found that hsa_circ_0065214 (termed as circSCAP) was significantly decreased. Mechanistically, circSCAP directly binds to the SF3A3 protein, facilitating the reduction of SF3A3 by promoting its ubiquitin-proteasome-mediated degradation, which enhances the expression of MDM4-S to finally activate its downstream p53 signaling.	 Kaplan-Meier analysis showed that patients with low level of circSCAP had a significantly poor prognosis.	Yes	 Gain- and loss-of-function experiments suggested that circSCAP played an important role in NSCLC cell proliferation, cell migration and apoptosis. 	35365208
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-512-3p/CORO1C)	CCK8//qRT-PCR//RIP//Western Blot	 Circ_0020123 expression was aberrantly upregulated in NSCLC tissues and cell lines.Circ_0020123 acted as a molecular sponge for miR-512-3p. Circ_0020123 silencing-induced effects in NSCLC cells were largely reversed by the knockdown of miR-512-3p. miR-512-3p interacted with the 3' untranslated region (3'UTR) of CORO1C. CORO1C overexpression largely reversed miR-512-3p accumulation-induced influences in NSCLC cells. Circ_0020123 positively regulated CORO1C expression by sponging miR-512-3p in NSCLC cells.		Yes	Circ_0020123 interference markedly restrained cell proliferation, migration, invasion, angiogenesis and autophagy and induced cell apoptosis of NSCLC cells. Circ_0020123 knockdown suppressed xenograft tumor growth in vivo.	35388975
hsa_circ_0120376	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-148b-3p/CEP55 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that circ_0120376 was markedly overexpressed in NSCLC, and its overexpression was positively associated with increased T stage and lymph node metastasis of the patients.  Circ_0120376 could adsorb miR-148b-3p to reduce miR-148b-3p expression, and circ_0120376 could increase CEP55 expression via adsorbing miR-148b-3p. 	We found that circ_0120376 was markedly overexpressed in NSCLC, and its overexpression was positively associated with increased T stage and lymph node metastasis of the patients. 	Yes	Functional experiments unveiled that circ_0120376 enhanced the proliferation, migration and invasion of NSCLC cells and impeded apoptosis, while knocking down circ_0120376 remarkably suppressed the malignant features of NSCLC cells mentioned above. 	35549631
hsa_circ_0001955	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction( miR-769-5p/EGFR axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//BrdU//Transwell Assay	 Circ_0001955 expression was up-regulated in NSCLC tissues and cell lines, and its overexpression was strongly associated with increased tumor TNM stage and lymph node metastasis. Circ_0001955 directly targeted miR-769-5p and negatively regulated its expression. EGFR, a target gene of miR-769-5p, could be indirectly and positively regulated by circ_0001955. Correlation analysis indicated that circ_0001955 was negatively correlated with miR-769-5p expression, while circ_0001955 was positively correlated with EGFR expression. Circ_0001955 facilitates the proliferation and represses the apoptosis of NSCLC cells by modulating miR-769-5p/EGFR axis.	 Circ_0001955 expression was up-regulated in NSCLC tissues and cell lines, and its overexpression was strongly associated with increased tumor TNM stage and lymph node metastasis.	Yes	 Circ_0001955 overexpression enhanced the proliferation and restrained the apoptosis in NSCLC cells, whereas knocking down circ_0001955 exerted the opposite effects. 	35920610
hsa_circ_0079530	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell line	Interaction(miR-584-5p/THBS2)	qRT-PCR//Western Blot	 Circ_0079530 was highly expressed in NSCLC tissues and cell lines. Circ_0079530 silence showed the opposite effects on the above malignant biological behaviors. Mechanistic analysis showed that circ_0079530 functioned as a sponge of miR-584-5p to relieve the suppressive action of miR-584-5p on its target THBS2.		Yes	 Circ_0079530 overexpression facilitated proliferation, migration, and invasion whereas it restrained the apoptosis of NSCLC cells.Additionally, circ_0079530 knockdown impeded the growth of xenografts in vivo.	36382967
hsa_circ_0079530	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(Hsa_circ_0079530/AQP4 Axis )	CCK8//qRT-PCR//Western Blot	Circ_0079530 expression was increased in NSCLC tissues and radioresistant samples. Circ_0079530 was verified as a miR-409-3p sponge, and miR-409-3p downregulation mitigated the effects of circ_0079530 interference on NSCLC cell malignancy and radiosensitivity. AQP4 was directly targeted by miR-409-3p. MiR-409-3p restrained cell proliferation, migration, and invasion, and enhanced radiosensitivity by decreasing AQP4 expression. Notably, circ_0079530 silence decreased AQP4 expression by regulating miR-409-3p expression.		Yes	Circ_0079530 knockdown restrained cell proliferation, migration, and invasion, and facilitated radiosensitivity. Circ_0079530 silence decreased tumor growth with or without radiation treatment.	35896371
circFAM126A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells 	Interaction(miR-613/IRS2)	CCK8//qRT-PCR//Western Blot	CircFAM126A was obviously overexpressed in NSCLC tissues and cells when compared with controls.  In addition, IRS2 was a target gene of miR-613. Overexpression of miR-613 exerted carcinoma inhibitor role in NSCLC by inhibition of IRS2 expression.Mechanistically, circFAM126A could function as a miRNA sponge for miR-613 to regulate the expression of IRS2, thereby regulating proliferation, migration, invasion, apoptosis, and cell cycle arrest in NSCLC cells.		Yes	 The loss-of-functional experiments suggested that knockdown of circFAM126A suppressed proliferation, migration and invasion, as well as caused apoptosis and cell cycle arrest in NSCLC cells, which was abolished by silencing of miR-613. Consistently, the silencing of circFAM126A also functioned anti-tumorigenic roles in nude mice in vivo. 	35397054
hsa_circ_0006006	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-924/SRSF7 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	Circ_0006006 was increased in NSCLC tissues and cells. Follow-up mechanism experiments depicted that circ_0006006 sponged miR-924 and miR-924 inhibitor rescued the circ_0006006 knockdown-mediated inhibition effect on the progression of NSCLC. Additionally, the inhibition effect of circ_0006006 knockdown on SRSF7 expression was reversed by miR-924 inhibitor. Moreover, the suppressive effect of miR-924 on NSCLC progression was reversed by SRSF7 overexpression. 		Yes	 Loss-of-function assays demonstrated that circ_0006006 silencing repressed proliferative ability, cell migration and invasion, and angiogenesis, as well as promoted cell apoptosis, in A549 and H1299 cells. Xenograft tumor experiment unveiled that circ_0006006 knockdown inhibited tumor growth in vivo.	35037349
circENTPD7	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and paired non-tumor tissues	Expression(highly expressed)	CCK8//qRT-PCR//ELISA//Western Blot	CircENTPD7 was upregulated in NSCLC and high expression levels of circENTPD7 predicts the poor survival rate of NSCLC cells. In NSCLC tissues, circENTPD7 was inversely correlated with PTEN protein but not mRNA. In NSCLC tissues, overexpression of circENTPD7 resulted in downregulation of PTEN, but did not alter the expression of PTEN mRNA. Cell proliferation analysis showed that overexpression of circENTPD7 promoted the proliferation of NSCLC cells and reduced the inhibitory effects of overexpression of PTEN on cell proliferation. CircENTPD7 may suppress the accumulation of PTEN to promote cell proliferation in NSCLC.	CircENTPD7 was upregulated in NSCLC and high expression levels of circENTPD7 predicts the poor survival rate of NSCLC cells.	Yes	In NSCLC tissues, overexpression of circENTPD7 resulted in downregulation of PTEN, but did not alter the expression of PTEN mRNA. Cell proliferation analysis showed that overexpression of circENTPD7 promoted the proliferation of NSCLC cells and reduced the inhibitory effects of overexpression of PTEN on cell proliferation.	35993557
circSCN8A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Regulation(miR-1290/ACSL4 axis)	IHC//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In this study, we found that circSCN8A expression was down-regulated in NSCLC tissues and cells. Low circSCN8A expression was positively associated with aggressive clinicopathological characteristics and poor prognosis in NSCLC patients. CircSCN8A suppressed cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and blocked tumor growth in vivo. Moreover, circSCN8A promoted cell ferroptosis in NSCLC. Mechanistically, circSCN8A acted as a competing endogenous RNA (ceRNA) by sponging miR-1290 to enhance the expression of long-chain acyl-CoA synthetase-4 (ACSL4). Furthermore, the knockdown of ACSL4 or overexpression of miR-1290 reversed the effect of circSCN8A on facilitating ferroptosis and inhibiting cell proliferation and metastasis. In summary, circSCN8A represses cell proliferation and metastasis in NSCLC by regulating the miR-1290/ACSL4 axis to induce ferroptosis. Thus, circSCN8A may represent a promising therapeutic target against NSCLC.	Low circSCN8A expression was positively associated with aggressive clinicopathological characteristics and poor prognosis in NSCLC patients.	Yes	CircSCN8A suppressed cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and blocked tumor growth in vivo. Moreover, circSCN8A promoted cell ferroptosis in NSCLC. Mechanistically, circSCN8A acted as a competing endogenous RNA (ceRNA) by sponging miR-1290 to enhance the expression of long-chain acyl-CoA synthetase-4 (ACSL4). Furthermore, the knockdown of ACSL4 or overexpression of miR-1290 reversed the effect of circSCN8A on facilitating ferroptosis and inhibiting cell proliferation and metastasis.	36482742
hsa_circ_100876	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Expression[highly expressed]	qRT-PCR	CircRNA_100876 expression was upregulated (P<0.05) and was negatively correlated with survival outcome (P<0.05) in ESCC. 	CircRNA_100876 expression was upregulated (P<0.05) and was negatively correlated with survival outcome (P<0.05) in ESCC. 	Yes	Inhibition of proliferation, migration, invasion, and epithelial-mesenchymal transition progression was confirmed after circRNA_100876 depletion.	30425526
hsa_circ_0006948	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	Regulation[miR-490-3p/HMGA2 axis]	qRT-PCR	 We first screened circRNA expression profiles using a circRNA microarray, and found that the expression of a novel circRNA, hsa_circ_0006948, is increased in 153 ESCC tissues and cell lines compared with noncancerous tissues and cell lines. Furthermore, we analyzed the relationship between hsa_circ_0006948 and miR-490-3p through bioinformatics, luciferase reporter assays, RNA immunoprecipitation and qRT-PCR. We found that hsa_circ_0006948 could bind directly to miR-490-3p which targets the 3'UTR of the oncogene HMGA2 to induce EMT. In conclusion, hsa_circ_0006948 was overexpressed in ESCC tissues and promoted cancer progression, and it could induce EMT by enhancing HMGA2 by sponging miR-490-3p, suggesting that hsa_circ_0006948 could be a biomarker for ESCC.	 Additionally, high hsa_circ_0006948 levels were positively associated with lymphatic metastasis and poor prognosis.	Yes	 Functionally, the assays indicated that cell proliferation, migration and invasion were promoted by hsa_circ_0006948 both in vitro and in vivo. 	31881015
hsa_circ_0006168	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	Interaction[sponges miR-100 and regulates mTOR]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Microarray//Transwell Assay	.Our results suggested that, hsa_circ_0006168 was remarkably increased not only in ESCC tissues but also in cell lines compared with those in normal cases. Mechanically, it was discovered in this study that hsa_circ_0006168 might regulate the expression of Mammalian Target of Rapamycin (mTOR) by sponging microRNA-100 (miR-100). Taken together, hsa_circ_0006168 can promote ESCC proliferation, migration and invasion through the competing endogenous RNA (ceRNA) mechanism, which has been first confirmed in our results. In ESCC, hsa_circ_0006168 can serve as a potential diagnostic biomarker and therapeutic target.	Besides, high hsa_circ_0006168 expression was positively connected with lymph node metastasis and TNM stage of ESCC patients.	Yes	In vitro, the proliferation, invasion and migration capacities of ESCC cells were suppressed through down-regulating hsa_circ_0006168 expression.	31229921
hsa_circ_0000654	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues,cell lines	Interaction[miR-149-5p/IL-6/STAT3 pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//BrdU//Transwell Assay	 Circ_0000654 was significantly upregulated in ESCC tissues and cell lines, and its high expression was remarkably associated with an increased T stage and local lymph node metastasis in ESCC patients.Circ_0000654 was identified as a sponge of miR-149-5p and facilitated ESCC progression by indirectly activating the IL-6/STAT3 signaling pathway. Additionally, knocking down circ_0000654 strikingly repressed ESCC growth and metastasis in vivo. In summary, circ_0000654 functions as an oncogenic circRNA in ESCC and accelerates ESCC progression via adsorbing miR-149-5p and activating the IL-6/STAT3 signaling pathway.		Yes	Circ_0000654 overexpression and knockdown experiments revealed that circ_0000654 regulated ESCC cell proliferation, migration, invasion, and apoptosis in vitro. 	31778020
circSMAD7	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	blood,ESCC tissues	Expression[lower expressed]	qRT-PCR	The expression of circ-SMAD7 was validated to be significantly down-regulated in ESCC plasmas in comparison with normal controls, showing a high negative correlation with TNM stage (P = 0.000) and lymphatic metastasis (P = 0.000). Moreover, circ-SMAD7 was significantly down-regulated in ESCC tissues compared to adjacent normal tissues.	The expression of circ-SMAD7 was validated to be significantly down-regulated in ESCC plasmas in comparison with normal controls, showing a high negative correlation with TNM stage (P = 0.000) and lymphatic metastasis (P = 0.000). 	Yes	Furthermore, Loss-of-function and gain-of-function experiments revealed that the expression level of circ-SMAD7 affected the proliferation and migration of ESCC cell lines.	30611100
hsa_circ_0000337	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction[bind to miR-670-5p ]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 hsa_circ_0000337 was significantly upregulated in ESCC tissues compared to adjacent normal-appearing tissues (P<0.0001).  Bioinformatics predicted and luciferase reporter assay verified that hsa_circ_0000337 could bind to miR-670-5p, a ncRNA involved in carcinogenesis. 		Yes	 Knockdown of hsa_circ_0000337 significantly inhibited cell proliferation, migration, and invasion in TE-1 and KYSE-150 cell lines. 	30881124
circTTC17	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC cells, plasma, and tissues	Expression[highly expressed]	CCK8//qRT-PCR//Wound Healing Assay	The expression level of circ-TTC17 was found to be significantly higher in ESCC cells, plasma, and tissues compared with normal cases. 		Yes	 In vitro experiments indicated that circ-TTC17 promoted proliferation and migration of ESCC cells.	30519852
circZDHHC5	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues,blood	regulation[miR-217/ZEB1 Axis]	qRT-PCR//Luciferase Report Assay//FISH	 circ-ZDHHC5, rather than linear ZDHHC5 mRNA, rose in the tissues of patients with ESCC, plasma, and ESCC cell lines in comparison with normal controls. It provides a novel perceptivity for the treatment of ESCC suggesting that circ-ZDHHC5 could impact on ESCC progression by sponging miR-217 with ZEB1.		Yes	Knockdown of circ-ZDHHC5 inhibited tumorigenesis in ESCC cells, and the co-transfection of si-circ-ZDHHC5 and miR-217 mimics further enhanced the above effect.	33392180
hsa_circ_0120816	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	regulation[inhibiting miR-1305 and releasing TXNRD1]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	Experimental investigations revealed that circ0120816 was the highest upregulated circRNA in ESCC tissues and that this non-coding RNA acted as a miR-1305 sponge in enhancing cell viability, cell proliferation, and cell adhesion as well as repressing cell apoptosis in ESCC cell lines.This research confirmed that circ0120816 played an active role in promoting ESCC development by targeting miR-1305 and upregulating oncogene TXNRD1.		Yes	 Furthermore, silencing circ0120816 was found to repress ESCC tumor growth and metastasis in vivo.	33292234
hsa_circ_6448-14	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	interaction[miR-455-3p]	qRT-PCR//RNA Pull-Down	hsa_circRNA6448-14 was significantly upregulated in ESCC tissues and cell lines. hsa_circRNA6448-14 functioned as a miRNA sponge to competitively bind miR-455-3p, and hsa_circRNA6448-14 expression negatively correlated with that of miR-455-3p.	 hsa_circRNA6448-14 upregulation was correlated with poor differentiation, advanced pTNM stage, poor disease-free survival (DFS), and poor overall survival (OS). 	Yes	Elevated hsa_circRNA6448-14 promoted cell proliferation, migration, invasion, and inhibited apoptosis in vitro.	32805720
circLPAR3	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cells	interaction[sponging miR-375/miR-433 ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	CircLPAR3 was upregulated in ESCC tissues and cells, and its high expression was related to the poor prognosis of ESCC patients.CircLPAR3 might play an oncogenic role in ESCC through sponging miR-375/miR-433 to promote HMGB1 expression, which might provide a theoretical basis for circLPAR3 to become a biomarker for ESCC therapy.	CircLPAR3 was upregulated in ESCC tissues and cells, and its high expression was related to the poor prognosis of ESCC patients.	Yes	CircLPAR3 was a stable cyclic transcript, mainly located in the cytoplasm, and its knockdown hindered the proliferation, migration and invasion of ESCC cells and inhibited ESCC tumor growth in vivo. 	32801782
circNTRK2	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	regulation[NRIP1 ,miR-140-3p]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	CircNTRK2 was highly expressed in ESCC tissues and cells. CircNTRK2 promoted ESCC progression by regulating miR-140-3p/NRIP1 pathway. 	High expression of circNTRK2 was correlated with advanced TNM stage, lymph node metastasis and short survival. 	Yes	Knockdown of circNTRK2 inhibited ESCC cell proliferation, invasion and epithelial-mesenchymal transition (EMT), and accelerated apoptosis in vitro.	32653032
hsa_circ_0006220	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells and tissues	Interaction(miR-203-3p/RGS17 )	EdU Staining//CCK8//qRT-PCR//Bioinformatics Analysis//Transwell Assay	The expression of circ_0006220 was elevated in NSCLC cells and tissues, and high circ_0006220 expression was significantly associated with unfavorable clinicopathological indicators. Furthermore, miR-203-3p was identified as a downstream target of circ_0006220, and circ_0006220 could sponge miR-203-3p; RGS17 was identified as a downstream target of miR-203-3p and was positively modulated by circ_0006220.	The expression of circ_0006220 was elevated in NSCLC cells and tissues, and high circ_0006220 expression was significantly associated with unfavorable clinicopathological indicators.	Yes	In addition, it was revealed that circ_0006220 overexpression facilitated NSCLC cell growth, migration, and invasion, whereas knocking down circ_0006220 had contrary effects. 	35041543
hsa_circ_0074027	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-335-5p/CUL4B )	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 High expression of circ_0074027 was found in NSCLC tissues and cells.Circ_0074027 acted as a sponge of miR-335-5p. The effect of circ_0074027 knockdown on NSCLC progression was weakened by miR-335-5p inhibition. Moreover, CUL4B was a target gene of miR-335-5p. CUL4B overexpression reversed the inhibitory effects on cell viability, cell cycle process, and colony formation and the promotional effect on cell apoptosis caused by miR-335-5p in NSCLC.		Yes	Circ_0074027 knockdown suppressed cell viability, cell cycle process, and colony formation and promoted apoptosis in NSCLC cells in vitro and inhibited tumor growth in vivo.	32580576
hsa_circ_0008797	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-301a-3p/SOCS2)	RNA Pull-Down//ISH//Tunel//CCK8//RIP//Luciferase Report Assay//Transwell Assay	circ_0008797 was low expressed in NSCLC tissues and cell lines, associating with poor outcome (p <.05).  circ_0008797 attenuated malignant phenotype of NSCLC cells by sponging miR-301a-3p. circ_0008797 facilitated SOCS2 expression by sponging miR-301a-3p. SOCS2 knockdown partially reversed the inhibitory effect of miR-301a-3p inhibition on NSCLC cells malignant phenotype (p <.05). circ_0008797 attenuated NSCLC prolifearion and metastasis in vivo (p <.05).		Yes	 circ_0008797 inhibited proliferation, migration, invasion, and glycolysis, but enhanced apoptosis of NSCLC cells (p <.05).	35305058
hsa_circ_0000520	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-1258/AKT3 Axis)	CCK8//qRT-PCR//Western Blot	circ_0000520 was upregulated in NSCLC. miR-1258 was identified as the downstream target of circ_0000520. miR-1258 overexpression weakened the effect of circ_0000520 overexpression on NSCLC cells. miR-1258 targeted and inhibited AKT3. circ_0000520 positively regulated the AKT3 expression in NSCLC cells by sponging miR-1258.	Highly expressed circ_0000520 is linked to the NSCLC patient's advanced TNM stage and lymph node metastasis.	Yes	circ_0000520 overexpression facilitated NSCLC cell growth, migration, and invasion.	36593867
hsa_circ_0001666	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-1184/miR-548I/AGO1 axis)	Wound Healing Assay//Migration Assay//RIP//FISH//Luciferase Report Assay//Invasion Assay	Herein, we discovered that a circRNA, hsa_circ_0001666 (circ0001666), was highly expressed in NSCLC tissues and cell lines, and it was positively correlated with NSCLC tumor pathological grade and lymph node metastasis. Mechanistically, circ0001666 could act as a sponge to miR-1184/miR-548I and upregulate the expression of AGO1, thereby promoting the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR signaling pathway in NSCLC cells. 	Herein, we discovered that a circRNA, hsa_circ_0001666 (circ0001666), was highly expressed in NSCLC tissues and cell lines, and it was positively correlated with NSCLC tumor pathological grade and lymph node metastasis. Moreover, Kaplan-Meier survival analysis implied that NSCLC patients with high circ0001666 expression were negatively correlated with favorable survival. 	Yes	Functionally, circ0001666 could promote migration and invasion of NSCLC cells in vitro and in vivo.	35284630
circSHKBP1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Interaction( miR-1294/PKM2 axis)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//ELISA//Colony Formation Assay	 circSHKBP1 was found to be upregulated in NSCLC tissues and cell lines and was enriched in exosomes derived from NSCLC cells. miRNA-1294 was identified as a target for circSHKBP1, and circSHKBP1 upregulated PKM2 expression by sponging miR-1294.  Exosomal circSHKBP1 regulated glycolysis through PKM2 in a HIF-1α-dependent manner in NSCLC cells and promoted M2 polarization and macrophage recruitment. Moreover, exosomal circSHKBP1 promoted NSCLC cell growth, metastasis, and M2 infiltration in vivo. Thus, exosomal circSHKBP1 participated in the progression of NSCLC via the miR-1294/PKM2 axis. circSHKBP1 may be potential biomarker for the diagnosis and treatment of NSCLC.		Yes	Exosomal circSHKBP1 enhanced the proliferation, migration, invasion, and stemness of NSCLC cells. 	35229026
circLIFR	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-429/CELF2/PTEN/AKT-signaling pathways )	CCK8//qRT-PCR//Colony Formation Assay//EdU Staining	CircLIFR, circular, and stable transcript in NSCLC cells, was decreased more than 2 folds in NSCLC tissues and cells than controls (P < 0.0001).  Importantly, overexpression of circLIFR impeded cell proliferation, migration, invasion, and inactivated protein kinase B (AKT)/phosphatase and tensin homolog (PTEN)-signaling pathways while enhanced apoptosis and cell-cycle arrest in NSCLC cells, which was overturned by upregulation of miR-429 or silencing of CELF2. Furthermore, the upregulation of circLIFR inhibited NSCLC tumor growth in vivo.		Yes	 Importantly, overexpression of circLIFR impeded cell proliferation, migration, invasion, and inactivated protein kinase B (AKT)/phosphatase and tensin homolog (PTEN)-signaling pathways while enhanced apoptosis and cell-cycle arrest in NSCLC cells, which was overturned by upregulation of miR-429 or silencing of CELF2. Furthermore, the upregulation of circLIFR inhibited NSCLC tumor growth in vivo.	36104590
circPITX1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-30e-5p/ITGA6 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	circ-PITX1 was substantially up-regulated in NSCLC tissues and cells, and circ-PITX1 up-regulation was correlated with NSCLC patients' poor survival.  Mechanistically, circ-PITX1 acted as a sponge of miR-30e-5p, which targeted the 3'untranslated region (UTR) of ITGA6. Knockdown of circ-PITX1 or overexpressing miR-30e-5p reduced ITGA6/PI3K/AKT axis. 	circ-PITX1 was substantially up-regulated in NSCLC tissues and cells, and circ-PITX1 up-regulation was correlated with NSCLC patients' poor survival. 	Yes	Functionally, circ-PITX1 overexpression or miR-30e-5p inhibition markedly facilitated proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), reduced apoptosis, and enhanced ITGA6/PI3K/AKT expression in NSCLC cells, whereas circ-PITX1 knockdown or miR-30e-5p up-regulation resulted in the opposite results.	35007184
hsa_circ_0025039	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-636/CORO1C axis)	CCK8//qRT-PCR//Western Blot	The expression of circ_0025039 and CORO1C was significantly increased, while miR-636 was decreased in NSCLC tissues and cells compared with controls. The neoplasm formation was repressed after circ_0025039 silencing. Additionally, circ_0025039 acted as a sponge for miR-636, which was found to target CORO1C. Importantly, the contribution of circ_0025039 to NSCLC progression was mediated by miR-636/CORO1C axis. 		Yes	 Circ_0025039 depletion repressed NSCLC cell proliferation, migration, invasion, tube-forming capacity, and sphere formation ability, but induced cell apoptosis.	35034254
hsa_circ_0007385	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-337-3p/LMO3 )	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Circ_0007385 expression was notably enhanced in NSCLC tissues and cell lines.  Circ_0007385 acted as a sponge for microRNA-337-3p (miR-337-3p), and circ_0007385 overexpression-mediated effects were largely overturned by the overexpression of miR-337-3p in NSCLC cells. MiR-337-3p interacted with the 3' untranslated region (3'UTR) of LIM-only protein 3 (LMO3). Circ_0007385 up-regulated LMO3 level by absorbing miR-337-3p in NSCLC cells. LMO3 overexpression largely reversed miR-337-3p overexpression-induced influences in NSCLC cells. 		Yes	Circ_0007385 facilitated the proliferation but suppressed the apoptosis of NSCLC cells. Circ_0007385 knockdown significantly restrained the growth of xenograft tumors in vivo.	36426731
hsa_circ_0006677	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC samples and cells	Interaction(miR-1245a/SATB2 )	qRT-PCR//Western Blot	We observed the downregulation of circ_0006677 in NSCLC samples and cells. Molecular mechanism experiments exhibited that circ_0006677 functioned as a miR-1245a sponge and mediated SATB2 expression through adsorbing miR-1245a. Either miR-1245a overexpression or SATB2 knockdown weakened circ_0006677 overexpression-mediated repression on proliferation, invasion, migration, and stemness.		Yes	Functionally, circ_0006677 overexpression decreased xenograft tumor growth and restrained NSCLC cell proliferation, invasion, migration, stemness, and induced NSCLC cell apoptosis in vitro.	35081869
hsa_circ_0007385	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC cells and tissues	Interaction(miR-493-3p/RAB22A axis)	CCK8//qRT-PCR//Western Blot	Expression of circ_0007385 and RAB22A increased, whereas miR-493-3p level was decreased in NSCLC tissues in contrast to that in normal tissues. Mechanically, circ_0007385 acted as a miR-493-3p sponge to modulate RAB22A expression. Moreover, circ_0007385 could regulate the development of NSCLC by sponging miR-493-3p to regulate the expression of RAB22A.		Yes	 For functional analysis, circ_0007385 deficiency inhibited cell proliferation and stemness, whereas it promoted cell apoptosis in NSCLC cells. In addition, circ_0007385 silence also attenuated tumor growth in vivo.	34989145
hsa_circ_0006427	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-346/VGLL4 Pathway)	qRT-PCR	Circ_0006427 expression was down-regulated in NSCLC tissues and cells, and circ_0006427 suppressed multiplication, migration, invasion and EMT of NSCLC cells.  miR-346 expression was upregulated in NSCLC tissues and cells, and miR-346 worked as a target of circ_0006427. VGLL4 was down-regulated in NSCLC tissues and cells, and knockdown of VGLL4 accelerated multiplication, migration, invasion and EMT of NSCLC cells. Circ_0006427 enhanced VGLL4 expression by competitively binding with miR-346.		Yes	Circ_0006427 expression was down-regulated in NSCLC tissues and cells, and circ_0006427 suppressed multiplication, migration, invasion and EMT of NSCLC cells. 	35717572
hsa_circ_0002476	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-1182/TFAM axis)	CCK8//qRT-PCR//Western Blot	Circ_0002476 was overexpressed in NSCLC tissues and cells.Circ_0002476 could sponge miR-1182, and miR-1182 inhibitor reversed the influence induced by circ_0002476 knockdown. Moreover, TFAM was targeted by miR-1182, and miR-1182 hindered NSCLC cell progression by regulating TFAM. Additionally, circ_0002476 silencing could reduce NSCLC tumor growth by miR-1182/TFAM. 		Yes	Circ_0002476 knockdown suppressed NSCLC cell proliferation and invasion, while promoted apoptosis and mtDNA damage.	36056804
circCAMSAP1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC lung tissues and cell lines	Interaction( circCAMSAP1/miR-1182/BIRC5 axis)	qRT-PCR//Western Blot	Overexpression of circCAMSAP1 has been demonstrated in NSCLC lung tissues and cell lines.Furthermore, a luciferase assay revealed that circCAMSAP1 could regulate baculoviral inhibitor of apoptosis protein (IAP) repeat containing 5 (BIRC5, also known as survivin) expression by directly binding to miR-1182. However, BIRC5 without 3' untranslated regions (3'UTR) could reverse the influence of downregulated circCAMSAP1 on proliferation and apoptosis in NSCLC. Together, our findings reveal a novel mechanism by which the circCAMSAP1/miR-1182/BIRC5 axis promotes NSCLC progression.		Yes	We also found that downregulated circCAMSAP1 repressed cell proliferation and increased apoptosis of NSCLC cells in vitro and suppressed xenograft tumor growth in vivo.	35132928
circPLK1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC patients and cells	Interaction(miR-1294/HMGA1 axis)	qRT-PCR//Western Blot	The Kaplan-Meier survival analysis revealed that a high expression level of circPLK1 was associated with a poorer prognosis in NSCLC patients. Molecular analyses demonstrated that circPLK1 directly targets miR-1294 and negatively regulates its activity. And circPLK1 overexpression facilitates the progression of NSCLC by negatively regulating miR-1294 level and maintaining a high-level expression of HMGA1 (High Mobility Group Protein A1). Our study suggests that circPLK1 upregulation plays an important role in NSCLC progression by targeting miR-1294/HMGA1 axis. 	The Kaplan-Meier survival analysis revealed that a high expression level of circPLK1 was associated with a poorer prognosis in NSCLC patients. 	Yes	Exosomes extracted from NSCLC serum could promote the replication, migration, and invasion of NSCLC cells and suppress apoptotic cell death. The overexpression of circPLK1 also promotes the malignant phenotype of NSCLC cells. 	35114891
hsa_circ_0006423	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue and cell line	Interaction(miR-492)	CCK8//qRT-PCR	We found has_circ_0006423 is lower expressed in NSCLC and miR-492 is opposite, has_circ_0006423 and miR-492 has diagnostic value in NSCLC.cThis effect may be due to the combination of has_circ_0006423 and miR-492 affecting the progression of NSCLC.		Yes	 In A549 and NCI-H1299 cells, hsa_circ_0006423 inhibited the proliferation, migration, and invasion of NSCLC cells by sponging miR-492 and accelerating NSCLC cell apoptosis. 	35962012
hsa_circ_0016760	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-876-3p/NOVA2 Axis)	CCK8//qRT-PCR	Circ_0016760 and NOVA2 were upregulated, while miR-876-3p expression was decreased in NSCLC tissues and cells.Circ_0016760 acted as a sponge of miR-876-3p, and miR-876-3p could target NOVA2. Circ_0016760 might play vital roles in NSCLC by regulating miR-876-3p/NOVA2 axis. Circ_0016760 could promote the malignant development of NSCLC through miR-876-3p/NOVA2 axis, at least in part.		Yes	Circ_0016760 depletion suppressed NSCLC cell proliferation and metastasis in vitro, as well as hampered tumor growth in vivo. 	35239092
circRAD23B	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-142-3p/MAP4K3 axis)	CCK8//qRT-PCR//Western Blot	 Circ-RAD23B was shown to be upregulated in NSCLC tissues and cells.  Knockdown of circ-RAD23B inhibited proliferation, migration, invasion, angiogenesis and promoted cell cycle arrest and apoptosis in NSCLC cells, and circ-RAD23B knockdown also impeded tumor growth in vivo. 		Yes	 Knockdown of circ-RAD23B inhibited proliferation, migration, invasion, angiogenesis and promoted cell cycle arrest and apoptosis in NSCLC cells, and circ-RAD23B knockdown also impeded tumor growth in vivo. 	35106926
hsa_circ_0017639	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation(PI3K/AKT signaling pathway)	CCK8//qRT-PCR//Western Blot	 Circ_0017639 expression was remarkably high in the NSCLC tissues and cell lines. We further showed that circ_0017639 knockdown suppressed the cellular development via PI3K/AKT cascade inactivation. 		Yes	 The transfection experiments showed that circ_0017639 overexpression was able to promote proliferative, migratory, and invasive properties of NSCLC cells, while sh-circ_0017639 showed opposing effects. 	35000535
hsa_circ_0007385	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-1253/FAM83A axis)	CCK8//qRT-PCR//Western Blot	Circ_0007385 was upregulated in NSCLC tissues and cells. In addition, miR-1253 was a direct target of circ_0007385, and miR-1253 reversed the inhibitory effects of circ_0007385 on cell proliferation and stemness in NSCLC cells. Moreover, FAM83A was a direct target of miR-1253, and miR-1253 suppressed NSCLC cell proliferation and stemness by targeting FAM83A. Exosomal circ_0007385 promoted NSCLC cell proliferation and stemness by regulating miR-1253/FAM83A axis.		Yes	Knockdown of circ_0007385 inhibited NSCLC cell proliferation and stemness, while exosomal circ_0007385 facilitated NSCLC cell proliferation and stemness. Furthermore, circ_0007385 knockdown inhibited tumor growth in vivo. 	34620741
circSFMBT2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-7-5p/ADAM10 axis)	CCK8//Flow Cytometry//EdU Staining//Transwell Assay	The expression levels of circ-SFMBT2 and ADAM10 were increased in NSCLC tissues and cell lines, while decreased the expression of miR-7-5p. circ-SFMBT2 was negatively correlated with miR-7-5p, while miR-7-5p was negatively correlated with ADAM10.circ-SFMBT2 could target miR-7-5p, and ADAM10 was the target gene of miR-7-5p. The combined effect of silencing circ-SFMBT2 and inhibition of miR-7-5p, as well as miR-7-5p overexpression and ADAM10 overexpression could promote cell proliferation, clone formation and invasion, and also suppress cell apoptosis. 		Yes	Silencing the overexpression of circ-SFMBT2 and miR-7-5p could inhibit cell proliferation, clone formation and invasion, and also promote apoptosis. Silencing circ-SFMBT2 could inhibit the growth of transplanted tumors.	35076912
circTP53	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues,cell lines	regulation[miR-876-3p/CDKL3 axis]	Western Blot//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	In our study, we found circTP53 was significantly up-regulated in colorectal cancer tissues from patients and in colorectal cell lines.  In conclusion, circTP53 was highly expressed in colorectal cancer tissues, and promoted colorectal cancer progression via modulating miR-876-3p/CDKL3 axis.		Yes	 At last, we suggested that circTP53 knockdown could inhibit colorectal cancer progression in vivo.	33232736
circTBL1XR1	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	regulation[CircTBL1XR1/miR-424 axis ]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	circTBL1XR1 was highly expressed in colon cancer patients.circTBL1XR1 was highly expressed in colon cancer, and miR-424 was poorly expressed in colon cancer cells. circTBL1XR1 regulates the expression of Smad7 through miR-424, thereby affecting the malignant progression of colorectal cancer.		Yes	In vivo and in vitro experimental results showed that overexpression of circTBL1XR1 enhanced the proliferation, migration, and invasion of colon cancer cells. After lowering circTBL1XR1, the ability of migration and invasion of colon cancer cells was significantly reduced. 	33209488
circFOXO3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	Interaction(miR-545-3p/miR-506-3p/HMGB3 )	qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis//Western Blot	Here, we show thatcircFOXO3 in NSCLC promotes the proliferation, migration and invasion of NSCLC cells, thereby promoting tumor growth. We further find that circFOXO3 sponges miR-545-3p/miR-506-3p that bind to 3'-UTR of HMGB3 mRNA, which constitutes the major network fulfilling the circFOXO3's promoting effect. 		Yes	Here, we show thatcircFOXO3 in NSCLC promotes the proliferation, migration and invasion of NSCLC cells, thereby promoting tumor growth. 	35038619
hsa_circ_0006508	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer samples and cells	Interaction( miR-1272)	qRT-PCR//Western Blot//ChIP	Upregulated circ_0006508 and downregulated miR-1272 were observed in colorectal cancer samples, which was associated with the TNM stage and overall survival.  Functional assays demonstrated that the hypoxia-induced upregulated circ_0006508 and downregulated miR-1272 promoted the viability and Warburg effect of colorectal cancer in vitro. Mechanistically, HIF-1α-induced circ_0006508 could directly sponge miR-1272, which played a suppressive role in glycolysis.	Upregulated circ_0006508 and downregulated miR-1272 were observed in colorectal cancer samples, which was associated with the TNM stage and overall survival. 	Yes	 Functional assays demonstrated that the hypoxia-induced upregulated circ_0006508 and downregulated miR-1272 promoted the viability and Warburg effect of colorectal cancer in vitro. 	36397308
circMERTK	CircRNA	Homo sapiens	Colorectal Neoplasms	TAMs	Interaction( circMERTK/miR-125a-3p/IL-10 axis)	qRT-PCR//Western Blot	Of note, the expression of circMERTK was remarkably overexpressed in TAMs. The ISH assay displayed that the expressions of circMERTK were mainly overlapped with macrophages marker CD68, and the abundance of circMERTK in CRC tissues was much higher than that in matched normal tissues.  Mechanically, TAM-like cell could exert immunosuppressive activity via circMERTK/miR-125a-3p/IL-10 axis.		Yes	Functionally, circMERTK knockdown resulted in attenuated CD8+ T cell apoptosis in the co-culture assay, indicating that circMERTK could have an impact on the immunosuppressive activity of TAM-like cell. 	36163585
circPLXNB1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-4701-5p)	qRT-PCR//MTT//Western Blot//Transwell Assay	The results showed that gene expression of circ_PLXNB1 in CRC tissues was significantly downregulated.  Mechanistically, circ_PLXNB1 exerted its functional effects by binding with miR-4701-5p. Moreover, TUSC1 siRNA partially abolished the suppressive effect of the miR-4701-5p inhibitor or circ_PLXNB1 on CRC cell malignant behaviors.		Yes	Overexpression of circ_PLXNB1 inhibited the malignant behaviors of CRC cells, as manifested by the decrease in cell proliferation, cell invasion, migration, and EMT. 	35434854
hsa_circ_0011385	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues or cells 	Interaction( miR-330-3p/MYO6 axis)	In Vivo Experiment//qRT-PCR//Luciferase Report Assay//Western Blot	 Circ_0011385 and MYO6 expression were dramatically upregulated, while miR-330-3p expression was downregulated in CRC tissues or cells compared with control groups.Circ_0011385 was associated with miR-330-3p, and miR-330-3p targeted MYO6. Circ_0011385 knockdown inactivated MEK1/2/ERK1/2 signaling pathway by miR-330-3p/MYO6 axis.	Circ_0011385 expression was associated with tumor size, tumor-node-metastasis stage (TNM) stage and lymph node metastasis of CRC patients. 	Yes	 Circ_0011385 silencing or MYO6 absence repressed cell proliferation, migration and invasion, whereas induced cell apoptosis in CRC. Additionally, miR-330-3p inhibitor or MYO6 overexpression attenuated the repressive impacts of circ_0011385 silencing on CRC process.	35091088
circRHOBTB3	CircRNA	Homo sapiens	Colorectal Neoplasms	 tissue samples 	Expression(highly expressed)	IF	 circRHOBTB3 levels were increased in the sera but was downregulated in tissue samples in CRC, and the downregulation was associated with poor prognosis.	 circRHOBTB3 levels were increased in the sera but was downregulated in tissue samples in CRC, and the downregulation was associated with poor prognosis.	Yes	Furthermore, circRHOBTB3 acts a tumor-suppressive circRNA by repressing metabolic pathways, intracellular ROS production in CRC.	35148775
circATAD1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-618 )	CCK8//qRT-PCR//Colony Formation Assay	 Circ-ATAD1 was upregulated in CRC and predicted poor survival.  In addition, circ-ATAD1 was inversely correlated with mature miR-618 but not premature miR-618.  In CRC cells, circ-ATAD1 overexpression decreased the level of mature miR-618 but not premature miR-618. A direct interaction between circ-ATAD1 and miR-618 was observed. Moreover, circ-ATAD1 overexpression reduced the inhibitory effects of miR-618 overexpression on cell proliferation.	 Circ-ATAD1 was upregulated in CRC and predicted poor survival. 	Yes	A direct interaction between circ-ATAD1 and miR-618 was observed. Moreover, circ-ATAD1 overexpression reduced the inhibitory effects of miR-618 overexpression on cell proliferation.	35505304
hsa_circ_0006174	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR‑1205/CCBE1/Wnt pathway)	Western Blot//Tunel//CCK8//qRT-PCR//Luciferase Report Assay	 Circ_0006174 showed a notable upregulation in CRC tissues and cell lines and its overexpression was linked to larger tumor diameter and advanced T stage of CRC patients. Mechanistically, circ_0006174 could decoy miR‑1205 to up‑modulate CCBE1 expression and Wnt pathway‑related proteins (c‑Myc and cyclin D1). Circ_0006174 is an oncogenic circRNA, which participates in the promotion of CRC progression by regulating the miR‑1205/CCBE1/Wnt pathway.	 Circ_0006174 showed a notable upregulation in CRC tissues and cell lines and its overexpression was linked to larger tumor diameter and advanced T stage of CRC patients. 	Yes	Circ_0006174 knockdown significantly suppressed cell growth and metastatic potential and promoted cell apoptosis in vitro. Circ_0006174 knockdown accelerated the lung metastasis in vivo. 	35674190
circCDC6	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor samples and cells	Interaction(miR-3187-3p/PRKAA2)	IHC//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	CircCDC6 showed poor expression in CRC tumor samples and cells.  MiR-3187-3p was targeted by circCDC6, and miR-3187-3p depletion also repressed CRC cell growth and glycolysis. PRKAA2 was a downstream target of circCDC6/miR-3187-3p pathway, and circCDC6 upregulated PRKAA2 expression via targeting miR-3187-3p. PRKAA2 knockdown rescued the functional effects of circCDC6 ectopic expression.		Yes	CircCDC6 ectopic expression repressed CRC cell proliferation, survival and glycolysis energy metabolism. CircCDC6 overexpression in vivo impeded tumor development in animal models. 	35438362
circTDRD3	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(HIF1α/PTBP1/circTDRD3/miR-1231/HIF1α axis)	ISH//qRT-PCR//RNA Pull-Down	 The expression of circTDRD3 was highly expressed in CRC tissues and positively correlated with overall survival, tumor size, lymph node invasion and clinical stage.  Mechanistically, circTDRD3 promoted HIF1α expression by sponging miR-1231, which facilitated CRC progression. Meanwhile, HIF1α directly combined with TDRD3 promoter to increase the expression of TDRD3 pre-mRNA. Then HIF1a-induced PTBP1 accelerated the formation of circTDRD3. 	 The expression of circTDRD3 was highly expressed in CRC tissues and positively correlated with overall survival, tumor size, lymph node invasion and clinical stage. 	Yes	 CircTDRD3 facilitated CRC cell proliferation, migration and metastasis in vitro and in vivo. 	36418471
circCAPRIN1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue specimens	Interaction(STAT2 )	ChIP//Western Blot//ISH//qRT-PCR//FISH//IHC//IF	 Among circRNAs, circCAPRIN1 was most significantly upregulated in CRC tissue specimens. circCAPRIN1 expression was positively correlated with the clinical stage and unfavorable prognosis of CRC patients.Further mechanistic assays demonstrated that circCAPRIN1 directly bound signal transducer and activator of transcription 2 (STAT2) to activate ACC1 transcription, thus regulating lipid metabolism and facilitating CRC tumorigenesis.	 Among circRNAs, circCAPRIN1 was most significantly upregulated in CRC tissue specimens. circCAPRIN1 expression was positively correlated with the clinical stage and unfavorable prognosis of CRC patients.	Yes	Downregulation of circCAPRIN1 suppressed proliferation, migration, and epithelial-mesenchymal transition of CRC cells, while circCAPRIN1 overexpression had opposite effects.RNA sequencing and gene ontology analysis indicated that circCAPRIN1 upregulated the expressions of genes involved in CRC lipid metabolism. Moreover, circCAPRIN1 promoted lipid synthesis by enhancing Acetyl-CoA carboxylase 1 (ACC1) expression. 	36328987
circKIAA1199	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-34c-5p/MSI1 )	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of circ_KIAA1199 was elevated in CRC. MiR-34c-5p was a target of circ_KIAA1199. The effects of circ_KIAA1199 downregulation were reversed by miR-34c-5p deficiency. In addition, MSI1 was a target of circ_KIAA1199, and the inhibitory effects of miR-34c-5p restoration on CRC cell proliferation, survival, migration and invasion were reversed by MSI1 overexpression. Circ_KIAA1199 positively regulated MSI1 expression by targeting miR-34c-5p.		Yes	 Circ_KIAA1199 downregulation suppressed CRC cell proliferation, survival, migration and invasion. 	34387591
hsa_circ_0000395	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC samples and cell lines	Interaction(miR-432-5p/MYH9)	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	Circ_0000395 was strongly expressed in CRC samples and cell lines. Mechanistically, circ_0000395 sequestered miR-432-5p to regulate MYH9 expression. Furthermore, miR-432-5p knockdown reversed circ_0000395 silencing-mediated effects on CRC cell malignant phenotypes. MYH9 overexpression counteracted the inhibiting effects of miR-432-5p upregulation on CRC cell malignant phenotypes. Additionally, CRC cells derived from exosomal circ_0000395 promoted cancer cell malignant phenotypes.		Yes	Also, circ_0000395 repressed CRC growth in mouse models in vivo and induced CRC cell apoptosis, restrained CRC cell proliferation, migration, invasion, and EMT in vitro. 	35759156
circALG1	CircRNA	Homo sapiens	Colorectal Neoplasms	peripheral blood and tumour tissues of patients	Interaction(miR-342-5p/PGF )	qRT-PCR//FISH//RIP//Transwell Assay	CircALG1 was highly expressed in both the peripheral blood and tumour tissues of patients with CRC and was closely associated with CRC metastasis. Further mechanistic studies showed that circALG1 upregulated the expression of placental growth factor (PGF) by binding to miR-342-5p and that m6A modification enhanced the binding of circALG1 to miR-342-5p and promoted its ceRNA function.		Yes	CircALG1 overexpression promoted the migration and invasion of CRC cells, and circALG1 silencing and reduction of the circALG1 m6A modification level inhibited CRC cell migration and invasion. In vivo experiments further confirmed the prometastatic role of circALG1 in CRC. 	35305647
circIFT80	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and tumor cells	Interaction(miR-142, miR-568, and miR-634/ Wnt/β-catenin pathway)	qRT-PCR//Wound Healing Assay//Luciferase Report Assay	 In this present study, we found that circIFT80 was abnormally overexpression in colorectal cancer tissues and tumor cells.  In conclusion, our work reveals the impacts of circIFT80 as ceRNA in the progression of CRC, by which sponging miR-142, miR-568, and miR-634 enhanced the expression levels of β-catenin and activation Wnt/β-catenin pathway. 		Yes	 While knockout circIFT80 in HT29 cell or SW480 cells, the proliferation, and migration of the cells were inhibited, the cell cycle was arrested in G2/M phase, and the cell apoptosis was increased. 	35783013
hsa_circ_0000467	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues and cells	Regulation(miR-330-5p-Dependent Regulation of TYRO3)	qRT-PCR//IHC//Luciferase Report Assay//RIP	Circ_0000467 was a stable circRNA and was highly expressed in CRC tumor tissues and cells. Silencing of circ_0000467 could inhibit the proliferation, migration, invasion, and glycolysis and accelerated the apoptosis of CRC cells in vitro and hindered tumor growth in vivo. Mechanistically, circ_0000467 directly interacted with miR-330-5p and circ_0000467 depletion inhibited CRC cell malignant progression by regulating miR-330-5p. Furthermore, TYRO3 was a target of miR-330-5p and circ_0000467 upregulated TYRO3 expression by sponging miR-330-5p. Moreover, TYRO3 overexpression counteracted the inhibitory effect of miR-330-5p overexpression or circ_0000467 knockdown on CRC cell progression. Altogether, circ_0000467 knockdown suppressed CRC cell malignant development through modulating the miR-330-5p/TYRO3 network, providing a novel molecular target of CRC therapy.		Yes	Silencing of circ_0000467 could inhibit the proliferation, migration, invasion, and glycolysis and accelerated the apoptosis of CRC cells in vitro and hindered tumor growth in vivo.	35039980
hsa_circ_0039857	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(hsa_circ_0039857/miR-338-3p/RAB32 axis)	Western Blot//Transfection//qPCR//PCR//Bioinformatics Analysis//IF	This study demonstrated that circ_0039857 knockdown suppressed CRC malignant progression through miR-338-3p/RAB32 axis. Most importantly, this will help us to better understand the circRNA network in CRC, and may find potential biomarkers and targets for CRC clinical treatment.	We revealed that circ_0039857 was significantly enhanced in CRC. Circ_0039857 was stabler than linear RNA in cells and valuable for the disease diagnosis.	Yes	In addition, circ_0039857 knockdown inhibited proliferation and promoted apoptosis. Mechanistically, circ_0039857 positively regulated the expression of RAB32 via sponging miR-338-3p.	36539702
hsa_circ_0022340	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(HNRNPC/EBF1/SYT7 or miR-382-5p/ELK1 axis)	qRT-PCR//RIP//Western Blot	Results showed that Circ_0022340 was highly expressed in CRC cells. Circ_0022340 was formed from exon 5 to 6 of the synaptotagmin 7 (SYT7). Silencing of circ_0022340 suppressed CRC cell proliferation and migration. Functionally, circ_0022340 recruited heterogeneous nuclear ribonucleoprotein C (HNRNPC) to stabilize EBF1 mRNA and thereby activated SYT7. Moreover, circ_0022340 targeted miR-382-5p to up-regulate ETS transcription factor ELK1 (ELK1). It is concluded that Circ_0022340 promoted colorectal cancer progression via recruiting HNRNPC to stabilize EBF1 mRNA and thereby activated SYT7 or miR-382-5p/ELK1 axis, which might provide a novel target for CRC treatment.		Yes	Silencing of circ_0022340 suppressed CRC cell proliferation and migration. Functionally, circ_0022340 recruited heterogeneous nuclear ribonucleoprotein C (HNRNPC) to stabilize EBF1 mRNA and thereby activated SYT7.	36495510
hsa_circ_0068464	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells and tissues	Interaction(miR-383/Wnt/β-catenin pathway)	Western Blot//qRT-PCR//FISH//RIP//MTT//Luciferase Report Assay//Transwell Assay	The results revealed that circ_0068464 was abnormally up-regulated in CRC cells and tissues. Further, the binding interaction between circ_0068464 and microRNA-383 (miR-383) was verified by dual-luciferase assay and RNA immunoprecipitation assay. And miR-383 was significantly down-regulated in CRC tissues and cells. Interfering with miR-383 expression reversed the inhibitory effect of circ_0068464 knockdown on CRC cells. In conclusion, circ_0068464 targets miR-383 to regulate Wnt/β-catenin pathway activation, thereby promoting the development of CRC.		Yes	Knockdown of circ_0068464 could inhibit CRC cell migration and proliferation and promoted apoptosis while suppressing the expression of Wnt/β-catenin pathway-related proteins (β-catenin, cyclin D1, C-myc and LEF-1). In addition, tumorigenic assays in nude mice confirmed that circ_0068464 downregulation significantly inhibited tumor growth and lung metastasis.	35168468
hsa_circ_0084927	CircRNA	Homo sapiens	Colorectal Neoplasms	 COAD tissues and cell lines	Interaction(has_circ_0084927/miR-106b-5p/VEGFA)	CCK8//qRT-PCR	Our study found that hsa_circ_0084927 is highly expressed in COAD tissues and cell lines. In addition, we effectively constructed a ceRNA: network has_circ_0084927/miR-106b-5p/VEGFA. 		Yes	Plasma hsa_circ_0084927 can be used as a diagnostic marker for COAD patients; hsa_circ_0084927 can promote the proliferation, migration and invasion of COAD cells. 	35493197
hsa_circ_0040809	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-330-3p/RUNX1)	qRT-PCR//Bioinformatics Analysis	Two DEcircRNAs (hsa_circ_0040809 and hsa_circ_0000467) were identified and validated in CRC tissues and cell lines. The results of MTs and Transwell experiments showed that hsa_circ_0040809 and hsa_circ_0000467 promoted CRC proliferation and migration.  Bioinformatics analysis screened 3 miRNAs (miR-326, miR-330-5p, and miR-330-3p) and 2 mRNAs (FADS1 and RUNX1), and a ceRNA network was constructed. In knockdown of hsa_circ_0040809 HCT-116 cells, the expression of miR-330-3p was significantly upregulated, while RUNX1 was significantly downregulated. In knockdown of hsa_circ_0000467 HCT-116 cells, the expressions of miR-326 and miR-330-3p were upregulated, while FADS1was downregulated.		Yes	Two DEcircRNAs (hsa_circ_0040809 and hsa_circ_0000467) were identified and validated in CRC tissues and cell lines. The results of MTs and Transwell experiments showed that hsa_circ_0040809 and hsa_circ_0000467 promoted CRC proliferation and migration. 	36339002
hsa_circ_0006732	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction( miR-127-5p/RAB3D axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Bioinformatics Analysis//Transwell Assay	It was found that hsa_circ_0006732 was highly expressed in CRC tissues and cell lines.Further mechanistic investigations proved that hsa_circ_0006732 functioned as a competitive endogenous RNA (ceRNA) by directly sponging of miR-127-3p, which further affected the expression of Ras-related protein Rab-3D (Rab3D). 		Yes	 Downregulation of hsa_circ_0006732 suppressed the proliferation, migration, invasion and EMT of CRC cells. 	35616807
hsa_circ_0066351	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell lines and tissues	Expression(lower expressed)	qRT-PCR//Colony Formation Assay	We proved that hsa_circ_0066351 was significantly downregulated in CRC cell lines and tissues (P < 0.001), and was negatively associated with distant metastasis (P < 0.01). 	 Significantly, the expression of hsa_circ_0066351 was associated with better survival in patients with CRC.	Yes	 Function assays showed that hsa_circ_0066351 could inhibit CRC cells proliferation.	36405685
hsa_circ_0000826	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(AUF1)	qRT-PCR//RIP//Western Blot	Here, we report that hsa_Circ_0000826 (Circ_0000826), a circRNA with significantly reduced expression level in CRC tissues, is associated with a poor prognosis in patients. Furthermore, Circ_0000826 could target AU-rich element RNA-binding protein 1 (AUF1). AUF1, known as heterogeneous nuclear ribonucleoprotein D (hnRNP D), could bind to the c-MYC 3'-UTR and promote c-MYC expression. When Circ_0000826 binds to AUF1, it competitively inhibits the binding of AUF1 to the c-MYC 3'-UTR, which inhibits the c-MYC expression and cell proliferation. 	Here, we report that hsa_Circ_0000826 (Circ_0000826), a circRNA with significantly reduced expression level in CRC tissues, is associated with a poor prognosis in patients. T	Yes	The silencing of Circ_0000826 promotes the proliferation of CRC cells. Conversely, the overexpression of Circ_0000826 restricted CRC cell proliferation both in vitro and in vivo. 	35940521
circPTK2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-136-5p/YTHDF1)	CCK8//qRT-PCR//RIP//Western Blot	In our study, circPTK2 abundance was enhanced in CRC and associated with liver metastasis, clinical stage and chemoresistance.  In conclusion, circPTK2 interference suppressed CRC proliferation, migration, invasion and chemoresistance via regulating miR-136-5p and YTHDF1.	In our study, circPTK2 abundance was enhanced in CRC and associated with liver metastasis, clinical stage and chemoresistance. 	Yes	 CircPTK2 knockdown constrained cell proliferation, migration, invasion, resistance to 5-FU and oxaliplatin, and the Wnt/β-catenin signaling.  In addition, we confirmed that circPTK2 silence reduced xenograft tumor growth.	34974791
circIFT80	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC patient serum and CRC cells	Interaction(miR-296-5p/MSI1 Axis)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Circ_IFT80 was upregulated in exosomes derived from CRC patient serum and CRC cells. Additionally, circ_IFT80 acted as a sponge of miR-296-5p, and miR-296-5p reversed the effects of circ_IFT80 on tumorigenesis and radiosensitivity. Moreover, MSI1 was a direct target of miR-296-5p. Furthermore, miR-296-5p overexpression inhibited tumorigenesis and promoted radiosensitivity by downregulating MSI1.		Yes	Exosomal circ_IFT80 or circ_IFT80 overexpression facilitated tumorigenesis by increasing cell proliferation and reducing apoptosis, and inhibited radiosensitivity via promoting colony formation and inhibiting apoptosis. Exosomal circ_IFT80 also accelerated tumor growth in vivo.	33658855
circASS1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells and tissues	Interaction(miR-1269a/VASH1 axis)	Western Blot//Wound Healing Assay//Tunel//qRT-PCR//MTT//Luciferase Report Assay	circASS1 expression was decreased in CRC cells and tissues, and circASS1 overexpression suppressed CRC cell proliferation, invasion and migration. circASS1 adsorbed miR-1269a and regulated its expression, and VASH1 was a target protein of miR-1269a.circASS1 overexpression decreased cell proliferation, invasion and migration, but enhanced cell apoptosis in HT29 cells, which was reversed by co-transfection with miR-1269a mimic or short hairpin RNA-VASH1. 		Yes	circASS1 expression was decreased in CRC cells and tissues, and circASS1 overexpression suppressed CRC cell proliferation, invasion and migration. 	34504600
circFAT1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-520b/ UHRF1 Axis or miR-302c-3p/ UHRF1 Axis)	CCK8//qRT-PCR//Western Blot	The levels of circFAT1 and UHRF1 were increased, as well as the levels of miR-520b and miR-302c-3p were decreased in CRC tissues and cells. Interestingly, circFAT1 was a sponge of miR-520b and miR-302c-3p, and miR-520b and miR-302c-3p could target UHRF1. Both miR-520b overexpression and miR-302c-3p overexpression inhibited CRC cell growth. Furthermore, both miR-520b knockdown and miR-302c-3p depletion weakened the effect of circFAT1 knockdown on the growth of CRC cells.		Yes	 CircFAT1 knockdown suppressed cell proliferation, cycle, and glycolysis as well as induced apoptosis.Besides, circFAT1 depletion repressed tumor growth in vivo. 	32379550
circEIF3K	CircRNA	Homo sapiens	Colorectal Neoplasms	exosome	Interaction(miR-214/PD-L1 axis)	CCK8//qRT-PCR//Western Blot	We found that hypoxia could induce secretion of circEIF3K exosome. Besides, we observed that circEIF3K knockdown evidently impaired tumor growth in mice. TCGA dataset analysis showed that low expression of circEIF3K was observed in normal tissues and associated with prolonged survival time. Finally, PD-L1 was confirmed as important target for miR-214 in CRC.	Besides, we observed that circEIF3K knockdown evidently impaired tumor growth in mice. TCGA dataset analysis showed that low expression of circEIF3K was observed in normal tissues and associated with prolonged survival time. 	Yes	Conditioned medium (CM) and exosome from circEIF3K knockdown CAF significantly attenuated proliferation, invasion and tube formation of HCT116 or SW620 cells, which could be reverted by miR-214 under hypoxia treatment. 	34412616
hsa_circ_0101802	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues and cells	Interaction(miR-1236-3p/MACC1 axis)	CCK8//qRT-PCR//Western Blot	Our results showed that circ_0101802 was highly expressed in CRC tumor tissues and cells.  In summary, our results revealed that circ_0101802 functioned as a tumor promoter in CRC, which could facilitate CRC proliferation, migration and invasion via regulating the miR-1236-3p/MACC1 axis.		Yes	Functional experiments suggested that circ_0101802 knockdown could inhibit the proliferation, migration and invasion of CRC cells in vitro and CRC tumorigenesis in vivo. 	34294360
circKRT6C	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	Interaction(miR-485-3p/PDL1 )	In Vivo Experiment//qRT-PCR//Luciferase Report Assay//Western Blot	 circ-KRT6C was overexpressed in colorectal cancer tissues and cells, and its level was associated with overall survival time of patients with colorectal cancer. circ-KRT6C could increase PDL1 expression by functioning as an miR-485-3p sponge, which promoted malignant progression and immune evasion of colorectal cancer cells. 		Yes	The suppression of circ-KRT6C suppressed growth, migration, invasion, and immune escape while stimulating apoptosis in colorectal cancer cells, which was abolished by shortage of miR-485-3p. In addition, overexpression of miR-485-3p repressed malignant progression and immune evasion of colorectal cancer by targeting PDL1, implying that PDL1 was a functional target of miR-485-3p. A xenograft experiment also suggested that circ-KRT6C inhibition could repress tumor growth in vivo. 	33771844
circIL4R	CircRNA	Homo sapiens	Colorectal Neoplasms	 sera and tissues from CRC patients	Interaction(miR-761/TRIM29)	qRT-PCR//IHC//ChIP	 CircIL4R was upregulated in CRC cell lines and in sera and tissues from CRC patients and was positively correlated with advanced clinicopathological features and poor prognosis. Mechanistically, circIL4R was regulated by TFAP2C and competitively interacted with miR-761 to enhance the expression of TRIM29, thereby targeting PHLPP1 for ubiquitin-mediated degradation to activate the PI3K/AKT signaling pathway and consequently facilitate CRC progression.	 CircIL4R was upregulated in CRC cell lines and in sera and tissues from CRC patients and was positively correlated with advanced clinicopathological features and poor prognosis. 	Yes	 Functional experiments demonstrated that circIL4R promotes CRC cell proliferation, migration, and invasion via the PI3K/AKT signaling pathway. 	34922544
hsa_circ_0087862	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-142-3p/BACH1 )	CCK8//qRT-PCR//FISH//RIP//ChIP	 Circ_0087862 was highly expressed in CRC tissues and cell lines. miR-142-3p inhibition weakened the impact of circ_0087862 knockdown on CRC cells. Circ_0087862 regulated BACH1 expressions by targeting miR-142-3p. Circ_0087862 regulates BACH1 expressions through sponging miR-142-3p, and promotes the proliferation, migration, and invasion of CRC cells.		Yes	 Knocking down circ_0087862 significantly restrained the multiplication, migration and invasion of CRC cells.	34390174
circN4BP2L2	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(miR-340-5p/CXCR4 axis)	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	 Our data indicated that circN4BP2L2 expression was increased in CRC tissues and cell lines.Mechanistic studies revealed that circN4BP2L2 acted as a molecular sponge of miR-340-5p to competitively promote CXCR4 expression. Furthermore, inhibition of miR-340-5p reversed the anti-cancer effects of circN4BP2L2 or CXCR4 silencing. 		Yes	Notably, inhibition of circN4BP2L2 effectively inhibited proliferation, migration, and invasion of LoVo cells, and inhibited tumor growth and metastasis in vivo, whereas the forced expression of circN4BP2L2 facilitated the proliferation, migration, and invasion of HT-29 cells.	34326457
circMMP1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-1238)	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We identified circMMP1 (hsa_circ_0024109) as a frequently upregulated circRNA in both CRC tissues and cells. The results demonstrated that circMMP1 promoted the growth and metastasis of CRC by sponging miR-1238 and upregulating the expression of matrix metalloproteinase 1 (MMP1), MMP2, and MMP9 expression.		Yes	Both in vitro and in vivo experiments demonstrated that circMMP1 knockdown significantly inhibited the proliferation and metastasis of CRC. 	34532478
hsa_circ_0026416	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues and cell lines	Interaction( miR-545-3p/MYO6)	CCK8//qRT-PCR//Flow Cytometry//Western Blot	The expression of circ_0026416 was increased in CRC tumor tissues and cell lines.MiR-545-3p was a target of circ_0026416, and rescue experiments indicated that circ_0026416 knockdown blocked CRC development by enriching miR-545-3p. In addition, miR-545-3p targeted MYO6 and inhibited MYO6 expression. 		Yes	Circ_0026416 downregulation inhibited CRC cell proliferation, colony formation, migration, invasion, and EMT but induced cell apoptosis in vitro, and circ_0026416 knockdown also blocked tumor growth in vivo. 	34645476
circRUNX1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-485-5p/SLC38A1 axis)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	 CircRUNX1 was upregulated in CRC tissues and cells compared with normal tissues and cells. CircRUNX1 directly sponged miR-485-5p, which negatively modulated SLC38A1 expression in CRC cells. Moreover, miR-485-5p overexpression repressed the malignant behaviours of CRC cells, with SLC38A1 elevation overturned the impacts.		Yes	CircRUNX1 deficiency restrained CRC cell colony formation, migration, invasion and glutaminolysis and induced apoptosis in vitro as well as blocked tumour growth in vivo. The effects of circRUNX1 knockdown on CRC cell colony formation, migration, invasion, apoptosis and glutaminolysis were reversed by miR-485-5p inhibition. 	33769559
hsa_circ_3823	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-30c-5p/TCF7 axis)	CCK8//qRT-PCR//IHC//IF	Circ3823 was evidently highly expressed in CRC and high circ3823 expression predicted a worse prognosis of CRC patients. Mechanism analysis showed that circ3823 act as a competing endogenous RNA of miR-30c-5p to relieve the repressive effect of miR-30c-5p on its target TCF7 which upregulates MYC and CCND1, and finally facilitates CRC progression. 	Circ3823 was evidently highly expressed in CRC and high circ3823 expression predicted a worse prognosis of CRC patients. 	Yes	 Functional experiments in vitro and in vivo indicated that circ3823 promote CRC cell proliferation, metastasis and angiogenesis.	34172072
circPLCE1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(SRSF2/PLCE1 )	qRT-PCR//Bioinformatics Analysis//Western Blot	 In this study, we found that circPLCE1 was more significantly down-regulated in CRC tissues compared with that in adjacent normal tissues.  Mechanistically, circPLCE1 directly bound to the SRSF2 protein, repressing SRSF2-dependent PLCE1 pre-RNA splicing, resulting in the progression of CRC. Individually mutating the binding sites of circPLCE1 abolished the inhibition of PLCE1 mRNA production.		Yes	 However, circPLCE1 knockdown suppressed CRC cell proliferation, migration and invasion and increased apoptosis. Nude mouse experiments showed that ectopic expression of circPLCE1 dramatically increased tumour growth in vivo. 	34173324
hsa_circ_0104103	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(HuR and miR-373-5p)	RNA Pull-Down//Western Blot//RIP//Luciferase Report Assay//IHC	We identified circ0104103, which is strongly downregulated in CRC tissues and cell lines. Mechanistically, circ0104103 binds to HuR, a functional RNA-binding protein commonly expressed in CRC. HuR binds to the 3'UTR of LACTB mRNA to facilitate stabilization and increase its expression. Moreover, circ0104103 was verified as a competing endogenous RNA (ceRNA) via negative regulation of miR-373-5p to increase LACTB expression, resulting in inhibiting the occurrence and progression of CRC.		Yes	Functional studies revealed that circ0104103 inhibited CRC cell growth, migration, and invasion both in vitro and in vivo. 	36562402
hsa_circ_102049	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miRNA-455-3p)	qRT-PCR//Luciferase Report Assay	The results demonstrated that hsa_circRNA_102049 was highly expressed in both CRC tissues and cell lines, which was associated with enhanced CRC cell proliferation, migration and invasion. Moreover, the results indicated that the circular RNA, hsa_circRNA_102049, may function as a tumor promoter in CRC via directly sponging miRNA-455-3p.		Yes	The results demonstrated that hsa_circRNA_102049 was highly expressed in both CRC tissues and cell lines, which was associated with enhanced CRC cell proliferation, migration and invasion.	35222721
circLRCH3	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(miRNA-223/LPP Axis)	Transwell Assay//qRT-PCR//Luciferase Report Assay//Western Blot	We found that the expression level of circLRCH3 was downregulated in CRC cells and negatively correlated with miR-223. In contrast, overexpression of miR-223 and depletion of LPP severally abrogated the tumor suppressive roles of circLRCH3 and miR-223 knockdown in CRC cells in vitro. The xenograft experiments in nude mice also proved the antitumor effect of circLRCH3.		Yes	The overexpression of circLRCH3 or silencing of miR-223 inhibited the growth, invasion, and migration of CRC cells, but promoted their apoptosis.The xenograft experiments in nude mice also proved the antitumor effect of circLRCH3.	35611368
hsa_circ_0007334	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction( miR-577/KLF12 axis )	qRT-PCR	 Circ_0007334 and KLF12 were increased, and miR-577 was decreased in CRC tissues and cells.Also, circ_0007334 expression was upregulated in CRC cell-derived exosomes.Mechanically, circ_0007334 could regulate KLF12 expression by sponging miR-577. 		Yes	Circ_0007334 deficiency repressed cell viability, colony formation, migration, invasion, and angiogenesis in CRC cells.Circ_0007334 downregulation or exosomal circ_0007334 silencing blocked CRC tumor growth in vivo. 	34459455
hsa_circ_0000467	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-326 and miR-330-3p/FADS1)	qRT-PCR//Bioinformatics Analysis	Two DEcircRNAs (hsa_circ_0040809 and hsa_circ_0000467) were identified and validated in CRC tissues and cell lines. The results of MTs and Transwell experiments showed that hsa_circ_0040809 and hsa_circ_0000467 promoted CRC proliferation and migration.  Bioinformatics analysis screened 3 miRNAs (miR-326, miR-330-5p, and miR-330-3p) and 2 mRNAs (FADS1 and RUNX1), and a ceRNA network was constructed. In knockdown of hsa_circ_0040809 HCT-116 cells, the expression of miR-330-3p was significantly upregulated, while RUNX1 was significantly downregulated. In knockdown of hsa_circ_0000467 HCT-116 cells, the expressions of miR-326 and miR-330-3p were upregulated, while FADS1was downregulated.		Yes	Two DEcircRNAs (hsa_circ_0040809 and hsa_circ_0000467) were identified and validated in CRC tissues and cell lines. The results of MTs and Transwell experiments showed that hsa_circ_0040809 and hsa_circ_0000467 promoted CRC proliferation and migration. 	36339002
circHIPK2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-485-5p/HSP90 )	qRT-PCR//Luciferase Report Assay//Western Blot	circHIPK2 expression was upregulated in patients with CRC compared with paracancerous tissues. In contrast, patients with high circHIPK2 expression had lower overall survival rate and disease-free survival rate than those with low circHIPK2 expression.circHIPK2 promoted CRC progression. miR-485-5p reduced CRC progression. miR-485-5p, as the target of circHIPK2 in CRC model, played a role in promoting CRC progression and expediting HSP90 ubiquitination. HSP90 ubiquitination by miR-485-5p can promote cell proliferation. 	 In contrast, patients with high circHIPK2 expression had lower overall survival rate and disease-free survival rate than those with low circHIPK2 expression.	Yes	circHIPK2 promoted CRC progression. miR-485-5p reduced CRC progression. miR-485-5p, as the target of circHIPK2 in CRC model, played a role in promoting CRC progression and expediting HSP90 ubiquitination. HSP90 ubiquitination by miR-485-5p can promote cell proliferation. 	36017914
hsa_circ_0106714	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	regulation[Hippo-YAP signaling]	Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Transwell Assay	Findings revealed that circ0106714 and DLG2 were significantly downregulated, while miR-942-5p was significantly upregulated in human CRC tissues and cell lines. In sum, circ0106714 could suppress CRC by sponging miR-942-5p and releasing DLG2, thus promoting YAP phosphorylation.		Yes	 However, circ0106714 upregulation significantly suppressed tumor progression in vivo and inhibited the malignancy phenotypes of tumor cells in vitro by targeting miR-942-5p. 	33128289
circPTK2	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells	Interaction(circPTK2/miR-506-3p/AKT2 axis )	qRT-PCR//MTT//Colony Formation Assay//Western Blot	 The expressions of circPTK2 and AKT2 were elevated in CRC cells, with a concomitant reduction of miR-506-3p.  The circPTK2/miR-506-3p/AKT2 axis plays a novel and essential role in promoting CRC progression, providing potential targets for CRC therapeutic modality.		Yes	 The knockdown of circPTK2 suppressed the proliferation, migration, and invasion of CRC cells.	36156852
hsa_circ_104916	CircRNA	Homo sapiens	Colonic Neoplasms	CRC tissues,cell lines(Caco-2, LoVo, SW480, HT-29 and HCT116)	Expression[Expression[lower expressed]-expression]	CCK8//qRT-PCR//Western Blot//Transwell Assay	In the present study, we show that circRNA_104916 is Expression[down-expression]regulated in colorectal cancers as compared to the adjacent normal tissues.	The expression of circRNA_104916 is negatively correlated with the tumor size, T stage and lymphatic metastasis. Patients with higher relative circRNA_104916 expression have a better post-operative disease-free survival as compared with those with lower relative expression.	Yes	Additionally, overexpression of circRNA_104916 significantly sExpression[Expression[up-expression]-expression]presses migration and invasion of tumor cells by inhibiting the epithelial-mesenchymal transition. 	30844715
hsa_circ_0001038	CircRNA	Homo sapiens	Colonic Neoplasms	CC tissues,cell lines	Interaction[activating CNNM3 and MACC1]	qRT-PCR//Luciferase Report Assay	 We found that hsa_circ_0001038 was highly expressed in CC cells and tissues and elevated hsa_circ_0001038 was closely related to the clinical severity including lymph node invasion and myometrial invasion.For mechanism investigation, hsa_circ_0001038 could sponge miR-337-3p to release its suppression on cyclin-M3 (CNNM3) and metastasis-associated in colon cancer 1 (MACC1), thereby promoting CC cell growth and invasive potential, respectively. In conclusion, hsa_circ_0001038 plays an oncogenic role in CC cells partly by activating CNNM3 and MACC1.	 We found that hsa_circ_0001038 was highly expressed in CC cells and tissues and elevated hsa_circ_0001038 was closely related to the clinical severity including lymph node invasion and myometrial invasion.In addition, overexpressed hsa_circ_0001038 correlated with unfavorable outcome in CC patients.	Yes	Knockdown of hsa_circ_0001038 attenuated cell growth, migration, and invasion but induced cell apoptosis. 	31809842
circPIP5K1A	CircRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissue	Interaction[inhibiting miR-1273a]	qRT-PCR//Transwell Assay//Western Blot	CircPIP5K1A was significantly upregulated in colon cancer tissue relative to their adjacent normal tissues.Bioinformatics prediction program predicted that the association of circPIP5K1A with miR-1273a, as well as AP-1, IRF-4, CDX-2, and Zic-1. Subsequent studies showed that overexpression of circPIP5K1A augmented the expression of AP-1 but attenuated the expression of IRF-4, CDX-2, and Zic-1. Reciprocally, overexpression of miR-1273a abrogated the oncogenic function of circPIP5K1A in colon cancers.		Yes	Knockdown of circPIP5K1A in colon cancer cells impaired cell viability and suppressed cell invasion and migration, while enforced expression of circPIP5K1A exhibited the opposite effects on cell migration. 	31558874
hsa_circ_0020095	CircRNA	Homo sapiens	Colonic Neoplasms	CC tissues and cells	regulation[miR-487a-3p/SOX9 axis]	qRT-PCR	We demonstrated that circ_0020095 was highly expressed in CC tissues and cells. Circ_0020095 functions as an oncogene to accelerate CC cell proliferation, invasion, migration and cisplatin resistance through the miR-487a-3p/SOX9 axis, which could be a promising target for CC treatment.		Yes	The proliferation, migration, invasion, and cisplatin resistance of CC were suppressed by silencing circ_0020095 in vitro and in vivo or by ectopic expression of miR-487a-3p in vitro.	33520987
hsa_circ_100859	CircRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	regulation[miR-217-HIF-1α pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	It was identified that circRNA_100859 was overexpressed in colon cancer tissues and promoted cell proliferation and inhibited cell apoptosis. In addition, the circRNA_100859-miR-217-HIF-1α axis may serve as a novel diagnostic and prognostic biomarker for patients with colon cancer.		Yes	It was identified that circRNA_100859 was overexpressed in colon cancer tissues and promoted cell proliferation and inhibited cell apoptosis.	32644049
hsa_circ_000166	CircRNA	Homo sapiens	Colonic Neoplasms	CC tissue and cell lines	regulation[miR-330-5p/ELK1]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	hsa_circRNA_000166 was significantly upregulated in the human CC tissue and in the CC cell lines.The data of this study demonstrated that the hsa_circRNA_000166 could upregulated the expression of gene ELK1 by sponging miR-330-5p, which may contribute to a better understanding of the regulatory circRNA/miRNA/mRNA network and CC pathogenesis.		Yes	Knockdown of hsa_circRNA_000166 reduced cell viability, colony formation, migration and invasion in vitro and decreased tumor size and weight in vivo.	32606768
circFNDC3B	CircRNA	Homo sapiens	Colonic Neoplasms	CC cell lines and tissues	regulation[Snail]	Wound Healing Assay//CCK8//qRT-PCR//FISH//Transwell Assay	CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues.By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC.	The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. 	Yes	 Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. 	32241279
hsa_circ_0001313	CircRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cell lines	regulation[Circ-0001313/miRNA-510-5p/AKT2 axis ]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//EdU Staining	Consistent with the microarray analysis, circ-0001313 was highly expressed in colon cancer tissues and cell lines. In conclusion, our study revealed that circ-0001313 regulates the pathogenesis of colon cancer by sponging miRNA-510-5p to upregulate AKT2 expression.		Yes	Knockdown of circ-0001313 attenuated proliferative ability, but induced apoptosis of colon cancer cells.	32051753
circSMARCA5	CircRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Interaction(miR-552)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	Our data presented that circSMARCA5 was under-expressed in colon cancer tissues.		Yes	 Transfection with overexpressing circSMARCA5 plasmid restrained growth, migration and invasion of colon cancer cells. 	33749508
circPPP1R12A	CircRNA	Homo sapiens	Colonic Neoplasms	CC tissues and cells	Interaction(miR-375/CTNNB1 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our results showed that circPPP1R12A was a highly expressed circRNA in CC tissues and cells. MiR-375 could be sponged by circPPP1R12A, and its inhibitor could reverse the inhibition of circPPP1R12A silencing on CC progression. Furthermore, CTNNB1 was a target of miR-375, and its overexpression also abolished the suppression of miR-375 on CC progression. Moreover, circPPP1R12A indirectly regulated CTNNB1 expression by sponging miR-375. 		Yes	Silenced circPPP1R12A suppressed the proliferation, promoted the apoptosis, and inhibited the migration and invasion of CC cells. MiR-375 could be sponged by circPPP1R12A, and its inhibitor could reverse the inhibition of circPPP1R12A silencing on CC progression. 	33595945
hsa_circ_0038718	CircRNA	Homo sapiens	Colonic Neoplasms	 CC tumor 	Interaction(miR-195-5p/Axin2/Wnt/β-catenin signaling pathway)	qRT-PCR//Transwell Assay//RIP//Western Blot	circ_0038718 was highly expressed in CC and could sponge miR-195-5p in cytoplasm. Axin2 was a downstream target of miR-195-5p and could regulate the Wnt/β-catenin signaling pathway. Axin2 expression was modulated by circ_0038718/miR-195-5p. 		Yes	Silencing circ_0038718 suppressed the proliferative, migratory and invasive abilities of CC cells, while the promoting effect of high circ_0038718 expression on CC cells was reversed upon miR-195-5p over-expression. 	34706645
hsa_circ_0085315	CircRNA	Homo sapiens	Colonic Neoplasms	CC patients	Interaction(miR-1200/MAP3K1 signaling pathway)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 Our results showed that the higher circRNA_0085315 expression led to the poorer prognosis of CC patients. In conclusion, circRNA_0085315 serves as a ceRNA and promotes CC progression through the activation of the MAPK signaling pathway mediated via the miR-1200/MAP3K1 axis, suggesting that circRNA_0085315 may be a promising diagnostic and therapeutic target for CC.		Yes	MAP3K1-overexpression or miR-1200 mimics prevented the suppression on the enhanced cell proliferation, migration, and invasion caused by circRNA_0085315-overexpression. circRNA_0085315 increased the phosphorylation levels of JNK, p38, and ERK1/2 by stimulating MAP3K1 up-regulation caused by miR-1200 inhibition.	35230926
circHADHA	CircRNA	Homo sapiens	Colonic Neoplasms	colon cancer cells and tissues	Interaction( miR-361/ATG13)	qRT-PCR//Luciferase Report Assay//Tunel	We explored that circRNA HADHA (circHADHA) was upregulated in plasma from polyp patients, whereas it was downregulated in plasma from colon cancer patients.CircHADHA increased the expression of ATG13 via miR-361 in both colon epithelial and cancer cells. ATG13 knockdown reduced autophagy even in the presence of circHADHA in colon cancer cells.		Yes	Overexpression of circHADHA promoted autophagy in colon epithelial cells. Moreover, in colon cancer cells, overexpression of circHADHA promoted autophagy, whereas it inhibited cell proliferation and colony formation. 	36313671
circPPFIA1s	CircRNA	Homo sapiens	Colonic Neoplasms	KM12L4 cells	Interaction(miR-155-5p/CDX1 and HuR/RAB36)	qRT-PCR//RIP	By analyzing circRNA microarray data, we identified two anti-metastatic circRNAs generated from PPFIA1 with different length, which named circPPFIA1-L (long) and -S (short). They were significantly downregulated in liver metastatic KM12L4 cells compared to primary KM12C cells.  circPPFIA1s were found to function as sponges of oncogenic miR-155-5p and Hu antigen R (HuR) by an ASO pulldown experiment. circPPFIA1s upregulated tumor-suppressing CDX1 expression and conversely downregulated oncogenic RAB36 by decoying miR-155-5p and by sequestering HuR, respectively.		Yes	knockdown of circPPFIA1s in KM12C enhanced metastatic potential and increased liver metastasis. Conversely, overexpression of circPPFIA1s weakened metastatic potential and inhibited liver metastasis.	36224588
circCSPP1	CircRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cell lines	Interaction(miR-431/ROCK1 and miR-431/ZEB1)	qRT-PCR//RIP//Western Blot	It was found that circCSPP1 expression was significantly upregulated in colon cancer tissues and cell lines. Mechanistically, circCSPP1 was found to bind with miR-431. In addition, ROCK1 and ZEB1 were identified as the target genes of miR-431. Rescue experiments further confirmed the interaction between circCSPP1, miR-431, ROCK1 and ZEB1. Moreover, circCSPP1 promoted the expression level of ROCK1, cyclin D1, cyclin-dependent kinase 4, ZEB1 and Snail, and lowered the E-cadherin expression level.		Yes	 Overexpression of circCSPP1 significantly promoted the proliferation, migration and invasion of colon cancer cells, whereas silencing of circCSPP1 exerted opposite effects	35101080
circABCB10	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues	Interaction[negatively regulated miR-1271, miR-1252 and miR-203]	qRT-PCR	 Circ-ABCB10 was upregulated in tumor tissues compared with adjacent tissues, and presented with good value in distinguishing tumor tissues from adjacent tissues (AUC = 0.766, 95% CI: 0.690-0.842).	Circ-ABCB10 high expression was correlated with poor differentiation, large tumor size and advanced International Federation of Gynecology and Obstetrics (FIGO) stage in EOC patients. As for survival, circ-ABCB10 was correlated with worse OS.	Yes	In vitro experiments revealed that circ-ABCB10 was upregulated and promoted cell proliferation but reduced cell apoptosis, and negatively regulated miR-1271, miR-1252 and miR-203 in EOC cells.	31381507
circMUC16	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues	interaction[ATG13 and miR-199a]	Western Blot//qRT-PCR//FISH//RNA-seq//IHC	CircMUC16 had increased expression in EOC tissues as compared to healthy ovarian tissues.  This study demonstrated that circMUC16 regulated Beclin1 and RUNX1 by sponging miR-199a-5p. The data suggested that circMUC16 could be a potential target for EOC diagnosis and therapy.	The expression of circMUC16 was linked to the progression in stage and grade of EOC.	Yes	Hence, silencing circMUC16 suppressed autophagy flux of SKOV3 cells. In contrast, ectopic expression of circMUC16 promoted autophagy flux of A2780 cells.	32111227
hsa_circ_0072995	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissue samples and cell lines 	regulation[miR-147a/CDK6 axis]	qRT-PCR//Luciferase Report Assay//Western Blot	Circ_0072995 was up regulated in EOC afflicted tissues and cell lines (HO8910 and A2780), and was mainly located in the cytoplasm.  Our results revealed that circ_0072995 promoted EOC progression through the circ_0072995/miR-147a/CDK6 axis and may represent a strategy for treatment of EOC afflicted patients.	The expression of circ_0072995 was associated with the pathological grade of EOC for respective patients.	Yes	 Functional experiments revealed that circ_0072995 promoted EOC cell proliferation, migration, induced apoptosis, as well as enhanced tumorigenesis in vivo.	32877369
circPPP1R12A	CircRNA	Homo sapiens	Colonic Neoplasms	CC tissues,cell lines(cell lines HT-29, HCT-116, SW480, SW620, LoVo, SW48, DLD-1, Caco2 and HCT-15,NCM460)	Interaction[Hippo-YAP signaling ]	qRT-PCR//FISH//Western Blot//Microarray	We firstly screened the expression profiles of human circRNAs in CC tissues and found that the expression of hsa_circ_0000423 (termed as circPPP1R12A) was significantly increased in CC tissues. Moreover, we identified that circPPP1R12A-73aa promoted the tumor pathogenesis and metastasis of CC via activating Hippo-YAP signaling pathway. 	 Kaplan-Meier analysis showed that patients with higher levels of circPPP R 2A had a significantly shorter overall survival.	Yes	By gain- and loss-of-function approaches, the results suggested that circPPP1R12A played a critical role in proliferation, migration and invasion of CC cells.	30925892
hsa_circ_0003602	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-149-5p/SLC38A1 Axis)	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Circ_0003602 was upregulated in CRC tissues and cell lines. Moreover, circ_0003602 directly interacted with miR-149-5p to negatively regulate its expression, and circ_0003602 knockdown suppressed the malignant behaviors of CRC cells largely by upregulating miR-149-5p. MiR-149-5p directly bound to the 3' untranslated region of SLC38A1 to induce its degradation, and miR-149-5p overexpression reduced the malignant potential of CRC cells largely by downregulating SLC38A1. Circ_0003602 positively regulated SLC38A1 expression by sponging miR-149-5p in CRC cells.		Yes	Circ_0003602 silencing suppressed CRC cell viability, migration, invasion, angiogenesis, and glutaminolysis; induced cell apoptosis in vitro; and blocked tumor growth in vivo. 	36148577
circZC3HAV1	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells	Interaction(miR-146b-3p/TBC1D9 )	Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	 circZC3HAV1 was significantly downregulated in CRC cells.  As for the mechanism, circZC3HAV1 competitively bound with microRNA-146b-3p (miR-146b-3p) to enhance the expression of TBC1 domain family member 9 (TBC1D9). Rescue assays demonstrated circZC3HAV1 sponged miR-146b-3p and upregulated TBC1D9 to restrict migration and invasion of CRC cells.		Yes	circZC3HAV1 overexpression hampered CRC cell migratory and invasive abilities.	36164444
hsa_circ_0101802	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(miR-665/DVL3 Signaling)	qRT-PCR//Luciferase Report Assay//RIP	The expression of DVL3 and circ_0101802 was elevated in CRC tissues and cell lines, and high levels of DVL3 and circ_0101802 were closely associated with short survival time of CRC patients. miR-665 was an intermediary molecule between circ_0101802 and DVL3, and circ_0101802 could positively regulate DVL3 protein expression by sponging miR-665 in CRC cells. DVL3 overexpression partly overturned miR-665 overexpression-mediated anti-tumor effects in CRC cells. 	The expression of DVL3 and circ_0101802 was elevated in CRC tissues and cell lines, and high levels of DVL3 and circ_0101802 were closely associated with short survival time of CRC patients. 	Yes	 Circ_0101802 silencing restrained the proliferation, migration, and tube formation abilities and induced the apoptosis of CRC cells. Circ_0101802 silencing-induced anti-tumor effects in CRC cells were partly reversed by DVL3 overexpression. Circ_0101802 knockdown significantly suppressed xenograft tumor growth in vivo. 	35314912
circEXOC6B	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation(HIF1A-RRAGB-mTORC1)	RNA Pull-Down//ChIP//CCK8//qRT-PCR//FISH//RIP//IF	 circEXOC6B was downregulated in CRC tissues, and its lower expression was associated with poor prognosis of patients. Mechanistically, circEXOC6B inhibited the heterodimer formation of RRAGB by binding to it, thereby suppressing the mTORC1 pathway and HIF1A level. In addition, HIF1A upregulated the transcription of RRAGB by binding to its promoter region. Altogether, the results demonstrated that a HIF1A-RRAGB-mTORC1 positive feedback loop drives tumor progression in CRC, which could be interrupted by circEXOC6B.		Yes	Functional experiments showed that circEXOC6B inhibited growth and increased the 5-fluorouracil-induced apoptosis of CRC cells in vitro and in vivo.	35739524
circIGF1R	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miR-362-5p/HMGB3-Mediated Wnt/β-Catenin Signal Pathway)	CCK8//qRT-PCR//RIP//IHC//Transwell Assay	Circ-IGF1R was up-regulated in CRC tissues and cells.Circ-IGF1R interacted with miR-362-5p and miR-362-5p inhibitor attenuated the anti-tumor effects of circ-IGF1R downregulation on CRC cells. HMGB3 acted as a downstream target for miR-362-5p, and circ-IGF1R facilitated the malignant behaviors of CRC cells by regulating HMGB3. Circ-IGF1R activated the Wnt/β-catenin pathway via targeting miR-362-5p/HMGB3 axis. 		Yes	 Knockdown of circ-IGF1R inhibited proliferation, migration, invasion and glycolysis but induced apoptosis of CRC cells. Tumor growth in vivo was reduced after knockdown of circ-IGF1R.	36542208
circREEP3	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(circREEP3-FKBP10 axis)	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ELISA	Here, circREEP3 is found to be upregulated in CRC tissues. Mechanistically, circREEP3 recruits the chromatin remodeling protein CHD7 to FKBP10 promoter and activates its transcription. Moreover, circREEP3 restricts RIG-1-dependent antitumor immunity. FKBP10 is highly expressed in CRC tissues and associated with poor prognosis. FKBP10 ectopic expression partially rescues the potential of proliferation and metastasis in circREEP3-deficient CRC cells. 	 circREEP3 upregulation predicts poor patient survival.	Yes	circREEP3 knockout suppresses CRC tumorigenesis and metastasis, and impairs stem cell-like phenotype. 	35233964
hsa_circ_0001955	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-583/FGF21 Axis)	RNA Pull-Down//Tunel//CCK8//qRT-PCR//FISH	We found that hsa_circ_0001955 showed characteristics of upregulated circRNA in CRC. Furthermore, hsa_circ_0001955 was a miR-583 sponge and FGF21 was directly targeted by miR-583. In addition, we found that downregulation of miR-583 promoted hsa_circ_0001955-mediated CRC cell malignancy in vitro. In contrast, FGF21 elevation promoted miR-583-regulated CRC cell malignancy in vitro.		Yes	Further analysis indicated that hsa_circ_0001955 elevation facilitated CRC cell malignancy in vitro and promoted tumor growth in vivo. 	35602296
hsa_circ_0000375	CircRNA	Homo sapiens	Colorectal Neoplasms	clinical CRC tissue and serum samples and CRC cell lines	Interaction(miR-1182)	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	Downregulated circ_0000375 and circ_0011536 expression was observed in CRC tissues in GSE126095, clinical CRC tissue and serum samples and CRC cell lines.  Furthermore, miR-1182 and miR-1246, which were overexpressed in CRC tissues in GSE41655, GSE49246 and GSE115513, were verified as target miRNAs of circ_0000375 and circ_0011536, respectively, by luciferase reporter assays. 		Yes	Circ_0000375 and circ_0011536 overexpression inhibited the proliferation, migration and invasion of CRC cells.	35611198
hsa_circ_0011536	CircRNA	Homo sapiens	Colorectal Neoplasms	clinical CRC tissue and serum samples and CRC cell lines	Interaction(miR-1246)	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	Downregulated circ_0000375 and circ_0011536 expression was observed in CRC tissues in GSE126095, clinical CRC tissue and serum samples and CRC cell lines.  Furthermore, miR-1182 and miR-1246, which were overexpressed in CRC tissues in GSE41655, GSE49246 and GSE115513, were verified as target miRNAs of circ_0000375 and circ_0011536, respectively, by luciferase reporter assays. 		Yes	Circ_0000375 and circ_0011536 overexpression inhibited the proliferation, migration and invasion of CRC cells.	35611198
circFNDC3B	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(FXR2/RNF41)	qRT-PCR//Wound Healing Assay//RNA Pull-Down//Western Blot	Mechanistically, studies revealed that YTHDC1 facilitated cytoplasmic translocation of m6A-modified circFNDC3B, and circFNDC3B enhanced RNF41 mRNA stability and expression via binding to FXR2. circFNDC3B promoted ASB6 degradation through RNF41-mediated ubiquitination. Functional studies showed that silencing of RNF41 counteracted circFNDC3B-suppressed CRC stemness and metastasis, and ASB6 overexpression reversed circFNDC3B- or RNF41-mediated regulation of CRC stemness and metastasis.	 Downregulated circFNDC3B was associated with unfavorite survival in CRC patients, and circFNDC3B overexpression suppressed CRC stemness and metastasis.	Yes	 Downregulated circFNDC3B was associated with unfavorite survival in CRC patients, and circFNDC3B overexpression suppressed CRC stemness and metastasis.	36446779
hsa_circ_0000231	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC primary tissues and cells	Interaction(miR-375/IGF2BP3/CCND2)	qRT-PCR//RNA Pull-Down//Western Blot	 We acquired data through circRNA microarray profiles, showing that the expression of hsa_circ_0000231 was upregulated in CRC primary tissues compared to adjacent normal tissues, which was indicated poor prognosis of patients with CRC. The mechanistic analysis showed that hsa_circ_0000231 might, on the one hand, act as a competing endogenous RNA of miR-375 to promote cyclin D2 (CCND2) and, on the other hand, bind to the IGF2BP3 protein to prevent CCND2 degradation.	 We acquired data through circRNA microarray profiles, showing that the expression of hsa_circ_0000231 was upregulated in CRC primary tissues compared to adjacent normal tissues, which was indicated poor prognosis of patients with CRC. 	Yes	 Functional analysis indicated that inhibition of hsa_circ_0000231 in CRC cell lines could suppress CRC cell proliferation as well as tumorigenesis in vitro and in vivo. 	35033075
circLDLR	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells 	Interaction(miR-30a-3p/SOAT1 axis)	qRT-PCR//RIP//FISH	 In our study, high expression of circLDLR was found in CRC tissues and cells and was closely associated with the malignant progression and poor prognosis of CRC patients.  Mechanistically, we showed that circLDLR competitively binds to miR-30a-3p and prevents it from reducing the SOAT1 level, facilitating the malignant progression of CRC.	 In our study, high expression of circLDLR was found in CRC tissues and cells and was closely associated with the malignant progression and poor prognosis of CRC patients. 	Yes	 We demonstrated that circLDLR boosts growth and metastasis of CRC cells in vitro and in vivo, and modulates cholesterol levels in vitro. 	35821230
hsa_circ_0001666	CircRNA	Homo sapiens	Colorectal Neoplasms	HT-29 and HCT-116 cell lines	Interaction(microRNA-1229/ Wnt/β-catenin signaling pathway )	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	 In addition, circ_0001666 expression levels negatively regulated those of miR-1229, whereas miR-1229 expression did not affect circ_0001666, in both the HT-29 and HCT-116 cell lines. Furthermore, a luciferase reporter assay confirmed that miR-1229 directly bound to circ_0001666. In the HT-29 cell line, miR-1229 overexpression activated the Wnt/β-catenin pathway, and promoted cell proliferation, invasion and stemness, while suppressing cell apoptosis. In addition, miR-1229 overexpression reversed the effects of circ_0001666 overexpression. 		Yes	 The protein expression level of proteins in the Wnt/β-catenin pathway was also examined. In both HT-29 and HCT-116 cell lines, circ_0001666 overexpression increased apoptosis, whilst inhibiting cell proliferation and invasion, and reducing the frequency of CD133+ cells. By contrast, circ_0001666 knockdown reduced apoptosis, but increased cell proliferation and the number of CD133+ cells. However, cell invasion remained unaffected. 	35836485
circTMEM59	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tumor tissues and cells	Interaction( miR-410-3p/HOXD8 axis)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay	 CircTMEM59 was lowly expressed in CRC tumor tissues and cells.  MiR-410-3p could be sponged by circTMEM59, and its mimic also reversed the inhibition effect of circTMEM59 on CRC cell proliferation and metastasis. Also, HOXD8 was targeted by miR-410-3p, and its knockdown abolished the negative regulation of miR-410-3p inhibitor on CRC cell proliferation and metastasis. Furthermore, circTMEM59 inhibited CRC tumor growth by overexpressing HOXD8 through sponging miR-410-3p.		Yes	Upregulation of circTMEM59 repressed CRC cell proliferation, migration and invasion. 	35426617
hsa_circ_0045932	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue samples and cells	Interaction(miR-873-5p/HK2 )	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	 Hsa_circ_0045932 was overexpressed in CRC tissue samples and cells.vHK2 was targeted by miR-873-5p, and hsa_circ_0045932 regulated HK2 expression through targeting miR-873-5p. Overexpression of HK2 reversed the repressive effect of hsa_circ_0045932 knockdown on CRC cell malignant behaviors.		Yes	 Hsa_circ_0045932 knockdown repressed CRC cell proliferation, invasion, migration, and glycolysis abilities in vitro.  MiR-873-5p could be sponged by hsa_circ_0045932, and its inhibitor also reversed the inhibitory effect of hsa_circ_0045932 knockdown on CRC cell progression. Furthermore, the pro-tumor role of hsa_circ_0045932 in vivo was also confirmed using animal experiments.	35949038
circPITHD1	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell line and tissues	Interaction(miR-590-5p/HK2 Axis)	In Vivo Experiment//qRT-PCR//Luciferase Report Assay	The data showed that circ-PITHD1 expression increased in a CRC cell line and tissues, which indicated that circ-PITHD1 functioned in CRC progression. Luciferase reporter results confirmed that both miR-590-5p and hexokinase 2 (HK2) were circ-PITHD1 downstream targets. HK2 overexpression or miR-590-5p suppression reversed CRC cell proliferation and invasion after silencing of circ-PITHD1 by regulation of glycolysis. 		Yes	circ-PITHD1 downregulation inhibited CRC invasion and proliferation in the experiments.	36276867
hsa_circ_0052184	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer cell lines and tissues	Interaction(miR-604/HOXA9 Axis)	qRT-PCR//Luciferase Report Assay//Western Blot	 Expression of circ_0052184 was significantly increased in colorectal cancer cell lines and tissues.  miR-604 was targeted by circ_0052184. The downstream target of miR-604 was HOXA9, and silencing circ_0052184 inhibited HOXA9 expression. The existence of the circ_0052184/miR-604/HOXA9 regulatory network in colorectal cancer was validated. circ_0052184 promoted the occurrence and development of colorectal cancer by targeting the miR-604/HOXA9 axis.		Yes	 Silencing circ_0052184 affected the proliferation, migration, and invasion of colorectal cancer cells. 	36065412
circFADS2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells 	Interaction(miR-498/S100A16)	qRT-PCR//Western Blot//Cell Cycle Assay//Transwell Assay	circ-FADS2 was found to be significantly upregulated in CRC tissues, when compared with paired normal tissues. By inhibiting miR-498 expression, circ-FADS2 promoted S100A16 expression leading to the activation of the AKT pathway, resulting in CRC progression. 	 Higher circ-FADS2 expression was associated with advanced stages, lymphatic metastasis, and reduced overall survival (OS). 	Yes	In addition, silencing circ-FADS2 markedly inhibited the proliferation and invasion of CRC and increased the percentage of cancer cells in the G1 phase in vitro. Reducing circ-FADS2 decreased SW480 cell proliferation in vivo. 	36696241
hsa_circ_0003215	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-663b/DLG4/G6PD axis)	CCK8//qRT-PCR//RNA Pull-Down//Transwell Assay	The novel circ_0003215 was identified at low levels in CRC and was negatively correlated with larger tumor size, higher TNM stage, and lymph node metastasis. The decreased level of circ_0003215 was resulted from the RNA degradation by m6A writer protein YTHDF2.  Moreover, circ_0003215 regulated the expression of DLG4 via sponging miR-663b, thereby inducing the metabolic reprogramming in CRC. Mechanismly, DLG4 inhibited the PPP through the K48-linked ubiquitination of glucose-6-phosphate dehydrogenase (G6PD). 	The novel circ_0003215 was identified at low levels in CRC and was negatively correlated with larger tumor size, higher TNM stage, and lymph node metastasis. 	Yes	A series of functional assays demonstrated that circ_0003215 inhibited cell proliferation, migration, invasion, and CRC tumor metastasis in vivo and in vitro.	36127319
circTMEM59	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-668-3p/ID4 Axis)	Western Blot//Tunel//qRT-PCR//FISH//RIP	This research primarily revealed that circTMEM59 was greatly downregulated in CRC tissues and cell lines via qRT-PCR. Furthermore, circTMEM59 also repressed the metastatic behaviors of CRC cells. Further study revealed that circTMEM59 played the role of competing endogenous RNAs (ceRNAs) by binding to miR-668-3p to increase the expression of inhibitor of DNA binding 4 (ID4) in CRC. 	In addition, the decreased expression of circTMEM59 was closely related to adverse clinicopathological characteristics and the shorter survival time of CRC patients. 	Yes	Then, a further study found that the overexpression of circTMEM59 suppressed cell growth and accelerated the cell death of CRC via a series of experiments in vitro and in vivo. 	35656024
hsa_circ_0001535	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal tissues and cells	Interaction(miR-485-5p/LASP1 Axis )	qRT-PCR//Western Blot	 Circ_0001535 was significantly upregulated in colorectal tissues and cells. This knockdown also induced apoptosis by sponging miR-485-5p and upregulating LASP1 expression.		Yes	Circ_0001535 knockdown suppressed the malignant behavior of colorectal cells such as proliferation, invasion, stemness, and tumor growth in vivo. 	36172827
circFAT1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-619-5p/FOSL2)	Flow Cytometry//qRT-PCR//Transwell Assay//Western Blot	Circ-FAT1 and FOSL2 were highly expressed in CRC tissues and cells. Mechanistically, circ-FAT1 acted as a sponge for miR-619-5p to up-regulate the expression of FOSL2, which was confirmed to be a target of miR-619-5p. A series of rescue experiments demonstrated that miR-619-5p inhibition or FOSL2 overexpression reversed the inhibitory action of circ-FAT1 silencing on CRC cell malignant phenotypes mentioned above. 		Yes	 Functionally, knockdown of circ-FAT1 or FOSL2 suppressed CRC cell apoptosis, migration, invasion, and angiogenesis, but induced cell apoptosis in vitro. Pre-clinically, lentivirus-mediated circ-FAT1 knockdown inhibited the tumorigenesis of CRC xenografts in nude mice via regulating miR-619-5p and FOSL2. 	35034245
circFAM120B	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-645/TGFBR2)	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of circFAM120B was decreased in CRC tissues and cells. MiR-645 was a target of circFAM120B, and miR-645 restoration reversed the effects of circFAM120B overexpression. In addition, TGFBR2 was a target of miR-645, and miR-645 inhibition-suppressed CRC cell proliferation, migration/invasion and glycolysis were restored by TGFBR2 knockdown. Moreover, circFAM120B activated the expression of TGFBR2 by targeting miR-645. TGFBR2 also blocked tumor growth in vivo by targeting the miR-645/TGFBR2 axis. 		Yes	CircFAM120B overexpression blocked CRC cell proliferation, migration/invasion, and glycolysis metabolism.	34381772
hsa_circ_0029803	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction( miR-216b-5p/SKIL axis.)	qRT-PCR//IHC//Luciferase Report Assay//Western Blot	Circ_0029803 expression was enhanced in CRC tissues and cells, and the 5-year overall survival rate of patients with high circ_0029803 expression was substantially reduced. Mechanically, circ_0029803 could serve as miR-216b-5p sponge to regulate its expression, and miR-216b-5p knockdown reversed the inhibition of si-circ_0029803 on the malignant behaviors of CRC cells. Additionally, as the target mRNA of miR-216b-5p, SKIL could counteract the inhibitory effect of miR-216b-5p on the development of CRC cells.	Circ_0029803 expression was enhanced in CRC tissues and cells, and the 5-year overall survival rate of patients with high circ_0029803 expression was substantially reduced. 	Yes	 Circ_0029803 depletion retarded proliferation, migration, invasion, EMT and glycolysis of CRC cells in vitro as well as the tumor growth in vivo. 	34479589
circCOG2	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues, plasmas, and exosomes	Interaction(miR-1305/TGF-β2/SMAD3 pathway)	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	 We found that circCOG2 was increased in CRC tissues, plasmas, and exosomes. Upregulated circCOG2 promoted CRC proliferation, migration, and invasion through the miR-1305/TGF-β2/SMAD3 pathway, and this effect could be transmitted from CRC cells with the high metastatic potential to CRC cells with low metastatic potential by exosomes. 		Yes	Upregulated circCOG2 promoted CRC proliferation, migration, and invasion through the miR-1305/TGF-β2/SMAD3 pathway, and this effect could be transmitted from CRC cells with the high metastatic potential to CRC cells with low metastatic potential by exosomes. 	34635639
hsa_circ_0008285	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	regulation[miR-382-5p/PTEN axis]	qRT-PCR//Luciferase Report Assay//Western Blot	First, the downregulated expression of circ_0008285 in CRC tissues and cell lines was confirmed using RT-qPCR analysis. Mechanistically, by using RNA-sequencing, bioinformatics analysis, dual-luciferase reporter assay, and western blotting, we determined that circ_0008285 suppressed the PI3K/AKT pathway via the miR-382-5p/PTEN axis. 	 In addition, the expression level of circ_0008285 was inversely correlated with tumor size, lymphatic metastasis, and tumor-node-metastasis (TNM) stage through clinicopathological parameter analysis.	Yes	Functionally, knockdown of circ_0008285 promoted CRC cell proliferation and migration in vitro. 	32423803
hsa_circ_0056618	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tumor tissues and CRC cell lines	regulation[miR-206,CXCR4,VEGF-A]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circ_0056618 was elevated in CRC tumor tissues and CRC cell lines, which was related to poor diagnosis for CRC patients. We found that circ_0056618 could promote cell proliferation, migration and angiogenesis through sponging with miR-206 and upregulating CXCR4 and VEGF-A in CRC, which might provide a novel potential therapeutic target for treating CRC.	We found that circ_0056618 was elevated in CRC tumor tissues and CRC cell lines, which was related to poor diagnosis for CRC patients. 	Yes	Circ_0056618 inhibition inhibited proliferation, angiogenesis and migration of HT29 cells, and repressed protein levels of Cyclin D1, VEGF-A and N-cadherin and increased E-cadherin.	32373955
circAPLP2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-485-5p/FOXK1 Axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	circAPLP2 expression was enhanced in CRC tissues and cells.circAPLP2 knockdown inhibited CRC progression through regulating miR-485-5p/FOXK1 axis, providing a novel avenue for treatment of CRC.		Yes	circAPLP2 knockdown or miR-485-5p overexpression suppressed cell proliferation, migration, and invasion, whereas it promoted apoptosis in CRC cells, which was reversed by upregulating FOXK1.	32343603
hsa_circ_0060745	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue	regulation[Circ_0060745/miR-4736/CSE1L axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC	 We showed that circ_0060745 was upregulated in CRC, and was associated with unfavorable clinicopathological characteristics.The Circ_0060745/miR-4736/CSE1L axis might be a novel target for the treatment of CRC.		Yes	We also showed that circ_0060745 acted as an oncogene and promoted CRC cell proliferation and metastasis.	32273712
hsa_circ_101951	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue and cell lines	regulation[ KIF3A-mediated EMT pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay	The results indicated that circRNA_101951 was increased in CRC tissues and cell lines.In addition, the downregulation of circRNA_101951 blocked the KIF3A-mediated epithelial-mesenchymal transition (EMT) pathway, which was detected by examining the expression levels of KIF3A and EMT related proteins. 		Yes	The downregulation of circRNA_101951 inhibited cell proliferation and colony formation as well as cell migration and invasion of CRC cell lines. 	32266033
circVAPA	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues	regulation[miR-125a/CREB5 axis]	Flow Cytometry//qRT-PCR//RIP//Transwell Assay	CircVAPA level was up-regulated in CRC tumor tissues.Our studies disclosed that circVAPA knockdown suppressed CRC cells cycle progression, migration, invasion and glycolysis partly by modulating miR-125a/CREB5 axis, suggesting a potential therapeutic strategy for CRC treatment.		Yes	CircVAPA knockdown repressed CRC cells cycle progression, migration, invasion and glycolysis.	32256212
circDENND4C	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	regulation[miR-760/GLUT1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	The expression of circDENND4C and GLUT1 was upregulated in colorectal cancer tissues and cells. CircRNA circDENND4C accelerated proliferation, migration, and glycolysis of colorectal cancer cells through regulating GLUT1 by sponging miR-760.		Yes	Functionally, the knockdown of circDENND4C suppressed proliferation, migration, and glycolysis of colorectal cancer cells. Similarly, silence of GLUT1 also inhibited cell proliferation, migration, and glycolysis.	32196590
circHUEW1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	interaction[Sponging miR-486]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we demonstrate that the expression of circHUEW1 is upregulated in CRC tissues. Mechanistically, we demonstrated that circHUWE1 could sponge miR-486 and the downregulation of miR-486 could reverse the cancer suppressive effects caused by silencing circHUWE1.	 High expression of circHUEW1 was significantly associated with lymphovascular invasion (P =0.036), lymph node metastasis (P =0.017), distant metastasis (P =0.024), and TNM stage (P =0.009). 	Yes	 Silencing circHUWE1 significantly inhibited the proliferation, migration and invasion capacity of CRC cells in vitro.	32021287
circPRTM5	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	interaction[miR-377,E2F3 ]	qRT-PCR//Luciferase Report Assay//Western Blot	The expression of CircPRTM5 in CRC tissues was significantly higher than that in adjacent tissues.CircPRTM5 exerts critical regulatory role in CRC progression by sponging miR-377 to induce E2F3 expression.		Yes	The results indicate that knockdown of CircPRTM5 can significantly inhibit the proliferation of CRC cells. 	32020730
circPTK2	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	Expression[highly expressed]	ISH//qRT-PCR	 CircPTK2 was elevated in CRC tissues and positively associated with tumor growth and metastasis.	 CRC patients with increased circPTK2 expression were positively correlated with poorer survival rates. 	Yes	Furthermore, our studies showed that circPTK2 could promote EMT of CRC cells in vitro and in vivo by binding to vimentin protein on sites Ser38, Ser55 and Ser82. 	31973707
hsa_circ_0004277	CircRNA	Homo sapiens	Colorectal Neoplasms	tissue samples and cell lines 	interaction[miR-512-5p,PTMA]	qRT-PCR//Microarray	High circ-0004277 expression was then verified in tissue samples and cell lines of colorectal cancer via qRT-PCR. In summary, our study showed that circ-0004277 promoted the proliferation of colorectal cancer cells as a miR-512-5p sponge to upregulate the PTMA expression.	Kaplan-Meier analysis was used for identifying the association between circ-0004277 expression and the overall survival rate of colorectal cancer patients. 	Yes	From a functional perspective, circ-0004277 knockdown accelerated cell apoptosis and restrained cell proliferation of colorectal cancer. 	31960446
hsa_circ_0001178	CircRNA	Homo sapiens	Colorectal Neoplasms		regulation[ZEB1 ]	qRT-PCR	Mechanistic study revealed that hsa_circ_0001178 acted as a competing endogenous RNA (ceRNA) for miR-382/587/616 to upregulate ZEB1 (a key trigger of epithelial-to-mesenchymal transition), thereby promoting CRC metastatic dissemination. 	CRC patients with high hsa_circ_0001178 were more prone to have metastatic clinical features, advanced TNM stage and adverse prognosis. 	Yes	Stable knockdown of hsa_circ_0001178 significantly weakened CRC cell migratory and invasive capabilities in vitro as well as lung and liver metastases in vivo.	31747371
hsa_circ_0000218	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[ miR-139-3p/RAB1A axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//BrdU//Colony Formation Assay	We demonstrated that circ_0000218 was notably upregulated in CRC tissues and cell lines, and its high expression level was markedly linked to the increase of T staging and local lymph node metastasis.Collectively, this study suggested that circ_0000218 upregulated RAB1A and promoted CRC proliferation and metastasis via sponging miR-139-3p.	We demonstrated that circ_0000218 was notably upregulated in CRC tissues and cell lines, and its high expression level was markedly linked to the increase of T staging and local lymph node metastasis.	Yes	Circ_0000218 overexpression enhanced the proliferation and metastasis of CRC cells while knocking down circ_0000218 caused the opposite effects. 	31598673
circMET	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-410-3p)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Notably, circMET is substantially upregulated in CRC cell lines and could promote cell proliferation and growth. 		Yes	Notably, circMET overexpression significantly increased cell proliferation and colony formation in SW480 cells 	34929287
hsa_circ_0074027	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells 	Interaction(microRNA‑525‑3p)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 CircRNA‑0074027 was upregulated in CRC tissues, while miR‑525‑3p expression was reduced.	 In addition, patients with CRC and circRNA‑0074027 overexpression were more likely to have low tumor differentiation, lymph node metastasis and advanced TMN stage.	Yes	Deletion of circRNA‑0074027 could suppress cell proliferation and metastasis through up-regulating p53 expression and forbidding epithelial‑mesenchymal transition signaling pathway. 	33760126
circEGFR	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	Interaction( miR-106a-5p/DDX5 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Here, we confirmed that the level of circEGFR was significantly increased in CRC tissues compared to matched adjacent non-tumor tissues, and a high level of circEGFR was correlated with poor clinicopathological characteristics and poor prognosis in patients with CRC.	a high level of circEGFR was correlated with poor clinicopathological characteristics and poor prognosis in patients with CRC	Yes	 Moreover, increased circEGFR expression promoted CRC cell proliferation, migration, and invasion in vitro. Mechanistically, circEGFR acted as a ceRNA for miR-106a-5p to relieve the repressive effect of miR-106a-5p on DDX5 mRNA. Moreover, circEGFR enhanced DDX5 expression, thereby upregulating p-AKT levels. 	34320120
hsa_circ_0084615	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines 	Interaction(miR-599)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_0084615 was up-regulated in CRC and was correlated with poor overall survival rate and advanced clinical stage of CRC patients. 	Circ_0084615 was up-regulated in CRC and was correlated with poor overall survival rate and advanced clinical stage of CRC patients.	Yes	Functional assays validated that depletion of circ_0084615 impeded CRC cell proliferation, migration and invasion. Circ_0084615 acted as a molecular sponge for miR-599 to repress its expression. DNMT3A was a downstream target of miR-599. 	34091391
hsa_circ_100146	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(MicroRNA 149/HMGA2 Axis )	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	circRNA 100146 was upregulated in CRC tissues and cells.		Yes	 circRNA 100146 knockdown inhibited cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro and impeded tumor growth in vivo Also, miR-149 was negatively regulated by circRNA 100146 and was targeted to HMGA2 and mediated its expression.	33257506
hsa_circ_0000467	CircRNA	Homo sapiens	Colorectal Neoplasms	 colorectal cancer tissues	Interaction(miR-382-5p/EN2 axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	In this study, circRNA microarray analysis was utilized to screen differentially expressed circRNA in colorectal cancer (CRC) and circ_0000467 was identified as one circRNA whose expression was significantly upregulated in CRC. 		Yes	The depletion of circ_0000467 expression was found to impede the multiplication, migration, invasion, and epithelial-mesenchymal transition (EMT) processes in CRC cells	33685351
hsa_circ_0005615	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[upregulating TNKS,Wnt/β-catenin pathway]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	Herein, we explored the expression profiles of circRNAs in 5 paired samples of CRC patients by microarray and noted a circRNA, hsa_circ_0005615 (circ5615), was significantly upregulated in CRC tissues. Our results indicated that circ5615 exerted oncogenic function as competing endogenous RNA (ceRNA) of miR-149-5p to release TNKS and activated Wnt/β-catenin pathway.		Yes	Studies in vitro and in vivo demonstrated that knockdown of circ5615 in cancer cells inhibited proliferation and cell cycle acceleration, while overexpression promoted malignant phenotypes.	32393760
hsa_circ_0007142	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	interaction[CDC25A,miR-122-5p]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The levels of circ_0007142 and CDC25A were enhanced and the level of miR-122-5p was declined in CRC tissues and cells, while the level of DOCK1 had no fluctuation.Circ_0007142 modulated CDC25A expression to promote CRC progression by sponging miR-122-5p.		Yes	Circ_0007142 knockdown impeded cell proliferation, colony formation, migration, and invasion in CRC cells by regulating miR-122-5p. 	32431519
hsa_circ_0003266	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-503-5p/PDCD4 )	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_0003266 was significantly lowly expressed in CRC tissues and cell lines. PDCD4 was a direct target of miR-503-5p and circ_0003266 promoted PDCD4 expression by competitively sponging miR-503-5p.		Yes	Circ_0003266 overexpression markedly repressed CRC cell proliferation, migration, and invasion, and accelerated the cell apoptosis, but its overexpression promoted the malignant phenotypes of CRC cells.	33726686
hsa_circ_0001946	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[ miR-135a-5p/EMT axis]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Our data showed that the expression of circ_0001946 was upregulated in CRC tissues, which was negatively correlated with tumor size, histologic grade, lymphatic metastasis, and TMN stage, and patients with circ_0001946 overexpression were more likely to have a poor prognosis.  To summarize, this study revealed that circRNA_0001946 might act as a tumor promoter by activating the miR-135a-5p/EMT axis and may be a promising treatment target for CRC.	Our data showed that the expression of circ_0001946 was upregulated in CRC tissues, which was negatively correlated with tumor size, histologic grade, lymphatic metastasis, and TMN stage, and patients with circ_0001946 overexpression were more likely to have a poor prognosis. 	Yes	 In addition, in vitro experiments showed that silencing circ_0001946 inhibited the epithelial-mesenchymal transition (EMT) pathway and markedly suppressed CRC cell growth, migration, and invasion. 	32508871
hsa_circ_0026416	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC patient tissues	regulation[miR-346/NFIB axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Hsa_circ_0026416 was markedly upregulated in CRC patient tissues and plasma and was a poor prognosis in CRC patients. Hsa_circ_0026416 promotes the progression of CRC via the miR-346/NFIB axis and may represent a potential biomarker for diagnosis and therapy in CRC.	Hsa_circ_0026416 was markedly upregulated in CRC patient tissues and plasma and was a poor prognosis in CRC patients. 	Yes	 Functionally, hsa_circ_0026416 promotes cell proliferation, migration and invasion both in vitro and in vivo. 	33061846
hsa_circ_0000231	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-502-5p/MYO6 axis]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	Hsa_circ_0000231 expression was dramatically upregulated while miR-502-5p was obviously downregulated in CRC tissues and cells compared with control groups.Hsa_circ_0000231 knockdown inhibited CRC progression and glycolysis by downregulating MYO6 expression through sponging miR-502-5p, which might provide a theoretical basis in further studying circ_0000231-directed therapy in CRC.		Yes	Functionally, hsa_circ_0000231 knockdown repressed cell glycolysis, proliferation, migration and invasion, and induced cell apoptosis, whereas these effects were decreased by miR-502-5p inhibitor.	32993655
circRAE1	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	regulation[miR-338-3p/TYRO3 axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We uncovered a novel circRNA Hsa_circ_0060967 (also known as circRAE1) that was remarkably increased in CRC tissues. We identified the network of circRAE1, miR-338-3p, and TYRO3 in CRC cells and determined that the increase in circRAE1 could serve as an oncogene by sponging miR-338-3p, which resulted in an upregulated TYRO3 expression. 	 The high circRAE1 level was positively associated with advanced tumor stage, lymph node metastasis, and tumor size. 	Yes	The loss-of-function assay showed that circRAE1 accelerated cell proliferation, migration, and invasion. 	32908453
circNOX4	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[microRNA-485-5p/CKS1B axis]	qRT-PCR//Luciferase Report Assay//RIP//Transwell Assay	The results demonstrated that the expression of circNOX4 was upregulated in CRC tissues and cell lines compared with that in adjacent normal tissues and a normal colon epithelial cell line, respectively. Collectively, the results of the present study demonstrated that circNOX4 may serve an oncogenic role in CRC by promoting the proliferation, migration, invasion and glycolysis of CRC cells via the miR‑485‑5p/CKS1B axis.		Yes	CircNOX4 silencing suppressed the proliferation, migration, invasion and glycolysis of CRC cells.	32901890
circFNDC3B	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[circFNDC3B-miR-97-5p-TIMP3 pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//ELISA//Colony Formation Assay//Invasion Assay	 Expression of circFNDC3B and TIMP3 levels in CRC tissues and cell lines were found to be low, whereas microRNA (miR)-937-5p expression was high in CRC.  In conclusion, our work reports a tumor-suppressing role for the circFNDC3B-miR-97-5p-TIMP3 pathway and suggests that circFNDC3B-enriched exosomes can inhibit angiogenesis and CRC progression.		Yes	In vivo CRC tumor growth, angiogenesis and liver metastasis were suppressed by circFNDC3B overexpression, circFNDC3B-enriched exosomes or miR-937-5p knockdown. 	32896063
hsa_circ_0044556	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression[highly expressed]	CCK8//qRT-PCR//Wound Healing Assay//Microarray	Hsa_circ_0044556 was highly expressed in CRC patients and was positively correlated with tumor stage and lymph node metastasis.	Hsa_circ_0044556 was highly expressed in CRC patients and was positively correlated with tumor stage and lymph node metastasis.	Yes	In CRC cell lines, the proliferation, migration, and invasion of cancer cells were inhibited by knocking down hsa_circ_0044556 expression.	32884449
circcse1l	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cell lines and tissue and serum	interaction[Binding to eIF4A3]	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	qRT-PCR assays showed that the levels of expression of circ_cse1l were lower in CRC cell lines and in tissue and serum samples from patients with CRC than in control samples.  The expression of circ_cse1l is downregulated in CRC. Furthermore, circ_cse1l downregulated PCNA expression by binding to eIF4A3, inhibiting the proliferation of CRC cells.	The expression of circ_cse11 in CRC tissues had clinical significance, as its level of expression was inversely associated with the depth of tumor invasion.	Yes	Overexpression of circ_cse1l in HT29 and HCT116 cells markedly reduced cell proliferation and metastasis.	32857753
circMAT2B	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell	regulation[miR-610/E2F1 axis]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 In our study, circMAT2B was found to be upregulated in CRC tissues and cell lines. Moreover, circMAT2B promoted CRC proliferation by regulating the miR-610/E2F1 axis, which may serve as a potential therapeutic target for CRC treatment.		Yes	Furthermore, the silencing of circMAT2B significantly inhibited proliferation. 	32848465
hsa_circ_0136666	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[miR-383/CREB1 Axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	circ_0136666 was aberrantly up-regulated in CRC tissues and cells, circ_0136666 deteriorated CRC through miR-383/CREB1 axis. circ_0136666/miR-383/CREB1 axis might be an underlying therapeutic target for CRC therapy.		Yes	 circ_0136666 was aberrantly up-regulated in CRC tissues and cells, and it promoted the proliferation and glycolysis and inhibited the apoptosis of CRC cells. circ_0136666 accelerated the progression of CRC through directly targeting and down-regulating miR-383. 	32821160
circTADA2A	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-374a-3p/KLF14 axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	CircTADA2A was abnormally down-regulated in CRC tissues and cell lines. CircTADA2A functioned as a tumor suppressor in CRC to inhibit the glycolysis and cell cycle and potentiate the apoptosis of CRC cells via miR-374a-3p/KLF14 axis.		Yes	CircTADA2A overexpression impeded CRC tumor growth in vivo. 	32799891
circMBOAT2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and serum 	interaction[sponging miR-519d-3p]	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	CircMBOAT2 is highly expressed in both CRC tissues and serum samples, and has a correlation with tumor stage. Also, circMBOAT2 regulated cell proliferation and migration by competitively binding to miR-519d-3p and targeting troponin-associated protein (TROAP) in CRC cells. 	CircMBOAT2 is highly expressed in both CRC tissues and serum samples, and has a correlation with tumor stage. 	Yes	 Further functional studies revealed that circMBOAT2 served as a microRNA (miRNA) sponge of miR-519d-3p and promoted the proliferation, migration, and invasion of CRC cells.	32796815
circUBAP2	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	regulation[miR-199a/VEGFA pathway]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression of circUBAP2 was upregulated in CRC tissues and cell lines, and depletion of circUBAP2 suppressed the cell proliferation, migration, and invasion of CRC. Our findings demonstrated that circUBAP2 facilitated CRC progression by sponging miR-199a to upregulate VEGFA. 		Yes	 The expression of circUBAP2 was upregulated in CRC tissues and cell lines, and depletion of circUBAP2 suppressed the cell proliferation, migration, and invasion of CRC.	32767322
hsa_circ_102209	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[hsa_circRNA_102209/miR-761/RIN1 signaling]	CCK8//qRT-PCR//Flow Cytometry	Our results revealed that expression of hsa_circRNA_102209 was remarkably increased in CRC tissues, where the levels of miR-761 were notably reduced (P < .05).More importantly, hsa_circRNA_102209/miR-761/RIN1 signaling may be a novel therapeutic target for the treatment of CRC patients.		Yes	 Knockdown of hsa_circRNA_102209 notably inhibited the proliferation, migration, invasion, and EMT of CRC cells (P < .05), whereas cell cycle arrest at G0/G1 phase and apoptosis were enhanced (P < .05). 	32706154
circCTNNA1	CircRNA	Homo sapiens	Colorectal Neoplasms	CC tissues	regulation[circCTNNA1/miR-149-5p/FOXM1 axis]	Flow Cytometry//qRT-PCR//Wound Healing Assay//Transwell Assay	 A novel circRNA, circCTNNA1, was significantly upregulated in CC, and its level was associated with advanced tumor-node-metastasis stage and poor prognosis of patients with CC.In summary, our study demonstrated that circCTNNA1 facilitated CC proliferation and invasion via the circCTNNA1/miR-149-5p/FOXM1 axis, and it might function as a novel diagnostic or therapeutic target for patients with CC.		Yes	The results revealed that circCTNNA1 promoted CC cell proliferation, migration, and invasion in vitro and in vivo.	32699205
circAGFG1	CircRNA	Homo sapiens	Colorectal Neoplasms	cell lines	regulation[YY1/CTNNB1]	qRT-PCR	In this study, circAGFG1 was upregulated in CRC cell lines. In brief, our findings uncovered that circAGFG1 modulated YY1/CTNNB1 axis to drive metastasis and stemness in CRC by sponging miR-4262 and miR-185-5p.		Yes	CircAGFG1 silencing significantly suppressed cell proliferation, migration, invasion, and stemness, while promoted cell apoptosis in CRC. Meanwhile, we found that circAGFG1 also accelerated CRC tumor growth and metastasis in vivo.	32681092
hsa_circ_0001806	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[COL1A1]	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	 Hsa_circ_0001806 was significantly upregulated in CRC tissues and correlated with TNM stage, depth of invasion, lymphatic metastasis and distant metastasis. CircRNA hsa_circ_0001806 may act as a promising therapeutic target by facilitating the stemness of CRC cells via activating the hsa_circ_0001806/miR-193a-5p/COL1A1 axis.	 Hsa_circ_0001806 was significantly upregulated in CRC tissues and correlated with TNM stage, depth of invasion, lymphatic metastasis and distant metastasis.	Yes	Hsa_circ_0001806 promoted the stemness of CRC cells, as evident by increasing sphere-formation ability, ALDH1 activity and stemness marker expression while had no effect on cell viability.	32636650
circSAMRCC1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and four cell lines 	regulation[circSMARCC1/miR-140-3p/MMPs axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of circSAMRCC1 in the CRC tissues and four cell lines is significantly increased, and circSMARCC1 and miR-140-3p are negatively correlated with expression level in the tissue. circSMARCC1 competitively combined with miR-140-3p and functioned through a circSMARCC1/miR-140-3p/MMPs axis as a CRC carcinogen, demonstrating its potential as a biomarker for CRC treatment.		Yes	 The downregulation of circSMARCC1 decreased CRC cell viability and suppressed metastasis in vitro and Inhibition of protein (MMP-2, MMP-9, VEGF) expression. 	32606978
circNOL10	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	interaction[sponging miR-135a-5p and miR-135b-5p]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	 CircNOL10 was decreased in CRC tissues and cells and was associated with poor outcomes.  In summary, our results showed that circNOL10 impeded CRC development by mediating proliferation, cell cycle, migration, and invasion by sponging miR-135a-5p and miR-135b-5p, which provided new understanding for CRC treatment.		Yes	Gain-of-functional experiment revealed that overexpression of circNOL10 constrained proliferation, cell-cycle progression, migration, and invasion of CRC cells, which was abolished by overexpression of miR-135a-5p or miR-135b-5p.	32606737
hsa_circ_0038646	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells and tissues	regulation[miR-331-3p/GRIK3]	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	Hsa_circ_0038646 was overexpressed in both CRC cells and tissues, and this aberrant expression was positively related with increasing tumor grade.The hsa_circ_0038646/miR-331-3p/GRIK3 axis may be a novel therapeutic and diagnostic target of CRC.		Yes	Knockdown of hsa_circ_0038646 significantly weakened human CRC cell proliferation and migration. 	32565953
hsa_circ_002144	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-615-5p)	Western Blot//Wound Healing Assay//CCK8//FISH//Flow Cytometry//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	Firstly, hsa_circRNA_002144 showed significantly elevation in both of CRC tissues and cell lines, and suggested closely associated with poor prognosis in patients. 	Firstly, hsa_circRNA_002144 showed significantly elevation in both of CRC tissues and cell lines, and suggested closely associated with poor prognosis in patients. 	Yes	Secondly, data from functional assays revealed that silence of hsa_circRNA_002144 inhibited CRC progression with reduced cell viability, proliferation, migration and invasion, while enhanced cell apoptosis. In addition, in vivo CRC growth and metastasis were also suppressed by knockdown of hsa_circRNA_002144. However, CRC progression was promoted with over-expression of hsa_circRNA_002144. Thirdly, hsa_circRNA_002144 colocalized with miR-615-5p in the cytoplasm of CRC cells, and decreased miR-615-5p expression.	33347535
hsa_circ_0031787	CircRNA	Homo sapiens	Colorectal Neoplasms	GEO(CRC)	Expression [highly expressed]	CCK8//RIP//Flow Cytometry//Luciferase Report Assay//Microarray//IF	Hsa_circ_0031787 expression levels in CRC were significantly increased and correlated with advanced TNM stage and lymph node metastasis in CRC patients. 	Hsa_circ_0031787 expression levels in CRC were significantly increased and correlated with advanced TNM stage and lymph node metastasis in CRC patients. 	Yes	Functional assays showed that hsa_circ_0031787 suppression reduced CRC cell proliferation and invasion in vitro and reduced tumor growth in vivo. 	34089272
circCDYL2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and  cell lines	Interaction(Ezrin)	Wound Healing Assay//Migration Assay//qRT-PCR//RNA-seq//Transwell Assay	Among the candidate circRNAs, circCDYL2 was the highest overexpressed circRNA in H-RKO compared to parental N-RKO cells. Furthermore, circCDYL2 expression was elevated in CRC tissues and cell lines. circCDYL2 was located in the cytoplasm of CRC cells and interacted with Ezrin to upregulate its protein levels, resulting in AKT phosphorylation. 		Yes	 Gain- and loss-of-function assays indicated that circCDYL2 enhanced the migration of CRC cells.	34485151
circEPB41L2	CircRNA	Homo sapiens	Colorectal Neoplasms	exosomes from colorectal cancer patients and cells	Interaction(miR-21-5p or miR-942-5p)	In Vivo Experiment//qRT-PCR//Luciferase Report Assay//RIP	CircEPB41L2 was downregulated in the exosomes from colorectal cancer patients and cells. CircEPB41L2 could sponge miR-21-5p or miR-942-5p. 		Yes	Overexpressed circEPB41L2 inhibited colorectal cancer cell proliferation, migration, invasion and promoted apoptosis, as well as suppressed the activity of PTEN/AKT signalling pathway. 	34022068
circCSPP1	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miR-431/LASP1 axis)	qRT-PCR//Tunel//Western Blot	Our data showed that circ-CSPP1 was significantly overexpressed in CRC tissues and cells. circ-CSPP1 directly targeted miR-431, and circ-CSPP1 knockdown modulated CRC cell progression in vitro via upregulating miR-431. Moreover, LIM and SH3 protein 1 (LASP1) was a functional target of miR-431 in modulating CRC cell malignant progression. 		Yes	The knockdown of circ-CSPP1 attenuated cell proliferation, migration, invasion and promoted apoptosis in vitro and weakened tumor growth in vivo. 	34124372
circMAPK14	CircRNA	Homo sapiens	Colorectal Neoplasms	cells and tissue samples 	Interaction(MKK6/FOXC1)	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//FISH//Transwell Assay	We identified that hsa_circ_0131663 (termed circMAPK14) showed significantly decreased expression level in cells and tissue samples of CRC, and was primarily localised in the cytoplasm. We also found that circMAPK14-175aa reduced nuclear translocation of MAPK14 by competitively binding to MKK6, thus facilitating ubiquitin-mediated degradation of FOXC1. Moreover, we described a positive feedback loop in CRC in which elevated FOXC1 expression was caused by reduced circMAPK14-175aa expression. 		Yes	A series of function experiments demonstrated that circMAPK14 influenced CRC progression and metastasis by encoding a peptide of 175 amino acids (termed circMAPK14-175aa). 	34709743
hsa_circ_0084927	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-20b-3p/GSTM5/ AKT/mTOR pathway.)	qRT-PCR//Wound Healing Assay//Western Blot	The expression of circ_0084927 was significantly increased in CRC tissues and cells, and it was higher in advanced-stage CRC compared with early-stage CRC. The expression of circ_0084927 is significantly increased in CRC and higher in advanced-stage CRC than in early-stage CRC. Moreover, circ_0084927 potentially regulates CRC cell migration and invasion via the miR-20b-3p/GSTM5/ AKT/mTOR pathway.	The expression of circ_0084927 was significantly increased in CRC tissues and cells, and it was higher in advanced-stage CRC compared with early-stage CRC. 	Yes	Knockdown of circ_0084927 inhibited the migration and invasion of HCT116 cells. Moreover, circ_0084927 was found to act as a sponge of miR-20b-3p. MiR-20b-3p activation reduced the circ_0084927 level, whereas miR-20b-3p inhibition increased the circ_0084927 level. 	34629820
circUBAP2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-582-5p/FOXO1 signaling)	RNA Pull-Down//Western Blot//qRT-PCR//FISH//IF	We find that circUBAP2 is upregulated in CRC tissues and cell lines to induce autophagy both in vitro and in vivo. Mechanistically, we uncover that circUBAP2 can directly interact with miR-582-5p and subsequently act as a microRNA sponge to regulate the expression of the miR-582-5p target gene forkhead box protein O1 (FOXO1) and downstream signaling molecules, which collectively advance the progression and metastasis of CRC. 		Yes	We find that circUBAP2 is upregulated in CRC tissues and cell lines to induce autophagy both in vitro and in vivo. The effects of circUBAP2 on migration, invasion, and proliferation may be partially related to autophagy. 	34416339
hsa_circ_0043278	CircRNA	Homo sapiens	Colorectal Neoplasms	tumor samples	Expression(lower expressed)	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We discovered that circular RNA hsa_circ_0043278 was significantly downregulated in tumor samples (P < 0.0001) as well as cell lines (P < 0.05). 		Yes	Moreover, we found that overexpression of hsa_circ_0043278 suppressed proliferation and migratory abilities while promoting apoptosis in colorectal cancer cells.	33568942
hsa_circ_0007142	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-455-5p/SGK1 axis)	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	Circ_0007142 and SGK1 levels were clearly increased, while miR-455-5p level was reduced in CRC tissues and cell lines. Circ_0007142 could sponge miR-455-5p to regulate SGK1 expression. Moreover, the effects of miR-455-5p on cell proliferation, apoptosis, migration and invasion could be partially reversed by SGK1 overexpression. Besides, circ_0007142 knockdown also suppressed the progression of CRC in vivo. 		Yes	Circ_0007142 silencing promoted cell apoptosis and inhibited cell proliferation, migration and invasion, while these effects of circ_0007142 were partially abolished by miR-455-5p inhibitor in CRC cells. 	32889894
circSMAD2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cell lines and tissues.	Interaction(miR-1258/RPN2 signaling pathway)	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	Hsa_circ_0000847 (circ_SMAD2) is a novel circRNA that was found to be elevated in CRC cell lines and tissues. Mechanistically, circ_SMAD2 elevated Ribophorin II (RPN2) levels by inhibiting miR-1258.	High circ_SMAD2 levels were positively correlated with CRC clinicopathological features. 	Yes	Functional assays revealed that circ_SMAD2 enhanced CRC cell invasion, proliferation, and tumor growth. 	33613755
circFAT1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues and CRC cell lines	Interaction(miR-30e-5p/ITGA6 Axis)	qRT-PCR//Luciferase Report Assay//Transwell Assay	qRT-PCR revealed that circFAT1(e2) in CRC tumor tissues was upregulated compared with that in adjacent normal tissues and was also upregulated in CRC cell lines. We demonstrated that circFAT1(e2) could sponge miR-30e-5p, which regulated the expression level of integrin α6 (ITGA6), the downstream target gene of miR-30e-5p. Rescue assays demonstrated that knockdown of miR-30e-5p enhanced CRC proliferation and migration via ITGA6. 		Yes	 The results showed that circFAT1(e2) silencing markedly suppressed CRC growth. Moreover, we identified circFAT1(e2) as a promoter of CRC metastasis. Knockdown of circFAT1(e2) evidently reduced HCT116 and RKO cell migration and invasion. 	34257702
hsa_circ_0006174	CircRNA	Homo sapiens	Colorectal Neoplasms	cancer tissues  and cell lines	Interaction(microRNA-142-3p)	qRT-PCR//Western Blot	Circ_0006174 was up-regulated in colorectal cancer tissues as well as in cell lines, and its high expression was remarkably associated with enlarged tumour volume and advanced tumour, node, metastasis stage of the patients. Circ_0006174 directly targeted and negatively regulated microRNA-142-3p expression, and X-linked inhibitor of apoptosis, a target gene of microRNA-142-3p, could be indirectly and positively modulated by circ_0006174.	Circ_0006174 was up-regulated in colorectal cancer tissues as well as in cell lines, and its high expression was remarkably associated with enlarged tumour volume and advanced tumour, node, metastasis stage of the patients.	Yes	Circ_0006174 overexpression enhanced colorectal cancer cell proliferation, migration and invasion, and inhibited colorectal cancer cell apoptosis; while knocking down circ_0006174 caused the opposite effects. 	34410163
hsa_circ_0089153	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-198/SUMO-specific peptidase 1 (SENP1) axis)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Our data showed that circ_0089153 was overexpressed in CRC tissues and cells. Mechanistically, circ_0089153 targeted miR-198, and the effects of circ_0089153 were mediated by miR-198. SENP1 was identified as a direct and functional target of miR-198. Circ_0089153 worked as a competing endogenous RNA (ceRNA) to post-transcriptionally regulate SENP1 expression by miR-198.		Yes	. Depletion of circ_0089153 repressed cell proliferation, sphere formation ability, and enhanced cell apoptosis, as well as inhibited tube formation in vitro. Moreover, circ_0089153 depletion diminished tumor growth in vivo. 	34516314
hsa_circ_002178	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells and tissues	Interaction(miR-542-3p/CREB1)	CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay	The circ_002178 and CREB1 expressions were up-regulated in the CRC cells and tissues, and the miR-542-3p expression was down-regulated (all P<0.05). Our molecular mechanism study revealed that circ_002178, as the molecular sponge of miR-542-3p, promotes CREB1 expression. The downregulation of miR-542-3p or the overexpression of CREB1 is able to partly weaken the inhibition of CRC cells through the circ_002178 knockdown.		Yes	The circ_002178 knockdown inhibited the proliferation, invasion, colony formation, and glycolysis of the CRC cells in vitro, but the overexpression of circ_002178 induced the opposite result (both P<0.05). 	34650680
hsa_circ_0136666	CircRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Interaction(miR-497/PD-L1 pathway)	Flow Cytometry//qRT-PCR//ELISA//IHC	The results showed that hsa_circ_0136666 and PD-L1 was increased in colorectal cancer cells while miR-497 was decreased in colorectal cancer cells when compared with normal colon epithelial cell line. Hsa_circ_0136666 was demonstrated to directly target miR-497, which also regulated PD-L1 by binding to its 3'UTR. Further mechanistic studies identified that hsa_circ_0136666 controlled cell proliferation and apoptosis via targeting miR-497 and regulating PD-L1 expression.		Yes	Of note, hsa_circ_0136666 stimulated Treg cells mediated by miR-497/PD-L1 axis and its downstream signal pathway in Treg cells. Finally, hsa_circ_0136666 was found to accelerate the tumor growth in vivo.	34320370
circRHOBTB3	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation(FUS and ADARB2)	Western Blot//qRT-PCR//RIP//IP//Transwell Assay	We identified circRHOBTB3 which is markedly downregulated in CRC tissues and cell lines. Mechanistically, circRHOBTB3 binds to HuR, which is a ubiquitously expressed and functional RNA-binding protein (RBP) in CRC development, and promotes β-Trcp1-mediated ubiquitination of HuR. Normally, HuR binds to the 3'UTR of target mRNAs to facilitate their stabilization, whereas the interaction between circRHOBTB3 and HuR degrades HuR to reduce the expression level of the downstream target PTBP1.	Furthermore, lower circRHOBTB3 levels were significantly associated with advanced clinical stages and greater risk of metastases. 	Yes	Overexpression of circRHOBTB3 suppresses tumor metastasis in CRC cells.	34158864
hsa_circ_0000372	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-495/IL6 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	Circ_0000372 was markedly upregulated in CRC, and its high expression was associated with the poor prognosis of CRC patients. Bioinformatics prediction and experimental verification proposed that circ_0000372 could sponge miR-495, and miR-495 could target IL6. Besides, the JAK2/STAT3 signaling pathway activation could be regulated by circ_0000372, miR-495 and IL6. 	Circ_0000372 was markedly upregulated in CRC, and its high expression was associated with the poor prognosis of CRC patients.	Yes	Silenced circ_0000372 was able to suppress CRC cell proliferation, migration and invasion in vitro and CRC tumor growth in vivo. 	33534412
hsa_circ_0026628	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(miR-346/SP1/ Wnt/β-catenin pathway)	RNA Pull-Down//ChIP//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//IF	We identified that hsa_circ_0026628 (circ_0026628), a circular RNA that originated from SP1 pre-mRNA, was upregulated in CRC cells.Mechanistically, circ_0026628 served as the endogenous sponge of miR-346 and FUS to elevate SP1 expression at the post-transcriptional level, thus strengthening the interaction between SP1 and β-catenin to activate the Wnt/β-catenin pathway.		Yes	 The results depicted that circ_0026628 functioned as a contributor to CRC cell proliferation, migration, EMT, and stemness. 	34420031
circCTNNA1	LncRNA	Homo sapiens	Colorectal Neoplasms	miR-363-3p/CXCL5 axis	Interaction(miR-363-3p)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircCTNNA1 and CXCL5 were highly expressed in CRC. Moreover, miR-363-3p could interact with CXCL5, and CXCL5 overexpression also could reverse the suppressive effect of miR-363-3p on CRC progression. 		Yes	Knockdown of circCTNNA1 could inhibit the proliferation, cell cycle, metastasis, and promote the apoptosis of CRC cells.  MiR-363-3p could be sponged by circCTNNA1, and the inhibition effect of circCTNNA1 silencing on CRC progression could be reversed by miR-363-3p inhibitor. Downregulation of circCTNNA1 also could hinder the tumor growth of CRC in vivo.	33640021
circNRIP1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR‑532‑3p)	qRT-PCR//Luciferase Report Assay	The results of the present study indicated that circNRIP1 was upregulated in CRC and its increased expression was associated with CRC progression. Bioinformatics analysis predicted that miR‑532‑3p was a direct target of circNRIP1, which was further confirmed by a dual‑luciferase reporter assay. miR‑532‑3p silencing reversed the effects of circNRIP1 knockdown on the sensitivity of 5‑FU in the chemotherapy of CRC. 		Yes	 Furthermore, overexpression of circNRIP1 promoted CRC cell proliferation, invasion and migration, while it inhibited apoptosis. Knockdown of circNRIP1 significantly enhanced the 5?FU?induced inhibition of the viability of HCT116 and SW480 cells. 	34396434
hsa_circ_0084615	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	Interaction(miR-599/ONECUT2 axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//IHC	Circ_0084615 was elevated in CRC tissues and was linked to TNM stages, lymph node metastasis, differentiation and overall survival rate. Circ_0084615 sponged miR-599 and miR-599 inhibition reversed circ_0084615 knockdown-mediated effects on CRC cell growth, motility and angiogenesis. ONECUT2 was identified as the target gene of miR-599. 		Yes	Circ_0084615 knockdown inhibited CRC cell proliferation, migration, invasion and angiogenesis in vitro and hampered tumorigenesis in vivo.	34253241
circGALNT16	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Regulation(SENP2-mediated hnRNPK-p53)	CCK8//qRT-PCR	 Circ-GALNT16 was downregulated in CRC and was negatively correlated with poor prognosis.Mechanistically, circ-GALNT16 could bind to the KH3 domain of heterogeneous nuclear ribonucleoprotein K (hnRNPK), which promoted the SUMOylation of hnRNPK. 		Yes	Circ-GALNT16 suppressed the proliferation and metastatic ability of CRC cells in vitro and in vivo.	34452628
hsa_circ_0040809	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-515-5p/DNMT1 axis)	CCK8//qRT-PCR//Western Blot	 In CRC tissues and cells, circ_0040809 and DNMT1 expression are markedly increased, whereas miR-515-5p expression is decreased. Mechanistically, circ_0040809 competitively binds to miR-515-5p to elevate DNMT1 expression. Rescue assay reveals that overexpressed miR-515-5p partly counteracts the tumor-facilitating impact of circ_0040809.	Also, high circ_0040809 expression is significantly linked to shorter overall survival. 	Yes	Cell function compensation experiments reveal that circ_0040809 silencing inhibits CRC cell proliferation and migration and promotes apoptosis, while circ_0040809 overexpression has the opposite effects. 	34438465
hsa_circ_0007919	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-942-5p/TET1 axis)	CCK8//qRT-PCR//Western Blot	 It was revealed that, in CRC tissues and cell lines, circ_0007919 and TET1 expressions were reduced whereas miR-942-5p expression was enhanced.  In addition, circ_0007919 could competitively bind with miR-942-5p to increase the expression of miR-942-5p's target gene TET1. 		Yes	 It was also revealed that circ_0007919 overexpression markedly suppressed CRC cell growth and migration. 	34906917
hsa_circ_0044556	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer samples and cells	Interaction(miR-665/Diaphanous Homolog 1 axis)	CCK8//qRT-PCR//Western Blot	Circ_0044556 was upregulated in colorectal cancer samples and cells. Our findings manifested that circ_0044556 functioned as an oncogenic circRNA in colorectal cancer by mediating the miR-665/Diaphanous Homolog 1 axis.		Yes	Silencing circ_0044556 inhibited cell proliferation, cell cycle progression, migration, invasion, and epithelial-mesenchymal transition in CRC cells. 	34822025
circASXL1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-1205)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	CircASXL1 and GRIK3 expression were apparently upregulated, and miR-1205 expression was downregulated in CRC tissues and cells relative to control groups.  Additionally, circASXL1 acted as a sponge for miR-1205, and miR-1205 was associated with GRIK3. 		Yes	CircASXL1 knockdown inhibited cell colony-forming ability, migration and invasion, whereas induced cell arrest at G0/G1 phase and cell apoptosis in CRC cells; however, these effects were attenuated by miR-1205 inhibitor.Furthermore, circASXL1 silencing hindered tumor formation by upregulating miR-1205 and downregulating GRIK3 expression.	34127015
hsa_circ_0062682	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues 	Interaction(miR-940/PHGDH Axis)	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	y online analyses and experimental validations, we showed that circ_0062682 expression was aberrantly increased in CRC tissues compared with paired normal tissues.  Mechanistically, we revealed that circ_0062682 could sponge miR-940 and identified D-3-phosphoglycerate dehydrogenase (PHGDH), a key oxidoreductase involved in serine biosynthesis, as a novel target of miR-940.	Increased expression of circ_0062682 in CRC notably correlated with a poor prognosis and advanced tumor stage.	Yes	Functional experiments showed that circ_0062682 knockdown reduced CRC growth both in vitro and in vivo. 	34957102
circRNF121	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-1224-5p/FOXM1 axis)	Wound Healing Assay//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Invasion Assay//Transwell Assay	Circ-RNF121 and FOXM1 expression were dramatically upregulated, while miR-1224-5p expression was downregulated in CRC tissues or cells compared with control groups. Additionally, circ-RNF121 acted as a sponge of miR-1224-5p and miR-1224-5p bound to FOXM1. 		Yes	 Circ-RNF121 silencing repressed cell proliferation, migration, invasion and glycolysis but induced cell apoptosis in CRC, which were attenuated by miR-1224-5p inhibitor.	34742305
circMFN2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-574-3p/IGF1R Signaling Axis)	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-MFN2 expression was elevated in CRC tissues and cells.MiR-574-3p could be sponged by circ-MFN2, and its inhibitor reversed the suppression effect of circ-MFN2 silencing on CRC progression. Moreover, IGF1R was a target of miR-574-3p, and its overexpression reversed the inhibition effect of miR-574-3p mimic on CRC progression. 		Yes	 Knockdown of circ-MFN2 restrained the proliferation, migration, invasion, and radioresistance of CRC cells in vitro. Furthermore, silenced circ-MFN2 also reduced the tumor volume and weight of CRC in vivo. 	34093664
hsa_circ_0007031	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC specimens (N = 50) and paracancerous normal colorectal tissues (N = 50) 	Interaction(miR-485-3p/MELK axis)	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining	Circ_0007031 and MELK expression were obviously increased, while miR-485-3p expression was decreased in CRC tissues and cells compared with normal colorectal tissues or cells.  Circ_0007031 controlled MELK expression via interacting with miR-485-3p.		Yes	Circ_0007031 knockdown repressed proliferation, whereas induced cell arrest at G0/G1 phase and apoptosis. On the opposite, circ_0007031 overexpression promoted cell proliferation and induced cell arrest at S phase. Furthermore, circ_0007031 contributed to tumor formation in vivo.	34322757
circSIRT1	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells and tissue	Interaction(eIF4A3)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay	The RT-qPCR results showed that circ-SIRT1 was highly expressed in CRC cells and tissue and was positively correlated with the depth of tumor invasion. We further found that EIF4A3 could bind to circ-SIRT1, and that overexpressing circ-SIRT1 decreased the abundance of EIF4A3 at the mRNAs of the EMT marker proteins N-cadherin and vimentin. 	The RT-qPCR results showed that circ-SIRT1 was highly expressed in CRC cells and tissue and was positively correlated with the depth of tumor invasion. 	Yes	Knocking down circ-SIRT1 inhibited the proliferation and invasion of CRC cells and EMT. 	34660182
circHERC4	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-556-5p/CTBP2/E-cadherin pathway)	CCK8//qRT-PCR//Western Blot	We demonstrated that circHERC4 was aberrantly elevated in CRC tissues (P < 0.001), and was positively associated with lymph node metastasis and advanced tumor grade (P < 0.01). Mechanistically, we revealed that circHERC4 inactivated the tumor suppressor, miR-556-5p, leading to the activation of CTBP2/E-cadherin pathway which promotes tumor metastasis in CRC.	Notably, the expression of circHERC4 was associated with worse survival in patients with CRC. 	Yes	Silencing of circHERC4 significantly inhibited the proliferation and migration of two highly aggressive CRC cell lines and reduced liver and lung metastasis in vivo. 	34781990
hsa_circ_0005927	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues or cells	Interaction(miR-942-5p/BATF2 Axis)	qRT-PCR//Western Blot	Circ_0005927 expression and the mRNA and protein expression of BATF2 were dramatically downregulated, while miR-942-5p expression was obviously upregulated in CRC tissues or cells compared with control groups.  Furthermore, circ_0005927 was a sponge of miR-942-5p, and miR-942-5p bound to BATF2. 		Yes	Circ_0005927 overexpression repressed cell colony-forming ability, migration and invasion, whereas induced cell apoptosis in CRC; however, these impacts were hindered by miR-942-5p mimic or BATF2 knockdown. 	33732022
hsa_circ_001659	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell	Regulation	qRT-PCR	ROC curve analysis demonstrated the predictive values and likelihood ratios of circ_001659 were satisfactory for the diagnosis of CRC, including patients in early-stage disease or patients with carcinoembryonic antigen (CEA)-negative status.  Mechanistically, circ_001659 was localized in the nucleus, recruited the RBBP5 to Vimentin promoter and increased H3K4 trimethylation level on the Vimentin promoter region, which epigenetically activated Vimentin transcription. 		Yes	We further investigated the oncogenic role of circ_001659. In vivo and in vitro experiments indicated that circ_001659 could promote CRC cell invasion and migration. 	33725570
circRAD23B	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miR-1205/TRIM44 axis)	CCK8//qRT-PCR//Western Blot	We identified that circRAD23B was overexpressed in CRC tissues and cells. Target analysis indicated that circRAD23B-targeted miR-1205 and TRIM44 were downstream genes of miR-1205. Moreover, the antitumor response of circRAD23B downregulation and miR-1205 overexpression was, respectively, achieved by increasing miR-1205 and decreasing TRIM44. 		Yes	CRC cell proliferation, cell cycle progression, and cell metastasis were inhibited, while apoptosis was promoted by downregulating circRAD23B. 	33634427
circDOCK1	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	Interaction(miR-132-3p/USP11  axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//IP//IHC//Transwell Assay	Circ_DOCK1 expression was enhanced in colorectal cancer tissues and cells. Circ_DOCK1 sponged miR-132-3p, and miR-132-3p silence mitigated the effect of circ_DOCK1 interference on cell growth, metastasis, and apoptosis. MiR-132-3p targeted USP11, and circ_DOCK1 could regulate USP11 level by miR-132-3p. 		Yes	Silencing circ_DOCK1 repressed cell growth, migration, and invasion, and facilitated apoptosis. 	33685455
circRASSF2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-195-5p/FZD4 axis )	CCK8//qRT-PCR//Western Blot	Our study reported that circRASSF2 was upregulated in CRC tissues and cells, and its high expression was related to the poor prognosis of CRC patients. Besides, our data revealed that circRASSF2 could sponge miR-195-5p, and miR-195-5p could target FZD4. The rescue experiments indicated that both miR-195-5p inhibitor and FZD4 overexpression could reverse the negative regulation of circRASSF2 silencing on CRC progression. Moreover, circRASSF2 could positively regulate the activity of Wnt/β-catenin signaling pathway by the miR-195-5p/FZD4 axis. 	Our study reported that circRASSF2 was upregulated in CRC tissues and cells, and its high expression was related to the poor prognosis of CRC patients. 	Yes	CircRASSF2 knockdown could inhibit proliferation, migration, invasion, and enhance apoptosis in CRC cells, and its overexpression had the opposite effect. 	33929991
hsa_circ_0115744	CircRNA	Homo sapiens	Colorectal Neoplasms	patients with CRC with liver metastasis	Interaction(miR-144/EZH2 axis)	qRT-PCR//Western Blot	We detected the upregulated expression of circ_0115744 in patients with CRC with liver metastasis (CRLM). Further investigation using a validation set indicated that circ_0115744 might be considered as a fingerprint for CRLM. Mechanistic analysis showed that circ_0115744 acted as a competing endogenous RNA of miR-144 to diminish the repressive effect of miR-144 on its target EZH2. 		Yes	Functionally, the overexpression of circ_0115744 significantly promoted the invasion of CRC cell lines, while decreased expression of circ_0115744 suppressed cell invasion in vitro. 	33591945
circNSUN2	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR‑181a‑5p/ROCK2 axis)	CCK8//qRT-PCR//Western Blot	The results revealed that circNSUN2 was highly expressed in CRC tissues and cell lines. Moreover, miR‑181a‑5p was revealed to be a target gene of circNSUN2, and the expression of ROCK2 was negatively regulated by miR‑181a‑5p. Knockdown of circNSUN2 inhibited proliferation and migration, and induced apoptosis of CRC cells and suppressed tumor growth by targeting miR‑181a‑5p to decrease ROCK2 expression. 		Yes	Knockdown of circNSUN2 inhibited the malignant biological behavior of CRC in vivo and in vitro. 	34080658
hsa_circ_1662	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction( YAP1/SMAD3 pathway)	RNA Pull-Down//Western Blot//ISH//FISH//RIP//IHC//IF	A novel circRNA, circ1662, exhibited significantly higher expression in CRC tissues than paired normal tissues.  Mechanistically, circ1662 directly bound to YAP1 and accelerated its nuclear accumulation to regulate the SMAD3 pathway. Additionally, circ1662 enhanced CRC invasion and migration depending on YAP1 and SMAD3. 	High circ1662 expression was correlated with poor prognosis and tumor depth in patients with CRC. 	Yes	Functionally, circ1662 promoted CRC cell invasion and migration by controlling EMT in vitro and in vivo.	33754062
hsa_circ_0001666	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell lines along and tissues	Interaction(miR-576-5p/PCDH10 axis)	CCK8//qRT-PCR	Hsa_circ_0001666 was downregulated in both CRC cell lines along with tumour tissues. Moreover, the mechanistic study showed that hsa_circ_0001666, acting as 'ceRNA' of miR-576-5p, prevented PCDH10 downregulation, as well as suppressed EMT and stemness of CRC cells, and the Wnt/β-catenin signalling pathway. 	higher expression level of hsa_circ_0001666 indicated a better clinical prognosis in patients with CRC.	Yes	Hsa_circ_0001666 knockdown significantly supported CRC cell proliferation along with invasion and inhibited cell apoptosis in vitro. Hsa_circ_0001666 knockdown accelerated the CRC growth and metastasis in vivo. 	34841662
circSPARC	CircRNA	Homo sapiens	Colorectal Neoplasms	the tissues and plasma of CRC patients	Regulation（JAK/STAT pathway ）	CCK8//qRT-PCR	CircSPARC was upregulated in both the tissues and plasma of CRC patients. Mechanistically, circSPARC sponged miR-485-3p to upregulate JAK2 expression and ultimately contribute to the accumulation of phosphorylated (p)-STAT3. Besides, circSPARC recruited FUS, which facilitated the nuclear translocation of p-STAT3.	High expression of circSPARC was associated with advanced TNM stage, lymph node metastases, and poor survival.	Yes	Silencing circSPARC inhibited CRC cell migration and proliferation in vitro and vivo. 	34074294
circMYH9	CircRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues	Expression [highly expressed]	qRT-PCR	We identified an intron-derived circRNA, circMYH9, which was significantly upregulated in CRC tissues. Mechanistically, circMYH9 destabilized the pre-mRNA of p53 by recruiting hnRNPA2B1 in the nucleus. hnRNPA2B1 bound to N6-methyladenosine sites on the 3' untranslated region of p53 pre-mRNA and maintained its stability. Moreover, a lack of amino acids led to an elevated level of ROS, resulting in increased HIF1α, which promoted circMYH9 expression by binding to the promoter region.	 A higher circMYH9 level correlated with shorter relapse-free survival and overall survival of CRC patients. 	Yes	 CircMYH9 promoted serine/glycine metabolism, the NAD + /NADH ratio, and glutathione recycling and inhibited reactive oxygen species (ROS) in a p53-dependent manner, impacting tumour growth.  Furthermore, in vivo AAV9-mediated transfection of circMYH9 could drive chemically-induced carcinogenesis by suppressing p53 in mice.	34496888
hsa_circ_0001073	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-582-3p/RGMB Axis)	CCK8//qRT-PCR//Transwell Assay	circ_0001073 was remarkably under-expressed in NSCLC tissues and cells.circ_0001073 directly bound to miR-582-3p and acted as a miRNA sponge to regulate RGMB expression. Besides, miR-582-3p overexpression or knockdown of RGMB remarkably reversed the malignant phenotypes of NSCLC cells induced by the up-regulation of circ_0001073 expression.		Yes	circ_0001073 overexpression impeded the multiplication, migration, and invasion and enhanced the apoptosis of NSCLC cells in vitro. 	34939762
circFARSA	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation( PI3K/AKT signaling pathway)	qRT-PCR//Western Blot//Transwell Assay//FISH	CircFARSA was significantly upregulated in NSCLC tissues, and the ectopic overexpression of circFARSA enhanced NSCLC cell metastasis. Mechanistically, exosomal circFARSA induced M2 polarization via PTEN ubiquitination and degradation, which further activated the PI3K/AKT signaling pathway. In addition, eIF4A3 promoted circRNA biogenesis and cyclization by binding to its flanking sequences.	CircFARSA was significantly upregulated in NSCLC tissues, and the ectopic overexpression of circFARSA enhanced NSCLC cell metastasis. 	Yes	Furthermore, NSCLC cell-derived exosomal circFARSA polarized the macrophages to a M2 phenotype. The NSCLC cells co-cultured with macrophages transfected with circFARSA or pre-treated with exosomal circFARSA showed enhanced EMT and metastasis	34119765
hsa_circ_0103552	CircRNA	Homo sapiens	Breast Neoplasms	BC and nontumor tissues,cell lines(BT‐20, T47D, MFC7, SKBR3 and MDA‐MB‐231, MCF10A)	Interaction[miR-1236]	qRT-PCR//Luciferase Report Assay//Cell Viability Assay	As data indicated, circ_0103552 was significantly elevated in BC tissue samples and cells. In addition, its expression correlates with clinical severity and dismal prognosis. Furthermore, circ_0103552 could facilitate cell growth, clone-forming ability, migration and invasion, and decrease apoptotic cells. For the mechanism exploration, circ_0103552 could directly sponge miR-1236 to execute oncogenic activities in BC cells. In summary, this study provides a novel circRNA in tumorigeneis and progression of BC and may help to develop effective therapeutic target for this devastating disease.		Yes	" The results revealed that
the viability of cells in cell lines MCF7 decreased
significantly after silencing of circ_0103552 (Figure 2C
and 2D). In MDA‐MB‐231 cells, cell proliferation ability was
strikingly elevated in the circ_0103552 overexpression
groExpression[Expression[up-expression]-expression] compared to empty vector groExpression[Expression[up-expression]-expression] (Figure 2C and
2D). Afterward, flow cytometric analyses were conducted in
two cell lines. As Figure 2E shows, after knockExpression[down-expression] of
circ_0103552 in MCF7 cell line, cell apoptotic rate was
remarkably boosted. Whereas, cell apoptosis was decreased
after circ_0103552 overexpressed. "	31056795
circACAP2	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[miR-29a/b-3p-COL5A1 axis]	CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	CircACAP2 expression was prominently elevated in tumorous tissues.Functionally and mechanistically, circACAP2 promoted breast cancer proliferation and motility by sponging miR-29a/b-3p and modulating COL5A1.		Yes	According to the results, cell proliferation and motility ability decreased and apoptosis ability increased after circACAP2 knockExpression[down-expression]. 	31863774
circUBE2D2	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues,cell lines	Interaction[Sponging miR-1236 and miR-1287]	CCK8//qRT-PCR//Luciferase Report Assay//IHC	 In the current study, we screened and identified a novel circRNA, circ-UBE2D2, which was highly expressed in BC cell lines and tissues and was closely related to aggressive clinical features and dismal prognosis. Mechanistically, circ-UBE2D2 was able to simultaneously function as molecular sponges of miR-1236 and miR-1287 to regulate the expression of their respective target genes. 		Yes	 Small interfering RNA (siRNA)-mediated circ-UBE2D2 silencing notably inhibited the proliferation, migration and invasion of BC cells, whereas circ-UBE2D2 overexpression displayed opposite effects. 	31336316
hsa_circ_100876	CircRNA	Homo sapiens	Breast Neoplasms	BC tissue	Interaction[adsorbing microRNA-361-3p]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	QRT-PCR results showed that circRNA_100876 level in BC tissues was conspicuously higher than that in the adjacent tissues.QRT-PCR revealed that microRNA-361-3p and circRNA_100876 showed a negative correlation in the expression level of genes in BC tissues. In addition, the results of the Luciferase reporter gene assay confirmed that circRNA_100876 can be targeted by microRNA-361-3p through their binding site.	Moreover, patients with a high expression of circRNA_100876 had a relatively lower overall survival rate. 	Yes	Compared with the NC group, the cell proliferation and invasion ability of circRNA_100876 knockdown group was conspicuously decreased.	31486496
hsa_circ_0072309	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[targeting miR-492]	qRT-PCR	hsa_circ_0072309 expression in breast cancer tissues was upregulated relative to that in adjacent normal tissues.The results of our mechanistic studies indicated that hsa_circ_0072309 could act as the sponge of miR-492, which exhibited increased expression in breast cancer tissues. Hsa_circ_0072309 suppressed breast cancer cell proliferation, migration, and invasion by inhibiting miR-492.		Yes	hsa_circ_0072309 overexpression dramatically inhibited the proliferation, migration, and invasion of breast cancer cells in vitro. In vivo assays revealed that the ectopic expression of hsa_circ_0072309 repressed breast cancer growth. 	30774431
hsa_circ_0006528	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[MAPK/ERK signaling pathway1]	qRT-PCR	We analyzed a cohort of 97 patients and found that circ_0006528 expression was significantly upregulated in human breast cancer tissues compared with that in adjacent non-tumorous tissues and was significantly associated with advanced tumor-node-metastasis (TNM) stage and poor prognosis.Further mechanistic studies revealed that circ_0006528 could sponge endogenous miR-7-5p and inhibit its activity. We also identified Raf1, which activates the MAPK/ERK signaling pathway, as a target of miR-7-5p and determined that circ_0006528 promotes breast cancer growth, invasion, and migration by promoting the expression of Raf1 and activates the MAPK/ERK pathway. 	We analyzed a cohort of 97 patients and found that circ_0006528 expression was significantly upregulated in human breast cancer tissues compared with that in adjacent non-tumorous tissues and was significantly associated with advanced tumor-node-metastasis (TNM) stage and poor prognosis.	Yes	 Downregulating circ_0006528 induced G2 phase arrest and cell apoptosis. 	31072375
hsa_circ_0004771	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[ ZEB2 signaling pathway]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	 hsa_circ_0004771 and Zinc finger E-box binding homeobox 2 (ZEB2) expression levels were up-regulated and positively correlated in breast cancer tumor tissues. 		Yes	Knockdown of hsa_circ_0004771 and ZEB2 served as equally authentic of miR-653 mimics to induce growth inhibition and apoptosis in breast cancer cells.	30979827
circDENND4C	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[miR-200b/c ]	qRT-PCR//Transwell Assay//RIP//Western Blot	 circDENND4C highly expressed in breast cancer was up-regulated in response to hypoxia.circDENND4C was validated as a sponge of miR-200b and miR-200c. Deficiency of miR-200b or miR-200c reversed the suppressive effect of circDENND4C knockdown on breast cancer progression. Moreover, silence of circDENND4C reduced xenograft tumor growth by increasing miR-200b and miR-200c.		Yes	Knockdown of circDENND4C decreased glycolysis, migration and invasion in breast cancer cells under hypoxia.	31488193
hsa_circ_001569	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction[PI3K-AKT pathway ]	qRT-PCR//Western Blot	 We found that hsa_circ_001569 expression was significantly up-regulated in both BC tissues and cell lines.Besides, molecular mechanistic study revealed that depression of hsa_circ_001569 impeded the activation of PI3K-AKT signaling in BC cells. Our results indicated that hsa_circ_001569 upregulation was associated with BC lymph-node metastasis, clinical stage, and poor prognosis. Hsa_circ_001569 might contribute to progression of BC by modulating PI3K-AKT pathway.	Overexpression of hsa_circ_001569 was associated with Lymph node metastasis, advanced clinical stage and shorter overall survival.Multivariate assay confirmed that hsa_circ_001569 expression was an independent prognostic factor for 5-year overall survival. 	Yes	Furthermore, functional investigations revealed that knockdown of hsa_circ_001569 significantly suppressed the growth and metastatic potentials of BC cells.	31104012
circPLK1	CircRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction[sponging miR-296-5p]	qRT-PCR//Microarray	 CircPLK1 was significantly upregulated in TNBC and associated with poor survivals.CircPLK1-miR-296-5p-PLK1 axis regulates tumor progression by ceRNA mechanism in TNBC, indicating that circPLK1 may serve as a prognostic factor and novel therapeutic target for TNBC.	 CircPLK1 was significantly upregulated in TNBC and associated with poor survivals.	Yes	CircPLK1 knockdown inhibited cell growth and invasion in vitro as well as tumor occurrence and metastasis in vivo.	31337246
circTADA2A-E6	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[miR-203a-3p/SOCS3 axis]	Western Blot//FISH//qRT-PCR//Luciferase Report Assay//Microarray	We detected two circRNAs, circTADA2A-E6 and circTADA2A-E5/E6, which were among the top five differentially expressed circRNAs in breast cancer. They were consistently and significantly decreased in a large cohort of breast cancer patients, and their downregulation was associated with poor patient survival for TNBC.circTADA2A-E6 preferentially acted as a miR-203a-3p sponge to restore the expression of miRNA target gene SOCS3, resulting in a less aggressive oncogenic phenotype. circTADA2As as promising prognostic biomarkers in TNBC patients, and therapeutic targeting of circTADA2As/miRNA/mRNA network may be a potential strategy for the treatment of breast cancer.	We detected two circRNAs, circTADA2A-E6 and circTADA2A-E5/E6, which were among the top five differentially expressed circRNAs in breast cancer. They were consistently and significantly decreased in a large cohort of breast cancer patients, and their downregulation was associated with poor patient survival for TNBC.	Yes	 Especially, circTADA2A-E6 suppressed in vitro cell proliferation, migration, invasion, and clonogenicity and possessed tumor-suppressor capability.	30787278
circBMPR2	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	Regulation[ circBMPR2/miR-553/USP4 Axis]	Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	 In this study, we identified a novel circRNA (named circBMPR2) whose expression was lower in breast cancer tissues with metastasis. Mechanistically, we demonstrated that circBMPR2 could abundantly sponge miR-553 and that miR-553 overexpression could attenuate the inhibitory effects caused by circBMPR2 overexpression. We also found that ubiquitin-specific protease 4 (USP4) was a direct target of miR-553, which functions as a tumor suppressor in breast cancer. Our findings demonstrated that circBMPR2 might function as a miR-553 sponge and then relieve the suppression of USP4 to inhibit the progression and tamoxifen resistance of breast cancer. Targeting this newly identified circRNA may help us to develop potential novel therapies for breast cancer patients.		Yes	Functionally, we found that circBMPR2 knockdown effectively enhanced cell proliferation, migration, and invasion. Moreover, circBMPR2 knockdown promoted tamoxifen resistance of breast cancer cells through inhibiting tamoxifen-induced apoptosis, whereas circBMPR2 overexpression led to decreased tamoxifen resistance. 	31302495
circKDM4C	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Expression[lower expressed]	qRT-PCR//Luciferase Report Assay//RIP	 Furthermore, we analyzed a cohort of breast cancer patients and found that circKDM4C expression was decreased in breast cancer tissues, and lower circKDM4C expression was associated with poor prognosis and metastasis in breast cancer. 		Yes	 Functionally, we demonstrated that circKDM4C significantly repressed breast cancer proliferation, metastasis	31406252
circFBXL5	CircRNA	Homo sapiens	Breast Neoplasms	 cell lines	Interaction[sponging miR-660]	CCK8//RIP//Colony Formation Assay//Microarray	We confirmed the expression of circFBXL5 and found that circFBXL5 was upregulated in breast cancer cell lines, especially in MDA‐MB‐453 and MDA‐MB‐231 (Figure ​(Figure1D).1D).  Collectively, our study highlighted the regulatory function of the circFBXL5/miR-660/SRSF6 pathway in breast cancer progression, which could be potential therapeutic targets for breast cancer.		Yes	"To investigate circFBXL5 functions in breast cancer, we knocked down circFBXL5 successful by si‐circFBXL5#1 (Figure ​(Figure2A).2A). CCK‐8 assay revealed that circFBXL5 down‐regulation suppressed cell proliferation (Figure ​(Figure2B).2B). And knockdown of circKIF4A suppressed breast cancer cell colony formation ability (Figure ​(Figure22C).
"	31729134
hsa_circ_0136666	CircRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction[miR-1299 and targeting CDK6]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Transwell Assay	It was displayed that hsa_circ_0136666 was greatly increased in breast cancer. In conclusion, it was revealed that Upregulation of hsa_circ_0136666 promoted breast cancer progression by sponging miR-1299 and targeting CDK6.		Yes	Meanwhile, its Upregulation repressed breast cancer proliferation, migration and invasion capacity, which could be reversed by the increase of hsa_circ_0136666. 	30993801
hsa_circ_0001283	CircRNA	Homo sapiens	Breast Neoplasms	Breast cancer tissue	interaction[MiR-187/HIPK3 Axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Downregulation of circRNA-0001283 expression was observed in breast cancer tissue samples.Finally, we showed that circRNA-0001283 positively regulated HIPK3 expression by sponging miR-187. 		Yes	Ectopic expression of circRNA-0001283 remarkably suppressed cell viability and invasion, and induced apoptosis in breast cancer cells.	32066649
circSETD2	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[ miR-155-5p/SCUBE2 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 circ_SETD2 and SCUBE2 were downregulated, while miR-155-5p was upregulated in BC tissues and cells.Therefore, circ_SETD2 curbed BC progression via upregulating SCUBE2 via binding to miR-155-5p.		Yes	Both circ_SETD2 and SCUBE2 elevation arrested cell cycle progression, inhibited cell proliferation, migration, and invasion, and accelerated cell apoptosis in BC cells. Moreover, circ_SETD2 upregulation repressed BC growth in vivo.	33336052
circNR4A1	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines,peripheral blood	Expression[lower expressed]	CCK8//qRT-PCR//Western Blot	 The expression of circNR4A1(Hsa-circ-0026352) was lower in breast cancer tissues, peripheral blood and breast cancer cell lines than in adjacent normal tissues, healthy individuals' peripheral blood and human breast epithelial cells. 		Yes	Over-expression of circNR4A1 in MCF-7 cells inhibited the cell proliferation, promoted cell apoptosis and blocked the cell cycle in G1/S phase. 	33325363
hsa_circ_0069094	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-591/HK2 axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay	 In the present study, we verified that circ_0069094 was upregulated in BC tissues and cells.In conclusion, these results indicated that circ_0069094 facilitated cell malignancy and glycolysis by upregulating HK2 through adsorbing miR-591, suggesting that circ_0069094 might be a prognostic biomarker and therapeutic target for BC.		Yes	Functional analysis revealed that circ_0069094 silencing induced apoptosis, curbed proliferation, and reduced glycolysis in BC cells in vitro, but circ_0069094 overexpression had an opposing influence. Also, circ_0069094 knockdown reduced BC growth in vivo.	33309838
circSLC8A1	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	regulation[PTEN/PI3k/Akt pathway]	Western Blot//Colony Formation Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	We demonstrated that circSLC8A1 was significantly down-regulated in breast cancer tissues and cell lines, of which expression was negatively correlated with clinical severity and dismal prognosis. In summary, circSLC8A1/miR-671 regulates breast cancer progression through PTEN/PI3k/Akt signaling, which may provide efficient therapeutic target for this devastating cancer.	We demonstrated that circSLC8A1 was significantly down-regulated in breast cancer tissues and cell lines, of which expression was negatively correlated with clinical severity and dismal prognosis. 	Yes	 Overexpression of circSLC8A1 suppressed cell proliferation, migration and invasion in vitro, and inhibited tumor growth in vivo. 	33301895
circCER	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[miR‑136/MMP13 axis]	CCK8//qRT-PCR//Western Blot	The results revealed that circRNA‑CER and matrix metalloproteinase 13 (MMP13) were Expression[Expression[up-expression]-expression]regulated, whereas miR‑136 was Expression[down-expression]regulated in breast cancer tissues compared with adjacent non‑tumor tissues.		Yes	the results demonstrated that silencing of circRNA-CER efficiently sExpression[Expression[up-expression]-expression]pressed the expression of circRNA-CER (Fig. 2B). In addition, the results from the CCK-8 and Transwell assays indicated that knockExpression[down-expression] of circRNA-CER significantly sExpression[Expression[up-expression]-expression]pressed proliferation (Fig. 2C) and migration (Fig. 2D) of MCF-7 cells.	30816475
circASS1	CircRNA	Homo sapiens	Breast Neoplasms	cell lines(MCF-7, MDA-MB-231)	Expression[Expression[lower expressed]-expression]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Microarray	CircASS1 in MDA-MB-231 is Expression[down-expression]regulated comparing to MCF-7, and overexpression of circASS1 could sExpression[Expression[up-expression]-expression]press invasion and migration. While silence, it could promote invasion and migration.		Yes	CircASS1 in MDA-MB-231 is Expression[down-expression]regulated comparing to MCF-7, and overexpression of circASS1 could sExpression[Expression[up-expression]-expression]press invasion and migration. While silence, it could promote invasion and migration.	30657346
circPRMT5	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	regulation[ circ-PRMT5/miR-509-3p/TCF7L2 axis]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//RNA Pull-Down	Circ-PRMT5 is up-regulated in breast cancer tissues and cells.  Overall, our data indicate that the circ-PRMT5/miR-509-3p/TCF7L2 axis can aggravate the malignant character of breast cancer cells by the regulation of the PI3K/AKT pathway.		Yes	Functionally, knockdown of circ-PRMT5 suppresses cell proliferation and angiogenesis and increases cell apoptosis in breast cancer.	33277756
hsa_circ_001783	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue,cell line	Interaction[sponging miR-200c-3p]	RIP//Luciferase Report Assay	 Here we systematically analyzed the circular RNAs in breast cancer based on their characteristic in sponging disease-specific miRNAs and identified hsa_circ_001783 as a top ranked circRNA in our computation and verified its high expression in both breast cancer cells and cancer tissue. .Importantly, hsa_circ_001783 promoted progression of breast cancer cells via sponging miR-200c-3p.		Yes	Knockdown of this circRNA remarkably inhibited the proliferation and invasion of breast cancer cells.	30670688
circPGD	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-16-5p/ABL2)	Western Blot//Wound Healing Assay//Migration Assay//CCK8//FISH//qRT-PCR//Flow Cytometry//IF//Luciferase Report Assay//IHC//Transwell Assay	Compared with the control, circPGD and ABL2 expression increased within GC tissues and cells, and the miR-16-5p level was decreased. Mechanistically, circPGD sponged miR-16-5p for relieving miR-16-5p suppression on the corresponding target ABL2 via the SMAD2/3 and YAP signaling pathways. 		Yes	 Functionally, circPGD promoted cell proliferation, migration and suppressed apoptosis in vitro. 	36104322
circSKA3	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-520h/CDC42)	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Overexpression of circ_SKA3 was validated in GC tissues and cells.  Circ_SKA3 directly bound to miR-520h, and circ_SKA3 regulated CDC42 expression through miR-520h. Circ_SKA3 exerted regulatory effects on GC cell behaviors by inhibiting miR-520h. Furthermore, CDC42 was a functional target of miR-520h in regulating GC cell behaviors.		Yes	 The down-regulation of circ_SKA3 suppressed proliferation, cell cycle progression, colony formation, migration, invasion, and promoted cell apoptosis in vitro, as well as weakening tumor growth in vivo. 	36134741
circRPPH1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells	Interaction(miR-375/SLC7A11 axis)	RIP//Luciferase Report Assay	Moreover, circRPPH1 promoted the stemness of gastric cancer cells dependent on the miR-375/SLC7A11. 		Yes	Moreover, circRPPH1 promoted the stemness of gastric cancer cells dependent on the miR-375/SLC7A11. 	36190453
circDNMT1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction( miR-576-3p/HIF-1α axis )	RNA Pull-Down//Western Blot//Migration Assay//CCK8//FISH//qRT-PCR//Luciferase Report Assay//Invasion Assay	circDNMT1 was successfully identified and shown to be overexpressed in GC tissues and cell lines. circDNMT1 functioned as an oncogenic factor by sponging miR-576-3p. HIF-1α was negatively regulated by miR-576-3p via binding its mRNA 3' untranslated region. circDNMT1 promoted malignant behaviors and metabolic reprogramming of GC by targeting the miR-576-3p/HIF-1α axis both in vitro and in vivo.	The expression levels of circDNMT1 were correlated with pathological T stage, pathological TNM stage and shorter survival time of GC patients. 	Yes	 circDNMT1 knockdown inhibited the proliferation, migration, invasion and glycolysis of GC cells. 	35712504
hsa_circ_0005758	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-1229-3p/GCNT4 feedback loop)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 Circ_0005758 expression was decreased in GC tissues and cells, re-expression of circ_0005758 induced apoptosis and suppressed proliferation, migration, invasion and angiogenesis in GC cells in vitro, and impeded xenograft tumor growth in nude mice. Circ_0005758 acts as a tumor suppressor to impede gastric cancer progression via miR-1229-3p/GCNT4 axis, implying that therapeutic targeting of circ_0005758 may better to prevent gastric cancer.		Yes	 Circ_0005758 expression was decreased in GC tissues and cells, re-expression of circ_0005758 induced apoptosis and suppressed proliferation, migration, invasion and angiogenesis in GC cells in vitro, and impeded xenograft tumor growth in nude mice. 	35970245
hsa_circ_0017728	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines 	Interaction(miR-149/IL-6/STAT3 signaling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	 Our results demonstrated that the hsa_circ_0017728 expression level was up-regulated in GC tissues and cell lines and closely associated with poor overall survival and pathological differentiation, higher TNM stage and lymph node metastasis.  We also discovered that hsa_circ_0017728 might serve as a ceRNA to sponge miR-149 and indirectly regulated the IL-6/STAT3 signaling pathway in GC cell proliferation and apoptosis.	 Our results demonstrated that the hsa_circ_0017728 expression level was up-regulated in GC tissues and cell lines and closely associated with poor overall survival and pathological differentiation, higher TNM stage and lymph node metastasis. 	Yes	. Knockdown of hsa_circ_0017728 had the ability to cause inhibition of cell proliferation and migration and elevate the cell apoptosis rate in GC cells. 	36457988
circCOL1A2	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(miR-1286/USP10/RFC2 )	RNA Pull-Down//Western Blot//Wound Healing Assay//Co-IP//qRT-PCR//FISH//RIP//IF//Luciferase Report Assay//Transwell Assay	 Our results found circCOL1A2 to be not only upregulated in GC cells, but that it also propels the migration and invasion of GC cells. CircCOL1A2 functions as a competing endogenous RNA (ceRNA) by sequestering microRNA-1286 (miR-1286) to modulate ubiquitin-specific peptidase 10 (USP10), which in turn spurs the migration and invasion of GC cells by regulating RFC2.CircCOL1A2 sponges miR-1286 to promote cell invasion and migration of GC by elevating the expression of USP10 to downregulate the level of RFC2 ubiquitination. 		Yes	 Our results found circCOL1A2 to be not only upregulated in GC cells, but that it also propels the migration and invasion of GC cells. CircCOL1A2 sponges miR-1286 to promote cell invasion and migration of GC by elevating the expression of USP10 to downregulate the level of RFC2 ubiquitination. 	35791074
circSFMBT2	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	Interaction(miR-885-3p/CHD7 pathway)	Wound Healing Assay//Colony Formation Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Transwell Assay	 Circ-SFMBT2 and CHD7 were upregulated, whereas miR-885-3p was downregulated in gastric cancer tissues and cells.  In mechanism analysis, circ-SFMBT2 regulated CHD7 expression by sponging its target miRNA, miR-885-3p. Rescue experiments manifested that miR-885-3p inhibition reversed the effects of circ-SFMBT2 knockdown, and CHD7 overexpression abolished the antitumor role of miR-885-3p overexpression. Moreover, circ-SFMBT2 knockdown inactivated the Wnt/β-catenin signaling pathway. 		Yes	 In functional assay, circ-SFMBT2 knockdown suppressed gastric cancer cell viability, colony formation ability, migration, invasion and oxidative stress but induced apoptosis, and circ-SFMBT2 downregulation also blocked tumor growth in vivo. 	34387601
hsa_circ_0000218	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(hsa_circ_0000218/hsa-miR-139-3p/SOX4 )	RNA Pull-Down//Western Blot//Luciferase Report Assay//qRT-PCR	circ_0000218 and SOX4 were highly expressed, whereas miR-139-3p was lowly expressed in GC cells.Moreover, circ_0000218 negatively regulated miR-139-3p in GC cells. miR-139-3p overexpression inhibited proliferation and induced apoptosis in GC cells, but these effects were reversed by SOX4 overexpression. 		Yes	circ_0000218 knockdown inhibited GC cell proliferation, promoted apoptosis and enhanced cleaved-Caspase3 expression in GC cells, whereas miR-139-3p knockdown reversed these effects. 	35185288
hsa_circ_0005230	CircRNA	Homo sapiens	Stomach Neoplasms	 130 cases of GC tissues and cell line	Interaction(miR-1299/RHOT1 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 This study validated that hsa_circ_0005230 was significantly up-regulated in 130 cases of GC tissues using qRT-PCR, and clinicopathological feature analysis revealed that its high expression was positively associated with histological grade, lymph node metastasis, TNM stages, and poor prognosis. In mechanism studies, bioinformatics analyses were used to predict the hsa_circ_0005230/miR-1299/RHOT1 axis and hsa_circ_0005230 may serve as a sponge for miR-1299 and indirectly regulate the expression of RHOT1. The regulated relationships between the molecules on the axis were verified using qRT-PCR and correlation analysis. Dual-luciferase reporter gene assay has been used to verify the binding site between miR-1299 and RHOT1. WB (Western blotting) and IHC (Immunohistochemical) were used to verify that RHOT1 may play the role of oncoprotein and affect the biological behavior of GC.	 This study validated that hsa_circ_0005230 was significantly up-regulated in 130 cases of GC tissues using qRT-PCR, and clinicopathological feature analysis revealed that its high expression was positively associated with histological grade, lymph node metastasis, TNM stages, and poor prognosis.	Yes	In vitro, functional experiments showed that silencing hsa_circ_0005230 significantly decreased GC cell proliferation, invasion and migration capabilities. In addition, the major proteins of EMT (epithelial-mesenchymal transition) relevance have changed.	35170374
hsa_circ_0006282	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells, gastritis tissues, and gastric cancer tissues	Interaction(hsa-miR-136-5p/PTEN/AKT pathway)	Western Blot//CCK8//qRT-PCR//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	Hsa_circ_0006282 was down expressed in gastric cancer cells, gastritis tissues, and gastric cancer tissues. Besides, Western blot showed that the levels of protein kinase B (AKT) and cyclin-dependent kinase 2 (CDK2) were significantly increased and decreased after knockdown and up-regulation of hsa_circ_0006282, respectively, while phosphatase and tensin homolog deleted on chromosome ten (PTEN) was significantly opposite regulated. Finally, hsa_circ_0006282 promoted the expression of PTEN by sponging hsa-miR-136-5p.		Yes	The abilities of cell proliferation, cell migration and resistance to apoptosis were enhanced after hsa_circ_0006282 was downregulated, while overexpression of hsa_circ_0006282 got opposite results. 	35794253
hsa_circ_0006470	CircRNA	Homo sapiens	Stomach Neoplasms	AGS cells	Interaction(miR-1234/TP53I11 axis)	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//EdU Staining//Transwell Assay	The data indicated that hsa_circ_0006470 expression was downregulated in AGS cells. Moreover, miR-1234 was bound to hsa_circ_0006470 and TP53I11 was targeted by miR-1234. Furthermore, OE of hsa_circ_0006470 inhibited the tumorigenesis of GC via the regulation of the miR-1234/TP53I11 axis. 		Yes	In addition, overexpression (OE) of hsa_circ_0006470 could inhibit the viability and proliferation of GC cells.  Moreover, OE of hsa_circ_0006470 inhibited the migration of GC cells and induced G1 cell cycle phase arrest. 	36190397
hsa_circ_0075825	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-432-5p/SOX9)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Circ_0075825 expression was raised in GC tissues and cell lines. SOX9 was identified as one of the direct target genes of miR-432-5p, and circ_0075825 repressed the expression of miR-432-5p, to induce the expression of SOX9. Furthermore, miR-432-5p overexpression counteracted the promoting effect of circ_0075825 on the malignancy of GC cells.		Yes	Circ_0075825 overexpression promoted the proliferative, migrative and invasive abilities of GC cells, while inhibiting apoptosis, while depletion of circ_0075825 suppressed the malignant biological behaviors of GC cells. 	35395444
hsa_circ_0001190	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-586/SOSTDC1 Axis)	RNA Pull-Down//Western Blot//Tube Formation Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The levels of circ_0001190 and SOSTDC1 were downregulated, and the miR-586 level was increased in GC. Circ _0001190 served as a miR-586 sponge to adjust the expression of SOSTDC1. Additionally, miR-586 could promote the advancement of GC by interfering SOSTDC1. Exosomal circ_0001190 overexpression inhibited the development of GC by miR-586/SOSTDC1 axis, which proposed a potential targeted therapy for GC cure.		Yes	For functional assay, circ _0001190 overexpression inhibited cell vitality, cell proliferation, angiogenesis, cell migration and invasion, whereas stimulated cell apoptosis in GC cells. 	35138469
hsa_circ_0110940	CircRNA	Homo sapiens	Stomach Neoplasms	human gastric cancer cells	Interaction(miR-1178-3p/SLC38A6 Axis)	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	 We found the significant upregulation of circ_0110940 in human gastric cancer cells AGS and MKN45.  Circ_0110940 binded with miR-1178-3p, which further targeted SLC38A6 3'UTR. Circ_0110940 degraded miR-1178-3p, and miR-1178-3p degraded SLC38A6. Thus, circ_0110940 has a positive effect on SLC38A6 expression. 		Yes	 Circ_0110940 was a stable circRNA and exerted an antiproliferative and proapoptotic effect in AGS and MKN45.	35813866
circPFKP	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues & GC cells	Interaction(miR-644 and regulating ADAMTSL5 expression)	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircPFKP is downregulated in GC tissues, and overexpression of circPFKP inhibits malignant behavior in GC cells. Bioinformatics predicted that circPFKP could bind to miR-644, and miR-644 could target disintegrin-like and metalloprotease domain-containing thrombospondin type 1 motif-like 5 (ADAMTSL5). Overexpression of circPFKP enhances the expression of ADAMTSL5 by decreasing the expression of miR-644 to suppress the growth of xenograft GC tumors in vivo and in vitro. In conclusion, the circPFKP/miR-644/ADAMTSL5 regulatory pathway inhibited the malignant progression of GC. These findings may extend our understanding of the effects of circRNAs on cancer development and provide novel targets for the diagnosis of GC.		Yes	Overexpression of circPFKP enhances the expression of ADAMTSL5 by decreasing the expression of miR-644 to suppress the growth of xenograft GC tumors in vivo and in vitro.	35587154
hsa_circ_0001658	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and GC cell lines	Interaction(miR-182/RAB10)	Flow Cytometry//qRT-PCR//Cell Viability Assay//Western Blot	Circ_0001658 was identified to be aberrantly expressed in GC tissues and was demonstrated in GC cell lines (AGS and HGC27) in vitro.MiR-182 bound to circ_0001658 and RAB10. Moreover, upregulated RAB10 neutralized the effects of miR-182 on cell viability, autophagy, and apoptosis of GC cells. Silencing circ_0001658 restrained cell viability, suppressed autophagy, and promoted apoptosis of GC cells by sponging miR-182 to suppress the expression of RAB10. Therefore, circ_0001658 may be a potential therapeutic target for GC.		Yes	Circ_0001658 and RAB10 were upregulated, whereas miR-182 was suppressed in AGS and HGC27 cells. GC cell viability and autophagy were inhibited and apoptosis was promoted after circ_0001658 knockdown, and the cellular functions were reversed by downregulating miR-182. 	35030981
hsa_circ_0005230	CircRNA	Homo sapiens	Breast Neoplasms	BC tissue specimens and cell lines	Regulation[miR-618/ CBX8 Signal Pathway]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	circ_0005230 was overexpressed in BC tissue specimens and cell lines.circ_0005230/miR-618/CBX8 axis might play a key role in BC tumorigenesis and development.	In addition, circ_0005230 could be regarded as a prognostic predictor in BC patients.	Yes	In vitro and in vivo data demonstrated the cell growth promoting role of circ_0005230.	30504704
hsa_circ_0052112	CircRNA	Homo sapiens	Breast Neoplasms	MDA-MB-231 cells	interaction[miR-125a-5p]	qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	 Hsa_circ_0052112 expression was significantly higher in MDA-MB-231 cells than that in MCF-7 cells.Hsa_circ_0052112 could directly sponge to miR-125a-5p; overexpression of miR-125a-5p significantly inhibited breast cancer cells migration and invasion. 		Yes	Overexpression of hsa_circ_0052112 promoted cell migration and invasion in breast cancer. Inversely, down-regulation of hsa_circ_0052112 suppressed breast cancer cells migration and invasion.	30257349
circPLK1	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-4500/IGF1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	CircPLK1 and IGF1 were upregulated and miR-4500 was downregulated in BC tissues and cells. CircPLK1 silence inhibited BC cell growth, migration and invasion by regulating miR-4500/IGF1 axis, suggesting circPLK1/miR-4500/IGF axis might be a potential therapeutic target.		Yes	Interference of circPLK1 inhibited BC cell growth, migration and invasion, which was reversed by overexpression of IGF1.	33298061
circUBR1	CircRNA	Homo sapiens	Breast Neoplasms	 BC tumor tissues	regulation[miR-1299/CCND1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 Our results revealed that circ-UBR1 was upregulated in BC, and its silencing could inhibit BC cell proliferation, metastasis, and promote apoptosis in vitro, as well as restrain BC tumor growth in vivo.Our data indicated that circ-UBR1 might play a pro-cancer role in BC progression by regulating the miR-1299/CCND1 axis.		Yes	 Our results revealed that circ-UBR1 was upregulated in BC, and its silencing could inhibit BC cell proliferation, metastasis, and promote apoptosis in vitro, as well as restrain BC tumor growth in vivo.	33259864
circPTCD3	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction(miR-198)	In Vivo Experiment//RNA Pull-Down//IHC//Wound Healing Assay//FISH//MTT//Luciferase Report Assay//PCR//Colony Formation Assay//Transwell Assay	In the present study, we identified a novel circRNA termed as circPTCD3 which was indicated to be significantly up-regulated in breast cancer tissues and cell lines.  Furthermore, we identified that circPTCD3 was able to target miR-198 in breast cancer cell. miR-198 has the function of inhibiting proliferation and migration of breast cancer cells which can be reversed by circPTCD3.		Yes	The results revealed that ectopic expression of circPTCD3 promoted the cell proliferation, migration and colony formation ability of breast cancer cells. Constantly, silencing of circPTCD3 inhibited those of breast cancer cells.	34785951
circKIF4A	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	regulation[miR-152/ZEB1 axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	CircKIF4A and ZEB1 were conspicuously upregulated and miR-152 was markedly reduced in BC tissues and cells. Silencing of circKIF4A hampered cell metastasis and promoted apoptosis by regulating ZEB1 via sponging miR-152 in BC.		Yes	Deficiency of circKIF4A repressed migration, invasion and induced apoptosis of BC cells. 	32408908
hsa_circ_103809	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[PI3K/AKT signaling pathway]	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	 The expression of circ_103809 in breast cancer was overexpressed.circ_103809 accelerated breast cancer progression via regulating PI3K/AKT signaling.		Yes	 circ_103809 was proved to promote cell proliferation in breast cancer progression. In addition, circ_103809 was also involved in repressing cell apoptosis and accelerating cell cycle progression in vitro.	32382325
circNFIC	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	interaction[sponging miR-658]	qRT-PCR	 Our study highlighted the regulatory function of the circNFIC/miR-658/UPK1A pathway in breast cancer progression, which could be a potential therapeutic target for breast cancer.	 Kaplan-Meier survival analysis revealed that low levels of circNFIC were related to poor outcome of breast cancer.	Yes	 Further experiments revealed that overexpressing circNFIC suppressed breast cancer cell proliferation and migration to the lung.	32368305
circHMCU	CircRNA	Homo sapiens	Breast Neoplasms	cell line and breast cancer tissues	interaction[let-7 Family]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining	In the present study we found a circRNA termed circHMCU whose expression was associated with poor prognosis. It was upregulated in cell lines with high metastatic potential compared with its parental cell line and in breast cancer tissues compared with normal tissues.  Finally, let-7 microRNAs could rescue the functions of circHMCU in breast cancer via suppressing the expression of MCY, HMGA2, and CCND1. 		Yes	In vitro results proved that circHMCU could significantly promote proliferation, migration, and invasion abilities of breast cancer cells via affecting the G1 phase cell cycle checkpoint and the epithelial-mesenchymal transition (EMT) pathway. Further in vivo studies showed that overexpression of circHMCU contributed to rapid proliferation and lung metastasis of breast cancer. 	32330870
circSCYL2	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Expression[lower expressed]	qRT-PCR//RNA-seq//Transwell Assay	The current study identified that circSCYL2 was downregulated in breast cancer tissues and cell lines, and that circSCYL2 overexpression inhibited cell migration and invasion. 		Yes	The current study identified that circSCYL2 was downregulated in breast cancer tissues and cell lines, and that circSCYL2 overexpression inhibited cell migration and invasion. 	32236616
circCDYL	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues 	regulation[miR-1275-ATG7/ULK1-autophagic axis ]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	An autophagy associated circRNA circCDYL was elevated by 3.2 folds in BC tissues as compared with the adjacent non-cancerous tissues, circCDYL promotes BC progression via the miR-1275-ATG7/ULK1-autophagic axis and circCDYL could act as a potential prognostic and predictive molecule for breast cancer patients.		Yes	Moreover, circCDYL enhanced the malignant progression of BC cells in vitro and in vivo.	32213200
hsa_circ_0068033	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues	regulation[hsa_circ_0068033/miR-659 axis]	ISH//qRT-PCR	 The results suggested that the expression of hsa_circ_0068033 was downregulated in BC tissues, and its expression was markedly correlated with tumor size (P=0.021), and the Tumor, Node, and Metastasis stage (P=0.023). Collectively, this study revealed for the first time that hsa_circ_0068033 acts as a tumor suppressor gene in BC, and the hsa_circ_0068033/miR-659 axis participates in the progression of BC.	 The results suggested that the expression of hsa_circ_0068033 was downregulated in BC tissues, and its expression was markedly correlated with tumor size (P=0.021), and the Tumor, Node, and Metastasis stage (P=0.023). 	Yes	Functionally, in-vitro experiments demonstrated that overexpression of hsa_circ_0068033 could inhibit the growths, clone formation, invasion and migration of MCF-7 and MDA-MB-231 cells while activating the intrinsic apoptotic pathway to induce apoptosis. 	32184627
hsa_circ_0008039	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	regulation[miR-515-5p/CBX4 axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Hsa_circ_0008039 was upregulated in BC tissues and cells, and expedited proliferation, migration and invasion of BC cells. These findings implicated that hsa_circ_0008039 contributed to proliferation, migration and invasion in vitro and promoted tumor growth in vivo by miR-515-5p/CBX4 axis in BC, suggesting a potential therapeutic strategy for BC treatment.		Yes	CBX4 was highly expressed in BC tissues and cells, and contributed to proliferation, migration and invasion of BC cells.	32141558
circRNF20	CircRNA	Homo sapiens	Breast Neoplasms	BC samples	regulation[ miR-487a/HIF-1α/HK2]	Microarray	CircRNA microarray sequencing revealed that circRNF20 was one of the upregulated transcripts in BC samples.In conclusion, this finding illustrates the vital roles of circRNF20 via the circRNF20/ miR-487a/HIF-1α/HK2 axis in breast cancer progress and Warburg effect, providing an interesting insight for the BC tumorigenesis.	 Increased circRNF20 level predicted the poor clinical outcome in BC specimens. 	Yes	 Functionally, circRNF20 promoted the proliferation and Warburg effect (aerobic glycolysis) of BC cells.	32094325
hsa_circ_0007255	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-335-5p/SIX2 axis]	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0007255 and SIX2 were overexpressed, but miR-335-5p was diminished in BC tissues and cells.Circ_0007255 functioned as a novel oncogene in the progression of BC by regulating miR-335-5p/SIX2 axis, and might be a promising biomarker for BC treatment.		Yes	 Circ_0007255 absence inhibited oxygen consumption, colony formation, cell migration and invasion, and these effects were particularly abrogated via miR-335-5p upregulation in BC cells.	31962380
circVAPA	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	interaction[sponging miR-130a-5p]	qRT-PCR//Wound Healing Assay//MTT//Transwell Assay	 We discovered that circVAPA was dysregulated in breast cancer tissues and cells.CircVAPA may promote migration and invasion capacity of breast cancer via harboring miR-130a-5p.		Yes	Ectopic circVAPA regulated breast cancer migration, invasion and proliferation.	31920104
circNFATC3	CircRNA	Homo sapiens	Breast Neoplasms	cell lines 	Regulation(up regulation)	Migration Assay//CCK8//qRT-PCR//RNA-seq//Invasion Assay	Breast and ovarian cancer cells showed a greater abundance of circNFATC3 compared to normal breast cell lines, lung fibroblast cells, and LCL cells.		Yes	The knockdown of circNFATC3 induces a reduction in cell proliferation, invasion, migration, and oxidative phosphorylation. Gain-of-function of circNFATC3 in MDA-MB-231 and SK-OV-3 cells show a significant increase in cell proliferation, migration, and respiration. 	33816459
circSCRIB	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer specimens	Expression [highly expressed]	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//cell invasion assay//Colony Formation Assay	Among these three circRNAs, circSCRIB (hsa_circ_0001831) was the most enriched in the breast cancer panel.		Yes	To test this, we generated a hsa_circ_0001831 expression construct. We found that there was decreased SCRIB mRNA production but increased cancer cell proliferation, migration, and invasion. In comparison, an exonic sequence construct did not affect mRNA splicing but decreased protein translation, leading to increased E-cadherin expression and decreased expression of N-cadherin and vimentin. 	34365033
circMMP11	CircRNA	Homo sapiens	Breast Neoplasms	 LR breast cancer tissues and cells	Interaction(MiR-1307-3p/SMG1 Axis)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-MMP11 and ANLN were highly expressed, and miR-153-3p was decreased in LR breast cancer tissues and cells.		Yes	Furthermore, circ-MMP11 knockdown promoted lapatinib sensitivity by repressing cell viability, colony number, migration, invasion, and boosting apoptosis in LR breast cancer cells. Circ-MMP11 deficiency improved the drug sensitivity of breast cancer in vivo. 	34295807
circNINL	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(miR-921/ADAM9 axis)	RNA Pull-Down//Western Blot//Co-IP//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	We found that the expression of circNINL increased while the expression of miR-921 decreased in BC tissues and cell lines, and their anomalous expressions were associated with malignant features and poor prognostic of BC. 	We found that the expression of circNINL increased while the expression of miR-921 decreased in BC tissues and cell lines, and their anomalous expressions were associated with malignant features and poor prognostic of BC.	Yes	Then, we demonstrated that circNINL could interact with miR-921 and facilitate BC cells malignant process including proliferation acceleration, migration enhancement and apoptosis evasion via sponging miR-921 in vitro. 	33479730
circSEPT9	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells 	Interaction(microRNA-149-5p )	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC	Results showed that circSEPT9 and SLC1A5 expression were significantly upregulated, while miR-149-5p was downregulated in BC tissues and cells as compared with paracancerous normal breast tissues and human normal breast cells.		Yes	 Knockdown of circSEPT9 or SLC1A5 inhibited glutamine uptake and cell proliferation, but induced cell apoptosis in BC cells. SLC1A5 overexpression relieved circSEPT9 silencing-induced repression of BC cell malignancy. 	34738502
circRASSF2	CircRNA	Homo sapiens	Breast Neoplasms	The paired samples of 70 BC	Interaction(miR-1205/HOXA1 axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	According to our study, it is found that circRASSF2 sequences contain miR-1205 binding sites, and Homeobox gene A1 (HOXA1) is the target gene of miR-1205.	Additionally, it is found that circRASSF2 expression had a positive correlation with distant metastasis, lymph node metastasis, TNM stage, differentiation and tumor size, and that overall survival (OS) and progression-free survival (PFS) of circRASSF2 high expression BC patients were inferior to those with low circRASSF2 expression. 	Yes	 In vitro study, an overt decrease was detected in the proliferation, clone formation ability, migration and invasion of breast cancer cells in cells when circRASSF2 was knocked down.	34180753
circTPGS2	CircRNA	Homo sapiens	Breast Neoplasms	metastatic BC tissues and cell lines	Interaction(miR-7/TRAF6/NF-κB axis)	ChIP//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	High circ-TPGS2 was observed in metastatic BC tissues and cell lines in comparison to respective normal controls, which was linked to poor overall and recurrence-free survival. In terms of mechanism, circ-TPGS2 acted as a sponge of miR-7 and elevated TRAF6, leading to p65 phosphorylation and nuclear translocation, ultimately activating NF-κB signalling. 	 which was linked to poor overall and recurrence-free survival. 	Yes	Overexpression of circ-TPGS2 notably promoted cell migration, while silencing of circ-TPGS2 resulted in an opposite trend.	34036857
hsa_circ_0103552	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(MicroRNA-515-5p)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_0103552 expression was found to be remarkably up-modulated in breast cancer tissues and cells,  Mechanistically, circ_0103552 could sponge miR-515-5p and restrained its expression in breast cancer cells. 		Yes	 circ_0103552 overexpression facilitated the multiplication, migration, and invasion of breast cancer cells, while knocking down circ_0103552 induced the opposite effects.	34707022
hsa_circ_0000526	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer samples	interaction[Sponging miR-492]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Circ_0000526 expression in breast cancer samples was downregulated, which was correlated with unfavorable pathological indexes.Circ_0000526 served as a tumor suppressor, which could function as the sponge of miR-492, an oncogenic microRNA, in breast cancer, and enhance the expression of tumor suppressor SOCS2 indirectly.		Yes	 It significantly inhibited the proliferation and metastasis of breast cancer cells, and facilitated apoptosis. 	32391718
hsa_circ_0000515	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues	regulation[microRNA-296-5p/CXCL10 axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	 We collected 340 cancerous tissues surgically resected from BC patients and found hsa_circ_0000515 was upregulated in BC tissues and associated with poor prognosis of BC.RNA pull-down and dual-luciferase reporter gene assays showed that hsa_circ_0000515 binds miR-296-5p, preventing it from repressing CXCL10 expression.		Yes	Silencing of hsa_circ_0000515 impaired cell cycle progression, cell proliferation, and invasion, attenuated inflammatory response, and reduced the proangiogenetic potential of BC cells.	32446265
hsa_circ_0008039	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-140-3p/SKA2 axis]	Western Blot//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	We found that circ_0008039 and SKA2 were upregulated in BC tissues and cells, while miR-140-3p was downregulated. In conclusion, circ_0008039 downregulation suppressed BC cell proliferation, migration, invasion, and glycolysis partially through regulating the miR-140-3p/SKA2 axis, providing an important theoretical basis for treatment of BC.		Yes	 Knockdown of circ_0008039 suppressed BC cell proliferation, migration, invasion, and glycolysis. 	33244865
hsa_circ_103809	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	regulation[Sponging MicroRNA-532-3p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	Then, our data showed that circRNA_103809 was down-regulated in breast cancer tissues in contrast to adjacent non-tumor tissues, and the relative expression level of circRNA_103809 was closely associated with distant metastasis size, TNM stage, HER-2 status and overall survival time. Taken together, this study showed that circRNA_103809 could inhibit cell proliferation and metastasis in breast cancer by sponging miR-532-3p, and circRNA_103809 might be a prospective target of breast cancer therapy.	Then, our data showed that circRNA_103809 was down-regulated in breast cancer tissues in contrast to adjacent non-tumor tissues, and the relative expression level of circRNA_103809 was closely associated with distant metastasis size, TNM stage, HER-2 status and overall survival time.	Yes	In addition, our in vitro assays showed that the overexpression of circRNA_103809 could significantly inhibit epithelial-mesenchymal transition (EMT) pathway, then suppress breast cancer cell proliferation and metastasis ability. 	32499818
hsa_circ_0061825	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-593-3p/FGFR3 axis]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our data indicated that circ_0061825 was overexpressed in BC tissues and cells, and it was mainly localized in the cytoplasm of BC cells. Our current work provided evidence that circ_0061825, an up-regulated circRNA in BC, regulated BC malignant progression at least in part through targeting the miR-593-3p/FGFR3 axis, illuminating a novel therapeutic target for BC management.		Yes	Circ_0061825 knockdown hampered BC cell viability, colony formation, migration, invasion, cell cycle progression and enhanced cell apoptosis in vitro and weakened tumor growth in vivo.	33177875
hsa_circ_0072995	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	interaction[sponging miR-149-5p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Circ_0072995 and SHMT2 were up-regulated in breast cancer tissues and cell lines.This study demonstrated that circ_0072995 promoted cell malignant phenotypes and anaerobic glycolysis in breast cancer via up-regulating SHMT2 through sponging miR-149-5p, indicating a promising molecular target for breast cancer treatment.		Yes	Circ_0072995 and SHMT2 were up-regulated in breast cancer tissues and cell lines, and knockdown of circ_0072995 or SHMT2 suppressed cell malignant properties and anaerobic glycolysis; importantly, SHMT2 overexpression attenuated the anticancer action of circ_0072995 knockdown in breast cancer.Additionally, xenograft analysis showed circ_0072995 silencing suppressed tumor growth via regulating SHMT2 and miR-149-5p in vivo.	33173349
hsa_circ_0003645	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cell lines	regulation[miR-139-3p/HMGB1 Axis]	Flow Cytometry//qRT-PCR//Luciferase Report Assay	Circ_0003645 expression was conspicuously increased in both the breast cancer tissues and cell lines.Circ_0003645 functions as a ceRNA for miR-139-3p, which could upregulate HMGB1 and further promote cell proliferation in breast cancer.		Yes	Circ_0003645 knockdown inhibited cell proliferation and induced the apoptosis of breast cancer cells in vitro and in vivo. 	33116616
hsa_circ_0001785	CircRNA	Homo sapiens	Breast Neoplasms	BC cells	regulation[miR-942/SOCS3 signaling axis]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	"Results showed that the expressions of hsa_circ_0001785 were decreased in BC cells. In general, circular RNA hsa_circ_0001785 inhibits the proliferation, migration and invasion of BC cells by modulating the miR-942/SOCS3 signaling axis.
"		Yes	Hsa_circ_0001785 overexpression inhibited the proliferation, migration, invasion of BC cells and tumor growth in nude mice. 	33054543
hsa_circ_0000043	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	regulation[miR-136-Smad3 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	Our results show that the expression of circ_0000043 is up-regulated in BC tissues and cell lines. In conclusion, our study demonstrates that circ_0000043 promote the progression of BC via regulating the miR-136-Smad3 axis.		Yes	The proliferation, migration, invasiveness, and epithelial-mesenchymal transition of BC cells were significantly inhibited by knockdown of circ_0000043, and overexpression of circ_0000043 had the opposite effects.	33043682
circABCC4	CircRNA	Homo sapiens	Breast Neoplasms	tumor tissues	regulation[NF-κB and Wnt/β-catenin signal pathways]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The expression of circABCC4 was far great in tumor tissues than in normal tissues.CircABCC4 knockdown repressed breast cancer cells viability, migration, and invasion by up-regulating miR-154-5p via inhibiting NF-κB and Wnt/β-catenin signal pathways.		Yes	Knockdown of circABCC4 could subdue cell viability, migration, invasion, and enhance apoptosis in breast cancer cell lines.	33023375
hsa_circ_0000518	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-326/FGFR1 axis]	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_0000518 and FGFR1 were upregulated while miR-326 was downregulated in BC tissues and cells.Circ_0000518 facilitated BC development via regulation of the miR-326/FGFR1 axis, suggesting that circ_0000518 might be a promising target for BC treatment.		Yes	Circ_0000518 silencing impeded tumor growth in vivo and induced cell cycle arrest, apoptosis, cured proliferation, colony formation, migration, and invasion of BC cells in vitro. 	33000910
hsa_circ_002178	CircRNA	Homo sapiens	Breast Neoplasms	cancer tissues or BrCa cells	regulation[miR-1258/KDM7A Axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//H&E Staining//Colony Formation Assay//Transwell Assay	 In this investigation, the expression levels of circ_002178 in cancer tissues or BrCa cells were significantly upregulated compared with those in paracancer tissues or normal cells. Taken together, targeting the circ_002178/miR-1258/KDM7A axis may be a prospective strategy for the diagnosis and therapies of BrCa in the future.	High expression of circ_002178 was correlated with the low survival rate, clinical tumor size, lymph node metastasis, and tumor, nodes, and metastases grade. After	Yes	 Besides, the overexpression of circ_002178 also significantly promoted the growth, invasion, and migration of BrCa cells. 	32951449
circWWC3	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[Ras signaling pathway,]	Microarray	circWWC3 is highly expressed in breast cancer tissues and is associated with the poor prognosis of breast cancer patients. Our findings reveal that ZEB1-mediated upregulation of circWWC3 promotes breast cancer progression through activating Ras signaling pathway, which provides a potential therapeutic target and prognostic biomarker for breast cancer.	circWWC3 is highly expressed in breast cancer tissues and is associated with the poor prognosis of breast cancer patients. 	Yes	 Silencing of circWWC3 significantly suppresses the proliferation, migration, and invasion of breast cancer cells.	32916598
hsa_circ_0000291	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	regulation[miR-326/ETS1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We demonstrated that circ_0000291 was significantly upregulated in BC, and its high expression was positively correlated with T stage and local lymph node metastasis. In conclusion, circ_0000291 is the novel oncogenic circRNA and promotes BC progression via modulating the miR-326/ETS1 axis.	We demonstrated that circ_0000291 was significantly upregulated in BC, and its high expression was positively correlated with T stage and local lymph node metastasis. 	Yes	Functional assays validated that circ_0000291 promoted BC cell proliferation, migration and invasion. 	32869935
circZFR	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[miR-578/HIF1A axis]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 Our data indicated that circZFR was overexpressed in BC tissues and cells, and the increased circZFR level predicted poor prognosis of BC patients. Our findings first identified that the silencing of circZFR suppressed BC malignant progression in vitro via the regulation of the miR-578/HIF1A axis, providing evidence for the crucial involvement of circZFR in BC pathogenesis.	 Our data indicated that circZFR was overexpressed in BC tissues and cells, and the increased circZFR level predicted poor prognosis of BC patients.	Yes	CircZFR silencing or miR-578 overexpression repressed BC cell viability, colony formation, migration, invasion, and glycolysis and enhanced cell apoptosis in vitro. CircZFR silencing also hampered tumor growth in vivo. 	32831653
circHIPK3	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues	regulation[miR-193a/HMGB1/PI3K/AKT signaling]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay	Upregulation of CirCHIPK3 was identified in BC, which predicted a worse prognosis in BC patients.CirCHIPK3 regulated miR-193a/HMGB1/PI3K/AKT signaling to facilitate BC development and progression, providing a novel therapeutic target for BC.	Upregulation of CirCHIPK3 was identified in BC, which predicted a worse prognosis in BC patients.	Yes	 Furthermore, it was found that CirCHIPK3 facilitated cell proliferation, migration, and invasion in BC by regulating miR-193a/HMGB1/PI3K/AKT signaling. CirCHIPK3 acted as a sponge for miR-193a to facilitate HMGB1 expression. si-CirCHIPK3 also inhibited tumor growth of BC in nude mice. 	32767499
circIQCH	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	regulation[circIQCH-miR-145-DNMT3A axis]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	circIQCH was upregulated in breast cancer tissues, especially in the metastatic sites.  In summary, our study demonstrated the pivotal role of circIQCH-miR-145-DNMT3A axis in breast cancer growth and metastasis via the mechanism of competing endogenous RNAs.		Yes	Knockdown of circIQCH inhibited breast cancer cell proliferation and migration to lung.	32756009
hsa_circ_000554	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues	regulation[microRNA-182/ZFP36 axis]	qRT-PCR	 Low expression of circRNA_000554 and ZFP36, and high miR-182 expression were determined in the clinical BC tissues.Taken together, the present study confirms that circRNA_000554 functioned as an inhibitor of EMT in BC and suggests a molecular mechanism that circRNA_000554 bound to miR-182 to upregulate ZFP36 in this process.		Yes	After that, in order to evaluate the effects of circRNA_000554, miR-182, and ZFP36 on cellular process, we evaluated in vitro epithelial-mesenchymal transition (EMT) and in vivo tumor growth after delivering a series of overexpression plasmids, mimic, inhibitor, or shRNAs into BC cells. 	32729957
hsa_circRPPH1_015	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues	regulation[Impairing miRNA-326-Mediated ELK1 Inhibition]	RNA Pull-Down//Western Blot//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	hsa_circRPPH1_015 expression was upregulated in BC tissues.  hsa_circRPPH1_015 could bind to miRNA-326 that negatively regulates ELK1. 		Yes	Tumor growth of MCF-7 cells in vivo was reduced in nude mice lack of endogenous hsa_circRPPH1_015 expression. 	32670874
circMMP11	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer cell lines and tissues	regulation[miR-1204]	qRT-PCR//Luciferase Report Assay	The expression of one of the top upregulated circRNAs, circMMP11, was confirmed by qRT-PCR in both breast cancer cell lines and tissues.  The circMMP11/miR-1204/MMP11 axis regulates breast cancer progression via a competitive endogenous RNA (ceRNA) mechanism.		Yes	 The inhibition of circMMP11 suppressed cell proliferation and migration of BC. 	32655792
circEIF3M	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[circEIF3M/ miR-33a/ cyclin D1 axis]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	 It was found that circEIF3M was markedly upregulated in triple-negative breast cancer as compared to adjacent nontumor tissue, These findings showed that circEIF3M promotes triple-negative breast cancer progression via the circEIF3M/ miR-33a/ cyclin D1 axis.		Yes	It was found that circEIF3M was markedly upregulated in triple-negative breast cancer as compared to adjacent nontumor tissue, and that circEIF3M promoted triple-negative breast cancer cell proliferation, migration, and invasion.	32652519
hsa_circ_1073	CircRNA	Homo sapiens	Breast Neoplasms	BC cells (BCCs) and tissues	Expression[lower expressed]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	 Low circ-1073 expression was discovered in BCCs and BC tissues compared with normal mammary epithelial cells and peritumoural tissues, respectively.	 Circ-1073 downregulation was significantly associated with an unfavourable prognosis, including a shorter RFS, in BC patients. 	Yes	Circ-1073 overexpression significantly inhibited BCC proliferation and induced apoptosis by increasing Cleaved Caspase-3/9 levels.	32636640
circDDX17	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	interaction[ miR-605 ]	qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	In this study, low circDDX17 expression was observed in breast cancer tissues and cell lines.We identified the downregulation of circDDX17 in breast cancer, and circDDX17 acted as a tumour suppressor by inhibiting proliferation and promoting apoptosis through its function as a sponge of miR-605 in breast cancer, indicating that it serves as a potential biomarker and a therapeutic target for breast cancer.	Moreover, circDDX17 expression was inversely associated with the clinicopathological parameters of tumour grade and advanced TNM stage (p<0.05).	Yes	Functionally, overexpressed circDDX17 inhibited cell proliferation and colony formation and promoted cell apoptosis in breast cancer.	32633371
hsa_circ_0119412	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-1298-5p/ZBED3 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Invasion Assay	Our data revealed that hsa_circ_0119412 and ZBED3 expression was upregulated in GC, while miR-1298-5p expression was downregulated.Mechanistically, hsa_circ_0119412 sponges miR-1298-5p, which regulates ZBED3 expression. Silencing hsa_circ_0119412 inhibits the progression of GC, at least in part, by targeting the miR-1298-5p/ZBED3 axis.		Yes	Both the knockdown of hsa_circ_0119412/ZBED3 and miR-1298-5p overexpression inhibited GC cell growth and invasion, and enhanced cell apoptosis, while miR-1298-5p interference or ZBED3 overexpression showed the opposite trend.	35200111
hsa_circ_0000190	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-382-5p/ZNRF3)	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Circ_0000190 was down-regulated in GC tissues and cell lines. MiR-382-5p was a target of circ_0000190, and circ_0000190 suppressed GC progression partly via serving as miR-382-5p sponge. ZNRF3 was a target of miR-382-5p, and miR-382-5p accelerated the proliferation, motility and restrained the ferroptosis of GC cells partly via regulating ZNRF3. 	 Low expression of circ_0000190 predicted dismal prognosis in GC patients.	Yes	Circ_0000190 overexpression inhibited the proliferation, migration and invasion and promoted Erastin- or ras selective lethal 3 (RSL3)-mediated ferroptosis in GC cells. Circ_0000190 overexpression restrained xenograft tumor growth in vivo. 	35037032
circDIDO1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(MiR-1307-3p/SOCS2 Axis)	Migration Assay//RIP//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	CircDIDO1 inhibited GC progression by regulating the expression of the signal transducer inhibitor SOSC2 through sponging miR-1307-3p.  Overexpression of circDIDO1 or SOSC2 antagonized the oncogenic role of miR-1307-3p. 		Yes	Compared with PBS and RGD-Exo-vector treatment, RGD-Exo-circDIDO1 treatment significantly inhibited the proliferation, migration and invasion of GC cells while promoted cell apoptosis. 	35864511
hsa_circ_0110389	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-127-5p/miR-136-5p-SORT1 pathway)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, hsa_circ_0110389 was identified as a novel upregulated circRNA in malignant-transformed GC cells through RNA-seq, and subsequent quantitative real-time PCR verified that hsa_circ_0110389 was significantly increased in GC tissues and cells. In addition, hsa_circ_0110389 was identified to sponge both miR-127-5p and miR-136-5p and SORT1 was validated as a direct target of miR-127-5p and miR-136-5p through multiple mechanism assays; moreover, hsa_circ_0110389 sponged miR-127-5p/miR-136-5p to upregulate SORT1 expression and hsa_circ_0110389 promoted GC progression through the miR-127-5p/miR-136-5p-SORT1 pathway.		Yes	 Knockdown and overexpression assays demonstrated that hsa_circ_0110389 regulates proliferation, migration, and invasion of GC cells in vitro.  Finally, hsa_circ_0110389 knockdown suppressed GC growth in vivo.	34162830
circhsa2	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(hsa-miR-944/PPM1E axis)	Western Blot//Bioinformatics Analysis//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In this study, we demonstrated that a specific circRNA, circHAS2, was upregulated in GC tissues and cells and was positively correlated with tumor metastasis.In addition, hsa-miR-944 interacted with protein phosphatase, Mg2+/Mn2+-dependent 1E (PPM1E), and was found to be a target gene of circHAS2. 		Yes	In vitro experiments demonstrated that circHAS2 knockdown or the addition of hsa-miR-944 mimics inhibited the proliferation, migration, and invasion ability of GC cells and affected the epithelial-mesenchymal transition. The upregulation of PPM1E reversed the effects of circHAS2 knockout on GC cells. 	34556632
circRNF111	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-876-3p/KLF12 )	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-RNF111 was higher expressed in GC tissues and cells than normal tissues and cells. Circ-RNF111 positively regulated KLF12 expression via absorbing miR-876-3p. MiR-876-3p downregulation reversed the impacts of circ-RNF111 silencing on GC cell malignant phenotypes. MiR-876-3p overexpression repressed GC cell growth, metastasis and glycolysis, inhibited apoptosis and arrested cell cycle, while KLF12 elevation weakened the effects. 		Yes	Silencing of circ-RNF111 restrained cell viability, colony formation, migration, invasion, cell cycle process and glycolysis and induced apoptosis in GC cells in vitro. Besides, circ-RNF111 knockdown inhibited tumor growth in vivo.	34461926
circBFAR	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	Interaction(miR-513a-3p/hexokinase 2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	The results showed that circBFAR exhibited higher expression in GC tissues and cell lines. circBFAR was proven to promote GC proliferation by targeting the miR-513a-3p/hexokinase 2 (HK2) axis. 		Yes	Inhibition of circBFAR also led to a significant decrease in the glycolysis levels. 	33979737
hsa_circ_0074027	CircRNA	Homo sapiens	Stomach Neoplasms	 GC cell lines	Interaction(EIF4A3 )	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	The results revealed that circ_0074027 was highly expressed in GC cell lines in the form of a closed loop.  Furthermore, EIF4A3 was predicted to be targeted by circ_0074027 and a positive association was identified between them. The overexpression of EIF4A3 reversed the effects of circ_0074027 on the proliferation and motility of GC cells. 		Yes	In addition, circ_0074027-knockdown inhibited cellular proliferation and motility. 	34457059
circURI1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(hnRNPM)	In Vivo Experiment//RNA Pull-Down//Northern Blot//Western Blot//Wound Healing Assay//RIP//Transwell Assay	CircURI1 exhibits the significantly higher expression in GC compared with paraGC and inhibitory effects on cell migration and invasion in vitro and GC metastasis in vivo. Mechanistically, circURI1 directly interacts with heterogeneous nuclear ribonucleoprotein M (hnRNPM) to modulate alternative splicing of genes, involved in the process of cell migration, thus suppressing GC metastasis. 		Yes	CircURI1 exhibits the significantly higher expression in GC compared with paraGC and inhibitory effects on cell migration and invasion in vitro and GC metastasis in vivo. 	34385309
hsa_circ_0005654	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell	Interaction( miR-363 /sp1)	In Vivo Experiment//ChIP//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//H&E Staining//Transwell Assay	 We observed that circ0005654 was enhanced in GC tissues and cells. It was also established that circ0005654 served as a miR-363 sponge and enhanced sp1 expression. Furthermore, sp1 promoted GC carcinogenesis by regulating myc transcription to potentiate the Wnt/β-catenin pathway.	Overexpression of circ0005654 was correlated with a poor long-term prognosis in patients with GC. 	Yes	. Functionally, silencing of circ0005654 remarkably suppressed GC cell proliferation, migration and invasiveness in vitro and tumorigenesis and metastases in vivo.	34499009
circCOL6A3_030	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	Expression(lower expressed)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//H&E Staining//IHC//Transwell Assay	 circCOL6A3_030 was down-regulated in GC tissues and cell lines, while circCOL6A3_030 was up-regulated in GC with distant lymph node metastasis.To sum up, our study showed that circCOL6A3_030 promoted GC cell migration by encoding a small peptide called circCOL6A3_030_198aa. 		Yes	 The migration of circCOL6A3_030 silenced GC cells was significantly inhibited in both SGC-7901 and BGC-823 cell lines. Importantly, in vivo assay, silencing circCOL6A3_030 could reduce liver metastases from gastric cancer cells. 	34595992
hsa_circ_0023409	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-542-3p/IRS4/PI3K/AKT Pathway)	In Vivo Experiment//ISH//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//FISH//Luciferase Report Assay//H&E Staining//IHC//EdU Staining//Transwell Assay	The results showed that hsa_circ_0023409 was mainly located in cytoplasm and highly expressed in GC tissues and cells.  Mechanism studies demonstrated that hsa_circ_0023409 upregulated IRS4 via sponging miR-542-3p in GC cells. Furthermore, IRS4 overexpression activated the PI3K/AKT pathway and reversed the inhibitory effect of hsa_circ_0023409 knockdown on the PI3K/AKT pathway. 	 Moreover, hsa_circ_0023409 showed positive correlation with tumor size, histological grade, and tumor-node-metastasis staging of GC patients.	Yes	Functional studies showed that hsa_circ_0023409 promoted cell viability, proliferation, migration, and invasion and suppressed apoptosis in GC.	33439739
circAFF2	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cell lines and tissues	Interaction(miR-6984-5p/ ANTXR 1.)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	 The result showed that circAFF2 expression was significantly increased in gastric cancer cell lines and tissues. In vivo studies showed that knockdown of circAFF2 delayed tumor growth. Furthermore, we revealed that circAFF2 functioned as a sponge to absorb miR-6984-5p and elevated the expression of ANTXR 1.		Yes	The knockdown of circAFF2 dramatically suppressed the cell migration, invasion and proliferation of gastric cancer cells.	33722777
hsa_circ_100290	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells and 102 GC tissues	Interaction(miR-29b-3p/ITGA11 axis and is regulated by EIF4A3)	Western Blot//Bioinformatics Analysis//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 The expression of circRNA_100290 was significantly upregulated in GC cells and 102 GC tissues, and high circRNA_100290 expression in GC was closely related to Borrmann's type, lymph node metastasis and tumour-node-metastasis stage. Mechanistically, a dual-luciferase reporter assay confirmed the direct interaction between circRNA_100290 and miR-29b-3p, which targets ITGA11, an oncogene that is closely related to epithelial-mesenchymal transition (EMT). In addition, EIF4A3, an RNA-binding protein (RBP), could inhibit the formation of circRNA_100290 by binding to the flanking sites of circRNA_100290. 	 The expression of circRNA_100290 was significantly upregulated in GC cells and 102 GC tissues, and high circRNA_100290 expression in GC was closely related to Borrmann's type, lymph node metastasis and tumour-node-metastasis stage.	Yes	In vitro, knockdown of circRNA_100290 in AGS and HGC-27 cells significantly inhibited cell proliferation, migration, and invasion. 	34182990
circHN1	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-302b-3p/ROCK2 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 We observed that circ_HN1 and ROCK2 were upregulated while miR-302b-3p was downregulated in GC tissues and cells. Circ_HN1 sponged miR-302b-3p to regulate ROCK2 expression. MiR-302b-3p inhibitor reversed circ_HN1 silencing-mediated influence on the malignant behaviors of GC cells. Furthermore, ROCK2 overexpression restored miR-302b-3p mimic-mediated impacts on cell malignant behaviors in GC cells.		Yes	Circ_HN1 silencing slowed tumor growth in vivo and impeded cell proliferation migration, invasion, and facilitated cell apoptosis in GC cells in vitro.	32949310
hsa_circ_0002570	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(MiR-587/VCAN )	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Wound Healing Assay//Tunel//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 Circ-0002570 expression was distinctly increased in GC tissues compared to adjacent normal specimens, and GC patients with higher circ-0002570 expressions displayed a short survival.Mechanistically, miR-587 was sponged by circ-0002570. VCAN expression in NSCLC was directly inhibited by miR-587. Overexpression of circ-0002570 prevented VCAN from miR-587-mediated degradation and thus facilitated GC progression.	 Circ-0002570 expression was distinctly increased in GC tissues compared to adjacent normal specimens, and GC patients with higher circ-0002570 expressions displayed a short survival.	Yes	Functionally, knockdown of circ-0002570 resulted in the inhibition of cell proliferation, migration, and invasion, and suppressed tumor growth in vivo. 	34692507
circPTPDC1	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells, tissues, and serum	Interaction( Mir-139-3p / ELK1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Invasion Assay//Migration Assay//CCK8//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Microarray//Colony Formation Assay//Bioinformatics Analysis	 Then we demonstrated that circ-PTPDC1 was up-regulated in GC cells, tissues, and serum. We further revealed that circ-PTPDC1 promotes the proliferation, migration, and invasion of GC cell lines via sponging miR-139-3p by regulating ELK1. 	Its overexpression was positively correlated with age, invasion depth, advanced clinical stages, and worse survival in patients with GC.	Yes	We further revealed that circ-PTPDC1 promotes the proliferation, migration, and invasion of GC cell lines via sponging miR-139-3p by regulating ELK1.  Importantly, we identified that circ-PTPDC1 promotes tumor upgrowth and metabasis in vivo. 	34803498
hsa_circ_0000423	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-582-3p/DIXDC1 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	In the present study, we demonstrated that circ_0000423 was highly expressed in GC. Moreover, miR-582-3p was confirmed as a direct target of circ_0000423, and an upstream regulator of DIXDC1. MiR-582-3p inhibition or DIXDC1 overexpression could reverse the above-mentioned effects of knocking down circ_0000423 on GC cells. 		Yes	Circ_0000423 knockdown suppressed GC cell viability, migration and invasion. 	34898351
hsa_circ_0021087	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-184/FOSB )	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	 Circ_0021087 and FOSB were lowly expressed in GC, whereas miR-184 had an opposite result.  Circ_0021087 could elevate FOSB expression by adsorbing miR-184. MiR-184 mimic reversed the inhibitory influence of circ_0021087 overexpression on GC cell malignancy. Also, FOSB knockdown offset the suppressive impact of miR-184 silencing on GC cell malignancy.		Yes	Circ_0021087 overexpression repressed GC cell proliferation and epithelial-mesenchymal transition (EMT) in xenograft models in vivo and induced GC cell apoptosis, repressed GC cell proliferation, EMT, migration and invasion in vitro. 	34076278
circHIPK3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-637/AKT1 Pathway)	CCK8//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	Quantitative real-time PCR (qRT-PCR) was employed to found that circHIPK3 markedly increased in GC tissues and cell lines. Then the bioinformatics tool predicted the downstream target of circHIPK3, and it was proved by the dual-luciferase report experiment. According to the results of bioinformatics analysis and experimental data, it was clarified that circHIPK3 acted as a sponge of miR-637, releasing its direct target AKT1. 		Yes	And low expression of circHIPK3 suppressed the GC cells growing and metabolizing.	33680975
circACC1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-29c-3p/FOXP1 network )	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	This study demonstrated that circACC1 is upregulated in GC tissues, and its upregulation predicts poorer OS in GC patients.  A mechanistic study revealed that the pro-oncogenic effect of circACC1 was mainly caused by binding to miR-29c-3p, thus regulating expression of its downstream target FOXP1. 	This study demonstrated that circACC1 is upregulated in GC tissues, and its upregulation predicts poorer OS in GC patients. 	Yes	Upregulation of circACC1 promoted GC cell proliferation, as indicated by CCK-8 and colony formation assays. 	33887587
hsa_circ_0072309	CircRNA	Homo sapiens	Stomach Neoplasms	GC cell lines 	Regulation(PI3K/AKT/PPARγ/PTEN signaling pathway)	Western Blot//Migration Assay//qRT-PCR//Cell Viability Assay//Colony Formation Assay//Invasion Assay	 In the present study, hsa_circ_0072309 was downregulated in GC cell lines and its overexpression inhibited the proliferation, migration and invasion of GC cells. In addition, hsa_circ_0072309 overexpression induced activation of the peroxisome proliferator‑activated receptor γ (PPARγ)/PTEN pathway and inhibition of PI3K/AKT signaling. The present findings suggested that hsa_circ_0072309 inhibited proliferation, invasion and migration of gastric cancer cells via the inhibition of PI3K/AKT signaling by activating the PPARγ/PTEN signaling pathway.		Yes	 In the present study, hsa_circ_0072309 was downregulated in GC cell lines and its overexpression inhibited the proliferation, migration and invasion of GC cells.	33760104
hsa_circ_0035445	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues, plasma of gastric cancer patients, and gastric cancer cells	Expression(lower expressed)	CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	Hsa_circ_0035445 was lowly expressed in gastric cancer tissues, plasma of gastric cancer patients, and gastric cancer cells. 	The expression level of hsa_circ_0035445 in gastric cancer tissues was relationship with tumor size and distant metastasis.	Yes	The AUC of hsa_circ_0035445 in tissues and plasma was 0.68 and 0.86, respectively. Upregulation of hsa_circ_0035445 suppressed the proliferation and migration, promoted apoptosis, and blocked cells at G0/G1 phase.Downregulation of hsa_circ_0035445 promoted the proliferation and migration, suppressed apoptosis, and blocked cells at S phase. 	33830559
circFAM73A	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues	Interaction(miR-490-3p/HMGA2 )	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining//ChIP	 Elevated circFAM73A expression was confirmed in GC tissues, and higher circFAM73A predicted poor prognosis in GC patients. Mechanistically, circFAM73A promoted GC malignancy by regulating miR-490-3p/HMGA2 in a positive feedback loop and recruiting HNRNPK to facilitate β-catenin stabilization. Moreover, HMGA2 further enhanced E2F1 and HNRNPL activity, which in turn promoted circFAM73A expression.		Yes	 The upregulation of circFAM73A enhanced CSC-like properties in GC, thus facilitating cell proliferation, migration, and cisplatin resistance. 	33731207
circNFATC3	CircRNA	Homo sapiens	Stomach Neoplasms	 GC cells	Interaction(miR-23b-3p axis )	In Vivo Experiment//IHC//Western Blot//FISH//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	As a consequence, upregulation of RAI14 and circNFATC3 or downregulation of miR-23b-3p was associated with poor prognosis in patients with GC. circNFATC3 had a co-localization with miR-23b-3p in the cytoplasm in GC tissue cells and could act as a sponge of miR-23b-3p in GC cell line. 		Yes	Silencing of circNFATC3 inhibited cell growth and in vivo tumorigenesis by upregulating miR-23b-3p and downregulating RAI14. 	33840258
hsa_circ_0043691	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-1294/PBX3 )	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The levels of hsa_circ_0043691 and PBX3 were upregulated, whereas miR-1294 expression was diminished in GC tissues and cells. Mechanistically, hsa_circ_0043691 was directly bound to miR-1294 to modulate PBX3 expression. Besides, silencing of hsa_circ_0043691 impeded tumor growth in vivo.		Yes	 Hsa_circ_0043691 deficiency significantly inhibited GC cell progression and glutaminolysis metabolism. 	36371782
hsa_circ_0001017	CircRNA	Homo sapiens	Stomach Neoplasms	GC cell lines and GC tissues	Interaction(miR-197/RHOB signaling pathway)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Decreased hsa_circ_0001017 was discovered in GC, and upregulation of hsa_circ_0001017 notably repressed proliferation, migration, and invasion of GC cell lines.  We further certificated that hsa_circ_0001017 served as miR-197 sponge and suppressed the expression of miR-197. Moreover, hsa_circ_0001017 upregulation meaningfully accelerated RHOB expression in both gene and protein levels, and RHOB was a downstream target of miR-197.		Yes	Decreased hsa_circ_0001017 was discovered in GC, and upregulation of hsa_circ_0001017 notably repressed proliferation, migration, and invasion of GC cell lines. 	32740683
hsa_circ_100395	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	Interaction(miR-142-3p)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	circRNA_100395 expression was found to be increased in GC tissues and cell lines. However, miR-142-3p expression was significantly reduced. cirRNA_100395-overexpression had antitumor effects via regulating the miR-142-3p signaling pathway.	Besides, low expression levels of circRNA_100395 were associated with poor tumor differentiation, advanced Tumor-Node-Metastasis stage, lymph node metastasis and shorter overall survival time. 	Yes	Moreover, overexpression of circRNA_100395 suppressed cell proliferation, increased the apoptosis rate and suppressed cell invasion and migration by inhibiting the PI3K/AKT signaling pathway. 	33841580
hsa_circ_0004104	CircRNA	Homo sapiens	Stomach Neoplasms	GEO ( three paired GC tissues and normal samples in GSE141977)	Interaction(miR-539-3p/RNF2 Axis)	In Vivo Experiment//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Circ_0004104 was upregulated in GC, and its knockdown repressed the proliferation, metastasis, and glutaminolysis of GC cells in vitro and reduced GC tumor growth in vivo. Furthermore, we discovered that circ_0004104 could sponge miR-539-3p and miR-539-3p could target RNF2. 		Yes	 Circ_0004104 was upregulated in GC, and its knockdown repressed the proliferation, metastasis, and glutaminolysis of GC cells in vitro and reduced GC tumor growth in vivo. 	33449226
circCOL1A1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells and tissues	Interaction(miR-145)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Invasion Assay	The results showed that circCOL1A1 was highly expressed in both gastric cancer cells and tissues. circCOL1A1 regulated the expression of miR-145 by acting as a microRNA sponge, and the influence of circCOL1A1 could be abrogated by miR-145 mimics. 		Yes	Silence of circCOL1A1 inhibited the proliferation, migration, and invasion of gastric cancer cells. 	34631898
circDONSON	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-149-5p/LDHA Axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Our results suggested that circ-DONSON was highly expressed in GC tissues and cells. In terms of mechanism, circ-DONSON could sponge miR-149-5p, which could target LDHA in GC. 		Yes	Loss-functional assay results confirmed that silenced circ-DONSON could inhibit the proliferation, metastasis and angiogenesis, while enhance the apoptosis and radiosensitivity of GC cells. 	34409524
circPGPEP1	CircRNA	Homo sapiens	Stomach Neoplasms	51 paired GC tissues and adjacent normal tissues	Interaction(miR-1297 )	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_PGPEP1 was a highly expressed circRNA in GC.MiR-1297 could be sponged by circ_PGPEP1, and its expression was downregulated in GC. 		Yes	 Loss-of-function experiment indicated that circ_PGPEP1 silencing could induce cell cycle arrest and apoptosis, while inhibit proliferation, migration, and invasion in GC cells. 	33386518
hsa_circ_0044366	CircRNA	Homo sapiens	Stomach Neoplasms	The whole blood samples of GC 	Interaction(miR-29a)	CCK8//qRT-PCR//In Vivo Experiment//Migration Assay	We detected that exosomal circ29 was confirmed to be highly expressed in GC and can significantly impair the proliferation, migration, tube formation of HUVEC by exosomal communication. Interestingly, this effect could be blocked by the effect of miR-29a.		Yes	We detected that exosomal circ29 was confirmed to be highly expressed in GC and can significantly impair the proliferation, migration, tube formation of HUVEC by exosomal communication. 	33965787
hsa_circ_0000117	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(microRNA-337-3p/signal transducer and activator of transcription 3 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	In the present study, we observed increased hsa_circ_0000117 and signal transducer and activator of transcription 3 (STAT3) expression, while microRNA-337-3p (miR-337-3p) was decreased in GC cells. Hsa_circ_0000117 was also identified as a miR-337-3p sponge. 		Yes	Depleted hsa_circ_0000117 decreased GC proliferation and invasion. 	33896365
circDIDO1	CircRNA	Homo sapiens	Stomach Neoplasms	102 paired GC and adjacent non-cancerous tissues 	Interaction(PRDX2)	Co-IP//RIP//RNA-seq//In Vivo Experiment	circDIDO1 was down-regulated in GC tissues and its low levels were associated with larger tumor size, distal metastasis, and poor prognosis.Mechanistically, circDIDO1 encoded a novel 529aa protein that directly interacted with poly ADP-ribose polymerase 1 (PARP1) and inhibited its activity. CircDIDO1 also specifically bound to peroxiredoxin 2 (PRDX2) and promoted RBX1-mediated ubiquitination and degradation of PRDX2, which led to the inactivation of its downstream signaling pathways.	circDIDO1 was down-regulated in GC tissues and its low levels were associated with larger tumor size, distal metastasis, and poor prognosis.	Yes	CircDIDO1 overexpression inhibited while knockdown promoted GC cell proliferation, migration and invasion. CircDIDO1 overexpression suppressed GC growth and metastasis in mouse tumor models.	34384442
circDLG1	CircRNA	Homo sapiens	Stomach Neoplasms	distant metastatic lesions and gastric cancer tissues resistant to anti-PD-1 therapy 	Interaction(miR-141-3p)	In Vivo Experiment//Western Blot//ISH//Colony Formation Assay//Flow Cytometry//qRT-PCR//FISH//CCK8//Migration Assay//RIP//Luciferase Report Assay//Microarray//RNA-seq//IHC//Invasion Assay	circDLG1 was significantly upregulated in distant metastatic lesions and gastric cancer tissues resistant to anti-PD-1 therapy and was associated with an aggressive tumor phenotype and adverse prognosis in gastric cancer patients treated with anti-PD-1 therapy. Mechanistically, circDLG1 interacted with miR-141-3p and acted as a miRNA sponge to increase the expression of CXCL12, which promoted gastric cancer progression and resistance to anti-PD-1-based therapy.	circDLG1 was significantly upregulated in distant metastatic lesions and gastric cancer tissues resistant to anti-PD-1 therapy and was associated with an aggressive tumor phenotype and adverse prognosis in gastric cancer patients treated with anti-PD-1 therapy. 	Yes	Ectopic circDLG1 expression promoted the proliferation, migration, invasion, and immune evasion of gastric cancer cells. 	34911533
circHN1	CircRNA	Homo sapiens	Stomach Neoplasms	GEO (gastric cancer)	Interaction(miR-628-5p/Ecto-5'-nucleotidase competing endogenous RNA network)	In Vivo Experiment//RNA Pull-Down//Western Blot//Invasion Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	 Our data showed that circ_HN1 expression was enhanced in human gastric cancer. NT5E was a downstream effector of circ_HN1 function. NT5E was targeted and inhibited by miR-628-5p through the perfect complementary site in NT5E 3'UTR, and circ_HN1 affected NT5E expression through miR-628-5p competition. 		Yes	Depletion of circ_HN1 impeded cell proliferation, spheroid formation, invasion, and migration and promoted apoptosis in vitro, as well as diminished tumor growth in vivo. 	34637682
circMAPK1	CircRNA	Homo sapiens	Stomach Neoplasms	80 paired human GC and adjacent non-tumor tissues	Interaction(MAPK1-109aa)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//IF//Luciferase Report Assay//PCR//Colony Formation Assay//EdU Staining//Transwell Assay	In this study, we identified that circMAPK1 (hsa_circ_0004872) was downregulated in gastric cancer tissues compared with adjacent normal tissues. Our study revealed that circMAPK1 inhibits the malignant biological behavior of gastric cancer cells through its encoded protein MAPK1-109aa.	Importantly, lower circMAPK1 expression predicted poor survival in GC patients. 	Yes	CircMAPK1 inhibited the proliferation and invasion of gastric cancer cells in vitro and in vivo. 	33836754
hsa_circ_002059	CircRNA	Homo sapiens	Stomach Neoplasms	Human GC cell lines	Interaction(miR-182/MTSS1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	MTSS1 was found to be a direct target of miR-182 and circ_002059 upregulated MTSS1 expression by competitively sponging miR-182. 		Yes	 Overexpression of circ_002059 significantly inhibited, whereas knockdown of circ_002059 notably facilitated, cell proliferation and migration in GC cells. Circ_002059 inhibited GC cell xenograft tumor growth by regulating miR-182 and MTSS1 expression.	33686422
circLMO7	CircRNA	Homo sapiens	Stomach Neoplasms	Clinical tissue specimens	Interaction(miR-30a-3p/WNT2/β-Catenin pathway)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Wound Healing Assay//qRT-PCR//FISH//IF//RIP//Luciferase Report Assay//H&E Staining//Colony Formation Assay//EdU Staining//Transwell Assay	CircLMO7 acted as a miR-30a-3p sponge affecting the WNT2/β-Catenin pathway to promote the proliferation, migration and invasion of GC cells. 		Yes	CircLMO7 acted as a miR-30a-3p sponge affecting the WNT2/β-Catenin pathway to promote the proliferation, migration and invasion of GC cells. Moreover, animal results also showed that circLMO7 could promote GC growth and metastasis in vivo. 	33397440
circATP2B1	CircRNA	Homo sapiens	Stomach Neoplasms	Normal gastric tissues (GT), highly differentiated gastric adenocarcinoma cancer specimens (HDAC) and poorly differentiated gastric adenocarcinoma cancer specimens (PDAC)	Interaction(miR-326)	In Vivo Experiment//Western Blot//ISH//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay	Our data showed that circRNA circATP2B1 (also called hsa_circ_000826) was overexpressed in gastric cancer tissues instead of linear ATP2B1 mRNA, and it promoted aerobic glycolysis in gastric cancer cells. Bioinformatic Gene Ontology analysis showed that the potential downstream targets of circATP2B1 include the microRNA miR-326 gene cluster (miR-326-3p/miR-330-5p), which is functionally focused on cell growth and metabolic processes. 		Yes	Taken together, circATP2B1 captured miR-326-3p/miR-330-5p and decreased the suppression of PKM2 by miR-326-3p/miR-330-5p, thus aiding the aerobic glycolysis and proliferation of gastric cancer cells. 	33996547
circCORO1C	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-138-5p/KLF12 Axis)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_CORO1C and KLF12 were upregulated, while miR-138-5p was downregulated in GC tissues and cells. Circ_CORO1C targeted miR-138-5p, the inhibition of which could attenuate silenced circ_CORO1C-induced inhibitory effects on GC progression. MiR-138-5p repressed the aggressive malignant behaviors of GC cells by directly targeting KLF12.		Yes	Circ_CORO1C knockdown suppressed colony formation ability, viability, migration, invasion and EMT in GC cells, while promoted cell apoptosis in vitro.  Circ_CORO1C deficiency inhibited GC tumor growth in vivo.	34007212
circDNA2	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-149-5p/CCDC6 axis)	RNA Pull-Down//Western Blot//ISH//CCK8//qRT-PCR//Luciferase Report Assay//RNA-seq//Colony Formation Assay//EdU Staining	By performing quantitative real-time PCR and fluorescence in situ hybridization (FISH) assays with a human tissue microarray, circDNA2 was found to be highly expressed in GC tissues and associated with lymphatic invasion of GC patients. Mechanistically, circDNA2 acted as a microRNA (miR)-149-5p sponge, which was confirmed to target CCDC6 by RNA pulldown and dual-luciferase reporter assays and rescue experiments. Both low miR-149-5p expression and high CCDC6 expression were related to unfavorable prognosis in GC patients. 		Yes	Knockdown of circDNA2 expression suppressed the proliferation of GC cells by reducing CCDC6 expression. 	34552818
circNEK9	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-409-3p/MAP7 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	CircNEK9 was up-regulated in GC tissues and cell lines. CircNEK9 accelerated the proliferation, migration, and invasion of GC cells through targeting miR-409-3p/MAP7 axis. Plasma exosomal circNEK9 promoted the migration and invasion of recipient GC cells.		Yes	CircNEK9 interference suppressed the proliferation and motility of GC cells. CircNEK9 silencing enhanced microRNA-409-3p (miR-409-3p) level through direct interaction. CircNEK9 silencing-mediated influences on the proliferation and metastasis of GC cells were partly overturned by the interference of miR-409-3p. 	33449227
hsa_circ_0006470	CircRNA	Homo sapiens	Stomach Neoplasms	 GC cells	Interaction(miR-27b-3p)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay	The results showed that hsa_circ_0006470 expression was significantly elevated in GC cells, which was mainly distributed in cytoplasmic components and could directly bind with miR-27b-3p in GC cells. 		Yes	Silencing of hsa_circ_0006470 repressed cell proliferation, migration, and invasion, which may be through regulating miR-27b-3p/Receptor tyrosine kinase-like orphan receptor 1 (ROR1). Silencing of hsa_circ_0006470 also elevated LC3II and Beclin-1 and suppressed p62 protein abundances, which subsequently induced autophagy in AGS cells. 	34641696
hsa_circ_0043691	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissue and cells	Interaction(miR-873-3p-GART axis)	Western Blot//Bioinformatics Analysis//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	CircRNA_0043691 was upregulated in GC tissue. CircRNA_0043691 has potential putative binding sites with miR-873-3p. Moreover, CircRNA_0043691 positively regulated GART expression by sponging miR-873-3p.		Yes	 Knockdown of circRNA_0043691 decreased cell viability, migration, and invasion in GC cells.	34370061
circALPL	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cell	Interaction(miR-127-MTDH pathway)	In Vivo Experiment//Western Blot//CCK8//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	circALPL downregulation suppresses the invasion and proliferation ability of gastric cancer cells.  The results showed that circALPL promotes gastric cancer progression by sponging miR-127, thus upregulating MTDH. 		Yes	circALPL downregulation suppresses the invasion and proliferation ability of gastric cancer cells. 	34234862
circPTPN22	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues, cells, and plasma	Expression(highly expressed)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//circRNA-seq//Colony Formation Assay//Transwell Assay	 CircPTPN22 is up-regulated and positively correlated with metastasis in GC tissues, cells, and plasma. 	RT-qPCR results showed that circPTPN22 had good diagnostic efficacy and could be used to predict the prognosis of GC patients. 	Yes	 In vitro and vivo experiments showed that the downregulation of circPTPN22 could inhibit cell proliferation, migration, and invasion through the epithelial-mesenchymal transformation (EMT) pathway.	33430866
hsa_circ_0049447	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-324-5p)	In Vivo Experiment//IHC//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	We demonstrated that circ_0049447 was downregulated in GC (P < 0.001). Upregulation of miR-324-5p in GC specimens and direct binding between miR-324-5p with circ_0049447 proven by luciferase reporter assay indicated that circ_0049447 may inhibit GC by sponging certain miRNA.		Yes	 CCK-8 and colony formation assay showed that overexpression of circ_0049447 could inhibit the proliferation (P < 0.05). Transwell migration and invasion assay showed upregulated circ_0049447 could impede migration in GC cells (P < 0.05). In addition, overexpression of circ_0049447 could impede GC cell EMT. 	33883408
hsa_circ_0000064	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	Interaction(miR-621/SYF2 axis)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//BrdU//IHC//Transwell Assay	Cric_0000064 expression was elevated in GC tissues and cell lines. Circ_0000064 can participate in the GC progression via modulating miR-621/SYF2 axis. 		Yes	Knocking down cric_0000064 could inhibit the viability, migration, and invasion of GC cells. 	34245111
hsa_circ_0002360	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells 	Interaction( miR-629-3p/PDLIM4 )	Western Blot//qRT-PCR//ELISA//Colony Formation Assay//Invasion Assay//Transwell Assay	Circ0002360 was found to be upregulated in GC cells using QRT-PCR.Furthermore, miR-629-3p, a target miRNA of circ0002360, was the most suppressed miRNA following circ0002360 overexpression.  RNA immunoprecipitation (RIP), dual-luciferase reporter analyses, clone formation, transwell, DCFH-DA, and ELISA assays demonstrated that circ0002360-targeted miR-629-3p promotes cell proliferation and migration while inhibiting oxidative stress.  randomForest analysis indicated that PDLIM4 was the target gene of miR-629-3p, whose level was increased by circ0002360 but reversed by miR-629-3p mimics. 		Yes	 RNA immunoprecipitation (RIP), dual-luciferase reporter analyses, clone formation, transwell, DCFH-DA, and ELISA assays demonstrated that circ0002360-targeted miR-629-3p promotes cell proliferation and migration while inhibiting oxidative stress. 	35982735
circPRRX1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells	Interaction(circPRRX1/miR-596/ NKAP)	Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	Our data showed that circPRRX1 expression was elevated in human gastric cancer, and circPRRX1 could be transferred by exosomes from gastric cancer cells. Mechanistically, circPRRX1 directly regulated miR-596 expression, and exosomal circPRRX1 affected cell biological functions at least in part through miR-596. NKAP was identified as a direct target and functionally downstream effector of miR-596. 		Yes	Exosomal circPRRX1 affected cell proliferation, motility, invasion, and radiation sensitivity in vitro and tumor growth in vivo . 	36206097
hsa_circ_0006089	CircRNA	Homo sapiens	Stomach Neoplasms	GC samples and cell lines	Interaction(miR-143-3p/IGF1R axis)	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//BrdU//Bioinformatics Analysis//Transwell Assay	Circ_0006089 expression was up-regulated in GC samples and cell lines. Additionally, miR-143-3p was validated as a downstream target of circ_0006089, and circ_0006089 could positively regulate IGF1R expression via repressing miR-143-3p. Circ_0006089 is highly expressed in GC, and it promotes the malignancy of GC cells via modulating miR-143-3p/IGF1R axis, suggesting that circ_0006089 may serve as a promising therapeutic target for GC.	And high circ_0006089 expression was associated with shorter survival time in GC patients. 	Yes	 Circ_0006089 overexpression in GC cells significantly accelerated GC cell proliferation, migration and invasion, whereas circ_0006089 knockdown resulted in the opposite effects. 	35545863
circRELL1	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(circRELL1/miR-637/EPHB3 axis )	RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Herein, we discover circRNA RELL1, which has not been investigated in GC, and it is markedly downregulated in GC tissues, which is related with poor prognosis, more pronounced lymph node metastasis and poor TNM stage.Further mechanism investigation demonstrated that circRELL1 could sponge miR-637 and indirectly unregulated the expression of EPHB3 via modulating autophagy activation in GC. Additionally, circRELL1 can be transmitted by exosomal communication, and exosomal circRELL1 suppressed the malignant behavior of GC in vivo and in vitro. 	 Herein, we discover circRNA RELL1, which has not been investigated in GC, and it is markedly downregulated in GC tissues, which is related with poor prognosis, more pronounced lymph node metastasis and poor TNM stage.	Yes	After confirming the circular structure of circRELL1, we found that circRELL1 could block cell proliferation, invasion, migration, and anti-apoptosis in patients with GC by a series of in vivo and in vitro function-related studies. 	35027539
circTHBS1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-204-5p/INHBA)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//Transwell Assay	 The expression of circTHBS1 was significantly increased in GC and associated with poor prognosis. Mechanistically, circTHBS1 sponged miR-204-5p to promote the expression of Inhibin Subunit Beta A (INHBA). Moreover, circTHBS1 could enhance the HuR-mediated mRNA stability of INHBA, which subsequently activated the TGF-β pathway. 	 The expression of circTHBS1 was significantly increased in GC and associated with poor prognosis.	Yes	CircTHBS1 facilitated the malignant behavior and epithelial-to-mesenchymal transition of GC cells.	35338119
circCEA	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(p53/CDK1)	RNA Pull-Down//Western Blot//Tunel//qRT-PCR//FISH//IHC//IF	 Circ_CEA is significantly upregulated in GC tissues and cell lines.Mechanistically, circ_CEA interacts with p53 and cyclin-dependent kinases 1 (CDK1) proteins. It serves as a scaffold to enhance the association between p53 and CDK1. As a result, circ_CEA promotes CDK1-mediated p53 phosphorylation at Ser315, then decreases p53 nuclear retention and suppresses its activity, leading to the downregulation of p53 target genes associated with apoptosis. These findings suggest that circ_CEA protects GC cells from stress-induced apoptosis, via acting as a protein scaffold and interacting with p53 and CDK1 proteins.		Yes	Circ_CEA knockdown suppresses GC progression, and enhances stress-induced apoptosis in vitro and in vivo. 	36167685
circARID1A	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(circARID1A-IGF2BP3-SLC7A5)	RNA Pull-Down//Western Blot//CCK8//RIP//FISH//qRT-PCR//EdU Staining	We identified a novel circRNA, circARID1A, that can bind to IGF2BP3 protein.  CircARID1A was significantly upregulated in GC tissues compared with noncancerous tissues and positively correlated with tumor length, tumor volume, and TNM stage. Mechanistically, circARID1A served as a scaffold to facilitate the interaction between IGF2BP3 and SLC7A5 mRNA, finally increasing SLC7A5 mRNA stability. Additionally, circARID1A was able to directly bind SLC7A5 mRNA through complementary base-pairing and then formed the circARID1A-IGF2BP3-SLC7A5 RNA-protein ternary complex and promoted the proliferation of GC via regulating AKT/mTOR pathway.	 CircARID1A was significantly upregulated in GC tissues compared with noncancerous tissues and positively correlated with tumor length, tumor volume, and TNM stage.	Yes	 CircARID1A knockdown inhibited the proliferation of GC cells in vitro and in vivo and circARID1A played an important role in the oncogenic function of IGF2BP3. 	35986300
hsa_circ_0000437	CircRNA	Homo sapiens	Stomach Neoplasms	GC cell 	Regulation( Ser/Arg-rich splicing factor 3)	FISH	 Hsa_circ_0000437 regulated GC cell proliferation, invasion, migration and apoptosis by targeting Ser/Arg-rich splicing factor 3 (SRSF3) and inhibiting programmed cell death 4 (PDCD4). 		Yes	 The ectopic expression of hsa_circ_0000437 dramatically promoted tumor growth in nude mice in vivo. 	36109630
circZNF131	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-186-5p/PFKFB2 Axis)	IHC//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Expression analysis indicated that circZNF131 was upregulated in GC tissues and cells in a stable structure.Mechanically, miR-186-5p was a target of circZNF131, and miR-186-5p could bind to PFKFB2. Rescue experiments presented that miR-186-5p inhibition reversed the effects of circZNF131 knockdown on GC cell growth and glycolysis, and PFKFB2 overexpression abolished the impacts of miR-186-5p restoration on GC cell progression. Moreover, circZNF131 could positively modulate PFKFB2 expression via sponging miR-186-5p.		Yes	Functional analyses showed that circZNF131 knockdown suppressed GC cell colony formation ability, migration, invasion and glycolysis metabolism, and induced cell apoptosis.In vivo, circZNF131 knockdown hindered GC tumor growth by regulating the miR-186-5p/PFKFB2 axis. 	35059934
hsa_circ_0000654	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction( miR-149-5p/INHBA)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 circ_0000654 and INHBA were up-regulated but miR-149-5p was down-regulated in GC.circ_0000654 absorbed miR-149-5p to target INHBA.circ_0000654 silence or miR-149-5p overexpression limited the growth of GC tumors in vivo. Obviously, circ_0000654 facilitates the growth of GC cells through absorbing miR-149-5p to up-regulate INHBA.		Yes	Silencing circ_0000654inhibited the progress of GC cell biology. Oppositely, restoring circ_0000654 enhanced the growth of GC cells. Inhibiting miR-149-5p rescued down-regulated circ_0000654-induced anti-tumor effect on GC. 	35100076
circPDIA4	CircRNA	Homo sapiens	Stomach Neoplasms	tissues	Interaction(DHX9)	RNA Pull-Down//Western Blot//Wound Healing Assay//Co-IP//CCK8//qRT-PCR//RIP//IF//Luciferase Report Assay//RNA-seq//Colony Formation Assay//Transwell Assay	Clinically, circPDIA4 was significantly upregulated in malignant tissues and was associated with poor survival of patients with gastric cancer.  In the nucleus, circPDIA4 interacted with DHX9 as a decoy and repressed its inhibitory functions on circRNA biogenesis to boost expression of multiple oncogenic circRNAs, which promoted gastric cancer progression. 	Clinically, circPDIA4 was significantly upregulated in malignant tissues and was associated with poor survival of patients with gastric cancer. 	Yes	 Elevated expression of circPDIA4 promoted distant metastasis in various mouse xenograft models in vivo and accelerated cancer cell invasion in vitro. 	36562654
circHN1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-485-5p/GSK3A pathway)	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	In both GC tissues and cells, circ-HN1 expression was upregulated, and its silencing suppressed cellular processes. Moreover, circ-HN1 served as a sponge of miR-485-5p, which was reduced in patients with GC and negatively regulated by circ-HN1 in GC cells. Inhibition of miR-485-4p abolished the biological functions induced by the silencing of circ-HN1. Additionally, miR-485-5p targeted GSK3A in GC, whose expression was elevated in tumor tissues and was negatively correlated with miR-485-5p in tumor cells. GSK3A rescued the inhibition of miR-485-5p in the cellular processes. 		Yes	In both GC tissues and cells, circ-HN1 expression was upregulated, and its silencing suppressed cellular processes.	34607506
hsa_circ_0061276	CircRNA	Homo sapiens	Stomach Neoplasms	plasma	Interaction(hsa-miR-7705)	Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	The results show that plasma hsa_circ_0061276 copy number showed a trend of a gradual decrease when comparing healthy controls to the early cancer group and advanced gastric cancer group.Through bioinformatic analyses combined with cellular experiments, it was found that hsa_circ_0061276 inhibited the growth of gastric cancer by binding to hsa-miR-7705.		Yes	Overexpression of hsa_circ_0061276 inhibited the growth and migration of gastric cancer cells.	36620570
circBGN	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(IL6/STAT3 signaling pathway)	Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 Our results showed that circBGN expression was significantly elevated in GC tissues and cells. Furthermore, circBGN can directly bind to miR-149-5p, thereby preventing miR-149-5p from binding to its target mRNA [IL6 mRNA], thus activating IL6/STAT3 signaling pathway. Rescue assays indicated that circBGN regulates GC cell proliferation and invasion by upregulating miR-149-5p/IL6 axis output. 		Yes	Knockdown of circBGN dramatically suppressed GC cell proliferation and invasion in vitro. Xenograft experiments revealed that knockdown of circBGN delayed tumor growth in vivo. 	36250950
hsa_circ_0091741	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells and their exosomes 	Interaction(miR-330-3p/TRIM14/Dvl2/Wnt/β-catenin axis)	Tunel//CCK8//RIP//Luciferase Report Assay//CO-IP	GC cells and their exosomes were characterized by upregulated circ_0091741 expression.circ_0091741 obstructed the binding of miR-330-3p to TRIM14 and increased the expression of TRIM14. TRIM14 could cause activation of the Wnt/β-catenin signaling pathway by stabilizing Dvl2.		Yes	circ_0091741 transferred by GC cell-derived exosomes induced the autophagy and OXA resistance of GC cells.	36323918
hsa_circ_0000592	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(MiR-1179 was a direct target of circ_0000592, and circ_0000592 silencing-mediated effects in GC cells were partly reversed by the knockdown of miR-1179. MiR-1179 interacted with the 3' untranslated region (3'UTR) of ANXA4. Circ_0000592 silencing reduced ANXA4 expression partly by upregulating miR-1179 in GC cells. ANXA4 overexpression partly overturned circ_0000592 knockdown-induced effects in GC cells.)	RNA Pull-Down//Western Blot//Bioinformatics Analysis//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	 Circ_0000592 expression was elevated in GC tissues and cells. MiR-1179 was a direct target of circ_0000592, and circ_0000592 silencing-mediated effects in GC cells were partly reversed by the knockdown of miR-1179. MiR-1179 interacted with the 3' untranslated region (3'UTR) of ANXA4. Circ_0000592 silencing reduced ANXA4 expression partly by upregulating miR-1179 in GC cells. ANXA4 overexpression partly overturned circ_0000592 knockdown-induced effects in GC cells.		Yes	Circ_0000592 knockdown hampered cell proliferation, migration, invasion and glycolysis of GC cells. 	34459457
hsa-circ-0052001	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues.	Regulation(MAPK )	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	We found that compared with normal gastric mucosa epithelial cells and adjacent paracancer tissues, hsa-circ-0052001 was overexpressed in GC cells and tissues. Mechanistically, hsa-circ-0052001 promoted the carcinogenesis of GC cells via the MAPK signal pathway.	Also, the hsa-circ-0052001 level was linked to patient clinicopathological characteristics of GC. 	Yes	Cell proliferation and metastatic ability were inhibited in gastric cancer cells when hsa-circ-0052001 was knocked down in vitro and cancer growth in vivo. 	36453441
hsa_circ_0001013	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-136/TWSG1 )	Northern Blot//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//FISH//EdU Staining//Transwell Assay	Circ_0001013 was predicted to be up-regulated in GC by microarray profiling, which was confirmed by RT-qPCR detection in GC tissues and cells.  miR-136 was poorly expressed, and TWSG1 was highly expressed in GC tissues. Mechanistically, circ_0001013 bound to miR-136, which negatively targeted TWSG1 in the GC cells. 		Yes	Silencing circ_0001013 or TWSG1 or over-expressing miR-136 led to decreased GC cell proliferation, migration, invasion, and cell cycle arrest and enhanced apoptosis. Furthermore, silencing circ_0001013 resulted in diminished TWSG1 expression and inhibited transplanted tumor growth in the nude mice.	35958507
hsa_circ_0006089	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-143-3p/PTBP3 axis and PI3K/AKT signaling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 Circ_0006089 expression was increased in GC. MiR-143-3p specially bound to circ_0006089 and PTBP3 was targeted by miR-143-3p. Moreover, circ_0006089 could regulate PTBP3 expression and the PI3K/AKT pathway by sponging miR-143-3p. Circ_0006089 knockdown also suppressed tumor growth.		Yes	 Circ_0006089 downregulation suppressed the proliferation and metastasis and induced apoptosis of GC cells, which was counteracted by miR-143-3p inhibition or PTBP3 overexpression. In addition, circ_0006089 overexpression could promote GC progression.	35844201
circPCSK5	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells 	Expression(highly expressed)	Other	The expression of circPCSK5 was significantly upregulated in GC tissues and cells (P < 0.001, P < 0.01). 	The expression level of circPCSK5 was positively correlated with tumor size, vascular invasion, lymph node metastasis and AJCC stage of GC (P < 0.05). The overall survival and disease-free survival were significantly lower in GC patients with high circPCSK5 expression than in those with low circPCSK5 expression (P < 0.001). 	Yes	 Knockdown of circPCSK5 significantly inhibited the proliferation, migration and invasion of HGC27 cells (P < 0.01), increased the expressions of E-cadherin, and decreased the expression of N-cadherin and vimentin (P < 0.01). CircPCSK5 overexpression promoted the proliferation, migration and invasion of MKN45 cells (P < 0.01), reduced E-cadherin expression and increased N-cadherin and vimentin expressions (P < 0.01).	36329577
hsa_circ_0005529	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction(miR-873-5p/ZEB1 )	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 hsa_circ_0005529 was strongly expressed in gastric cancer where it stimulated tumorigenic behavior.  Furthermore, hsa_circ_0005529 was shown to promote ZEB1 expression by sponging miR-873-5p, an inhibitor of ZEB1 expression.		Yes	 hsa_circ_0005529 was strongly expressed in gastric cancer where it stimulated tumorigenic behavior. 	36305048
hsa_circ_0006089	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells,	Interaction(miR-361-3p/TGFB1)	IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA//Colony Formation Assay	circ_0006089 had been found to be upregulated in GC tissues and cells, and it could act as an miR-361-3p sponge.  TGFB1 was targeted by miR-361-3p, and its overexpression reversed the effects of miR-361-3p on GC cell function. Also, circ_0006089 promoted TGFB1 expression via sponging miR-361-3p. 		Yes	 circ_0006089 knockdown suppressed GC proliferation, metastasis, glycolysis, angiogenesis, and increased apoptosis, while this effect could be revoked by miR-361-3p inhibitor. Animal experiments showed that silenced circ_0006089 inhibited GC tumorigenesis through the miR-361-3p/TGFB1 pathway.	35347818
hsa_circ_0026344	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-590-5p/PDCD4 axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay//Transwell Assay	Circ_0026344 expression was underexpressed in GC tissues and cells, which was associated with clinicopathological characteristics such as tumour size, tumor-node-metastasis stage and lymph node metastasis.Circ_0026344 could act as a competing endogenous RNA of miR-590-5p to negatively modulate its expression, and this miRNA could mitigate the impact of circ_0026344 on GC cells. In addition, PDCD4 was identified as the downstream target of miR-590-5p, and PDCD4 expression was positively modulated by circ_0026344.	Circ_0026344 expression was underexpressed in GC tissues and cells, which was associated with clinicopathological characteristics such as tumour size, tumor-node-metastasis stage and lymph node metastasis.	Yes	Circ_0026344 overexpression restrained the malignant biological behaviours of GC cells, while circ_0026344 knockdown functioned oppositely. 	35640631
circEVI5	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction( miR-4793-3p/FOXO1)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Cycle Assay//EdU Staining	 circEVI5 was significantly downregulated in GC tissues and cells, and low circEVI5 expression was correlated with poor prognosis. Moreover, bioinformatics prediction showed that circEVI5 binds to miR-4793-3p, while FOXO1 may be a target of miR-4793-3p. Pull-down assays, RNA immunoprecipitation (RIP) assays, luciferase assays, and western blot were used to confirm the interactions between circEVI5, miR-4793-3p, and FOXO1. 	 circEVI5 was significantly downregulated in GC tissues and cells, and low circEVI5 expression was correlated with poor prognosis.	Yes	 Gain of function experiments indicated that circEVI5 could inhibit GC cell proliferation and retard the cell cycle. 	34354043
hsa_circ_001988	CircRNA	Homo sapiens	Stomach Neoplasms	341 GC patients	Interaction(miR-197-3p/FBXW7 )	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Wound Healing Assay//Migration Assay//qRT-PCR//RIP//Cell Viability Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	We first found that the expression of hsa_circ_001988 was decreased in 341 GC patients that was related to World Health Organization histological types, Lauren types, and tumor invasion depth (p < .05). Mechanistically, hsa_circ_001988 attenuated the miR-197-3p expression possibly due to its molecular sponge effect, and then, positively promoted FBXW7 expression. 	We first found that the expression of hsa_circ_001988 was decreased in 341 GC patients that was related to World Health Organization histological types, Lauren types, and tumor invasion depth (p < .05). 	Yes	Silencing of hsa_circ_001988 facilitated proliferation, colony formation, migration, and invasion of GC cells, while overexpression of hsa_circ_001988 reversed the effect on GC progression in vitro. Additionally, the results of subcutaneous xenotransplanted tumor model demonstrated that overexpressing hsa_circ_001988 significantly suppressed the subcutaneous tumor growth in vivo. 	32592202
hsa_circ_0000144	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(MiR-217)	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The circ_0000144 expression was obviously upregulated in GC tissues and cells. Moreover, circ_0000144 sponged miR-217, and rescue assays revealed that silencing miR-217 expression reversed the inhibitory effect of circ_0000144 knockdown on the progress of GC. 		Yes	 Silencing of circ_0000144 inhibited cell proliferation, migration and invasion of GC cells, but ectopic expression of circ_0000144 showed the opposite results.	33958507
hsa_circ_0006282	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-144-5p/YWHAB axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0006282 level was increased in GC tissues and cells compared to normal tissues and cells.  For mechanism analysis, circ_0006282 was identified to function as the sponge for miR-144-5p to positively regulate YWHAB expression in GC cells. Moreover, miR-144-5p inhibition or YWHAB overexpression effectively reversed the impacts of circ_0006282 knockdown on GC cell growth and motility. 		Yes	 Silencing of circ_0006282 restrained GC cell proliferation, migration and invasion. Additionally, circ_0006282 knockdown blocked tumor growth of GC in vivo.	33536789
hsa_circ_0027599	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-21-5p/RUNX1 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//H&E Staining//Colony Formation Assay//Transwell Assay	Circ_0027599 and RUNX1 were downregulated in GC tissues and cells.For mechanism analysis, circ_0027599 positively regulated RUNX1 expression via functioning as the sponge for miR-21-5p. RUNX1 inhibition reversed circ_0027599 overexpression mediated malignant behaviours of GC cells. 	 Circ_0027599 level was associated with the overall survival of GC patients. 	Yes	Circ_0027599 or RUNX1 overexpression inhibited GC cell viability, colony formation, migration, invasion and cell cycle process in vitro. Moreover, circ_0027599 overexpression repressed tumour growth in vivo.	34032284
hsa_circ_0008434	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissue	Interaction(miR-6838-5p)	Western Blot//Wound Healing Assay//Colony Formation Assay//CCK8//qRT-PCR//RNA-seq//IHC//Transwell Assay	We found that hsa_circ_0008434 was one of the most upregulated circRNAs in GC tissue versus normal tissue. Further in vitro testing indicated that by acting as a miRNA sponge for miR-6838-5p, hsa_circ_0008434 promotes the expression of USP9X and further increases the proliferation, migration, and invasion of GC cells. In addition, animal studies indicated that hsa_circ_0008434 could promote tumour growth in vivo.		Yes	Further in vitro testing indicated that by acting as a miRNA sponge for miR-6838-5p, hsa_circ_0008434 promotes the expression of USP9X and further increases the proliferation, migration, and invasion of GC cells. In addition, animal studies indicated that hsa_circ_0008434 could promote tumour growth in vivo.	34856948
circPRKDC	CircRNA	Homo sapiens	Stomach Neoplasms	GC samples and cells	Interaction(miR-493-5p/IRS2)	IHC//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircPRKDC was upregulated in GC samples, and circPRKDC silencing restrained GC cell viability, metastasis, and EMT and suppressed GC tumor growth. Besides, miR-493-5p was a target of circPRKDC, and the repressive impact of circPRKDC knockdown on GC development was neutralized by miR-493-5p inhibition. Moreover, miR-493-5p targeted IRS2 and IRS2 addition rescued the effects of circPRKDC depletion on GC progression. Finally, circPRKDC knockdown could regulate IRS2 expression by targeting miR-493-5p. 		Yes	CircPRKDC was upregulated in GC samples, and circPRKDC silencing restrained GC cell viability, metastasis, and EMT and suppressed GC tumor growth.	34605348
circSMAD4	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(CTNNB1/wnt/β-catenin pathway)	RNA Pull-Down//IHC//Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//Colony Formation Assay//EdU Staining//ChIP	 Circ_SMAD4 expression was potentiated in GC. Mechanically, nuclear circ_SMAD4 recruited TCF4 to facilitate CTNNB1 transcription, while cytoplasmic circ_SMAD4 sequestered miR-1276 to prevent the silence of CTNNB1 mRNA, leading to activation of Wnt/β-catenin pathway. 		Yes	 Circ_SMAD4 depletion impeded GC cell growth in vitro and restrained tumorigenesis in vivo. 	33458917
hsa_circ_0051620	CircRNA	Homo sapiens	Stomach Neoplasms	 tumoral tissues and cell lines 	Interaction(miR-338-3p/ADAM17)	Western Blot//Migration Assay//CCK8//qRT-PCR//RNA-seq//Invasion Assay	qRT-PCR results indicated that circ_0051620 in GC was over-expressed in tumoral tissues and cell lines compared to the normal controls. Moreover, miR-338-3p was confirmed to be the target of circ_0051620. Overall overexpression of miR-338-3p inhibited the cell migration, invasion through inhibiting ADAM17 in GC cells.		Yes	Moreover, miR-338-3p was confirmed to be the target of circ_0051620. Overall overexpression of miR-338-3p inhibited the cell migration, invasion through inhibiting ADAM17 in GC cells.	35413598
hsa_circ_0009910	CircRNA	Homo sapiens	Stomach Neoplasms	GC tumor tissues and cells	Interaction(miR-361-3p/SNRPA axis.)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 Circ_0009910 and SNRPA were upregulated in GC tumor tissues and cells. Circ_0009910 could sponge miR-361-3p, and miR-361-3p could target SNRPA. Further experiments confirmed that circ_0009910 positively regulated SNRPA by sponging miR-361-3p. 		Yes	Knockdown of circ_0009910 or SNRPA could inhibit GC cell proliferation, migration, invasion, glycolysis, and promote apoptosis.	35098410
hsa_circ_0007360	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction(miR-762/ IRF7 Axis)	IHC//Western Blot//Flow Cytometry//FISH//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In summary, our results revealed that activation of the circ0007360/miR-762/IRF7 axis is a novel mechanism for the attenuation of gastric cancer progression.		Yes	In summary, our results revealed that activation of the circ0007360/miR-762/IRF7 axis is a novel mechanism for the attenuation of gastric cancer progression.	35252169
hsa_circ_0044301	CircRNA	Homo sapiens	Stomach Neoplasms	 tissues and cancer cells	Interaction(Hsa-miR-188-5p/DAXX Axis and MAPK Pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//IF//RNA-seq//Luciferase Report Assay//Microarray//IHC//Transwell Assay	CircRNA-0044301 was upregulated in tissues and cancer cells compared to its levels in controls, related to patient prognosis, and its specific siRNA-vivo could slow tumor growth.On the mechanism, it acted as a sponge of miRNA-188-5p, could regulate the downstream target DAXX, and modulated the effect of GDC-0994 on ERK1/2 and 5-FU in cells. 	CircRNA-0044301 was upregulated in tissues and cancer cells compared to its levels in controls, related to patient prognosis, and its specific siRNA-vivo could slow tumor growth.	Yes	CircRNA-0044301 was upregulated in tissues and cancer cells compared to its levels in controls, related to patient prognosis, and its specific siRNA-vivo could slow tumor growth.	36077718
hsa_circ_0000285	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-1278/FN1 axis )	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	 Hsa_circ_0000285 was significantly overexpressed in the GC tissues.  Hsa_circ_0000285 sponged miR-1278. Inhibition of miR-1278 in vitro reversed the effects of hsa_circ_0000285 silencing on GC progression. MiR-1278 targeted FN1, and silencing FN1 neutralized the effects of miR-1278 inhibitors on GC progression.		Yes	 Silencing hsa_circ_0000285 inhibited cell proliferation and invasion, promoted apoptosis, and inhibited tumor development. 	35535385
hsa_circ_0008287	CircRNA	Homo sapiens	Stomach Neoplasms	 gastric cancer cells	Interaction(miR-548c-3p/CLIC1 r)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Transwell Assay	 circ_0008287, an upregulated circRNA in gastric cancer cells, augmented the viability as well as invasive and migratory potentials of gastric cancer cells. By competitively binding to miR-548c-3, circ_0008287 increased the expression of CLIC1, which impaired the function of CD8 + T cells and promoted their apoptosis. 		Yes	 circ_0008287, an upregulated circRNA in gastric cancer cells, augmented the viability as well as invasive and migratory potentials of gastric cancer cells. After downregulation of circ_0008287, in vivo tumorigenesis and metastasis were suppressed.	35905561
hsa_circ_0008035	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-1256/CEACAM6 axis)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	Circ_0008035 and CEACAM6 were significantly high-expressed in GC tissues and cells.MiR-1256 was a target of circ_0008035. The inhibition effect of circ_0008035 knockdown on the malignant behavior of GC cells could be reversed by miR-1256 inhibitor. In addition, CEACAM6 was a target of miR-1256. Overexpression of CEACAM6 partially restored the inhibitory effect of miR-1256 on cell progression. 		Yes	Silencing of circ_0008035 reduced GC cell proliferation, migration, and invasion while enhancing apoptosis. Animal experiments confirmed the anti-tumor effect of circ_0008035 knockdown in vivo. 	35220873
hsa_circ_0000081	CircRNA	Homo sapiens	Stomach Neoplasms	 tissues and cells 	Interaction( hsa-miR-423-5p/PDPK1 )	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//Transwell Assay	 Using quantitative reverse transcription polymerase chain reaction (qRT-PCR), hsa_circ_0000081 (circRNA-0000081) expression was found to be up-regulated in tissues and cells and was negative correlated with patients' survival time.Finally, dual luciferase reporter, RNA immunoprecipitation, qRT-PCR, and western blotting assays were used to verify the targeting relationship between circRNA-000081 and miRNA-423-5p or miRNA-423-5p and 3-phosphoinositide-dependent kinase 1 (PDPK1). 	 Using quantitative reverse transcription polymerase chain reaction (qRT-PCR), hsa_circ_0000081 (circRNA-0000081) expression was found to be up-regulated in tissues and cells and was negative correlated with patients' survival time.	Yes	Moreover, the knockdown or overexpression of circRNA-000081 could influence the proliferation, migration, and invasion potential of GC. 	35302432
hsa_circ_0067934	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(miR‑1301‑3p/KIF23 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 The results demonstrated that circ_0067934 expression was upregulated in GC cells, and circ_0067934 silencing significantly inhibited GC cell proliferation, migration and invasion. In conclusion, circ_0067934 may regulate the proliferation, invasion and migration of GC cells via the miR‑1301‑3p/KIF23 signaling axis, which may represent a novel therapeutic target for GC metastasis.		Yes	 The results demonstrated that circ_0067934 expression was upregulated in GC cells, and circ_0067934 silencing significantly inhibited GC cell proliferation, migration and invasion.	35475447
circMYBL2	CircRNA	Homo sapiens	Stomach Neoplasms	 GC cells	Interaction( miR-92b)	BrdU//RNA Pull-Down//Northern Blot	 We found that GC tissues exhibited increased mature miR-92b levels but decreased precursor miR-92b and circ-MYBL2 levels.  Circ-MYBL2 was detected in both the nucleus and cytoplasm in GC cells, and it directly interacted with precursor miR-92b. Moreover, circ-MYBL2 overexpression increased precursor miR-92b expression and decreased mature miR-92b level.		Yes	Furthermore, miR-92b (mature) increased GC cell proliferation, and circ-MYBL2 decreased GC cell proliferation and suppressed the effect of miR-92b on GC cell proliferation.	35644224
circFOXK2	CircRNA	Homo sapiens	Breast Neoplasms	BC cells with high metastatic ability	Interaction(IGF2BP3/miR-370 axis)	Migration Assay//FISH//Luciferase Report Assay//RNA-seq//Invasion Assay	The results showed that circRNA circFOXK2 was significantly increased in BC cells with high metastatic ability, and the upregulation of circFOXK2 was correlated with poor clinicopathological characteristics. Also. circFOXK2 could act with IGF2BP3, an RNA-binding protein, and miR-370 to synergistically promote BC metastasis. 	 the upregulation of circFOXK2 was correlated with poor clinicopathological characteristics	Yes	Functional experiments demonstrated that overexpression of circFOXK2 promoted migration and invasion of BC cells. 	34329193
circCDYL	CircRNA	Homo sapiens	Breast Neoplasms	HER2+ breast cancer tissue	Interaction(miR-92b-3p)	Western Blot//ISH//CCK8//qRT-PCR//FISH//Luciferase Report Assay	CircCDYL was high-expressed in HER2+ breast cancer tissue, similar with that in HER2- breast cancer tissue.  CircRNA pull down and miRNA deep-sequencing demonstrated the binding of miR-92b-3p and circCDYL. Interestingly, circCDYL did not act as miR-92b-3p sponge, but was degraded in miR-92b-3p-dependent silencing manner. 	Clinically, expression of circCDYL and miR-92b-3p was associated with clinical outcome of HER2+ breast cancer patients.	Yes	Over-expression of circCDYL promoted proliferation of HER2+ breast cancer cells but not through miR-1275-ULK1/ATG7-autophagic axis.	34395434
hsa_circ_0001944	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-142-5p/NFAT5 )	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay	Circ_0001944 was highly expressed in NSCLC, and NSCLC patients with high expression of circ_0001944 had a worse prognosis. Circ_0001944 was verified as a decoy for microRNA (miR)-142-5p, which targeted NFAT5 (nuclear factor of activated T cells 5). MiR-142-5p was downregulated while NFAT5 was upregulated in NSCLC. Both miR-142-5p inhibition and NFAT5 overexpression offset the suppressive impact of circ_0001944 silencing on proliferation, migration, invasion, and glycolysis of NSCLC cells. 	Circ_0001944 was highly expressed in NSCLC, and NSCLC patients with high expression of circ_0001944 had a worse prognosis. 	Yes	Circ_0001944 silencing decreased xenograft tumor growth in vivo and repressed proliferation, migration, invasion, and glycolysis of NSCLC cells in vitro.	34040437
circSEC31A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	interaction[Sponging miR-376a]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our data indicated that circSEC31A and SEC31A were upregulated in NSCLC tissues and cells.Our findings first identified that the knockdown of circSEC31A suppressed NSCLC malignant progression at least partly through modulating SEC31A expression by acting as a miR-376a sponge, providing a novel molecular target of NSCLC therapy.		Yes	CircSEC31A knockdown suppressed NSCLC cell migration, invasion, glycolysis and promoted apoptosis in vitro, as well as hindered tumor growth in vivo.	33204164
circTHBS1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[sponging miR-129-5p and regulating SOX4 expression]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining	 The expression of circTHBS1 was markedly higher in NSCLC patients than that in control group, and it was increased in patients with metastatic NSCLC compared with that in patients with non-metastatic NSCLC.  CircTHBS1 promotes the proliferation and inhibits the apoptosis of NSCLC cells through targeting miR-129-5p and regulating SOX4 expression.		Yes	 Moreover, the proliferative ability of the cells was weakened notably after transfection with small interfering (Si)-CircTHBS1, but it was enhanced remarkably after transfection with CircTHBS1-overexpression vector (OE).	33099906
circNFIX	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-212-3p/ADAM10 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our data revealed that circNFIX was overexpressed in NSCLC and predicted poor prognosis of NSCLC patients.: Our findings first identified that the knockdown of circNFIX, a highly expressed circRNA in NSCLC, exerted a repressive role in NSCLC malignant progression at least in part through targeting the miR-212-3p/ADAM10 axis, illuminating a novel understanding of circRNA regulation in NSCLC.	Our data revealed that circNFIX was overexpressed in NSCLC and predicted poor prognosis of NSCLC patients.	Yes	CircNFIX knockdown suppressed NSCLC cell viability, migration, invasion and glycolysis in vitro and hampered tumor growth in vivo.	33061643
circDENND2A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[MiR-34a/CCNE1 Signaling]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Here, we demonstrated that circDENND2A was down-regulated in NSCLC samples.We thought this study indicated that circDENND2A/miR-34a/CCNE1 may be a potential therapeutic target for NSCLC.		Yes	Loss-of-function assays showed circDENND2A knockdown suppressed cell growth via inducing cell cycle arrest and apoptosis and inhibited cell migration and invasion. 	33033491
hsa_circ_100876	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		regulation[miR-636/RET axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	CircRNA_100876 knockdown notably suppressed the progression of NSCLC through regulation of miR-636/RET axis, which may serve as a potential target for treatment of NSCLC.		Yes	Silencing of circRNA_100876 notably inhibited the proliferation of NSCLC cells. Moreover, downregulation of circRNA_100876 significantly induce the apoptosis of NSCLC cells via mediation of apoptosis-related proteins. In addition, silencing of circRNA_100876 significantly inhibited migration and invasion of NSCLC cells.	33030101
circHIPK3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	regulation[circHIPK3/miR-107/BDNF axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results showed that circHIPK3 expression was upregulated in NSCLC cells.  These results indicate that circHIPK3 promotes tumor progression through a new circHIPK3/miR-107/BDNF axis, which offers potential markers and medical treatment for NSCLC.		Yes	 circHIPK3 knockdown inhibited the migration and proliferation of NSCLC cells by promoting the expression of miR-107.	33015172
circMEMO1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,blood	regulation[miR-101-3p/KRAS axis]	qRT-PCR//MTT//RNA Pull-Down//RIP	Circ-MEMO1 was up-regulated in NSCLC, and high expression of circ-MEMO1 predicted poor prognosis in NSCLC patients.  Circ-MEMO1 facilitated the progression and glycolysis of NSCLC through regulating miR-101-3p/KRAS axis.	Circ-MEMO1 was up-regulated in NSCLC, and high expression of circ-MEMO1 predicted poor prognosis in NSCLC patients. 	Yes	Circ-MEMO1 accelerated the proliferation, cell cycle progression, and glycolytic metabolism and inhibited the apoptosis of NSCLC cells.	33005174
hsa_circ_0000376	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[ miR-1182/NOVA2 Network]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Circ_0000376 was upregulated in NSCLC, and its high expression was related to the poor overall survival of NSCLC patients.Circ_0000376 promoted NSCLC progression by regulating the miR-1182/NOVA2 axis, suggesting that circ_0000376 might be a potential biomarker for NSCLC treatment.	Circ_0000376 was upregulated in NSCLC, and its high expression was related to the poor overall survival of NSCLC patients.	Yes	However, silencing of circ_0000376 could inhibit the glycolysis, viability, migration, and invasion of hypoxia-induced NSCLC cells. 	32922073
hsa_circ_0000735	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	regulation[miR-940/BMPER Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_0000735 was upregulated and significantly correlated with overall survival in patients with NSCLC.Circ_0000735 regulated proliferation, migration, invasion, and glycolysis in NSCLC cells by targeting miR-940/BMPER axis.	 Circ_0000735 was upregulated and significantly correlated with overall survival in patients with NSCLC.	Yes	In addition, the loss-of-functional experiments revealed that knockdown of circ_0000735 repressed proliferation, migration, invasion and glycolysis of NSCLC cells and tumor growth in vivo, which was overturned by overexpression of BMPER.	32922033
hsa_circ_102179	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	regulation[miR-330-5p/HMGB3 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 CircRNA_102179 was overexpressed in NSCLC tissues and cells compared with normal lung tissues and human bronchial epithelial cells (HBEs). Our results reveal that circRNA_102179 facilitates the proliferation, migration, and invasion of NSCLC cell via modulating miR-330-5p/ HMGB3 axis in NSCLC cells.		Yes	 The down-regulation of circRNA_102179 markedly reduced the proliferation, migration, and invasion of NSCLC cells. 	32911346
hsa_circ_103993	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	regulation[miR-1271/ERG signaling pathway]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	CircRNA_103993 and ERG were significantly up-regulated while miR-1271 was significantly down-regulated in NSCLC cells.The CircRNA_103993 /miR-1271/ ERG axis had an important effect on the proliferation and apoptosis of NSCLC cells.		Yes	Knockdown of CircRNA_103993 and high expression of miR-1271 significantly inhibited NSCLC cell proliferation and promoted apoptosis. 	32894545
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[THBS2,miR-590-5p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The expression of circ_0020123 was upregulated in NSCLC tissues and cells.Circular RNA circ_0020123 regulated THBS2 by sponging miR-590-5p to promote cell proliferation and migration and inhibit cell apoptosis in NSCLC cells.		Yes	Functionally, circ_0020123 downregulation inhibited the proliferation and migration and promoted the apoptosis of NSCLC cells. 	32831647
circEPSTI1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[ inhibiting TRIM24 via miR-1248 upregulation]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	 We found that circEPSTI1 expression was significantly elevated in NSCLC. In summary, our data demonstrate that downregulation of circEPSTI1 represses the proliferation and invasion of NSCLC by inhibiting TRIM24 via miR-1248 upregulation.		Yes	 In vitro experiments elucidated that knockdown of circEPSTI1 caused a significant reduction in NSCLC cell proliferation and invasion. 	32828310
circEPSTI1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells 	regulation[miR-145/HMGB3 Axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 CircEPSTI1 was abnormally up-regulated in NSCLC tissues and cells in comparison with that in normal tissues and cells.CircEPSTI1 aggravated the progression of NSCLC through elevating the expression of HMGB3 via sponging miR-145.	The high expression of circEPSTI1 was associated with the low survival rate of NSCLC patients.	Yes	CircEPSTI1 accelerated the proliferation, colony formation and motility of NSCLC cells in vitro. CircEPSTI1 silencing restrained the NSCLC tumor growth in vivo.	32801908
circSLC7A6	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues	regulation[circ-SLC7A6/miR-21 axis]	RNA Pull-Down//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Transwell Assay	 Circ-SLC7A6 was significantly downregulated in NSCLC tissues in comparison to para-carcinoma tissues. Overall, our study demonstrates that circ-SLC7A6 is a novel tumor suppressor in NSCLC, targeting circ-SLC7A6/miR-21 axis may be a promising treatment for NSCLC patients.	Low circ-SLC7A6 was closely associated with larger tumor size, lymph node metastasis, advanced clinical stage and adverse outcome.	Yes	Importantly, in vivo xenograft tumor experiments showed that reintroduction of circ-SLC7A6 retarded tumor growth as well as decreased lung metastatic nodules. 	32794418
circARHGAP10	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues, cells, and serum-derived exosomes	regulation[miR-638/FAM83F Axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	circARHGAP10 was upregulated in NSCLC tissues, cells, and serum-derived exosomes. Inhibition of serum-derived exosomes-mediated circARHGAP10 curbed NSCLC progression through the miR-638/FAM83F axis.		Yes	circARHGAP10 depletion repressed proliferation, migration, invasion, and glycolysis of NSCLC cells in vitro, and curbed tumor growth in vivo. 	32783691
circRACGAP1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues, cells	regulation[miR-144-5p/CDKL1 signaling pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//EdU Staining	CircRACGAP1 was highly expressed and miR-144-5p was inhibited both in NSCLC tissues and cell lines, suggesting their negative correlation in NSCLC. In summary, our study revealed a novel machinery of circRACGAP1/miR-144-5p/CDKL1 for the NSCLC tumorigenesis and development, providing potential diagnostic and therapeutic targets for NSCLC.		Yes	 Knockdown of circRACGAP1 suppressed cell proliferation via arresting the cell cycle.	32778770
circMAGI3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues, cells	regulation[miR-515-5p/HDGF]	qRT-PCR	Clinically, circMAGI3 was significantly up-regulated in NSCLC tissue and cells, which was closely correlated with unfavorable outcome for NSCLC patients.Collectively, this research identified the oncogenic role of circMAGI3 in the tumorigenesis through miR-515-5p/HDGF axis, providing a vital theoretical basis for treatment of NSCLC.	Clinically, circMAGI3 was significantly up-regulated in NSCLC tissue and cells, which was closely correlated with unfavorable outcome for NSCLC patients.	Yes	 Functionally, circMAGI3 promoted the glycolysis and proliferation of NSCLC cells.	32774748
hsa_circ_0067934	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[ miR-1182/KLF8 axis and activating Wnt/β-catenin pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Transwell Assay	We found that circ_0067934 and KLF8 were up-regulated, while miR-1182 was down-regulated in NSCLC tissues and cells. In conclusion, Circ_0067934 acted as a competing endogenous RNA to facilitate NSCLC progression by regulating the miR-1182/KLF8 axis and activating Wnt/β-catenin pathway.		Yes	Circ_0067934 knockdown blocked proliferation, migration, invasion and EMT and induced apoptosis in NSCLC cells. 	32768951
hsa_circ_0000376	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue 	regulation[repressing miR-384]	CCK8//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	Circ_0000376 expression in NSCLC clinical samples was up-regulated and this was linked to unfavorable pathological parameters.Mechanically, circ_0000376 overexpression could bind with miR-384 and repress its expression.		Yes	 Circ_0000376 markedly accelerated the proliferation and metastasis, and enhanced chemoresistance of NSCLC cells.	32716343
circBIRC6	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC patient samples and cell lines	interaction[targeting miR-4491]	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	We found that expression levels of circ-BIRC6 in NSCLC patient samples and cell lines were elevated. These findings demonstrate that circ-BIRC6 functions as a critical regulator of proliferation and apoptosis via binding to and negatively regulating miR-4491, suggesting that circ-BIRC6 might be a potential target for treatment of NSCLC.		Yes	Small interfering RNA (siRNA)-mediated circ-BIRC6 knockdown suppressed cell proliferation, colony formation, migration and invasion, and promoted apoptosis in NCI-H460 and A549 cells. 	33177288
hsa_circ_0001869	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	interaction[sponging miR-638 and promoting FOSL2 expression]	IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//FISH//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	The data advised that hsa_circ_0001869 expression was increased in NSCLC cell lines and tissues.Present investigation discovered that hsa_circ_0001869 enhanced NSCLC progression via sponging miR-638 and promoting FOSL2 expression. 	High hsa_circ_0001869 expression had negatively correlation with the NSCLC patients prognosis.	Yes	hsa_circ_0001869 downregulation decreased tumor proliferation, invasion and migration by promoting miR-638 expression and decreasing FOSL2 expression. 	33221767
circLDLRAD3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-137/SLC1A5 axis]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this study, we found that circ-LDLRAD3 was high-expressed and miR-137 was low-expressed in NSCLC tissues and cells compared to their normal counterparts, which showed negative correlations in NSCLC tissues. Taken together, this in vitro study found that knock-down of circ-LDLRAD3 inhibited the development of NSCLC by regulating miR-137/SLC1A5 axis.		Yes	 In addition, knock-down of circ-LDLRAD3 and miR-137 overexpression promoted NSCLC cell apoptosis, and inhibited cell proliferation and invasion.	32658600
hsa_circ_0001313	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell line	regulation[microRNA-452/HMGB3/ERK/MAPK Axis]	qRT-PCR	Abnormally elevated circ0001313 and decreased miR-452 in NSCLC cells were observed.We highlighted that silencing of circ0001313 blunted the ERK/MAPK pathway via the miR-452/HMGB3 axis, thereby inhibiting NSCLC cell proliferation and invasion.		Yes	Circ0001313 silencing or miR-452 overexpression significantly reduced NSCLC cell proliferation and invasion.	33328759
circZFR	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and corresponding adjacent normal lung tissues,cell line (HBE A549, H460, H1703, PC9 and H1299)	Interaction[miR-101-3p;CUL4B]	CCK8//qRT-PCR//Transwell Assay//FISH	 Our results showed that circZFR expressions were significantly Expression[Expression[up-expression]-expression]regulated in NSCLC tissues and cell lines. KnockExpression[down-expression] of circZFR significantly inhibited the cell proliferation, migration and invasion of NSCLC cells in vitro. Furthermore, we demonstrated that circZFR acted as a sponge to absorb microRNA-101-3p (miR-101-3p) and promoted cullin 4B (CUL4B) expression		Yes	 KnockExpression[down-expression] of circZFR significantly inhibited the cell proliferation, migration and invasion of NSCLC cells in vitro.	31407591
F-circSR1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines(H1299 and A549)	Regulation[Expression[Expression[highly expressed]-expression]-regulated]	qRT-PCR//Wound Healing Assay//MTT//Transwell Assay	Transwell migration assays show that both F-circSRs significantly promoted cell migration in both cells (Fig. 2d), which were further confirmed by wound healing assays (Fig. 2e, f). 		Yes	Functional studies through gain- and loss-of-function strategies showed that both F-circSRs promote cell migration in lung cancer cells, whereas they have little effect on cell proliferation. 	31118036
F-circSR2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines(H1299 and A550)	Regulation[Expression[Expression[highly expressed]-expression]-regulated]	qRT-PCR//Wound Healing Assay//MTT//Transwell Assay	Transwell migration assays show that both F-circSRs significantly promoted cell migration in both cells (Fig. 2d), which were further confirmed by wound healing assays (Fig. 3e, f).		Yes	Functional studies through gain- and loss-of-function strategies showed that both F-circSRs promote cell migration in lung cancer cells, whereas they have little effect on cell proliferation. 	31118036
hsa_circ_0003645	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumor tissues, cell lines(16HBE, H358, H1299, H1581, and A549)	Interaction[miR-1179/TMEM14A pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The data demonstrated an Expression[Expression[up-expression]-expression]regulation of circ_0003645 in patients' tissue specimens and cells. Moreover, circ_0003645 acted as a ceRNA to sponge miR-1179, which resulted in the elevation of TMEM14A expression and facilitated cell progression.	Overexpression of circ_0003645 in tissues was related to advanced TNM stages, positive lymph node invasion and unfavorable prognosis for the patients with NSCLC. 	Yes	 In addition, gain and loss of function assays uncovered that circ_0003645 functioned as an oncogene in NSCLC cells. 	30853176
circFOXM1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[ circ-FOXM1/miR-1304-5p/PPDPF/MACC1 signaling]	Other	The results indicated that circ-FOXM1 overexpression was observed in NSCLC tissues and closely associated with lymph node invasion, higher TNM stage, and unfavorable prognosis.Mechanistically, miR-1304-5p was discovered as a direct target of circ-FOXM1. Circ-FOXM1 Expression[Expression[up-expression]-expression]regulated the level of pancreatic progenitor cell differentiation and proliferation factor (PPDPF) and metastasis-associated in colon cancer 1 (MACC1) by sponging miR-1304-5p, thereby increasing the proliferation and invasion of NSCLC cells. 	The results indicated that circ-FOXM1 overexpression was observed in NSCLC tissues and closely associated with lymph node invasion, higher TNM stage, and unfavorable prognosis	Yes	Furthermore, knockExpression[down-expression] and ectopic expression of circ-FOXM1 significantly inhibited and promoted the growth, migration and invasion of NSCLC cells, respectively.	30954221
circPIP5K1A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell line	Interaction[miR-600/HIF-1α]	FISH//Luciferase Report Assay//PCR	The data demonstrated that circPIP5K1A expression was increased in NSCLC cells.The circPIP5K1A may function as an miR-600 sponge to facilitate NSCLC proliferation and metastasis by promoting HIF-1α. A bifluorescein reporter experiment confirmed that miR-600 was the circPIP5K1A target, and miR-600 interacted with the 3' untranslated region of HIF-1α. These results show that circPIP5K1A acted as a tumor promoter through a novel circPIP5K1A/miR-600/HIF-1α axis, which provides candidate markers and therapeutic targets for NSCLC.		Yes	The circPIP5K1A knockdown sExpression[up-expression]pressed NSCLC cell metastasis and proliferation by promoting expression of miR-600. Overexpression of miR-600 inhibited HIF-1α-mediated metastasis and proliferation of NSCLC cell by downregulating the endothelial mesenchymal transition-related proteins, Snail and vimentin, and Expression[up-expression]regulating E-cadherin.	31241217
hsa_circ_0026134	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Interaction[ sponging miR-1256 and miR-1287]	qRT-PCR//Luciferase Report Assay	 Circ_0026134 was frequently upregulated in NSCLC samples and cell lines. For the part of mechanism exploration, miR-1256 and miR-1287 were proved to be sponged by circ_0026134. Rescue experiments further indicated that the oncogenic role of circ_0026134 was dependent on its regulation of miR-1256 and miR-1287. 		Yes	 Furthermore, we observed that downregulation of circ_0026134 attenuated NSCLC cell proliferation and metastatic properties and induced cell apoptosis. The overexpression of circ_0026134 in NSCLC cells caused the opposite effect.	30970529
circFGFR1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[sponging miR-381-3p]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Here, we report that circFGFR1 is upregulated in NSCLC tissues, and circFGFR1 expression is associated with deleterious clinicopathological characteristics and poor prognoses for NSCLC patients.Mechanistically, circFGFR1 could directly interact with miR-381-3p and subsequently act as a miRNA sponge to upregulate the expression of the miR-381-3p target gene C-X-C motif chemokine receptor 4 (CXCR4), which promoted NSCLC progression and resistance to anti-programmed cell death 1 (PD-1)- based therapy.		Yes	Forced circFGFR1 expression promoted the migration, invasion, proliferation, and immune evasion of NSCLC cells.	31815619
circHIPK3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissue	Regulation[MIR124-3p-STAT3-PRKAA/AMPKα signaling]	qRT-PCR//Western Blot	Mechanistically, we uncovered that autophagy was induced upon loss of circHIPK3 via the MIR124-3p-STAT3-PRKAA/AMPKa axis in STK11 mutant lung cancer cell lines (A549 and H838). STAT3 abrogation as well as transfection with a MIR124-3p mimic, recapitulated the induction of autophagy. We also demonstrated antagonistic regulation on autophagy between circHIPK3 and linear HIPK3 (linHIPK3). We therefore propose that the ratio between circHIPK3 and linHIPK3 (C:L ratio) may reflect autophagy levels in cancer cells. We observed that a high C:L ratio (>0.49) was an indicator of poor survival, especially in advanced-stage NSCLC patients. These results support that circHIPK3 is a key autophagy regulator in a subset of lung cancer and has potential clinical use as a prognostic factor. The circular RNA HIPK3 (circHIPK3) functions as an oncogene and autophagy regulator may potential use as a prognostic marker and therapeutic target in lung cancer.		Yes	. Our results provided evidence that silencing of circHIPK3 significantly impaired cell proliferation, migration, invasion and induced macroautophagy/autophagy. 	31232177
hsa_circ_000984	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	We found that hsa_circ_000984 was highly expressed in NSCLC tissues and cell lines and correlated with advanced TNM stage and lymph nodes metastasis. Moreover, hsa_circ_000984 displayed its oncogenic roles by modulating the activation of Wnt/β-catenin pathway, which was demonstrated by measuring the expression levels of, β-catenin, c-myc, and cyclin D1.	We found that hsa_circ_000984 was highly expressed in NSCLC tissues and cell lines and correlated with advanced TNM stage and lymph nodes metastasis. The clinical assays indicated that patients with high hsa_circ_000984 expression had shorter overall survival and disease-free survival. 	Yes	The functional investigations showed that the knockdown of hsa_circ_000984 suppressed NSCLC cells proliferation, migration, invasion, and EMT. 	31081091
circZKSCAN1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Interaction[circ-ZKSCAN1/miR-330-5p/FAM83A feedback loop]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Our results showed that circ-ZKSCAN1 was significantly up-regulated in NSCLC. Importantly, circ-ZKSCAN1 can act as a sponge of carcinogenic miR-330-5p to increase the expression of FAM83A, resulting in the inhibition of MAPK signal transduction pathway, thus promoting the progress of NSCLC. Interestingly, the increase in FAM83A expression caused by circ-ZKSCAN1 overexpression could in turn promote the expression of circ-ZKSCAN1.	Our results showed that circ-ZKSCAN1 was significantly up-regulated in NSCLC, closely related to malignant characteristics and poor prognosis, and clinically related to tumor size and clinical stage. 	Yes	 Subsequent experiments showed that circ-ZKSCAN1 could inhibit the growth of NSCLC cells in vitro and in vivo.	32010565
hsa_circ_0004015	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[circ_0016760/miR-1183/PDPK1 signaling pathway ]	qRT-PCR//Luciferase Report Assay	Here, we identified hsa_circ_0004015 was upregulated in NSCLC tissues, and was associated with the poor overall survival rate of NSCLC patients.In conclusion, circ_0016760/miR-1183/PDPK1 signaling pathway might play vital roles in the tumorigenesis of NSCLC.	Here, we identified hsa_circ_0004015 was upregulated in NSCLC tissues, and was associated with the poor overall survival rate of NSCLC patients.	Yes	Knockdown of hsa_circ_0004015 significantly decreased cell viability, proliferation, and invasion, whereas overexpression exhibited opposed effects in vivo and in vitro. 	30509491
hsa_circ_0023404	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Regulation[miR-217/ZEB1 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The expression of hsa_circ_0023404 was upregulated in NSCLC tissues, as well as in NSCLC cell lines. hsa_circ_0023404 promotes the proliferation, migration and invasion of NSCLC cells by regulating miR-217/ZEB1 axis, providing a fresh perspective on circRNAs in NSCLC development.	 High hsa_circ_0023404 expression predicted short overall survival in NSCLC. 	Yes	Functionally, knockdown of hsa_circ_0023404 inhibited the proliferation, migration and invasion of NSCLC cells.	31496723
hsa_circ_0078767	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[ inhibiting miR-330-3p]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Transwell Assay	Circ_0078767 and RASSF1A were downregulated, while miR-330-3p was upregulated in NSCLC tissues than that in adjacent tissues.Circ_0078767 could suppress NSCLC progression by inhibiting miR-330-3p, which thereby increased RASSF1 levels.		Yes	The overexpression of circ_0078767 and RASSF1A or the underexpression of miR-330-3p significantly suppressed NSCLC cell viability, cell cycle progression and invasion while also significantly promoting cell apoptosis. Additionally, these modulations significantly suppressed in vivo tumour growth.	30507050
hsa_circ_0000003	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Regulation[miR-338-3p/IRS2 axis]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//BrdU//Transwell Assay	The expression of circ_0000003 was significantly high in NSCLC tissues and cell lines.Circ_0000003 promotes the proliferation and metastasis of NSCLC cells via modulating miR-338-3p/IRS2 axis.	The expression of circ_0000003 was significantly high in NSCLC tissues and cell lines, and its high expression level was notably correlated with lymph node metastasis andTNM staging.	Yes	In vitro experiments showed that overexpression of circ_0000003 facilitated the proliferation, migration, invasion and inhibited the apoptosis of NSCLC cells, while the knockdown of circ_0000003 had the opposite effect.In vivo experiments revealed that knockdown of circ_0000003 impeded tumor growth and metastasis.	31736412
circSATB2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Expression[highly expressed]	qRT-PCR//FISH//Luciferase Report Assay//Western Blot	Data from the investigation showed that circSATB2 was highly expressed in NSCLC cells and tissues.		Yes	Furthermore, circSATB2 can be transferred by exosomes and promote the proliferation, migration and invasion of NSCLC cells, as well as induce abnormal proliferation in normal human bronchial epithelial cells.	32493389
hsa_circ_101237	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell line	interaction[miRNA-490-3p/MAPK1 axis]	CCK8//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	The study found an elevation in the expression of Hsa_circRNA_101237 in both NSCLC tissues and cell line. To sum up, as revealed by the study, hsa_circRNA_101237 promoted the expression of MAPK1 via miRNA-490-3p sponge, thus affecting the NSCLC as an important onco-circRNA.	 High Hsa_circRNA_101237 expression predicted poor survival in NSCLC.	Yes	Meanwhile, we found that hsa_circRNA_101237 expression sponged miR-490-3p to enhance MAPK1 expression, thus significantly promoting NSCLC cell lines proliferation, migration, and invasion.	32494004
hsa_circ_0016760	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell line	interaction[sponging miR-145-5p/FGF5]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 Hsa_circ_0016760 was aberrantly upregulated in NSCLC, which was associated with poor prognosis of patients (P<0.05).In conclusion, hsa_circ_0016760 exacerbated the malignant development of NSCLC by sponging miR‑145‑5p/FGF5.	 Hsa_circ_0016760 was aberrantly upregulated in NSCLC, which was associated with poor prognosis of patients (P<0.05).	Yes	Hsa_circ_0016760 silencing suppressed NSCLC cell proliferation, migration and invasion in vitro (P<0.01).	33416186
hsa_circ_0004050	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	regulation[ERK/JNK signaling pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	The expression of hsa_ circ_0004050 was significantly lower in tumor tissues than that in para-carcinoma tissues in NSCLC patients.  In terms of its mechanism, hsa_circ_0004050 could markedly increase the protein expression of DUSP9 via targeting miR-1233-3p in A549 cells, thereby inhibiting the ERK/JNK signaling pathway.	 The expression of hsa_circ_0004050 was significantly correlated with TNM stage, tumor size and lymph node metastasis. The results of survival analysis showed that the survival time of patients with a high expression of hsa_circ_0004050 was obviously prolonged.	Yes	According to the results of phenotype assay, hsa_circ_0004050 could promote apoptosis and inhibit proliferation of A549 cells. 	33348975
hsa_circ_0007580	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-545-3p]	Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	Hsa_circ_0007580 was upregulated in NSCLC tumor tissues, and the expression of its host gene (protein kinase Ca) correlated negatively with overall survival.Dual luciferase reporter assays indicated that miR-545-3p can bind to hsa_circ_0007580 (suggesting that hsa_circ_0007580 sponges miR-545-3p) and to protein kinase Ca (suggesting that miR-545-3p directly inhibits this gene).	Hsa_circ_0007580 was upregulated in NSCLC tumor tissues, and the expression of its host gene (protein kinase Ca) correlated negatively with overall survival.	Yes	Knocking down hsa_circ_0007580 inhibited proliferation and invasion by NSCLC cells and induced their apoptosis. 	32681720
circMET	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-145-5p/CXCL3 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//IHC//Transwell Assay	In this study, the present results demonstrated that circMET expression was significantly higher in NSCLC tissues than in peritumoral tissues using quantitative real-time polymerase chain reaction.  Collectively, circMET regulates the miR-145-5p/CXCL3 axis and serves as a novel, promising diagnostic and prognostic biomarker in patients with NSCLC.	 Notably, NSCLC patients with a large tumor diameter, poor differentiation and lymphatic metastasis had high RNA levels of circMET. Moreover, high circMET expression served as an independent risk factor for short overall survival (OS) and progression-free survival (PFS) in NSCLC patients.	Yes	Next, we validated that circMET overexpression can enhance NSCLC cell proliferation, metastasis, and immune evasion in vitro.	32614785
hsa_circ_0053063	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines 	Interaction(hsa-miR-330-3p/PDCD4 axis)	Western Blot//qRT-PCR//FISH//MTT//Luciferase Report Assay//Colony Formation Assay	Hsa_circ_0053063 was mainly located in the cytoplasm and activated in BC tissues and cell lines.  In conclusion, hsa_circ_0053063 inhibits breast cancer cell proliferation via hsa_circ_0053063/hsa-miR-330-3p/PDCD4 axis, which may provide a new therapeutic target for BC patients.		Yes	Moreover, hsa_circ_0053063 inhibited cell viability, proliferation, and progression of BC through the negative regulation of miR-330-3p. 	33744861
hsa_circ_0003222	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and LCSCs	Interaction(miR-527)	In Vivo Experiment	We found that hsa_circ_0003222 was highly expressed in NSCLC tissues and LCSCs.  	Higher levels of hsa_circ_0003222 were associated with the stage, metastasis, and survival rate of patients with NSCLC.	Yes	Reduced levels of hsa_circ_0003222 decreased tumor cell proliferation, migration, invasion, stemness-like properties, and chemoresistance. The silencing of hsa_circ_0003222 was found to downregulate PHF21B expression and its downstream, β-catenin by relieving the sponging effect of miR-527. 	34433810
hsa_circ_0000735	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumor tissues 	Interaction(miR-635/FAM83F axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0000735 was a highly expressed circRNA in NSCLC. 		Yes	Silenced circ_0000735 could inhibit NSCLC cell proliferation, migration, invasion, glycolysis, and increase apoptosis. MiR-635 could be sponged by circ_0000735, and its inhibitor could reverse the regulation of circ_0000735 silencing on NSCLC progression. 	33560141
hsa_circ_0000517	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissues and cells	Interaction(miR-330-5p/YY1 signal pathway)	RNA Pull-Down//qRT-PCR//Western Blot	The results demonstrated that circ_0000517 was highly expressed in lung cancer tissues and cells, and overexpression of circ_0000517 was negatively correlated with the prognosis of NSCLC patients. Further study found that circ_0000517 targeted miR-330-5p and miR-330-5p targeted YY1. 	 overexpression of circ_0000517 was negatively correlated with the prognosis of NSCLC patients.	Yes	Silencing of circ_0000517 significantly inhibited the proliferation, glycolysis, and glutamine decomposition of NSCLC cells in vitro and repressed the growth of xenografted tumors in vivo. Moreover, knockdown of circ_0000517 attenuated the expression of PCNA, HK2, LDHA, ASCT2, and GLS1. 	34405943
hsa_circ_0006349	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissues and NSCLC cell lines	Interaction(microRNA-98/MKP1 Axis)	Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay	Circ_0006349 and MKP1 were upregulated, and miR-98 was poorly expressed in the collected tumor tissues and the acquired NSCLC cell lines. Circ_0006349 was identified as a sponge for miR-98 to elevate MKP1 expression. 		Yes	Silencing of circ_0006349 suppressed proliferation and increased apoptosis of Calu-3 and H1299 cells, and it reduced glycolysis, glucose uptake, and the production of lactate in cells. Upon circ_0006349 knockdown, further downregulation of miR-98 or upregulation of MKP1 restored the malignant behaviors of cells.	34604211
circPITX1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Forty-one paired NSCLC tumor tissues and adjacent normal tissues	Interaction(miR-1248/CCND2 Axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	 Circ-PITX1 was upregulated in NSCLC and its silencing could inhibit the proliferation, migration, invasion, cell cycle process, glycolysis, glutamine metabolism, and promote the apoptosis of NSCLC cells in vitro, as well as reduced tumor growth in vivo. In the terms of mechanism, we found that circ-PITX1 could act as a sponge of miR-1248, and miR-1248 could target CCND2.		Yes	 Circ-PITX1 was upregulated in NSCLC and its silencing could inhibit the proliferation, migration, invasion, cell cycle process, glycolysis, glutamine metabolism, and promote the apoptosis of NSCLC cells in vitro, as well as reduced tumor growth in vivo. 	33727831
hsa_circ_0089823	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Sixty-seven NSCLC samples and 18 adjacent non-cancer samples	Interaction(miRNA/SOX4 axis)	Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Colony Formation Assay//IF	Circ_0089823, an up-regulated circRNA (5.4-fold, P = 0.0017), was further investigated through loss-of-function and gain-of-function. Furthermore, SOX4, a tumor-promoting transcription factor, was highly expressed in NSCLC tissues and positively regulated by circ_0089823. Bioinformatic analysis revealed several potential binding sites for miR-507, miR-557, miR-579-3p and miR-1287-5p in circ_0089823 and SOX4 3'-untranslated region, which was later confirmed by luciferase reporter assay.	The circ_0089823 level in NSCLC samples was related to the gender, tumor size, pathological type, TNM stage and smoking history.	Yes	 Knockdown of circ_0089823 suppressed cell proliferation, induced cell cycle arrest and apoptosis of NSCLC cells in vitro. Additionally, circ_0089823-silenced xenografts grew much slowly. On the contrary, its over-expression promoted the malignant behaviors of NSCLC cells.	34311177
hsa_circ_0001287	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue specimens 	Interaction(miR-21/PTEN axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//Colony Formation Assay//Transwell Assay	We reported that circ_0001287 expression was down-modulated in NSCLC tissues and cell lines. Circ_0001287 could adsorb miR-21 and repress its expression, and indirectly up-modulate PTEN expression in NSCLC cells. 	Besides, circ_0001287 low expression was associated with low differentiation and positive lymph node invasion of NSCLC. 	Yes	Circ_0001287 overexpression suppressed the multiplication, migration, invasion, and radioresistance of NSCLC cells, whereas circ_0001287 knockdown promoted the above phenotypes.	33467964
circUSP7	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	Interaction(miR-934.)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ELISA//IHC	The expression levels of circUSP7 were higher in human NSCLC tissues than in matched adjacent nontumour tissues. Increased levels of circUSP7 indicate poor clinical prognosis and CD8+ T cell dysfunction in patients with NSCLC.   Furthermore, circUSP7 inhibits CD8+ T cell function by upregulating the expression of Src homology region 2 (SH2)-containing protein tyrosine phosphatase 2 (SHP2) via sponging miR-934. Finally, we show that circUSP7 may promote resistance to anti-PD1 immunotherapy in NSCLC patients.		Yes	The circUSP7 found in NSCLC patient plasma is predominantly secreted by NSCLC cells in an exosomal manner, and circUSP7 inhibits IFN-γ, TNF-α, Granzyme-B and Perforin secretion by CD8+ T cells. 	34753486
hsa_circ_0008037	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Interaction(miR-433-3p/NUCKS1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	 Circ_0008037 was upregulated in NSCLC tissues and cells. Mechanically, circ_0008037 regulated nuclear ubiquitous casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) expression via sponging miR-433-3p.		Yes	 Circ_0008037 downregulation reduced tumor growth in vivo and repressed proliferation, migration, invasion, and decreased the Warburg effect of NSCLC cells in vitro. 	34850570
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-142-3p/ZFX axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//migration assay//Luciferase Report Assay//Invasion Assay	 Our results showed that circ_0020123 was upregulated in NSCLC, and its knockdown could suppress NSCLC cell proliferation, migration, invasion, and promote apoptosis.  In addition, circ_0020123 silencing inhibited NSCLC tumorigenesis by the miR-142-3p/ZFX axis.		Yes	 Our results showed that circ_0020123 was upregulated in NSCLC, and its knockdown could suppress NSCLC cell proliferation, migration, invasion, and promote apoptosis. 	33633466
hsa_circ_0069244	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC patients	Interaction(miR-346-5p/XPC axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//BrdU	We reported that circ_0069244 was remarkably down modulated in NSCLC and was linked to shorter survival and poor tumor histological grade in NSCLC patients. Furthermore, miR-346-5p was unveiled to be a downstream target of circ_0069244, and miR-346-5p specifically modulated XPC expression. 	We reported that circ_0069244 was remarkably down modulated in NSCLC and was linked to shorter survival and poor tumor histological grade in NSCLC patients.	Yes	Functionally, circ_0069244 repressed NSCLC cell proliferation and migration. 	34228324
circDTL	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC cells	Interaction(miR-1287-5p/GPX4 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay	CircDTL was found to be upregulated and acted as an oncogene in NSCLC cells. It was identified that circDTL exerts its oncogenic effects via the circDTL/miR-1287-5p/GPX4 axis and GPX4 inhibits both ferroptosis and apoptosis. 		Yes	Knockdown of circDTL promoted both apoptosis and ferroptosis of NSCLC cells. Finally, this study showed that silencing of circDTL promoted the sensitivity of NSCLC cells to chemotherapeutic agents and inhibited the growth of tumors in vivo.	34621297
hsa_circ_0000677	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	non-small cell lung cancer (NSCLC) patients	Interaction(microRNA-106b-5p/CCND1 )	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//IF	 Here, we show that circular RNA circ_0000677 was overexpressed and correlated with poor prognosis in non-small cell lung cancer (NSCLC) patients.  In mechanism, circ_0000677 acted as a sponge of microRNA-106b and further regulated CCDND1 gene expression in NSCLC cells by dual luciferase activity assay and their expression examination. 	 Here, we show that circular RNA circ_0000677 was overexpressed and correlated with poor prognosis in non-small cell lung cancer (NSCLC) patients. 	Yes	 Functionally, circ_0000677 knockdown markedly inhibited proliferation of NSCLC cells by observing of immunofluorescence staining of Ki67, clone formation assay, and xenograft experiments. 	34519258
hsa_circ_0074027	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-2467-3p/RHOA )	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	 Circ_0074027 expression was prominently elevated in NSCLC tissues and cell lines. Circ_0074027 interacted with miR-2467-3p, and RHOA was a target of miR-2467-3p in NSCLC cells. RHOA silencing blocked the malignant potential of NSCLC cells. 		Yes	Circ_0074027 knockdown or miR-2467-3p overexpression suppressed cell proliferation, migration and invasion and facilitated cell apoptosis of NSCLC cells. Circ_0074027 silencing restrained the malignant phenotypes of NSCLC cells largely through up-regulating miR-2467-3p. Circ_0074027 knockdown notably blocked xenograft tumor growth in vivo.	33687619
circIGF2BP3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Expression(highly expressed)	Western Blot//CCK8//qRT-PCR//RIP//IP//IHC	We demonstrated that circIGF2BP3 (hsa_circ_0079587) expression was increased in NSCLC and negatively correlated with CD8+ T cell infiltration. Collectively, the PKP3/PD-L1 signature and the infiltrating CD8+ T cell status stratified NSCLC patients into different risk groups.		Yes	Functionally, elevated circIGF2BP3 inactivated cocultured T cells in vitro and compromised antitumor immunity in an immunocompetent mouse model, and this effect was dependent on CD8+ T cells. 	34416901
circPIP5K1A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues, serum samples, and cells	Interaction(miR-101/ABCC1 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_PIP5K1A and ABCC1 were overexpressed and miR-101 was downregulated in NSCLC tissues, serum samples, and cells. MiR-101 was a direct target of circ_PIP5K1A, and its knockdown reversed the effects of circ_PIP5K1A silence on inhibition of NSCLC progression and promotion of cisplatin sensitivity. Moreover, ABCC1 was a downstream target of miR-101, and miR-101 overexpression inhibited the progression of NSCLC cells and increased cisplatin sensitivity by targeting ABCC1. 		Yes	 Knockdown of exosomal circ_PIP5K1A inhibited NSCLC cell proliferation, migration, and invasion and promoted apoptosis and cisplatin sensitivity. Likewise, circ_PIP5K1A downregulation inhibited tumor growth. 	33570734
circGLIS3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-644a/PTBP1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Cell Apoptosis Assay//Invasion Assay//IF	In current study, circGLIS3 was found to be highly expressed in NSCLC tissues and cell lines and high circGLIS3 level was correlated to malignant characteristics and poor prognosis of NSCLC. In conclusion, CircGLIS3 functions as an oncogene via sponging multiple tumor-suppressive miRNAs in NSCLC. A circGLIS3/miR-644a/PTBP1 positive feedback loop exists in the tumorigenesis and development of NSCLC.	In current study, circGLIS3 was found to be highly expressed in NSCLC tissues and cell lines and high circGLIS3 level was correlated to malignant characteristics and poor prognosis of NSCLC.	Yes	Functional experiments suggested that circGLIS3 promoted proliferation, migration and invasion and arrested apoptosis of NSCLC cells in vitro.CircGLIS3 also participated in the in vivo process by accelerate NSCLC tumor growth and metastasis.	33520363
circSLC8A1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-106b-5p /FOXJ3 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	CircSLC8A1 was found to be downregulated in NSCLC tissues and cell lines.Further investigations shown that circSLC8A1 was able to bind to miR-106b-5p as well as inhibit the expression of miR-106b-5p in NSCLC cells. Furthermore, we found that forkhead box J3 (FOXJ3) to be a target gene of miR-106b-5p in NSCLC cells. Knockdown of FOXJ3 reversed the inhibitory effects of miR-106b-5p inhibitor on cell proliferation and invasion.		Yes	Overexpression of circSLC8A1 significantly inhibited the proliferation and invasion of NSCLC cells.	34724864
hsa_circ_0002360	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Expression(highly expressed)	Western Blot//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	We found that circ_0002360 expression was raised in NSCLC tissues. High circ_0002360 expression predicted a short overall survival time for NSCLC patients. MiR-127-5p, miR-145-5p, miR-585-3p, and miR-758-3p were the targets of circ_0002360, and circ_0002360 could regulate MMP16 expression by competitively binding with the above miRNAs. 	We found that circ_0002360 expression was raised in NSCLC tissues. High circ_0002360 expression predicted a short overall survival time for NSCLC patients. 	Yes	Circ_0002360 overexpression promoted NSCLC cell proliferative, migrative, and invasive abilities, and circ_0002360 depletion worked oppositely. 	34747300
circCCND1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer cells and patients	Interaction(miR-187-3p/FGF9 )	qRT-PCR	We observed that circCCND1 was significantly upregulated in lung cancer cells and patients. 		Yes	circCCND1 knockdown attenuated cell proliferation and induced apoptosis under cisplatin treatment.  Mechanistically, circCCND1 interacted with miR-187-3p to regulate reactive oxygen species and FGF9 in NSCLC cells. Finally, miR-187-3p was demonstrated to rescue circCCND1 knockdown-modulated chemoresistance of NSCLC cells. 	33733860
F-circEA1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NCI-H3122 cells 	Interaction(ALK)	Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//Cell Viability Assay//IHC//Invasion Assay//Transwell Assay	Our study confirmed the existence of fusion circEA1 (F-circEA1) in NCI-H3122 cells (carrying the EML4-ALK1 gene), F-circEA1 was expressed both in the cytoplasm and nucleus as determined by fluorescence in situ hybridization (FISH) and Sanger sequencing. 		Yes	CCK8 and transwell assays showed that F-circEA1 was beneficial to cell proliferation, metastasis, and invasion. Overexpression of F-circEA1 can also promote cell proliferation, migration and invasion in A549 and SPCA1 cells (non-small cell lung cancer cell line not carrying the EML4-ALK1 gene). 	34633654
hsa_circ_0008594	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	10 NSCLC tissues and 10 adjacent tissues	Interaction(miR-760)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	A total of 455 dysregulated circRNAs in NSCLC tissues versus adjacent tissues and 353 dysregulated circRNAs in NSCLC tissues with LNM versus those without LNM were discovered.		Yes	Subsequent experiments showed that circ_0008594 promoted H23 and H460 cell proliferation and invasion but affected stemness less and negatively regulated miR-760 via direct binding. 	34858831
circLARP4	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines (including NCI-H1299, NCI-H522, NCI-H23, NCI-H358, and NCI-H1650)	regulation[sponging miR-21-5p]	CCK8//qRT-PCR//Luciferase Report Assay	Circ-LARP4 expression was decreased in NSCLC cell lines (including NCI-H1299, NCI-H522, NCI-H23, NCI-H358, and NCI-H1650) compared with human normal lung epithelial cell line. Circ-LARP4 is decreased and suppresses cell proliferation while promoted apoptosis by sponging miR-21-5p in NSCLC.		Yes	Circ-LARP4 overexpression inhibited cell proliferation while promoted apoptosis in NCI-H1650 cells, whereas circ-LARP4 knockdown increased cell proliferation while decreased apoptosis in NCI-H1299 cells.	32614609
circCDYL	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues, plasma, and cell lines.	Interaction(miR-185-5p)	IHC//Western Blot//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay	The decreased level of circCDYL was observed in NSCLC patients’ tissues and plasma, which was also downregulated in NSCLC cell lines. 		Yes	Forced expression of circCDYL inhibited cell viability, proliferation and induced apoptosis in A549 cells. Luciferase assay verified that circCDYL could bind with miR-185-5p and confirmed that TNRC6A was a downstream target of miR-185-5p. Overexpression of miR-185-5p or silencing of TNRC6A could inhibit the anti-tumor effect of circCDYL in A549 cells via regulating the ERK1/2 signal.	33531835
circTUBA1C	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[sponging miR-143-3p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In the present study, we found that the expression of circTUBA1C was significantly upregulated in NSCLC tissues.Taken together, these findings indicated the important role of circTUBA1C/miR-143-3p axis in NSCLC, which may provide a potential target for NSCLC therapy.		Yes	The loss-of function assays suggested that circTUBA1C deficiency notably hampered cell proliferation as well as accelerated cell apoptosis in NSCLC.	32599139
hsa_circ_0000353	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[ miR-411-5p,FOXO1]	Western Blot//CCK8//qRT-PCR//BrdU//Colony Formation Assay//Transwell Assay	Circ_0000353 was significantly down-regulated in NSCLC tissues and cell lines,Circ_0000353 repressed the proliferation, migration, and invasion of NSCLC cells via inhibition of miR-411-5p and up-regulation of FOXO1.	Circ_0000353 was significantly down-regulated in NSCLC tissues and cell lines, and the decreased expression was significantly linked to the increased clinical stage, larger tumor volume, and metastasis. 	Yes	The circ_0000353 over-expression restrained the proliferation, migration, and invasion of NSCLC cells in vitro.	32568175
hsa_circ_0000284	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-377-3p-mediated PD-L1 promotion]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	As for the biological characterization, circ_0000284 was highly stable and localized in the cytoplasm.Thus, our results unraveled that circ_0000284 facilitated the progression of NSCLC by up-regulating the PD-L1 expression as a competing endogenous RNA (ceRNA) of miR-377, possibly developing a different perspective in understanding the molecular pathogenesis of NSCLC.	 Circ_0000284 was up-regulated in NSCLC and could predict poor prognosis of NSCLC patients.	Yes	Both in vitro and in vivo, down-regulation of circ_0000284 refrained tumorigenesis of NSCLC.	32550825
hsa_circ_0072088	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-377-5p/NOVA2 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	GSE101586 dataset and the analysis of tissue specimens showed that circ_0072088 was aberrantly upregulated in tumor tissues of lung cancer and NSCLC.Circ_0072088 facilitated the proliferation and metastasis of NSCLC cells through upregulating NOVA2 via functioning as a competitive endogenous RNA (ceRNA) for miR-377-5p.		Yes	Circ_0072088 interference caused marked suppression on the proliferation and motility of NSCLC cells.	32524752
hsa_circ_0109320	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues or cells	regulation[MiR-595/E2F7 Axis]	qRT-PCR//Transwell Assay//Western Blot	 The results of present study indicated that circ_0109320 expression in NSCLC patients was upregulated significantly in tumor tissues compared with tissues adjacent to carcinoma. Circ_0109320/miR-595/E2F2 axis may exert a pivotal role in the pathological mechanism of NSCLC progression, and it has potential application in the future treatment of NSCLC.	Upregulated circ_0109320 level was significantly associated with TNM stages as well as lymph node metastasis of NSCLC.	Yes	Moreover, downregulation of circ_0109320 attenuated proliferation and invasion while promoting apoptosis in NSCLC cells.	32508344
circSEC31A	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-520a-5p/GOT-2 axis]	CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	 In this study, we found that hsa_circ_0001421 (circ-SEC31A) was upregulated in NSCLC tissues and cell lines. Mechanistically, we demonstrated that silencing circ-SEC31A downregulated GOT-2 expression by relieving the sponging effect of miR-520a-5p, which resulted in significantly reduced malate-aspartate metabolism in NSCLC cells. 	 Increased circ-SEC31A expression in NSCLC was significantly correlated with malignant characteristics and served as an independent risk factor for the post-surgical overall survival of NSCLC patients.	Yes	Reduced circ-SEC31A expression in NSCLC decreased tumor cell proliferation, migration, invasion, and malate-aspartate metabolism.	32499446
hsa_circ_100565	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[HMGA2 ,miR-506-3p]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Circ_100565 was upregulated in NSCLC, and its high expression was positively associated with the poor overall survival of NSCLC patients.Circ_100565 increased HMGA2 expression to promote proliferation, migration and invasion in NSCLC via absorbing miR-506-3p.	Circ_100565 was upregulated in NSCLC, and its high expression was positively associated with the poor overall survival of NSCLC patients.	Yes	Silencing of circ_100565 suppressed the proliferation, migration and invasion of NSCLC cells in vitro and reduced the tumor growth of NSCLC in vivo.	32425695
circPSMC3	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-182-5p/NME2 Axis]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay	Compared with adjacent normal tissues, the expression of circPSMC3 in NSCLC tissues was decreased. CircPSMC3 inhibits the invasion and migration of NSCLC cells through the miR-182-5p/NME2 signaling pathway.	Lower circPSMC3 expression was closely associated with lymph node metastasis and higher TNM stage in NSCLC patients.	Yes	Biological function analysis suggested that circPSMC3 inhibits the invasion and migration of H1299 cells through upregulating the expression of NME2. 	32386284
hsa_circ_001010	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	interaction[miR-5112,CDK4]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Results showed that the expressions of circRNA_001010 and CDK4 were upregulated in human NSCLC tissues and cells.The bioinformatics prediction and Luciferase assay demonstrated that by sponging with miR-5112, circRNA_001010 can serve as a ceRNA for miR-5112 to further regulate the expression of CDK4.		Yes	qRT-PCR and CCK-8 assay showed that circRNA_001010 expression is associated with the proliferation of NSCLC cells, and that upregulated circRNA_001010 contributed to cell proliferation of A549. Transwell assay showed that circRNA_001010 was associated with the migration ability of tumor cells, and that increased expression of circRNA_001010 promoted the migration and invasion of NSCLC cells. 	32373963
hsa_circ_0087862	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC patients	regulation[miR-1253/RAB3D Axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Transwell Assay	hsa_circ_0087862 was significantly up-regulated in NSCLC patients, which was associated with poor prognosis (P < 0.05).  hsa_circ_0087862 acted as an oncogene in NSCLC by targeting miR-1253/RAB3D.	hsa_circ_0087862 was significantly up-regulated in NSCLC patients, which was associated with poor prognosis (P < 0.05). 	Yes	hsa_circ_0087862 down-regulation prominently weakened NSCLC cells viability, migration, invasion and enhanced apoptosis (P < 0.01).  hsa_circ_0087862 overexpression exhibited the opposite results in NSCLC cells. 	32308420
circBIRC6	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and NSCLC cells	interaction[sponging microRNA-145]	qRT-PCR	We found that circBIRC6 was upregulated in primary human NSCLC tissues and NSCLC cells, whereas its potential target, miR-145, was downregulated. From our data we conclude that circBIRC6 overexpression promotes NSCLC cell progression, possibly by sponging miR-145.		Yes	In A549 NSCLC cells and primary human NSCLC cells, shRNA-induced silencing of circBIRC6 potently inhibited their growth, proliferation, migration and invasion. 	32297303
circCCDC66	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	regulation[miR-33a-5p/KPNA4 axis]	ChIP//Western Blot//Tunel//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In this study, circCCDC66 in NSCLC cells was highly expressed. Briefly, STAT3-induced circCCDC66 upregulation accelerates NSCLC progression via miR-33a-5p/KPNA4 axis, suggesting circCCDC66 as a promising biomarker in NSCLC treatment.		Yes	 Downregulation of circCCDC66 impaired cell proliferation, migration and invasion whereas boosted cell apoptosis in NSCLC.	32151944
hsa_circ_103762	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell	Expression[highly expressed]	CCK8//qRT-PCR	 In our study, circRNA_103762 expression was upregulated in NSCLC tissues and cell.		Yes	 Knockdown of circRNA_103762 can inhibited cell proliferation, migration and invasion in NSCLC.	32118311
circNT5E	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	interaction[sponging microRNA-134]	qRT-PCR//RNA Pull-Down	 We show that circNT5E levels are significantly elevated in human NSCLC tissues and cells, correlating with downregulation of its potential targets, miR-134, miR-422a and miR-338. In A549 and primary NSCLC cells, circNT5E shRNA inhibited cancer cell growth, proliferation and migration, whiling inducing apoptosis activation. Importantly, circNT5E shRNA was ineffective in miR-134-overexpressed A549 cells. Collectively, circNT5E promotes human NSCLC cell progression possibly by sponging miR-134.		Yes	 We show that circNT5E levels are significantly elevated in human NSCLC tissues and cells, correlating with downregulation of its potential targets, miR-134, miR-422a and miR-338. In A549 and primary NSCLC cells, circNT5E shRNA inhibited cancer cell growth, proliferation and migration, whiling inducing apoptosis activation.Conversely, ectopic circNT5E overexpression promoted A549 cell progression in vitro. 	32096481
hsa_circ_0014130	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[miR-136-5p,BCL2]	qRT-PCR//Luciferase Report Assay//Western Blot	"The level of hsa_circ_0014130 was significantly upregulated in NSCLC tissues. In addition, hsa_circ_0014130 functions as a tumor promoter in NSCLC to promote tumor growth through upregulating Bcl-2 partially via ""sponging"" miR-136-5p."		Yes	 Downregulation of hsa_circ_0014130 markedly inhibited the proliferation and invasion of A549 cells via inducing apoptosis. In addition, downregulation of hsa_circ_0014130 inhibited the tumorigenesis of subcutaneous A549 xenograft in mice in vivo. 	32060230
circGFRA1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[circGFRA-miR-188-3p-PI3K/AKT regulatory pathway]	CCK8//qRT-PCR//Colony Formation Assay//RIP	The expression of circGFRA1 and miR-188-3p was detected in NSCLC tissues by RT-qPCR and it was found that circGFRA1 was highly expressed and miR-183-3p was lowly expressed in NSCLC tissues. Our study elaborated a novel circGFRA-miR-188-3p-PI3K/AKT regulatory pathway, providing a potential diagnostic biomarker and therapeutic target for NSCLC.		Yes	Overexpression of cirGFRA1 enhanced NSCLC progression while miR-188-3p overexpression inhibited it by CCK8 and colony formation analysis. In vivo tumor xenograft model, circGFRA1 and miR-188-3p synergistically regulated the proliferation of NSCLC tumors.	32021297
circCDR1as	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-219a-5p/SOX5 axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircCDR1as expression was elevated in NSCLC tissues and cells in comparison to the matched controls.Knockdown of circCDR1as inhibited the progression of NSCLC by decreasing cell viability, migration and invasion and increasing apoptosis by upregulating miR-219a-5p and downregulating SOX5.		Yes	 Interference of circCDR1as led to obvious inhibition of cell viability, migration and invasion and increase of apoptosis in NSCLC cells.	31917898
hsa_circ_0014130	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-142-5p/IGF-1 Axis]	RNA Pull-Down//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	Circ_0014130 was abnormally highly expressed in NSCLC tissues and cells.Our results indicated that the silencing circ_0014130 inhibited NSCLC cell proliferation and promoted cell apoptosis by upregulating miR-142-5p and downregulating IGF-1 expression.		Yes	After shRNA interfering circ_0014130 of NSCLC cells H1299 and A549, the NSCLC cell proliferation was inhibited and the cell apoptosis was promoted. 	31916848
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC specimens and adjacent normal samples	Interaction[miR-488-3p;ADAM9 ]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	We found circ_0020123 was higher in NSCLC samples than the normal counterparts (Fig. 1B). In addition, similar results were found in NSCLC cells compared with 16HBE (Fig. 1C). For the mechanism exploration, circ_0020123 could sponge miR-488-3p to release its inhibition on ADAM9 expression. Moreover, the functional role of circ_0020123 is partly dependent on its regulation of ADAM9 proved by rescue assays. Taken together, our findings provide the possibility that circ_0020123 may be a new target for NSCLC prognosis prediction and therapy.	As Table 1 demonstrated, TNM stage (P = 0.037) and lymph node invasion (P = 0.029) were two circ_0020123 associated clinical factors in the patients with NSCLC. Other clinical features such as smoking status and differentiation grade were not linked to circ_0020123 expression. Kaplan-Meier analysis showed that high level of circ_0020123 was obviously in connection with a decrease in patients’ overall survival (Fig. 1D). Further cox regression analysis demonstrated the independent prognostic role of circ_0020123 in the patients with NSCLC (P = 0.031, Table 2).	Yes	Functionally, silencing of circ_0020123 distinctly sExpression[Expression[up-expression]-expression]pressed the growth, migration and invasion and inhibited the apoptosis of A549 cells. On the contrary, when circ_0020123 expression was ectopically expressed, the above effects were significantly strengthened in H1299 cell line.	31153639
circPRMT5	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cancer and adjacent normal tissues,cell lines(HBE, NSCLC,A549, 95-D, HCC827, H1299,SK-MES-1)	Regulation[miR-377/382/498-EZH2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	As shown in Fig. 1A, circ-PRMT5 was significantly overexpressed in NSCLC tissues in comparison to para-carcinoma normal tissues. Also, the uniformly up-regulated circ-PRMT5 was observed in five NSCLC cell lines as compared with normal human bronchial epithelial HBE cells Overall, our data indicate that circ-PRMT5 is an oncogenic circRNA in NSCLC that can promote the growth of NSCLC via regulation of miR-377/382/498-EZH2 axis.	 	Yes	Stable knockdown of circ-PRMT5 dramatically weakened the proliferative capacities of NSCLC cells both in vitro and in vivo.	31479715
hsa_circ_100146	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC and matched paracancerous tissues,cell lines(16HBE,A549, H446, H1299, 95-D,H460,HEK-293T)	Expression[highly expressed]	Western Blot//qRT-PCR//FISH//Luciferase Report Assay//RNA-seq	Data from the current investigation showed that circRNA 100146 is highly expressed in non-small cell lung cancer (NSCLC) cell lines and the chemically induced malignant transformed bronchial cell line, 16HBE-T, as well as 40 paired tissue samples of NSCLC.  	 	Yes	Suppression of circRNA 100146 inhibited the proliferation and invasion of cells and promoted apoptosis.	30665425
circWHSC1	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues	Interaction(miR-195-5p/FASN/AMPK/mTOR Axis )	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//IHC//Transwell Assay	As shown by the result, circWHSC1 was up-regulated in BC tissues versus adjacent non-tumor tissues.Collectively, CircWHSC1 acted as an oncogene to expedite BC evolvement by modulating the miR-195-5p/FASN/AMPK/mTOR pathway.	circWHSC1 overexpression was correlated with higher tumor stages, lymphatic metastasis and worse survival of BC patients. 	Yes	 Functionally, overexpressing circWHSC1 amplified proliferation, migration and invasion of BC cell lines and boosted xenograft tumor growth in nude mice. 	35070947
hsa_circ_0084927	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell	Interaction(miR-142-3p/ERC1 pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	High levels of circ_0084927 and ERC1 and low levels of miR-142-3p were detected in the BC tissues and cells. miR-142-3p is the target of circ_0084927. Overexpression of miR-142-3p could inhibit BC cell proliferation, colony formation, and cell invasion and induce apoptosis of the BC cells (all P<0.05), and the effects of miR-142-3p knockout on the BC cells could be reversed by silencing circ_0084927. miR-142-3p could target ERC1. Both ERC1 silencing and circ_0084927 knockout in the BC cells could achieve the tumor-suppressing effect, and this effect could be more remarkable under simultaneous ERC1 silencing and circ_0084927 knockout (all P<0.05).		Yes	Knockdown of circ_0084927 promoted apoptosis and inhibited proliferation, colony formation, and invasion of BC cells (all P<0.05), whereas overexpression of circ_0084927 in the BC cells achieved the opposite effects. 	34150003
hsa_circ_0001667	CircRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction(miR-4458/NCOA3 )	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0001667 knockdown inhibited MCF-7/ADM and MDA-MB-231/ADM cell proliferation, migration, invasion and ADM resistance. MiR-4458 was a target of circ_0001667, and its expression was decreased in ADM-resistant tumor tissues and cells. MiR-4458 inhibition reversed the effects of circ_0001667 knockdown. In depth, NCOA3 was a target of circ_0001667, and circ_0001667 knockdown weakened NCOA3 expression by releasing miR-4458.		Yes	Circ_0001667 knockdown inhibited MCF-7/ADM and MDA-MB-231/ADM cell proliferation, migration, invasion and ADM resistance. 	34227151
circYY1	CircRNA	Homo sapiens	Breast Neoplasms	BC TISSUES	Interaction(miR-769-3p/YY1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	CircYY1 and YY1 were upregulated in BC, while miR-769-3p had an opposing result. CircYY1 acted as a sponge for miR-769-3p, which targeted YY1. CircYY1 sponged miR-769-3p to modulate YY1 expression. Both miR-769-3p inhibition and YY1 upregulation antagonized circYY1 silencing-mediated influence on malignancy and glycolysis of BC cells.	Also, BC patients with high circYY1 expression had a poor prognosis. 	Yes	Downregulation of circYY1 decreased xenograft tumor growth in vivo. Both circYY1 inhibition and miR-769-3p elevation constrained BC cell viability, colony formation, migration, invasion, and glycolysis in vitro. 	33603460
circNOL10	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	Regulation(PDCD4)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay	Circ-NOL10 is downregulated in breast cancer and associated with aggressive characteristics and shorter survival time. Furthermore, circ-NOL10 binds multiple miRNAs to alleviate carcinogenesis by regulating PDCD4. CASC3 and metadherin (MTDH) can bind directly to circ-NOL10 with characterized motifs. Accordingly, ectopic expression or depletion of CASC3 or MTDH leads to circ-NOL10 expression changes, suggesting that these two RBPs modulate circ-NOL10 in cancer cells. 	Circ-NOL10 is downregulated in breast cancer and associated with aggressive characteristics and shorter survival time. 	Yes	Upregulation of circ-NOL10 promotes apoptosis, decreases proliferation, and inhibits invasion and migration. 	34729247
hsa_circ_0001598	CircRNA	Homo sapiens	Breast Neoplasms	BC tissue	Interaction(miR-1184/PD-L1 signaling)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	We observed upregulation of circ_0001598 in BC tissues, especially in trastuzumab-resistant BC samples.We further identified that miR-1184 is a functional target of circ_0001598. Moreover, it was found that programmed death-ligand 1 (PD-L1) was a direct target of miR-1184.		Yes	 The oncogenic effects of circ_0001598 in promoting BC cell growth, trastuzumab-resistance, PD-L1 expression, and escaping of CD8 T cell killing were abolished after the restoration of miR-1184.	34559381
hsa_circ_0000517	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cells	Interaction( miR-326)	qRT-PCR//Luciferase Report Assay//Western Blot	Hsa_circ_0000517 was upregulated in breast cancer tissues and cells. Hsa_circ_0000517 acted as a sponge of miR-326 to suppress its expression. miR-326 inhibition abolished the effects of hsa_circ_0000517 knockdown on the malignant behaviors of breast cancer cells.  		Yes	Hsa_circ_0000517 knockdown inhibited cell proliferation, colony formation ability, and invasion and triggered apoptosis in breast cancer cells.	34619576
circABCB10	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction(miR-223-3p/PFN axis )	qRT-PCR//Luciferase Report Assay//Western Blot	CircABCB10 and PFN2 were elevated, while miR-223-3p was reduced in BC tissues and cells.  CircABCB10 sponged miR-223-3p, and PFN2 was a target of miR-223-3p in BC cells.  Besides, circABCB10 knockdown declined PFN2 in BC cells via miR-223-3p. 		Yes	CircABCB10 silencing inhibited cell proliferation, glycolysis, colony formation, and decreased IR resistance in BC cells by modulating miR-223-3p. Meanwhile, circABCB10 depletion restrained xenograft tumor growth in vivo. Also, miR-223-3p overexpression refrained cell proliferation, glycolysis, and colony formation while improving IR sensitivity in BC cells by regulating PFN2. 	32522014
hsa_circ_0001982	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells under hypoxia	Interaction(miR-1287-5p/MUC19 axis)	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay	The levels of circ_0001982 and MUC19 were upregulated, while miR-1287-5p was downregulated in BC tissues and cells under hypoxia.  Mechanistic studies discovered that circ_0001982 could act as a sponge for miR-1287-5p to enhance MUC19 expression in BC cells. In addition, circ_0001982 silencing reduced xenograft tumor growth by regulating miR-1287-5p/MUC19 axis.		Yes	 Knockdown of circ_0001982 hindered glycolysis, cell viability, migration, and invasion of BC cells under hypoxia.	34082777
hsa_circ_0068631	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(EIF4A3/c-Myc axis)	In Vivo Experiment//RNA Pull-Down//IHC//Transwell Assay//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//FISH//RIP//MTT//Colony Formation Assay//IF	In this study, we demonstrate that hsa_circ_0068631, a circRNA generated from the transferrin receptor (TFRC), is upregulated in BC tissues and cell lines. Mechanistically, an RNA pull-down assay and RNA immunoprecipitation assay revealed that eukaryotic translation initiation factor 4A3 (EIF4A3) could bind to hsa_circ_0068631 and c-Myc mRNA. Additionally, the expression of hsa_circ_0068631 was positively correlated with c-Myc, and the upregulation of hsa_circ_0068631 was a crucial factor for the dysregulation of c-Myc. Through an actinomycin D assay, we confirmed that the mRNA stability of c-Myc was influenced by hsa_circ_0068631 and EIF4A3. Furthermore, hsa_circ_0068631 could recruit EIF4A3 to increase c-Myc mRNA stability.		Yes	Knockdown of hsa_circ_0068631 inhibited the proliferation and migration of BC cells in vitro and in vivo. 	34513299
circKLHL24	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-1204/ ALX4 Network)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	 circKLHL24 and ALX4 were downregulated, while miR-1204 was upregulated in breast cancer tissues and cells. miR-1204 bound to ALX4, and circKLHL24 sponged miR-1204 to upregulate ALX4. Cell viability, colony formation, migration/invasion, and glycolysis progression suppressed by miR-1204 deficiency were recovered by ALX4 knockdown. Besides, circKLHL24 blocked tumor growth in vivo by regulating miR-1204 and ALX4. 		Yes	circKLHL24 overexpression blocked cell viability, colony formation, migration/invasion, and glycolysis progression. circKLHL24 competitively targeted miR-1204, and miR-1204 reintroduction reversed the effects of circKLHL24 restoration. 	33781094
hsa_circ_0088088	CircRNA	Homo sapiens	Breast Neoplasms	 tumor tissues and cells	Interaction(miR-135-5p)	RNA Pull-Down//Western Blot//RIP//Luciferase Report Assay//Transwell Assay	hsa_circ_0088088 was upregulated in the tumor tissues and cells, and higher expression presented an unfavorable prognosis. EIF4A3 was found to positively regulate hsa_circ_0088088. Furthermore, we confirmed that hsa_circ_0088088 sponges miR-135-5p and directly targets miR-135-5p with respect to the cell growth and metastasis in MDA-MB-231 cells. 	hsa_circ_0088088 was upregulated in the tumor tissues and cells, and higher expression presented an unfavorable prognosis. 	Yes	 hsa_circ_0088088 overexpression promoted cell growth and metastasis in MDA-MB-231 cells. 	34463003
hsa_circ_0069718	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction(miR-590-5p/NFIB axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Circ_0069718 was up-regulated in BC tissues and cells.Mechanistically, circ_0069718 directly targeted miR-590-5p to up-regulate its target NFIB. Rescue experiments showed that miR-590-5p inhibition reversed the inhibitory effects of circ_0069718 knockdown on BC cell-aggressive oncogenic phenotypes; moreover, miR-590-5p re-expression restrained BC cell proliferation and mobility, which were abolished by NFIB up-regulation.		Yes	Knockdown of circ_0069718 suppressed BC cell apoptosis, migration, and invasion in vitro effectively.Besides that, circ_0069718 silencing hindered tumor growth via miR-590-5p/NFIB axis in vivo. 	34632534
circRPPH1	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-328-3p/HMGA2 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RNA-seq//migration assay//Luciferase Report Assay//Invasion Assay	Circ-RPPH1 expression was elevated and miR-328-3p was decreased in BC tissues and cells.		Yes	Circ-RPPH1 knockdown or miR-328-3p re-expression suppressed cell proliferation, migration, invasion and glycolysis but induced apoptosis in BC in vitro.	34593318
circARL8B	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-653-5p/HMGA2 Axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	CircARL8B was increased in BC tissues and cells. CircARL8B silencing inhibited cell viability, migration, invasion and fatty acid metabolism in BC cells in vitro and blocked tumor growth in vivo. MiR-653-5p was identified as the target of circARL8B and miR-653-5p was negatively modulated by circARL8B. The suppressive role of circARL8B silencing in BC cell progression was abolished by miR-653-5p downregulation. Moreover, HMGA2 was the target gene of miR-653-5p. HMGA2 overexpression abrogated the effect of miR-653-5p on BC cell development. In addition, circARL8B knockdown might block PGE2/PI3K/AKT/GSK-3β/Wnt/β-catenin pathway. Silencing of circARL8B inhibited cell viability, migration, invasion and fatty acid metabolism via miR-653-5p/HMGA2 axis in BC.		Yes	In addition, circARL8B knockdown might block PGE2/PI3K/AKT/GSK-3β/Wnt/β-catenin pathway.Silencing of circARL8B inhibited cell viability, migration, invasion and fatty acid metabolism via miR-653-5p/HMGA2 axis in BC.	34050452
hsa_circ_0005273	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(miR-200a-3p/YAP1 axis )	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//MTT//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	Hsa_circ_0005273 is over-expressed in BC tissues and cell lines, whereas miR-200a-3p expression is repressed.Importantly, hsa_circ_0005273 upregulated YAP1 expression and inactivated Hippo pathway via sponging miR-200a-3p to promote BC progression.		Yes	Depletion of hsa_circ_0005273 inhibited the progression of BC cells in vitro and in vivo, while overexpression of hsa_circ_0005273 exhibited the opposite effect. 	33436041
circACTN4	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(FUBP1 )	RNA Pull-Down//ChIP//Western Blot//ISH//Wound Healing Assay//Co-IP//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Cycle Assay//IHC//Invasion Assay//IF	CircACTN4 was significantly upregulated in breast cancer tissues and cells, its expression was correlated with clinical stage and poor prognosis of patients with BC. Further mechanistic research proved that circACTN4 could competitively bind to far upstream element binding protein 1 (FUBP1) to prevent the combination between FUBP1 and FIR, thereby activating MYC transcription and facilitating tumor progression of breast cancer. Furthermore, we found that upstream transcription factor 2 (USF2) might promote the biogenesis of circACTN4.	CircACTN4 was significantly upregulated in breast cancer tissues and cells, its expression was correlated with clinical stage and poor prognosis of patients with BC. 	Yes	Ectopic expression of circACTN4 strikingly facilitated the growth, invasion, and metastasis of breast cancer cells in vitro and in vivo.Whereas knockdown of circACTN4 revealed opposite roles. 	34116677
hsa_circ_001569	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	In the present study, it was demonstrated that expression levels of circ_001569 were significantly increased in NSCLC tissues compared with in adjacent normal tissues.Therefore, the results indicated that circ_001569 promoted cell proliferation by regulating the Wnt/β-catenin pathway in NSCLC, and circ_001569 may be a potential target of NSCLC treatment.	Increased circ_001569 expression was closely associated with tumor differentiation, lymph node metastasis and Tumor-Node-Metastasis classification in NSCLC. Patients that exhibited higher circ_001569 expression demonstrated a poorer survival outcome compared with patients with lower circ_001569 expression.	Yes	 Functional assay results indicated that the knockdown of circ_001569 inhibited the cell proliferation ability of NSCLC in vitro.	29928432
circMMP11	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells 	Interaction(miR-625-5p/ZEB2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	We found that circMMP11 and ZEB2 were overexpressed in BC tissues and cells compared with controls.Additionally, miR-625-5p, interacted with ZEB2, was a target of circMMP11 in BC cells. CircMMP11 regulated the expression of ZEB2 by targeting miR-625-5p. Knockdown of circMMP11-mediated effects on BC cells could be abolished by overexpression of ZEB2. 		Yes	The suppression of circMMP11 or ZEB2 repressed proliferation, migration, and invasion while induced apoptosis of BC cells. Consistently, silencing of circMMP11 impeded the tumor growth in vivo.	33632213
circRPPH1	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction(miR-542-3p/ARHGAP1 Pathway)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	pregulation of circ_RPPH1 and ARHGAP1, and downregulation of miR-542-3p were detected in BC tissues and cells.  circ_RPPH1 sponged miR-542-3p to upregulate ARHGAP1 expression, thereby affecting BC progression.		Yes	circ_RPPH1 knockdown or miR-542-3p introduction inhibited BC cell proliferation and metastasis, while promoted apoptosis in vitro. circ_RPPH1 sponged miR-542-3p to upregulate ARHGAP1 expression, thereby affecting BC progression. Moreover, depletion of circ_RPPH1 suppressed tumor growth in vivo.	34402683
circDNMT1	CircRNA	Homo sapiens	Breast Neoplasms	The paired tumor and paracancer tissues (n = 41) 	Interaction(miR-485-3p/ZEB1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	Circ-DNMT1 and ZEB1 levels were upregulated in breast cancer, and miR-485-3p was downregulated.  MiR-485-3p was negatively regulated by circ-DNMT1, and miR-485-3p knockdown mitigated the effect of circ-DNMT1 silence on breast cancer development. ZEB1 was targeted via miR-485-3p, miR-485-3p overexpression repressed cell colony formation, migration, and invasion and triggered apoptosis by decreasing ZEB1.		Yes	Circ-DNMT1 knockdown restrained cell colony formation, migration, and invasion and increased apoptosis. MiR-485-3p was negatively regulated by circ-DNMT1, and miR-485-3p knockdown mitigated the effect of circ-DNMT1 silence on breast cancer development. ZEB1 was targeted via miR-485-3p, miR-485-3p overexpression repressed cell colony formation, migration, and invasion and triggered apoptosis by decreasing ZEB1. Circ-DNMT1 silence reduced ZEB1 expression via regulating miR-485-3p. Circ-DNMT1 knockdown reduced xenograft tumor growth.	33403756
circIKBKB	CircRNA	Homo sapiens	Breast Neoplasms	bone-metastatic BC tissues	Regulation(NF-κB/bone remodeling factors signaling)	RNA-seq	We identified that a novel circRNA, circIKBKB, was upregulated significantly in bone-metastatic BC tissues. Mechanically, circIKBKB activated NF-κB pathway via promoting IKKβ-mediated IκBα phosphorylation, inhibiting IκBα feedback loop and facilitating NF-κB to the promoters of multiple bone remodeling factors. Moreover, EIF4A3, acted acting as a pre-mRNA splicing factor, promoted cyclization of circIKBKB by directly binding to the circIKBKB flanking region. 		Yes	Overexpressing circIKBKB enhanced the capability of BC cells to induce formation of bone pre-metastatic niche dramatically by promoting osteoclastogenesis in vivo and in vitro. 	34325714
circHIPK3	CircRNA	Homo sapiens	Breast Neoplasms	Bca tissues	Interaction( miR-326)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Transwell Assay	In BCa, the expression of circHIPK3 was up-regulated and that of miR-326 was down-regulated. MiR-326 was the direct target of circHIPK3, and was inversely correlated with circHIPK3 expression.		Yes	CircHIPK3 knockdown inhibited the cell proliferation, invasion, and migration. MiR-326 was the direct target of circHIPK3, and was inversely correlated with circHIPK3 expression. 	34152928
hsa_circ_0008673	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-153-3p/CFL2 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0008673 and CFL2 expressions were upregulated, while miR-153-3p expression was downregulated in breast cancer tissues and cells compared with adjacent normal breast tissues and cells, respectively. circ_0008673 served as a sponge of miR-153-3p. And circ_0008673 was proved to regulate breast cancer cell malignancy by sponging miR-153-3p. MiR-153-3p was found to modulate breast cancer cell carcinogenesis via targeting CFL2. 		Yes	Circ_0008673 overexpression promoted cell proliferation, migration and invasion, and repressed cell apoptosis, while circ_0008673 silencing had opposite effects. 	34324029
circMETTL3	CircRNA	Homo sapiens	Breast Neoplasms	  breast cancer tissues	Interaction(miR-31-5p/CDK1 axis. )	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Herein, we report circMETTL3, which has not been explored in breast cancer, and it is markedly upregulated in breast cancer. Mechanism investigation showed that circMETTL3 might act as a competing endogenous RNA (ceRNA) of miR-31-5p and upregulate its target cyclin-dependent kinases (CDK1). Moreover, m6A modification of circMETTL3 might affect its expression. 		Yes	Moreover, we uncovered that circMETTL3 could facilitate cell proliferation, migration and invasion in breast cancer. 	33867838
circNOL10	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-767-5p / SOCS2/JAK/STAT signaling)	IHC//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	CircNOL10 was down-regulated in BC tissues and cells. CircNOL10 repressed BC development via inactivation of JAK2/STAT5 signaling by regulating miR-767-5p/SOCS2 axis.	Low expression of circNOL10 was associated with larger tumor size, advanced TNM stage, lymph node metastasis and unfavorable prognosis.	Yes	Overexpression of circNOL10 inhibited cell proliferation, migration, invasion and EMT in vitro and slowed xenograft tumor growth in vivo. 	33397365
hsa_circ_0025202	CircRNA	Homo sapiens	Breast Neoplasms	cancer tissues	Interaction(miR-182-5p/FOXO3a Axis )	Western Blot//Migration Assay//RIP//Luciferase Report Assay//Colony Formation Assay	hsa_circ_0025202, a circRNA that was significantly downregulated, was selected for further investigation. Using a large cohort of clinical specimens, we found that hsa_circ_0025202 exhibited low expression in cancer tissues and was negatively correlated with lymphatic metastasis and histological grade. Bioinformatics and luciferase reporter assays verified that hsa_circ_0025202 could act as a miRNA sponge for miR-182-5p and further regulate the expression and activity of FOXO3a. 		Yes	Gain- and loss-of-function assays indicated that hsa_circ_0025202 could inhibit cell proliferation, colony formation, and migration and increase cell apoptosis and sensitivity to tamoxifen. 	31153828
hsa_circ_0043278	CircRNA	Homo sapiens	Breast Neoplasms	BC cell lines	Interaction(miR-455-3p/EI24 signalling pathway)	Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	sa_circ_0043278 was downregulated in BC cell lines.  Hsa_circ_0043278 expression was negatively correlated with that of miR-455-3p. In addition, mechanistic investigation proved that hsa_circ_0043278 directly bound to miR-455-3p and regulated EI24 and NF-κB expression in BC cells.		Yes	 Furthermore, overexpression of hsa_circ_0043278 notably decreased BC cell viability and inhibited BC cell migration and invasion in vitro and suppressed tumour growth in vivo. Downregulation of hsa_circ_0043278 led to the opposite results. 	34800978
circRGPD6	CircRNA	Homo sapiens	Breast Neoplasms	metastatic breast cancer stem cells	Interaction(miR-26b/YAF2 Axis)	IHC//Microarray	Targeted expression of circRGPD6 via human telomerase reverse transcriptase (hTERT) promoter-driven VP16-GAL4-woodchuck hepatitis virus post-transcriptional regulatory element (WPRE)-integrated systemic amplifier delivery composite vector (TV-circRGPD6) significantly inhibited expression of stem-cell marker CD44 and increased expression of the DNA damage marker p-H2AX.		Yes	Targeted expression of circRGPD6 via human telomerase reverse transcriptase (hTERT) promoter-driven VP16-GAL4-woodchuck hepatitis virus post-transcriptional regulatory element (WPRE)-integrated systemic amplifier delivery composite vector (TV-circRGPD6) significantly inhibited expression of stem-cell marker CD44 and increased expression of the DNA damage marker p-H2AX.	32950105
circHIPK3	CircRNA	Homo sapiens	Breast Neoplasms	Bca cells 	Interaction(miR-326)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	 The circular structure of circHIPK3 was abundantly expressed in the cytoplasm and was up-regulated in BCa. MiR-326 interacted with circHIPK3 and the two were negatively correlated. 		Yes	Silenced circHIPK3 suppressed malignant phenotype of BCa cells.  Overexpressed circHIPK3 promoted cell viability, proliferation, migration and invasion, but inhibited apoptosis. Moreover, overexpressed circHIPK3 promoted the expressions of EMT-related genes and antiapoptotic genes, but inhibited proapoptotic gene expressions.Overexpressed circHIPK3 promoted tumor growth and Ki-67 levels, inhibited apoptosis in vivo. 	34135597
hsa_circ_0000442	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tumor tissues	Interaction(miR-148b-3p/PTEN/PI3K/Akt axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	In this study, the results showed a lower expression of circ_0000442 in breast cancer tumor tissues compared with the adjacent normal tissues. Subsequently, circ_0000442 was found to acted as the sponge of miR-148b-3p in breast cancer cells, thus exerting the tumor-suppressive effects. In the subsequent mechanism study, results showed that miR-148b-3p directly targeted PTEN, a well-known tumor suppressor which negatively regulats PI3K/Akt pathway, thus promoting tumor growth in breast cancer. Overall, this study for the first time identified the tumor-suppressive role of circ_0000442 in breast cancer and found PTEN as a novel direct target of miR-148b-3p. The regulatory role of circ_0000442/miR-148b-3p/PTEN/PI3K/Akt axis was preliminarily confirmed in breast cancer cells and mouse models. 		Yes	Overall, this study for the first time identified the tumor-suppressive role of circ_0000442 in breast cancer and found PTEN as a novel direct target of miR-148b-3p. The regulatory role of circ_0000442/miR-148b-3p/PTEN/PI3K/Akt axis was preliminarily confirmed in breast cancer cells and mouse models. 	32891771
circTFF1	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction(miR-338-3p/FGFR1 Axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Circ-TFF1 was overexpressed in BC tissues and cells. Circ-TFF1 acted as a sponge of miR-338-3p, and the effects of circ-TFF1 knockdown on BC cell proliferation, apoptosis, invasion, and glycolysis were abolished by miR-338-3p inhibition. FGFR1 was confirmed to be a target gene of miR-338-3p, and miR-338-3p played a tumor-suppressive role in BC by targeting FGFR1. 		Yes	 Circ-TFF1 knockdown inhibited cell proliferation, invasion and glycolysis and induced apoptosis in BC cells. 	34219206
circRPPH1	CircRNA	Homo sapiens	Breast Neoplasms	cancerous tissue 	Interaction(miR-512-5p-STAT1 axis)	Western Blot//Wound Healing Assay//FISH//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircRPPH1 expression was higher in the cancerous tissue compared to paired adjacent tissue.  In addition, circRPPH1 was mainly localized in cytoplasm and played the role of miR-512-5p sponge. By sequestering miR-512-5p from the 3'-UTR of STAT1, circRPPH1 inhibited the suppressive role of miR-512-5p, stabilized STAT1 mRNA in BC and finally affected BC progression.		Yes	Further in vitro and in vivo experiments indicated that circRPPH1 acted as an oncogene in BC. 	34873163
hsa_circ_0000511	CircRNA	Homo sapiens	Breast Neoplasms	BC tissue samples and cell line	Interaction(miR‑326/TAZ axis)	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_0000511 abundance was abnormally elevated in BC tissue samples and cell lines compared with in matched normal cases.miR‑326 was a direct target of circ_0000511, and circ_0000511 silencing‑mediated effects in BC cells were largely reversed by the knockdown of miR‑326. miR‑326 directly bound to TAZ mRNA, and TAZ accumulation largely attenuated miR‑326 overexpression‑induced effects in BC cells. 		Yes	Circ_0000511 interference suppressed the proliferation, migration and invasion, and induced apoptosis of BC cells. 	33649821
circNOLC1	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	Interaction(miR-365a-3p /STAT3 axis)	RNA Pull-Down//Western Blot//Migration Assay//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Invasion Assay	The expression of circNOLC1 was induced in breast cancer tissues compared with the non-tumor tissues. Regarding to the mechanism, circNOLC1 functioned as a competing endogenous RNAs (ceRNAs) for microRNA-365a-3p (miR-365a-3p) and the inhibition of miR-365a-3p rescued circNOLC1 depletion-repressed proliferation and cancer stem cell activity of breast cancer. MiR-365a-3p targeted signal transducer and activator of transcription 3 (STAT3) in breast cancer cells and circNOLC1 enhanced STAT3 expression by sponging miR-365a-3p. 		Yes	The silencing of circNOLC1 was able to repress the viability of breast cancer cells. Meanwhile, the numbers of colony formation were suppressed by circNOLC1 knockdown in breast cancer cells. The inhibition of circNOLC1 reduced the invasion and migration ability of breast cancer cells. The mRNA and protein levels of E-cadherin were enhanced but Vimentin levels were reduced by the silencing of circNOLC1. The repression of circNOLC1 decreased the side population (SP) ratio in breast cancer cells. Meanwhile, the sphere formation ability of breast cancer cells was attenuated by the silencing of circNOLC1. The levels of ATP-binding cassette (ABC) superfamily G member 2 (ABCG2), c-Myc, B cell-specific Moloney murine leukemia virus integration site 1 (Bmi1), and SRY-box transcription factor 2 (Sox2) were repressed by the depletion of circNOLC1 in the cells. 	34789263
hsa_circ_0069094	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-661/HMGA1 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	Hsa_circ_0069094 and HMGA1 expression were significantly upregulated, while miR-661 expression level was downregulated in breast cancer tissues and cells relative to adjacent normal breast tissues or MCF-10A cells. Mechanistically, hsa_circ_0069094 regulated HMGA1 by sponging miR-661.		Yes	Functionally, hsa_circ_0069094 knockdown inhibited cell glycolysis, proliferation, migration and invasion, whereas induced cell apoptosis in breast cancer, which was decreased by miR-661 inhibitor.	33929992
circRPPH1	CircRNA	Homo sapiens	Breast Neoplasms	BC patients and cells	Interaction(miR-296-5p/FOXP4 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	According to the results, up-regulation of circRPPH1 was closely correlated with the poor prognosis of BC patients. In addition, circRPPH1 could sponge miR-296-5p to enhance FOXP4 expression in BC cells. miR-296-5p inhibition or FOXP4 overexpression restored the malignant properties of circRPPH1-silenced BC cells. Thus, circRPPH1 promoted BC malignant progression through regulating miR-296-5p/FOXP4 axis, indicating a possible novel therapeutic strategy involving circRNA for BC patients.	According to the results, up-regulation of circRPPH1 was closely correlated with the poor prognosis of BC patients. 	Yes	 Functional experiments showed that knockdown of circRPPH1 repressed BC cell growth, migration, invasion, glycolysis, and in vivo tumor growth.	34377235
circCARM1	CircRNA	Homo sapiens	Breast Neoplasms	 BCSC exosomes	Interaction(miR-1252-5p/PFKFB2)	In Vivo Experiment//Western Blot//CCK8//FISH//RIP//Luciferase Report Assay//Cell Cycle Assay	circCARM1 was higher in BCSC exosomes than it in the parent breast cancer cells.  Further investigation demonstrated that BCSC exosomes circCARM1 played an important role in breast cancer cell glycolysis by miR-1252-5p/PFKFB2. 		Yes	 Further investigation demonstrated that BCSC exosomes circCARM1 played an important role in breast cancer cell glycolysis by miR-1252-5p/PFKFB2. 	35027669
hsa_circ_0048764	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-1296-5p/TRIM14 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 It was revealed that circ_0048764 expression was remarkably up-regulated in BC tissues and cells, and circ_0048764 expression was associated with TNM stage and tumor size.  Mechanistically, circ_0048764 directly targeted miR-1296-5p and could negatively modulate its expression in BC cells. Besides, miR-1296-5p could reverse the influence of circ_0048764 on BC viability, migration, invasion and apoptosis. Moreover, TRIM14 was confirmed to be a downstream target of miR-1296-5p. Circ_0048764 positively regulated TRIM14 expression in BC cells via targeting miR-1296-5p. 	 It was revealed that circ_0048764 expression was remarkably up-regulated in BC tissues and cells, and circ_0048764 expression was associated with TNM stage and tumor size. 	Yes	 Functionally, overexpression of circ_0048764 significantly promoted BC cell proliferative, migrative and invasive abilities and inhibited apoptosis, while circ_0048764 knockdown exerted the opposite effects. 	34787066
circRNF10	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and  NK cells against BC cells	Interaction(miR-934/PTEN/PI3k-Akt Axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//FISH//RNA-seq//Colony Formation Assay//Invasion Assay//Transwell Assay	 In the current study, we discovered that hsa_circ_0028899 (also called circRNF10) was significantly reduced in BC tissues, and a higher level of circRNF10 was markedly related to a favorable prognosis. These data suggest that circRNF10 serves as a molecular sponge for miR-934 to further regulate PTEN expression and PI3k/Akt/MICA signaling in vitro and tumor growth in vivo. 	 In the current study, we discovered that hsa_circ_0028899 (also called circRNF10) was significantly reduced in BC tissues, and a higher level of circRNF10 was markedly related to a favorable prognosis. 	Yes	 The results of CCK8, colony formation, Transwell, ELISA, and NK cell-mediated cytotoxicity assays indicated that increased circRNF10 expression could significantly repress the proliferation, invasion, and migration of BC cells and enhance the killing efficiency of NK cells against BC cells. 	36497344
circPRMT5	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissue, MCF-10A cells	Expression(highly expressed)	CCK8//qRT-PCR//migration assay//Invasion Assay//Transwell Assay	 CircPRMT5 expression in BC tissue was higher than that in adjacent normal breast tissue. Consistently, the expression level of circPRMT5 was also elevated in serum samples collected from BC patients when compared with healthy controls. And in multiple breast cancer cell lines, circPRMT5 was upregulated as compared to normal breast epithelial MCF-10A cells. 	CircPRMT5 expression level was correlated with tumor size, TNM stage, lymph node metastasis distant metastasis, but no correlation was observed with ER, PR, HER2 status. 	Yes	Overexpression of circPRMT5 promoted the proliferation, invasion, and migration of MCF7 cells; while the knockdown of circPRMT5 inhibited cell proliferation, invasion, and migration.	36161608
hsa_circ_0000129	CircRNA	Homo sapiens	Breast Neoplasms	BC samples and cell lines	Interaction( miR-485-3p/SPIN1 )	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 Circ_0000129 was overexpressed in BC samples and cell lines.  Mechanically, circ_0000129 interacted with miR-485-3p to mediate the inhibiting effect of miR-485-3p on SPIN1. Silenced miR-485-3p expression weakened the inhibiting effect of circ_0000129 knockdown on BC cell malignant behaviors. Also, forced SPIN1 expression weakened miR-485-3p upregulation mediated effects on BC cell malignant behaviors.		Yes	 Functionally, circ_0000129 silencing reduced cell proliferation, migration, invasion, and promoted cell apoptosis, as well as induced HUVEC angiopoiesis in vitro. Furthermore, circ_0000129 knockdown decreased BC cell growth in mouse xenograft models.	36426627
circIRAK3	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(miR-603/KIF2A axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	We observed higher levels of circ_IRAK3 in BC tissues and cell lines than their respective controls. Mechanistically, circ_IRAK3 could modulate kinesin family member 2A (KIF2A) expression through acting as a microRNA (miR)-603 sponge. miR-603 silencing impaired the effects of circ_IRAK3 inhibition on the malignant behaviors of BC cells. Also, the repressive effects of miR-603 mimic on the malignant behaviors of BC cells were weakened by KIF2A overexpression.		Yes	 Functional experiments presented that circ_IRAK3 silencing induced BC cell apoptosis, curbed cell proliferation, migration, and invasion in vitro, and decreased tumor growth in vivo.	35164763
hsa_circ_0000514	CircRNA	Homo sapiens	Breast Neoplasms	bc tissues and cell lines	Interaction(miR-296-5p/CXCL10 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//Transwell Assay	We demonstrated that circ_0000514 and CXCL10 expressions were raised in bc tissues and cell lines while miR-296-5p expression was declined.Mechanistically, miR-296-5p was identified as the downstream target of circ_0000514 and could be inhibited by circ_0000514. Moreover, CXCL10 was the target of miR-296-5p, whose expression could be indirectly and positively regulated by circ_0000514.		Yes	Circ_0000514 knockdown could inhibit the proliferation, migration and invasion of bc cells and miR-296-5p overexpression also suppressed the malignant phenotypes of bc cells. 	34528678
circROBO1	CircRNA	Homo sapiens	Breast Neoplasms	BC cells	Interaction( circROBO1/KLF5/FUS)	In Vivo Experiment//RNA Pull-Down//Wound Healing Assay//Migration Assay//CCK8//RIP//RNA-seq//Invasion Assay//ChIP	In this study, upregulated expression of circROBO1 was found in BC-derived liver metastases and was correlated with poor prognosis. Further research revealed that circROBO1 could upregulate KLF5 by sponging miR-217-5p, allowing KLF5 to activate the transcription of FUS, which would promote the back splicing of circROBO1. Therefore, a positive feedback loop comprising circROBO1/KLF5/FUS was formed. More importantly, we found that circROBO1 inhibited selective autophagy of afadin by upregulating KLF5.	In this study, upregulated expression of circROBO1 was found in BC-derived liver metastases and was correlated with poor prognosis. 	Yes	Knockdown of circROBO1 strikingly inhibited the proliferation, migration, and invasion of BC cells, whereas overexpression of circROBO1 showed the opposite effects. Moreover, overexpression of circROBO1 promoted tumor growth and liver metastasis in vivo.	35073911
hsa_circ_0001429	CircRNA	Homo sapiens	Breast Neoplasms	human breast cancer cell lines BT474, SKBr-3, ZR-75-30, and MCF7	Interaction(miR-205/KDM4A )	CCK8	hsa_circ_000 1429 may upregulate the KDM4A gene by adsorbing miR-205. Therefore, it will promote the proliferation, migration, and invasion of breast cancer cells and inhibit their apoptosis.		Yes	hsa_circ_000 1429 may upregulate the KDM4A gene by adsorbing miR-205. Therefore, it will promote the proliferation, migration, and invasion of breast cancer cells and inhibit their apoptosis.	35833065
hsa_circ_0000442	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-1229-3p/ZBTB1 axis)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Circ_0000442 expression was downregulated and miR-1229-3p expression was upregulated in BC tissues and cells.  Circ_0000442 directly interacted with miR-1229-3p. The anti-tumor role of circ_0000442 was attributed to the sponge effect on miR-1229-3p. ZBTB1 was a downstream target for miR-1229-3p. Downregulation of miR-1229-3p blocked the malignant behaviors in BC cells by elevating the expression of ZBTB1. Circ_0000442 regulated the ZBTB1 level by targeting miR-1229-3p, and it inhibited tumor growth of BC in vivo by mediating the miR-1229-3p/ZBTB1 axis. 		Yes	Circ_0000442 repressed proliferation, migration, invasion and glycolysis but promoted apoptosis in BC cells.	35394175
hsa_circ_0069094	CircRNA	Homo sapiens	Breast Neoplasms	tissues and cells of breast cancer	Interaction(miR-758-3p/ZNF217 )	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Hsa_circ_0069094 and ZNF217 were highly expressed, while miR-758-3p was poorly expressed in tissues and cells of breast cancer.  Hsa_circ_0069094 competed with ZNF217 for the binding site of miR-758-3p, and hsa_circ_0069094 positively regulated ZNF217 expression by competitively binding to miR-758-3p. Hsa_circ_0069094 knockdown also blocked solid tumor growth in mice. Collectively, Hsa_circ_0069094 played oncogenic effects in breast cancer by activating the expression of ZNF217 via competitively binding to miR-758-3p, which might be a novel strategy for breast cancer suppression.		Yes	Hsa_circ_0069094 knockdown or ZNF217 knockdown inhibited cell proliferation, invasion and migration and induced cell apoptosis and cell cycle arrest in breast cancer cells. The inhibitory effects of hsa_circ_0069094 knockdown on cell malignant behaviors were abolished by ZNF217 overexpression. 	36356557
hsa_circ_0002082	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cell lines	Interaction(miR-508-3p/CENPF axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	Hsa_circ_0002082 expression was higher in BC tissues and cell lines.Mechanistically, hsa_circ_0002082 targeted miR-508-3p, which was confirmed to be decreased in BC. MiR-508-3p overexpression suppressed BC cell malignant phenotypes, moreover, inhibition of miR-508-3p attenuated the anticancer action of hsa_circ_0002082 silencing on BC cells. Besides that, miR-508-3p targeted CENPF, CENPF was highly expressed in BC, CENPF up-regulation reversed the suppressive impacts of miR-508-3p on BC cell growth and metastasis. 		Yes	 Functionally, knockdown of hsa_circ_0002082 induced apoptosis and suppressed proliferation and metastasis in BC cells in vitro.  Besides, hsa_circ_0002082 silencing impeded BC growth in nude mice.	36161346
hsa_circ_0039960	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction(miR-1178/PRMT7 axis)	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//PCR//Cell Cycle Assay//Bioinformatics Analysis	 The results showed that circ_0039960 and PRMT7 were both up-regulated, while miR-1178 was down-regulated, in BC tissues and cells. Moreover, we validated that circ_0039960 positively mediated PRMT7 expression via directly targeting to miR-1178. The inhibition of miR-1178 and overexpression of PRMT7 reversed the effect of circ_0039960 knockdown on BC cell growth and Warburg effect.		Yes	 Silencing circ_0039960 effectively inhibited cell viability and Warburg effect of BC cells, also, induced cell cycle arrest and apoptosis. 	35597500
hsa_circ_0089153	CircRNA	Homo sapiens	Breast Neoplasms	BCa patients and cells	Interaction(miR-2467-3p/E2F6)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	The up-modulated circ_0089153 indicated an unfavorable survival of BCa patients. circ_0089153 was miR-2467-3p sponge. Low miR-2467-3p expression indicated a worse survival of BCa patients. miR-2467-3p overexpression reduced BCa cells proliferation, migration, invasion and EMT (P < .05). circ_0089153 enhanced BCa cells proliferation, migration, invasion and EMT by sponging miR-2467-3p (P < .05). E2F6 was directly suppressed by miR-2467-3p. E2F6 high expression in BCa patients associated with worse survival. circ_0089153 knockdown suppressed in vivo BCa cells growth and lung metastasis (P < .01). circ_0089153 was an oncogene in breast cancer, which enhanced proliferation and metastasis through sponging miR-2467-3p/E2F6.	The up-modulated circ_0089153 indicated an unfavorable survival of BCa patients. 	Yes	circ_0089153 knockdown attenuated BCa cells proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) (P < .01).	35225430
circEZH2	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(FUS/circEZH2/KLF5/CXCR4 )	In Vivo Experiment	In our research, circEZH2 was proved to be upregulated in liver metastases in BC and predicted the worse prognosis in breast cancer patients. Moreover, circEZH2 could adsorb miR-217-5p to upregulate KLF5 thus leading to activate FUS transcription which would facilitate the back-splicing program of circEZH2. Meanwhile, KLF5 could upregulated CXCR4 transcriptionally to accelerate epithelial and mesenchymal transition of breast cancer.	In our research, circEZH2 was proved to be upregulated in liver metastases in BC and predicted the worse prognosis in breast cancer patients.	Yes	Overexpression of circEZH2 notably accentuated the vitality and invasion of BC cells, whereas knockdown of circEZH2 elicited the literally opposite effects. Besides, overexpressed circEZH2 promoted tumorigenesis and liver metastasis in vivo. 	36224562
hsa_circ_0041732	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction(miR-541-3p/RelA/GLI4 )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	According to experimental results, significant upregulation of circ_0041732 was confirmed in breast cancer tissues and cell lines. E2F4 was proved to transcriptionally modulate circ_0041732.circ_0041732 could sponge miR-541-3p to enhance expression levels of RelA and GLI4, thus activating NFκB and Hedgehog pathways and affecting breast cancer cell proliferation, cell cycle, and apoptosis. In all, E2F4-mediated circ_0041732 could activate RelA/NFκB and GLI4/Hedgehog signaling pathways via modulation on miR-541-3p/RelA/GLI4 to promote breast cancer progression.		Yes	 Moreover, circ_0041732 was validated to accelerate breast cancer cell proliferation and impede G2-M arrest and cell apoptosis, and the oncogenic role of circ_0041732 in breast cancer was further verified via in vivo experiments. 	35838496
hsa_circ_0006014	CircRNA	Homo sapiens	Breast Neoplasms	breast tumor samples and cells	Interaction(miR-885-3p/NTRK2/PIK3CA/AKT axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	In this study, we found higher expression of hsa_circ_0006014 in breast tumor samples than in matched adjacent normal samples, and its expression was positively correlated with histological grade (grade iii). Mechanistically, there were confirmed binding sites between hsa_circ_0006014 and miR-885-3p, and hsa_circ_0006014 promoted breast cancer cell proliferation partially by sponging miR-885-3p and influenced CDK2/CCNE1 and CDK4/6/CCND1. Furthermore, we found that hsa_circ_0006014 regulated NTRK2 through miR-885-3p to modulate the PIK3/AKT signaling pathway. Our results demonstrated that hsa_circ_0006014 promotes breast cancer progression by sponging miR-885-3p to regulate the NTRK2/PIK3CA/AKT axis.	In this study, we found higher expression of hsa_circ_0006014 in breast tumor samples than in matched adjacent normal samples, and its expression was positively correlated with histological grade (grade iii). 	Yes	Phenotypically, hsa_circ_0006014 promoted the proliferation of MDA-MB-231 and MCF-7 breast cancer cells.	35383130
hsa_circ_0067934	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and NSCLC cells 	Expression[highly expressed]	qRT-PCR	The results of the present study demonstrated that the expression levels of circ-0067934 were significantly increased in non-small cell lung cancer (NSCLC) tissues and NSCLC cells compared with that in adjacent normal tissues and a normal human bronchial epithelium cell line, as assessed using reverse transcription-quantitative polymerase chain reaction. 	 Increased expression levels of circ-0067934 were associated with lymph node metastasis and advanced tumor stage in patients with NSCLC. Increased levels of circ-0067934 were significantly associated with the poor overall survival (OS) time of patients with NSCLC compared with low circ-0067934 expression levels, as assessed using Kaplan-Meier estimator survival curves and log-rank tests. 	Yes	The results demonstrated that the proliferative ability was significantly inhibited when circ-0067934 was knocked down in NSCLC cells.	30344708
hsa_circ_0003998	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[hsa_circ_0003998/miR-326/Notch1 pathway ]	qRT-PCR//Luciferase Report Assay	hsa_circ_0003998/miR-326/Notch1 pathway regulates the progression of NSCLC.	Hsa_circ_0003998 upregulation was associated with larger tumor size and lymph node metastasis and also correlated with shorter overall survival of NSCLC patients. 	Yes	Functional experiments showed knockdown of hsa_circ_0003998 restrained cell proliferation and invasion in NSCLC cells.	30237723
hsa_circ_0033155	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissue	Expression[lower expressed]	qRT-PCR	In the present study, it was demonstrated that the expression level of hsa_circ_0033155 was significantly downregulated in NSCLC tissue and the expression of hsa_circ_0033155 correlated with lymphatic metastasis.	In the present study, it was demonstrated that the expression level of hsa_circ_0033155 was significantly downregulated in NSCLC tissue and the expression of hsa_circ_0033155 correlated with lymphatic metastasis.	Yes	 In order to further investigate the possible role of hsa_circ_0033155 in NSCLC progression, circRNA was overexpressed in NSCLC cells and it was observed that the overexpression of hsa_circ_0033155 significantly decreased cell proliferation, colony formation and migration, and elevated the level of phosphatase and tensin homolog deleted on chromosome 10, a tumor suppressor in many types of tumor. 	30214545
hsa_circ_0020123	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cancer tissues	Regulation[hsa_circ_0020123-miR-144-ZEB1/EZH2 axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Herein, a novel functional circRNA hsa_circ_0020123 had been identified in NSCLC progression in this study, and elevated hsa_circ_0020123 expression could be observed in cancer tissues compared with that in matched normal lung tissues.	Moreover, up-regulation of hsa_circ_0020123 was recognized to be closely associated with a poor differentiation degree, lymph node metastasis, a high TNM stage and dismal prognosis for NSCLC patients.	Yes	Typically, knockdown of hsa_circ_0020123 could inhibit the NSCLC growth and metastasis both in vitro and in vivo, which could be reversed by the hsa_circ_0020123 overexpression.	30210911
hsa_circ_0007534	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue samples and cell lines	Expression[highly expressed]	qRT-PCR	The results indicated that hsa_circ_0007534 was up-regulated in both NSCLC tissue samples and cell lines and this up-regulation is linked to lymph node invasion and advanced TNM stage. 	The results indicated that hsa_circ_0007534 was up-regulated in both NSCLC tissue samples and cell lines and this up-regulation is linked to lymph node invasion and advanced TNM stage. Hsa_circ_0007534 could also function as an unfavorable prognostic indicator for the patients with NSCLC. 	Yes	For the part of functional assays, down-regulation of hsa_circ_0007534 suppressed cell growth, migratory and invasive capacities; facilitating cell apoptosis in A549 and H1299 cells. 	30017736
circTFF1	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction( miR-129-2-3p/IRAK1 Axis)	In Vivo Experiment//IHC//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Circ-TFF1 and IRAK1 were significantly high expressed in BC tissues and cells.MiR-129-2-3p was a target of circ-TFF1. Silencing of circ-TFF1 inhibited the malignant behavior of BC cells by releasing miR-129-2-3p. In addition, IRAK1 was a target of miR-129-2-3p. Overexpression of IRAK1 partially restored the inhibitory effect of miR-129-2-3p on cell progression. 		Yes	Silencing of circ-TFF1 reduced the proliferation, migration, invasion and tube formation, while increased the apoptosis of MDA-MB-361 and SK-Br-3 cells. Animal experiments confirmed the anti-tumor effect of circ-TFF1 knockdown in vivo. 	35279761
circBRWD3	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-142-3p_miR-142-5p/RAC1/PAK1 signaling)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	qRT-PCR analysis revealed that circBRWD3 expression was dramatically upregulated in BC tissues, a feature that was positively correlated with the poor prognosis of patients with BC. Further, mechanistic studies elucidated that circBRWD3 sponged both miR-142-3p and miR-142-5p to modulate RAC1 expression, which subsequently activated the RAC1/PAK1 signaling to facilitate the tumorigenesis and progression of BC. 		Yes	CircBRWD3 knockdown repressed cell proliferation and metastasis, while promoting cell apoptosis in vitro. Consistently, an in vivo circBRWD3 deficiency model exhibited suppressed tumor metastasis and oncogenesis. On the other hand, circBRWD3 overexpression promoted cancer cell activity and tumorigenesis.	36443711
hsa_circ_0001583	CircRNA	Homo sapiens	Breast Neoplasms	MCF-7 cells	Regulation	qRT-PCR//MTT//Colony Formation Assay	Functional experiments showed that depletion of circ_0008812 and circ_0001583 could significantly inhibit the proliferation of MCF-7 cells.		Yes	Functional experiments showed that depletion of circ_0008812 and circ_0001583 could significantly inhibit the proliferation of MCF-7 cells.	36200070
hsa_circ_0102273	CircRNA	Homo sapiens	Breast Neoplasms	BC tumor tissues and cells	Interaction(miR-1236-3p/PFKFB3 axis)	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	 Our data showed that circ_0102273 was highly expressed in BC tumor tissues and cells, and its downregulation could inhibit BC cell proliferation, metastasis and glycolysis. PFKFB3 could be targeted by miR-1236-3p, and its expression could be positively regulated by circ_0102273. In addition, miR-1236-3p could suppress BC cell proliferation, metastasis and glycolysis, while this effect could be abolished by PFKFB3. Furthermore, circ_0102273 knockdown also had been discovered to reduce BC tumorigenesis in vivo. 		Yes	MiR-1236-3p was confirmed to be sponged by circ_0102273, and its inhibitor could reverse the negative regulation of sh-circ_0102273 on BC cell proliferation, metastasis and glycolysis. 	35266884
hsa_circ_0001955	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	Interaction(miR-1299/GLUT1 pathway)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Upregulation of circ_0001955 was detected in breast cancer.MiR-1299 was a target of circ_0001955, and its repression reversed the effects of circ_0001955 knockdown. Moreover, circ_0001955 targeted miR-1299 to positively regulate GLUT1 expression. GLUT1 overexpression reversed the effects of miR-1299 enrichment. GLUT1 knockdown was verified to block tumor growth in vivo.		Yes	Knockdown of circ_0001955 inhibited breast cancer cell proliferation, migration, invasion, angiogenesis and glycolysis. 	35174654
hsa_circ_002172	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-296-5p/CXCL12 axis)	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Upregulation of circ_002172 and CXCL12 and downregulation of miR-296-5p occurred in BC tissues and cells.. Circ_002172, as a miR-296-5p sponge, upregulated expression CXCL12. Moreover, Ectopic expression of circ_002172 inhibited cytotoxic T lymphocytes (CTL) infiltration to promote the immune escape of BC. 		Yes	Circ_002172 promoted the oncogenic phenotypes of BC cells in vitro and growth of tumors in vivo, which was reversed by knockdown of CXCL12 expression. 	35240495
circADAM9	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells 	Interaction(miR-383-5p/PFN2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	We found that circ-ADAM9 was upregulated in breast cancer tissues and cells compared to controls.  The functional effects of circ-ADAM9 were related to miR-383-5p, a target of circ-ADAM9. Overexpression of miR-383-5p-mediated malignant behaviors and radiosensitivity of breast cancer cells were dependent on PFN2.		Yes	 Inhibition of circ-ADAM9 expression impaired proliferation, migration, and invasion, but increased radiosensitivity and apoptosis in breast cancer cells; 	36205752
hsa_circ_0008784	CircRNA	Homo sapiens	Breast Neoplasms	TNBC cells	Interaction(miR-506-3p/CTNNB1)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	 It was found that circ_0008784 regulates Wnt/β-catenin signaling pathway, and augments TNBC cell progression via sponging miR-506-3p to modulate catenin beta 1 (CTNNB1). 		Yes	 Circ_0008784 activates Wnt/β-catenin pathway to affect the proliferation and apoptosis of TNBC cells. 	36436315
hsa_circ_0047604	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue	Interaction(miR-548o-DACH1 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	In this work, hsa_circ_0047604 expressed lower in breast cancer tissue and played the role of sponge of miR-548o.By this way, hsa_circ_0047604 could upregulate DACH1 to inhibit breast cancer. 		Yes	 In conclusion, this study revealed that hsa_circ_0047604 acted as a tumor suppressor and regulated breast cancer progression via hsa_circ_0047604-miR-548o-DACH1 axis, which might provide a therapeutic method for breast cancer.	35097124
circSEMA4B	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cell lines	Interaction(miR-330-3p/PDCD4 axis)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Co-IP//qRT-PCR//RIP//MTT//Luciferase Report Assay//ELISA//Colony Formation Assay//Transwell Assay	 Both circSEMA4B and SEMA4B-211aa were remarkably downregulated in BC tissues and cell lines. Of note, SEMA4B-211aa inhibited the generation of PIP3 by binding to p85, thereby inhibiting the phosphorylation of AKT (Thr308). CircSEMA4B inhibited the phosphorylation of AKT (Ser473) through miR-330-3p/PDCD4 axis. 	Low expression of circSEMA4B was positively associated with TNM stage, tumor size, lymph node metastasis, and distant metastasis of BC patients. 	Yes	 The functional investigation showed that circSEMA4B and SEMA4B-211aa could significantly inhibit the proliferation and migration of BC in vivo and in vitro. 	36115854
circHIPK3	CircRNA	Homo sapiens	Breast Neoplasms	 BC cell	Interaction(miR-124-3p/MTDH axis)	IHC//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay	HIPK3s were mainly in forms of circRNAs and were highly expressed in the BC cell derived exosomes, which could be absorbed by the recipient ECs. Furthermore, MTDH was proved to be the responsible gene in this process which was regulated by miR-124-3p, the local miRNA sponged by the exosomal circHIPK3.circHIPK3 enclosed in the BC cell-derived exosomes enhanced MTDH expression in the endothelial cell by sponging miR-124-3p, favoring the tube formation in ECs, which might serve as a therapeutic target for anti-angiogenesis therapy for breast cancer.		Yes	 The cell viability and angiogenesis in ECs were enhanced when treated with circHIPK3s and decreased when treated with circHIPK3-si. 	35460835
circATXN7	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cells	Interaction(miR-149-5p/HOXA11 pathway)	RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 CircATXN7 and HOXA11 levels were enhanced, whereas miR-149-5p level was declined in breast cancer tissues and cells. Additionally, circATXN7 upregulated HOXA11 via absorbing miR-149-5p, thereby inducing breast cancer cell progression and reducing doxorubicin sensitivity.		Yes	CircATXN7 silencing suppressed breast cancer development and doxorubicin resistance. 	34845164
circEPSTI1	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cells	Interaction(circEPSTI1/miR-145/ERBB3 Axis)	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay//Transwell Assay	 CircEPSTI1 was upregulated in the HER2-positive breast cancer tissues and cells.Mechanistically, circEPSTI1 directly targeted miR-145, and miR-145 was a downstream mediator of circEPSTI1 in modulating the proliferation, migration, and invasion of SKBR3 and BT474 cells.  ERBB3 was identified as a direct and functional target of miR-145 in HER2-positive breast cancer cells. 		Yes	Knockdown of circEPSTI1 inhibited SKBR3 and BT474 cell proliferation, migration, and invasion. 	36059813
hsa_circ_0008812	CircRNA	Homo sapiens	Breast Neoplasms	MCF-7 cells	Regulation	qRT-PCR//MTT//Colony Formation Assay	Functional experiments showed that depletion of circ_0008812 and circ_0001583 could significantly inhibit the proliferation of MCF-7 cells.		Yes	Functional experiments showed that depletion of circ_0008812 and circ_0001583 could significantly inhibit the proliferation of MCF-7 cells.	36200070
circRAD54L2	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer cells.	Interaction(miR-888 family/PDK1 axis)	Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay	This study identified and characterized the circRAD54L2 originating from exon 1, 2, 3, and 4 of the RAD54L2 gene. Importantly, we found that circRAD54L2, rather than RAD54L2 linear mRNA, was significantly upregulated in breast cancer cell lines. Furthermore, we found that inhibiting circRAD54L2 expression markedly reduced the invasion, metastasis, and proliferation of breast cancer cells via sponging of the miR-888 family, which downregulated the expression of pyruvate dehydrogenase kinase 1 (PDK1).Our results showed that circRAD54L2 could regulate PDK1 expression by sponging the miR-888 family competing for the ceRNA mechanism, indicating that circRAD54L2 may act as an essential upstream regulator and providing further mechanistic evidence to support the notion that circRAD54L2/miR-888s/PDK1 is a promising therapeutic target in the treatment of breast cancer.		Yes	Furthermore, we found that inhibiting circRAD54L2 expression markedly reduced the invasion, metastasis, and proliferation of breast cancer cells via sponging of the miR-888 family, which downregulated the expression of pyruvate dehydrogenase kinase 1 (PDK1).	36334805
circWAC	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Regulation(miR-599/E2F3 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	CircWAC was up-regulated in BC tissues and cell lines. CircWAC knockdown restrained the proliferation, migration, invasion, and glycolysis and promoted the apoptosis of BC cells. CircWAC acted as miR-599 sponge, and miR-599 interference largely reversed circWAC silencing-induced effects in BC cells. MiR-599 interacted with the 3' untranslated region (3'UTR) of E2F3, and miR-599 overexpression-induced suppressive effect on cellular malignant potential was overturned by the accumulation of E2F3 in BC cells. Eukaryotic initiation factor 4A3 (eIF4A3) induced the expression of circWAC in BC cells. CircWAC knockdown suppressed xenograft tumor growth in vivo. 		Yes	CircWAC knockdown suppressed xenograft tumor growth in vivo. 	34989110
circLARP4	CircRNA	Homo sapiens	Breast Neoplasms	cells	Expression(highly expressed)	Western Blot//CCK8//qRT-PCR//ELISA//Transwell Assay	Results Compared with the control group, circ_LARP4 overexpression group showed an upregulation in the expression of circ_LARP4, decreased cell proliferation, and down-regulated expression of ki67.  It also reported the up-regulated expression of p21, smaller tumor stem cell bullet size, and decreased the expression of OCT4 and SOX2, together with the decreased number of invaded cells, decreased expression of VEGF and N-cadherin, increased expression of E-cadherin, and decreased levels of iNOS and IL-1β.		Yes	Results Compared with the control group, circ_LARP4 overexpression group showed an upregulation in the expression of circ_LARP4, decreased cell proliferation, and down-regulated expression of ki67.  It also reported the up-regulated expression of p21, smaller tumor stem cell bullet size, and decreased the expression of OCT4 and SOX2, together with the decreased number of invaded cells, decreased expression of VEGF and N-cadherin, increased expression of E-cadherin, and decreased levels of iNOS and IL-1β.	35365990
circKDM4B	CircRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	Interaction(miR-675/NEDD4L axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//IP//ELISA//Transwell Assay	 It was significantly decreased in breast cancer tissues compared with adjacent non-tumor tissues. In addition, the overexpression of circKDM4B inhibited cell migration and invasion in vitro, while knockdown of circKDM4B induced the opposite effects. In vivo, circKDM4B suppressed tumor growth and metastasis. Mechanically, circKDM4B sponged miR-675 to upregulate the expression of NEDD4-like E3 ubiquitin protein ligase (NEDD4L), which catalyzes ubiquitination of PI3KCA, thereby inhibiting PI3K/AKT and VEGFA secretion. 		Yes	In addition, the overexpression of circKDM4B inhibited cell migration and invasion in vitro, while knockdown of circKDM4B induced the opposite effects. In vivo, circKDM4B suppressed tumor growth and metastasis.  Additionally, circKDM4B inhibited migration and tube formation of human umbilical vein endothelial cells (HUVECs) in vitro and angiogenesis in vivo.	35145234
circCCDC85A	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction(miR-550a-5p/MOB1A)	Western Blot//Bioinformatics Analysis//Wound Healing Assay//Migration Assay//CCK8//FISH//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The expression of circCCDC85A in breast cancer tissues was obviously lower than that in normal breast tissues. Moreover, enforced expression of circCCDC85A inhibits the oncogenic activity of miR-550a-5p and increases the expression of MOB1A targeted by miR-550a-5p. Further molecular mechanism research showed that circCCDC85A may act as a molecular sponge for miR-550a-5p, thus restoring miR-550a-5p-mediated targeting repression of tumor suppressor MOB1A in breast cancer cells.		Yes	 Over-expression of circCCDC85A substantially inhibited the proliferative, migrative, and invasive ability of breast cancer cells, while knocking down of circCCDC85A enhanced the aforementioned properties of breast cancer cells. 	34983617
hsa_circ_0012673	CircRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction(miR-576-3p/SOX4 Axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Herein, we found that the expression of hsa_circ_0012673 was upregulated in breast cancer tissues and cell lines.Mechanistically, hsa_circ_0012673 sponged miR-576-3p to stabilize SRY-box transcription factor 4 (SOX4), and thereby facilitating breast cancer cell proliferation, migration and invasion. Collectively, our study identified the oncogenic properties of hsa_circ_0012673/miR-576-3p/SOX4 axis in breast cancer, providing potential and exploitable diagnostic and therapeutic molecules for breast cancer.		Yes	Knockdown of hsa_circ_0012673 using RNA interference technique suppressed the proliferation, migration, and invasion of breast cancer cells. 	35794450
circZFR	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(miR-223-3p/FABP7)	In Vivo Experiment//Western Blot//CCK8//Luciferase Report Assay//Transwell Assay	 The expression levels of circ_ZFR and FABP7 were higher in BC tissues and cell lines, whereas miR-223-3p expression was lower. Furthermore, circ_ZFR might act as a sponge for miR-223-3p to regulate FABP7 expression, thereby promoting the progression of BC cells in vitro and in vivo.		Yes	 Knockdown of circ_ZFR or FABP7 in BC cells reduced proliferation, migration, invasion, and epithelial mesenchymal transition (EMT), and induced apoptosis in vitro, whereas the opposite effects were observed in circ_ZFR-overexpressed cells. 	35355424
hsa_circ_0000518	CircRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cell lines	Interaction(miR-1225-3p/SOX4 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	It was revealed that, circ_0000518 and SOX4 mRNA expression levels were up-modulated in BC tissues, while miR-1225-3p expression was down-modulated in BC tissues than that in adjacent tissues. Circ_0000518 was identified as a molecular sponge of miR-1225-3p, and it can up-regulate SOX4 mRNA expression via repressing miR-1225-3p. In conclusion, circ_0000518 is oncogenic in BC and functions through miR-1225-3p/SOX4 axis.		Yes	 Circ_0000518 overexpression or inhibition of miR-1225-3p remarkably enhanced the growth, migration as well as invasion of BC cells in vitro, whereas circ_0000518 knockdown or miR-1225-3p overexpression worked oppositely. 	35112991
circN4BP2L2	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC patients	Expression(lower expressed)	qRT-PCR//ELISA	 Plasma circN4BP2L2 was significantly downregulated in EOC patients.	 Decreased circN4BP2L2 was significantly associated with advanced tumor stage, worse histological grade, lymph node metastasis and distant metastasis in EOC. 	Yes	CircN4BP2L2 inhibited tumor cell migration and invasion in vitro. 	34980005
circATP2B4	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues	Interaction(miR-532-3p/SREBF1/PI3Kα/AKT axis)	qRT-PCR//RNA-seq//FISH	CircATP2B4 was upregulated in EOC tissues and positively correlated with ovarian cancer progression.Mechanistically, EV-packaged circATP2B4 in EOC could be transmitted to infiltrated macrophages and acted as competing endogenous RNA of miR-532-3p to relieve the repressive effect of miR-532-3p on its target SREBF1. Furthermore, circATP2B4 induced macrophage M2 polarization by regulating the miR-532-3p/SREBF1/PI3Kα/AKT axis, thereby leading to immunosuppression and ovarian cancer metastasis. 		Yes	 Functionally, circATP2B4 promoted carcinogenic progression and metastasis of EOC both in vitro and in vivo.	36512324
circRHOBTB3	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cells	Interaction(miR-23a-3p/PTEN)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//FISH	Furthermore, it revealed that circRHOBTB3 could serve as the ceRNA of miR-23a-3p to facilitate PTEN expression, suppress proliferation, G1/S transition, invasion, and promote apoptosis in EOC. 		Yes	Furthermore, it revealed that circRHOBTB3 could serve as the ceRNA of miR-23a-3p to facilitate PTEN expression, suppress proliferation, G1/S transition, invasion, and promote apoptosis in EOC. 	35650643
hsa_circ_100290	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	oral squamous cell carcinoma tissues	Interaction[ miR-378a,GLUT1]	qRT-PCR//Luciferase Report Assay//IHC	Reportedly, hsa_circular RNA (circRNA)_100290 (circ_SLC30A7) is significantly Expression[Expression[up-expression]-expression]regulated (fold change = 6.91, p < 0.0000001) in OSCC. The effect of miR-378a overexpression on OSCC cells was similar to those of circRNA_100290 silence. miR-378a directly bound to circRNA_100290 and GLUT1 3'-untranslated region, circRNA_100290 could remarkably relieve miR-378a-induced inhibition on GLUT1 via acting as a competing endogenous RNA (ceRNA). miR-378a inhibition remarkably attenuated the effect of circRNA_100290 silence on cell proliferation and glycolysis in OSCC cell lines.		Yes	Herein, the expression of circRNA_100290 and GLUT1 remarkably increased in oral tumor tissue specimens and cells.In OSCC cell lines, cell proliferation and glycolysis could be remarkably Expression[down-expression]regulated by circRNA_100290 silence, which could be rescued by GLUT1 overexpression.	31187488
hsa_circ_0007059	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue	Interaction[AKT/mTOR]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//EdU Staining	The circRNA hsa_circ_0007059 was downregulated in OSCC. Subsequently, hsa_circ_0007059 levels in OSCC tissues and cell lines were assessed by quantitative reverse-transcription chain reaction.Furthermore, nude mouse tumor formation was assessed to validate the tumor-sExpression[up-expression]pressive role of hsa_circ_0007059 in vivo. Finally, hsa_circ_0007059 was determined to alter cell growth via AKT/mTOR signaling, representing a potential prognostic/therapeutic target for OSCC.		Yes	 Importantly, hsa_circ_0007059 Expression[up-expression]regulation sExpression[up-expression]pressed cell growth, migration, and invasion, facilitating apoptosis of these cells. 	30680715
hsa_circ_102459	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Expression[lower expressed]	CCK8//Flow Cytometry//EdU Staining//qRT-PCR	 The results revealed that hsa_circRNA_102459 was significantly downregulated and hsa_circRNA_043621 was significantly upregulated in OSCC tissues.	Clinical stage, tumor differentiation, lymph node metastasis presented significant difference in regards to the expression of circRNA_043621 and circRNA_102459. 	Yes	 The in vitro experiments further demonstrated that upregulation of circRNA_102459 or downregulation of circRNA_043621 significantly suppressed TSCC1 cell proliferation, induced cell cycle G0/G1 phase arrest and promoted apoptosis.	31638251
hsa_circ_043621	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Expression[highly expressed]	CCK8//Flow Cytometry//EdU Staining//qRT-PCR	 The results revealed that hsa_circRNA_102459 was significantly downregulated and hsa_circRNA_043621 was significantly upregulated in OSCC tissues.	Clinical stage, tumor differentiation, lymph node metastasis presented significant difference in regards to the expression of circRNA_043621 and circRNA_102459. 	Yes	 The in vitro experiments further demonstrated that upregulation of circRNA_102459 or downregulation of circRNA_043621 significantly suppressed TSCC1 cell proliferation, induced cell cycle G0/G1 phase arrest and promoted apoptosis.	31638251
circPKD2	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Regulation[miR-204-3p/APC2 axis]	qRT-PCR	We found that downregulation of circ-PKD2 in OSCC correlated significantly with aggressive characteristics.In addition, circ-PKD2 was identified as a sponge for miR-204-3p and upregulated the expression of adenomatous polyposis coli 2 (APC2), which was the functional target of miR-204-3p. Moreover, circ-PKD2 attenuated the oncogenic effects of miR-204-3p-mediated APC2 on OSCC progression via multiple signaling pathways.		Yes	 Further analysis revealed that overexpression of circ-PKD2 inhibited OSCC cell proliferation, migration and invasion, induced apoptosis and cell cycle arrest, which were promoted by knockdown of circ-PKD2. 	31206208
circPVT1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues,cell lines	Regulation[circPVT1/miR‑125b axis]	CCK8//qRT-PCR	It was identified that circPVT1 was upregulated in OSCC cells and specimens.Mechanistically, it was demonstrated that circPVT1 possessed two targeting sites of microRNA (miRNA/miR)‑125b and could effectively sponge miR‑125b to release its downstream mRNA targets. Subsequently, the downstream target signal transducer and activator of transcription 3 (STAT3) was verified as a direct target of miR‑125b and STAT3 expression was regulated by the circPVT1/miR‑125b axis. CircPVT1 functioned as competing endogenous RNA (ceRNA) to increase the STAT3 level and cell proliferation through sponging miR‑125b. In conclusion, circPVT1 regulates cell proliferation and may serve as a promising therapeutic target for OSCC patients. Therefore, silencing of circPVT1 could be a future direction to develop a novel treatment strategy.		Yes	Knockdown of circPVT1 suppressed cell proliferation as evidenced by Cell Counting kit‑8 assay and elevated Ki‑67 expression.	31485648
hsa_circ_0005379	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction[EGFR pathway]	Flow Cytometry//qRT-PCR//Western Blot//Transwell Assay	We found that circRNA hsa_circ_0005379 expression is significantly lower in OSCC tissue compared to paired non-cancerous matched tissue and is associated with tumor size and differentiation. Mechanistic studies revealed that hsa_circ_0005379 may be involved in the regulation of the epidermal growth factor receptor (EGFR) pathway. Furthermore, we found that high expression of hsa_circ_0005379 could significantly enhance the sensitivity of OSCC to the cetuximab drug.	We found that circRNA hsa_circ_0005379 expression is significantly lower in OSCC tissue compared to paired non-cancerous matched tissue and is associated with tumor size and differentiation.	Yes	 Overexpression of hsa_circ_0005379 effectively inhibits migration, invasion, and proliferation of OSCC cells in vitro and suppresses OSCC growth in nude mice in vivo.	31035951
hsa_circ_0063772	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Expression[lower expressed]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	The expression of circular RNA hsa_circ_0063772 in OSCC tissues (9.38±0.34) was lower than that in adjacent tissues (11.30±0.31) (t=5.20, P<0.001), and the expression in OSCC cells (SCC15: 0.12±0.01; SCC25: 0.18±0.02; SCC9: 0.21±0.01; CAL27: 0.13±0.01) was significantly lower than that in human keratinocytes (1.02±0.02) (t(SCC15)=41.91, t(SCC25)=29.21, t(SCC9)=35.16, t(CAL27)=41.86, P<0.001).		Yes	Overexpression of hsa_circ_0063772 in SCC15 and CAL27 cells can affect tumor cell proliferation, cell counting assay showed that tumor cell proliferation ability in high expression group (SCC15: 0.76±0.01; CAL27: 0.74±0.02) were lower than empty group (SCC15∶1.22±0.04; CAL27: 0.99±0.03; t(SCC15)=12.58, t(CAL27)=6.97; P<0.05).	31378036
circIGHG	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	interaction[miR-142-5p/IGF2BP3 Signaling]	RNA Pull-Down//Northern Blot//Western Blot//CCK8//FISH//RIP//Luciferase Report Assay//IHC	Transcriptomic analyses identified a circRNA derived from IGHG locus (circIGHG) as significantly upregulated in OSCC and positively associated with poor prognosis of OSCC.Epithelial-mesenchymal transition was the main mechanism through which circIGHG/IGF2BP3 promotes metastasis of OSCC. 		Yes	Knockdown of circIGHG led to impaired expression of IGF2BP3 and attenuated aggressiveness of OSCC cells. 	33203701
circUHRF1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells and tissue	interaction[circUHRF1/miR-526b-5p/c-Myc/TGF-β1/ESRP1 feedback loop]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//qRT-PCR//FISH//RIP//RNA-seq//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Results showed that circUHRF1 was markedly upregulated in the OSCC cells and tissue, besides, the overexpression was closely correlated with the poor prognosis of OSCC patients. In conclusion, our research identified the oncogenic roles of circUHRF1 in the OSCC tumorigenesis and EMT via circUHRF1/miR-526b-5p/c-Myc/TGF-β1/ESRP1 feedback loop, shedding light on the pathogenic mechanism of circUHRF1 for OSCC and providing the potential therapeutic target.		Yes	Functionally, circUHRF1 promoted the proliferation, migration, invasion, and epithelial mesenchymal transformation (EMT) in vitro and the tumor growth in vivo. 	31570856
circSEPT9	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cell lines and tumour tissues	regulation[miR-1225/PKN2 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In this research, we found that circ_SEPT9 was highly expressed in OSCC cell lines and tumour tissues. Our study provides strong evidence that circ_SEPT9/miR-1225/PKN2 axis is a promising target for OSCC treatment.		Yes	Results showed that circ_SEPT9 promoted OSCC proliferation and tumour growth.	33090705
hsa_circ_009755	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues and OSCC cell lines	Expression[lower expressed]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The expression of hsa_circ_009755 was low in OSCC tissues and three OSCC cell lines.		Yes	 Silencing hsa_circ_009755 significantly enhanced the proliferation, migration, and invasion and suppressed the apoptosis of OSCC cells.	32956844
circGDI2	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells	regulation[MiR-424-5p/SCAI Axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our data indicated that circGDI2 was down-regulated in OSCC, and it could be transferred by the exosomes in OSCC cells. The present study had led to the identification of exosomal circGDI2 that regulated OSCC cell malignant behaviors through targeting the miR-424-5p/SCAI axis, highlighting circGDI2 as a novel exosome-based cancer biomarker and therapeutic agent for OSCC treatment.		Yes	 The up-regulation of exosomal circGDI2 weakened OSCC cell proliferation, migration, invasion and glycolysis. 	32943917
hsa_circ_0000199	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	exosomes 	Expression[highly expressed]	qRT-PCR	 Our results showed that the high level of circ_0000199 in circulating exosomes was significantly associated with betel quid chewing, tumor size, lymphatic metastasis, and TNM stage in patients with OSCC.		Yes	Overexpression of circ_0000199 promoted, while knockdown of circ_0000199 inhibited OSCC cell growth.	32792549
circPVT1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	regulation[Circ-PVT1/miR-106a-5p/HK2 axis ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 Circ-PVT1 was expressed with abnormal high level while miR-106a-5p was down-regulated in OSCC tissues and cells. Our works suggested that circ-PVT1 directly combined with miR-106a-5p to mediate HK2 level, consequently regulating cellular behaviors in OSCC as a tumor promoter.		Yes	Circ-PVT1 knockdown reduced OSCC cell growth, metastasis and glycolysis. 	32737775
hsa_circ_002178	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue	regulation[Akt/mTOR pathway]	CCK8//qRT-PCR	Our data showed that circRNA_002178 expression in OSCC tissue specimens was remarkably higher than that in adjacent ones.CircRNA_002178, over-expressed in OSCC tissues and cell lines, may promote the malignant progression of OSCC through activating the Akt/mTOR signaling pathway.	In comparison to patients in low circRNA_002178 expression group, patients in high expression group showed higher incidences of advanced pathological stage and distant metastasis, and a lower overall survival rate. 	Yes	Cell functional experiments revealed that knockdown of circRNA_002178 markedly attenuated the proliferation and migration ability of OSCC cells compared to the sh-NC group, and the consistent results were observed in the nude mouse experiment.	32572877
circMDM2	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue and cells	interaction[miR-532-3p/HK2]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//EdU Staining	Clinically, circMDM2 was overexpressed in OSCC tissue and cells, and the overexpression served as a poor prognostic factor for OSCC patients.  In conclusion, these findings demonstrated that circMDM2/miR-532-3p/HK2 axis promotes the proliferation and glycolysis of OSCC, rendering a potential diagnostic biomarker and prospective therapeutic target for OSCC.	Clinically, circMDM2 was overexpressed in OSCC tissue and cells, and the overexpression served as a poor prognostic factor for OSCC patients. 	Yes	Functionally, cellular experiments confirmed that circMDM2 accelerated OSCC cell proliferation and glycolysis in vitro and circMDM2 knockdown repressed the tumour growth in vivo. 	32410389
hsa_circ_0072387	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells and tissues	regulation[Downregulating miR-503-5p]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	hsa_circ_0072387 expression was significantly downregulated, and miR-503-5p was upregulated in OSCC cells and tissues. hsa_circ_0072387 inhibited OSCC progression by downregulating miR-503-5p, explicating that hsa_circ_0072387 could function as a novel potential therapeutic target for OSCC.		Yes	Gain of hsa_circ_0072387 or knockdown of miR-503-5p suppressed the cell proliferation, migration and invasion, EMT, and glycolysis in OSCC SCC-4 and HSC-3 cells.	32302508
hsa_circ_0001971	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	tumor tissues and cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	The expression of circ_0001971 was significantly increased in tumor tissues and cell lines.		Yes	Circ_0001971 knockdown inhibited cell proliferation, migration, and invasion but promoted cisplatin (DDP) sensitivity and cell apoptosis. 	32196598
hsa_circ_0055538	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	Oral squamous cell carcinoma tissues	Regulation[p53/Bcl-2/caspase signaling pathway]	CCK8//Wound Healing Assay//EdU Staining//Western Blot	Low hsa_circ_0055538 expression levels were verified in tumor tissues and OSCC cell lines.Importantly, nude mouse experiments showed that high expression of hsa_circ_0055538 inhibited tumor growth. Finally, hsa_circ_0055538 may affect the development of OSCC via the p53/Bcl-2/caspase signaling pathway.	Clinical data analysis showed that the expression level is related to the degree of tumor differentiation.	Yes	Lentiviral infection and siRNA transfection of SCC9 and CAL27 cell lines revealed that changes in circRNA expression significantly affected the malignant biological behavior of OSCC cells. 	30857544
hsa_circ_0004491	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC and normal tissue	Expression[Expression[lower expressed]-expression]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	qRT-PCR analysis revealed that hsa_circ_0004491 was significantly Expression[down-expression]regulated in OSCC tissues compared with paired normal tissues (P < 0.001), and this low expression was associated with lymph node metastasis (P = 0.0398; area under ROC curve = 0.7510). 		Yes	Hsa_circ_000449 silencing or overexpression significantly affected the invasion and migration abilities of OSCC cells.	31669576
circSPATA6	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	Interaction( miR-182)	qRT-PCR	CircSPATA6 and TRAF6 were declined, and miR-182 was elevated in OSCC cells. Mechanistically, circSPATA6 could modulate TRAF6 expression through sponging miR-182.		Yes	 Functionally, circSPATA6 impeded migration and invasion, and facilitated cell cycle arrest and apoptosis of OSCC cells. 	33654430
circCEP128	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cells	Interaction(microRNA-515-5p/SDC1 Axis)	qRT-PCR//MTT//Western Blot	 circCEP128 and SDC1 were highly expressed and miR-515-5p was low expressed in bladder cancer tissues and cells. circCEP128 loss increased miR-515-5p expression through direct interaction in bladder cancer cells. MiR-515-5p depletion mitigated the influences of circCEP128 knockdown on bladder cancer cell phenotypes. SDC1 was a direct target of miR-515-5p. circCEP128 positively regulated SDC1 expression via miR-515-5p. 		Yes	circCEP128 knockdown hindered cell proliferation, migration and invasion and promoted cell apoptosis in bladder cancer. 	33833571
circMYLK	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues and cells	Interaction(miR-34a/CCND3 )	qRT-PCR//Western Blot	CircMYLK was highly expressed in bladder cancer tissues and cells.CircMYLK contributed to the malignant development of bladder cancer cells partly through the miR-34a/CCND3 regulatory network, showing the significance of circMYLK in bladder cancer pathogenesis.		Yes	CircMYLK downregulation inhibited bladder cancer cell migration and invasion, and promoted cancer cell apoptosis and cell cycle arrest.	34056735
hsa_circ_0088036	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissues and cell lines	Interaction(miR-140-3p/FOXQ1 signaling)	qRT-PCR//RIP	Upregulated expression of hsa_circRNA_0088036 in BCa tissues and cell lines was positively correlated with overall survival and clinicopathologic characteristics. Mechanistically, hsa_circRNA_0088036 could directly interact with miR-140-3p and act as a miRNA sponge to modulate FOXQ1 expression. Knockdown of hsa_circRNA_0088036 inhibited the proliferation, migration, and metastasis of BCa cells via miR-140-3p/FOXQ1 signaling.	Upregulated expression of hsa_circRNA_0088036 in BCa tissues and cell lines was positively correlated with overall survival and clinicopathologic characteristics. 	Yes	 Knockdown of hsa_circRNA_0088036 inhibited the growth, migration, and invasion of BCa cells both in vivo and in vitro. 	35396504
circLAMA3	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues and cell lines	Interaction(MYC/CDK6)	qRT-PCR//Western Blot	The circular RNA (circRNA) circLAMA3 is significantly downregulated in bladder cancer tissues and cell lines. Mechanistically, circLAMA3 directly binds to and promotes the degradation of MYCN mRNA, thereby reducing the MYCN protein expression in bladder cancer cells. Decreased expression of the MYCN protein inhibits the promoter activity and expression of CDK6. Ultimately, circLAMA3 affects DNA replication by downregulating CDK6, resulting in G0/G1 phase arrest and inhibition of bladder cancer proliferation.		Yes	In this study, functional experiments demonstrated that circLAMA3 significantly inhibited the proliferation, migration, and invasion of bladder cancer cells and inhibited bladder cancer growth in vivo. 	35317525
hsa_circ_3323	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissues 	Interaction(miR-186-5p/APP axis)	qRT-PCR//RNA Pull-Down	The expression of circ3323 was higher in BCa tissues and cells than in normal samples. Mechanistically, we demonstrated that circ3323 acts as a sponge for miR-186-5p and promotes host gene APP's expression. 	miR-186-5p/APP axis	Yes	Experiments in vitro showed that the knockdown of circ3323 inhibited cell proliferation and impeded the metastasis of BCa cells. 	35362879
circFARSA	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC tissues and cell lines	Interaction(microRNA-330-5p)	qRT-PCR//Western Blot	 circFARSA expression was markedly upregulated in BC tissues and cell lines compared with that in normal bladder samples. Downregulating circFARSA expression slowed tumor growth in vivo and directly sponged miR-330 and inhibited its function in BC cells in vitro. Inhibiting miR-330 expression abolished the regulatory effects of circFARSA silencing on the tumor phenotypes of BC cells.		Yes	 Silencing circFARSA expression decreased BC cell proliferation, invasion, and migration but induced their apoptosis in vitro. 	35395756
circNCOR1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction(DDX39B/TGFβ-SMAD )	ISH	Here, we identify an intron-retained circRNA, circNCOR1, that is significantly downregulated in LN metastatic bladder cancer and is negatively associated with poor prognosis of patients.Nuclear retention of circNCOR1 was regulated by small ubiquitin-like modifier (SUMO)ylation of DDX39B, an essential regulatory factor responsible for circRNA nuclear-cytoplasmic transport. Reduced SUMO2 binding to DDX39B markedly increased circNCOR1 retention in the nucleus to suppress bladder cancer LN metastasis. 	Here, we identify an intron-retained circRNA, circNCOR1, that is significantly downregulated in LN metastatic bladder cancer and is negatively associated with poor prognosis of patients.	Yes	 Overexpression of circNCOR1 inhibited lymphangiogenesis and LN metastasis of bladder cancer in vitro and in vivo. 	35395674
circPTK2	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	Bca cell lines	Interaction(circPTK2/PABPC1/SETDB1 axis)	Western Blot//ISH//Bioinformatics Analysis//Transfection//qRT-PCR//RIP//FISH//PCR//IP//IHC//Invasion Assay//IF	 Herein, we identified an upregulated circRNA, circPTK2, which could regulate SETDB1 expression by analyzing the transcriptome by RNA-sequencing.Importantly, using circRNA pulldown assay and RNA-binding protein immunoprecipitation, we identified PABPC1 as a robust novel interacting protein of circPTK2. Mechanistically, circPTK2 could bind to PABPC1 and enhance its ability to stabilize SETDB1 mRNA, thereby specifically promoting SETDB1 expression and facilitating SETDB1-mediated epithelial-mesenchymal transition (EMT). 		Yes	Functionally, overexpression of the circPTK2-SETDB1 axis markedly promoted migration, invasion, and gemcitabine resistance in vitro and enhanced lymph node metastasis in vivo. 	36436682
circSPECC1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 Bca tissues and cell lines.	Interaction(miR-136-5p/GNAS axis)	qRT-PCR//RNA Pull-Down	In this study, we found that circSPECC1 was significantly up-regulated in Bca tissues and cell lines.  Mechanically, circSPECC1 sponged miR-136-5p to promote the mRNA and protein expression of GNAS. Besides, enforced expression of GNAS significantly reversed the proliferation and migration inhibition mediated by circSPECC1 suppression.	 Increased expression of circSPECC1 contribute to poor prognosis of Bca. 	Yes	Further tests showed that knockdown of circSPECC1 impaired the proliferation and migration of Bca cells.	35523104
circSTK39	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues and cell lines	Interaction(miR-135a-5p/NR3C2)	qRT-PCR//Wound Healing Assay//Transwell Assay	In this research, we first found a novel circRNA, circSTK39 (termed as has_circ_0001079), which was a downregulated gene based on the results of high-throughput RNA sequencing. Subsequently, we determined that the expression of circSTK39 in BCa tissues and their cell lines was significantly reduced. In conclusion, our results revealed that circSTK39 inhibited EMT of BCa cells through the miR-135a-5p/NR3C2 axis and may provide promising biomarkers for the diagnosis or prospective therapeutic targets for BCa.	 In addition, lower circSTK39 expression was strongly related to a worse prognosis for BCa patients. 	Yes	Next, we detected the biological functions of circSTK39 by using loss and gain experiments in vitro and in vivo. Ectopic expression of circSTK39 decreased cell proliferation, colony formation, and invasion capacities, while circSTK39 knockdown prevented the above phenotypes. 	36538242
circSHPRH	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa cells and tissues	Interaction(miR-942/BARX2 pathway)	qRT-PCR//Luciferase Report Assay	In this article, we showed that circSHPRH expression was obviously decreased in BCa tissues, compared with adjacent normal tissues. Mechanistic studies demonstrated that circSHPRH could combine with miR-942 and serve as a sponge of miR-942, which targets BARX2 in BCa cells. Rescue experiments showed that suppression of miR-942 or BARX2 overexpression could significantly abrogate the promoting effects of circSHPRH silencing on BCa cell proliferation and invasion. Furthermore, circSHPRH overexpression partly eliminated the suppressive effects of miR-942 on BARX2 expression. In addition, circSHPRH knockdown promoted activation of the Wnt/β-catenin signaling pathway by regulating BARX2. 	Moreover, a low circSHPRH level was positively correlated with a high grade, a high pathological stage, lymphatic metastasis and an unfavorable prognosis for BCa patients. 	Yes	Cell function studies indicated that silencing circSHPRH dramatically increased the proliferation, migration and invasion of BCa cells. 	35200157
hsa_circ_0000658	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissue samples and cell lines	Interaction(miR-498/HMGA2 axis)	qRT-PCR//FISH	 Circ_0000658 was highly expressed in BCa tissue samples and cell lines, which indicated a poor prognosis of BCa patients. Circ_0000658 competitively bound to miR-498 and thus restricted miR-498 expression. Meanwhile, circ_0000658 weakened the binding of miR-498 to the target gene HMGA2 and upregulated the HMGA2 expression. 	 Circ_0000658 was highly expressed in BCa tissue samples and cell lines, which indicated a poor prognosis of BCa patients. 	Yes	Circ_0000658 elevation or miR-498 knockdown augmented oncogenic phenotypes and EMT of BCa cells, corresponding to a reduction in the expression of β-catenin and E-cadherin as well as an increase in the expression of N-cadherin, Slug, Snail, ZEB1 and Twist. Inhibition of HMGA2 reversed the effects of circ_0000658 overexpression on tumor growth in vivo.	35031054
hsa_circ_0139402	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues 	Interaction(hsa-miR-326/PAX8 Signaling)	qRT-PCR//Western Blot	High-throughput sequencing result showed that the expression of hsa_circ_0139402 was highest in BC tissues and increased in metastatic tissues compared to that of nonmetastatic tissues.Bioinformatics analysis, dual-luciferase reporter, and RIP assay showed that hsa_circ_0139402 can bind to hsa-miR-326, and PAX8 is a direct target of hsa-miR-326 in BC cell. 		Yes	MTT assay, wound healing assay, and transwell assay revealed that sh-hsa_circ_0139402 could suppress BC cells' proliferation, invasion, and migration. Further, cytological studies found that hsa_circ_0139402 enhances BC cells' proliferation, migration, and invasion by targeting PAX8 via hsa-miR-326.	35154515
hsa_circ_0002099	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BLCA tissues and cells	Interaction(miR-217-5p/miR-103a-3p/KRAS axis-WNT/β-catenin axis)	CCK8//qRT-PCR//Luciferase Report Assay	The results indicated that Circ_0002099 was significantly upregulated in BLCA and could enhance the progression of BLCA in vivo and in vitro. Furthermore, dual-luciferase reporter assay and FISH assay revealed that Circ_0002099 could regulate miR-217-5p/miR-103a-3p/Kirsten RAS (KRAS) axis in BLCA. In addition, rescue experiments confirmed that miR-217-5p/miR-103a-3p could rescue the facilitative effect of Circ_0002099 on BLCA progression. 		Yes	The results indicated that Circ_0002099 was significantly upregulated in BLCA and could enhance the progression of BLCA in vivo and in vitro. 	36301978
hsa_circ_0000515	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC tissues and cell lines	Interaction(miR-542-3p/ILK axis)	qRT-PCR//Luciferase Report Assay//Western Blot	 Circ_0000515 and ILK expressions were significantly elevated in BC tissues and cell lines, while that of miR-542-3p was dramatically suppressed. Moreover, circ_0000515 knockdown inhibited pulmonary metastasis in vivo. Circ_0000515 was validated to adsorb miR-542-3p, and ILK was testified as the downriver target of miR-542-3p. Circ_0000515 could ascend ILK expression through repressing that of miR-542-3p.		Yes	 Knocking down circ_0000515 could significantly repress the growth, migration and aggressiveness of BC cells while overexpression of circ_0000515 showed opposite effects. 	35029589
circZNF609	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa cell lines and tissues	Interaction(miR-1200/CDC25B pathway)	qRT-PCR//FISH	CircZNF609 expression was increased significantly in BCa cell lines and tissues. Mechanistically, circZNF609 alleviated the inhibition effect on target CDC25B expression by sponging miR-1200. CircZNF609 promoted tumor growth through novel circZNF609/miR-1200/CDC25B axis, implying that circZNF609 has significant potential to act as a new diagnostic biomarker and therapeutic target in BCa. 	For BCa patients, increased expression of circZNF609 was correlated with a worse survival. 	Yes	 In vitro and in vivo, enforced expression of circZNF609 enhanced BCa cells proliferation, migration, and cisplatin chemoresistance. 	35567596
circDHTKD1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell line	Regulation(CXCL5)	qRT-PCR//IHC	 Mechanistically, circDHTKD1 directly interacted with miR-149-5p, and antagonized the repression of miR-149-5p on CXCL5. Furthermore, circDHTKD1-induced CXCL5 expression recruited and activated neutrophils, which participated in lymphangiogenesis by secreting VEGF-C. Our study supports circDHTKD1 as a promising diagnostic and therapeutic target for LN metastasis in BCa.		Yes	By analyzing the co-expression patterns of circDHTKD1 and differentially expressed mRNAs, we identified that circDHTKD1 facilitated lymphangiogenesis by upregulating CXCL5. 	35504887
hsa_circ_0003221	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BLCA cells	Interaction(miR-892b/DHCR24 )	qRT-PCR//RNA Pull-Down	Abnormal circ_0003221 upregulation was affirmed in BLCA. MiR-892b was identified as a target for circ_0003221. Reduction of miR-892b relieved si-circ_0003221-induced anti-tumor response in BLCA cells. In addition, miR-892b targeted DHCR24 and circ_0003221/miR-892b could regulate the level of DHCR24. The effects of si-circ_0003221 were also counteracted by DHCR24 overexpression.		Yes	BLCA cell proliferation, motility and glycolysis were impeded after circ_0003221 level was knocked down. 	36068004
hsa_circ_0002623	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell line	Interaction(miR-1276/SMAD2 axis)	qRT-PCR//Transwell Assay	We reported that, in BCa tissues and cell lines, circ_0002623 was upregulated, whereas miR-1276 was downregulated. Additionally, circ_0002623 could competitively bind with miR-1276 to increase the expression of SMAD2, the target gene of miR-1276. Furthermore, circ_0002623 could regulate the expression of TGF-β and WNT1 via modulating miR-1276 and SMAD2. 		Yes	 Circ_0002623 positively regulated BCa cell proliferation, migration, and cell cycle progression. 	35048477
circFOXO3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tumor and cell lines	Interaction( miR-214)	In Vivo Experiment//Western Blot//CCK8//RIP//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	CircRNA sequencing was conducted in OSCC tumor and tumor-side tissues, and the expression of circFOXO3 is found to be markedly increased in tumor tissues. CircFOXO3 is also highly expressed in several OSCC cell lines compared with human oral keratinocytes.		Yes	Transwell assay and colony formation showed that knockdown of circFOXO3 prevents the invasion and proliferation of oral cancer cells. Via bioinformatic research, miR-214 was found to be the target of circFOXO3 and correlate well with circFOXO3 both in vitro and in vivo. KDM2A was then validated by database analysis and luciferase assay to be the direct target of miR-214. 	34117688
circMTO1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tumor tissues and cells	Interaction(miR-320a)	RNA Pull-Down//ChIP//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	It was found that circMTO1 was upregulated in OSCC tumor tissues and cells. A novel circMTO1/miR-320a/ATRX axis was identified. Our results suggest that circMTO1 modulates ATRX expression to accelerate OSCC progression by sponging miR-320a.		Yes	It was found that circMTO1 knockdown inhibited OSCC cell proliferation, migration, and invasion. 	34738503
hsa_circ_0000052	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Interaction(miR-382-3p/PD-L1 axis)	qRT-PCR//Western Blot//FISH	 Our data demonstrate that circ_0000052 is oncogenic, and the circ_0000052/miR-382-3p/PD-L1 axis is critical in HNSCC progression. 		Yes	In addition to demonstrating that the IFN-γ/JAK2/STAT1 signalling pathway can induce PD-L1 overexpression in HNSCC, a novel mechanism by which upregulated circ_0000052 mediates PD-L1 overexpression was also demonstrated. To do this, circ_0000052 competitively binds to miR-382-3p and alleviates its repression of PD-L1. This leads to overexpression of PD-L1, causing the aggressiveness of the cells.	36515567
hsa_circ_0004872	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues and cells	Interaction(miR-424-5p)	qRT-PCR//Western Blot//RIP//Transwell Assay	The expression of circ_0004872 was significantly downregulated in OSCC tissues and cells, and the overexpression of circ_0004872 inhibited the proliferation, vitality, invasion, and glycolysis of OSCC cells, and promoted apoptosis. The expression of miR-424-5p was greatly upregulated in OSCC tissues and OSCC cells. circ_0004872 can adsorb miR-424-5p in OSCC cells, and circ_0004872 can reverse the promoting effect of miR-424-5p overexpression on the process of OSCC cells.		Yes	The expression of circ_0004872 was significantly downregulated in OSCC tissues and cells, and the overexpression of circ_0004872 inhibited the proliferation, vitality, invasion, and glycolysis of OSCC cells, and promoted apoptosis. 	35576499
circZDBF2	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells 	Interaction(miR-362-5p and miR-500b-5p/RNF145/CEBPB)	CCK8//qRT-PCR//Colony Formation Assay	 CircZDBF2 expressed at a high level in OSCC cells and it accelerated OSCC cell proliferation, migration, invasion as well as EMT (epithelial-mesenchymal transition) process.  Further, circZDBF2 sponged miR-362-5p and miR-500b-5p in OSCC cells to release their target ring finger protein 145 (RNF145). RNF145 expressed at a high level in OSCC cells and circZDBF2 facilitated RNF145 transcription by recruiting the transcription factor CCAAT enhancer binding protein beta (CEBPB). Moreover, RNF145 activated NFκB (nuclear factor kappa B) signaling pathway and regulated IL-8 (C-X-C motif chemokine ligand 8) transcription.		Yes	 CircZDBF2 expressed at a high level in OSCC cells and it accelerated OSCC cell proliferation, migration, invasion as well as EMT (epithelial-mesenchymal transition) process. 	35365168
hsa_circ_0014359	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues and cell lines 	Interaction(miR-149)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	We found that circ_0014359 was highly expressed in the OSCC tissues and cell lines compared to the normal controls (P<0.05).  The circ_0014359 can directly interact with the micro-RNA-149 (miR-149). Inhibition of miR-149 can rescue the inhibitory effects of circ_0014359 knock down on OSCC cells.	The expression of circ_0014359 was associated with the survival of patients (P<0.05). 	Yes	For the OSCC cell lines, circ_0014359 knock down induced apoptosis and inhibited migration, invasion, and epithelial-mesenchymal transition of OSCC cells (P<0.001). In vivo, silencing the circ_0014359 blocked the growth of OSCC tumors. 	35612554
hsa_circ_0005320	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues and cells	Interaction(circ_0005320-miR-486-3p/miR-637 axis )	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Circ_0005320 expression was higher in OSCC tissues and cells. Mechanistically, miR-486-3p or miR-637 were confirmed to be a target of circ_0005320. Moreover, the inhibitory effects of circ_0005320 silencing on OSCC growth were reversed by the inhibition of miR-486-3p or miR-637. We also found that circ_0005320-miR-486-3p/miR-637 axis mediated the activation of JAK2/STAT3 pathway. 		Yes	Knockdown of circ_0005320 suppressed OSCC cell growth, migration, invasion, and induced cell apoptosis in vitro, as well as impeded tumor growth in vivo. 	34967281
circCLK1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC patients and cell lines	Interaction(miR-18b-5p/Y-box protein 2 axis)	Flow Cytometry//qRT-PCR//Western Blot	We found that the expression of circ-CLK1 was significantly higher in OSCC patients and cell lines.However, inhibiting miR-18b-5p or overexpression of Y-box protein 2 (YBX2) can reverse the effect of circ-CLK1 knockdown on OSCC cells. Therefore, circ-CLK1 inhibited the apoptosis of OSCC cells through the miR-18b-5p/YBX2 axis, and these findings suggest that circ-CLK1 could be a potential therapeutic target for OSCC patients.		Yes	 Inhibition of circ-CLK1 reduced the viability and proliferation of OSCC cells while enhancing their apoptosis.	35156507
circGOLPH3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and normal paracancerous tissues	Interaction(miR-145-5p/lysine demethylase 2A (KDM2A) axis)	qRT-PCR//Western Blot	circGOLPH3 expression was upregulated in OSCC. circGOLPH3 downregulation inhibited cell growth, metastasis, and glycolysis in vitro, and in vivo experiments revealed that circGOLPH3 inhibited tumor growth. In addition, circGOLPH3 bound to miR-145-5p and competitively inhibited KDM2A expression, thereby regulating OSCC cell behaviors as well as glycolysis.		Yes	Knockdown of circGOLPH3 inhibited OSCC cell malignant phenotypes and glycolysis	36268878
circMYBL2	CircRNA	Homo sapiens	pancreatic adenocarcinoma	PA tissues and cells	Interaction(miR-19a )	qRT-PCR//Wound Healing Assay//Transwell Assay	Downregulation of circ-MYBL2 and upregulation of miR-19a were observed in PA. In conclusion, circ-MYBL2 was downregulated in PA and it downregulated miR-19a through methylation to suppress PA cell proliferation.		Yes	 In PA cells, circ-MYBL2 decreased the accumulation of miR-19a but increased its RNA gene methylation. Overexpression of circ-MYBL2 decreased PA cell proliferation and movement, while overexpression of miR-19a showed an opposite effect. In addition, circ-MYBL2 suppressed the role of miR-19a in cell proliferation, migration, and invasion. 	35387554
hsa_circ_0002577	CircRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Regulation[regulating miR-197/CTNND1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Here, we showed that hsa_circ_0002577 expression was significantly Expression[Expression[up-expression]-expression]regulated in EC tissues.In mechanism study, we revealed that hsa_circ_0002577 might act as a sponge for miR-197, and CTNND1 was revealed to be a target gene of miR-197. In addition, we revealed that the oncogenic effects of hsa_circ_0002577 were attributed to the regulation of miR-197/CTNND1/Wnt/β-catenin axis. 	and high hsa_circ_0002577 expression was associated with advanced FIGO stage, lymph node metastasis, and poor overall survival rate of EC patients.	Yes	In function assays, we demonstrated that hsa_circ_0002577 knockExpression[down-expression] significantly reduced EC cells proliferation, migration, invasion ability in vitro and decreased tumor growth in vivo. 	31081718
hsa_circ_0075960	CircRNA	Homo sapiens	Endometrial Neoplasms	cell lines	regulation[miR-361-3p/SH2B1]	CCK8//qRT-PCR//Wound Healing Assay//Luciferase Report Assay	We first determined that hsa_circ_0075960 is aberrantly expressed in EC cells.Our cumulative results revealed that the novel tumor regulator hsa_circ_0075960 functioned as a sponge for miR-361-3p/SH2B1 in EC cells and regulated the progression of EC through the modulation of miR-361-3p.		Yes	Then, we uncovered that the downregulation of hsa_circ_0075960 suppressed cell proliferation and promoted cell apoptosis of EC cells, suggesting that hsa_circ_0075960 could inhibit the progression of EC in vitro. 	33356989
hsa_circ_0109046	CircRNA	Homo sapiens	Endometrial Neoplasms	EC tissues,cell line	regulation[microRNA-105/SOX9/Wnt/β-catenin axis]	qRT-PCR	First, high expression of Circ_0109046 was found in EC tissues compared to the adjacent tissues, and it predicted unfavorable prognosis in patients. Similarly, high expression of Circ_0109046 was confirmed in EC cells relative to that in normal endometrial epithelial cells.This study evidenced that Circ_0109046 upregulates SOX9 expression through sponging miR105, leading to activation of Wnt/β-catenin signaling and the malignant growth of EC. This study may offer novel understanding in EC treatment.		Yes	Silencing of Circ_0109046 in AN3-CA cells inhibited proliferation and aggressiveness but increased apoptosis of cells. 	33220169
hsa_circ_0067835	CircRNA	Homo sapiens	Endometrial Neoplasms	endometrial tissues	interaction[sponges miR-324-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	We observed circ_0067835 was markedly elevated in endometrial cancer. In conclusion, circ_0067835 can compete with miR-324-5p, resulting in HMGA1 up-regulation, and therefore induce the development of endometrial cancer.		Yes	 Loss-of-functional assays revealed that circ_0067835 down-regulation significantly repressed RL95-1 and HEC-1B cell proliferation, migration and invasion. 	33169939
hsa_circ_0000043	CircRNA	Homo sapiens	Endometrial Neoplasms	 EC tissues and cells	regulation[miR-1271-5p/CTNND1 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Circ_0000043 and CTNND1 were highly expressed and miR-1271-5p was lowly expressed in EC tissues and cells.Circ_0000043 knockdown inhibited the progression of EC by regulating miR-1271-5p/CTNND1 axis, which might provide a promising circRNA-targeted therapy for EC.		Yes	 Knockdown of circ_0000043 inhibited the progression of EC by inhibiting cell proliferation, migration, invasion and tumor growth (in vivo) and promoting apoptosis.	33128584
circTNFRSF21	CircRNA	Homo sapiens	Endometrial Neoplasms	EC cells and tumor tissues	regulation[miR-1227-MAPK13/ATF2 axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Colony Formation Assay	 In this study, we found that circTNFRSF21 was highly expressed in EC cells and tumor tissues.  Mechanically, we showed that circTNFRSF21 acts as a sponge of miR-1227 in EC cells to rescue MAPK13/ATF2 signaling pathway activity.		Yes	In vitro and in vivo results showed that circTNFRSF21 was linked to increased EC cell growth and EC xenografts formation in nude mice. 	32299063
hsa_circ_0001610	CircRNA	Homo sapiens	Endometrial Neoplasms	 EC samples (n = 30) and cells	Interaction(miR-646-STAT3 axis)	qRT-PCR//Wound Healing Assay//Colony Formation Assay//Transwell Assay	circ_0001610 levels were upregulated in EC samples (n = 30) and cells.  miR-646 is targeted by circ_0001610, and miR-646 inhibition attenuated interference of circ_0001610-mediated suppression of EC development. STAT3 was modulated by miR-646, and miR-646 upregulation restrained EC progression by decreasing STAT3. circ_0001610 silencing reduced STAT3 levels by sponging miR-646 and reduced the growth of xenograft tumor established by EC cells.		Yes	circ_0001610 interference restrained cell proliferation, migration, and invasion, and promoted apoptosis. circ_0001610 downregulation constrained glycolysis through reducing glucose consumption, lactate production, and levels of adenosine triphosphate, extracellular acidification, hexokinase 2, and lactate dehydrogenase A, and increasing oxygen consumption rate. 	33822442
hsa_circ_0075960	CircRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Interaction(miR-202-5p/CTNND1 axis/Wnt/β-catenin)	qRT-PCR//Wound Healing Assay//Western Blot	 Circ_0075960 and CTNND1 were upregulated, while miR-202-5p was downregulated in EC. MiR-202-5p was targeted by circ_0075960 and it directly bound to CTNND1 3'UTR. The inhibition of circ_0075960 knockdown or miR-202-5p enrichment on EC cell proliferation and migration was reversed by miR-202-5p depletion or CTNND1 overexpression, respectively. Circ_0075960 targeted miR-202-5p to positively regulate CTNND1 expression. Moreover, circ_0075960 knockdown weakened the activity of Wnt/β-catenin signaling via targeting the miR-202-5p/CTNND1 axis.		Yes	Knockdown of circ_0075960 induced EC cell apoptosis, suppressed cell proliferation and migration, and repressed tumor growth in animal models. 	36424704
circWDR26	CircRNA	Homo sapiens	Endometrial Neoplasms	EC tissues or cell lines	Interaction(miR-212-3p/MSH2 axis)	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	The expression of circWDR26 in EC tissues or cell lines was higher than in the normal tissue or endometrial epithelial cells.  Mechanistically, circWDR26 targeted and suppressed the expression of miR-212-3p. We further found that MSH2 was the novel target of miR-212-3p and was upregulated by circWDR26 via inhibiting miR-212-3p. In vivo experiment demonstrated that circWDR26 was essential for EC tumor growth.		Yes	 Downregulation of circWDR26 resulted in attenuated proliferation, increased apoptosis, reduced migration and invasion of EC cells. 	35897048
hsa_circ_0000437	CircRNA	Homo sapiens	Endometrial Neoplasms	 EC tissues ands cells	Interaction(miR-626/CDKN1B Axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 Circ_0000437 expression was reduced in EC tissues, and the low expression of circ_0000437 was positively correlated with the lymph node metastasis and high TNM stage of EC patients. Circ_0000437 directly targeted miR-626 and negatively modulated miR-626 expression in EC cells. CDKN1B was identified as the downstream target of miR-626 in EC cells. Besides, CDKN1B overexpression of miR-626 knockdown reversed the effects of knocking down circ_0000437 on EC cells.		Yes	Knocking down circ_0000437 promoted the proliferation, invasion and EMT of EC cells.	35733309
circGNG7	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues andCAL27, CAL33, SCC4, SCC9, HN6, and HN30 cells	Interaction(HSP27-JNK/P38 MAPK signaling)	qRT-PCR	CircGNG7 was predominately localized to the cytoplasm, and its expression was downregulated in both HNSCC tissues andCAL27, CAL33, SCC4, SCC9, HN6, and HN30 cells. Our results revealed that a new intronic circRNA, circGNG7, functions as a strong tumor suppressor and that circGNG7/HSP27-JNK/P38 MAPK signaling is a novel mechanism by which HNSCC progression can be controlled.	 Low expression of circGNG7 was significantly correlated with poor prognosis in HNSCC patients.	Yes	Consistent with this finding, overexpression of circGNG7 strongly inhibited tumor cell proliferation, colony formation, in vitro migration, and in vivo tumor growth.	34498800
circOSBPL10	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-299-3p/CDK6 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	Circ_OSBPL10 was up-regulated in OSCC tissues and cells. Mechanistically, circ_OSBPL10 directly targeted miR-299-3p, and circ_OSBPL10 silencing affected cell functional properties in vitro by up-regulating miR-299-3p. CDK6 was a direct and functional target of miR-299-3p. The circ_OSBPL10/miR-299-3p axis regulated cell functional properties in vitro via CDK6. 		Yes	Silencing of circ_OSBPL10 hindered cell proliferation, cell cycle progression, colony formation, migration, invasion, and promoted apoptosis in vitro and diminished tumor growth in vivo. 	35180547
hsa_circ_0076977	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-802/MYO6)	qRT-PCR//Western Blot//Colony Formation Assay//Transwell Assay	Circular (circ)_0076977 was abnormally up-regulated in OSCC tissues and cell lines. miR-802 was a direct target of circ_0076977, and circ_0076977 knockdown restrained OSCC progression largely by up-regulating miR-802. miR-802 directly interacted with myosin VI (MYO6) mRNA, and MYO6 was negatively modulated by miR-802 in OSCC cells. miR-802 overexpression reduced the malignant potential of OSCC cells largely by down-regulating MYO6. Circ_0076977 could up-regulate MYO6 expression by absorbing miR-802 in OSCC cells.		Yes	Circ_0076977 absence inhibited the proliferation, angiogenesis, migration, and invasion and induced the apoptosis of oral squamous cell carcinoma (OSCC) cells. Circ_0076977 knockdown blocked xenograft tumor growth. 	36265392
circGDI2	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-454-3p/FOXF2 Axis)	qRT-PCR	CircGDI2 was a stable circRNA and was low expressed in OSCC tissues and cells.  MiR-454-3p could be sponged by circGDI2, and its overexpression could mitigate the suppressive effects of circGDI2 overexpression on OSCC progression. Meanwhile, circGDI2 positively regulated FOXF2 expression by targeting miR-454-3p.		Yes	CircGDI2 overexpression could effectively inhibit the proliferation, migration, invasion and promote apoptosis in OSCC cells, and suppress OSCC tumor growth in nude mice in vivo.	33603482
circPVT1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-143-3p/SLC7A11 axis )	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	CircPVT1 and SLC7A11 were upregulated, while miR-143-3p was downregulated in OSCC tissues and cells. CircPVT1 upregulated SLC7A11 expression via sponging miR-143-3p. SLC7A11 upregulation alleviated the effect of circPVT1 knockdown on OSCC cell progression. Besides, circPVT1 modulated MAPK signaling pathway by regulating miR-143-3p.		Yes	Silencing of circPVT1 or SLC7A11 suppressed proliferation, migration, and invasion and promoted apoptosis in OSCC cells. 	35624316
circKIAA0907	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	59 paired OSCC cancer tissues and adjacent normal tissues 	Interaction(miR-96-5p/UNC13C axis)	qRT-PCR//RNA Pull-Down//RIP//Western Blot	Circ-KIAA0907 was a stability circRNA with lowly expression in OSCC. In the terms of mechanism, circ-KIAA0907 could sponge miR-96-5p to regulate UNC13C expression. MiR-96-5p overexpression could reverse the inhibitory effect of circ-KIAA0907 on OSCC progression, and UNC13C knockdown also could overturn the suppressive effect of miR-96-5p inhibitor on OSCC progression. Animal experiments revealed that circ-KIAA0907 could reduce the tumor growth of OSCC by regulating the miR-96-5p/UNC13C axis.		Yes	Overexpressed circ-KIAA0907 could inhibit migration, invasion, and glycolysis, while promoting apoptosis and radiosensitivity in OSCC cells. 	33715625
circLPAR3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-643/HMGB2 Network)	qRT-PCR//Western Blot	Our data showed that circLPAR3 was highly expressed in OSCC tissues and cells.On the mechanism, we discovered that circLPAR3 could sponge miR-643 to positive regulate HMGB2. MiR-643 overexpression had an inhibition effect on OSCC progression, and its inhibitor could reverse the negative regulation of circLPAR3 knockdown on OSCC progression. In addition, overexpressed HMGB2 also reversed the suppressive effect of circLPAR3 silencing on OSCC progression. 		Yes	 CircLPAR3 silencing suppressed OSCC cell proliferation, metastasis and stemness, while promoted apoptosis.	34528144
hsa_circ_0004674	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction(microRNA-377-3p/THBS1 axis)	qRT-PCR//RIP	 Circ_0004674 and THBS1 levels were enhanced while miR-377-3p level was reduced in OSCC. Down-regulating Circ_0004674 restricted the growth of CAL27 cells in vivo and in vitro.  Restoring miR-377-3p, the target gene of Circ_0004674, destroyed CAL27 cell progression and tumor growth. miR-377-3p suppression rescued the effects of down-regulated Circ_0004674 on OSCC. THBS1 was negatively mediated by miR-377-3p.		Yes	 Down-regulating Circ_0004674 restricted the growth of CAL27 cells in vivo and in vitro. 	33621591
hsa_circ_0036988	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Expression(lower expressed)	CCK8//qRT-PCR	Hsa_circ_0036988 was significantly downregulated in OSCC tissues compared with adjacent normal tissues. Furthermore, the altered expression of hsa_circ_0036988 have an impact on the epithelial-to-mesenchymal transition (EMT)-related protein expression levels.	While low expression of hsa_circ_0036988 was highly correlated with lymph nodes metastasis. 	Yes	 Overexpression or knockdown of hsa_circ_0036988 significantly affected the proliferation, migration and invasion of OSCC cells.	33896837
circKRT1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Interaction(miR-495-3p/PDL1 axis)	qRT-PCR//RNA Pull-Down//RIP//Western Blot	CircKRT1 and PDL1 were highly expressed in OSCC tissues and cells. CircKRT1 sponged miR-495-3p and miR-495-3p targeted PDL1. OSCC progression and immune evasion were regulated by circKRT1 via the miR-495-3p/PDL1 axis. CircKRT1 also facilitated OSCC progression in vivo by regulating miR-495-3p and PDL1.		Yes	CircKRT1 knockdown repressed OSCC cell growth, migration, invasion, epithelial-mesenchymal transition, and CD8+ T-cell apoptosis, but enhanced CD8+ T cytotoxicity and percentage. The inhibitory effects of circKRT1 downregulation on OSCC progression and immune evasion were related to PDL1 expression inhibition. 	33675276
circBCL11B	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-579/LASP1 axis)	CCK8	We demonstrated that circBCL11B was significantly upregulated in OSCC tissues and cell lines, and the expression level was correlated with the malignancy. miR-145 was identified as a downstream target mediating the effect of circBCL11B by targeting LASP1. miR-145 negatively regulated LASP1 expression, which could be rescued by miR-145 inhibitor. Collectively, our study uncovered a functional role of circBCL11B/miR-579/LASP1 axis in OSCC.	We demonstrated that circBCL11B was significantly upregulated in OSCC tissues and cell lines, and the expression level was correlated with the malignancy. 	Yes	Silencing cirCBCL11B inhibited cell proliferation and migration, and also included cell apoptosis in OSCC cells. 	34288804
hsa_circ_0060927	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	NOM, OLK, and OSCC	Interaction(miR-195-5p/TRIM14 axis)	RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 The expression of hsa_circ_0060927 increased in NOM, OLK, and OSCC. The prediction of ceRNA network suggested that hsa_circ_0060927 could regulate the target gene TRIM14 through sponging miR-195-5p. AGO2 RIP indicated that hsa_circ_0060927 had a sponge mechanism. RNA pull-down and dual luciferase reporter gene assay suggested that hsa_circ_0060927 interacted with miR-195-5p.		Yes	Overexpression of hsa_circ_0060927 enhanced the ability of cell proliferation and migration, and decreased cell apoptosis capacity. 	35087744
hsa_circ_0001461	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cell lines and tumor tissues.	Interaction(miR-145/TLR4/NF-κB axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay	In this study, we confirmed that circ_0001461 was highly expressed in OSCC cell lines and tumor tissues. Mechanistically, we found circ_0001461 regulates OSCC cell proliferation, migration and invasion through sponging miR-145. Furthermore, circ_0001461 promotes the resistance of TNF-α-induced apoptosis of OSCC cells by modulating miR-145/TLR4/NF-κB pathway. 		Yes	Knocking down of circ_0001461 suppressed cell proliferation, migration and invasion in vitro, and repress xenograft tumor growth in vivo. 	34119822
circLPAR3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction(miR-513b-5p/VEGFC and AKT1)	CCK8//qRT-PCR//IHC	circ_LPAR3 was upregulated in OSCC. Circ_LPAR3 promoted VEGFC and AKT1 activity by sponging miR-513b-5p in OSCC cells.		Yes	Its knockdown in cells could decrease cell survival and mobility and in mice model, could inhibit the tumor growth and angiogenesis. 	34922206
circDHTKD1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-326/GAB1)	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//Transwell Assay	 Our expression analysis revealed that circDHTKD1 was upregulated in OSCC tissues and cells.Additionally, circDHTKD1 served as a microRNA-326 (miR-326) sponge and the function of circDHTKD1 was achieved by sponging miR-326 in OSCC cells. Also, miR-326 inhibited OSCC development via targeting GRB2-associated-binding protein 1 (GAB1).		Yes	circDHTKD1 knockdown was shown to impede OSCC cell growth and metastasis but motivate apoptosis. 	34287578
circCDR1as	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-876-5p/SLC7A11 )	qRT-PCR//Transwell Assay	CircCDR1as level was aberrantly elevated in OSCC tissues and cells. CircCDR1as directly targeted miR-876-5p and miR-876-5p interacted with SLC7A11. MiR-876-5p overexpression reversed the effects of circCDR1as elevation on OSCC cell autophagy, cell cycle, growth, motility, and apoptosis. 		Yes	Overexpression of circCDR1as promoted autophagy, cell cycle, proliferation, and metastasis and repressed apoptosis in OSCC cells.	34817912
hsa_circ_0011946	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cellsOSCC tissues and cells	Interaction(miR-216a-5p/BCL2L2 axis)	qRT-PCR//MTT//RNA Pull-Down//Western Blot	Circ_0011946 and BCL2L2 levels were increased, while miR-216a-5p level was decreased in OSCC tissues and cells. Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells. Circ_0011946 functioned as a sponge for miR-216a-5p, and BCL2L2 was targeted by miR-216a-5p. Besides, miR-216a-5p or BCL2L2 knockdown partly attenuated the inhibitory influences of circ_0011946 silence or miR-216a-5p overexpression on OSCC cell progression. Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo.		Yes	Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells.Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo.	34620126
circHIPK3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-381-3p-YAP1)	qRT-PCR//Western Blot//Transwell Assay	CircHIPK3 was elevated in OSCC tissues and cell lines, and decrease of circ-HIPK3 suppressed OSCC cell proliferation, invasion, migration and induced apoptosis in vitro as well as inhibited tumor growth in vivo. Rescue assay indicated circ-HIPK3 silence mediated OSCC progression inhibition by sponging miR-381-3p, which was a target of circ-HIPK3. Furthermore, miR-381-3p directly interacted with YAP1 and miR-381-3p inhibition could attenuate YAP1 deletion-induced suppression on cell malignant biological behavior in OSCC. Meanwhile, co-expression analysis showed circ-HIPK3 could regulate YAP1 expression by competing for miR-381-3p.		Yes	Rescue assay indicated circ-HIPK3 silence mediated OSCC progression inhibition by sponging miR-381-3p, which was a target of circ-HIPK3. 	33737493
circFOXK2	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	oral squamous cell carcinoma	Interaction(m6A-dependent IGF2BP3/GLUT1 axis)	MeRIP-seq	Here, m6A-circRNA epitranscriptomic microarray analysis revealed a high-expressed m6A-modified circFOXK2 (hsa_circ_0000816, from FOXK2 gene) in oral squamous cell carcinoma (OSCC).  Methylated RNA immunoprecipitation sequencing (MeRIP-Seq) demonstrated that a remarkable m6A modified site was installed on glucose transporter 1 (GLUT1) mRNA. Mechanistically, circFOXK2 promoted the GLUT1 mRNA stability through cooperating with insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in a m6A-dependent manner.		Yes	 For the biofunctions of OSCC, results revealed that circFOXK2 promoted the malignant phenotypes of OSCC cells. 	36127411
hsa_circ_0005050	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	Interaction(miR-23a-3p/miR-625-5p/STAT3 axis/ JAK/STAT3 signaling pathway)	RNA Pull-Down//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 According to the collected data, circ_0005050 was significantly up-regulated in OSCC cells compared to normal cells.As for mechanism analyses, circ_0005050 knockdown led to the reduction of STAT3 expression and JAK/STAT3 signaling pathway activity. Moreover, circ_0005050 competitively bound to miR-23a-3p and miR-625-5p to up-regulate STAT3, thus prompting malignant behaviors of OSCC cells.		Yes	Circ_0005050 depletion hampered proliferative ability of OSCC cells while promoting cell apoptotic ability. 	36155326
hsa_circ_0001971	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	Interaction(miR-186-5p/FNDC3B axis)	RIP//qRT-PCR//Bioinformatics Analysis	Our study displayed that circRNA_0001971 and FNDC3B were elevated in OSCC, whereas miR-186-5p was declined in OSCC.  In OSCC cells, circRNA_0001971 sponged miR-186-5p to enhance FNDC3B. Due to the interaction between circRNA_0001971, miR-186-5p, and FNDC3B, FNDC3B overexpression relieved the negative function of silencing circRNA_0001971 in OSCC cells.		Yes	Silencing circRNA_0001971 attenuated the malignancy of OSCC cells by suppressing proliferation, migration, and invasion.	35060189
hsa_circ_0049396	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC tissues and cells	Interaction(miR-663b/ENDOU axis)	qRT-PCR//RIP	 The expression of circ_0049396 and ENDOU was downregulated in OSCC tissues and cells, whereas miR-663b was upregulated. MiR-663b mimic enhanced the migratory and proliferative abilities of OSCC cells, but suppressed apoptosis. Furthermore, circ_0049396 or ENDOU overexpression partially reversed the malignant behavior of miR-663b-overexpressing OSCC cells.		Yes	 Circ_0049396 overexpression weakened OSCC cell proliferation and migration but enhanced their apoptosis. Circ_0049396 overexpression suppresses tumorigenesis in vivo. 	36581129
hsa_circ_0004491	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-2278/GNAS)	Western Blot//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	 Circ_0004491 was downregulated in OSCC tissues and cell lines. Circ_0004491 acted as a molecular sponge for miR-2278, and circ_0004491 overexpression-mediated effect was partly reversed by miR-2278 mimic in OSCC cells. MiR-2278 interacted with the 3'UTR of GNAS. Circ_0004491 contributed to GNAS level by sponging miR-2278 in OSCC cells. GNAS knockdown restored miR-2278 inhibitor-mediated effect in OSCC cells.		Yes	 Circ_0004491 overexpression suppressed the proliferation, migration and invasion whereas facilitated the apoptosis of OSCC cells.Circ_0004491 overexpression repressed xenograft tumor growth in vivo.	36643221
hsa_circ_0006948	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	Interaction( N-cadherin)	CCK8//qRT-PCR	 Circ_0006948 was upregulated in BC tissues and cell lines.  The key protein in the EMT signaling E-cadherin was upregulated by knockdown of circ_0006948 in BC cells, while N-cadherin, Vimentin, β-catenin and MMP-9 were downregulated. The interaction between circ_0006948 and N-cadherin was identified, and they were co-responsible for the malignant development of BC.	 High level of circ_0006948 indicated advanced tumor stage, high rates of lymph node metastasis and distant metastasis, and poor prognosis in BC. 	Yes	. Knockdown of circ_0006948 reduced proliferative and metastatic abilities in BC cells. 	34565009
hsa_circ_100984	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Interaction(miR‐432‐3p/ c‐Jun/YBX‐1/β‐catenin feedback loop)	qRT-PCR//RIP	 Here, we found that circ_100984 and YBX‐1 were high presented, while miR‐432‐3p was low presented in BC. Mechanistically, we revealed that circ_100984 served as a competing endogenous RNA that sponged miR‐432‐3p to indirectly regulate YBX‐1 and epithelial‐mesenchymal transition (EMT)‐related molecules. Moreover, we confirmed that YBX‐1 or c‐Jun acted as a transcription regulatory factor for β‐catenin or YBX‐1, respectively, in BC cells. Knockdown of YBX‐1 inhibited the expression of β‐catenin and c‐Jun, whereas downregulated c‐Jun inversely repressed the expression of YBX‐1 and β‐catenin.		Yes	Silencing of circ_100984 and YBX‐1 repressed BC tumor growth, migration, and invasion in vitro and in vivo.	33314480
circZFR	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa cell lines	Interaction(miR-545 and miR-1270)	qRT-PCR//Western Blot	The expression of CircZFR was up-regulated both in BCa tissues and in BCa cell lines, and was positively correlated with patient survival rates.On the other hand, overexpression of target miRNA supported that circZFR directly interact with miR-545 and miR-1270. Moreover, we demonstrated that circZFR promotes the progression of BCa by upregulating WNT5A's expression via sponging miR-545 and miR-1270.	The expression of CircZFR was up-regulated both in BCa tissues and in BCa cell lines, and was positively correlated with patient survival rates.	Yes	Blocking of circZFR's expression by RNA inhibitors suppressed the proliferation, migration and invasion of BCa cells both in vitro and in vivo. 	33928018
hsa_circ_0001756	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines 	Regulation( IGF2BP2-mediated RAB5A expression)	qRT-PCR//RNA Pull-Down//Co-IP	Herein, we detected the expression of hsa_circ_0001756 in OC tissues and cell lines with RT-qPCR assay, which showed that hsa_circ_0001756 was upregulated in OC tissues and cell lines. Moreover, RNA pull-down assay verified the binding between hsa_circ_0001756 and IGF2 mRNA binding protein 2 (IGF2BP2), and rescue experiments indicated that IGF2BP2 overexpression reversed the effects of has_circ_0001756 knockdown on OC cell functions. Co-IP assay verified IGF2BP2 could interact with RAB GTPase 5A (RAB5A) protein. 		Yes	We found that hsa_circ_0001756 knockdown inhibited OC cell proliferation, invasion and EMT. 	35113003
hsa_circ_0063804	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC patients and cells	Interaction(miR-1276/CLU axis)	CCK8//qRT-PCR//Western Blot	Circ_0063804 expression was up-regulated in OC patients and indicated poor prognosis (P < 0.05). Circ_0063804 had a stable circle structure.  CLU was directly inhibited by miR-1276 and up-regulated in OC patients. Circ_0063804 exacerbated malignant phenotype and resistance to cisplatin of OC cells in vitro by enhancing CLU expression via sponging miR-1276 (P < 0.01). Circ_0063804 silencing inhibited OC cells growth, resistance to cisplatin and Ki67 expression in vivo (P < 0.01).	Circ_0063804 expression was up-regulated in OC patients and indicated poor prognosis (P < 0.05). Circ_0063804 had a stable circle structure. 	Yes	Circ_0063804 enhanced proliferation, resistance to cisplatin and reduced apoptosis of OC cells (P < 0.01). miR-1276 was down-regulated in OC patients and sponged by circ_0063804. 	35687899
circRNF144B	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR-342-3p/FBXL11 )	In Vivo Experiment//qRT-PCR//FISH	 CircRNF144B was elevated in OC tissues with low autophagy levels, and associated with poor prognosis. Mechanistically, circRNF144B acts as a sponge for miR-342-3p and inhibits miR-342-3p-induced degradation of lysine demethylase 2 A (FBXL11) mRNA, leading to elevated FBXL11 protein levels. Elevated FBXL11 promoted the ubiquitination and degradation of Beclin-1, thus inhibiting autophagy. 	 CircRNF144B was elevated in OC tissues with low autophagy levels, and associated with poor prognosis. 	Yes	CircRNF144B promoted the malignant biological properties of OC cells, and inhibited the autophagy. 	36209140
circFNDC3B	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Regulation[miR-1178-3p/G3BP2/SRC/FAK axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//FISH	We found that circFNDC3B was dramatically downregulated in BC tissues and correlated with pathological T stage, grade, lymphatic invasion and patients' overall survival rate. Mechanistically, circFNDC3B could directly bind to miR-1178-3p, which targeted the 5'UTR of the oncogene G3BP2. Moreover, circFNDC3B acted as a miR-1178-3p sponge to suppress G3BP2, thereby inhibiting the downstream SRC/FAK signaling pathway.	We found that circFNDC3B was dramatically downregulated in BC tissues and correlated with pathological T stage, grade, lymphatic invasion and patients' overall survival rate. 	Yes	 Functionally, overexpression of circFNDC3B significantly inhibited proliferation, migration and invasion both in vitro and in vivo.	30458784
circUBXN7	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues 	Regulation[circUBXN7-miR-1247-3p-B4GALT3 regulatory network]	Western Blot//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Here, we identified a novel circular RNA, termed circUBXN7, which was significantly downregulated in BC tissues compared with matched nontumor tissues.The circUBXN7-miR-1247-3p-B4GALT3 regulatory network may provide a new perspective for gene-based treatment strategies for BC.	Importantly, we found that decreased circUBXN7 expression was associated with pathological stage, grade and poor prognosis of BC patients.	Yes	 Functional experiments showed that circUBXN7 overexpression dramatically inhibited proliferation, migration and invasion in vitro and suppressed tumor growth in vivo.	30312173
circCEP128	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	interaction[ miR-145-5p,SOX11 ]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	 In present study, circCEP128 and SOX11 were observed significantly up-regulated in bladder cancer tissues, while the expression of miR-145-5p was decreased in cancer samples compared to normal samples.  CircCEP128 functions as a ceRNA for miR-145-5p, which could up regulates SOX11 and further promotes cell proliferation and inhibits cell apoptosis of bladder cancer.		Yes	Knockdown of circCEP128 induced the inhibition of cell proliferation and the increased bladder cancer cell apoptosis rate.	30134837
circSLC8A1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	Regulation[circSLC8A1/miR-130b, miR-494/PTEN axis ]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the present study, we found that circSLC8A1 was down-regulated in bladder cancer tissues and cell lines, and circSLC8A1 expression was associated with the pathological stage and histological grade of bladder cancer. CircSLC8A1 acts as a tumor suppressor by a novel circSLC8A1/miR-130b, miR-494/PTEN axis, which may provide a potential biomarker and therapeutic target for the management of bladder cancer.		Yes	Over-expression of circSLC8A1 inhibited cell migration, invasion and proliferation both in vitro and in vivo.	31228937
hsa_circ_403658	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	Bladder cancer tissues  and the matched adjacent tissues,cell lines(CCC-HB-2,SW780, 5637, T24, J82 and RT4)	Interaction[LDHA]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Western Blot	has_circRNA_403658 expression was higher in bladder cancer tissues than in the matched adjacent tissues.In addition, has-circRNA-403658 was induced by HIF1α and silencing has-circRNA-403658 inhibited LDHA-mediated aerobic glycolysis, inhibiting bladder cancer cell growth.	 We demonstrated that has-circRNA-403658 was an important circRNA that upregulated in bladder cancer cells under hypoxia, and higher has-circRNA-403658 levels were associated with poorer survival outcome. 	Yes	Silencing has-circRNA-403658 in bladder cancer cells inhibited cell growth and induced cell apoptosis. 	31814891
circMTO1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and the matched adjacent tissues,cell lines (UMUC3, SVHUC1, T24, J82,5637,CCC-HB-2)	Interaction[ sponging miR-221]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	We found that circMTO1 was significantly decreased in bladder cancer tissues compared with adjacent tissues.Compared with CCC-HB-1 cells, the expression of circMTO1 was significantly downregulated in five bladder cancer cell lines.In addition, we also revealed that circMTO1 was able to sponge miR-221 and overexpression of circMTO1 negatively regulated the E-cadherin/N-cadherin pathway to inhibit bladder cancer cells' EMT by competing for miR-221.	 We first demonstrated that circMTO1 was an important circRNA frequently downregulated in bladder cancer tissue, and lower circMTO1 levels were positively correlated with bladder cancer patients' metastasis and poorer survival.	Yes	Ectopic expression of circMTO1 in bladder cancer cells inhibited cell's epithelial-to-mesenchymal transition (EMT) and metastasis.	30551873
circFoxo3	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer  tissues	Interaction[miR-191-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	circ-Foxo3 was Expression[down-expression]regulated in bladder cancer in vivo and in vitro, and was Expression[Expression[up-expression]-expression]regulated in response to apoptotic stress.  We further characterized the interaction between circ-Foxo3 and miR-191 and its functional impact on bladder cancer cells.		Yes	Overexpression of circ-Foxo3 promoted bladder cancer cell apoptosis in BBN mice and in human bladder cancer cell lines. 	31802888
circPTPRA	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	breast cancer tissues	Interaction[miR-636,KLF9]	qRT-PCR//Luciferase Report Assay//FISH	By using qRT-PCR analysis, we verified that circPTPRA is Expression[down-expression]-regulated in clinical BC specimens compared with the matched non-tumor samples, while correlation analyses showed that low circPTPRA expression is associated with poor prognosis, advanced tumor stage and larger tumor size.Cell transfection experiments showed that miR-636 promotes the proliferation of BC cells by decreasing the expression of Krüppel Like Factor 9 (KLF9) Expression[Expression[up-expression]-expression]on binding to the 3'UTR of its mRNA.Further analysis confirmed that circPTPRA competitively sponges miR-636 to Expression[Expression[up-expression]-expression]regulate the KLF9 expression, leading to decreased proliferation of BC cells.	By using qRT-PCR analysis, we verified that circPTPRA is Expression[down-expression]-regulated in clinical BC specimens compared with the matched non-tumor samples, while correlation analyses showed that low circPTPRA expression is associated with poor prognosis, advanced tumor stage and larger tumor size.	Yes	Based on these findings, we conducted functional assays and revealed that circPTPRA inhibits BC cell proliferation in vitro and tumor growth in vivo.	31821171
hsa_circ_0084606	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	breast cancer tissues	Expression[Expression[lower expressed]-expression]	CCK8//qRT-PCR//Luciferase Report Assay//RNA-seq//Transwell Assay	In high-grade BC tissues, 316 circRNAs were dysregulated compared with NCs (205 Expression[Expression[up-expression]-expression]regulated and 111 Expression[down-expression]regulated) and 244 circRNAs were dysregulated compared with low-grade BC tissues (109 Expression[Expression[up-expression]-expression]regulated and 135 Expression[down-expression]regu-lated). Further analysis indicated that 42 dysregulated circRNAs overlapped between the two groExpression[Expression[up-expression]-expression]s (Table I). As shown in Fig. 2A-G, the RT-qPCR results were consistent with the expression profiles of our high-throughput sequencing data, in which, hsa_circ_0137613 exhibited a high degree of Expression[down-expression]regulation.		Yes	The Transwell assays revealed that hsa_circ_0137606 knockExpression[down-expression] significantly promoted BC cell migration (Fig. 5D) and invasion (Fig. 5E) compared with the NC groExpression[Expression[up-expression]-expression]. In summary, hsa_circ_0137606 knockExpression[down-expression] promoted the proliferation and metastasis of BC cells in vitro.	30892069
circVANGL1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC tissues	Interaction[miR-605-3p/VANGL1 pathway]	CCK8//Luciferase Report Assay//Western Blot	We found that circ-VANGL1 was highly expressed in BC tissues compared with adjacent normal tissues.Mechanistically, we identified circ-VANGL1 as a sponge of miR-605-3p which targeted VANGL1 in BC cells. Through repressing miR-605-3p availability, circ-VANGL1 contributes to VANGL1 expression, consequently leading to BC cell proliferation, migration, and invasion. 	Furthermore, we showed that circ-VANGL1 could serve as a prognostic marker for patients with BC. 	Yes	Through functional experiments, we found that circ-VANGL1 knockExpression[down-expression] significantly sExpression[Expression[up-expression]-expression]pressed BC cell proliferation, cell cycle, migration, and invasion in vitro. Besides, circ-VANGL1 silence inhibited BC cell propagation in vivo.	30146736
hsa_circ_0058063	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Interaction[sponging miR-145-5p ]	qRT-PCR//Wound Healing Assay//MTT//Western Blot	Circ_0058063 was significantly overexpressed in BC tissues. Circ_0058063 repressed miR-145-5p, which inhibited the expression of CDK6. Downregulation of circ_0058063 or miR-145-5p transfection contributed to more cells arresting in G0/G1 stage. MiR-145-5p suppressed cell growth and migration ability in BC, whereas CDK6 exerted the opposite influence on these cellular events. In vivo experiment also indicated that tumor development in BALB/c nude mice was repressed remarkably when circ_0058063 was downregulated.		Yes	The downregulation of circ_0058063 impaired BC cell proliferation and migration ability but improved cell apoptosis ability. Circ_0058063 repressed miR-145-5p, which inhibited the expression of CDK6. Downregulation of circ_0058063 or miR-145-5p transfection contributed to more cells arresting in G0/G1 stage.	30362519
hsa_circ_0001361	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues , cell lines	Regulation[miR-491-5p/MMP9 axis]	qRT-PCR//Luciferase Report Assay//RNA-seq	 In this study, we focused on the upregulated circRNAs and identified a novel circular RNA, hsa_circ_0001361 (circ0001361), was expressed at high levels in BC tissues and cell lines based on RNA-Seq data and qRT-PCR analysis, and it was positively corelated with pathologic grade and muscle invasion. Mechanistically, RNA sequencing analysis indicated that MMP9 was upregulated in circ0001361-overexpressed BC cells, and MMP9 was verified to mediate circ0001361-induced cell migration and invasion. Furthermore, we demonstrated that circ0001361 could directly interact with miR-491-5p to upregulate MMP9 expression. Collectively, our findings indicate that circ0001361 plays oncogenic role in BC invasion and metastasis through targeting the miR-491-5p/MMP9 axis, and it might be a potential novel target for BC therapy.	Moreover, Kaplan-Meier survival analysis implied that BC patients with high circ0001361 expression level had a poor overall survival.	Yes	 Functionally, circ0001361 promoted BC cell invasion and metastasis both in vitro and in vivo, but had no effect on cell cycle and proliferation. 	31705065
hsa_circ_0001429	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction[binding miR-205-5p ]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Expressions of circ0001429 and VEGFA were up-regulated, whereas miR-205-5p expression was down-regulated in bladder cancer tissues in comparison with paired adjacent normal bladder tissues. Circ0001429 sponged miR-205-5p that targeted VEGFA, thereby modulating the protein level of VEGFA. Meanwhile, miR-205-5p restrained the cell viability and mobility and promoted the apoptosis in bladder cancer. Circ0001429 could accelerate cell propagation, migration and invasiveness through increasing VEGFA expression via miR-205-5p.		Yes	 Circ0001429 enhanced the propagation and metastasis abilities of T24 cells and 5637 cells in vitro, but reduced cell apoptosis.In vivo experiments revealed the inhibitor role of sh-circ0001429 in tumor growth and lung metastasis.	30909190
hsa_circ_0068871	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell lines	Interaction[targeting miR-181a-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	Hsa_circ_0068871 is over-expressed in BCa tissues and cell lines, whereas miR-181a-5p expression is repressed. Mechanistically, hsa_circ_0068871 upregulated FGFR3 expression and activated STAT3 by targeting miR-181a-5p to promote BCa progression.		Yes	 Depletion of has_circ_0068871 or upregulation of miR-181a-5p inhibited the proliferation and migration of BCa cells in vitro and in vivo.	30999937
circZFR	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues,cell lines	Regulation[miR-377/ZEB2 signaling]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	 First, we demonstrated that the expression of circZFR was higher in bladder cancer tissues and cells compared with adjacent non-tumor tissues and normal bladder epithelial cells.Mechanistically, we observed that circZFR could directly bind to miR-377 as sponge to promote ZEB2 expression in bladder cancer cells. In addition, rescue assays demonstrated that restoration of ZEB2 significantly impaired the suppressive effects of circZFR silencing on bladder cancer cells growth, migration and invasion. Taken together, our results illuminated that circZFR could be a prognostic biomarker in bladder cancer and exerted oncogenic roles through regulating miR-377/ZEB2 axis in bladder cancer, which indicated that circZFR could be a potential therapeutic target for bladder cancer patients treatment.		Yes	Functionally, knockdown of circZFR could significantly prohibit cell growth, migration and invasion, arrest cell cycle as well as promote apoptosis of bladder cancer cells in vitro study.	31746333
circCEP128	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder tissue,blood	Regulation[MAPK signaling pathway]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//CCK8//Luciferase Report Assay	Expression of miR-145-5p was decreased in cancer samples. Overexpression of miR-145-5p or knockdown of circCEP128 promoted MAKP signaling pathway and related proteins expression. In addition, knockdown of circCEP128 suppressed the growth of bladder cancer tumor tissues in vivo. Overexpression of circCEP128 promoted bladder cancer progression through modulating miR-145-5p and MYD88 via MAKP signaling pathway.		Yes	Knockdown of circCEP128 induced the inhibition of cell viability and mobility and cell cycle arrest. 	30939216
circNR3C1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues,cell lines	Interaction[sponging miR-27a-3p]	qRT-PCR	" In this study, we discovered that a circular RNA derived from NR3C1 (circNR3C1) was downregulated in bladder cancer tissues and cell lines according to RNA-Seq data and qRT-PCR analysis.Mechanistically, we demonstrated that circNR3C1 possessed four targeting sites of miR-27a-3p and could effectively sponge miR-27a-3p to suppress the expression of cyclin D1. Furthermore, we revealed that miR-27a-3p functioned as an oncogene through interacting with 5'UTR of cyclin D1 to enhance its expression, which led to promote cell cycle progression and proliferation in bladder cancer cells. Conclusively, our findings further confirm the hypothesis that circRNAs function as ""microRNA sponges"", and our data suggest that circNR3C1 and miR-27a-3p would be potential therapeutic targets for bladder cancer treatment."		Yes	Functionally, we found that overexpression of circNR3C1 could significantly inhibit cell cycle progression and proliferation of bladder cancer cells in vitro, as well as suppress tumor growth in vivo.	31255724
hsa_circ_0061140	CircRNA	Homo sapiens	Ovarian Neoplasms	OC samples and cells	Interaction(miR-361-5p/RAB1A)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 The circ_0061140 level was upregulated in OC samples and cells.		Yes	Downregulation of circ_0061140 impeded proliferation, migration, invasion, EMT, and angiogenesis of OC cells. 	35181843
circAHNAK	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	Interaction(miR-28/EIF2B5/ JAK2/STAT3 signaling pathway)	qRT-PCR//Wound Healing Assay//Western Blot	We reported that circAHNAK was decreased in ovarian cancer tissues. Mechanistically, circAHNAK acted as a miR-28 sponge. CircAHNAK deficiency resulted in the amassing of miR-28, which was elevated in ovarian cancer and promoted cancer cell malignancy. MiR-28 in turn inhibited EIF2B5 expression. Silence of EIF2B5 abolished the anticancer effects of miR-28 inhibitor. CircAHNAK overexpression retarded tumor growth in vivo, along with the decreased miR-28 and increased EIF2B, as well as EMT inhibition.		Yes	Forced expression of circAHNAK promoted apoptosis and inhibited cell proliferation, migration, invasion, EMT and JAK2/STAT3 signaling pathway.	35710311
hsa_circ_0030586	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cells	Interaction(miR-665/NR4A3 axis)	qRT-PCR//Bioinformatics Analysis	The expression of circ_0030586 was significantly decreased in BCa tissues and cells, as suggested by RT-qPCR. Circ_0030586 served as a competing endogenous RNA (ceRNA) for hsa-miR-665 to upregulate the expression of nuclear receptor subfamily 4 group A member 3 (NR4A3) which is a downstream target gene of miR-665 in BCa.		Yes	Colony formation, 5-Ethynyl-2'-deoxyuridine and sphere formation assays revealed that overexpression of circ_0030586 suppressed BCa cell proliferation and stemness in vitro. According to xenograft experiment, circ_0030586 overexpression suppressed tumor growth in vivo. 	34175686
circNFIX	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues, HUVECs	Interaction(miR-518a-3p/TRIM44 axis)	qRT-PCR//RNA Pull-Down//Western Blot	CircNFIX and TRIM44 expression were higher and miR-518a-3p was lower in OC tissues than in the adjacent tissues. OC-derived exosomal circNFIX positively regulated TRIM44 expression by targeting miR-518a-3p in HUVECs. OC-derived exosomal circNFIX promoted angiogenesis by regulating the Janus-activated kinase/signal transducer and activator of transcription 1 (JAK/STAT1) pathway via miR-518a-3p/TRIM44 axis in HUVECs.	Upregulated circNFIX and TRIM44 were significantly correlated with the tumor size and International Federation of Gynecology and Obstetrics (FIGO) stage of OC patients. 	Yes	 HUVECs treated OC-derived exosomes had higher proliferation, migration, and angiogenesis capacities than the control group. While OC-derived exosomal circNFIX silencing restrained HUVECs' proliferation, migration, and angiogenesis, compared with the OC-derived exosomes group. 	36448712
hsa_circ_0004712	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR-331-3p/FZD4 pathway)	Western Blot//Flow Cytometry//qRT-PCR//RIP//CCK8//IHC//Transwell Assay	In our results, hsa_circ_0004712 was aberrantly overexpressed in OC tissues and cells.Hsa_circ_0004712 directly targeted miR-331-3p whose inhibitors reversed the effects of hsa_circ_0004712 downregulation. FZD4 was targeted by miR-331-3p, and hsa_circ_0004712 could positively regulated FZD4 expression by targeting miR-331-3p. 		Yes	Downregulation of hsa_circ_0004712 impaired OC cell proliferation, colony formation, invasion and migration, and accelerated apoptosis. 	34507595
hsa_circ_0026123	CircRNA	Homo sapiens	Ovarian Neoplasms	 OVA tissues and cell lines	Interaction(miR‑124‑3p/EZH2 signaling pathway)	qRT-PCR//Luciferase Report Assay//FISH	The results confirmed that hsa_circ_0026123 expression was upregulated in OVA tissues and cell lines, while hsa_circ_0026123 silencing suppressed cell proliferation and migration. The results revealed that hsa_circ_0026123 silencing suppressed ovarian cancer cell progression via the miR‑124‑3p/EZH2 signaling pathway. 		Yes	it also suppressed the expression of cancer stem cell (CSC) differentiation?related markers in either in vivo or in vitro experiments. 	33416105
circCRIM1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer  tissues	Interaction( miR-383-5p/ZEB2 axis)	qRT-PCR//Wound Healing Assay//MTT//Western Blot	CircCRIM1 and CRIM1 had higher expression in ovarian cancer than in normal ovarian tissues, and both of them promoted ovarian cancer progression in vitro. CircCRIM1 and CRIM1 had a positive correlation relationship in the same cohort of ovarian cancer tissues. Bioinformatics predicted and dual luciferase assay confirmed circCRIM1 and CRIM1 bond with miR-145-5p, and circCRIM1 bond with miR-383-5p additionally. CircCRIM1 positively affected the expression of CRIM1. After circCRIM1 was over-expressed, miR-145-5p mimics transfection reversed the expression of CRIM1. Western blot discovered circCRIM1 positively affected the expression of zinc finger E-box binding homeobox 2 (ZEB2). 		Yes	CircCRIM1 and CRIM1 had higher expression in ovarian cancer than in normal ovarian tissues, and both of them promoted ovarian cancer progression in vitro.  In vivo circCRIM1 promoted the growth of tumors. 	34847936
circATRNL1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	Interaction(miR-378/Smad4 )	qRT-PCR//Luciferase Report Assay//RIP	circATRNL1 was decreased while miR-378 was increased in human ovarian cancer tissues and cells.circATRNL1 bound to miR-378 while miR-378 directly targeted Smad4. 		Yes	 Overexpression of circATRNL1 or knockdown of miR-378 suppressed angiogenesis and ovarian cancer cell proliferation, invasion, and migration via decreasing proliferation- and migration-related proteins via miR-378 or Smad4, respectively. Overexpression of circATRNL1 restrained ovarian cancer growth and abdominal metastasis in vivo.	33372356
hsa_circ_0072995	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR-122-5p/SLC1A5 Axis)	Flow Cytometry//qRT-PCR//RIP//Western Blot	Circ_0072995 was upregulated in OC tissues and cells in a stable structure.  Mechanistically, miR-122-5p was a direct target of circ_0072995, and its knockdown reversed the effects of circ_0072995 silence on inhibition of OC cell progression. Meanwhile, SLC1A5 was a downstream target gene of miR-122-5p, and miR-122-5p overexpression inhibited the progression of OC cells by targeting SLC1A5. Moreover, circ_0072995 positively regulated SLC1A5 expression via sponging miR-122-5p. 		Yes	Functional experiments indicated that circ_0072995 knockdown suppressed cell proliferation, migration, invasion and accelerated cell apoptosis of OC cells. 	34132956
hsa_circ_0000745	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(microRNA-3187-3p/ERBB4/PI3K/AKT axis)	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 Circ_0000745 and ERBB4 were abundantly expressed while miR-3187-3p was poorly expressed in OC tissues and cells.  Circ_0000745 sequestered miR-3187-3p and blocked its repressive effect on ERBB4.By contrast, artificial induction of circ_0000745 upregulation, miR-3187-3p upregulation and ERBB4 downregulation led to inverse trends in ES-2 cells. ERBB4 promoted the phosphorylation of the PI3K/AKT signaling pathway.		Yes	 Downregulation of circ_0000745 reduced proliferation, aggressiveness, epithelial-mesenchymal transition, and stemness of SK-OV-3 cells, but this reduction was blocked upon miR-3187-3p inhibition or ERBB4 upregulation.	34774079
hsa_circ_0002711	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cell line	Interaction(miR-1244/ROCK1 axis)	qRT-PCR//MTT//RIP	Circ_0002711 was upregulated in OC tissues and cell lines.Circ_0002711 contained binding sites with miR1244. Moreover, loss of miR-1244 undermined circ_0002711 downregulation-mediated function. ROCK1 contained binding sites with miR-1244. 		Yes	Circ_0002711 downregulation inhibited cell viability, colony formation ability and aerobic glycolysis.	33737494
hsa_circ_0025033	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR-184/LSM4)	qRT-PCR//IHC//Transwell Assay	" The expression of circ_0025033 and LSM4 was promoted in OC tissues and cells. Circ_0025033 knockdown or LSM4 knockdown blocked the ability of colony formation, migration/invasion and glycolysis metabolism in OC cells. In mechanism, circ_0025033 functioned as a ""competing endogenous RNA (ceRNA)"" to modulate LSM4 expression by targeting miR-184. LSM4 overexpression recovered the inhibitory effects on colony formation, migration/invasion and glycolysis metabolism caused by circ_0025033 knockdown. Moreover, circ_0025033 knockdown also inhibited tumor growth in vivo by regulating LSM4 and targeting miR-184."		Yes	Circ_0025033 knockdown or LSM4 knockdown blocked the ability of colony formation, migration/invasion and glycolysis metabolism in OC cells.	33285422
circATRNL1	CircRNA	Homo sapiens	Ovarian Neoplasms	 20 ovarian cancer tissues 	Expression(lower expressed)	CCK8//qRT-PCR	CircATRNL1 and circZNF608 were downregulated in 20 ovarian cancer tissues compared to normal tissues. CircATRNL1 and circZNF608 are mainly located in the cytoplasm of ovarian cancer cells, and circATRNL1 is a highly conserved circRNA.However, a luciferase reporter assay showed that only miR-152-5p was sequestered by circZNF608.Bioinformatics analysis and experiments indicated that circATRNL1 contains an internal ribosome entry site and an open reading frame encoding a 131 aa protein. 		Yes	 The overexpression of circATRNL1 and circZNF608 inhibits the proliferation and invasion of ovarian cancer cells. 	35281849
circZNF608	CircRNA	Homo sapiens	Ovarian Neoplasms	 20 ovarian cancer tissues 	Interaction(miR-152-5p)	CCK8//qRT-PCR	CircATRNL1 and circZNF608 were downregulated in 20 ovarian cancer tissues compared to normal tissues. CircATRNL1 and circZNF608 are mainly located in the cytoplasm of ovarian cancer cells, and circATRNL1 is a highly conserved circRNA.However, a luciferase reporter assay showed that only miR-152-5p was sequestered by circZNF608.Bioinformatics analysis and experiments indicated that circATRNL1 contains an internal ribosome entry site and an open reading frame encoding a 131 aa protein. 		Yes	 The overexpression of circATRNL1 and circZNF608 inhibits the proliferation and invasion of ovarian cancer cells. 	35281849
hsa_circ_0015756	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cells	Interaction(miR-145-5p/PSAT1 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	Circ_0015756 was highly expressed in OC tissues and cells. In a mechanical study, circ_0015756 directly bound to miR-145-5p, and inhibition of miR-145-5p reversed the effects of circ_0015756 knockdown on OC cells. Moreover, miR-145-5p directly targeted PSAT1, and miR-145-5p weakened OC cell growth, migration and invasion via targeting PSAT1. 		Yes	Knockdown of circ_0015756 suppressed cancer cell growth, migration and invasion in vitro, as well as impeded tumor growth in vivo.	36327671
hsa_circ_0078607	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cells	Interaction(miR-32-5p/SIK1 network)	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0078607 and SIK1 were downregulated in OC tissues and cells.Furthermore, SIK1 was a target of miR-32-5p, and circ_0078607 could regulate SIK1 by sponging miR-32-5p. The inhibitory effect of circ_0078607 on OC progression also could be reversed by SIK1 silencing. In vivo experiments showed that circ_0078607 reduced OC tumorigenesis by regulating the miR-32-5p/SIK1 axis.		Yes	 Overexpressed circ_0078607 and SIK1 could inhibit OC cell proliferation, migration, invasion, and promote apoptosis. MiR-32-5p could be sponged by circ_0078607, and its overexpression could reverse the suppressive effect of circ_0078607 on OC progression. 	34983607
hsa_circ_0000144	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cells and tissues	Interaction(miR-610/ELK3 )	qRT-PCR//Wound Healing Assay//RNA Pull-Down//Colony Formation Assay	Circ_0000144 was significantly upregulated in ovarian cancer cells and tissues.  This study further demonstrated that circ_0000144 downregulated ELK3 levels by sponging miR-610 in ovarian cancer cells. 		Yes	Circ_0000144 overexpression significantly promoted ovarian cancer cell proliferation, migration, and invasion. Moreover, circ_0000144 significantly promotes ovarian cancer tumorigenesis in vivo.	36243865
hsa_circ_0000497	CircRNA	Homo sapiens	Ovarian Neoplasms	22 samples 	Expression(highly expressed)	qRT-PCR//RNA-seq//Western Blot	Among them, hsa_circ_0000497 and hsa_circ_0000918 were significantly up-regulated in ASC. 		Yes	Functional analysis showed that both hsa_circ_0000497 and hsa_circ_0000918 promoted metastasis of EOC via epithelial-mesenchymal transition (EMT) in vitro. 	35538537
hsa_circ_0000918	CircRNA	Homo sapiens	Ovarian Neoplasms	22 samples 	Expression(highly expressed)	qRT-PCR//RNA-seq//Western Blot	Among them, hsa_circ_0000497 and hsa_circ_0000918 were significantly up-regulated in ASC. 		Yes	Functional analysis showed that both hsa_circ_0000497 and hsa_circ_0000918 promoted metastasis of EOC via epithelial-mesenchymal transition (EMT) in vitro. 	35538537
hsa_circ_0067934	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC samples and cells	Interaction(microRNA-545-3p/PPA1 axis )	RIP//qRT-PCR//Tunel	 Circ_0067934 was overexpressed in OC samples and associated with advanced tumor staging and lymph node metastasis. Circ_0067934 served as a sponge for miR-545-3p and diminished its suppressive effect on PPA1 translation. Artificial upregulation of PPA1 enhanced proliferation, invasion and DDP resistance of A2780/DDP cells, and it reduced phosphorylation of the pro-apoptotic JNK signaling.	 Circ_0067934 was overexpressed in OC samples and associated with advanced tumor staging and lymph node metastasis.	Yes	Downregulation of circ_0067934 reduced DDP resistance of the DDP-resistant A2780/DDP cell line and reduced cell proliferation and invasion, but the malignant behaviors of OC cells were restored after further miR-545-3p downregulation. 	35179434
hsa_circ_0000119	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cells and tissues	Interaction(miR-142-5p/CDH13 )	qRT-PCR//MTT	In this present study, our data shows that hsa_circ_0000119 and DNA methyltransferase 1 (DNMT1) was increased, while miR-142-5p was decreased in ovarian cancer. Moreover, the data proves that hsa_circ_0000119 negatively regulated miR-142-5p and cadherin 13 (CDH13) expression, but positively regulated DNMT1 expression. miR-142-5p could interact with hsa_circ_0000119 and DNMT1 3'-UTR. Silencing of DNMT1 could reverse the inhibition of hsa_circ_0000119 to miR-142-5p and CDH13 expression. Importantly, higher level of CDH13 promoter methylation existed in the ovarian tumors than that in matched normal tissues. DNA methyltransferase inhibitor could increase the expression of CDH13 in ovarian cancer cells. 		Yes	Overexpression of hsa_circ_0000119 promoted tumor growth, while silencing of hsa_circ_0000119 resulted in an opposite effects. Decreasing of hsa_circ_0000119 also notably inhibited the proliferation, migration, and invasion of the ovarian cancer cells. 	36482494
hsa_circ_0000471	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	Interaction(mir-135b-5p/dusp5 axis)	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	Circ_0000471 expression was down-regulated in OC tissues and cell lines. Circ_0000471 served as a molecular sponge for microRNA-135b-5p (miR-135b-5p), and circ_0000471 overexpression-mediated anti-tumor influences in OC cells were largely reversed by the overexpression of miR-135b-5p. Dual specificity phosphatase 5 (DUSP5) was a target of miR-135b-5p, and miR-135b-5p silencing-induced anti-tumor effects were largely counteracted by the interference of DUSP5. Circ_0000471 increased DUSP5 expression by sponging miR-135b-5p in OC cells.		Yes	 Circ_0000471 overexpression blocked the proliferation, migration, and invasion and triggered the apoptosis of OC cells. Circ_0000471 overexpression restrained the growth of xenograft tumors in vivo.	36369900
hsa_circ_0025033	CircRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer tissues and cells	Interaction(hsa_miR-370-3p/SLC1A5 axis)	qRT-PCR//Transwell Assay	circ_0025033 was upregulated in ovarian cancer; its knockdown induced proliferation, invasion, angiogenesis, glutamine metabolism, and apoptosis in vitro, and blocked tumor growth in vivo.  circ_0025033 regulated ovarian cancer cellular behaviors via sponging hsa_miR-370-3p. In parallel, SLC1A5 might abolish the anti-ovarian cancer role of hsa_miR-370-3p. Furthermore, circ_0025033 affected SLC1A5 via regulating hsa_miR-370-3p.		Yes	circ_0025033 was upregulated in ovarian cancer; its knockdown induced proliferation, invasion, angiogenesis, glutamine metabolism, and apoptosis in vitro, and blocked tumor growth in vivo. 	36273140
circVANGL1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	Regulation[miR-1184/IGFBP2 axis]	CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	The results showed that circVANGL1 was upregulated in both BC tissues and cell lines. Mechanistically, we demonstrated that circVANGL1 upregulated the expression of miR-1184 target gene insulin-like growth factor-binding protein 2 (IGFBP2) by sponging miR-1184, which promoted the aggressive biological behaviors of BC. Taken together, our results indicate that circVANGL1 acts as a tumor promoter through the novel circVANGL1/miR-1184/IGFBP2 axis. Hopefully, our study will provide new ideas for the clinical treatment of BC.		Yes	Silencing the expression of circVANGL1 suppressed cell invasion, migration, and proliferation during in vitro experiments.	31758655
circSMARCA5	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissue, cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot	Circ-SMARCA5 was overexpressed in tumor tissue compared to paired adjacent tissue and it was also overexpressed in TCCSUP, 5637, J82 and UM-UC-3 cells compared to normal human urothelial cell line SV-HUC-1. 		Yes	 In UM-UC-3 cells, cell proliferation ability, migration rate and invasion cell count were increased in Circ-SMARCA5(+) group compared to Control(+) group, while reduced in Circ-SMARCA5(-) group compared to Control(-) group. 	35116915
circCDYL	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	Interaction[down-regulating the expression of C-MYC]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Transwell Assay	It was found that circCDYL was low expressed in bladder cancer tissues and cell lines.Importantly, over-expression of circCDYL down-regulated the protein level of C-MYC in both EJ and T24T cells, while the mRNA level of C-MYC was not significantly reduced. Furthermore, over-expression of C-MYC could partly reverse the G0/G1 phase cell cycle arrest induced by circCDYL in bladder cancer cells. Our findings suggest that circCDYL functions as a tumor suppressor in bladder cancer by down-regulating the expression of C-MYC, and this circular RNA might be used as a new target for bladder cancer therapy.		Yes	Functionally, over-expression of circCDYL inhibited cell growth and migration.	30968727
circACVR2A	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues,cell lines	Regulation[miR-626/EYA4 axis]	RNA Pull-Down//qRT-PCR//FISH//Luciferase Report Assay//RNA-seq	The expression of circACVR2A was lower in bladder cancer tissues and cell lines.Our in vivo and in vitro data indicated that circACVR2A suppressed the proliferation, migration and invasion of bladder cancer cells. 	The down-regulation of circACVR2A was positively correlated with aggressive clinicopathological characteristics, and circACVR2A served as an independent risk factor for overall survival in bladder cancer patients after cystectomy.	Yes	Our in vivo and in vitro data indicated that circACVR2A suppressed the proliferation, migration and invasion of bladder cancer cells. 	31101108
circCASC15	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	regulation[CREB1]	qRT-PCR	The data from the microarray showed that hsa_circ_0075828 (named circCASC15) was most highly expressed in 5637 and T24 cells. circCASC15 was highly expressed in BC tissues and cells.Mechanistically, circCASC15 could act as miR-1224-5p sponge to activate the expression of CREB1 to promote cell proliferation in BC.		Yes	Overexpression of circCASC15 was closely associated with BC tumor stage and promoted cell proliferation significantly in vitro and in vivo.	31072448
circGLIS3	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cells	Interaction(miR-1273f)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Cell Apoptosis Assay//EdU Staining//Transwell Assay	In this study, we screened out a circRNA-circGLIS3 with a significant upregulation trend in both bladder cancer tissues and cells. Bioinformatics prediction results showed that circGLIS3 may be involved in multiple tumor-related pathways. Mechanically, circGLIS3 upregulates the expression of SKP1 by adsorbing miR-1273f and then promotes cyclin D1 expression, ultimately promoting the proliferation of bladder cancer cells. 		Yes	Function gain and loss experiments verified circGLIS3 can affect the proliferation, migration, and invasion of bladder cancer cells in vitro. Moreover, silencing circGLIS3 inhibited bladder cancer cell growth in vivo. 	33656636
hsa_circ_0000629	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	Interaction(MicroRNA-1290/CDC73)	CCK8//qRT-PCR//Flow Cytometry//EdU Staining	Circ_0000629 and CDC73 were reduced, and miR-1290 was significantly overexpressed in BC tissues and cells.		Yes	 Moreover, circ_0000629 significantly inhibited the development and metastasis of BC cells, but further overexpression of miR-1290 or knockdown of CDC73 attenuated the inhibitory effect of circ_0000629 on BC cells. 	33790645
hsa_circ_0007813	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	clinical tissue samples and cell lines	Interaction(miR-361-3p)	CCK8//qRT-PCR//Western Blot//Transwell Assay	Based on these findings from clinical tissue samples and cell lines, we assumed that hsa_circ_0007813 functioned a vital role in bladder cancer progression. 		Yes	Next, functional experiments revealed that knockdown of hsa_circ_0007813 inhibited proliferation, migration, and invasiveness of bladder cancer cells both in vitro and in vivo. Through extensive bioinformatic prediction and RNA pull-down assays, we identified hsa-miR-361-3p as a competing endogenous RNA of hsa_circ_0007813.	34365465
circPPP1CB	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Interaction(microRNA 409-5p)	RNA Pull-Down//Western Blot//Wound Healing Assay//Tube Formation Assay//Migration Assay//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//IF	CircPPP1CB is downregulated in BC and is negatively correlated with clinical stages and histological grades. 	CircPPP1CB is downregulated in BC and is negatively correlated with clinical stages and histological grades. 	Yes	Functionally, circPPP1CB modulated cell growth, metastasis, and epithelial-to-mesenchymal transition (EMT) process in vitro and in vivo. Mechanically, we performed various experiments to verify the circPPP1CB/miR-1307-3p/SMG1 regulatory axis. 	34595165
circEHBP1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	186 pairs of tumor tissues and NATs from patients with BCa 	Interaction(miR-130a-3p/TGFβR1/VEGF-D signaling)	CCK8//qRT-PCR	Novel circRNA circEHBP1 was markedly upregulated in bladder cancer and correlated positively with lymphatic metastasis and poor prognosis of patients with bladder cancer. circEHBP1 upregulated transforming growth factor beta receptor 1 (TGFBR1) expression through physically binding to miR-130a-3p and antagonizing the suppression effect of miR-130a-3p on the 3' UTR region of TGFBR1. 	Novel circRNA circEHBP1 was markedly upregulated in bladder cancer and correlated positively with lymphatic metastasis and poor prognosis of patients with bladder cancer. 	Yes	 Importantly, administration of VEGF-D neutralizing antibodies remarkably blocked circEHBP1-induced lymphangiogenesis and lymphatic metastasis in vivo. 	33545359
hsa_circ_100284	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	Bladder cancer tissues and tissues beyond 1 cm adjacent to the cancer tissues	Interaction(microRNA-217)	qRT-PCR//Western Blot	With prolonged contact time with arsenite, the expression level of circRNA-100284 in cells increased continuously (P < 0.05). Flow cytometry and CCK-8 showed that circRNA-100284 accelerated cell cycle transition and cell proliferation through miR-217.		Yes	Flow cytometry and CCK-8 showed that circRNA-100284 accelerated cell cycle transition and cell proliferation through miR-217.	33386469
circBIRC6	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC cell lines	Interaction(miR‑495‑3p/XBP1 signaling axis)	qRT-PCR//Wound Healing Assay//Transwell Assay	The results demonstrated that circ‑BIRC6 expression was upregulated in BC cell lines.  It was also identified that circ‑BIRC6 sponged miR‑495‑3p to regulate XBP1 expression.		Yes	Moreover, circ‑BIRC6 knockdown notably attenuated the proliferation, invasion, migration and EMT of BC cells, which was blocked by the miR‑495‑3p inhibitor. In addition, results from the xenograft experiments indicated that the knockdown of circ‑BIRC6 and miR‑495‑3p expression significantly inhibited tumor growth. 	34542161
circMBOAT2	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	Bca tissues	Interaction(miR-433-3p)	qRT-PCR//RNA Pull-Down//Transwell Assay	In this research, we identified that circMBOAT2 expression was increased in Bca tissues and positively corelated with unfavorable prognosis.  Mechanically, circMBOAT2 was predominantly spread in cytoplasm and it sponged miR-433-3p to strengthen CREB1 expression.	In this research, we identified that circMBOAT2 expression was increased in Bca tissues and positively corelated with unfavorable prognosis. 	Yes	In vitro assay demonstrated that suppression of circMBOAT2 impaired the proliferation and migration of Bca cells. 	34563754
circST6GALNAC6	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissues and cells	Interaction(miR-200a-3p /STMN1/EMT axis)	qRT-PCR//ChIP	circST6GALNAC6(hsa_circ_0088708) was downregulated in BCa tissues and cells.  Mechanistically, we showed that the SP1 transcription factor, which binds to the circST6GALNAC6 mRNA transcript, activates circST6GALNAC6 transcription. Next, we verified that circST6GALNAC6 serves as a sponge that directly binds miR-200a-3p to regulate stathmin (STMN1) expression. Furthermore, we found that STMN1 is involved in circST6GALNAC6/miR-200a-3p axis-regulated BCa EMT and metastasis. 		Yes	Overexpression of circST6GALNAC6 effectively inhibited the cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and suppressed BCa metastasis in vivo.	33568625
circRHOT1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tumor tissues and cell lines	Interaction(miR-3666/SMAD5)	qRT-PCR//ChIP	 Our findings suggest that circRHOT1 was highly expressed in BC tumor tissues and cell lines.  Subsequently, we conducted bioinformatics analysis followed by RNA pull-down, ChIP, and luciferase reporter assays, from which we found that circRHOT1 expression in BC cells could be regulated by ZNF652, and circRHOT1 could promote SMAD5 expression to regulate BC cell cellular progression by sponging miR-3666. 		Yes	 The results from CCK-8, EDU, Transwell migration, and NK cell-mediated cytotoxicity detection assays suggested that circRHOT1 knockdown could markedly suppress BC cell proliferation and migration level and could aggravate the sensitivity of BC cells to NK cells. 	34926705
circUBE2K	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Interaction(miR-516b-5p/ARHGAP5 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	High circUBE2K predicted unfavorable prognoses in BCs, as well as correlated with clinical features. Further studies showed that circUBE2K promoted BC progression via sponging miR-516b-5p and enhancing ARHGAP5 expression through regulating RhoA activity. Dual-luciferase reporter, FISH and RNA pulldown assays were employed to verify the relationships among circUBE2K/miR-516b-5p/ARHGAP5/RhoA axis.		Yes	CCK8, transwell, EdU and wound healing assays demonstrated down-regulating circUBE2K decreased BC cell phenotype as proliferation, invasion, and migration, respectively. 	34285193
hsa_circ_0014130	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	cells and tissues of bladder cancer	Interaction(miR-132-3p/KCNJ12 )	qRT-PCR//Western Blot	The expressions of hsa_circ_0014130 were markedly ameliorated in bladder cancer samples and linked with aggressive characteristics and unfavorable survival. The expression of hsa_circ_0014130 was tied to miR-132-3p in a negative manner with the cells and tissues of bladder cancer. The underlined data revealed that hsa_circ_0014130 exerted its biological roles by regulating miR-132-3p/KCNJ12 expression. 	The expressions of hsa_circ_0014130 were markedly ameliorated in bladder cancer samples and linked with aggressive characteristics and unfavorable survival. 	Yes	 Ectopic expression of hsa_circ_0014130 clearly enhanced the differentiation, proliferative, migratory, invasive potential of the cell in bladder cancer, and the development of tumor xenograft in vivo, while malignant biological behaviors were inhibited by hsa_circ_0014130 knockdown. 	34755307
hsa_circ_0001495	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cells	Interaction(miR-527/Robo1 )	qRT-PCR//Transwell Assay	 It was found that circ_0001495 was highly expressed in BCa tissues and cells, and was further correlated with poor prognosis in BCa patients.  In addition, circ_0001495 inhibited the activity of miR-527 by acting as a sponge to sponge miR-527, which further elevated the Robo1 expression. 	 It was found that circ_0001495 was highly expressed in BCa tissues and cells, and was further correlated with poor prognosis in BCa patients. 	Yes	Lastly, circ_0001495 was found to promote the proliferation, migration and invasion of BCa cells in vitro through the miR-527/Robo1 axis and promote the growth and metastasis of BCa tumors in vivo. 	34021307
circNT5E	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	Bca tissues	Interaction(miR-502-5p/HOXC8)	qRT-PCR//RNA Pull-Down	In this study, we observed that circNT5E expression was augmented in Bca tissues compared with that in adjacent normal tissues, and its expression level was positively associated with larger tumor size and lower survival rate. circNT5E was mainly distributed in the cytoplasm and it captured miR-502-5p to increase HOXC8 mRNA and protein expression. Moreover, decreased miR-502-5p obviously reversed the circNT5E silencing-mediated inhibition of Bca cell growth and migration.	In this study, we observed that circNT5E expression was augmented in Bca tissues compared with that in adjacent normal tissues, and its expression level was positively associated with larger tumor size and lower survival rate.	Yes	 Further experiments showed that suppression of circNT5E restrained the growth and metastasis of Bca cells in vitro. 	33758619
hsa_circ_0000326	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC cell lines and tissues	Interaction(miR-338-3p/miR-338-3p/ETS1/PI3K/AKT pathway)	qRT-PCR//Wound Healing Assay	Here, we found that circ_0000326 expression was significantly elevated in BC cell lines and tissues, and circ_0000326 could promote BC cell growth and migration, and inhibit apoptosis. Dual-luciferase reporter gene assay confirmed that circ_0000326 and ETS1 could bind directly to miR-338-3p. Furthermore, circ_0000326 sponged miR-338-3p and up-regulated ETS1 expression. ETS1 was associated with the activation of PI3K/AKT pathway. Moreover, circ_0000326 could activate PI3K/AKT pathway by miR-338-3p/ETS1 axis. 		Yes	Here, we found that circ_0000326 expression was significantly elevated in BC cell lines and tissues, and circ_0000326 could promote BC cell growth and migration, and inhibit apoptosis.	34889689
circPTPRA	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC cells	Interaction(IGF2BP1 )	qRT-PCR//RIP	We demonstrated that IGF2BP1 was predominantly binded with circPTPRA in the cytoplasm in BC cells. Importantly, circPTPRA downregulated IGF2BP1-regulation of MYC and FSCN1 expression via interacting with IGF2BP1. Moreover, the recognition of m6A-modified RNAs mediated by IGF2BP1 was partly disturbed by circPTPRA through its interaction with KH domains of IGF2BP1.		Yes	Ectopic expression of circPTPRA abolished the promotion of cell proliferation, migration and invasion of BC cells induced by IGF2BP1. 	33853613
circNUDT21	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	Interaction(miR-16-1-3p/MDM2/p53 axis)	CCK8//qRT-PCR	The circNUDT21 level was overexpressed in BC tissues and cell lines as compared to normal controls.Mechanistical analysis showed that circNUDT21 acted as a miR-16-1-3p sponge and that MDM2 was a potential downstream target of miR-16-1-3p. We further verified that overexpression of circNUDT21 was associated with elevated MDM2 and reduced p53 expression. CircNUDT21 promoted BC progression by acting as a sponge of miR-16-1-3p to activate the miR-16-1-3p/MDM2/p53 axis.		Yes	Overexpression and silencing of circNUDT21 promoted and inhibited, respectively, the proliferative and invasive abilities of BC cells. 	34703648
hsa_circ_0041103	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell lines	Interaction(miR-107/FOXK1 axis)	CCK8//qRT-PCR	Circ0041103 was abnormally upregulated in BCa tissues and cell lines. MiR-107 was the binding target of circ0041103, and FOXK1 was the downstream gene of miR-107. Overexpression of circ0041103 could reverse the inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells overexpressing miR-107.	 Its level was higher in BCa tissues with a larger tumor size, or worse tumor staging, or BCa cases with lymphatic metastasis.	Yes	Knockdown of circ0041103 inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells.	33629298
hsa_circ_0091017	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell lines	interaction[microRNA-589-5p]	CCK8//qRT-PCR//EdU Staining//Transwell Assay	QRT-PCR results revealed that the expression level of hsa_circ_0091017 was remarkably down-regulated in BCa tissues and cell lines, while the expression level of microRNA-589-5p was remarkably increased in BCa tissues and cells. The circular RNA hsa_circ_0091017 can inhibit the proliferation, migration and invasiveness of BCa cells by regulating the expression of microRNA-589-5p.		Yes	Overexpression of the circular RNA hsa_circ_0091017 in BCa cells can inhibit the proliferation, migration, and invasiveness of BCa cells. 	31957821
circFAM114A2	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	UCB tissue specimens and cell lines	regulation[circFAM114A2/miR-762/-NP63 axis]	qRT-PCR//FISH	In this study, we found circFAM114A2 was significantly downregulated both in UCB tissue specimens and cell lines, and the expression level was highly correlated with pathological TNM stage and grade.Taken together, our results demonstrated that circFAM114A2 might serve as a competing endogenous RNA (ceRNA) of miR-762 in regulating the expression of ∆NP63, thus suppressed UCB progression through circFAM114A2/miR-762/∆NP63 axis.	In this study, we found circFAM114A2 was significantly downregulated both in UCB tissue specimens and cell lines, and the expression level was highly correlated with pathological TNM stage and grade.	Yes	Functionally, overexpression of circFAM114A2 dramatically inhibited the migration, invasion and proliferation of UCB cells in vitro, and suppressed tumor growth in vivo. 	31969560
circRIP2	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues 	regulation[miR-1305/Tgf-β2/smad3 pathway]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	circRIP2 was identified as a conserved and dramatically repressed circular RNA in bladder cancer.Taken together, our study provides the first evidence that circRIP2 expresses differentially in bladder cancer and negatively along with the cancer progression; effective circRIP2 activity accelerates bladder cancer progression via inducing EMT by activating miR-1305/Tgf-β2/smad3 pathway.		Yes	In vitro and in vivo studies suggest that circRIP2 enables to promote bladder cancer progression via inducing EMT. 	32019579
circSEMA5A	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC tissues and cell lines	regulation[upregulating ENO1 and SEMA5A expression]	RNA Pull-Down//Western Blot//EdU Staining//qRT-PCR//FISH//RIP//migration assay//Luciferase Report Assay//Invasion Assay	In this study, we found that circSEMA5A was upregulated in BC tissues and cell lines.To sum up, circSEMA5A is upregulated in BC and facilitates BC progression by mediating miR-330-5p/ENO1 signaling and upregulating SEMA5A expression.		Yes	 In vitro data indicated that circSEMA5A promoted proliferation, suppressed apoptosis, facilitated migration, accelerated invasion, enhanced angiogenesis and promotes glycolysis of BC. 	33176280
hsa_circ_0137439	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Expression[highly expressed]	qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//Microarray//Cell Cycle Assay//Transwell Assay	We found that hsa_circ_0137439 was significantly upregulated in bladder cancer samples.Cell assays showed that hsa_circ_0137439 knockdown contributed to the inhibition of cell proliferation and migration via hsa_circ_0137439/miR-142-5p/ MTDH axis. 	Moreover, increased expression of hsa_circ_0137439 was correlated with higher tumor stage, higher tumor grade, higher lymph node status, and history of muscle-invasive bladder cancer (MIBC). Additionally, hsa_circ_0137439 in urine supernatant could serve as an independent prognostic predicator of recurrence-free survival and overall survival for patients with bladder cancer. 	Yes	Cell assays showed that hsa_circ_0137439 knockdown contributed to the inhibition of cell proliferation and migration via hsa_circ_0137439/miR-142-5p/ MTDH axis.	31777254
circZKSCAN1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues and cell lines	Regulation[miR-1178-3p/p21 axis]	RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//FISH//Luciferase Report Assay//Invasion Assay	Here, we found that circ-ZKSCAN1 was downregulated in BCa tissues and cell lines.Mechanistically, we demonstrated that circ-ZKSCAN1 upregulated p21 expression by sponging miR-1178-3p, which suppressed the aggressive biological behaviors in bladder cancer.	Circ-ZKSCAN1 levels were associated with survival, tumor grade, pathological T stage and tumor recurrence.	Yes	Overexpressed circ-ZKSCAN1 inhibits cell proliferation, migration, invasion and metastasis in vitro and in vivo.	31481066
circPICALM	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Interaction[sponges miR-1265]	Co-IP//qRT-PCR//Luciferase Report Assay	CircPICALM was downregulated in BC tissues.CircPICALM can inhibit BC metastasis and bind to miR-1265 to block its pro-invasion activity. 	CircPICALM was downregulated in BC tissues, and low circPICALM expression was related to advanced T stage, high grade, lymph node positivity and poor overall survival. 	Yes	Overexpression of circPICALM inhibited the metastasis of BC cells, and DHX9 negatively regulated circPICALM levels.	31648990
hsa_circ_0002024	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	Interaction[sponging miR-197-3p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that the expression of hsa_circ_0002024 was downregulated, but that of miR-197-3p was upregulated in BC tissues and cell lines.In conclusion, our data demonstrated that hsa_circ_0002024 suppresses cell proliferation, migration, and invasion in BC by sponging miR-197-3p.		Yes	Upregulation of hsa_circ_0002024 suppressed the proliferation, migration, and invasion of EJ and T24 cells.	30972190
hsa_circ_0006332	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction[modulating MYBL2 expression via miR-143]	qRT-PCR//Luciferase Report Assay//FISH	Direct Sanger sequencing and quantitative RT-PCR analysis showed that circ_0006332 was significantly upregulated in bladder cancer tissues.Our study demonstrates that circ_0006332 promotes the growth and progression of bladder cancer by modulating MYBL2 expression by acting as a sponge for miR-143. Circ_0006332 is thus a potential early diagnostic marker of bladder cancer.		Yes	Circ_0006332 knockdown increased E-cadherin levels and decreased Vimentin, CCNB1 and P21 protein expression. This suggests that circ_0006332 promotes epithelial-mesenchymal transition and cell cycle progression. In vivo experiments in nude mice showed that circ_0006332 knockdown bladder cancer cells form significantly smaller tumors than the controls.	31756170
hsa_circ_0000735	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cells	interaction[sponges miR-502-5p]	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	Circ_0000735 expression was increased in bladder cancer tissues and cells compared with paraneoplastic tissues and normal cells, and miR-502-5p expression was reduced (both P<0.05). Circ_0000735 can adsorb miR-502-5p to promote bladder cancer cell proliferation and invasion and inhibit apoptosis.		Yes	Circ_0000735 silencing prevented cell proliferation and invasion and facilitated apoptosis (all P<0.05).	33425100
hsa_circ_0004463	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder carcinoma tissue and cells	regulation[circ_0004463/miR-380-3p/FOXO1 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	circ_0004463 is significantly downregulated, whereas miR-380-3p is upregulated in bladder carcinoma tissue samples and cells. In conclusion, the circ_0004463/miR-380-3p/FOXO1 axis could regulate mitochondrial respiration and bladder cancer cell apoptosis via FOXO1 signaling.		Yes	Circ_0004463 overexpression inhibits cancer cell proliferation and mitochondrial respiration in bladder cancer cell lines, while miR-380-3p overexpression dramatically reverses the roles of circ_0004463 overexpression.	33283616
circRIMS1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissue and cell lines	regulation[ circRIMS1/miR-433-3p/CCAR1 regulatory axis ]	RNA Pull-Down//Western Blot//qRT-PCR//FISH//Transwell Assay	We further verified by qRT-PCR that circRIMS1 is upregulated in both bladder cancer tissue and cell lines.Taken together, our research demonstrated that circRIMS1 promotes tumor growth, migration, and invasion through the miR-433-3p/CCAR1 regulatory axis, representing a potential therapeutic target and biomarker in bladder cancer.		Yes	 Inhibition of circRIMS1 suppressed the proliferation, migration, and invasion of bladder cancer cells both in vitro and in vivo.	33230478
hsa_circ_100146	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	regulation[RNF2]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Our data showed that circRNA_100146 expression was increased in bladder cancer tissues and cell lines, and that high expression of circRNA_100146 was correlated with poor patient prognosis. Our findings indicate that circRNA_100146 functions as a sponge of miR-149-5p in promoting bladder cancer progression by regulating RNF2 expression and that circRNA_100146 may serve as a novel biomarker in human bladder cancer.	Our data showed that circRNA_100146 expression was increased in bladder cancer tissues and cell lines, and that high expression of circRNA_100146 was correlated with poor patient prognosis. 	Yes	 Upregulation of circRNA_100146 promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, whereas knockdown of circRNA_100146 displayed opposite effects on bladder cancer cells. 	33149615
circFUT8	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder tissues	regulation[miR-570-3p/KLF10 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//FISH//Luciferase Report Assay	 Quantitative real-time PCR analysis demonstrated that circFUT8 was downregulated in BCa tissues and correlated with patients' prognosis, histological grade, and lymph node (LN) metastasis.In conclusion, circFUT8 functions as a tumor suppressor in BCa cells by targeting the miR-570-3p/KLF10 axis and may serve as a potential biomarker and therapeutic target for the management of BCa patients with LN metastasis.	 Quantitative real-time PCR analysis demonstrated that circFUT8 was downregulated in BCa tissues and correlated with patients' prognosis, histological grade, and lymph node (LN) metastasis.	Yes	Functionally, gain- and loss-of-function assays indicated that circFUT8 inhibited the migration and invasion of BCa cell lines in vitro and LN metastasis in vivo.	32072011
hsa_circ_103809	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	regulation[miR-516a-5p/FBXL18 Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	circRNA_103809 was highly expressed in BC tissues and cell lines.circRNA_103809 promotes proliferation, migration, invasion and chemo-resistance of BC cells through regulating miR-516a-5p/FBXL18 axis.	CircRNA_103809 high expression was associated with a poor progression in BC patients.	Yes	CircRNA_103809 knockdown impaired the growth and metastasis of BC cells.	32922071
circBC048201	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cells	regulation[miR-1184/ITGA3 axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	circBC048201 was abnormally highly expressed in bladder cancer tissues and cells, and the interference with circBC048201 inhibited bladder cancer cell proliferation, migration, and invasion. In summary, our results showed that circBC048201 was abnormally highly expressed in bladder cancer tissues and cells, and the interference with circBC048201 inhibited the proliferation, migration, and invasion of bladder cancer cells through the miR-1184/ITGA3 axis.		Yes	circBC048201 was abnormally highly expressed in bladder cancer tissues and cells, and the interference with circBC048201 inhibited bladder cancer cell proliferation, migration, and invasion. 	32789658
hsa_circ_0008532	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC cell lines and tissues	regulation[miR-155-5p/miR-330-5p/MTGR1 axis]	Western Blot//FISH//qRT-PCR//RIP//Luciferase Report Assay	We found that circ_0008532 is upregulated in BC cell lines and tissues. Circ_0008532 may act as an oncogene in BC through a novel circ_0008532/miR-155-5p, miR-330-5p /MTGR1/Notch pathway axis, which in turn may provide potential biomarkers and a therapeutic target for the management of bladder cancer.		Yes	Moreover, overexpression of circ_0008532 promotes, and silencing of circ_0008532 inhibits the capacity for invasive in BC cells. 	32460831
circKIF4A	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	regulation[circKIF4A-miR-375/1231-NOTCH2 axis]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Detected by qRT-PCR analysis, circKIF4A was significantly upregulated in bladder cancer tissues and cell lines.Generally, our research unveils the essential role of circKIF4A-miR-375/1231-NOTCH2 axis in bladder cancer progression possibly via the competing endogenous RNA mechanism.		Yes	Functionally, knockdown of circKIF4A inhibited the proliferation and colony-formation ability of bladder cancer cells. 	32457613
hsa_circ_0067934	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues	regulation[miR-1304]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 circ_0067934 expression levels were significantly increased in bladder cancer tissues (P<0.001), which was associated with metastasis and a significantly decreased 5-year overall (P<0.05) and disease-free survival (P<0.05). In conclusion, circ_0067934 was demonstrated to increase bladder cancer cell proliferation, migration and invasion through promoting Myc expression levels via the suppression of miR-1304 expression.	 circ_0067934 expression levels were significantly increased in bladder cancer tissues (P<0.001), which was associated with metastasis and a significantly decreased 5-year overall (P<0.05) and disease-free survival (P<0.05).	Yes	In vitro, T24 cells in the small interfering RNA (si)circ_0067934 group demonstrated significantly reduced proliferation, migration and invasion abilities compared with the si negative control (siNC) group (P<0.01). 	32346439
circRGNEF	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	regulation[miR-548/KIF2C axis]	CCK8//qRT-PCR//FISH//Luciferase Report Assay//EdU Staining	 Expression profile analysis of human circRNAs in BC revealed that circRGNEF was upregulated significantly.In summary, the data illustrate that circRGNEF suppresses BC progression by functioning as a miR-548 sponge to enhance KIF2C expression.		Yes	The downregulation of circRGNEF suppressed BC cell metastasis and proliferation by targeting the miR-548/KIF2C axis in vitro and in vivo; these results were verified with luciferase reporter assays.	32305958
hsa_circ_102336	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissue samples and cell lines	interaction[sponging miR-515-5p]	qRT-PCR	Circ_102336 was identified to be sharply increased in both BC tissue samples and cell lines, and increased circ_102336 is correlated with a worse overall survival rate of BC patients.therefore, we suggested that circ_102336 indirectly regulate apoptosis and ABC transport pathways through miR-515-5p to finally modulate BC cell proliferation and chemo-resistance.	Circ_102336 was identified to be sharply increased in both BC tissue samples and cell lines, and increased circ_102336 is correlated with a worse overall survival rate of BC patients.	Yes	Overexpression of circ_102336 dramatically increased the cell proliferation viability of T24 and 5637 cells, while knockdown of circ_102336 exhibited opposite effects.	32208321
hsa_circ_0058063	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	regulation[miR-486-3p/FOXP4 axis]	qRT-PCR//Luciferase Report Assay//RIP	circRNA_0058063 was overexpressed in BC tissues compared with adjacent normal tissues.Taken together, circRNA_0058063 functions by sponging miR-486-3p in BC progression, which could act as a new biomarker and further developed to be a therapeutic target in BC.		Yes	 Knockdown of circRNA_0058063 dramatically decreased cell proliferation and invasion, and promoted apoptosis in 5637 and BIU-87 cell lines. 	32181485
hsa_circ_0032822	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tumor tissues	Interaction(miR-141/EF3 Signaling Axis)	In Vivo Experiment//qRT-PCR//Luciferase Report Assay//Western Blot	 In this study, we confirmed the upregulation of circ_0032822 in HNSCC tumor tissues. Mechanistic analysis showed that circ_0032822 acted as a competing endogenous RNA of miR-141 to diminish the repressive effect of miR-141 on its target E2F3. 		Yes	Functionally, the overexpression of circ_0032822 significantly promoted the proliferation of HNSCC cell lines along with the S phase arrest and reduced apoptosis, while downregulation of circ_0032822 has the opposite effect in vitro. 	33981611
circPARD3	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues and cell lines 	Interaction(circPARD3/miR-5194/ENO1)	CCK8//qRT-PCR//RIP//Western Blot	 Upregulated circPARD3 observed in HNSCC tissues and cell lines indicated the poor prognosis of patients. Mechanistically, circPARD3 harbored miR-5194, serving as a miRNA sponge, thereby increasing ENO1 expression. Moreover, ENO1 evidently reversed miR-5194-mediated attenuated malignant behaviors. 	 Upregulated circPARD3 observed in HNSCC tissues and cell lines indicated the poor prognosis of patients. 	Yes	Stable knockdown of circPARD3 dramatically exerted the suppressive effects on cell viability, proliferation, migration, and invasion, as well as glucose uptake and lactate production. 	35900705
circBNC2	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	 EOC tissues	Interaction(miR-223-3p/ LARP4 axis)	qRT-PCR	 The expression of circBNC2 and LARP4 was decreased in EOC tissues, while the expression of miR-223-3p was increased. CircBNC2 can sponge miR-223-3p, and LARP4 is the target of miR-223-3p.  In-vitro complement experiments showed that overexpression of circBNC2 significantly decreased the malignant behavior of EOC, while co-transfection of miR-223-3p mimics partially upregulated this change. Mechanically, circBNC2 regulates LARP4 expression in EOC cells by spongy miR-223-3p.		Yes	 In addition, LARP4 knockdown increased the proliferation, migration, and invasion of EOC cells inhibited by miR-223-3p inhibitor.	36730544
hsa_circ_0000253	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-1236-3p/SP1 axis)	BrdU//qRT-PCR	Circ_0000253 was upregulated in OS tissues and cell lines. Circ_0000253 targeted miR-1236-3p directly and negatively modulated its expression. SP1 was miR-1236-3p's target gene and positively regulated by circ_0000253.		Yes	 Circ_0000253 overexpression facilitated OS cell growth and suppressed apoptosis, whereas knocking down circ_0000253 inhibited OS cell growth and facilitated apoptosis. 	36444162
hsa_circ_0097271	CircRNA	Homo sapiens	Osteosarcoma	 OS samples and cells	Interaction(miR-640/MCAM Pathway)	qRT-PCR//Western Blot	Circ_0097271's expression was enhanced in OS samples and cells.  Circ_0097271 targeted miR-640 and negatively modulated miR-640 expression. MiR-640 was poorly expressed in OS, and its depletion recovered OS cell growth and migration that were repressed by circ_0097271 knockdown. MiR-640 bound to MCAM 3'UTR and thus suppressed MCAM expression. MCAM knockdown repressed OS cell growth and migration, while additional miR-640 depletion partially abolished the anticancer effects of MCAM knockdown in OS cells.		Yes	 The knockdown of circ_0097271 restrained OS cell growth and migration, and its downregulation also blocked solid tumor growth in vivo. 	36340580
hsa_circ_0051079	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(circ_0051079/miR-1286/MAFB axis )	qRT-PCR//Luciferase Report Assay	 Circ_0051079 expression was upregulated in OS. Circ_0051079 interacted with miR-1286, and the tumor-inhibitory function of si-circ_0051079 was abolished by miR-1286 inhibition in OS cells. MAFB served as a target for miR-1286. OS cell progression was suppressed by miR-1286 overexpression via downregulating MAFB. Circ_0051079/miR-1286 resulted in expression change of MAFB in OS cells. Silencing circ_0051079 inhibited tumor growth in vivo via regulating the miR-1286/MAFB axis.		Yes	Downregulation of circ_0051079 reduced OS cell proliferation, migration, invasion, and accelerated apoptosis. 	36153605
hsa_circ_0136666	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-1244/CEP55 axis)	qRT-PCR//Western Blot	Circ_0136666 expression was prominently elevated in OS tissues and cell lines.  Circ_0136666 negatively regulated miR-1244 expression by binding to it in OS cells. MiR-1244 overexpression suppressed the malignant behaviors of OS cells. CEP55 was a target of miR-1244 in OS cells. Circ_0136666 positively regulated CEP55 expression partly by sequestering miR-1244 in OS cells. 		Yes	Circ_0136666 absence restrained the proliferation, migration, invasion and glycolytic metabolism and promoted the apoptosis of OS cells. CEP55 overexpression largely reversed circ_0136666 silencing-mediated influences in OS cells. Circ_0136666 silencing significantly suppressed tumor growth in vivo.	36109749
circFOXM1	CircRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(miR-320a and miR-320b/Wnt signaling pathway)	qRT-PCR//RIP	High expression of circ-FOXM1 was detected in OS cell lines.  From the aspect of molecular mechanism, circ-FOXM1 was discovered to upregulate FOXM1 expression via sponging miR-320a and miR-320b, therefore activating Wnt signaling pathway. Besides, rescue experiments elucidated that circ-FOXM1 regulated cellular activities of OS cells via FOXM1. 		Yes	 Functionally, circ-FOXM1 knockdown inhibited the proliferation, migration and EMT process, whereas induced the apoptosis of OS cells. Further, in vivo assays supported that loss of circ-FOXM1 restrained OS tumor growth.	35799265
circNASP	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(miR-1253/FOXF1)	qRT-PCR//Luciferase Report Assay	In the present study, we screened out a novel circRNA termed circNASP which was significantly upregulated in OS tissues compared to adjacent normal tissues. Taken together, our findings demonstrated that circNASP contributes to malignant behaviors of OS cells by miR-1253/FOXF1 pathway, which suggested circNASP/miR-1253/FOXF1axis might be a potential therapeutic target.	Moreover, we showed that circNASP expression was positively correlated with tumor size and metastasis in OS patients.	Yes	 We found that circNASP knockdown dramatically inhibited the proliferation, cell cycle progression and invasion of OS cells. 	29678578
hsa_circ_0070441	CircRNA	Homo sapiens	Parkinson Disease	SH-SY5Y cells	Interaction(miR-626/IRS2 axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//ELISA	 The levels of circ_0070441 and IRS2 were increased while miR-626 expression was decreased in MPP+-treated SH-SY5Y cells in dose- and time-dependent manners.In summary, circ_0070441 aggravated MPP+-triggered neurotoxic effect in SH-SY5Y cells by regulating miR-626/IRS2 axis.		Yes	Depletion of circ_0070441 alleviated MPP+-triggered neuronal damage by regulating cell apoptosis and inflammation.	34748128
hsa_circ_0004381	CircRNA	Homo sapiens	Parkinson Disease	SK-N-SH cells	Interaction(miR-185-5p/RAC1 Axis)	qRT-PCR//ELISA	Hsa_circ_0004381 and RAC1 were increased, and miR-185-5p was decreased in MPP+-triggered SK-N-SH cells.  The mechanical analysis suggested that hsa_circ_0004381 served as a sponge of miR-185-5p to affect RAC1 expression. Hsa_circ_0004381 could contribute to MPP+-triggered neuron injury by targeting the miR-185-5p/RAC1 axis, which provided a novel insight into the pathogenesis and treatment of PD.		Yes	Moreover, hsa_circ_0004381 silencing promoted cell viability, and repressed apoptosis, inflammatory response, and oxidative stress in MPP+-treated SK-N-SH cells. 	35726081
circHIPK3	CircRNA	Homo sapiens	Parkinson Disease	human serum and cerebral fluids 	Interaction(miR-124-3p/STAT3/NLRP3 signaling pathway )	Western Blot//qRT-PCR//RIP//FISH//ELISA	 The expression of circHIPK3 in human serum and cerebral fluids was significantly higher than in controls, whereas miR-124 expression was drastically reduced.  In addition, lipopolysaccharide (LPS)-treated BV2 cells exhibited higher expression of circHIPK3 and lower miR-124 expression. The upregulation of circHIPK3 increased IL-6, IL-1β and TNF-α secretion in BV2 cells. The protein expressions of microglia markers (CD11b and Iba-1), as well as pyroptosis-related factors, NLRP3, caspase-1, and ASC, were also increased following the expression of circHIPK3. All these effects were reversed by the addition of miR-124.		Yes	The SH-SY5Y cells exhibited a significantly impaired viability and elevated apoptotic rate, along with an upregulation of circHIPK3 and a downregulation of miR-124 expression after being treated with supernatants collected from LPS-treated BV2 cells. 	36306116
circTLK1	CircRNA	Homo sapiens	Parkinson Disease	PD models	Interaction(miR-26a-5p/DAPK1)	qRT-PCR//Luciferase Report Assay	 The expression of circTLK1 was notably elevated in in vitro and in vivo PD models.MiR-26a-5p acts as a sponge of DAPK1 to mediate circTLK1 functions. Luciferase reporter gene assay confirmed the interaction between circTLK1 and miR-26a-5p as well as miR-26a-5p and DAPK1.		Yes	Knockdown of circTLK1 significantly improved cell viability, suppressed apoptosis and cytotoxicity, whereas inhibition of miR-16a-5p and overexpression of DAPK1 abolished these effects. 	35447224
circzip-2	CircRNA	Homo sapiens	Parkinson Disease	worms	Interaction [miR-60]	qRT-PCR//RNA-seq	We went on to sequence circzip-2 which is synthesized from functionally important gene zip-2. Studying RNAi-induced knockdown conditions of zip-2, we observed a reduced aggregation of α-synuclein protein along with an enhanced lifespan of the worms. We further carried out transcriptome analysis of zip-2 silenced worms, which suggested that zip-2 might be functioning via Daf-16 pathway. Further interaction studies revealed that circzip-2 possibly sponges microRNA molecule miR-60 towards asserting an important role in various processes associated with PD.		Yes	 Studying RNAi-induced knockdown conditions of zip-2, we observed a reduced aggregation of α-synuclein protein along with an enhanced lifespan of the worms. 	29363043
hsa_circ_0009910	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	 bone marrow aspiration	Interaction[miR-20a-5p]	RNA Pull-Down//CCK8//FISH//Luciferase Report Assay//Microarray	 Furthermore, we found that circ_0009910 was significantly upregulated in AML patients compared with iron-deficiency anemia patients. Further experiments in vitro and in vivo demonstrated that knockdown of circ_0009910 inhibited AML cell proliferation and induced apoptosis through sponging miR-20a-5p. Our findings firstly identify that circ_0009910 is significantly upregulated in AML bone marrow samples and might serve as a novel outcome biomarker for AML. Both circ_0009910 and miR-20a-5p may be potential therapeutic targets for future AML treatment.	 High circ_0009910 expression predicted a poor risk and outcome of AML patients. 	Yes	Further experiments in vitro and in vivo demonstrated that knockdown of circ_0009910 inhibited AML cell proliferation and induced apoptosis through sponging miR-20a-5p. 	30612066
hsa_circ_0079480	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute		regulation[miR-654-3p/HDGF axis]	CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining	In this analysis, hsa_circ_0079480, a novel circRNA, has been identified as being highly expressed in AML. In summary, hsa_circ_0079480 is highly expressed in AML and drives by tumor progression via regulation of hsa_circ_0079480/miR-654-3p/HDGF axis, indicating that hsa_circ_0079480 may function as a new treatment target for AML therapy.		Yes	 Loss-of-function assays showed that reduction of hsa_circ_0079480 decreased the growth and stimulated apoptosis of AML cells in vitro. 	33290265
hsa_circ_0002483	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow,cell line	regulation[miR-758-3p/MYC axis]	CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	 Circ_0002483 expression was elevated in AML patients and cells.Circ_0002483 knockdown repressed AML cell proliferation and promoted cycle arrest and apoptosis via controlling miR-758-3p/MYC axis.		Yes	Circ_0002483 silence constrained AML cell proliferation and facilitated cell cycle arrest and apoptosis. 	33283885
circPTK2	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow 	regulation[miR-330-5p/FOXM1 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	 Circ-PTK2 was highly expressed in AML. Circ-PTK2 promoted the proliferation and hampered the apoptosis of AML cells through targeting miR-330-5p/FOXM1 axis.		Yes	Circ-PTK2 interference suppressed the proliferation and triggered the apoptosis of AML cells.	33126007
circCRKL	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML cell lines and samples	Interaction(miR-196a-5p/miR-196b-5p/p27 axis)	qRT-PCR//RIP	The results indicated low circCRKL expression in AML cell lines and samples. In addition, bioinformatics tools and luciferase assays revealed that circCRKL could sponge miR-196a-5p and miR-196b-5p to promote the expression of p27. Furthermore, circCRKL inhibited AML cell proliferation via the miR-196a-5p/miR-196b-5p/p27 axis, suggesting a potential new target for AML therapy.		Yes	Moreover, the overexpression of circCRKL inhibited the proliferation and colony-forming ability of AML cells, while its silencing promoted them. 	34617876
hsa_circ_0005774	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	blood of pediatric AML patients and AML cells	Interaction(miR-192-5p/ULK1 ceRNA pathway)	qRT-PCR//Luciferase Report Assay//RIP	Real time-quantitative PCR revealed that circ_0005774 was highly expressed in blood of pediatric AML patients and AML cells (HL-60 and NB4), accompanied with downregulated miRNA-192-5p (miR-192-5p) which was a crucial tumor-associated and leukemia-related miRNA. Circ_0005774 was abundant in miRNA response element according to CSCD software, and miR-192-5p was identified as a target of circ_0005774, as evidenced by RNA immunoprecipitation and dual-luciferase reporter assays. Notably, ULK1 was a downstream target of miR-192-5p and indirectly modulated by circ_0005774. 		Yes	Accordingly, blocking circ_0005774 and/or overexpressing miR-192-5p could enhance apoptosis rate of HL-60 and NB4 cells, but suppress cell viability and cell cycle entrance, accompanied with depression of proliferation markers including proliferating cell nuclear antigen (PCNA), CyclinD1 and B cell lymphoma 2 (Bcl-2).	33735626
circSPI1	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients	Interaction(miR-1307-3p, miR-382-5p, and miR-767-5p)	CCK8//qRT-PCR//Western Blot	 Here, we found that circSPI1, the circular RNA derived from the SPI1 gene, is highly expressed in AML but not in normal counterparts. On one hand, circSPI1 contributes to myeloid differentiation of AML cells by interacting with the translation initiation factor eIF4AIII to antagonize PU.1 expression at the translation level. On the other hand, circSPI1 contributes to proliferation and apoptosis by interacting with miR-1307-3p, miR-382-5p, and miR-767-5p; this role is uncoupled with SPI1. 	 Finally, we illustrate the clinical significance of circSPI1 by showing that circSPI1-regulated genes are associated with the clinical outcome of AML patients.	Yes	 Unlike SPI1, a tumor suppressor and being lowly expressed in AML, we demonstrate that circSPI1 acts as an oncogene, evidenced by the observation that circSPI1 knockdown induces myeloid differentiation and apoptosis of AML cells.	33741901
hsa_circ_0001982	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells (MG63)	Interaction(miR-143)	qRT-PCR//Transwell Assay	The expression of hsa_circ_0001982 was significantly increased in OS tissues and cells (MG63), as in well as chemoresistant OS tissues and cells (MG63/Dox). By contrast, knockdown of hsa_circ_0001982 markedly reduced the resistance of MG63/Dox cells to doxorubicin (IC50 evidently reduced). Bioinformatic prediction showed that miR-143 was a target miRNA of hsa_circ_0001982, and a dual-luciferase reporter assay proved this. Further experiments revealed that miR-143 expression was notably downregulated in OS tissues, chemoresistant OS tissues, and MG63/Dox cells. Moreover, miR-143 was negatively correlated with hsa_circ_0001982 in OS cells and tissues.		Yes	Overexpression of hsa_circ_0001982 promoted proliferation, colony formation, migration, invasion, and multidrug resistance in MG63 cells.	35576496
circNRIP1	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines	Interaction(miR-1200/MIA2 )	qRT-PCR//IHC	CircNRIP1 was mainly localized in OS cell cytoplasm and significantly lower in OS cell lines than in normal human osteoblasts. miR-1200 was predicted as the sponge miRNA of circNRIP1 and directly interacted with circNRIP1 confirmed by the dual-luciferase reporter assay. Moreover, miR-1200 overexpression significantly alleviated the inhibitory effect of circNRIP1 on OS cells. A protein-coding gene MIA2 was identified as the miR-1200 targeting gene and reversely associated with miR-1200 expression in OS cells. Increase in MIA2 expression in a murine OS cell xenograft model was associated with circNRIP1 expression in inhibition of OS cell xenograft growth in vivo. 		Yes	 CircNRIP1 overexpression significantly inhibited OS cell proliferation, migration, and invasion in vitro. 	35812061
circPTK2	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML peripheral blood samples and cells	Interaction(miR-582-3p/ALG3 axis)	qRT-PCR//MTT//RIP	 CircPTK2 level was enhanced in AML peripheral blood samples and cells.Mechanically, circPTK2 functioned as the sponge for miR-582-3p to positively ALG3 expression in AML cells. Moreover, miR-582-3p inhibition ameliorated the impacts of circPTK2 knockdown on AML cell processes. MiR-582-3p overexpression regulated cell phenotypes by targeting ALG3.		Yes	CircPTK2 knockdown restrained AML cell proliferation and glycolysis and promoted cell apoptosis and cell cycle arrest. 	35980117
circSRSF4	CircRNA	Homo sapiens	Osteosarcoma	 osteosarcoma tissues and cell lines	Interaction( circSRSF4/miR-224/Rac1 axis)	CCK8//qRT-PCR	The expression of circSRSF4 was significantly higher in osteosarcoma tissues and cell lines.  A mechanistic study showed that circSRSF4 can be used as an miR-224 sponge to up-regulate the expression of Rac1, thereby promoting the development of osteosarcoma.		Yes	Down-regulating the expression of circSRSF4 in vitro significantly inhibited the proliferation, invasion, and migration of cells, and also reduced the expression of Rac1, while the overexpression of Rac1 and miR-224 inhibition could reverse these effects. The inhibition of circSRSF4 expression in vivo also attenuated tumor growth.	35682879
circMRPS35	CircRNA	Homo sapiens	Osteosarcoma	 osteosarcoma cells	Interaction(KAT6B/FOXO3)	qRT-PCR//Western Blot	Mechanically, the depletion of circMRPS35 reduced the enrichment of histone H3 lysine 23 acetylation (H3K23ac) on forkhead box O3 (FOXO3) promoter in osteosarcoma cells. The interaction of circMRPS35 and KAT6B was identified. The knockdown of KAT6B reduced the enrichment of H3K23ac on FOXO3 promoter in osteosarcoma cells. 		Yes	 The colony formation numbers and Edu-positive osteosarcoma cells were repressed by the overexpression of circMRPS35. Meanwhile, the overexpression of circMRPS35 increased the apoptosis rate of osteosarcoma cells. The expression levels of autophagy markers, including LC3 and Beclin1, were enhanced by the overexpression of circMRPS35 in osteosarcoma cells.The overexpression of circMRPS35 inhibited the tumor growth in vivo , whereas the depletion of KAT6B could reverse the effect in the mice. 	35503036
hsa_circ_0087302	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	Regulation(Wnt/β-catenin)	CCK8//qRT-PCR	Using RT-PCR, we confirmed that the expression of hsa_circ_0087302 in osteosarcoma cells was lower than that in osteoblasts. Furthermore, Western blotting experiments demonstrated that hsa_circ_0087302 affected the expression of cell cycle- and Wnt/β-catenin signaling pathway-related proteins.		Yes	Functional validation experiments revealed that hsa_circ_0087302 overexpression inhibited proliferation, cell cycle, migration, and invasion in osteosarcoma cells.	36035366
hsa_circ_0069117	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines	Interaction(miR-875-3p/PF4V1 )	qRT-PCR//Western Blot	We identified hsa_circ_0069117 as the most markedly dysregulated circRNA in OS cell lines.Bioinformatics analysis indicated that hsa_circ_0069117 might inhibit the expression of miR-875-3p, thereby promoting the expression of platelet factor 4 variant 1 (PF4V1).  Luciferase reporter gene assays confirmed the binding sites of miR-875-3p on hsa_circ_0069117 and PF4V1. 	The expression of miR-875-3p was negatively correlated to hsa_circ_0069117 and PF4V1 in clinical samples. 	Yes	Gain/loss-of-function and rescue assays further indicated that hsa_circ_0069117 could significantly promote the expression of PF4V1 by sponging miR-875-3p, thereby inhibiting the proliferation and migration of OS cells by suppressing ERK1 and AKT.	35062989
circCSPP1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction( miR-200c )	qRT-PCR//RNA Pull-Down	CircCSPP1 and premature miR-200c levels were increased while mature miR-200c level was decreased in OS. CircCSPP1 was detected in both the nuclear and cytoplasm fractions of OS cells. CircCSPP1 directly interacted with premature miR-200c. CircCSPP1 overexpression increased premature miR-200c level, glucose uptake, and cell proliferation, but decreased mature miR-200c level. MiR-200c overexpression suppressed the role of circCSPP1 in OS cells.		Yes	 CircCSPP1 overexpression increased premature miR-200c level, glucose uptake, and cell proliferation, but decreased mature miR-200c level. 	35713481
hsa_circ_0051079	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(miR-625-5p/TRIM66/Wnt/β-catenin)	qRT-PCR	 Circ_0051079 and TRIM66 expressions were significantly upregulated, but miR-625-5p was downregulated in OS tissues and cells compared with control groups. MiR-625-5p, a target miRNA of circ_0051079, participated in regulating circ_0051079-induced effects. Also, TRIM66 was identified as a target mRNA of miR-625-5p, and partially attenuated the inhibitory effects of miR-625-5p in OS cells. Circ_0051079 modulated the Wnt/β-catenin pathway through TRIM66 in vitro. Importantly, circ_0051079 silencing reduced TRIM66 expression by interacting with miR-625-5p.	Circ_0051079 expression was significantly associated with tumor-node-metastasis stage and tumor size of OS patients.	Yes	Circ_0051079 knockdown inhibited OS cell proliferation, migration and invasion, repressed angiogenesis but induced cell apoptosis, accompanied by the decreases of PCNA and Bcl-2 production and an increase of Bax production. Further, circ_0051079 depletion inhibited tumor formation in vivo.	35733786
hsa_circ_0001174	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cell lines	Interaction(miR-186-5p/MACC1 axis)	Western Blot//Bioinformatics Analysis//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	 the results were consistent with the sequencing data, and circ_0001174 was found to be significantly upregulated in 16 pairs of OS tissues and OS cell lines (fold change > 2.0, P value < 0.05). Additionally, circ_0001174 directly and negatively modulated the expression of miR-186-5p and positively regulated the expression of MACC1.		Yes	 Knockdown of circ_0001174 inhibited the proliferation, migration, and invasion of OS cells. 	35279159
circRASSF2	CircRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(miR-6838-5p)	CCK8//qRT-PCR	Compared with osteoblasts, OS cells showed lower expression of miR-6838-5p and higher expression of circRASSF2. The dual luciferase report confirmed that miR-6838-5p targeted IGF1R. Overexpression of IGF1R significantly blocked the anticancer effects of miR-6838-5p. The dual luciferase report verified that circRASSF2 targeted miR-6838-5p, and promoted the expression of IGF1R. Overexpression of circRASSF2 not only promoted the malignant biological behavior of OS cells, but also blocked the anticancer effects of miR-6838-5p. In OS tissue, circRASSF2 and IGF1R were upregulated, and the two were positively correlated. MiR-6838-5p was downregulated, which negatively correlated with both circRASSF2 and IGF1R. High levels of circRASSF2 were associated with higher stage and metastasis of OS.		Yes	Overexpression of IGF1R significantly blocked the anticancer effects of miR-6838-5p.	35242856
hsa_circ_0001017	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines & U2OS cells	Interaction(miR-145-5p)	qRT-PCR//MTT	A total of 241 CDECs, including 75 upregulated and 166 downregulated CDECs, were identified in three OS cell lines compared with normal vascular endothelial cells. PCR validation showed that hsa_circ_0000704, hsa_circ_0001017 and hsa_circ_0005035 were all highly expression in the three OS cell lines, compared with osteoblast cell lines (HECC, hFOB1.19 and HFF-1). Functionally, overexpression of circ_0001017 significantly promoted the cell proliferation, migration and invasion and decreased apoptosis in U2OS cells. Knockdown of circ_0001017 obtained the opposite results. Circ_0001017 may downregulate miR-145-5p through direct binding. Furthermore, the expression of miR-145-5p was negatively regulated by circ_0001017 in OS cells. In addition, further functional studies indicated that miR-145-5p inhibitor eliminated the effects caused by si-circ_0001017 in OS cells.		Yes	Functionally, overexpression of circ_0001017 significantly promoted the cell proliferation, migration and invasion and decreased apoptosis in U2OS cells. Knockdown of circ_0001017 obtained the opposite results.	35346268
circUBAP2	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(circ_UBAP2/miR-637/HMGB2 axis)	CCK8//qRT-PCR	Circ_UBAP2 showed high expression levels in OS tissues and cells, which was directly proportional to metastasis and clinical stage of OS. Furthermore, miR-637 served as a downstream target of circ_UBAP2, which played opposite roles to circ_UBAP2 in OS. More importantly, HMGB2 served as miR-637's downstream target. The xenograft experiments in nude mice also proved that knockdown of circ_UBAP2 could increase miR-637 expression, but decrease HMGB2 expression, thus alleviating OS progression. Mechanistically, circ_UBAP2 exerts a cancer-promoting effect on OS by downregulating miR-637 and upregulating the expression of HMGB2. 		Yes	The overexpression of circ_UBAP2 enhanced the growth, invasion, and migration of OS cells, but suppressed their apoptosis. In contrast, circ_UBAP2 silencing had opposite effects. 	35114890
circCYP51A1	CircRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(miR-490-3p/KLF12 axis)	qRT-PCR//Western Blot	 CircCYP51A1 and KLF12 expression were dramatically increased, whereas miR-490-3p was decreased in OS cells under hypoxia condition. CircCYP51A1 enhanced KLF12 expression by sponging miR-490-3p. MiR-490-3p inhibitor weakened the inhibition effect of circCYP51A1 knockdown on the progression of OS under hypoxia. Besides, overexpression of miR-490-3p inhibited cell progression of OS under hypoxia condition, while the effects were attenuated by KLF12 overexpression. 		Yes	Deficiency of circCYP51A1 hindered hypoxia-induced cell proliferation, migration, invasion and glycolysis in OS cells.	36276300
circCDK14	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cell lines	Interaction(miR-198/E2F2 axis)	Migration Assay//qRT-PCR//Cell Viability Assay//Invasion Assay//Transwell Assay	Our data revealed that circ-CDK14 was up-regulated and miR-198 was down-regulated in OS tissues and cell lines. Mechanistically, circ-CDK14 directly targeted miR-198. Moreover, miR-198 was a functional mediator of circ-CDK14 in regulating OS cell progression in vitro. E2F2 was a direct target of miR-198, and miR-198 overexpression regulated OS cell progression in vitro by down-regulating E2F2. Furthermore, circ-CDK14 regulated E2F2 expression by functioning as a sponge of miR-198 in OS cells.		Yes	 Circ-CDK14 silencing suppressed OS cell viability, migration, invasion, and glycolysis and promoted cell apoptosis in vitro, as well as diminished tumor growth in vivo.	35218724
hsa_circ_0078767	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines and tissues	Interaction(miR-889/KLF9 )	qRT-PCR	This study confirmed that circ_0078767 expression was reduced in OS cell lines and tissues. MicroRNA-889 (miR-889) was targeted and regulated by circ_0078767, and miR-889 could negatively modulate Kruppel-like factor 9 (KLF9) expression. Besides, circ_0078767 positively regulated KLF9 expression in OS cells via repressing miR-889. In conclusion, circ_0078767 enhances KLF9 expression by targeting miR-889 to inhibit OS progression.		Yes	Circ_0078767 overexpression remarkably inhibited OS cell growth, migration, invasion, epithelial-mesenchymal transition (EMT), and promoted apoptosis, whereas circ_0078767 knockdown resulted in the opposite effects. 	35758280
circFIRRE	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma cell lines and tissues	Interaction(miR-486-3p and miR-1225-5p/LUZP1)	Bioinformatics Analysis	In this article, a novel circular RNA, circFIRRE (hsa_circ_0001944) was screened out and identified from RNA-sequencing, and was upregulated in both osteosarcoma cell lines and tissues. Mechanistically, upregulated circFIRRE was induced by transcription factor YY1, and partially boosted the mRNA and protein level of LUZP1 by sponging miR-486-3p and miR-1225-5p.	Clinically, aberrantly upregulated circFIRRE portended higher metastatic risk and worse prognosis in osteosarcoma patients. 	Yes	" Functionally, in vitro, ex vivo and in vivo experiments demonstrated that circFIRRE could drive primary osteosarcoma progression and lung metastasis by inducing both tumor cells and blood vessels, we call as ""tumorigenic-angiogenic coupling"". "	35986280
circCTNNB1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Expression(highly expressed)	qRT-PCR//Northern Blot//Western Blot	Circ-CTNNB1 was highly expressed in OS tissues and predominantly detected in the nucleus of OS cells.  Mechanistically, circ-CTNNB1 interacted with RBM15 and subsequently promoted the expression of hexokinase 2 (HK2), glucose-6-phosphate isomerase (GPI) and phosphoglycerate kinase 1 (PGK1) through N6-methyladenosine (m6A) modification to facilitate the glycolysis process and activate OS progression.		Yes	Ectopic expression of circ-CTNNB1 promoted the growth, invasion, and metastasis of OS cells in vitro and in vivo. 	36181462
circTNPO1	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines 	Interaction(miR-338-3p)	CCK8//qRT-PCR	 The RNA expression of circTNPO1 in OS cell lines U2OS, HOS, MG63, 143B, ZOS and ZOSM were 2.73±0.27, 3.18±0.54, 4.33±0.52, 5.75±0.65, 4.50±0.49 and 3.96±0.35, respectively, higher than 1.00±0.09 in hFOB1.19 (P<0.001).CircTNPO1 promotes the proliferation and metastasis of OS by sponging miR-338-3p, which could be a new target for OS treatments.		Yes	CCK-8 assay revealed that after 48 h and 72 h, the absorbance of sh-circTNPO1 #1 was 0.81±0.05 and 1.09±0.06, while sh-circTNPO1 #2 143B cells was 0.84±0.04 and 1.2±0.04, which were sharply reduced compared with the control (1.00±0.06 and 1.49±0.06, P<0.001); after 48 h and 72 h, the absorbance of 143B cells transfected with circTNPO1 #1 and miR-338-3p (0.92±0.06 and 1.32±0.07) were higher than those of cells transfected with sh-circTNPO1 cells and miR NC (0.92±0.06 and 1.32±0.07, P<0.050). Wound healing assay demonstrated that the 24 hour-migration rates of sh-circTNPO1 #1 and sh-circTNPO1 #2 cells were (24.43±2.15)% and (39.70±4.20)% respectively, which were significantly lower than that of the control [(56.51±3.27)%, P<0.010]; the migration rates of sh-circTNPO1 #1+ miR NC and sh-circTNPO1 #1+ miR-338-3p inhibitor were (26.70±2.21)% and (46.10±5.71)%, with a significant difference (P<0.005). In xenograft tumor model, the weight and size of tumors in control, sh-circTNPO1 #1+ miR NC and sh-circTNPO1 #1+ miR-338-3p inhibitor mice were (458.80±158.10) mg, (262.50±82.09) mg, (395.40±137.60) mg and (593.00±228.40) mm(2,) (203.30±144.20) mm(2,) (488.60±208.60) mm(2,) respectively.  Compared with control, sh-circTNPO1 tumors were significantly smaller (P<0.01).	36164699
circAGFG1	CircRNA	Homo sapiens	Osteosarcoma	 osteosarcoma cells	Interaction(miR-302a/LATS2)	In Vivo Experiment//qRT-PCR	 The expression level of circAGFG1 was upregulated in osteosarcoma cells. CircAGFG1 was specifically bound to miR-302a to regulate the expression activity of miR-302a. MiR-302a specifically bound to the 3'UTR of LATS2 and inhibited the expression of LATS2. The overexpression of miR-302a reversed the effect of circAGFG1 on the proliferation, invasion, and migration of osteosarcoma cells. CircAGFG1 regulated the expression of LATS2 by miR-302a, thereby regulating the proliferation, migration, and invasion of osteosarcoma cells.		Yes	The downregulation of circAGFG1 inhibited the proliferation, invasion, and migration of osteosarcoma cells.  The overexpression of circAGFG1 enhanced the stemness of osteosarcoma cells. 	35958928
circLRP6	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR‑141‑3p/HDAC4/HMGB1 axis)	qRT-PCR//Luciferase Report Assay	The results confirmed that circ?LRP6 was highly expressed in OS tissues and cell lines. In addition, circ‑LRP6 negatively regulated the expression of miR‑141‑3p and, in turn, miR‑141‑3p negatively regulated HDAC4 and HMGB1 expression.		Yes	Functional assays revealed that circ?LRP6 knockdown inhibited the proliferation, migration and invasion of OS cells, whereas the inhibition of miR?141?3p or the overexpression of either HDAC4 or HMGB1 partly reversed the inhibitory effect of circ?LRP6 knockdown. 	35211755
circKIF4A	CircRNA	Homo sapiens	Osteosarcoma	OS cells and tissues	Interaction(miR-515-5p/SLC7A11)	qRT-PCR//Transwell Assay	 In both OS cells and tissues, circKIF4A (hsa_circ_0007255) was found to be upregulated. circKIF4A enhanced OS growth as well as metastasis by sponging miR-515-5p and by upregulating SLC7A11.		Yes	In vitro and in vivo, circKIF4A knockdown markedly suppressed OS proliferation as well as metastasis.	35579738
hsa_circ_0003732	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	Interaction(miR-377-3p/CPEB1 axis )	qRT-PCR//Western Blot	Circ_0003732 was upregulated in osteosarcoma tissues and cells. Meanwhile, miR-377-3p could bind to circ_0003732 and CPEB1 and miR-377-3p inhibitor could reverse the effects of circ_0003732 silence on osteosarcoma cell progression. Furthermore, CPEB1 overexpression could overturn the suppressive impacts of miR-377-3p on osteosarcoma progression. In addition, circ_0003732 silence restrained Wnt/β-catenin signaling pathway via regulating miR-377-3p in osteosarcoma cells. 		Yes	Knockdown of circ_0003732 suppressed osteosarcoma cell proliferation, migration, invasion and triggered cell apoptosis in vitro, as well as reduced osteosarcoma tumor growth in vivo. 	34407049
hsa_circ_0040823	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients and leukemia cells	Interaction(miR-516b/PTEN)	qRT-PCR//Western Blot	 circ_0040823 was significantly downregulated in AML patients and leukemia cells. circ_0040823 acted as a miR-516b sponge and regulated key cellular events in leukemia cells via downregulating miR-516b. Moreover, tumor suppressor phosphatase and tensin homolog (PTEN) was a downstream target of miR-516b. The inhibition of miR-516b impaired the proliferation capacity of leukemia cells and induced apoptosis, while PTEN deficiency attenuated these effects.		Yes	Overexpression of circ_0040823 inhibited AML cell proliferation, and induced apoptosis and cell cycle arrest.  Upregulation of circ_0040823 also repressed the growth of xenograft tumors in vivo.	34913223
hsa_circ_0059706	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	leukemia cells	Expression(lower expressed)	qRT-PCR	We found that circ_0059706 expression was significantly lower in AML patients than in controls (p < 0.001). Survival analysis of patients with AML divided into two groups according to high and low circ_0059706 expression showed that overall survival (OS) of patients with high circ_0059706 expression was significantly longer than that of those with low expression (p < 0.05). Further, female patients with AML and those aged >60 years old in the high circ_0059706 expression group had longer OS than male patients and those younger than 60 years. Multiple regression analysis showed that circ_0059706 was an independent factor-affecting prognosis of all patients with AML. To evaluate the prospects for application of circ_0059706 in machine learning predictions, we developed seven types of algorithm. The gradient boosting (GB) model exhibited higher performance in prediction of 1-year prognosis and 3-year prognosis, with AUROC 0.796 and 0.847. We analyzed the importance of variables and found that circ_0059706 expression level was the first important variables among all 26 factors included in the GB algorithm, suggesting the importance of circ_0059706 in prediction model. Further, overexpression of circ_0059706 inhibited cell growth and increased apoptosis of leukemia cells in vitro. 	We found that circ_0059706 expression was significantly lower in AML patients than in controls (p < 0.001). Survival analysis of patients with AML divided into two groups according to high and low circ_0059706 expression showed that overall survival (OS) of patients with high circ_0059706 expression was significantly longer than that of those with low expression (p < 0.05). Further, female patients with AML and those aged >60 years old in the high circ_0059706 expression group had longer OS than male patients and those younger than 60 years. Multiple regression analysis showed that circ_0059706 was an independent factor-affecting prognosis of all patients with AML. To evaluate the prospects for application of circ_0059706 in machine learning predictions, we developed seven types of algorithm. The gradient boosting (GB) model exhibited higher performance in prediction of 1-year prognosis and 3-year prognosis, with AUROC 0.796 and 0.847. We analyzed the importance of variables and found that circ_0059706 expression level was the first important variables among all 26 factors included in the GB algorithm, suggesting the importance of circ_0059706 in prediction model. 	Yes	urther, overexpression of circ_0059706 inhibited cell growth and increased apoptosis of leukemia cells in vitro.	36338954
circMAT2B	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 HNSCC tissues and cell lines	Interaction(miR-491-5p/ASCT2 axis)	CCK8//qRT-PCR	 Remarkably overexpressed circMAT2B was observed in HNSCC tissues and cell lines, of which high abundance was positively correlated with patients' poor prognosis.  miR-491-5p, interacted with ASCT2, was identified to be a downstream target of circMAT2B, thereby involving in circMAT2B-mediated biological effects. In summary, we draw a conclusion that circMAT2B could modulate the processes of cell proliferation, migration, invasion, and glutaminolysis of HNSCC cells partly via the miR-491-5p/ASCT2 axis by a molecular mechanism of competing endogenous RNA (ceRNA), implying an underlying circRNA-targeted therapy for HNSCC treatment.	 Remarkably overexpressed circMAT2B was observed in HNSCC tissues and cell lines, of which high abundance was positively correlated with patients' poor prognosis. 	Yes	Silencing of circMAT2B inhibited cell proliferation, migration, and invasion, as well as glutaminolysis. 	36219356
hsa_circ_0007534	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	Interaction[sponging miR-625 and miR-892b]	qRT-PCR//Luciferase Report Assay	As a result, circ_0007534 was overexpressed not only in PDAC tissues but also in a panel of PDAC cell lines, and this overexpression is closely associated with advanced tumor stage and positive lymph node invasion. Mechanistically, miR-625 and miR-892b were sponged by circ_0007534. The oncogenic functions of circ_0007534 is partly dependent on its regulation of miR-625 and miR-892b. 	As a result, circ_0007534 was overexpressed not only in PDAC tissues but also in a panel of PDAC cell lines, and this overexpression is closely associated with advanced tumor stage and positive lymph node invasion.	Yes	For the part of functional assays, circ_0007534 significantly increased cell proliferation, migratory, and invasive potential of PDAC cells.	30382592
circFOXK2	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues 	interaction[Sponging MiR-942]	RNA Pull-Down//qRT-PCR//circRNA-seq//RIP//Luciferase Report Assay	Among them, circFOXK2 was validated with significant upregulation in PDAC cells and 63% of primary tumors (53 of 84).circFOXK2 promoted cell growth, migration, and invasion and was involved in cell-cycle progression and apoptosis. circFOXK2 contained multiple miRNA binding sites, functioning as a sponge for miR-942, which in turn promoted expression of ANK1, GDNF, and PAX6. 		Yes	circFOXK2 promoted cell growth, migration, and invasion and was involved in cell-cycle progression and apoptosis.	32217695
circBFAR	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	regulation[ miR-34b-5p/MET/Akt axis]	qRT-PCR//RNA Pull-Down//EdU Staining//Transwell Assay	In the present study, we identified a novel circRNA (termed as circBFAR, hsa_circ_0009065) that was upregulated in a 208-case cohort of patients with PDAC. Additionally, circBFAR overexpression increased the expression of MET and activated downstream phosphorylation of Akt (Ser 473) and further activated the MET/PI3K/Akt signaling pathway, which ultimately promoted the progression of PDAC cells. 	The ectopic expression of circBFAR correlated positively with the tumor-node-metastasis (TNM) stage and was related to poorer prognosis of patients with PDAC.	Yes	Moreover, circBFAR knockdown dramatically inhibited the proliferation and motility of PDAC cells in vitro and their tumor-promoting and metastasis properties in in vivo models.	32375768
hsa_circ_000684	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 PDAC tissues and cells	Interaction(miR-145  )	CCK8//qRT-PCR//Bioinformatics Analysis	Expression of CircRNA_000684 and KLF5 was upregulated, whereas miR-145 expression was downregulated in PDAC tissues and cells. Taken together, the present study provided evidence clarifying that circRNA_000684 could downregulate miR-145 expression and elevate KLF5 to promote the progression of PDAC.		Yes	CircRNA_000684 repression or miR-145 elevation inhibited the proliferation, invasion and migration of PDAC cells and HUVEC angiogenesis, as evidenced by lower levels of MCM2, MMP2 and MMP9 and VEGFA. In-vivo, circRNA_000684 elevation or miR-145 repression promoted tumor growth.	33563550
circSLIT2	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 PDAC tissues and cells	Interaction( miR-510-5p/c-Myc/LDHA axis)	CCK8//qRT-PCR//ChIP	 Here, our study found that the novel circRNA circSLIT2 was significantly upregulated in PDAC tissues and cells. Mechanistically, circSLIT2 acted as miRNA sponge to target miR-510-5p/c-Myc axis. 	Clinically, ectopic high-expression of circSLIT2 was correlated with unfavorable prognosis of PDAC patients.	Yes	 Functional experiments demonstrated that circSLIT2 promoted the aerobic glycolysis and proliferation of PDAC cells in vitro, and circSLIT2 knockdown inhibited tumor growth in vivo. 	34168116
hsa_circ_0005105	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cell lines	Interaction(miR-20a-3p-COL11A1 axis)	Wound Healing Assay//qRT-PCR//RIP//IHC//Invasion Assay	 We found that circ-0005105 expression was upregulated in both PDAC tissues and cell lines. Mechanistically, circ-000510 served as a competing endogenous RNA (ceRNA) of miR-20a-3p and indirectly modulated COL11A1 expression, leading to activation of epithelial-mesenchymal transition (EMT). Rescue experiments suggested that the oncogenic activity of circ-0005105 was dependent on the modulation of the miR-20a-3p-COL11A1 axis. 	Higher circ-0005105 expression correlated positively with the malignant clinical phenotype and poor prognosis of patients with PDAC. 	Yes	 Gain- and loss-of-function analysis showed that circ-0005105 facilitated both in vitro and in vivo cellular proliferation and invasion.	34183642
circEYA3	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cells	Interaction(miR-1294/c-Myc axis)	qRT-PCR//FISH	CircEYA3 was elevated in PDAC tissues and cells, and a higher level of circEYA3 was significantly associated with a poorer prognosis in patients with PDAC.Mechanistically, circEYA3 functions as an endogenous miR-1294 sponge to elevate c-Myc expression, thus exerting its oncogenic functions.	CircEYA3 was elevated in PDAC tissues and cells, and a higher level of circEYA3 was significantly associated with a poorer prognosis in patients with PDAC.	Yes	Functionally, circEYA3 increased energy production via ATP synthesis to promote PDAC progression in vitro and in vivo.	34419070
circNEIL3	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cell lines	Interaction(miR-432-5p/ADAR1 axis )	qRT-PCR//RIP//Western Blot	CircNEIL3 was upregulated in PDAC and promoted the progression of PDAC cells both in vitro and in vivo. Moreover, we discovered that the circNEIL3/miR-432-5p/ADAR1 axis was correlated with the PDAC clinical stage and overall survival of PDAC patients, while ADAR1 may reduce the biogenesis of circNEIL3.	Moreover, we discovered that the circNEIL3/miR-432-5p/ADAR1 axis was correlated with the PDAC clinical stage and overall survival of PDAC patients, while ADAR1 may reduce the biogenesis of circNEIL3.	Yes	CircNEIL3 was upregulated in PDAC and promoted the progression of PDAC cells both in vitro and in vivo. 	33750389
circRHOBTB3	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC cell lines and tissues	Interaction(miR-600/NACC1)	qRT-PCR//RNA Pull-Down//IHC	 circRHOBTB3 is highly expressed in PDAC cell lines and tissues, which also promotes PDAC autophagy and then progression in vitro and in vivo. Mechanistically, circRHOBTB3 directly binds to miR-600 and subsequently acts as a miRNA-sponge to maintain the expression level of miR-600-targeted gene NACC1, which facilitates the autophagy response of PDAC cells for adaptation of proliferation via Akt/mTOR pathway.		Yes	 circRHOBTB3 is highly expressed in PDAC cell lines and tissues, which also promotes PDAC autophagy and then progression in vitro and in vivo. 	34416910
circMYOF	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDA clinical specimens and cell lines	Interaction(VEGFA/PI3K/AKT axis)	qRT-PCR//RNA Pull-Down//Western Blot//Transwell Assay	Real-time PCR indicated that it was highly expressed in PDA clinical specimens and cell lines. Gain-of- and loss-of-function assays showed that circMYOF induced progression in PDA. Mechanistically, RNA pull-down and luciferase reporter experiments elucidated that circMYOF, as a competing endogenous RNA for miR-4739, facilitated glycolysis via the VEGFA/PI3K/AKT pathway. Taken together, our findings indicate that circMYOF may work as a desirable biomarker and therapeutic target for PDA patients.		Yes	Gain-of- and loss-of-function assays showed that circMYOF induced progression in PDA. 	34811346
circRTN4	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 PDAC patients	Interaction(miR-497-5p-HOTTIP pathway)	CCK8//qRT-PCR//Western Blot	CircRTN4 was significantly upregulated in primary tumors from PDAC patients.The upregulated circRTN4 promotes tumor growth and liver metastasis in PDAC through the novel circRTN4-miR-497-5p-HOTTIP pathway. Also, circRTN4 stabilizes RAB11FIP1 to contribute EMT.		Yes	In vitro and in vivo functional studies revealed that circRTN4 promoted PDAC tumor growth and liver metastasis.	34983537
hsa_circ_0007367	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cells	Interaction( miR-6820-3p/YAP1 axis )	CCK8//qRT-PCR//IHC	We first identified that a novel circRNA, hsa_circ_0007367, was markedly upregulated in PDAC tissues and cells. Mechanistically, we confirmed that hsa_circ_0007367 could facilitate the expression of YAP1, a well-known oncogene, by sponging miR-6820-3p, which function as a tumor suppresser in PDAC cells. The results of ISH and IHC demonstrated that hsa_circ_0007367 and YAP1 were upregulated in PDAC tissues.In conclusion, our findings reveal that hsa_circ_0007367 acts as an oncogene via modulating miR-6820-3p/YAP1 axis to promote the progression of PDAC, and suggest that hsa_circ_0007367 may serve as a potential therapeutic target for treatment of PDAC.	Furthermore, clinical data showed that higher hsa_circ_0007367 expression was correlated with advanced histological grade and lymph node metastasis in PDAC patients. 	Yes	Functionally, in vivo and in vitro data indicated that hsa_circ_0007367 promotes the proliferation and metastasis of PDAC.	36008392
circUHRF1	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tumor tissues and cells	Interaction(IRF3/circUHRF1/miR-1306-5p/ARL4C axis)	CCK8//qRT-PCR//Western Blot	Here, our results found that circUHRF1 was highly expressed in PDAC tumor tissues compared with normal tissues.Our findings suggest that circUHRF1 regulated ARL4C expression to promote PDAC progression through sponging miR-1306-5p. The role of miR-1306-5p in PDAC cellular progression has been elucidated, and the expression association between miR-1306-5p and circUHRF1 or ARL4C in PDAC tissues was analyzed. Furthermore, circUHRF1 expression in PDAC cells could be transcriptionally regulated by IRF3. 		Yes	 CircUHRF1 knockdown influenced PDAC cell proliferation, apoptosis, migration and EMT level in vitro, and tumor growth in vivo. 	34983293
hsa_circ_0047744	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 PDAC tissues and cell lines	Interaction( miR-21/SOCS5 axis)	ISH//qRT-PCR//FISH	 We found that circRNA_0047744 was weakly expressed in PDAC tissues and cell lines.  Mechanistically, circ_0047744 could regulate SOCS5 expression by acting as a sponge of miR-21 to inhibit migration and invasion of PDAC cells. 	 The expression of circ_0047744 was negatively correlated with lymph node metastasis and positively correlated with overall survival in PDAC patients. 	Yes	 Functionally, the overexpression of circ_0047744 suppressed cell migration and invasion in vitro and in vivo. 	35334414
circCUL2	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 cancer-associated fibroblasts (CAFs)	Interaction(miR-203a-3p/MyD88/NF-κB/IL6 axis)	qRT-PCR//FISH	We identified that circCUL2 was specifically expressed in cancer-associated fibroblasts (CAFs) but not in cancer cells. Mechanistically, circCUL2 functioned as a ceRNA and modulated the miR-203a-3p/MyD88/NF-κB/IL6 axis, thereby further activating the STAT3 signaling pathway in pancreatic cancer cells to induce PDAC progression.	Moreover, the enrichment of circCUL2 in tumor tissues was significantly correlated with the poor prognosis of PDAC patients. 	Yes	Upregulation of circCUL2 expression in normal fibroblasts (NFs) induced the iCAF phenotype, and then iCAFs promoted PDAC progression through IL6 secretion in vitro. Furthermore, circCUL2-transduced NFs promoted tumorigenesis and metastasis of PDAC cells in vivo, which was blocked by an anti-IL6 antibody. 	35189958
hsa_circ_0006790	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC cells	Interaction(CBX7/S100A11)	Co-IP//qRT-PCR//RIP//FISH//ELISA//ChIP	Exo enhanced circ_6790 expression in PDAC cells. In conclusion, our results suggest that MSC-derived exosomal circ_6790 could downregulate S100A11 in PDAC cells and hamper immune escape via CBX7-catalyzed DNA hypermethylation.		Yes	 Knockdown of circ_6790 in Exo significantly attenuated the anti-tumor effect of Exo. 	35693076
hsa_circ_8924	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissue 	interaction[miR-518d-5p/519-5p ]	CCK8//qRT-PCR//Transwell Assay//Western Blot	CircRNA8924 is highly expressed in CC tissue and can be considered a competitive endogenous RNA of the miR-518d-5p/519-5p family to promote the malignant biological behavior of CC cells. 	The study demonstrated that the expression level of circRNA8924 in CC was significantly higher than that in the adjacent normal tissues (P < 0.001), and that it was also associated with tumor size, FIGO staging and myometrial invasion.	Yes	 The knockdown of circRNA8924 significantly inhibited the proliferation, migration and invasion of CC cells SiHa and HeLa. 	30007986
hsa_circ_0023404	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues 	Regulation[miR-136/TFCP2/YAP pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	In the present study, we found that circRNA hsa_circ_0023404 was significantly upregulated in CC tissues compared to adjacent normal tissues.Taken together, our study for the first time demonstrated the pivot role of hsa_circ_0023404 and revealed a novel regulatory loop of hsa_circ_0023404/miR-136/TFCP2/YAP axis in CC progression.	 And its overexpression was correlated with poor prognosis in CC patients.	Yes	 Functionally, we showed that knockdown of hsa_circ_0023404 significantly suppressed the proliferation, arrested the cell-cycle progression and inhibited cell migration and invasion in CC. 	29738762
hsa_circ_0000285	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	"cell lines((HeLa, SiHa, C4-1,C-33a,NC104)
C-33a))"	Interaction[regulating FUS]	CCK8//qRT-PCR//Cell Cycle Assay//Western Blot	 CircRNA_0000285 expression level was significantly higher in CC samples than that of corresponding normal tissues.CircRNA_0000285 could enhance the proliferation and metastasis of CC by up-regulating FUS, which might be a potential therapeutic target for CC treatment.		Yes	Moreover, the growth and migration abilities of CC cells were significantly inhibited after circRNA_0000285 was knocked down in vitro.	31696463
hsa_circ_0000515	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and the normal adjacent tissues,cell lines(H8,Hela, U14, SiHa, CaSki)	Interaction[up-regulation of ELK1 ]	Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay//Microarray//Transwell Assay	We first found that hsa_circ_0000515 was highly expressed in the cervical cancer tissues and cells.  Dual-luciferase reporter assay, RNA pull-down and RIP assays highlighted that hsa_circ_0000515 was able to act as a ceRNA of miR-326 to increase ELK1.	 	Yes	In vitro experiments exhibited that silencing of hsa_circ_0000515 or upregulation of miR-326 resulted in suppressed proliferation and invasion, along with induced apoptosis and autophagy of cervical cancer cells. 	31772143
hsa_circ_0030235	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissue,cell lines	Interaction[sponging miR-1253 and miR-1294]	CCK8//qRT-PCR//Transwell Assay	As a result, the data documented that circ_0030235 was upregulated in PDAC cell lines and cancerous tissues compared with HPDE and matched normal tissue specimens, respectively.Mechanistically, circ_0030235 directly sponges miR-1253 and miR-1294 in PDAC cells. What's more, the oncogenic properties of circ_0030235 was partly dependent on its suppression on miR-1253 and miR-1294. 	Overexpression of circ_0030235 in tumor samples is related to higher tumor stage and positive lymph node invasion. Additionally, analyses documented that high expression of circ_0030235 was associated with poor prognosis for PDAC patients. 	Yes	Knockdown of circ_0030235 by siRNAs inhibited cell growth, migratory and invasive potential, and promoted cell apoptosis. On the contrary, overexpression of circ_0030235 caused the opposite effect.	30591218
circASH2L	CircRNA	Homo sapiens	pancreatic ductal adenocarcinoma	pancreatic ductal adenocarcinoma tissues	Interaction[miR-34a,Notch 1]	qRT-PCR//Transwell Assay//EdU Staining//Microarray	We identified a circRNA (circ-ASH2L) based on our previous studies, detected its expression in different malignant cells and found that circ-ASH2L was highly expressed in pancreatic cells or tumor tissues and correlated with tumor malignancy.Further studies revealed that circ-ASH2L promoted tumor invasion, proliferation and angiogenesis by regulating miR-34a, thus regulate Notch 1 expression.	 Finally, we analyzed circ-ASH2L expression in clinical tissues and found that high circ-ASH2L expression was correlated with lymphatic invasion and TNM stage and was an independent risk factor for pancreatic patient survival.	Yes	"Moreover, Flow cytometry analysis showed that less cells stopped in G1 phase after overexpressing circ-ASH2L in Aspc-1 cells (Fig. ​(Fig.2i),2i), but silencing of circ-ASH2L arrested cell cycle in G1 phase in Capan-1 cells (Fig. ​(Fig.2j).2j). We further tested the effects of circ-ASH2L in angiogenesis. When HUVECs were transfected with circ-ASH2L, the tube-like structures were significantly enhanced compared to the normal or sh-circ-ASH2L groExpression[Expression[up-expression]-expression]s (Fig. ​(Fig.2k-l).2k-l). Together, the results above suggest that circ-ASH2L could promote invasion, proliferation and angiogenesis in PDAC.
"	31718694
circRNF220	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML cell lines	Interaction(miR-330-5p/SOX4 )	qRT-PCR//MTT//RNA Pull-Down//Transwell Assay	Expression detection identified that circRNF220 was overexpressed in AML.Target analysis indicated that circRNF220 directly targeted miR-330-5p, and the effects of si-circRNF220 were abrogated by miR-330-5p inhibitor. Moreover, circRNF220 targeted miR-330-5p to increase the expression of SOX4 and SOX4 promoted cell progression of AML.		Yes	In vitro experiments showed that silence of circRNF220 promoted cell apoptosis but impeded proliferation, cell cycle progression, invasion and glycolytic metabolism in AML cells. 	35611720
circBCAR3	CircRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues and cells 	Interaction( miR-27a-3p/TNPO1)	qRT-PCR//RIP	 CircBCAR3 was highly expressed in esophageal cancer tissues and cells and its expression was increased by hypoxia in vitro. Mechanistically, circBCAR3 can interact with miR-27a-3p by the competitive endogenous RNA mechanism to upregulate transportin-1 (TNPO1). Furthermore, our investigation indicated that splicing factor quaking (QKI) is a positive regulator of circBCAR3 via targeting the introns flanking the hsa_circ_0007624-formed exons in BCAR3 pre-mRNA. Hypoxia upregulates E2F7 to transcriptionally activate QKI.		Yes	 Silencing of circBCAR3 repressed the proliferation, migration, invasion, and ferroptosis of esophageal cancer cells in vitro, as well as inhibited the growth and metastasis of esophageal xenograft in mice in vivo. The hypoxia-induced promotive effects on esophageal cancer cell migration and ferroptosis were rescued by circBCAR3 knockdown.	35840974
hsa_circ_0003602	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML cell lines and tissues	Interaction(miR-502-5p/IGF1R axis)	qRT-PCR//RNA Pull-Down	 Hsa_circ_0003602 was upregulated and predicted poor survival in AML. Hsa_circ_0003602 sequestered miR-502-5p by functioning as a competitive endogenous RNA (ceRNA), thereby regulating IGF1R expression. Hsa_circ_0003602 acted as a tumor promoter in AML via miR-502-5p/IGF1R axis. 		Yes	Knockdown of hsa_circ_0003602 in AML cell lines induced the inhibition of proliferation, migration, and invasion and caused apoptosis.	34988853
hsa_circ_0059707	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	 AML patients and cell line	Interaction(miR-1287-5p)	qRT-PCR//Bioinformatics Analysis	In this study, we found that the expression levels of circ_0059707 were significantly decreased in AML patients with respect to normal controls (p < 0.001).Collectively, our research demonstrated that the down-regulation of circ_0059707 was highly evident in de novo AML patients. Our analysis also demonstrated that circ_0059707 inhibited cell growth and promoted apoptosis by up-regulating miR-1287-5p.	Low expression levels of circ_0059707 were also associated with a poor prognosis. 	Yes	Furthermore, circ_0059707 overexpression inhibited cell growth and promoted apoptosis in leukemia cells, compared with control cells. Circ_0059707- and empty plasmid-transfected cells were injected subcutaneously into BALB/c nude mice. We found that the tumor volume was significantly lower in mice in the circ_0059707 group than in control mice (p < 0.01). 	36135094
hsa_circ_0044907	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patient-derived BM and AML cells	Interaction(miR-186-5p/KIT)	qRT-PCR//MTT	Circ_0044907 was overexpressed in AML patient-derived BM and AML cells. Mechanically, circ_0044907 sponged miR-186-5p to block the inhibiting effect of miR-186-5p on KIT. Silenced miR-186-5p expression weakened circ_0044907 knockdown mediated suppression on AML cell viability, proliferation, and cycle progression. Also, forced KIT expression weakened miR-186-5p upregulation mediated inhibition on AML cell viability, proliferation, and cycle progression.	Furthermore, circ_0044907 could distinguish AML patients from healthy controls, and high circ_0044907 expression in BM had a poor prognosis for AML patients, implying that circ_0044907 served as a diagnostic and prognostic indicator for AML. 	Yes	Functionally, circ_0044907 silencing reduced cell viability, restrained cell proliferation, arrested cell cycle progression, and induced cell apoptosis in AML cells in vitro. Furthermore, circ_0044907 knockdown decreased AML cell growth in xenograft mouse models.	36004511
circNFIX	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow samples of AML patients, cell line	Interaction(miR-876-3p/TRIM31 axis)	qRT-PCR//RNA Pull-Down//Western Blot	 The expression level of circNFIX was significantly increased in the bone marrow samples of AML patients and AML cells when compared with normal controls.  In addition, circNFIX indirectly regulated TRIM31 through miR-876-3p. Further, TRIM31 overexpression counteracted the effect of circNFIX silencing on AML cell proliferation and apoptosis.		Yes	CircNFIX silencing inhibited AML cell proliferation and promoted apoptosis. Inhibition of miR-876-3p reversed the effect of circNFIX knockdown on AML cell progression.	36094501
circRAD23B	CircRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues	Interaction[sponging miR-5095]	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	In the present study, we found that circular RNA-RAD23B (circRAD23B) was upregulated in specimens of patients with esophageal cancer. Next, we identified microRNA-5095 (miR-5095) as a target of circRAD23B, and found that miR-5095 was negatively correlated to the expression of circRAD23B in esophageal cancer. In addition, circRAD23B facilitated expression of PARP2 and AKT2 by sponging miR-5095, which might underlie the growth of esophageal cancer. 		Yes	 Further investigation revealed that circRAD23B promoted proliferation and invasion of esophageal cancer cells.	31208717
hsa_circ_0023397	CircRNA	Homo sapiens	Esophageal Neoplasms	cell lines	regulation[miR-106b]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	Compared with that in normal human esophageal epithelial cell line HET-1A, the expression of hsa_circ_RNA0023397 was down-regulated in three esophageal cancer cell lines in vitro.Hsa_circ_RNA0023397 is down-regulated in esophageal cancer cells and can act as miR-106b to affect the biological function of esophageal cancer cells.		Yes	Overexpression of hsa_circ_RNA0023397 overtly inhibited KYSE-150 cell proliferation and promoted its apoptosis.	32964974
hsa_circ_0008717	CircRNA	Homo sapiens	Esophageal Neoplasms	EC cells	regulation[miR-203/Slug]	qRT-PCR//Luciferase Report Assay	 circRNA-0008717 expression was significantly upregulated in EC cells, and miR-2031 expression was decreased. The proliferation, invasion, and migration of EC cells were enhanced by circRNA-0008717 sponging the miR-203 to increase Slug expression.		Yes	Moreover, si-circRNA-0008717 or si-Slug inhibited the proliferation, migration, and invasion of EC cells. 	32953799
circPRKCI	CircRNA	Homo sapiens	Esophageal Neoplasms	EC tissues and cells	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	We observed that circPRKCI and PARP9 were upregulated while miR-186-5p was downregulated in EC tissues and cells. CircPRKCI regulated cell malignancy and radioresistance through modulating the miR-186-5p /PARP9 axis in EC, which provided a might target for EC treatment.		Yes	Furthermore, circPRKCI knockdown decreased tumor growth in vivo and constrained cell viability, colony formation, cell cycle progression, elevated cell radiosensitivity in EC cells in vitro. 	32739469
hsa_circ_0003340	CircRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer cells,tissues 	regulation[miR-564/TPX2 ]	qRT-PCR//Western Blot	Firstly, we found the expression levels of circ3340 are higher in ESCC and two esophageal cancer cells than in adjacent normal tissues and Het-1a cells. Downregulation of circ3340 had a negative influence on EC1 and EC9706 cells by affecting the miR-564/TPX2 pathway. 		Yes	Moreover, knockdown of circ3340 or enhancement of miR-564 expression had similar effects in EC1 and EC9706 cells, i.e., inducing cell apoptosis, inhibiting cell proliferation, and arresting cell invasion.	32535036
hsa_circ_0006168	CircRNA	Homo sapiens	Esophageal Neoplasms	EC tumors and cells	regulation[miR-384/RBBP7 axis via activation of S6K/S6 pathway]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Circ_0006168 and RBBP7 were over-expressed while miR-384 was low-expressed in EC tumors and cells.Abundance of circ_0006168 contributes to cell proliferation, migration, invasion, and glycolysis in EC by competitively sponging miR-384 to facilitate RBBP7 expression, representing prospective targets for EC therapy.		Yes	The repression of circ_0006168 attenuated cell proliferation, migration, invasion, and glycolysis in EC.	31957828
circAGFG1	CircRNA	Homo sapiens	Esophageal Neoplasms	ESCC cell lines	Interaction(miR-4306 )	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	CircAGFG1 was observably upregulated in ESCC cell lines. Mechanistic analysis evidenced that circAGFG1 might act as a competitive endogenous RNA of miR-4306 to relieve the repressive effect of miR-4306 on its target MAPRE2.		Yes	Besides, circAGFG1 silencing hindered ESCC cell development in vitro, and these effects were enhanced by miR-4306 overexpression or MAPRE2 silencing.	34461454
circVIM	CircRNA	Homo sapiens	Esophageal Neoplasms	EC tissues or cells	Interaction(miR-124/PD-L1 axis)	qRT-PCR//Western Blot	Significant upregulation of circ-VIM and PD-L1 and downregulation of miR-124 were detected in EC tissues or cells.  Circ-VIM sponged miR-124 and released its suppression on the downstream target PD-L1. 		Yes	By modulating miR-124/PD-L1 axis, silencing circ-VIM and applying sevoflurane both inhibited immune escape and multiple oncogenic activities of EC in vitro, and suppressed xenograft growth and lung metastases in vivo. The inactivation of Ras/ERK signaling pathway was involved in suppression of malignant phenotypes by silencing circ-VIM and sevoflurane treatment.	34018092
hsa_circ_0000554	CircRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues 	Interaction(miR-485-5p/FERMT1)	qRT-PCR//Western Blot	Circ_0000554 and FERMT1 expression was enhanced in esophageal cancer tissues and radioresistant esophageal cancer tissues. Importantly, circ_0000554 served as a sponge for miR-485-5p in esophageal cancer cells. And FERMT1 acted as a downstream target for miR-485-5p. Additionally, circ_0000554 modulated FERMT1 expression via miR-485-5p. 		Yes	Both circ_0000554 and FERMT1 repression blocked cell colony formation, migration, invasion and elevated cell radiosensitivity and apoptosis in esophageal cancer cells. 	33470617
hsa_circ_0004370	CircRNA	Homo sapiens	Esophageal Neoplasms	 EC tissues and cells	Interaction(miR-1301-3p/COL1A1 axis)	qRT-PCR//RNA Pull-Down	We discovered that circ_0004370 was remarkably upregulated in EC tissues and cells.Moreover, we explored its regulatory mechanism and found that circ_0004370 directly bound to miR-1301-3p and COL1A1 was verified as a target of miR-1301-3p.		Yes	Knockdown of circ_0004370 inhibited cell proliferation, migration as well as invasion, and promoted apoptosis in vitro, while its effect was rescued by miR-1301-3p inhibition.  And circ_0004370 mediated the EMT process in EC cells. 	33506107
circSFMBT2	CircRNA	Homo sapiens	Esophageal Neoplasms	EC samples and cells	Interaction(miR-107/SLC1A5 axis)	qRT-PCR//RNA Pull-Down//Transwell Assay	 Circ-SFMBT2 was overexpressed in EC samples and cells. Circ-SFMBT2 targeted miR-107 and the regulation of circ-SFMBT2 was achieved by sponging miR-107. SLC1A5 was a target of miR-107, and it worked as an oncogene in EC cells. 		Yes	. Circ-SFMBT2 downregulation inhibited EC cell proliferation, invasion and glutamine metabolism.	34530825
hsa_circ_0086414	CircRNA	Homo sapiens	Esophageal Neoplasms	 EC tissues and cells	Interaction(miR-1290/SPARCL1 pathway)	qRT-PCR//Luciferase Report Assay	Results showed that circ_0086414 and SPARCL1 expression were significantly downregulated, while miR-1290 was upregulated in EC tissues and cells. Besides, circ_0086414 acted as a miR-1290 sponge and regulated EC cell processes by binding to the miRNA. MiR-1290 also participated in EC malignant progression through SPARCL1. 	EC patients with low circ_0086414 expression had a poor prognosis. 	Yes	 Increasing circ_0086414 expression led to decreased EC cell proliferation, invasion and glycolysis and increased cell apoptosis, accompanied by a decrease of N-cadherin expression and an increase of E-cadherin expression. Also, the enforced expression of circ_0086414 delayed tumor tumorigenesis. 	35549806
hsa_circ_0058063	CircRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues	Interaction(miR-377-3p/HOXA1 axis)	Flow Cytometry//qRT-PCR//Wound Healing Assay	Circ_0058063 and HOXA1 were upregulated, while miR-377 was downregulated in esophageal cancer. Circ_0058063 targeted miR-377-3p, and HOX4 was a target of miR-377-3p. 		Yes	Knockdown of circ_0058063 inhibited migration, invasion and proliferation and promoted apoptosis of esophageal cancer cells. MiR-377-3p inhibition or HOXA1 overexpression could restore the effect of si-circ_0058063 on esophageal cancer cells. Knockdown of circ_0058063 repressed the growth of esophageal cancer tumors in vivo.	36729977
hsa_circ_0001273	CircRNA	Homo sapiens	Esophageal Neoplasms	 EC tumor tissues and cells	Interaction(miR-622/SLC1A5 signaling axis)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay	 Circ_0001273 was upregulated in EC tumor tissues and cells.MiR-622 was targeted by circ_0001273, and its inhibition reversed the functional effects of circ_0001273 knockdown. SLC1A5 was a target gene of miR-622, and circ_0001273 targeted miR-622 to positively regulate SLC1A5 expression. The inhibitory effects of miR-622 enrichment on EC cell proliferation, migration, EMT and glutamine metabolism were recovered by SLC1A5 overexpression.		Yes	 Knockdown of circ_0001273 repressed EC cell proliferation, migration, epithelial-mesenchymal transition (EMT) and glutamine metabolism. Circ_0001273 knockdown also blocked tumor development in animal models.	35567340
circPOLR1C	CircRNA	Homo sapiens	Esophageal Neoplasms	EC cell and tissues	Interaction(miR-361-3p )	qRT-PCR//Transwell Assay//FISH	Highly expressed circPOLR1C in EC was related to tumor differentiation and invasion. The enrichment of miR-361-3p was higher than that of other targeted miRNAs. circPOLR1C adsorbed miR-361-3p to regulate apoptosis- and EMT-related genes and partially reversed the tumor suppressive effect of miR-361-3p, which was lowly expressed in EC tissues. Silencing the target genes of miR-361-3p also inhibited the malignant development of EC cells.	Highly expressed circPOLR1C in EC was related to tumor differentiation and invasion.	Yes	 circPOLR1C silencing inhibited circPOLR1C expression and EC cell malignant function, while circPOLR1C overexpression promoted the growth of transplanted tumors and lung metastasis.	36590309
hsa_circ_0001060	CircRNA	Homo sapiens	Osteosarcoma	OS tumor tissues	Interaction(miR-203a-5p-TRIM21 or miR-208b-5p-MAP3K5 or miR-203a-5p-PRKX)	qRT-PCR//Wound Healing Assay//Colony Formation Assay	We previously found that circ_0001060 was highly expressed in OS tumor tissues. Using bioinformatics analysis, we built three circRNA-miRNA-mRNA regulatory modules (circ_0001060-miR-203a-5p-TRIM21, circ_0001060-miR-208b-5p-MAP3K5, and circ_0001060-miR-203a-5p-PRKX), suggesting that these signaling axes may be involved in the inhibitory effect of circ_0001060 on OS. 	 In this work, we identified that high level expression of circ_0001060 was significantly associated with late clinical stage, larger tumor volume, higher frequency of metastasis, and poor prognosis in OS patients.	Yes	Furthermore, we confirmed that silencing circ_0001060 inhibited the proliferation and migration of OS cell. 	36580535
circDOCK1	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cell lines	Interaction( miR-936/LEF1 axis)	qRT-PCR//RIP	Increased circDOCK1 and LEF1, and decreased miR-936 were found in OS tissues and cell lines. Bioinformatics analysis exhibited that circDOCK1 acted as a sponge for miR-936 and LEF1 was a downstream target of miR-936. Moreover, circDOCK1 functions through modulation of the miR-936/LEF1 axis.		Yes	Furthermore, circDOCK1 silencing might suppress OS cell proliferation, migration, invasion, and angiogenesis in vitro.	36147545
hsa_circ_0078767	CircRNA	Homo sapiens	Osteosarcoma	 osteosarcoma tissues and cells	Interaction(miR-330-3p/CDK14 )	qRT-PCR//IHC//H&E Staining	 Aberrant abundance of circ_0078767 was found in both osteosarcoma tissues and cells, relating to dismal prognosis in patients with osteosarcoma. Additionally, miR-330-3p targeted and decreased CDK14 expression whereby motivating the malignant phenotypes of osteosarcoma cells. Through in vivo experiments, we further confirmed that circ_0078767 targeted miR-330-3p to upregulate CDK14, whereby strengthening the in vivo tumorigenic and metastatic ability of osteosarcoma cells. 	 Aberrant abundance of circ_0078767 was found in both osteosarcoma tissues and cells, relating to dismal prognosis in patients with osteosarcoma. 	Yes	 Functionally, circ0078767 strengthened the proliferation, invasiveness, and migration of osteosarcoma cells, which could be neutralized by miR-330-3p. 	35307379
hsa_circ_0000282	CircRNA	Homo sapiens	Osteosarcoma	OSA tissues and cell lines	regulation[miR-192/XIAP axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//BrdU	Circ_0000282 was highly expressed in OSA tissues and cell lines, which represented positive correlation with Enneking stage of OSA patients and negative correlation with tumor differentiation degree. Circ_0000282 was a novel oncogenic circRNA in OSA. Circ_0000282/miR-192/XIAP axis regulated OSA cell proliferation apoptosis with competitive endogenous RNA mechanism.	Circ_0000282 was highly expressed in OSA tissues and cell lines, which represented positive correlation with Enneking stage of OSA patients and negative correlation with tumor differentiation degree.	Yes	In vitro experiments confirmed that overexpression of circ_0000282 markedly facilitated OSA cell proliferation and repressed cancer cell apoptosis in comparison to control group. Besides, knockdown of circ_0000282 repressed OSA cell proliferation and promoted apoptosis. 	33097010
hsa_circ_0086996	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue	interaction[miR-125b-5p]	Northern Blot//Western Blot//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay	Hsa_circ_0086996 (Circ_0086996) was found to upregulated in tumor tissue compared to adjacent tissue.Our study discovers that Circ_0086996 acts as miR-125b-5p sponge to mediate the tumorigenicity, which could act as a potential biomarker for the osteosarcoma and provides a novel insight for the mechanism in osteosarcoma. Circ_0086996 knockdown also induced cell cycle arrest in G0/G1 phaseand promoted cell apoptosis in SAOS2 and MG-63 cells.		Yes	Circ_0086996 knockdown significantly suppressed cell proliferation, migration, and invasion.	33053498
hsa_circ_0028171	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[circ_0028171/miR-218-5p/IKBKB axis]	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We found that circ_0028171 displayed a remarkably higher expression in both OS tissues and cell lines. our research reveals that circ_0028171 might promote the malignant behavior of OS tissues through miR-218-5p/IKBKB axis, which could be a potential novel marker for early diagnosis of OS.		Yes	Knockdown of circ_0028171 suppressed OS tumor growth in vitro and in vivo, while up-regulated circ_0028171 remarkably enhanced cell proliferation, migration and invasion abilities in OS.	33041665
hsa_circ_0001721	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	regulation[miR-372-3p/MAPK7 Axis]	Flow Cytometry//qRT-PCR//RIP//MTT//Transwell Assay	The levels of circ_0001721 and MAPK7 were upregulated in osteosarcoma tissues and cells, while miR-372-3p was downregulated.Circ_0001721 promoted osteosarcoma development through the miR-372-3p/MAPK7 axis.		Yes	Knockdown of circ_0001721 inhibited glycolysis, cell proliferation, cell migration, invasion and epithelial-to-mesenchymal transition (EMT), and promoted apoptosis.	32982424
circITGA7	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[miR-370/PIM1 Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circITGA7 was upregulated in OS tissues and cell lines.In summary, this study shows that circITGA7 promotes OS proliferation and metastasis via miR-370/PIM1.		Yes	 Knockdown of circITGA7 weakened the cell's ability to proliferate and metastasize.	32963582
hsa_circ_0001649	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	interaction[miR-338-5p, miR-647 and miR-942]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Circ_0001649 was low-expressed in OS tissues and cell lines.Circ_0001649 suppressed OS cell proliferation and STAT pathway and induced apoptosis through sponging miR-338-5p, miR-647 and miR-942.		Yes	Circ_0001649 overexpression suppressed U2OS and HOS cell viability and survival fraction, and induced apoptosis presented as the increasing levels of Apaf-1, cleaved-caspase-3 and cleaved-caspase-9. 	32954926
circXPR1	CircRNA	Homo sapiens	Osteosarcoma	OS tissue	regulation[miR-214-5p/DDX5 axis]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay	We identified one upregulated circRNA (Circ-XPR1), and RT-PCR was performed to further confirm the expression abundance in OS tissue. Therefore, the Circ-XPR1/miR-214-5p/DDX5 axis may serve as a potential therapeutically relevant target for OS.		Yes	Knockdown of Circ-XPR1 significantly reduced the proliferation of OS cells. Gain- and loss-of-function studies showed that Circ-XPR1 promoted OS cell proliferation by sponging miR-214-5p to regulate DDX5 expression.	32920730
circSIPA1L1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[miR-379-5p/MAP3K9 Axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Circ_SIPA1L1 abundance was aberrantly elevated in OS tissues and cell lines.  Circ_SIPA1L1 promoted the progression of OS via miR-379-5p/MAP3K9 axis.		Yes	Circ_SIPA1L1 accelerated the proliferation and metastasis abilities of OS cells. 	32897735
circCCDC66	CircRNA	Homo sapiens	Osteosarcoma	OS tissue samples and OS cell lines 	regulation[circCCDC66/miR-338-3p/PTP1B axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	High circCCDC66 expression level was found in OS patient-derived tissue samples and OS cell lines by qRT-PCR.. Collectively, our findings demonstrated that circCCDC66 contributed to malignant behaviors of OS cells by miR-338-3p/PTP1B pathway, which suggested circCCDC66/miR-338-3p/PTP1B axis might be a potential therapeutic target.		Yes	Through functional experiments, we found that circCCDC66 knockdown promoted the inhibition of cell proliferation and metastatic of OS cell lines.	32851074
hsa_circ_0010220	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	regulation[miR-503-5p/CDCA4 axis]	Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Invasion Assay//Transwell Assay	Circ_0010220 expression was markedly increased in osteosarcoma cells.  In conclusion, we indicated circ_0010220 can be an important biomarker for osteosarcoma via regulating miR-503-5p and CDCA4.		Yes	Additionally, knockdown of circ_0010220 significantly depressed tumor growth. CCK-8 analysis indicated that down-regulation of circ_0010220 inhibited osteosarcoma cells proliferation. Flow cytometry assay showed that knockdown of circ_0010220 induced cell apoptosis and blocked cell cycle in the G1 phase. 	32827680
hsa_circ_0008934	CircRNA	Homo sapiens	Osteosarcoma	cell line	regulation[sponging miR-145-5p to enhance E2F3 expression]	qRT-PCR//Tunel//Western Blot	Hsa_circ_0008934 expression was significantly elevated in SaOS2 and MG63 cells. Elevated hsa_circ_0008934 expression promotes the proliferation and migration of osteosarcoma cells by sponging miR-145-5p to enhance E2F3 expression.		Yes	Hsa_circ_0008934 silencing significantly reduced proliferation, enhanced apoptosis, blocked cell cycle progression, and impaired migration and invasion capacities of SaOS2 cells. Opposite cellular alterations were achieved by overexpressing hsa_circ_0008934 in MG63 cells.	32822848
hsa_circ_0008035	CircRNA	Homo sapiens	Osteosarcoma	OSA tissues and cells,serum 	regulation[upregulating microRNA-375]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	 Our results demonstrated that hsa_circ_0008035 was overexpressed in serum of OSA patients, OSA tissues and cells.  In conclusion, silencing hsa_circRNA_0008035 exerted repressive function on OSA cell growth and migration and Notch pathway by accelerating miR-375.		Yes	Silencing hsa_circRNA_0008035 impeded OSA cell growth and migration, while hsa_circ_0008035 facilitated cell behaviors of hFOB1.19 cells. 	32779548
circHIPK3	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines	regulation[miR-637/STAT3 Axis ]	qRT-PCR	In this study, we performed experiments with the human OS cell lines and the results showed that the expression of circHIPK3 in OS cell lines was significantly upregulated compared to that in the normal cell line.  In conclusion, our research uncovered an important role of the circHIPK3/miR-637/STAT3 pathway in the migration and invasion of OS cells and suggested that circHIPK3 may be a prognostic marker and a promising therapeutic target for OS.		Yes	 In addition, the results showed that circHIPK3 could promote the migration, invasion, and growth of OS cells.	32775413
circFAT1(e2)	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[circFAT1(e2)/miR-181b/HK2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In the present study, we identified a circRNA circFAT1(e2) with an upregulated expression level in OS tissues. On the whole, our study indicated that circFAT1(e2) exerted oncogenic roles in OS and suggested the circFAT1(e2)/miR-181b/HK2 axis might be a potential therapeutic target.		Yes	 By functional experiments, we found that circFAT1(e2) depletion significantly suppressed the proliferation and reduced migration in OS. 	32733938
circCNST	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	interaction[Sponging miR-421]	qRT-PCR//MTT//RIP//FISH	As a result, we found that the expression levels of circCNST were dramatically increased in OS tissues and cell lines as compared with the adjacent normal tissues, and it was associated with tumor size and poor survival in OS patients. In conclusion, our findings demonstrate that circCNST promotes the tumorigenesis of OS cells by sponging miR-421, and provides a potential biomarker for patients with OS.	As a result, we found that the expression levels of circCNST were dramatically increased in OS tissues and cell lines as compared with the adjacent normal tissues, and it was associated with tumor size and poor survival in OS patients.	Yes	Knockdown of circCNST repressed cell viability, colony formation, and xenograft tumor growth, while restored expression of circCNST reversed these effects.	32693639
hsa_circ_0005909	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-936/HMGB1 axis]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Circ_0005909 level was upregulated in OS tissues and cells. Circ_0005909 inhibition impeded the progression of OS via downregulating HMGB1 via sponging miR-936.		Yes	OS patients with high circ_0005909 expression had a lower survival rate. Circ_0005909 inhibition reduced tumor growth in vivo and constrained cell viability, colony formation, migration, invasion, and EMT of OS cells in vitro. 	32684842
hsa_circ_100284	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[downregulating PTEN and EMP1]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 Circ100284 had a high level in OS tissues. Circ100284 promotes the progression of OS cells by downregulating PTEN and EMP1.	The high expression of circ100284 was positively correlated with tumor size, pathological stage, and lung metastasis, and negatively correlated with patient survival time. 	Yes	Knocking down circ100284 in OS cells damaged the cell viability and invasiveness, blocked cell cycle, and promoted cell apoptosis. 	32633341
circEIF4G2	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	interaction[Sponging miR-218]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The present study identified that a novel circRNA circEIF4G2 was upregulated in OS tissues and cells. Mechanically, we found that circEIF4G2 could directly bind to miR-218, and miR-218 mediated the effect of circEIF4G2 knockdown on OS progression.		Yes	Loss-of-function assays showed that circEIF4G2 knockdown significantly suppressed OS cell proliferation, migration, and invasion.	32596384
hsa_circ_0003732	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[miR-545/CCNA2 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//EdU Staining	In the present study, we showed that hsa_circ_0003732 was up-regulated in OS tissues and elevated level of hsa_circ_0003732 was linked to poor prognosis of OS patients.Altogether, our findings demonstrate that hsa_circ_0003732 promotes OS cells proliferation via miR-545/CCNA2 axis and imply hsa_circ_0003732 may be a potential prognosis biomarker and therapeutic target for OS.	In the present study, we showed that hsa_circ_0003732 was up-regulated in OS tissues and elevated level of hsa_circ_0003732 was linked to poor prognosis of OS patients.	Yes	Functional investigation indicated that hsa_circ_0003732 promoted proliferation of OS cells. 	32537647
circUBAP2	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-641/YAP1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The level of circUBAP2 was significantly upregulated in OS tissues and cells compared with normal tissues and cells, which was contrary to the expression of miR-641.Knockdown of circUBAP2 impeded proliferation and invasion of OS cells by downregulating the expression of YAP1 via sponging miR-641.		Yes	Downregulation of circUBAP2 suppressed proliferation and invasion of OS cells and weakened the process of epithelial-mesenchymal transition (EMT).	32528231
circXPO1	CircRNA	Homo sapiens	Osteosarcoma	OC tissues	regulation[regulate XPO1 expression]	qRT-PCR//Microarray	 Elevation of circ-XPO1 and XPO1 mRNA was identified in OS tissue specimens and cells by qRT-PCR.Taken together, we found that circ-XPO1 regulated the expression of XPO1 through sponging miRNAs as a competing endogenous (ceRNA), providing the possibility that circ-XPO1 might play as a new therapeutic target for OS.	In addition, enhanced expression of circ-XPO1 and XPO1 mRNA both correlated with poor prognosis for the patients with OS, as estimated by Kaplan-Meier analysis. 	Yes	Functionally, circ-XPO1 and XPO1 both facilitated the growth and invasion and decreased the apoptosis of OS cells.	33091396
circECE1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells 	regulation[c-Myc/TXNIP axis]	qRT-PCR//IHC//Western Blot	 We found that CircECE1 is highly expressed in OS tissues and cells and that CircECE1 knockdown suppresses tumor proliferation and metastasis both in vitro and in vivo.  CircECE1 regulates the Warburg effect through the c-Myc/TXNIP axis.		Yes	 We found that CircECE1 is highly expressed in OS tissues and cells and that CircECE1 knockdown suppresses tumor proliferation and metastasis both in vitro and in vivo. 	33106166
circMGEA5	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(miR-153-3p and miR-8084)	qRT-PCR//ChIP	CircMGEA5 was significantly upregulated in metastatic OS tissues compared to primary tissues. Mechanistically, circMGEA5 acted as a competing endogenous RNA (ceRNA) to directly sponge miR-153-3p and miR-8084, resulting in increasing ZEB1 and Snail expression, respectively, thereby inducing EMT and metastasis. In turn, ZEB1 and Snail were capable to bind to circMGEA5 promoter, activating circMGEA5 transcription, thus forming a positive feedback loop.	High circMGEA5 was positively related with shorter overall and disease-free survival time. 	Yes	Knockdown of circMGEA5 suppressed OS cell migration, invasion, and epithelial-mesenchymal transition (EMT). 	36564929
circCRIM1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	regulation[miR-432-5p/HDAC4 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	In OS tissues and cells, circCRIM1 was differentially up-regulated.  Our findings elucidated the oncogenic function of circCRIM1 in OS via the regulation of the miR-432-5p/HDAC4 axis, affording a novel view about how circRNA participated in OS development.		Yes	Functionally, cell proliferation, migration and invasion were suppressed while autophagy was promoted after circCRIM1 was down-regulated in OS cells.	33116874
hsa_circ_0000264	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues and cells	Interaction(hsa-let-7b-5p/HMGA2 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	hsa_circ_0000264 was upregulated in HNSCC tissues and cells, and its loop structure was confirmed. Mechanistically, hsa_circ_000026 upregulation can upregulate the expression of high mobility group AT-hook 2 (HMGA2) by sponging hsa-let-7b-5p, which in turn promotes HNSCC progression.		Yes	Knockdown of hsa_circ_0000264 inhibited the migration, invasion, and epithelial-to-mesenchymal transition of HNSCC cells in vivo and in vitro.	36214613
circFAT1	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	interaction[ miR-375]	qRT-PCR//FISH//Western Blot	In this study, we observed significant upregulation of circFAT1 originating from exon 2 of the FAT1 gene in human osteosarcoma tissues and cell lines.Mechanistic studies revealed that circFAT1 contains a binding site for the microRNA-375 (miR-375) and can abundantly sponge miR-375 to upregulate the expression of Yes-associated protein 1. 		Yes	 Inhibition of circFAT1 effectively prevented the migration, invasion, and tumorigenesis of osteosarcoma cells in vitro and repressed osteosarcoma growth in vivo. 	30514309
hsa_circ_0002052	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Regulation[miR-1205/APC2 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the present study, we identified a novel circRNA hsa_circ_0002052 significantly downregulated in osteosarcoma (OS) tissues and cell lines. Our study suggested hsa_circ_0002052/miR-1205/APC2/Wnt/β-catenin axis might be a potential target for OS therapy.		Yes	Functionally, we showed that hsa_circ_0002052 overexpression significantly suppressed OS cell proliferation, migration and invasion while promoting apoptosis in vitro.	29852168
circMMP9	CircRNA	Homo sapiens	Osteosarcoma	Osteosarcoma tissues	Regulation[miR-1265/CHI3L1 Axis]	CCK8//qRT-PCR//Transwell Assay	circMMP9 was overexpressed in cancer tissues.		Yes	Overexpressed circMMP9 was correlated with advanced tumor stage and predicted poor prognosis. circMMP9 knockExpression[down-expression] exhibited a tumor-sExpression[Expression[up-expression]-expression]pressive phenotype via sExpression[Expression[up-expression]-expression]pressing proliferation, migration and invasion.	31754311
hsa_circ_0001785	CircRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction[sponging miR-1200 to Expression[highly expressed]regulate HOXB2]	qRT-PCR//Luciferase Report Assay//EdU Staining//Western Blot	Consistent with the microarray analysis, circ-0001785 was highly expressed in osteosarcoma cell lines. Furthermore, we confirmed that circ-0001785 competitively bound to miR-1200, thus Expression[Expression[up-expression]-expression]-regulating its target gene HOXB2. Western blot analyses revealed that circ-0001785 regulated the PI3K/Akt signaling and Bcl-2 family pathway in osteosarcoma. 		Yes	KnockExpression[down-expression] of circ-0001785 attenuated proliferative ability, but induced the apoptosis of osteosarcoma cells. 	31116090
hsa_circ_0102049	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction[sponging miR-1304-5p]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Circ_0102049 was overexpressed in both OS specimens and cells. 	Moreover, the level of circ_0102049 in OS patients was markedly correlated with larger tumor size, pulmonary metastasis and poor prognosis	Yes	Circ_0102049 remarkably accelerated cell proliferation, migration and invasion but attenuated cell apoptosis in OS cells analyzed by gain/loss of function experiments.	31727503
hsa_circ_0000502	CircRNA	Homo sapiens	Osteosarcoma	OS tissue,cell lines	Interaction[sponging miR-1238]	CCK8//qRT-PCR//Transwell Assay	Circ_0000502 was identified upregulated in both OS tissue specimens and cells. For mechanism exploration, circ_0000502 could directly sponge microRNA (miR)-1238, and the oncogenic functions of circ_0000502 is partially dependent on its regulation of miR-1238 proved by rescue assays. In summary, this study might help to develop rational predictive and therapeutic target for patients with OS.	 In addition, its expression predicts clinical severity and unfavorable prognosis in the 63 recruited patients with OS.	Yes	Circ_0000502 facilitated cell proliferation, migration, and invasion in OS cells and inhibited cell apoptosis. The animal study further confirmed the in vitro results. 	30525215
circORC2	CircRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction[miR-19a]	RNA Pull-Down//Western Blot//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	This research showed that circ_ORC2 was generally up-regulated in various osteosarcoma cell lines, and mainly distributed in the cytoplasm.Circ_ORC2 had the binding site of miR-19a, and its expression was positively correlated with miR-19a expression. RIP experiments showed that circ_ORC2 could bind to Ago2 protein. RNA pull-down using biotinylated circ_ORC2 or miR-19a showed that circ_ORC2 could directly interact with miR-19a, and dual luciferase reporter gene assay also confirmed that miR-19a could bind to circ_ORC2. After circ_ORC2 knockdown, miR-19a expression was down-regulated, but the downstream target gene PTEN expression was up-regulated, and the phosphorylation level of Akt was reduced, which indicated that circ_ORC2 enhanced the inhibition of miR-19a on PTEN expression by combining miR-19a. When co-transfected with circ_ORC2 siRNA and miR-19a mimics or PTEN siRNA, the above cell biological behaviors did not change significantly. Therefore, circ_ORC2 binds with miR-19a and enhances its expression, thereby inhibiting downstream PTEN expression and activating Akt pathway to promote osteosarcoma cell growth and invasion. 		Yes	Further functional experiments showed that after circ_ORC2 knockdown, cell proliferation and invasion decreased, while the apoptosis level increased. 	31103262
hsa_circ_0001721	CircRNA	Homo sapiens	Osteosarcoma	OS tissue,cell lines	Interaction[sponging miR-569 and miR-599]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	We found that circ_0001721 was enhanced in OS tissue samples and cell lines and the overexpression of circ_0001721 is closely related to clinical severity.		Yes	 What's more, loss-of-function and gain-of-function assays demonstrated circ_0001721 facilitates cell progression in OS. 	30396080
circSAMD4A	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction[ circSAMD4A/miR-1244/MDM2]	CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Then, we identified a novel circRNA(circ_101356/circ_0004846, we named circSAMD4 in the present study) and found it was highly expressed in the OS tissues compared to adjacent non-cancerous tissues.In mechanism, circSAMD4A could sponge miR-1244 in OS cells. Moreover, we verified that MDM2 was a target of miR-1244. In conclusion, circSAMD4A/miR-1244/MDM2 regulatory loop might be a promising therapeutic target for OS treatment.		Yes	Furthermore, we indicated that circSAMD4A promoted OS proliferation in vivo and in vitro. 	31200957
circANKIB1	CircRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction[SOCS3/STAT3 pathway]	RIP//Luciferase Report Assay//RNA Pull-Down	 Further studies have shown that circ_ANKIB1 has binding sites for miR-19b, and both molecules were generally upregulated in osteosarcoma cells.Circ_ANKIB1 promoted miR-19b expression, inhibited the expression of the downstream target gene SOCS3, and then activated the STAT3 pathway. When cotransfected with circ_ANKIB1 siRNA, and miR-19b mimics, the expression of SOCS3 and the phosphorylation level of STAT3 did not change significantly.When cotransfected with circ_ANKIB1 siRNA and miR-19b mimics or SOCS3 siRNA, the cell proliferation, apoptosis, and invasion levels did not change significantly, suggesting that circ_ANKIB1 could affect the STAT3 pathway and osteosarcoma cell growth and invasion by enhancing the regulation of miR-19b on the downstream target gene SOCS3. 		Yes	Continuous detection of cell growth and invasion showed that the downregulation of circ_ANKIB1 or miR-19b significantly inhibited cell proliferation and invasion, but increased the apoptotic level. 	31667786
circLRP6	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction[regulating KLF2 and APC levels ]	Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Invasion Assay//ChIP	 CircLRP6 level markedly increased in OS tissues.  Collectively, circLRP6 was highly expressed in OS and served as an oncogene by binding to LSD1 and EZH2 to inhibit expressions of KLF2 and APC.	Besides, OS patients with high expression of circLRP6 showed shorter disease-free survival and over-all survival than those with low expression. 	Yes	 CircLRP6 knockdown suppressed proliferative, migratory and invasive rates of OS cells.	31396323
circMYO10	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues, cell lines	Regulation[miR-370-3p/RUVBL1 axis]	RNA Pull-Down//Western Blot//qRT-PCR//FISH//Luciferase Report Assay//IP	CircMYO10 was significantly upregulated, while miR-370-3p was downregulated, in osteosarcoma cell lines and human osteosarcoma samples. CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to promote chromatin remodeling and thus enhances the transcriptional activity of β-catenin/LEF1 complex, which indicates that circMYO10 may be a potential therapeutic target for osteosarcoma treatment.		Yes	 Silencing circMYO10 inhibited cell proliferation and EMT in vivo and in vitro.	31665067
hsa_circ_0003998	CircRNA	Homo sapiens	Osteosarcoma	steosarcoma tissue and cell lines	Interaction[binding to miR-197-3p ]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Compared to normal control tissues and cells, the expression of circ-0003998 was significantly up-regulated in both osteosarcoma tissue samples and cell lines.Meanwhile, circ-0003998 up-regulates the expression of KLF10 by binding to miR-197-3p, thereby promoting osteosarcoma cell growth and invasion, and accelerating the progression of osteosarcoma.	Highly-expressed circ-0003998 was significantly associated with poor overall survival of patients with osteosarcoma. 	Yes	In vitro experiments revealed that the down-regulation of circ-0003998 significantly inhibited the proliferative ability and invasiveness of osteosarcoma cells. 	31858530
circCAMSAP1	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	interaction[miR-145-5p,FLI1 ]	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//Colony Formation Assay//CCK8//qRT-PCR//Luciferase Report Assay//RNA-seq//IHC//Transwell Assay	We found that circCAMSAP1, also named hsa_circ_0004338, is significantly upregulated in human osteosarcoma tissues and cell lines, and it is positively correlated with osteosarcoma development. Furthermore, we validated that circCAMSAP1 functions in osteosarcoma tumorigenesis through a circCAMSAP1/miR-145-5p/friend leukemia virus integration 1 (FLI1) pathway.		Yes	Silencing of circCAMSAP1 effectively suppresses osteosarcoma cell growth, apoptosis, migration, and invasion. 	33664993
circHIPK3	CircRNA	Homo sapiens	Osteosarcoma	OS tissue samples and OS cell lines	regulation[miR-637/HDAC4 signaling]	qRT-PCR//FISH//Transwell Assay	It was revealed that circHIPK3 expression was upregulated in OS tissue samples and OS cell lines. It was demonstrated that circHIPK3 promoted OS cell proliferation, migration and invasion by modulating miR‑637/HDAC4 signaling.		Yes	Using loss‑of‑function proliferation and Transwell assays, the present study revealed that circHIPK3‑knockdown suppressed OS cell proliferation, migration and invasion.	33416147
hsa_circ_03955	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue	regulation[miR-3662/Metadherin Pathway]	qRT-PCR	Circ-03955 was significantly upregulated, and miR-3662 was downregulated in osteosarcoma.All these findings demonstrate that the presence of circ-03955 promotes EMT in osteosarcoma by acting as miR-3662 sponge-mediated MTDH expression.		Yes	 Circ-03955 silencing inhibited the growth and metastasis of osteosarcoma.	33312941
hsa_circ_0000658	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[miR-1227/IRF2 axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//IHC//Transwell Assay	The results of this study revealed that circ-0000658 exhibits low levels in OS tissues and cell lines. Conclusively, circ-0000658 modulates biological function of OS cells through the miR-1227/IRF2 axis. 		Yes	 Moreover, circ-0000658 repression promoted cell cycle, proliferation, invasion and migration but inhibited the apoptosis of OS cells.	33264494
hsa_circ_0032462	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	regulation[Promoting KIF3B Expression]	qRT-PCR//Wound Healing Assay//Invasion Assay//Migration Assay	Using real-time polymerase chain reaction, we verified the elevated expression of circ_0032462 in osteosarcoma cells than normal cells.In addition, kinesin family member 3B inhibition was found to inhibit circ_0032462-induced enhanced osteosarcoma cell progression.		Yes	Functional validation experiments revealed that circ_0032462 overexpression promoted proliferation, migration, and invasion in osteosarcoma cells, whereas circ_0032462 silencing was observed to inhibit cancer cell progression (proliferation, migration, and invasion).	33153390
hsa-circ-0001146	CircRNA	Homo sapiens	Osteosarcoma	Osteosarcoma tissues	regulation[has-circ-0001146/miR-26a-5p/MNAT1 network ]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	Osteosarcoma tissues showed higher MNAT1 and has-circ-0001146 expression than adjacent normal tissues, although the expression of MNAT1 was not significantly up-regulated in sarcomas according to TCGA databases. The present study confirmed that has-circ-0001146 blocked miR-26a-5p targeting MNAT1 in osteosarcoma cells, thereby promoting the malignant behaviours of osteosarcoma cells.		Yes	The depletion of has-circ-0001146 or MNAT1 or the increase of miR-26a-5p inhibited osteosarcoma cell viability and invasion, and increased apoptosis. 	32453410
hsa_circ_0136666	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[miR-593-3p/ZEB2 pathway]	CCK8//qRT-PCR//Transwell Assay	hsa_circ_0136666 was shown to be upregulated in OS and correlated with advanced stage and poor prognosis.  Additionally, we identified hsa_circ_0136666 was a molecular sponge for miR-593-3p to facilitate ZEB2 expression.	hsa_circ_0136666 was shown to be upregulated in OS and correlated with advanced stage and poor prognosis. 	Yes	Functional investigation using CCK8, colony formation assay and Transwell assay demonstrated that hsa_circ_0136666 promoted OS proliferation, migration and invasion, but inhibited cell death. 	32424109
hsa_circ_0000337	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines	regulation[miR-4458/BACH1 pathway]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Circ_0000337 expression was upregulated in OS cell lines and it silence hindered OS cell proliferation and migration. This research for the first time documented that circ_0000337 promoted OS progression via sponging miR-4458 and thus elevating BACH1 expression, offering rational therapeutic target for OS.		Yes	Circ_0000337 expression was upregulated in OS cell lines and it silence hindered OS cell proliferation and migration.	32390598
hsa_circ_0002052	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[miR-382/STX6 axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 The results of this research manifested that relative to that in non-tumor controls, circ-0002052 level was raised in OS tissues.	Up-regulated circ-0002052 was associated with advanced stage, tumor size, and metastasis. Additionally, circ-0002052 elevation indicated a low survival rate in OS patients and silencing of circ-0002052 suppressed proliferation, migration, and invasion of OS cells.	Yes	Additionally, circ-0002052 elevation indicated a low survival rate in OS patients and silencing of circ-0002052 suppressed proliferation, migration, and invasion of OS cells. 	32274658
circRAB3IP	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cells	Interaction(miR-580-3p/TWIST1 axis)	CCK8//qRT-PCR	.In the present study, We found that circRAB3IP was highly expressed in OS tissues and OS cells. Moreover, circRAB3IP directly binds to miR-580-3p. TWIST1 is directly targeted by miR-580-3p. We also demonstrated that circRAB3IP act as the sponge of miR-580-3p to promote TWIST1 expression. CircRAB3IP promotes OS cells proliferation, migration, and invasion through modulating miR-580-3p/TWIST1 axis. 	High levels of circRAB3IP was correlated with advanced TNM stage, distant metastasis. 	Yes	CircRAB3IP knockdown inhibited cell proliferation, migration, and invasion.Moreover, circRAB3IP facilitated tumor formation in vivo. 	34224315
hsa_circ_0102049	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines	Interaction(miR-520g-3p/PLK2 axis)	CCK8//qRT-PCR	 Although circ_0102049 has been found to be highly expressed in OS cell lines. Here, we found that silence of circ_0102049 could significantly exacerbate the tumorigenesis of OS in vivo through sponging microRNA-520g-3p. Polo-like kinase 2 (PLK2) was predicted to be a target of miR-520g-3p, and luciferase reporter assay revealed that overexpression of miR-520g-3p dramatically suppressed the expression of PLK2, whereas miR-520g-3p inhibitor promoted the PLK2 expression.		Yes	Moreover, the silence of circ_0102049 could markedly promote the proliferation, invasion, migration and cell-cycle promotion while inhibiting the apoptosis of OS cell line MG63 cells in vitro through regulating miR-520g-3p/PLK2 axis. 	34060415
circATRNL1	CircRNA	Homo sapiens	Osteosarcoma	 osteosarcoma tissues and cells	Interaction(miR-409-3p/LDHA)	qRT-PCR//FISH	 Results indicated that expression of circATRNL1 was higher in osteosarcoma tissues and cells. Mechanistically, circATRNL1 up-regulated the expression level of LDHA, which was also targeted by miR-409-3p. Therefore, circATRNL1 exerted the accelerative roles of osteosarcoma aerobic glycolysis through miR-409-3p/LDHA axis.	The high-expression of circATRNL1 was significantly correlated with aggressive features and acted as an independent risk factor for osteosarcoma patients' overall survival. 	Yes	 Functionally, our findings demonstrate that circATRNL1 promotes the osteosarcoma aerobic glycolysis in vitro.	34635009
circFOXP1	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues 	Interaction(microRNA -127-5p/CDKN2AIP signaling pathway)	qRT-PCR//Western Blot	We found that circFOXP1 expression was increased in osteosarcoma, and could promote angiogenesis in osteosarcoma through upregulating CDKN2AIP expression. Moreover, circFOXP1 could directly bind to miR-127-5p, which further targets CDKN2AIP directly. 		Yes	We found that circFOXP1 expression was increased in osteosarcoma, and could promote angiogenesis in osteosarcoma through upregulating CDKN2AIP expression. 	34637672
circCRIM1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR-513)	qRT-PCR//Luciferase Report Assay	 The results demonstrated that the expression of circCRIM1 was notably decreased both in OS tissues and cell lines. Further mechanistic studies indicated that circCRIM1 served as a competing endogenous RNA (ceRNA) of miR-513, leading to decreases in the proliferation, migration, and invasion of OS cells. Taken together, our data uncovered a significant role of the circCRIM1/miR-513 pathway in the proliferation, migration, and invasion of OS cell lines and suggested that circCRIM1 may serve as a possible therapeutic target for OS treatment.	Depressed circCRIM1 expression was correlated with lymph node metastasis, advanced FIGO stage, and low overall survival of OS patients. 	Yes	In addition, the results indicated that circCRIM1 could decrease the migration, invasion, and growth of OS cells. 	34480205
hsa_circ_0008932	CircRNA	Homo sapiens	Osteosarcoma	 OS tumors,	Interaction(miR-145-5p)	qRT-PCR	 The results suggested that circ_0008932 was upregulated in most primary OS tumors, suggesting that circ_0008932 is associated with the development of OS. A luciferase reporter assay revealed that circ_0008932 may downregulate microRNA (miR)-145-5p through direct binding. Furthermore, the expression of miR-145-5p was negatively correlated with circ_0008932 levels in OS specimens. In addition, further functional studies indicated that miR-145-5p inhibitors eliminated the effects caused by si-circ_0008932 in OS cells. 		Yes	 In the in vitro assays, si-circ_0008932 inhibited the proliferation, migration and invasion of OS cells, while apoptosis was promoted. 	34504560
circVRK1	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Interaction(miR-337-3p/ZNF652 axis)	qRT-PCR//Transwell Assay	We demonstrated that circVRK1 was a stable circular transcript localized in the cytoplasm of osteosarcoma cells, and the down-regulation of circVRK1 in osteosarcoma tissues was related to poor outcome of patients. Mechanistically, circVRK1 was assumed to be a microRNA sponge for miR-337-3p, and ZNF652 was the downstream gene of miR-337-3p. CircVRK1 overexpression or miR-337-3p knockdown accelerated ZNF652 expression, and up-regulated miR-337-3p efficiently abolished the promotion of ZNF652 induced by circVRK1. 	We demonstrated that circVRK1 was a stable circular transcript localized in the cytoplasm of osteosarcoma cells, and the down-regulation of circVRK1 in osteosarcoma tissues was related to poor outcome of patients. 	Yes	Meanwhile, over-expressed circVRK1 obviously restrained the growth, migration, and invasion of osteosarcoma in vitro and in vivo. 	34424826
circNRIP1	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	Interaction(miR-532-3p/AKT3/PI3K/AKT Axis)	qRT-PCR//Luciferase Report Assay//Transwell Assay	circNRIP1 was upregulated in osteosarcoma tissues and cells.  Co-culture data showed that BMSC-EVs could transfer circNRIP1 into osteosarcoma cells where it competitively bound to miR-532-3p and weakened miR-532-3p's binding ability to AKT3. By this mechanism, the PI3K/AKT signaling pathway was activated and the malignant characteristics of osteosarcoma cells were stimulated.		Yes	Overexpression of circNRIP1 promoted the proliferative, migratory, and invasive potential of osteosarcoma cells. 	34660257
hsa_circ_0007534	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-219a-5p/SOX5 axis)	qRT-PCR//RIP	The levels of circ_0007534 and SOX5 were increased, while the miR-219a-5p level was decreased in OS tissues and cells.Circ_0007534 targeted miR-219a-5p, and miR-219a-5p interacted with SOX5. Furthermore, circ_0007534 regulated the growth of OS cells through modulating the levels of miR-219a-5p and SOX5.		Yes	Circ_0007534 knockdown repressed the proliferation, colony formation, migration, and invasion in OS cells. 	33552887
circATP2A2	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	Regulation(miR-335-5p/MYH9)	qRT-PCR//Western Blot	 circATP2A2 and MYH9 were upregulated while miR-335-5p was downregulated in OS. circATP2A2 accelerated OS cell malignancy and glycolysis through upregulating MYH9 via sponging miR-335-5p, offering a promising target for OS treatment.	OS patients with high circATP2A2 expression displayed a shorter overall survival and the area under curve of circATP2A2 was 0.77, manifesting that circATP2A2 might be a diagnostic and prognostic biomarker. 	Yes	circATP2A2 silencing repressed OS cell proliferation and glycolysis in vivo and constrained OS cell proliferation, glycolysis, migration, and invasion in vitro.	34901459
circATAD1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(miR-154-5p)	qRT-PCR//RNA Pull-Down	Circ-ATAD1 was overexpressed in OS compared to non-tumor tissues and was detected in the nuclei of OS cells.  Mature miR-154-5p, but not premature miR-154-5p, was downregulated in OS tissues compared to non-tumor tissues and was inversely correlated with circ-ATAD1.n OS cells, circ-ATAD1 overexpression decreased the expression of mature miR-154-5p, but not premature miR-154-5p. 		Yes	Transwell assay analysis showed that circ-ATAD1 overexpression increased cell invasion and migration, and mature miR-154-5p overexpression suppressed these cell behaviors. 	34857012
hsa_circ_0000073	CircRNA	Homo sapiens	Osteosarcoma	 OS cell lines 	Interaction(miR-1252-5p/CCNE2 and MDM2 )	qRT-PCR//Western Blot	hsa_circ_0000073 was highly expressed in OS cell lines and could promote OS progression, including proliferation, migration, invasion, and cell cycle in vitro as well as tumorigenesis in vivo. Mechanically, hsa_circ_0000073 could readily downregulate the expression of CCNE2 and MDM2 through miR-1252-5p. 		Yes	hsa_circ_0000073 was highly expressed in OS cell lines and could promote OS progression, including proliferation, migration, invasion, and cell cycle in vitro as well as tumorigenesis in vivo. 	34568326
hsa_circ_0032463	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cell lines	Interaction(MicroRNA 498/LEF1 Axis)	qRT-PCR//Luciferase Report Assay	 Our findings revealed that circ_0032463 expression was upregulated in OS tissues and cell lines. Overall, this research suggested that circ_0032463 could promote OS development by regulating the miR-498/LEF1 axis.		Yes	We also found that circ_0032463 interacted with miR-498, thereby reducing the expression of miR-498 in OS cells. Experimental results indicated that miR-498 could directly target LEF1 in OS cells and that circ_0032463 could abrogate the tumor-inhibitory effect of miR-498 by upregulating LEF1 in OS. More specifically, by binding to miR-498 and inhibiting LEF1 expression, circ_0032463 promoted the migration and proliferation abilities of OS cells and suppressed the apoptosis ability of OS cells.	34096776
circPVT1	CircRNA	Homo sapiens	Osteosarcoma	OS cell 	Interaction(miR-423-5p/Wnt5a/Ror2 signaling pathway)	qRT-PCR//Western Blot	circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p.		Yes	Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	33369809
hsa_circ_0010220	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cells	Interaction(miR-198/Syntaxin 6 axis)	qRT-PCR//RNA Pull-Down//RIP	Circ_0010220 was elevated in osteosarcoma tissues and cells, and was related to the lower survival rate of osteosarcoma patients. Mechanistic research revealed that miR-198 is a target of circ_0010220, and directly targets STX6. Moreover, circ_0010220 upregulated the expression of STX6 by sponging miR-198 to regulate cell proliferation, migration, invasion, cell cycle, and apoptosis.	Circ_0010220 was elevated in osteosarcoma tissues and cells, and was related to the lower survival rate of osteosarcoma patients. 	Yes	Circ_0010220 knockdown inhibited cell proliferation, migration and invasion, but induced cell cycle arrest and apoptosis in vitro. Besides, circ_0010220 silence curbed the growth of xenograft osteosarcoma tumors in vivo. 	33996428
hsa_circ_0005721	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction(miR-16-5p/TEP1)	qRT-PCR//Transwell Assay	hsa_circ_0005721 was upregulated in osteosarcoma tissues and cell lines.Serving as a ceRNA, hsa_circ_0005721 upregulated the linear transcript TEP1 by competitively binding miR-16-5p, thus exerting its biological functions in regulating osteosarcoma development.		Yes	 Knockdown of hsa_circ_0005721 suppressed proliferative and metastatic rates of U-2OS and Saos-2 cells, and stimulated apoptosis. 	34565023
hsa_circ_0000527	CircRNA	Homo sapiens	Osteosarcoma	hFOB1.19 cells	Regulation(miR-646/ARL2 axis)	CCK8//qRT-PCR	We demonstrated that circ_0000527 sponges miR-646 in osteosarcoma cells and that ARL2 is a target gene of miR-646. MiR-646 expression was decreased and ARL2 was overexpressed in osteosarcoma cells (SAOS-2, HOS, MG-63 and U2OS) compared to hFOB1.19 cells. Overexpression of circ_0000527 was demonstrated to induce ARL2 expression in MG-63 cells. We showed that miR-646 was downregulated in osteosarcoma specimens compared to that of non-tumor specimens and that the level of circ_0000527 was negatively correlated with miR-646 expression in osteosarcoma specimens. The elevated expression of circ_0000527 was shown to promote cell growth and cell cycle progression by modulating miR-646 expression. The ectopic expression of circ_0000527 was shown to promote cell growth, cell cycle progression and the secretion of inflammatory mediators by modulating ARL2. The present study suggested that the circ_0000527/miR-646/ARL2 axis may be a potential treatment target for osteosarcoma.		Yes	Overexpression of circ_0000527 was demonstrated to induce ARL2 expression in MG-63 cells. 	33617480
circCNST	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-578-LDHA/PDK1 ceRNA networks)	qRT-PCR//MTT	 Circ-CNST was upregulated in human OS tissues and cells, accompanied with downregulation of miR-578 and upregulation of LDHA and PDK1. There were negative correlations between miR-578 expression and circ-CNST or LDHA/PDK1 in OS tissues.  Physically, miR-578 was targeted by circ-CNST, and miR-578 could target LDHA/PDK1. 	 Moreover, high circ-CNST/LDHA/PDK1 or low miR-578 might predict shorter overall survival, advanced TNM stages, and lymph node metastasis. 	Yes	Functionally, blocking circ-CNST and restoring miR-578 enhanced apoptosis rate and suppressed cell proliferation, colony formation, migration, and invasion in 143B and U2OS cells, accompanied with decreased glucose consumption, lactate production, and adenosine triphosphate (ATP)/adenosine diphosphate (ADP) ratio. Furthermore, in vivo growth of U2OS cells was retarded by silencing circ-CNST. 	33962616
circITCH	CircRNA	Homo sapiens	Osteosarcoma	 40 paired OS tissue and normal tissue samples	Interaction(miR-524/RASSF6 axis)	Flow Cytometry//qRT-PCR//Transwell Assay	Down-regulation of circITCH and RASSF6, as well as the up-regulation of miR-524, was revealed in OS by investigating 40 paired OS tissue and normal tissue samples. circITCH sponged miR-524 to up-regulate RASSF6, causing OS progression inhibition and DXR resistance reduction. 		Yes	 Overexpression of circITCH lowered the cell viability, IC50 value of DXR, migration and invasion, whereas it facilitated apoptosis of OS cells. Additionally, circITCH up-regulation reduced tumor growth in vivo.	34151476
hsa_circ_0032463	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cell lines	Interaction(miR‑330‑3p/PNN axis)	qRT-PCR//Transwell Assay	The findings indicated that circ_0032463 and PNN were highly expressed in OS tissues and OS cell lines, and that they facilitated cell proliferation, viability, invasion and adhesion, but attenuated cell apoptosis in OS cells. It was also noted that circ_0032463 inhibited miR‑330‑3p to upregulate PNN expression. In conclusion, this study confirmed that by regulating the miR‑330‑3p/PNN axis,		Yes	The findings indicated that circ_0032463 and PNN were highly expressed in OS tissues and OS cell lines, and that they facilitated cell proliferation, viability, invasion and adhesion, but attenuated cell apoptosis in OS cells. 	33786605
circCDK14	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-520a-3p/GAB1 axis)	Transwell Assay//qRT-PCR//Colony Formation Assay//Western Blot	Circ_CDK14 and GAB1 expression was upregulated, while miR-520a-3p was downregulated in OS tissues and cells.  Circ_CDK14 could sponge miR-520a-3p. miR-520a-3p targeted GAB1 to repress OS cell proliferation and metastasis.		Yes	 Circ_CDK14 depletion hindered OS cell proliferation, metastasis, and tumorigenesis while facilitated apoptosis, which were all ameliorated by miR-520a-3p inhibition. Circ_CDK14 knockdown blocked OS tumor growth in vivo. 	34348465
hsa_circ_0008259	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-21-5p)	CCK8//qRT-PCR//Transwell Assay//FISH	Circ_0008259 expression and PDCD4 expression were down-regulated and miR-21-5p expression was elevated in the OS tissues and cells.Besides, PDCD4 was validated as the target gene of miR-21-5p, and circ_0008259 could competitively bind to miR-21-5p, thus up-regulating PDCD4 expression in OS cells.		Yes	 Functional experiments showed that circ_0008259 overexpression significantly inhibited the proliferation and metastatic potential of OS cells and promoted the apoptosis. 	34905503
circARF3	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma cell lines and tumor tissues	regulation[miR-1299,CDK6 ]	qRT-PCR//Luciferase Report Assay	In this study we found that circ_ARF3 were highly expressed in osteosarcoma cell lines and tumor tissues.In general, our study demonstrated that in the OS, highly expressed circ_ARF3 acts as a sponge of miR-1299 to inhibit miR-1299 mediated CDK6 downregulation which further promoted OS pathogenesis.		Yes	Knocking down circ_ARF3 greatly ceased OS cell growth, impaired cell colony formation and halted cell cycle transition from G1 to S phase. 	32240746
hsa_circ_0008792	CircRNA	Homo sapiens	Osteosarcoma	 osteosarcoma cells	regulation[Hsa-miR-711/ZFP1]	Flow Cytometry//Wound Healing Assay//Transwell Assay	Hsa_circ_0008792 is expressed at low levels in osteosarcoma cells, and up-regulation of hsa_circ_0008792 could suppress osteosarcoma cell migration and invasion and promote apoptosis.Osteosarcoma is suppressed by hsa_circ_0008792/hsa-miR-711/ZFP1 axis.		Yes	Hsa_circ_0008792 is expressed at low levels in osteosarcoma cells, and up-regulation of hsa_circ_0008792 could suppress osteosarcoma cell migration and invasion and promote apoptosis.	32210583
hsa_circ_0001105	CircRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[miR-766/YTHDF2 signaling pathway]	Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	Data showed that circ_0001105 and YTHDF2 were significantly lower, while miR-766 was higher in OS tissues compared to adjacent tissues.Our findings suggest that circ_0001105 inhibits OS progression, at least partially, by regulating miR-766/YTHDF2 signaling pathway.	 Low expression of circ_0001105 or YTHDF2 was associated with poor survival of OS patients as demonstrated by the Kaplan-Meier analysis.	Yes	 Ectopic overexpression of circ_0001105 or YTHDF2 significantly suppressed OS cell viability and invasion through regulating miR-766. Last, overexpression of circ_0001105 significantly attenuated in vivo tumor growth.	32161468
hsa_circ_0060428	CircRNA	Homo sapiens	Osteosarcoma	cells	regulation[RPBJ]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	 In present study, we identified an elevated expressed circ-0060428 in osteosarcoma cells.Altogether, we confirmed the up-regulated circ-0060428 could improve the proliferation and survival of osteosarcoma cells by sponging miR-375 to upregulate RBPJ expression. 		Yes	The results of CCK-8 and flow cytometry assay showed that circ-0060428 promoted cell proliferation and reduced cell apoptosis of osteosarcoma cells.	32130980
circPVT1	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[ miR-205-5p/c-FLIP Axis ]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	circPVT1 and c-FLIP were highly expressed, while miR-205-5p was lowly expressed in OS tissues and cell lines.  Our study demonstrated circPVT1 functions as a sponge for miR-205-5p to promote c-FLIP expression, thereby enhancing EMT and inducing OS invasion and metastasis in vitro, implying that circPVT1 might be a potential therapeutic target for further clinical therapy of OS.		Yes	Knockdown of circPVT1 repressed cell proliferation, migration and invasion via inhibiting epithelial-mesenchymal transition (EMT) in OS. 	32110097
circEPSTI1	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	regulation[circEPSTI1-miR-892b-MCL1 axis ]	qRT-PCR	We found that circEPSTI1 was significantly upregulated in osteosarcoma. Thus, the circEPSTI1-miR-892b-MCL1 axis affected osteosarcoma progression through the miRNA sponging mechanism. 		Yes	Inhibition of circEPSTI1 suppressed the osteosarcoma cancer cell proliferation and migration in vitro.	31702512
circPIP5K1A	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Interaction(miR-515-5p/YAP axis)	Western Blot//Flow Cytometry//IF//Luciferase Report Assay//Cell Viability Assay//Transwell Assay	CircPIP5K1A expression was significantly enhanced in clinical osteosarcoma tissues compared with the adjacent normal tissues. 		Yes	The depletion of circPIP5K1A by siRNA repressed osteosarcoma cell viabilities and induced osteosarcoma cell apoptosis. The suppression of circPIP5K1A attenuated the capabilities of invasion and migration of osteosarcoma cells. The circPIP5K1A knockdown increased E-Cadherin expression and decreased Vimentin expression in osteosarcoma cells. 	34774083
circUBAP2	CircRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(miR‑204‑3p/HMGA2 axis)	Western Blot//Flow Cytometry//qRT-PCR//CCK8//RIP//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	The results demonstrated that circUBAP2 expression was significantly upregulated in OS tissues and cell lines compared with paracancerous tissues and hFOB1.19 cells, respectively.	 In addition, high circUBAP2 expression levels in patients with OS were associated with a lower survival rate compared with lower expression levels in patients with OS.	Yes	 The functional assays revealed that circUBAP2 knockdown significantly inhibited OS cell proliferation, migration and invasion, but increased OS cell apoptosis compared with the small interfering RNA‑negative control (si‑NC) group. The dual‑luciferase reporter and RIP assay results confirmed that circUBAP2 bound to miR‑204‑3p. 	33650644
circUSP34	CircRNA	Homo sapiens	Osteosarcoma	OS cells (KHOS and 143B cell lines)	Interaction(miR-16-5p )	qRT-PCR//FISH//Western Blot	Based on the inhibited effect of miR-16-5p reported on OS, circUSP34 was analyzed as a sponge of miR-16-5p via Starbase. 		Yes	We found that circUSP34 promoted the proliferation, migration, and invasion of OS in vitro and in vivo. Function assays showed that the malignancy of OS cells, including proliferation, migration, and invasion, was inhibited after knocking out circUSP34. 	34592064
circFAM120B	CircRNA	Homo sapiens	Osteosarcoma	OS tissue and cell lines	Interaction(miR-1205/PTBP1 axis)	CCK8//qRT-PCR//RNA Pull-Down	CircFAM120B and the transcription factor, PTBP1 were elevated in OS tissue and cell lines, while miR-1205 was poorly expressed.  CircFAM120B also appeared to function as an miR-1205 sponge, as miR-1205 bound to PTBP1. Interestingly, overexpressed PTBP1 (or miR-1205 inhibition) reversed the inhibitory effects mediated by circFAM120B downregulation in OS cells.		Yes	Silenced circFAM120B significantly suppressed in vitro OS cell proliferation and invasion, and inhibited in vivo tumor growth.	34716285
hsa_circ_0002137	CircRNA	Homo sapiens	Osteosarcoma	osteosarcoma tumours 	Interaction(miR-433-3p/ IGF1R axis)	qRT-PCR//Luciferase Report Assay//Transwell Assay	In our study, we implicated a circRNA hsa_circ_0002137, which was higher expressed in osteosarcoma tumours compared with paracancerous tissue. In conclusion, it was demonstrated that circ_0002137 could restrain the progression of OS through regulating miR-433-3p/IGF1R axis.		Yes	 It was proved that down-regulation of circ_0002137 suppressed the progress of OS, including cell invasion, cell cycle and cell apoptosis. 	33621401
circSIPA1L1	CircRNA	Homo sapiens	Osteosarcoma	human OS samples and OS cell lines	Interaction( miR-411-5p/RAB9A Signaling Pathway )	qRT-PCR//Luciferase Report Assay	Our study confirmed circSIPA1L1 to be upregulated in both human OS samples and OS cell lines. Mechanistically, circSIPA1L1 could serve as a miR-411-5p molecular sponge to increase RAB9A expression, which was confirmed to be a tumor promoter mediating carcinogenesis.		Yes	 Silencing of circSIPA1L1 attenuated the vitality, invasion, migration and proliferation of OS cell lines both in vivo and in vitro. miR-411-5p inhibition or RAB9A overexpression reversed the anti-tumor effects caused by circSIPA1L1 knockdown. Briefly, circSIPA1L1 could function as a driver gene in OS and initiate OS tumorigenesis through the miR-411-5p/RAB9A signaling pathway, which might become a potential therapeutic biomarker for OS treatment.	33968929
hsa_circ_001422	CircRNA	Homo sapiens	Osteosarcoma	OS cell lines and tissues 	Interaction(miR-195-5p/FGF2/PI3K/Akt axis)	qRT-PCR//RNA-seq	We characterized a novel and abundant circRNA, circ_001422, that promoted OS progression. Circ_001422 expression was dramatically increased in OS cell lines and tissues compared with noncancerous samples. Mechanistically, competitive interactions between circ_001422 and miR-195-5p elevated FGF2 expression while also initiating PI3K/Akt signaling. These events enhanced the malignant characteristics of OS cells.	 Higher circ_001422 expression correlated with more advanced clinical stage, larger tumor size, higher incidence of distant metastases and poorer overall survival in OS patients.	Yes	Circ_001422 knockdown markedly repressed the proliferation and metastasis and promoted the apoptosis of OS cells in vivo and in vitro, whereas circ_001422 overexpression exerted the opposite effects. 	34271943
hsa_circ_103801	CircRNA	Homo sapiens	Osteosarcoma	 OS patients' tissues	Interaction(miR-3388-3p-HIF-1/Rap1/PI3K-Akt pathway)	qRT-PCR//Western Blot	The results showed that the expression level of circRNA_103801 was significantly up-regulated in OS patients' tissues. The results of the luciferase reporter assay suggested that circRNA_103801 could be combined with miR-338-3p, and the RT-qPCR revealed that the miR-338-3p level in OS cells after knockdown of circRNA_103801 was elevated compared with the control group. The results of Western blotting suggested that the expression levels of HIF-1, Rap1, PI3K, and Akt were elevated in OS cells. 		Yes	 Inhibiting the expression level of circRNA_103801 could attenuate the proliferation, migration, and invasion abilities of OS cells. In addition, the down-regulated expression level of circRNA_103801 could induce cell apoptosis. 	34157832
circMTO1	CircRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction(miR-630/KLF6 axis)	qRT-PCR//Western Blot	Here, we measured 20 circRNAs which were downregulated in osteosarcoma tissues using circRNA microarray. CircMTO1 expression was decreased in osteosarcoma cell lines. Bioinformatics analysis showed that circMTO1 serves as a sponge for miR-630 and KLF6 is a direct target of miR-630. Furthermore, circMTO1 functions through regulation of miR-630/KLF6 axis.		Yes	Besides, circMTO1 could inhibit cell proliferation, migration and invasion, and induced apoptosis in osteosarcoma cells. 	33506896
circANKIB1	CircRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	Interaction(miR-217/PAX3 axis)	qRT-PCR	CircANKIB1 and PAX3 were high-expressed, whereas miR-217 was low-expressed in OS tissues and cells. MiR-217 was a direct target of circANKIB1, and its inhibition reversed the inhibitory effect of circANKIB1 knockdown on the progression of OS cells. Moreover, PAX3 was a direct target of miR-217, and miR-217 exerted the anti-tumor role in OS cells by targeting PAX3. F		Yes	 Knockdown of circANKIB1 inhibited the progression of OS by reducing cell proliferation, migration, invasion, and tumor growth (in vivo), and inducing apoptosis. 	33552886
circMUC16	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cells	Interaction(miR-1182/S100B signaling pathway)	Wound Healing Assay//qRT-PCR//RIP//MTT//Transwell Assay	Propofol inhibited ovarian cancer cell proliferation, glycolysis metabolism, migration and invasion, which were partly recovered by circ_MUC16 overexpression.  Circ_MUC16 was downregulated in Propofol-treated ovarian cancer cells.  MiR-1182 was a target of circ_MUC16, and circ_MUC16 knockdown-inhibited cell proliferation, glycolysis metabolism, migration and invasion were partly restored by miR-1182 inhibition. In addition, S100B was a target of miR-1182, and miR-1182-suppressed cell proliferation, glycolysis metabolism, migration and invasion were partly restored by S100B overexpression.		Yes	Propofol inhibited ovarian cancer cell proliferation, glycolysis metabolism, migration and invasion, which were partly recovered by circ_MUC16 overexpression. Besides, circ_MUC16 knockdown enhanced the effects of Propofol to further inhibit tumor growth in vivo. 	34837947
circPTK2	CircRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer tissues 	Interaction(miR-639/FOXC1 )	qRT-PCR//IF//IHC//FISH	Circ-PTK2 expression was significantly higher in the ovarian cancer tissues compared with normal ovary tissues (P < 0.001).  The RNA level of miR-639 was negatively correlated to cell proliferation and migration, whereas the mRNA level of FOXC1 was positively correlated to those processes. miR-639 mimics reversed the function of circ-PTK2 overexpression; however, interference of FOXC1 mRNA also reversed the function of circ-PTK2.		Yes	Overexpression of circ-PTK2 enhanced tumor formation and was correlated to expression of EMT pathway markers. 	34034740
hsa_circ_0013958	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cells	Interaction(miR-637/PLXNB2 Axis)	IHC//Western Blot//CCK8//qRT-PCR//RIP//Colony Formation Assay	Circ_0013958 and PLXNB2 were upregulated, while miR-637 was downregulated in OC tissues and cells. Circ_0013958 acted as a sponge for miR-637 to regulate the expression of PLXNB2 in OC cells.  And miR-637 targeted PLXNB2 to suppress OC cell proliferation, migration, and invasion. Moreover, circ_0013958 silencing blocked OC tumor growth in vivo.  Circ_0013958 knockdown impeded OC development through modulating the miR-637/PLXNB2 axis, highlighting a therapeutic target for OC.		Yes	The repression effects of circ_0013958 knockdown on cell proliferation, migration, invasion, and apoptosis in OC cells were partly attenuated by the miR-637 inhibitor. 	34367233
circPRKCI	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[regulating E2E7]	qRT-PCR//FISH	 The level of circ-PRKCI was significantly higher in HCC tissues than in tumor adjacent tissues, and in HCC cell lines than in cells lines of esophageal, liver, stomach, and colon cancers.And clinical data suggested that the distribution of circ-PRKCI rose with the depth of invasion, lymph node metastasis, distant metastasis, and TNM stage, indicating that circ-PRKCI may affect the survival and prognosis of patients with HCC by regulating E2E7.	 The level of circ-PRKCI was significantly higher in HCC tissues than in tumor adjacent tissues, and in HCC cell lines than in cells lines of esophageal, liver, stomach, and colon cancers.And clinical data suggested that the distribution of circ-PRKCI rose with the depth of invasion, lymph node metastasis, distant metastasis, and TNM stage, indicating that circ-PRKCI may affect the survival and prognosis of patients with HCC by regulating E2E7.	Yes	 A series of functional tests showed that circ-PRKCI substantially inhibited cell apoptosis and promoted cell invasion. 	31086464
circMAT2B	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[ miR-338-3p/PKM2 Axis]	RNA Pull-Down//Luciferase Report Assay//RIP//FISH	CircMAT2B expression was up-regulated in HCC tissues and cell lines.CircMAT2B promoted HCC progression by enhanced glycolysis by activating the circMAT2B/miR-338-3p/PKM2 axis under hypoxia, which may provide a therapeutic target for HCC.	 HCC patients with high circMAT2B expression had shortened overall survival. 	Yes	 Functional assays were performed in HCC cells, HCC organoids, and nude mice to explore the tumor-promoting roles of circMAT2B in HCC.	31004447
circVAPA	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	circVAPA was upregulated in HCC cell lines and circVAPA depletion was associated with decreased HCC cell proliferation. This study revealed that circVAPA contributes to HCC cell proliferation through sponging miR-377-3p and thereby disinhibiting PSAP, shedding light on a new insight into HCC initiation and progression.		Yes	circVAPA was upregulated in HCC cell lines and circVAPA depletion was associated with decreased HCC cell proliferation.	31368365
hsa_circ_0005075	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[sponging miR-335]	qRT-PCR	We found circ_0005075 was upregulated in HCC tissues. Our data provide evidence that circ_0005705 promotes the HCC progression by sponging miR-335 and further regulating MAPK1 expression.		Yes	HCC progression was suppressed by downregulation of circ_0005075 in vitro and in vivo, and the suppression was partially reversed by inhibition of microRNA-335 (miR-335) expression.	31054187
circZFR	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[ regulating miR-3619-5p/CTNNB1 axis and activating Wnt/β-catenin pathway]	qRT-PCR	 We then detect the expression of circZFR in HCC tissues using qRT-PCR.  In summary, our findings indicated that circZFR may exert carcinogenic role in HCC through regulating miR-3619-5p/CTNNB1 axis and activating Wnt/β-catenin pathway. These findings may provide a novel perspective for the treatment of hepatocellular carcinoma.	Furthermore, Kaplan-Meier method and log rank test revealed that high expression of circZFR was associated with the poor prognosis of patients with HCC. 	Yes	Subsequently, loss-of-function assay indicated that circZFR knockdown significantly suppressed cell proliferation and epithelial-mesenchymal transition (EMT) in HCC.	30468709
hsa_circ_0003418	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 The expression level of circ_0003418 was downregulated in HCC tissues and cell lines, and the level correlated with tumor size, TNM stage and HBsAg level in HCC patients.	 The expression level of circ_0003418 was downregulated in HCC tissues and cell lines, and the level correlated with tumor size, TNM stage and HBsAg level in HCC patients.	Yes	 circ_0003418 knockdown promoted HCC cells' proliferation, migration, and invasion. 	31807029
hsa_circ_0015756	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[ miR-7]	MTT//Luciferase Report Assay	The expression level of circ_0015756 was increased and the expression level of miR-7 was diminished in cancerous liver tissues relative to noncancerous liver tissues.  Importantly, we showed circ_0015756 could up-regulate FAK via targeting miR-7.		Yes	Circ_0015756 knockdown was shown to increase the expression of miR-7, reduce the proliferation, invasion, migration and resistance to apoptosis, and down-regulate the expression of FAK in HCC. These in vitro findings were reproduced in vivo that circ_0015756 knockdown decreased HCC xenograft growth.	31522588
hsa_circ_0000885	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[upregulating Caprin1]	Western Blot//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay	Circ_0000885 was highly expressed in HCC tissues than that in adjacent samples.The expression of circ_0000885 was also higher in HCC cell lines. Circ_0000885 could enhance cell proliferation and regulate cell cycle of HCC by promoting Caprin1.	 The miR-532-5p expression was associated with lymphatic metastasis and TNM stage. 	Yes	The cell growth ability of HCC cells was inhibited after circ_0000885 was silenced.	31599409
circEPHB4	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[inhibition of HIF-1α ]	qRT-PCR	The expression of circ-EPHB4 was found to be downregulated in HCC tumor tissues.In conclusion, circ-EPHB4 is a tumor inhibitor in HCC and functions by inhibiting HIF-1α expression.		Yes	The expression of circ-EPHB4 was found to be downregulated in HCC tumor tissues, whereas circ-EPHB4 overexpression suppressed cell viability, induced apoptosis, and inhibited cell migration and invasion in Huh7 and HepG2 cells.	30644610
circLARP4	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[miR-761/RUNX3/p53/p21 signaling ]	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining	Downregulated circLARP4 level was observed in HCC tissues and cell lines.  Our study revealed the role of circLARP4/miR-761/RUNX3/p53/p21 signaling in HCC progression, providing a potential survival predictor and therapeutic candidate for HCC.	Low expression level of circLARP4 independently predicted poor survival outcome. 	Yes	 Gain-of-function and loss-of-function assays demonstrated that circLARP4 suppressed HCC cell proliferation, mediated cell cycle arrest and induced senescence in vitro. 	30520539
circZFR	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[miR-511/AKT1 axis ]	Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of circZFR was enhanced and the expression of miR-511 was down-regulated in HCC tissues and cells. circZFR promotes HCC progression by directly down-regulating miR-511 to activate AKT1 signaling, suggesting that circZFR is a potential target in HCC treatment. Targeting circZFR may provide therapeutic benefits for HCC.		Yes	 Functionally, circZFR silencing or miR-511 overexpression suppressed cell proliferation, migration and invasion, and induced apoptosis of HCC cells. 	31147216
hsa_circ_104348	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[miR-187-3p/RTKN2 axis, Wnt/β-catenin pathway]	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//IF//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In the present study, we clarified that hsa_circRNA_104348 was dramatically upregulated in HCC tissues and cells.  Taken together, these findings indicated that circular RNA hsa_circRNA_104348 might function as a competing endogenous RNA (ceRNA) to promotes HCC progression by targeting miR-187-3p/RTKN2 axis and activating Wnt/β-catenin pathway.	 Patients with HCC displaying high hsa_circRNA_104348 level possessed poor prognosis.	Yes	 Has_circ_104348 facilitated proliferation, migration, and invasion, meanwhile suppressed apoptosis of HCC cell.	33311442
circASAP1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	interaction[miR-326/miR-532-5p-MAPK1/CSF-1 signaling ]	circRNA-seq	CircASAP1 was overexpressed in HCC cell lines with high metastatic potential and in metastatic HCCs.We identified circASAP1 as a key regulator of HCC metastasis that acts on miR-326/miR-532-5p-MAPK1/CSF-1 signaling and serves as a prognostic predictor in patients with HCC.		Yes	In vitro, circASAP1 promoted cell proliferation, colony formation, migration, and invasion, and in vivo, it enhanced tumor growth and pulmonary metastasis.	31838741
hsa_circ_0014717	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue and cells	regulation[miR-668-3p/BTG2 Axis]	RNA Pull-Down//Western Blot//CCK8//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	It was shown that circ_0014717 was significantly decreased in HCC.  In conclusion, our findings illustrated a novel circ_0014717/miR-668-3p/BTG2 regulatory signaling pathway in HCC.		Yes	Then, we observed overexpression of circ_0014717 obviously repressed HCC cell growth, migration and invasion.	33598424
hsa_circ_0004277	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines,blood	Expression[highly expressed]	qRT-PCR//Transwell Assay	 We found that circ-0004277 was significantly upregulated in HCC cells, tissues, and plasma exosomes compared to that in normal controls. 		Yes	Overexpression of circ-0004277 enhanced the proliferation, migration, and epithelial-mesenchymal transition (EMT) of HCC cells in vivo and in vitro.	33511111
circARNT2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	regulation[miR-155-5p/PDK1 Axis]	qRT-PCR	The qRT-PCR analysis was to investigate the expression pattern of circARNT2 in HCC patient tissues and cell lines. In summary, our study demonstrated that circARNT2 modulates cisplatin resistance through miR-155-5p/PDK1 pathway.		Yes	In vitro experiments showed that knockdown of circARNT2 inhibited cell proliferation and enhances the cisplatin sensitivity of HCC cells. 	33425483
circPVT1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-377/TRIM23 Axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	 CircPVT1 and TRIM23 levels were elevated, while miR-377 was decreased in HCC.CircPVT1 aggravated the progression of HCC by upregulating TRIM23 via sponging miR-377.		Yes	CircPVT1 knockdown restrained proliferation and glycolysis, but enhanced apoptosis in HCC cells. 	33364841
hsa_circ_102272	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Expression[highly expressed]	CCK8//qRT-PCR//Luciferase Report Assay	 CircRNA_102272 expression was upregulated in HCC tissues and cells.		Yes	CircRNA_102272 knockdown suppressed HCC cell proliferation and decreased cisplatin-resistance.	33324096
circSMYD4	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[sponging miR-584-5p]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircSMYD4 was down-regulated in HCC tissues and cells, and was not easily affected by RNase R and Actinomycin D.CircSMYD4 prevents the development of HCC through regulating multiple signaling pathways such as metastasis and apoptosis by sponging miR-584-5p.		Yes	 Up-regulation of circSMYD4 inhibited the proliferation, invasion and migration and promoted the apoptosis of HCC cells in vitro, while it inhibited tumor growth, promoted apoptosis-related proteins, and suppressed alpha-fetoprotein (AFP) levels in vivo.	33292243
hsa_circ_0006916	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues and cells	regulation[miR-337-3p/STAT3 axis]	qRT-PCR//Luciferase Report Assay//RIP	Hsa_circ_0006916 was substantially overexpressed in hepatocellular carcinoma tissues and cells.Our data suggest a novel hsa_circ_0006916/miR-337-3p/STAT3 axis in hepatocellular carcinoma, and provide a new target for treatment.	High levels of hsa_circ_0006916 in hepatocellular carcinoma patients were associated with advanced clinical characteristics.	Yes	Down-regulation of hsa_circ_0006916 decreased the growth and invasion of hepatocellular carcinoma cells in vitro. 	33292166
hsa-circ-0046600	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[miR-640/HIF-1α Signalling Pathway]	qRT-PCR//Western Blot//Luciferase Report Assay//FISH	The expression level of hsa-circ-0046600 in HCC tissue was significantly higher than that in adjacent normal tissue (P < 0.05) and was associated with tumour size, TNM stage and pathological vascular invasion.hsa-circ-0046600 is present mainly in the cytoplasm and promotes the expression of proteins such as HIF-1α by competitively binding to miR-640 in HCC, thereby affecting the malignant biological behaviour of liver cancer cells.	The expression level of hsa-circ-0046600 in HCC tissue was significantly higher than that in adjacent normal tissue (P < 0.05) and was associated with tumour size, TNM stage and pathological vascular invasion.	Yes	Moreover, the downregulated expression of hsa-circ-0046600 significantly inhibited the migration of HepG2 and SK-HEP-1 cells.	31807009
circPCNX	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[Inhibiting miR-506]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	We observed that circPCNX and Pecanex were significantly upregulated in tumor tissues of patients with HCC and correlated with clinicopathological variables or prognosis of HCC patients. Mechanistic investigations suggested that both circPCNX and Pecanex 3'UTR could bind to miR-506 and subsequently inhibited the miR-506-induced anticarcinogenic effect in HCC.		Yes	 Functional investigations showed circPCNX and Pecanex could promote the viability of HCC cells.	32099459
circHIPK3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	regulation[sponging miR-338-3p to induce ZEB2 expression]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	CircHIPK3 expression is significantly upregulated during HCC development.CircHIPK3 plays a regulatory role in metastatic HCC by sponging miR-338-3p to induce ZEB2 expression, thus promoting EMT procession.		Yes	Overexpression of circHIPK3 promotes cell migration, invasion, and metastases in vitro and in vivo. 	33247421
hsa_circ_0085616	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Expression[highly expressed]	qRT-PCR//Western Blot//Transwell Assay	We found that hsa_circ_0085616 was highly expressed in all HCC cell lines compared to the normal liver cell line.  Moreover, the protein levels of β-catenin, p-ERK, and p-AKT, which play important roles in the typical proliferation pathway, were also affected by the expression of hsa_circ_0085616.		Yes	Upregulation or downregulation of hsa_circ_0085616 expression could strengthen or weaken the proliferative ability of HCC cells in vitro. 	31496798
hsa_circ_0008450	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor and corresponding nontumor tissue	Interaction[sponging miR-548p]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of circ_0008450 is Expression[Expression[up-expression]-expression]regulated in HCC tissue specimens and cell lines.In addition, circ_0008450 was proved to be a sponge of miR-548p. The oncogenic role of circ_0008450 was partially attributed to its sExpression[Expression[up-expression]-expression]pression on miR-548p.	Patients with a high circ_0008450 expression usually bear a lower 5-year survival rate.	Yes	Silencing of circ_0008450 in Huh-7 cells inhibited cell viability, migration, and invasion, whereas cell apoptosis was increased. Conversely, its overexpression in HepG2 cells leads to absolutely inverse results.	30556306
circADD3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues 	Interaction[EZH2]	Co-IP//qRT-PCR//RIP//Microarray//ChIP	Here, we performed circRNA microarray expression profile in four paired HCC and normal tissues, and found that circ-ADD3, a novel circRNA derived from linear ADD3 exon 4 to exon 12, was significantly Expression[down-expression]regulated in HCC, which was further validated in 112 matched HCC and paracancerous tissues. Mechanistically, circ-ADD3 was capable of reinforcing the interaction between CDK1 and EZH2, resulting in increased EZH2 ubiquitination and subsequent degradation via phosphorylation at Thr-345 and Thr-487 sites. The decreased EZH2 markedly increased the expression of a cohort of anti-metastatic genes, including circ-ADD3, by reducing H3K27me3 levels on their promoter regions, which formed a regulatory circuit, thereby dampening HCC metastasis. 	As shown in Table 1, patients with metastatic characteristics exhibited lower circ-ADD3 expression than patients without metastatic characteristics. Moreover, low circ-ADD3 expression was positively correlated with worse overall and progression-free survival (Figure 2C, ​,2D).2D). 	Yes	Functionally, exogenous expression of circ-ADD3 dramatically weakened HCC cell invasion and metastasis both in vitro and in vivo.	31497351
hsa_circ_101280	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues	Interaction[regulating miR-375/JAK2]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	 After screening differentially expressed circRNAs in HCC tissues through Gene Expression Omnibus data analysis, hsa_circ_101280 was found to be highly expressed, and its high expression was verified in HCC cell lines with qRT-PCR along with the low expression of its downstream miRNA miR-375. JAK2 was identified as a downstream mRNA target of miR-375 by RNA pull-down and dual-luciferase reporter gene assays, its expression in HCC cell lines were positively regulated by hsa_circ_101280 and negatively by miR-375 expression.		Yes	Colony formation and flow cytometry assays showed that both hsa_circ_101280 silencing and miR-375 overexpression restrained proliferation and promoted apoptosis in HCC cells. Furthermore, the silencing of hsa_circ_101280 significantly inhibited the growth of HCC xenografts in nude mice, with the downregulated expression of JAK2. Overall, both the in vitro and in vivo studies revealed that hsa_circ_101280 largely facilitated the tumorigenesis of HCC, characterized by the promoted proliferation and suppressed apoptosis of HCC cells, by sponging miR-375 and upregulating JAK2.	30302825
circSETD3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[microRNA-421]	qRT-PCR//Luciferase Report Assay//RNA-seq//RIP	CircSETD3 (hsa_circRNA_0000567/hsa_circRNA_101436) was significantly downregulated in HCC tissues and cell lines.rthermore, we demonstrated that circSETD3 acts as a sponge for miR-421 and verified that mitogen-activated protein kinase (MAPK)14 is a novel target of miR-421.	Low expression of circSETD3 in HCC tissues significantly predicted an unfavourable prognosis and was correlated with larger tumour size and poor differentiation of HCC in patients. 	Yes	In vitro experiments showed that circSETD3 inhibited the proliferation of HCC cells and induced G1/S arrest in HCC cells. In vivo studies revealed that circSETD3 was stably overexpressed in a xenograft mouse model and inhibited the growth of HCC. 	30795787
hsa_circ_103809	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[regulating miR-377-3p/FGFR1/ERK axis]	qRT-PCR	 Our results suggested that hsa_circRNA_103809 was overexpressed in HCC patients.The investigations of molecular showed that hsa_circRNA_103809 could elevate the protein expression of a miR-377-3p target, fibroblast growth factor receptor 1 (FGFR1), through interacting with miR-377-3p and decreasing its expression level. Additionally, in vivo assays revealed hsa_circRNA_103809 short hairpin RNA served as a tumor suppressor through downregulating FGFR1 in HCC. This study systematically investigated novel regulatory signaling of hsa_circRNA_103809/miR-377-3p/FGFR1 axis, providing insights into hepatocellular carcinoma treatment from bench to clinic.		Yes	hsa_circRNA_103809 knockdown remarkably inhibited the proliferation, cycle progression, and migration of HCC cells.	31317555
circBIRC6	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue,cell lines	Regulation[miR-3918/Bcl2 axis]	Western Blot//CCK8//FISH//Flow Cytometry//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circ-baculoviral IAP repeat-containing (BIRC)6 was upregulated in HCC tissue samples and cells; this was associated with the overall survival of HCC patients.Additionally, circ-BIRC6 overexpression negatively regulated the expression of microRNA miR-3918, which was identified as an inhibitor of B cell lymphoma (Bcl)2. The tumor-suppressive effect of circ-BIRC6 deletion was abrogated by inhibiting miR-3918.		Yes	circ-BIRC6 knockdown reduced HCC cell proliferation, migration, and invasion and enhanced their apoptosis. 	30931701
hsa_circ_0008450	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells lines	Regulation[microRNA-214-3p/EZH2 Axis ]	CCK8//qRT-PCR//Wound Healing Assay//Luciferase Report Assay	hsa_circ_0008450 was significantly increased in HCC tissues and cells. Mechanically, hsa_circ_0008450 promoted the expression of EZH2 protein through sponging miR-214-3p. Knockdown of circ_0008450 suppressed tumorigenesis of HCC cells in vivo.		Yes	Furthermore, knockdown of hsa_circ_0008450 in HCC cells inhibited cell proliferation, invasion, and migration.	31695501
hsa_circ_0001955	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCCtissues	Interaction[sponging miR-516a-5p]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Colony Formation Assay	We revealed that circ_0001955, TRAF6 and MAPK11 levels were increased, while miR-516a-5p levels were decreased in HCC tumor tissues compared to adjacent normal tissues.Circ_0001955 was identified as a sponge for miR-145-5p and miR-516a-5p, and TRAF6 and MAPK11 were demonstrated to be two target genes of miR-516a-5p. In conclusion, circ_0001955 facilitated HCC tumorigenesis by sponging miR-516a-5p to release TRAF6 and MAPK11 expression.		Yes	Knockdown of circ_0001955 repressed HCC tumor growth in vitro and in vivo, while overexpression of circ_0001955 exhibited the opposite effect. 	31822654
hsa_circ_0000267	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction[sponging miR-646]	Flow Cytometry//qRT-PCR//CCK8//Colony Formation Assay//Transwell Assay	As a result, circ_0000267 was enhanced in HCC tissues and cell lines.Mechanistically, circ_0000267 could directly sponge miR-646 to exert its oncogenic properties. In summary, we identified a novel HCC-associated circRNA in the progression of this fatal disease.	This upregulation is associated with patients' clinical severity and poor prognosis.	Yes	Functionally, circ_0000267 could facilitate cell growth, migration and invasion and attenuate cell apoptosis in HCC cells. 	30719761
circHIAT1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues 	Regulation[miR-3171/PTEN axis]	qRT-PCR//FISH	 CircHIAT1 was expressed at a significantly low level in cancerous samples.Mechanistically, circHIAT1 acted as the miR-3171 sponge to upregulate PTEN in HCC. Finally, rescue assays demonstrated the role of circHIAT1/miR-3171/PTEN pathway in regulating HCC cell growth. Taken together, this study revealed the novel mechanism of circHIAT1 in HCC.	Based on Kaplan-Meier survival analysis, we determined a positive correlation between the downregulation of circHIAT1 and the poor overall survival of HCC patients.	Yes	Both in vitro and in vivo experiments demonstrated the suppressive effect of circHIAT1 on the HCC cell growth.	31108351
hsa_circ_0078710	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue,cell lines	Interaction[sponging microRNA-31]	qRT-PCR	 Has_circ_0078710 was significantly unregulated in HCC tissues and cells.Furthermore, overexpression of has_circ_0078710 in HCC could up-regulate HDAC and CDK2 levels by sponging miR-31, simultaneously mediating the expression of cell cycle components (cyclin A, cyclin D1, CDK4) and negative cell cycle regulator p21.	Moreover, HCC patients with high level of has_circ_0078710 had the advance stage (TNM III-IV). 	Yes	In vitro and in vivo functional studies showed that overexpression of has_circ_0078710 in HepG2, SMMC-7721 cell lines significantly promoted cell proliferation, migration, invasion and tumor growth by inducing the cell cycle progression.	30342168
circDB	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	blood	Regulation[USP7/Cyclin A2 signaling pathway]	Western Blot//qRT-PCR//Luciferase Report Assay//IHC//EdU Staining//IF	 It was observed that exosome circ-deubiquitination (circ-DB) is upregulated in HCC patients with higher body fat ratios.Moreover, in vitro and in vivo studies showed that exo-circ-DB promotes HCC growth and reduces DNA damage via the suppression of miR-34a and the activation of deubiquitination-related USP7. Finally, the results showed that the effects of adipose exosomes on HCC cells can be reversed by knockdown of circ-DB. These results indicate that exosome circRNAs secreted from adipocytes promote tumor growth and reduce DNA damage by suppressing miR-34a and activating the USP7/Cyclin A2 signaling pathway.		Yes	Moreover, in vitro and in vivo studies showed that exo-circ-DB promotes HCC growth and reduces DNA damage via the suppression of miR-34a and the activation of deubiquitination-related USP7. 	30546088
hsa_circ_0002124	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	liver cancer tissues,cell lines	Interaction[MAPK pathway]	Flow Cytometry//qRT-PCR//Western Blot//Transwell Assay	Hsa_circ_0002124 was highly expressed in the HCC cells and liver cancer tissues. KEGG and interaction network analysis of hsa_circ_0002124 indicated that hsa_circ_0002124 could be a molecular sponge of miRNAs, which regulates the key protein expressions in the MAPK pathway. The p-JNK/JNK, p-ERK/ERK, p-P38/P38, and c-Myc expressions in knockdown hsa_circ_0002124-treated 97H cells were significantly lower than in normal 97H cells, whereas these expressions in overexpressed hsa_circ_0002124-treated 97H cells were significantly higher than in mock vector-treated 97H cells.		Yes	Moreover, the knockdown hsa_circ_0002124 in 97H cells resulted in the repression of cell proliferation, cell invasion, and migration, with simultaneous promotion of cell apoptosis and cell cycle transformation.The opposing situations of cell function could be detected in overexpressed hsa_circ_0002124 in 97H cells. 	35116769
circPTGR1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	blood	Interaction[miR449a-MET pathway]	qRT-PCR//Western Blot	 LM3 exosomes enhanced the cell migration and invasion potential of HepG2 and 97 L cells. CircPTGR1, a circRNA with three isoforms, was specifically expressed in exosomes from 97 L and LM3 cells, upregulated in serum exosomes from HCC patients and was associated with the clinical stage and prognosis. Bioinformatics, co-expression analysis, and a luciferase assay indicated that circPTGR1 competed with MET to target miR449a.		Yes	 Knockdown of circPTGR1 expression suppressed the migration and invasion of HepG2 and 97L cells induced by co-culturing with LM3 exosomes.	30630697
circSMARCA5	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression[lower expressed]	qRT-PCR	 The expression of circSMARCA5 was significantly downregulated in HCC tissues compared with para-carcinoma tissues. 	CircSMARCA5 levels were correlated with tumor differentiation (p = 0.023), Tumor-node-metastasis (TNM) stage (p = 0.001), cancer invasion (p = 0.004), as well as cancer diameter (p = 0.018).	Yes	 In vitro cell experiments revealed that overexpression of circSMARCA5 resulted in inhibited proliferation, increased apoptosis and suppressed invasion.	30716279
hsa_circ_0070269	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[miR-182/NPTX1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the present study, we identified a novel circRNA (hsa_circ_0070269) was significantly decreased in HCC tissues and cell lines. Mechanistically, hsa_circ_0070269 increased NPTX1 expression via sponging miR-182 in HCC cells, which inhibited aggressive tumor behavior. Taken together, our findings suggest that hsa_circ_0070269 might play an important role in HCC development via miR-182/NPTX1 axis, therefore could serve as a potential therapeutic target for HCC treatment.	low hsa_circ_0070269 expression was positively associated with advanced tumor stage, lymph node metastasis, and poor overall survival.	Yes	Hsa_circ_0070269 overexpression suppressed proliferation and invasion of HCC cells in vitro and reduced tumor growth in vivo. 	31606623
hsa_circ_0000502	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[targeting microRNA-124]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	QRT-PCR results indicated that the level of circ_0000502 in HCC tissues was significantly higher than that in adjacent ones. QRT-PCR results revealed that the expression of miR-124 and circ_0000502 mRNA in HCC tissues was negatively correlated. Also, the result of luciferase reporter gene assay demonstrated that circ_0000502 could be targeted by miR-124 via this binding site.	 Compared with patients with low expression of circ_0000502, patients with high expression of circ_0000502 had a lower overall survival rate compared with the negative control (NC) group.	Yes	The proliferation, invasion and migration ability of circ_0000502 knockdown group significantly decreased, while on the contrary cell apoptosis increased.	31983112
hsa_circ_100338	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[circRNA-100338/miR-141-3p/RHEB axis ]	CCK8//qRT-PCR//IHC//Western Blot	The circRNA expression profiles based on the RNA-seq data indicated that circRNA-100338 was significantly up-regulated in tumor tissues, as compared with non-tumor tissues (P-value < 0.001, Figure 1A). In conclusion, elevated circRNA-100338 activates mTOR signaling pathway in HCC via circRNA-100338/miR-141-3p/RHEB axis and associates with poor prognosis of hepatitis B-related HCC patients.		Yes	Cell proliferation assay demonstrated that knockdown of circRNA-100338 in highly metastatic potential HCC cell lines could significantly reduce the cancer cell proliferation (Figure 1B). Consistently, overexpression of circRNA-100338 in two HCC cell lines with low metastatic potential could increase cancer cell proliferation (P < 0.05, Figure 1C).	31157168
hsa_circ_0021093	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[miR-766-3p/MTA3 axis]	qRT-PCR	Upregulation of circ_0021093 was found in HCC tumor samples and cells. In conclusion, the circ_0021093/miR-766-3p/MTA3 regulatory axis may be an effective therapeutic target for HCC.		Yes	Furthermore, downregulated circ_0021093 attenuated cell growth, migration and invasion but increased cell apoptosis.	31330234
circGSK3B	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cell lines	regulation[circGSK3B-miR-1265-CAB39 axis]	qRT-PCR//RNA Pull-Down//RIP	We found that circGSK3B was highly expressed in HCC tissues and HCC cell lines.In summary, we proved that the circGSK3B-miR-1265-CAB39 axis can promote the proliferation, migration, invasion of HCC cells, indicating that circGSKB may serve as a promising diagnostic and prognostic marker in HCC.	Additionally, the expression level of circGSK3B significantly correlated with HCC tumor size and vascular invasion. 	Yes	Functionally, we confirmed that circGSK3B can promote the proliferation, migration, and invasion of HCC cells in vivo and in vitro.	33262952
circSOD2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues	regulation[JAK2/STAT3 signaling pathway]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 In accordance with previous sequencing results, here, we demonstrated that circSOD2 was highly expressed in HCC tumor tissues compared with normal liver tissues. The novel signaling axis circSOD2/miR-502-5p/DNMT3a/JAK2/STAT3/circSOD2 provides a better understanding of HCC tumorigenesis. 		Yes	 SiRNA mediated circSOD2 suppression impaired liver cancer cell growth, cell migration, prohibited cell cycle progression and in vivo tumor growth.	33234142
circE2F2	CircRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and cell line	Interaction(HuR/E2F2)	qRT-PCR//RIP//Western Blot	The results showed that one of the circRNAs (termed circE2F2) was significantly upregulated in OC tissues and cell lines, and high circE2F2 expression was associated with poor survival in OC patients.  In circE2F2-deficient cells, the half-life of the E2F2 mRNA was significantly shorter than that in the control group, indicating that sufficient circE2F2 expression could strengthen the stability of the E2F2 mRNA. Further analysis revealed that circE2F2 could bind to RNA-binding protein Hu antigen R (HuR). 	The results showed that one of the circRNAs (termed circE2F2) was significantly upregulated in OC tissues and cell lines, and high circE2F2 expression was associated with poor survival in OC patients. 	Yes	The knockdown of circE2F2 in OC cells suppressed cell proliferation, migration, invasion, and cellular glucose metabolism.	33894314
hsa_circ_0001445	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-942-5p/ALX4 axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	Herein, circ_0001445 was decreased and miR-942-5p was increased in HCC tissues and cells. In conclusion, circ_0001445 played a negative role in HCC progression by modulating miR-942-5p/ALX4 axis, which might provide a novel target for HCC therapy.		Yes	Circ_0001445 overexpression or miR-942-5p inhibition repressed cell cycle process, migration, invasion, epithelial-mesenchymal transition and glycolysis in HCC cells. 	32856218
hsa_circ_0046599	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-1258/RPN2 Network]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Circ_0046599 was highly expressed in HCC tissues and cells, and its knockdown could suppress HCC cell proliferation, migration, invasion and glycolysis process.Our results provided new evidence that circ_0046599 could promote the progression of HCC by increasing RPN2 expression via sponging miR-1258.		Yes	Circ_0046599 was highly expressed in HCC tissues and cells, and its knockdown could suppress HCC cell proliferation, migration, invasion and glycolysis process.	32801909
hsa_circ_101141	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-1297/ROCK1 Pathway]	Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	In the present study, we found that the expression of human circ_101141 was upregulated in HCC tissues and cells.aken together, these findings indicated that circRNA circ_101141 acted as a ceRNA to facilitate tumorigenesis of HCC by regulating miR-1297/ROCK1 pathway.		Yes	In addition, downregulation of circ_101141 dramatically inhibited cell proliferation, migration, and invasion in HCC cells. 	32787581
hsa_circ_0000517	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	regulation[miR-326/SMAD6 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	Hsa_circ_0000517 and SMAD6 were up-regulated while miR-326 was down-regulated in HCC tissues and cells. Hsa_circ_0000517 depletion repressed HCC advancement via regulating the miR-326/SMAD6 axis.		Yes	Hsa_circ_0000517 down-regulation repressed cell proliferation, colony formation, migration, and invasion, and induced cell cycle arrest in HCC cells in vitro, and constrained tumor growth in vivo. 	32774154
hsa_circ_4911	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	human umbilical vein endothelial cells	Expression[lower expressed]	qRT-PCR//RNA-seq	 Subsequently, we validated the expression of the candidate circRNAs using RT?qPCR, and selected two of the most downregulated circRNAs among them, circ_4911 and circ_4302. 		Yes	Next, through circRNA overexpression experiments, we demonstrated that overexpression of circ_4911 and circ_4302 both inhibited the proliferation and migration of HUVECs, and arrested cells at the GO/G1 stage, while promoting adhesion. 	32700752
hsa_circ_4302	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	human umbilical vein endothelial cells	Expression[lower expressed]	qRT-PCR//RNA-seq	 Subsequently, we validated the expression of the candidate circRNAs using RT?qPCR, and selected two of the most downregulated circRNAs among them, circ_4911 and circ_4302. 		Yes	Next, through circRNA overexpression experiments, we demonstrated that overexpression of circ_4911 and circ_4302 both inhibited the proliferation and migration of HUVECs, and arrested cells at the GO/G1 stage, while promoting adhesion. 	32700752
hsa_circ_103809	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	regulation[circRNA-103809/miR-1270/PLAGL2 axis]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	CircRNA-103809 was highly expressed in HCC cell lines.Thereafter, we verified the tumor-facilitating effect of circRNA-103809/miR-1270/PLAGL2 axis on biological behaviors of HCC cells.		Yes	 After interfering circRNA-103809, the proliferation, migration, invasion and epithelial-to-mesenchymal transition process were all hindered in HCC cells. 	32683589
hsa_circ_0091579	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-490-5p/CASC3 Axis]	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	circ_0091579 and CASC3 were upregulated, while miR-490-5p was downregulated in HCC tissues and cells.circ_0091579 promoted cell proliferation, migration, invasion, and glycolysis partially through miR-490-5p/CASC3 axis in HCC cells.		Yes	Silencing of either circ_0091579 or CASC3 suppressed cell proliferation, migration, invasion, and glycolysis in HCC cells.	32673066
circNFATC3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-548I,NFATC3 ]	qRT-PCR//Transwell Assay	Overall, the circNFATC3 can sponge miR-548I to protect NFATC3 itself, then it regulates hepatoma cell function via the JNK, c-Jun, AKT, and mTOR signaling pathways, and the circNFATC3 can be a tumor-repressor on HCC.		Yes	 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, apoptotic, and transwell assay proved that circNFATC3 can inhibit hepatoma cell proliferation, apoptosis, and migration/invasion in vitro. Mouse xenograft assay demonstrated that circNFATC3 suppressed tumor size and weight and reduced lung metastasis in vivo, and vice versa.	32667692
circKIAA1429	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tumor tissues	regulation[m6A-YTHDF3-Zeb1]	qRT-PCR	In this study, we found hsa_circ_0084922, which came from KIAA1429, named circ_KIAA1429, was upregulated in HCC cells and tumor tissues. This study revealed that circ_KIAA1429 could accelerate HCC advancement, maintained the expression of Zeb1 through the mechanism of m6A-YTHDF3-Zeb1 in HCC. 		Yes	 Overexpression of circ_KIAA1429 can facilitate HCC migration, invasion, and EMT process. However, knockdown of circ_KIAA1429 lead to the opposite results.	32653519
hsa_circ_0026134	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and cell lines	regulation[miR-127-5p expression]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	hsa_circ_0026134 expression was increased in HCC samples and cell lines.Down-regulation of hsa_circ_0026134 suppressed TRIM25- and IGF2BP3-mediated HCC cell proliferation and invasion via promotion of miR-127-5p expression, which have been confirmed by luciferase reporter assay.		Yes	Down-regulation of hsa_circ_0026134 attenuated HCC cell proliferation and metastatic properties. 	32648571
hsa_circ_0005394	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-507/E2F3 and miR-515-5p/CXCL6 Signaling Pathways]	qRT-PCR//Luciferase Report Assay	circ_0005394 expression was higher in HCC tissues and cells than noncancerous samples and normal cell line, respectively.Rescue assay indicated that circ_0005394 facilitated HCC growth and invasion by regulating miR-507/E2F3 and miR-515-5p/CXCL6 signaling pathways.	High expression of circ_0005394 was associated with larger tumor size, more advanced TNM stages, and poorer overall survival for the patients with HCC. 	Yes	Gain/loss-of function assays demonstrated its oncogenic role in cell growth, apoptosis, migration, and invasion.	32636641
circPTN	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tumor tissues and cell lines	interaction[ Sponges miR-326]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//EdU Staining	Our results indicated that circPTN was upregulated in human hepatocellular carcinoma tumor tissues and cell lines, compared with paratumor tissues and immortalized normal liver cell line.Our study indicates that circPTN acts as an oncogenic factor via sponging miR-326 in HCC.		Yes	 circPTN could significantly promote HCC tumor growth according to gain-and loss-of-function assays.	32581550
hsa_circ_0000515	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[regulating MAPK10]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_0000515 was highly expressed in HCC tissues and cell lines. Circ_0000515 aggravates the malignant progression of HCC by downregulating MAPK10.	High level of circ_0000515 predicted advanced stage, high incidence of lymphatic metastasis, and low disease-free survival and overall survival in HCC.	Yes	Knockdown of circ_0000515 attenuated proliferative and migratory abilities in Hep3B and MHCC88H cells.	32572915
hsa_circ_0101145	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-548c-3p/LAMC2 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Transwell Assay	 The data demonstrated that hsa_circ_0101145 was significantly upregulated in both HCC tissues and cell lines. . In summary, the findings illustrated that hsa_circ_0101145 silencing suppressed HCC progression by functioning as an miR-548c-3p sponge to enhance LAMC2 expression. 		Yes	Downregulation of hsa_circ_0101145 suppressed HCC proliferation as well as metastasis by targeting the miR-548c-3p/LAMC2 axis, which was examined using luciferase reporter and RNA pulldown assays. Silencing of hsa_circ_0101145 suppressed the epithelial-mesenchymal transition in HCC.	32554866
hsa_circ_0003998	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[ circ0003998/miR-143-3p/FOSL2 axis and circ0003998 /PCBP1/CD44v6 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Compared with adjacent normal liver tissues (ANL), circ0003998 expression was significantly upregulated in PVTT tissues and HCC tissues, and its expression correlates with the aggressive characteristics of HCC patients.Circ0003998 promotes EMT of HCC by circ0003998/miR-143-3p/FOSL2 axis and circ0003998 /PCBP1/CD44v6 axis.		Yes	Further assays suggested that circ0003998 promoted EMT of HCC both in vitro and in vivo. 	32552766
circMTO1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	liver cancer tissues and cell lines	regulation[miR-9-5p/NOX4 Axis]	CCK8//qRT-PCR//Transwell Assay//Western Blot	CircMTO1 were down-regulated in the liver cancer tissues and cell lines compared to their respective normal controls. 		Yes	 Overexpression of circMTO1 and NOX4 inhibited proliferation and migration of hepatoma cells, while the overexpression of miR-9-5p had the opposite effects. In contrast, overexpression of circMTO1 and NOX4 promoted apoptosis, while that of miR-9-5p decreased the cell apoptosis rates.	32547227
circGprc5a	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues or cells	regulation[YAP1/TEAD1 signaling pathway]	CCK8//qRT-PCR//Western Blot	CircGprc5a was highly expressed in liver cancer, and closely related poor survival of patients with liver cancer. CircGprc5a promoted the development of HCC by inhibiting the expression of miR-1283 and activating the YAP1/TEAD1 signaling pathway.	CircGprc5a was highly expressed in liver cancer, and closely related poor survival of patients with liver cancer. 	Yes	Knockout of circGprc5a inhibited proliferation of HCC and induced apoptosis. 	32547082
circZNF566	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[ circZNF566/ miR-4738-3p /TDO2 axis]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	CircZNF566 was significantly upregulated in HCC tissues and cell lines.	High circZNF566 expression in HCC tissues was positively correlated with clinicopathological features and poor prognosis.	Yes	 Functionally, in vitro experiments showed that circZNF566 promoted HCC cell migration, invasion, and proliferation, whereas in vivo experiments showed that circZNF566 promoted tumorigenesis and metastasis. 	32532962
circCSPP1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	interaction[sponging miR-577]	ISH//Wound Healing Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In HCC patients and cells, circ-CSPP1 was aberrantly expressed, and its upregulation predicted poor prognosis, and closely correlated with tumor size and TNM stage.These findings revealed that circ-CSPP1 contributed to HCC progression by positively regulating CCNE2 via miR-577, thus established its potential as new a prognostic and therapeutic marker for HCC patients.	 In HCC patients and cells, circ-CSPP1 was aberrantly expressed, and its upregulation predicted poor prognosis, and closely correlated with tumor size and TNM stage.	Yes	Moreover, overexpression of circ-CSPP1 promoted HCC cell viability, colony formation, migration, and invasion in vitro. Knockdown of circ-CSPP1 showed contrary results. 	32514247
circIL4R	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-541-3p/GPX4 network]	RNA Pull-Down//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	CircIL4R was abnormally overexpressed in HCC tissues and cells. Our data suggested that circIL4R served for a tumor promoter and ferroptosis inhibitor in HCC by the miR-541-3p/GPX4 network.		Yes	 CircIL4R knockdown impeded oncogenesis and expedited ferroptosis of HCC cells.	32808701
hsa_circ_0000517	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues and cell lines	regulation[miR-326/IGF1R axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 circ_0000517 expression was elevated in hepatocellular carcinoma tissues and cell lines. circ_0000517 knockdown repressed hepatocellular carcinoma development in vitro and in vivo by modulating miR-326 and IGF1R.		Yes	 circ_0000517 knockdown suppressed cell viability, colony formation, migration, invasion and glycolysis.	32863763
hsa_circ_0001955	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells and tissues	regulation[miR-145-5p/NRAS Axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Transwell Assay	hsa_circ_0001955 ranked as the top three most upregulated DECs in GEO: GSE78520, GSE94508, and GSE97332. Collectively, our findings demonstrate the oncogenic roles of the hsa_circ_0001955/miR-145-5p/NRAS axis in HCC, which may represent a potential therapeutic target for HCC. Moreover, hsa_circ_0001955 expression in HCC cells and tissues was significantly higher than that in corresponding normal controls. 		Yes	Functional experiments revealed that knockdown of hsa_circ_0001955 markedly inhibited proliferation, migration, and invasion of HCC, and its overexpression led to the opposite effects. 	33230448
circMYLK	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR29a/KMT5C Signaling Pathway]	qRT-PCR//Luciferase Report Assay//Western Blot//FISH	circMYLK was determined to be significantly upregulated in HCC tissues and cells.Our current study demonstrated that circMYLK promotes HCC progression by acting as a competing endogenous RNA of miR-29a, which regulates the downstream oncogene KMT5C.		Yes	 Suppression of circMYLK repressed HCC cell proliferation, migration, and invasion while increasing apoptosis. 	32904604
circTMEM45A	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[MicroRNA-665 ]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Microarray	We found that the level of circTMEM45A was significantly upregulated in HCC and was positively correlated with clinicopathological features and poor prognosis of patients with HCC.Mechanistically, circTMEM45A acted as a miR-65 sponge to relieve the repressive effect of miR-665 on its target IGF2. 	We found that the level of circTMEM45A was significantly upregulated in HCC and was positively correlated with clinicopathological features and poor prognosis of patients with HCC.	Yes	 Functionally, circTMEM45A promoted cell mobility in vitro, as well as in vivo tumorigenesis.	33230434
circLRIG3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[EZH2/STAT3 signaling]	ChIP//Co-IP//CCK8//qRT-PCR//RIP//EdU Staining//Transwell Assay	Circ-LRIG3 was notably upregulated in HCC and promoted HCC cell proliferation, migration, invasion and reduced apoptosis. Circ-LRIG3 formed a ternary complex with EZH2 and STAT3, facilitating EZH2-induced STAT3 methylation and subsequent phosphorylation, resulting in the activation of STAT3 signaling.	Clinically, high circ-LRIG3 was closely linked with aggressive clinicopathological features and was identified as an independent risk prognostic factor of overall survival.	Yes	Circ-LRIG3 was notably upregulated in HCC and promoted HCC cell proliferation, migration, invasion and reduced apoptosis. The animal models showed that exogenous expression of circ-LRIG3 enhanced tumorigenicity and metastasis in vivo, whereas these effects were blocked after treatment with C188-9, a specific STAT3 small-molecule inhibitor. 	33222697
hsa_circ_0008305	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	interaction[binding to miR-186 and inducing TMED2]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Currently, our data showed that circ_0008305 was highly elevated in HCC cell lines and 30 paired tissue samples of HCC.  Mechanistically, we demonstrated that circ_0008305 up-regulated TMED2 expression by sponging miR-186, which resulted in significantly induced HCC progression in vitro and in vivo. 		Yes	As evidenced, suppression of circ_0008305 repressed HCC cell growth significantly. Meanwhile, up-regulation of circ_0008305 significantly reduced HCC cell growth.	33210454
circFAT1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-30a-5p/REEP3 pathway]	Western Blot//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Transwell Assay	In the present study, we found that circFAT1 expression is up-regulated in HCC tissues and cells.In conclusion, circFAT1 sponges miR-30a-5p to regulate the expression of REEP3, thus promoting hepatocarcinogenesis.	 In addition, circFAT1 level is positively correlated with TNM stage and tumour size. 	Yes	The results show that circFAT1 inhibition reduces the proliferation and invasion of HCC cells and tumorigenesis in vivo, whereas REEP3 overexpression reverses these processes. 	33179443
hsa_circ_1306	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-584-5p/CDK16 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay	we found has_circRNA_001306 (circ_1306) was up-regulated in HCC tissues and cell lines.Altogether, our findings suggested that circ_1306 could promoter HCC progress by miR-584-5p/CDK16 axis, which provided a novel marker for HCC diagnosis and treatment.		Yes	Knockdown the expression circ_1306 significantly suppressed HCC cell proliferation and induced the cell apoptosis in vitro and in vivo.	33135290
hsa_circ_0039053	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	interaction[combining with miR-637]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Herein, hsa_circ_0039053 was upregulated in HCC tissues and cell lines. Collectively, our study confirmed that hsa_circ_0039053 could be regarded as a competing endogenous RNA (ceRNA) to positively modulate the expression of USP21 combining with miR-637, which provided a potential target in HCC treatment.		Yes	 Downregulation of hsa_circ_0039053 decreased the invasion and proliferative ability of tumors in vitro and as well as tumor growth in vivo.	33123285
hsa_circ_102559	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-130a-5p,ANXA2]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 First, analysis of HCC-related circRNA expression profile GSE97332 and HCC patients showed a significant upregulation of hsa_circ_102559 in HCC tissues.	Upregulation of hsa_circ_102559 in HCC cells was associated with the metastatic properties.	Yes	 Second, hsa_circ_102559 significantly promoted HCC metastasis, while knockdown of hsa_circ_102559 reversed the promotive effects on HCC progression. Lastly, xenograft experiment was established and results indicated that knockdown of hsa_circ_102559 inhibited HCC growth and metastasis through the downregulation of ANXA2.	33121269
circUGGT2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-526b-5p/RAB1A Axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 We observed that circUGGT2 and RAB1A were upregulated while miR-526b-5p was downregulated in HCC tissues and cells. CircUGGT2 silencing inhibited HCC development via modulating the miR-526b-5p/RAB1A axis, providing a possible target for HCC treatment.		Yes	CircUGGT2 silencing suppressed tumor growth in vivo and curbed proliferation, colony formation, cell cycle progression, migration, and invasion of HCC cells in vitro.	33116877
circCDR1as	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-1287/Raf1 and MEK/ERK pathways]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Expression of circ_CDR1as and Raf1 is elevated, while miR-1287 expression is decreased in HCC. Circ_CDR1as depletion inhibits HCC cell proliferation and metastasis by miR-1287/Raf1 and MEK/ERK pathways, highlighting a promising molecular target for HCC treatment.		Yes	Depletion of circ_CDR1as or Raf1 could inhibit proliferation and metastasis of HCC cells. 	33061591
hsa_circ_0004018	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissues,cell lines	regulation[hsa_circ_0004018/miR-626/DKK3 regulatory axis]	RNA Pull-Down//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 We found that the expression of hsa_circ_0004018 was lower in tumor tissues than in their paired non-tumor tissues from 28 out of 41 HCC patients.Similarly, hsa_circ_0004018 was downregulated in HCC cell lines. We revealed that hsa_circ_0004018/miR-626/DKK3 regulatory axis may be a possible novel therapeutic target for HCC.	The difference in the expression between tumor tissues and non-tumor tissues was statistically significant (p<0.001). Further analysis revealed that such lower expression in tumor tissues was much more common in bigger tumor size group (≥5cm) compared with the smaller tumor size group (<5cm) (85% vs 42%, p=0.0007).	Yes	Furthermore, hsa_circ_0004018 blocked xenograft tumor growth in vivo through inhibiting Wnt/β-catenin signaling pathway by targeting miR-626/DKK3.	33061423
hsa_circ_0091581	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue samples and cell lines	regulation[miR-591/FOSL2 Axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ_0091581 was highly expressed in HCC tissue samples and cell lines in contrast to that in adjacent normal tissue samples and THLE-2 cell line. Circ_0091581 acted as an oncogene to enhance the viability, colony formation, metastasis and cell cycle and inhibit the apoptosis of HCC cells through targeting miR-591/FOSL2 axis.		Yes	Circ_0091581 accelerated the viability, colony formation, metastasis, and cell cycle, while it impeded the apoptosis of HCC cells. Circ_0091581 interference notably suppressed HCC tumor growth in vivo.	33040214
hsa_circ_102	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	interaction[as a sponge of miR-182 and miR-184]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	We found that a novel circular RNA, circ-102,166, was down-regulated in HCC and that its expression level was significantly associated with multiple clinicopathologic characteristics, as well as the clinical prognosis of HCC patients.  Down-regulation of circ-102,166 enhanced the proliferation and invasion of HCC cells by releasing the oncomiRs miR-182 and miR-184.	We found that a novel circular RNA, circ-102,166, was down-regulated in HCC and that its expression level was significantly associated with multiple clinicopathologic characteristics, as well as the clinical prognosis of HCC patients. 	Yes	In vitro and in vivo experiments revealed that circ-102,166 overexpression significantly inhibited the proliferation, invasion, migration and tumorigenicity of HCC cells. 	33034848
hsa_circ_166	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	interaction[as a sponge of miR-182 and miR-184]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	We found that a novel circular RNA, circ-102,166, was down-regulated in HCC and that its expression level was significantly associated with multiple clinicopathologic characteristics, as well as the clinical prognosis of HCC patients.  Down-regulation of circ-102,166 enhanced the proliferation and invasion of HCC cells by releasing the oncomiRs miR-182 and miR-184.	We found that a novel circular RNA, circ-102,166, was down-regulated in HCC and that its expression level was significantly associated with multiple clinicopathologic characteristics, as well as the clinical prognosis of HCC patients. 	Yes	In vitro and in vivo experiments revealed that circ-102,166 overexpression significantly inhibited the proliferation, invasion, migration and tumorigenicity of HCC cells. 	33034848
hsa_circ_104566	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	interaction[sponged miR-338-3p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//FISH//Luciferase Report Assay//Transwell Assay	First, the high expression of hsa_circ_104566 was found in HCC tissues, which was significantly associated with poor prognosis in HCC patients.  In conclusion, hsa_circ_104566 sponged miR-338-3p to promote HCC progression, providing a potential therapeutic target for cancer intervention.	First, the high expression of hsa_circ_104566 was found in HCC tissues, which was significantly associated with poor prognosis in HCC patients. 	Yes	 Second, Hsa_circ_104566 promoted HCC progression by decreasing apoptosis and E-cadherin, while increasing cell viability, proliferation, migration, invasion, and N-cadherin. On the other hand, HCC progression was suppressed by knockdown of hsa_circ_104566.	33028110
hsa_circ_0004913	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-184/HAMP axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Circ_0004913 was downregulated in HCC, and its expression impeded cell proliferation, migration, and invasion, EMT, and glycolysis in HCC cells.Circ_0004913 could inhibit JAK2/STAT3/AKT signaling pathway and tumor growth in vivo by regulating the miR-184/HAMP axis. 		Yes	Circ_0004913 was downregulated in HCC, and its expression impeded cell proliferation, migration, and invasion, EMT, and glycolysis in HCC cells.	33021399
hsa_circ_0038718	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[sponging miR-139-3p]	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that circ-0038718 was frequently elevated in HCC specimens and cell lines.Rescue experiments suggested the oncogenic activity of circ-0038718 was partially exerted via modulating miR-139-3p expression. Inhibition of miR-139-3p abrogated the regulatory effect of circ-0038718 in HCC cells.	High expression levels of circ-0038718 were correlated with unfavorable prognosis in HCC patients. 	Yes	Furthermore, we demonstrated that knockdown of circ-0038718 attenuated HCC cell proliferation and metastatic abilities, while overexpression of circ-0038718 resulted the converse effect. Silencing circ-0038717 inhibited HCC xenograft tumor development in vivo.	33008587
circHIPK3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-582-3p/DLX2 axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	Circ_HIPK3 and DLX2 levels were enhanced, and miR-582-3p level was reduced in HCC tissues and cells. Circ_HIPK3 facilitated HCC progression by mediating miR-582-3p/DLX2 pathway, suggesting a new potential biomarker for HCC treatment.		Yes	Silencing of circ_HIPK3 impeded proliferation, migration and invasion and expedited apoptosis in HCC cells. 	32977948
hsa_circ_0005785	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-578/APRIL Axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	Herein, we explored the functions and potential mechanisms of hsa_circ_0005785 in HCC, which was aberrantly overexpressed in HCC and related to HCC patients' TNM stage and overall survival. Moreover, targeting to the hsa_circ_0005785/miR-578/APRIL regulatory pathway might be a promising diagnostic and therapeutic strategy for HCC clinical practice.	Herein, we explored the functions and potential mechanisms of hsa_circ_0005785 in HCC, which was aberrantly overexpressed in HCC and related to HCC patients' TNM stage and overall survival. 	Yes	. Moreover, hsa_circ_0005785 depletion could repress proliferation and metastasis of the HCC cell in vitro, lead to cell apoptosis and cell-cycle arrest, and restrain HCC cell growth in vivo.	32974140
circFBLIM1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC serum exosomes and HCC cells	regulation[miR-338/LRP6 Axis]	Flow Cytometry//qRT-PCR//MTT	ircFBLIM1 was highly expressed in HCC serum exosomes and HCC cells. CircFBLIM1 facilitated HCC progression and glycolysis via modulating the miR-338/LRP6 axis, which may provide promising therapeutic targets for HCC.		Yes	Inhibition of circFBLIM1 confined HCC glycolysis and progression. CircFBLIM1 knockdown blocked tumorigenesis in vivo. 	32907351
circADAMTS13	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[miR-484]	CCK8//qRT-PCR//Luciferase Report Assay//RNA-seq	CircADAMTS13, derived from Exon 13-14 of the ADAMTS13 gene, was significantly Expression[down-expression]regulated in HCC tumor tissues.  Bioinformatic analysis and luciferase reporter assays further revealed that circADAMTS13 directly interacts with microRNA (miR)-484. Rescue experiments showed that miR-484 mimics can reverse the tumor-sExpression[Expression[up-expression]-expression]pressing roles of circADAMTS13 in HCC.		Yes	 Furthermore, clinicopathological analysis revealed that Expression[Expression[up-expression]-expression]-regulation of circADAMTS13 was negatively associated with tumor size but positively associated with prognosis. In addition, overexpression of circADAMTS13 could markedly inhibit HCC cell proliferation in vitro.	30537115
circTRIM33	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues,cell line	Interaction[MicroRNA-191 ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Here, we found that circTRIM33-12, is Expression[down-expression]regulated in HCC tissues and cell lines. Mechanistically, we demonstrated that circTRIM33-12 Expression[Expression[up-expression]-expression]regulated TET1 expression by sponging miR-191, resulting in significantly reduced 5-hydroxymethylcytosine (5hmC) levels in HCC cells.	The Expression[down-expression]regulation of circTRIM33-12 in HCC was significantly correlated with malignant characteristics and served as an independent risk factor for the overall survival (OS) and recurrence-free survival (RFS) of patients with HCC after surgery. 	Yes	The reduced expression of circTRIM33-12 in HCC cells increases tumor proliferation, migration, invasion and immune evasion. 	31153371
hsa_circ_0001649	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines(HHCC, H-97, HepG2, HuH-7, Li-7, SMMC-7721, HepG2.2.15 and HL-7702)	Interaction[miR-127-5p, miR-612 and miR-4688]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//RNA-seq	Results showed that circ-0001649 was markedly decreased in hepatocellular carcinoma cell lines and tumor tissues. More importantly, we confirmed that circ-0001649 regulated cellular behaviors of HCC cells by targeting SHPRH. Furthermore, we determined that circ-0001649 served as a ceRNA to sponge miR-127-5p, miR-612 and miR-4688, thus activating SHPRH.		Yes	Overexpression of circ-0001649 greatly inhibited proliferation and migration of HCC in vitro and in vivo.	31137016
hsa_circ_0003892	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cells	Interaction(miR-326/LASP1 axis)	Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	 Circ_0003892 expression was raised in PTC tissues and cells, which was significantly interrelated with larger tumor size and extrathyroidal extension in PTC sufferers.Additionally, miR-326 was a downstream target of circ_0003892, and miR-326 overexpression weakened the promoting effect of circ_0003892 overexpression on the malignant progression of PTC. MiR-326 specifically inhibited LASP1. Circ_0003892 positively regulated LASP1 expression by targeting miR-326.	 Circ_0003892 expression was raised in PTC tissues and cells, which was significantly interrelated with larger tumor size and extrathyroidal extension in PTC sufferers.	Yes	Overexpression of circ_0003892 significantly promoted the malignant biological behaviors of PTC cells. 	36394255
circFAM53B	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cells	Interaction(miR-183-5p-CCDC6)	qRT-PCR//MTT//Luciferase Report Assay//RIP	Our data showed that circ_FAM53B expression was reduced in PTC tissues and cells.  Circ_FAM53B repressed miR-183-5p expression. MiR-183-5p re-expression reversed the effects of circ_FAM53B on cell behaviors. MiR-183-5p targeted and inhibited CCDC6, and circ_FAM53B upregulated CCDC6 through miR-183-5p competition. MiR-183-5p knockdown repressed cell proliferation, migration, invasion, and tube formation and facilitated apoptosis by upregulating CCDC6. Furthermore, circ_FAM53B reduced tumor growth in vivo. Collectively, our findings suggest that circ_FAM53B affects PTC cell biological behaviors via the miR-183-5p-CCDC6 axis.		Yes	Circ_FAM53B expression restrained proliferation, migration, and invasion and triggered apoptosis of PTC cells, as well as hindered HUVEC tube formation. 	35598218
hsa_circ_0082003	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Expression(highly expressed)	CCK8//qRT-PCR//Wound Healing Assay//Colony Formation Assay	RT-qPCR validation demonstrated that hsa_circ_0082003 expression was significantly increased in PTC tissues and correlated with poor clinicopathological parameters.	RT-qPCR validation demonstrated that hsa_circ_0082003 expression was significantly increased in PTC tissues and correlated with poor clinicopathological parameters.Receiver operating characteristic curve analysis showed that hsa_circ_0082003 had good performance for diagnosing PTC and judging whether it was accompanied by lymph node metastasis. 	Yes	Knockdown of hsa_circ_0082003 inhibited PTC cell proliferation, migration, and invasion. Tumor formation assays in vivo showed that downregulation of hsa_circ_0082003 significantly suppressed the growth of PTC.	36115894
hsa_circ_0002111	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Interaction(miR-363-3p/HMGB1 axis)	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	It was found that the expression of circ_0002111 was enhanced in PTC tissues and cells. For mechanism analysis, circ_0002111 adjusted the expression of HMGB1 by sponge adsorption of miR-363-3p. Moreover, miR-363-3p inhibitor regained the influence of cellular malignant phenotype caused by circ_0002111 knockdown. Additionally, miR-363-3p overexpression impacted the cell functions by targeting HMGB1 in PTC. 		Yes	 Silencing circ_0002111 apparently retarded the viability, proliferation, invasion and tube formation, as well as expedited the apoptosis of PTC cells. Besides, circ_0002111 knockdown impeded the growth of the tumor in vivo.	36136992
circNRIP1	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and PTC cell lines	Interaction(miR-653-5p/PBX3 axis)	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	circNRIP1 significantly increased in PTC tissues and PTC cell lines than that in normal ones.circNRIP1 was a miR-653-5p sponge; miR-653-5p knockdown reversed the suppressive role of circNRIP1 silence in PTC progression. PBX3, a target of miR-653-5p, was positively medicated through circNRIP1 via competitively sponging miR-653-5p.	Higher circNRIP1 expression was associated with the TNM stage and poorer overall survival. 	Yes	circNRIP1 knockdown attenuated the malignant progression of PTC, specifically by inhibiting proliferation and invasion/migration and promoting apoptosis. Knockdown of circNRIP1 attenuated the PTC tumor progression via miR-653-5p/PBX3 axis.	35646117
hsa_circ_000926	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues	Interaction[bind to miR-411 to up-regulate CDH2]	Western Blot//qRT-PCR//Luciferase Report Assay//RNA-seq//Transwell Assay	The expression of circ_000926, miR-411, and cadherin 2 (CDH2) was up-regulated or down-regulated in RCC cells to unearth their effects on the biological behaviors of RCC cells.circ_000926 was highly expressed in RCC tissues and cell lines, whereas CDH2 was verified to be a target of miR-411. As a competing endogenous RNA, circ_000926 could directly bind to miR-411 to up-regulate CDH2.		Yes	Down-regulation of circ_000926 resulted in inhibited growth, migration, and invasion abilities of RCC cells, as well as suppressed epithelial-mesenchymal transition and tumor growth. 	31476285
hsa_circ_0039569	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues	Interaction[miR-34a-5p/CCL22]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 Hsa_circ_0039569 (circ_0039569) was verified to be up-regulated in RCC and cells compared with the controls by real time RT-PCR.The molecular mechanism of circ_0039569 in RCC cells showed that circ_0039569 promoted RCC progression by up-regulating CCL22 expression via down-regulating miR-34a-5p.		Yes	The assays of cellular functions showed that circ_0039569 down-regulation suppressed the proliferation and metastasis of RCC cells. 	31497210
hsa_circ_001287	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	regulation[miR-144-targeted CEP55]	qRT-PCR//RIP//Western Blot	 circ_001287 and CEP55 were highly expressed while miR-144 was decreased in RCC tissues and cell lines. circ_001287 can up-regulate CEP55 by binding to miR-144, which resulted in increased proliferative, invasive and migratory capacities and tumor growth in vivo. In addition, down-regulation of miR-144 was also observed to promote these biological activities.		Yes	circ_001287 can up-regulate CEP55 by binding to miR-144, which resulted in increased proliferative, invasive and migratory capacities and tumor growth in vivo.	33256799
hsa_circ_400068	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC plasma exosomes, tissue samples and cells	regulation[miR-210-5p/SOCS1 axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Upregulation of circ_400068 was detected in RCC plasma exosomes, tissue samples and cells.Collectively, the present findings provided a novel insight into the crucial regulatory functions of circ_400068 in RCC, and the circ_400068/miR‑210‑5p/SOCS1 axis could be a candidate therapeutic target for the treatment of patients with RCC.		Yes	Additionally, treatment with exosomal circ_400068 promoted the proliferation and inhibited the apoptosis of healthy kidney cells, which were abrogated by short hairpin RNA?circ_400068. 	33173957
hsa_circ_001504	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues	regulation[circ_001504/miR-149/NUCB2 feedback loop]	CCK8//qRT-PCR//Flow Cytometry	RT-qPCR results showed that circ_001504 was highly expressed in RCC tissues, whereas miR-149 was poorly expressed.Collectively, reduced expression of circ_001504 lowered NUCB2 expression by sponging miR-149, thereby attenuating RCC progression, providing insight into circ_001504/miR-149/NUCB2 feedback loop into RCC treatment.		Yes	Interestingly, downregulation of circ_001504 suppressed malignant phenotypes in RCC cells, and upregulation of miR-149 exerted a similar effect.	33110207
circPTCH1	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC cell lines and tumor samples	regulation[miR-485-5p/MMP14 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	We observed that circPTCH1 was up-regulated in RCC cell lines and tumor samples,  circPTCH1 promotes RCC metastasis via the miR-485-5p/MMP14 axis and activation of the EMT process. 	We observed that circPTCH1 was up-regulated in RCC cell lines and tumor samples, and higher levels of circPTCH1 were significantly correlated with worse patient survival, advanced Fuhrman grade and greater risk of metastases.	Yes	Elevated circPTCH1 expression led to increased migration and invasion of RCC cells both in vitro and in vivo whereas silencing circPTCH1 decreased migration and invasion and impeded the epithelial-mesenchymal transition (EMT) of RCC cells.	32929380
circNUP98	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues	regulation[miR-567/ PRDX3 axis]	qRT-PCR//Western Blot	 CircNUP98 was up-regulated in both RCC tissues and cell lines, and high expression of circNUP98 was correlated with poor prognosis of RCC patients.CircNUP98 acts as an oncogene by a novel STAT3/circ NUP98/miR-567/PRDX3 axis, which may provide a potential biomarker and therapeutic target for the treatment of RCC.	 CircNUP98 was up-regulated in both RCC tissues and cell lines, and high expression of circNUP98 was correlated with poor prognosis of RCC patients.	Yes	Silencing of circSMC3 inhibited the proliferation and promoted the apoptosis in a caspase-dependent manner in RCC cells.	32729669
hsa_circ_001842	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	regulation[microRNA-502-5p,SLC39A14]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	 Our initial in silico microarray-based analysis identified that circRNA circ_001842 was highly expressed in RCC. These observations imply the involvement of circ_001842 in RCC pathogenesis through a miR-502-5p-dependent SLC39A14 mechanism, suggesting circ_001842 is a potential target for RCC treatment.		Yes	circ_001842 was found to elevate SLC39A14 expression by binding to miR-502-5p, consequently resulting in augmented RCC cell proliferation, migration and invasion, as well as EMT in vitro and tumour growth in vivo. 	32729666
hsa_circ_0001368	CircRNA	Homo sapiens	Carcinoma, Renal Cell	carcinoma cells and tissues	interaction[miR-492 and LATS2]	qRT-PCR//Western Blot	The qRT-PCR results indicate that the circ_0001368 expression level was downregulated in the carcinoma cells and tissues of the renal cell.Large tumor suppressor kinase 2 (LATS2) was confirmed by Targetscan as a target gene of miR-492. 		Yes	The transwell and CCK8 assays showed that circ_0001368 suppressed cell proliferation and invasion in the ACHN and 786-O cells.	32428698
circMYLK	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues 	regulation[miR-513a-5p/VEGFC signalling ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we observed that circMYLK is notably up-regulated in RCC. In summary, our findings demonstrate that circMYLK has an oncogenic role in RCC growth and metastasis by modulating miR-513a-5p/VEGFC signalling. 	 Increased circMYLK expression led to a larger tumour size, distant metastasis and poor prognosis of RCC patients.	Yes	 Moreover, circMYLK silencing repressed RCC growth and metastasis in vitro and in vivo.	32342645
circMTO1	CircRNA	Homo sapiens	Carcinoma, Renal Cell	cell lines	regulation[miR9/LMX1A Axis]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	In the research, we selected a highly expressed novel circular RNAs named circMTO1 in renal cell carcinomas.In conclusion, circMTO1 suppresses renal cell carcinoma progression by circMTO1/miR9/ LMX1A, indicating that circMTO1 may be a potential target in renal cell carcinoma therapy.		Yes	We investigated the roles of circMTO1 and found that circMTO1 overexpression could suppress cell proliferation and metastases in both A497 and 786-O renal cancer cells, while silencing of circMTO1 could promote the progression in SN12C and OS-RC-2 renal cancer cells. 	32207384
hsa_circ_0035483	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction( miR-31-5p-Mediated HMGA1 Upregulation)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Circ_0035483 expression was upregulated in RCC tissues and cells. MiR-31-5p was identified as a target of circ_0035483 and miR-31-5p upregulation was related to the function of circ_0035483 knockdown in RCC cells. Additionally, miR-31-5p targeted HMGA1 and inhibited the malignant behaviors of RCC cells by negatively regulating HMGA1. 		Yes	 The inhibitory effects on RCC cell proliferation, migration, invasion, EMT and glycolysis were induced after circ_0035483 was downregulated. Moreover, HMGA1 expression was regulated by circ_0035483 via targeting miR-31-5p. Circ_0035483 also affected tumor growth in vivo by relying on the miR-31-5p/HMGA1 axis.	33531839
circSDHC	CircRNA	Homo sapiens	Carcinoma, Renal Cell	patients with RCC	Interaction(CDKN3/E2F1 axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	Clinically, high circSDHC expression was correlated with advanced TNM stage and poor survival in patients with RCC. Analysis of the mechanism underlying the effects of circSDHC in RCC demonstrated that it binds competitively to miR-127-3p and prevents its suppression of a downstream gene, CDKN3, and the E2F1 pathway, thereby leading to RCC malignant progression. Furthermore, knockdown of circSDHC caused decreased CDKN3 expression and E2F1 pathway inhibition, which could be rescued by treatment with an miR-127-3p inhibitor.	Clinically, high circSDHC expression was correlated with advanced TNM stage and poor survival in patients with RCC. 	Yes	Further, circSDHC promoted tumor cell proliferation and invasion, both in vivo and in vitro.	33468140
circAMOTL1L	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction(miR-92a-2-5p/KLLN Pathway)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	qRT-PCR showed the downregulation of circAMOTL1L in RCC tissues and cell lines. Conclusively, our findings demonstrate that circAMOTL1L has an antioncogenic role in RCC growth by modulating the miR-92a-2-5p-KLLN pathway. 	The decrease in circAMOTL1L expression correlated with the tumor stage, metastasis, and poor prognosis in patients with RCC. 	Yes	Functional experiments revealed that circAMOTL1L inhibited cell proliferation and increased apoptosis in RCC cells. Subcutaneous implantation with circAMOTL1L-overexpressing cells in nude mice decreased the growth ability of the xenograft tumors.	34646428
circCCDC66	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC specimens and cell lines 	Interaction(miR-129-5p/LARP1 )	Western Blot//CCK8//qRT-PCR//IHC//EdU Staining//Transwell Assay	We observed that circ-CCDC66 expression was upregulated in PTC specimens and cell lines and was correlated with poor clinical characteristics of PTC patients. Mechanistically, miR-129-5p was a target gene of circ-CCDC66 and was downregulated in PTC tissues. LARP1, a downstream target of miR-129-5p, was upregulated in PTC tissues.	We observed that circ-CCDC66 expression was upregulated in PTC specimens and cell lines and was correlated with poor clinical characteristics of PTC patients.	Yes	Moreover, in vitro experiments demonstrated that knockdown of circ-CCDC66 markedly suppressed the proliferative, migratory, and invasive capacities of PTC cells.  In addition, we confirmed that inhibition of circ-CCDC66 could repress xenograft tumor growth. 	35264065
hsa_circ_104565	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissue and cell 	Interaction(miR-134/ELF2 axis)	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	We found that circRNA_104565 was highly expressed in PTC tissue and cell and promoted cell proliferation in vitro and in vivo.  In addition, circRNA_104565 promoted cell proliferation in PTC by regulating the miR-134/ELF2 axis.		Yes	We found that circRNA_104565 was highly expressed in PTC tissue and cell and promoted cell proliferation in vitro and in vivo. 	33500653
hsa_circ_104718	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines(SMMC-7721, HepG2, MHCC-LM3, and SK-Hep1)	Regulation[microRNA-218-5p/TXNDC5 signaling pathway]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay	The present study aims at investigating the role of circRNA-104718 in HCC progression, which has been observed to be significantly Expression[Expression[up-expression]-expression]-regulated in HCC tissues.	We found that, higher expression of circRNA-104718 also leds to a poor prognosis in HCC patients.Using luciferase binding assays and RNA immunoprecipitation studies, we identified circRNA-104718 is physically associated and co-expressed with microRNA (miR)-218-5p in HCC.Mechanistically, we demonstrated that circRNA-104718 functions as a competing endogenous RNAs (ceRNAs) and competes with thioredoxin domain-containing protein 5 (TXNDC5) mRNA and directly binds to miR-218-5p. 	Yes	In vivo studies on a nude mice model showed that circRNA-104718 overexpression could increase the tumor size and the rate of metastasis. Silencing of circRNA-104718 could decrease both the tumor size and metastasis significantly.	31278132
hsa_circ_0067934	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Interaction(miR-1301-3p/HMGB1 axis)	Tunel//Colony Formation Assay//qRT-PCR//Luciferase Report Assay//IHC	We found that circ_0067934 was upregulated in PTC tissues and cell lines.  Moreover, circ_0067934 acted as a molecular sponge for miR-1301-3p, and depletion of miR-1301-3p abrogated the effects of circ_0067934 knockdown in PTC cells. In addition, HMGB1 was a target of miR-1301-3p, and miR-1301-3p overexpression inhibited the malignant effects of PTC cells via suppressing HMGB1. Furthermore, knockdown of circ_0067934 suppressed HMGB1 expression, PI3K/Akt, and MAPK activation by sponging miR-1301-3p.		Yes	Knockdown of circ_0067934 inhibited growth, colony formation, migration, invasion, EMT, and tumor xenograft growth, and induced apoptosis of PTC cells. In nude mice, circ_0067934 depletion repressed tumor xenograft growth of PTC cells.	34704451
hsa_circ_0008274	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Regulation[AMPK/mTOR signaling pathway ]	Western Blot//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	We found that has_circ_0008274 was significantly upregulated in PTC tissues, and the level of has_circ_0008274 was negatively associated with TNM stage and lymph node metastasis. Has_circ_0008274/ AMPK/mTOR axis may be a novel therapeutic candidate target in PTC treatment.	We found that has_circ_0008274 was significantly upregulated in PTC tissues, and the level of has_circ_0008274 was negatively associated with TNM stage and lymph node metastasis. 	Yes	Loss-of-function assay indicated that knockdown of has_circ_0008274 suppressed PTC cells proliferation and invasion in vitro. 	30575918
hsa_circ_0004458	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Regulation[miR-885-5p,RAC1]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	Our results indicated that hsa_circ_0004458 was upregulated in PTC tissues and cells, while silencing of hsa_circ_0004458 suppressed PTC cell proliferation and promoted PTC cell cycle arrest and apoptosis in vitro. We found that hsa_circ_0004458 promoted the progression of PTC by inhibition of miR-885-5p and activation of RAC1, and hsa_circ_0004458 may serve as a potential therapeutic target and biomarker for PTC.		Yes	Our results indicated that hsa_circ_0004458 was upregulated in PTC tissues and cells, while silencing of hsa_circ_0004458 suppressed PTC cell proliferation and promoted PTC cell cycle arrest and apoptosis in vitro. Tumor formation assay in nude mice showed that knockdown of hsa_circ_0004458 by siRNAs inhibited the growth of PTC tumor in vivo. 	30086127
circFOXM1	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues, cell lines	Interaction[Sponging miR-1179]	qRT-PCR//Luciferase Report Assay	In this study, circFOXM1 was observed to be upregulated in PTC tissues and cell lines.Bioinformatics analysis predicted that there is a circFOXM1/miR-1179/high-mobility group box 1 (HMGB1) axis in PTC. A dual luciferase reporter system validated the direct interaction of circFOXM1, miR-1179, and HMGB1.	A lower level of UPF1 was observed in glioma tissues in the more advanced stage with a larger tumor size.	Yes	circFOXM1 downregulation inhibited tumor growth of PTC in vitro and in vivo.	31951855
circBACH2	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues, cell lines	Interaction[sponging miR-139-5p]	qRT-PCR//Luciferase Report Assay//FISH	We found that circBACH2 was highly expressed in PTC tissues and PTC cell lines.Mechanistically, we confirmed that circBACH2 could directly bind to miR-139-5p and relieve suppression of the target LMO4.		Yes	Functionally, we found that inhibiting circBACH2 expression decreased cell proliferation, migration, and invasion. Finally, down-regulating circBACH2 suppressed the growth of PTC xenografts in nude mice.	30796202
circPVT1	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Interaction[sponging miR-126]	qRT-PCR	High expression of circPVT1 was shown in PTC tissues and cells and was associated with poor outcomes of patients.CircPVT1 knockdown inhibited PTC progression by sponging miR-126. This may indicate circPVT1 as a novel target for treatment of PTC.	High expression of circPVT1 was shown in PTC tissues and cells and was associated with poor outcomes of patients.	Yes	Knockdown of circPVT1 suppressed viability, migration and invasion but induced apoptosis in PTC cells.	35520785
circPSD3	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tumor tissues	regulation[miR-637/HEMGN axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_PSD3 was aberrantly up-regulated in PTC tumor tissues compared with adjacent normal tissues. Circ_PSD3/miR-637/HEMGN signaling axis might be a potential target for PTC therapy.		Yes	Circ_PSD3 and HEMGN promoted the cell cycle progression, proliferation and metastasis and impeded the apoptosis of PTC cells.	33203523
hsa_circ_0058124	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	regulation[miR-370-3p/LMO4 axis]	qRT-PCR//Luciferase Report Assay	The expression of circ_0058124 was enhanced in PTC tissues and cells. Circ_0058124 promoted the development of PTC by mediating the miR-370-3p/LMO4 axis, and circ_0058124, functioned as an oncogene in PTC, might be used as a promising biomarker for PTC diagnosis and treatment.		Yes	Circ_0058124 knockdown inhibited viability, colony formation, migration and invasion and promoted apoptosis of PTC cells.	33061633
circEIF3I	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	regulation[ circEIF3I/miR-149/KIF2A axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 We found that the expression of circEIF3I was significantly upregulated in PTC tissues compared to adjacent normal tissues.This study suggested circEIF3I/miR-149/KIF2A axis might be a potential therapeutic target.	 CircEIF3I expression was positively associated with tumor size, TNM stage and metastasis. 	Yes	 CircEIF3I knockdown remarkably suppressed the proliferation, migration and invasion of PTC cells. 	32368390
hsa_circ_0007694	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	pericarcinomatous tissues	Expression[lower expressed]	qRT-PCR	 We identified a circRNA, hsa_circ_0007694 that was down-regulated in PTC tissues compared to pericarcinomatous tissues.		Yes	Over-expression of hsa_circ_0007694 promoted apoptosis and inhibited proliferation, migration, and invasion in PTC cells in vitro, and decreased tumor growth in vivo.	32355548
hsa_circ_0005273	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	regulation[circ_0005273/miR-1183/SOX2 axis]	CCK8//qRT-PCR	Gene Expression Omnibus datasets (GSE93522) and qRT-PCR (quantitative real-time PCR) analyses showed that circ_0005273 were upregulated in PTC tissues and cell lines.In conclusion, circ_0005273 functioned as a tumor promoter of PTC via circ_0005273/miR-1183/SOX2 axis, suggesting a novel biomarker and therapeutic target for PTC.	Moreover, circ_0005273 was located in the cytoplasm of PTC cells and suggested poor prognosis in PTC patients.	Yes	In vivo and in vitro functional assays indicated that knockdown of circ_0005273 inhibited PTC tumor growth and progression, respectively.	31693489
circNRIP1	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cells 	Interaction(mir-195-5p )	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	CircRNA NRIP1 was over-expressed in PTC tissues and cells and the high levels of CircRNA NRIP1 were correlated with advanced PTC stage. In conclusion, CircRNA NRIP1 promoted PTC progression by accelerating PTC cells proliferation, invasion and tumor growth, while impeding apoptosis by way of sponging miR-195-5p and regulating the P38 MAPK and JAK/STAT pathways.	CircRNA NRIP1 was over-expressed in PTC tissues and cells and the high levels of CircRNA NRIP1 were correlated with advanced PTC stage.	Yes	 Depletion of CircRNA NRIP1 inhibited PTC cell proliferation, invasion, while accelerated apoptosis. 	34689819
hsa_circ_0008274	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	Tissue samples included 60 tumor tissues and 60 matched normal tissues	Interaction(miR-154-3p)	qRT-PCR//Luciferase Report Assay	Our data showed that the high levels of circ_0008274 and SLC7A11 were associated with poor prognosis of PTC patients.Mechanistically, circ_0008274 modulated SLC7A11 expression by acting as a sponge of miR-154-3p. 	Our data showed that the high levels of circ_0008274 and SLC7A11 were associated with poor prognosis of PTC patients.	Yes	 The knockdown of circ_0008274 or SLC7A11 enhanced PTC cell apoptosis and repressed cell migration and adhesion in vitro. Circ_0008274 knockdown suppressed tumor growth in vivo. 	33473055
hsa_circ_0001666	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC clinical samples and cell lines	Interaction(miR‑330‑5p/miR‑193a‑5p/miR‑326/ETV4 pathway)	qRT-PCR//Western Blot//RIP//FISH	The results demonstrated that hsa_circ_0001666 was upregulated in both PTC clinical samples and cell lines. Additionally, luciferase reporter assays showed that hsa_circ_0001666 and ETS variant transcription factor 4 (ETV4) shared common binding sites with three microRNAs [(miRNA/miR)‑330‑5p, miR‑193a‑5p and miR‑326]. Knockdown of these miRNAs separately reversed the inhibitory effect of hsa_circ_0001666 small interfering RNAs on PTC tumor aggressiveness, and ETV4 overexpression also induced a similar effect to that of miRNA inhibitors.	 Its expression was associated with lymph node metastasis of patients with PTC.	Yes	Knocking down hsa_circ_0001666 expression inhibited cell proliferation, as evidenced by decreased cell viability, arrest of cell cycle progression at the G1 phase and an increase in cell cycle‑associated proteins. Apoptosis rates and expression levels of pro‑apoptotic proteins were also increased by silencing hsa_circ_0001666. In xenograft experiments, the oncogenic effect of hsa_circ_0001666 on tumor growth was verified. 	33760216
circLDLR	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cell lines	Interaction(miR-637/LMO4 Axis)	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	In this study, circLDLR was found to be markedly upregulated in PTC tissues and cell lines, and knockdown of circLDLR inhibited PTC cell proliferation, migration, and invasion but induced apoptosis in vitro. Moreover, circLDLR acted as a sponge for miR-637, and miR-637 interference reversed the anticancer effects of circLDLR knockdown on PTC cells. LMO4 was verified to be a target of miR-637; LMO4 upregulation abolished miR-637 mediated inhibition of cell growth and metastasis in PTC. Additionally, circLDLR could indirectly modulate LMO4 via acting as a sponge of miR-637 in PTC cells. 		Yes	In this study, circLDLR was found to be markedly upregulated in PTC tissues and cell lines, and knockdown of circLDLR inhibited PTC cell proliferation, migration, and invasion but induced apoptosis in vitro. 	34925640
hsa_circ_0062389	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines. 	Interaction(miR-1179/high mobility group box 1 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	Besides, miR-1179 was a downstream molecule of circ_0062389. Furthermore, miR-1179 inhibitors could partially reverse the above effect of knocking down circ_0062389 on PTC cells. It was also confirmed that HMGB1 was a direct target of miR-1179 and mediated the effects of circ_0062389 and miR-1179 in PTC. 	 The high expression of circ_0062389 was related to large tumor size and positive lymphatic metastasis. 	Yes	Knocking down circ_0062389 could inhibit the proliferation, migration and EMT process of PTC cells. 	33926347
circPVT1	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Interaction(miR-195/VEGFA/ Wnt/β-catenin signaling pathway)	qRT-PCR//Western Blot	 The results of RT-PCR showed that the expression level of circPVT1 was significantly upregulated in PTC tissues and cell lines.  Besides, miR-195 could both bind to PVT1 and VEGFA, while PVT1 could promote the expression of VEGFA by binding to miR-195. Downregulation of VEGFA expression in PTC cells revealed weakened cell proliferation, migration, and invasion capacities, and restrained Wnt/β-catenin signaling pathway. 		Yes	After downregulating circPVT1 expression in PTC cells, the abilities of cell proliferation, migration, and invasion were obviously suppressed, and the Wnt/β-catenin signaling pathway was also repressed. 	34927541
hsa_circ_007293	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	serum and cell culture media	Interaction(microRNA-653-5p/paired box 6 axis)	CCK8//qRT-PCR//Wound Healing Assay	Results showed that circ007293 was enriched in exosomes derived from PTC patient serum and cell culture media. Additionally, circ007293 could competitively bind with miR-653-5p to regulate PAX6 expression. Notably, miR-653-5p overexpression or PAX6 inhibition suppressed the malignant effects of exosomal circ007293. 		Yes	 Moreover, circ007293 could enter PTC cells through exosomes, and exosomal circ007293 promoted PTC cell epithelial-mesenchymal transition, invasion, migration, and proliferation. circ007293 knockdown reversed the malignant phenotype of PTC cells in vitro.	34866540
hsa_circ_0039411	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	papillary thyroid carcinoma tissues and cell lines	Interaction(miR-423-5p/SOX4 signaling)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	 Circ_0039411 was highly expressed in papillary thyroid carcinoma tissues and cell lines compared with adjacent normal tissues and NTHY-ORI3.1 cells. MiR-423-5p was a target of circ_0039411 in papillary thyroid carcinoma cells. Circ_0039411 knockdown-mediated effects in papillary thyroid carcinoma cells were largely overturned by the silence of miR-423-5p. MiR-423-5p bound to the 3' untranslated region (3'UTR) of SOX4. SOX4 overexpression largely reversed circ_0039411 silencing-mediated effects in papillary thyroid carcinoma cells. Circ_0039411 positively regulated SOX4 expression by sponging miR-423-5p in papillary thyroid carcinoma cells. 		Yes	Circ_0039411 interference suppressed the colony formation ability, migration, invasion, and glycolysis but promoted the apoptosis of papillary thyroid carcinoma cells. Circ_0039411 silencing notably suppressed the growth of xenograft tumors in vivo.	34738852
hsa_circ_0054537	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction(circ_0054537/miR-640/NPTX2 ceRNA pathway)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//IHC//ChIP	we found circ_0054537 was upregulated in RCC tissues and cells, and distributed throughout the cytoplasm. 		Yes	 functional effects of circ_0054537 in RCC were detected using cell counting kit-8, transwell, flow cytometry and glycolysis stress test and adenosine Triphosphate (ATP) assays. The results uncovered that circ_0054537 knockdown inhibited cell proliferation, migration, invasion, autophagy and glycolysis, but promoted apoptosis in RCC cells. Notably, circ_0054537 was identified as a ceRNA for microRNA (miR)-640, and miR-640 could target neuronal pentraxin-2 (NPTX2), as evidenced by dual-luciferase reporter assay and RNA immunoprecipitation assay.RCC cell growth in vivo was retarded by circ_0054537 silence.	34565284
circNTNG1	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction( circNTNG1/miR-19b-3p/HOXA5 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	In all three circRNA datasets, circNTNG1, which was frequently deleted in RCC, showed significantly low expression in the tumor group. Next, the sponge effect of circNTNG1 on miR-19b-3p and the inhibition of HOXA5 by miR-19b-3p were validated. GSEA analysis indicated that HOXA5 could inactivate the epithelial–mesenchymal transition (EMT) process, and this inactivation was mediated by HOXA5-induced SNAI2 (Slug) downregulation. Finally, it was confirmed that the Slug downregulation was caused by HOXA5, along with the DNA methyltransferase DNMT3A, binding to its promoter region and increasing the methylation level.	Clinically, circNTNG1 expression was associated with RCC stage and Fuhrman grade, and it also served as an independent predictive factor for both OS and RFS of RCC patients.	Yes	The basic properties of circNTNG1 were characterized, and phenotype studies also demonstrated the inhibitory effect of circNTNG1 on RCC cell aggressiveness.	36536414
hsa_circ_0037866	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction( miR-384/CBX5)	CCK8//qRT-PCR	Circ_0037866 is a stable circRNA and was found to be increased in RCC tissues and cells.Mechanistically, circ_0037866 could function as a sponge for miR-384 to elevate the expression of its target CBX5. Furthermore, a series of rescue experiments showed that miR-384 inhibition reversed the anticancer effects of circ_0037866 knockdown on RCC cells; besides that, miR-384 restoration suppressed RCC cell growth and mobility, which were attenuated by CBX5 overexpression.		Yes	Functionally, circ_0037866 silencing suppressed RCC cell survival, invasion, and migration in vitro, and impeded RCC cell tumorigenesis in the subcutaneous xenograft model. 	35249038
circSDHC	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC tissues and cell lines	Interaction(miR-130a-3p/CEP55 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	We observed an observable elevation in circSDHC expression in RCC tissues and cell lines.Mechanically, circSDHC modulated centrosomal protein 55 (CEP55) expression by functioning as a miR-130a-3p sponge. Also, miR-130a-3p silencing offset circSDHC knockdown-mediated impacts on malignant phenotypes and angiogenesis of RCC cells. Furthermore, exogenetic expression of CEP55 counteracted miR-130a-3p overexpression-mediated effects on malignant phenotypes and angiogenesis of RCC cells.		Yes	Functionally, circSDHC silencing decreased xenograft tumor growth and induced RCC cell apoptosis, repressed RCC cell proliferation, angiogenesis, migration, and invasion in vitro. 	35506422
hsa_circ_0083429	CircRNA	Homo sapiens	Osteoarthritis	human chondrocytes	Interaction(Mir-346/ SMAD3 Axis)	qRT-PCR//Western Blot	In our study, we found that Circ0083429 regulates the homeostasis of the extracellular matrix (ECM) in human chondrocytes. In conclusion, Circ0083429 regulates the ECM via the regulation of the downstream miRNA-346/SMAD3 in human chondrocytes, which provides a new therapeutic strategy for OA.		Yes	Mechanistically, Circ0083429 affects OA by regulating the mRNA level of SMAD3 through the sponging of microRNA (miRNA)-346. Injecting adeno-associated virus Circ0083429 into the intra-junction of the mouse knee alleviated OA.	33520980
hsa_circ_0128846	CircRNA	Homo sapiens	Osteoarthritis	OA cartilage tissues	Interaction(miR-127-5p/NAMPT axis)	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay	Circ_0128846 and NAMPT were upregulated and miR-127-5p was downregulated in OA cartilage tissues. Moreover, circ_0128846 positively regulated NAMPT expression by sponging miR-127-5p. Furthermore, miR-127-5p promoted cell viability and suppressed apoptosis, inflammation, and ECM degradation in OA chondrocytes by directly targeting NAMPT.		Yes	Knockdown of circ_0128846 increased cell viability and inhibited apoptosis, inflammation and ECM degradation in OA chondrocytes, while these effects were reversed by downregulating miR-127-5p.	33975612
hsa_circ_0037658	CircRNA	Homo sapiens	Osteoarthritis	CHON-001 cells	Expression(highly expressed)	CCK8//qRT-PCR//Cell Apoptosis Assay//Western Blot	The results indicated that hsa_circ_0037658 was significantly upregulated in IL-1β-treated CHON-001 cells.		Yes	The silencing of hsa_circ_0037658 could protect CHON-001 cell injury against IL-1β. Moreover, hsa_circ_0037658 shRNA reversed IL-1β-induced cell growth inhibition via inducing cell autophagy. Furthermore, knockdown of hsa_circ_0037658 notably alleviated the symptom of OA in vivo. 	32980988
circFAM160A2	CircRNA	Homo sapiens	Osteoarthritis	OA tissue	Interaction(miR-505-3p and SIRT3)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	We found that miR-505-3p was upregulated and circFAM160A2 was downregulated in OA. While overexpression of circFAM160A2 decreased the production of extracellular matrix (ECM) degrading enzymes and ameliorated chondrocyte apoptosis and mitochondrial dysfunction, inhibition of miR-505-3p could reverse the protective effect of circFAM160A2 on the OA phenotype both in vitro and in vivo. 		Yes	While overexpression of circFAM160A2 decreased the production of extracellular matrix (ECM) degrading enzymes and ameliorated chondrocyte apoptosis and mitochondrial dysfunction, inhibition of miR-505-3p could reverse the protective effect of circFAM160A2 on the OA phenotype both in vitro and in vivo.	34646424
circNFKB1	CircRNA	Homo sapiens	Osteoarthritis	inflamed chondrocytes and osteoarthritic cartilage	Interaction(NFKB1)	qRT-PCR//IHC//RNA Pull-Down//IF	We identified a highly upregulated circRNA, termed as circNFKB1 in inflamed chondrocytes and osteoarthritic cartilage.  Mechanistically, circNFKB1 interacted with α-enolase (ENO1), regulated the expression of its parental gene NFKB1 and sustained the activation of NF-κB signaling pathway in chondrocytes. 		Yes	Furthermore, knockdown of circNFKB1 inhibited extracellular matrix (ECM) catabolism and rescued IL-1β impaired ECM anabolism whereas ectopic expression of circNFKB1 significantly promoted chondrocytes degradation in vitro. Moreover, intraarticular injection of adenovirus-circNFKB1 in mouse joints triggered spontaneous cartilage loss and OA development. 	35945200
hsa_circ_0114876	CircRNA	Homo sapiens	Osteoarthritis	 OA tissues, chondrocytes	Interaction(miR-1227-3p/ADAM10 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ELISA	Circ_0114876 and ADAM10 were upregulated and miR-1227-3p was decreased in OA tissues and LPS-treated chondrocytes. Mechanistically, circ_0114876 functioned in human chondrocytes through targeting miR-1227-3p and ADAM10. Furthermore, miRNA-1227-3p inhibitor reversed the effect of circ_0114876 knockdown on the OA chondrocytes, and ADAM10 overexpression reversed the effect of miR-1227-3p mimic on the OA chondrocytes.		Yes	Low expression of circ_0114876 promoted proliferation and inhibited apoptosis, inflammation, and extracellular matrix of the LPS-treated chondrocytes. 	36436795
circCDK14	CircRNA	Homo sapiens	Osteoarthritis	chondrocytes, OA cartilage tissues	Interaction(miR-1183/KLF5 )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	CircCDK14 and KLF5 expression were significantly decreased, while miR-1183 was increased in OA cartilage tissues and IL-1β-treated chondrocytes in comparison with controls. Additionally, miR-1183 was targeted by circCDK14, and miR-1183 mimics reversed circCDK14-mediated actions in IL-1β-treated chondrocytes. The knockdown of KLF5, a target mRNA of miR-1183, also rescued the effects of miR-1183 inhibitors in IL-1β-induced chondrocytes. Moreover, circCDK14 could induce KLF5 expression by interacting with miR-1183. 		Yes	 CircCDK14 overexpression attenuated the inhibitory effect of IL-1β treatment on cell proliferation and the promoting effects on cell apoptosis and extracellular matrix degradation. 	35723551
circNT5C2	CircRNA	Homo sapiens	Osteoarthritis	 OA tissues and in a cell model	Interaction(miR-142-5p/NAMPT axis)	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//EdU Staining	We reported that circ-NT5C2 and NAMPT were greatly upregulated, and miR-142-5p level was constrained in OA tissues and in a cell model. The targeting relationship of miR-142-5p with either circ-NT5C2 or NAMPT was confirmed. Knockdown of miR-142-5p reversed the suppressive effects of circ-NT5C2 silencing on the OA progression in vitro, and NAMPT overexpression also attenuated the effects of miR-142-5p upregulation in an OA cell model. 		Yes	Circ-NT5C2 silencing alleviated IL-1β-induced inhibitory effects on chondrocyte proliferation and ECM generation, meanwhile the promotional role of IL-1β on chondrocyte apoptosis and inflammation was also weakened.	36540014
hsa_circ_0022383	CircRNA	Homo sapiens	Osteoarthritis	 OA patients and  chondrocytes	Interaction(miR-3619-5p/SIRT1 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA//EdU Staining	Circ_0022383 expression was lower in the cartilages of OA patients and IL-1β-induced primary chondrocytes. Mechanistically, circ_0022383 acted as a sponge for miR-3619-5p, which was verified to target SIRT1. Rescue experiments showed that miR-3619-5p up-regulation reversed the protective effects of circ_0022383 on IL-1β-stimulated chondrocytes. Additionally, miR-3619-5p inhibition abolished IL-1β-induced apoptosis, inflammation and ECM degeneration in chondrocytes, which were counteracted by SIRT1 silencing.		Yes	 Functionally, ectopic overexpression of circ_0022383 alleviated IL-1β-induced proliferation arrest, apoptosis, the release of IL-6 and TNF-α, as well as the decrease of ACAN and COL2A1 and the increase of ADAMTS5 level in chondrocytes.	36194985
hsa_circ_0043947	CircRNA	Homo sapiens	Osteoarthritis	chondrocytes	Interaction(miR-671-5p/RTN3 )	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	Interleukin 1β (IL-1β) stimulation up-regulated the expression of circ_0043947 in chondrocytes. Circ_0043947 interacted with miR-671-5p, and miR-671-5p silencing largely reversed circ_0043947 knockdown-mediated protective effects in IL-1β-induced chondrocytes. miR-671-5p interacted with the 3' untranslated region (3'UTR) of RTN3. miR-671-5p overexpression attenuated IL-1β-induced injury in chondrocytes, and these protective effects were largely overturned by the overexpression of RTN3. Circ_0043947 acted as a molecular sponge for miR-671-5p to up-regulate RTN3 level in chondrocytes.		Yes	 IL-1β treatment restrained the viability and proliferation and induced the apoptosis, extracellular matrix degradation and inflammatory response of chondrocytes partly by up-regulating circ_0043947. 	35331286
circSCAPER	CircRNA	Homo sapiens	Osteoarthritis	chondrocytes	Interaction(miR-127-5p/TLR4 axis )	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//ELISA	CircSCAPER was increased in OA cartilages and IL-1β-induced chondrocytes. Mechanistically, circSCAPER acted as a sponge for miR-127-5p to positively regulate TLR4 expression in chondrocytes. IL-1β treatment reduced miR-127-5p expression but up-regulated TLR4 expression, re-expression of miR-127-5p suppressed IL-1β-caused chondrocyte injury, which was abolished by TLR4 overexpression. Moreover, miR-127-5p inhibition reversed the protective action of circSCAPER knockdown on chondrocytes under IL-1β treatment.		Yes	Functionally, knockdown of circSCAPER attenuated IL-1β-evoked apoptosis, ECM degradation, inflammation and oxidative stress in vitro. CircSCAPER up-regulation in OA cartilages was discovered to be accompanied by decreased miR-127-5p and increased TLR4. 	35993243
hsa_circ_001569	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue specimens and cells	interaction[miR-411-5p and miR-432-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results indicated that circ_001569 was overexpressed in HCC tissue samples and cells. More importantly, circ_001569 could directly sponge miR-411-5p and miR-432-5p. 	This overexpression is correlated with larger tumor size, advanced TNM stages and unfavorable prognosis in the patients with HCC.	Yes	Additionally, circ_001569 significantly facilitated HCC cell growth, migration and invasion. The animal studies further confirmed thein vitroresults. 	30086881
circRHOT1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and adjacent normal tissues	Interaction[ initiation of NR2F6]	Northern Blot//ISH//qRT-PCR//RIP//FISH	We identified circRHOT1 (hsa_circRNA_102034) as a conserved and dramatically upregulated circRNA in HCC tissues.Taken together, circRHOT1 inhibits HCC development and progression via recruiting TIP60 to initiate NR2F6 expression, indicating that circRHOT1 and NR2F6 may be potential biomarkers for HCC prognosis.	HCC patients displaying high circRHOT  level possessed poor prognosis. 	Yes	Through in vitro and in vivo experiments, we demonstrated circRHOT1 significantly promoted HCC growth and metastasis.	31324186
hsa_circ_5692	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC and adjacent non-tumor tissues,cell lines(Huh-7、SMMC-7721、HCCLM3、MHCC997H , HepG2)	Interaction[ circRNA-5692-miR-328-5p-DAB2IP regulatory pathway  ]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay	It was notable that the circRNA-5692 was encoded by the GLIS2 gene and most significantly downregulated in five HCC tissues and HCC cells. In conclusion, the circRNA-5692-miR-328-5p-DAB2IP regulatory pathway inhibits the progression of HCC. Our findings may provide potential new targets for the diagnosis and therapy of HCC.	 	Yes	Moreover, circRNA-5692 overexpression inhibited the growth of xenograft HCC tumors in vivo by decreasing miR-328-5p expression to enhance DAB2IP expression.	31776329
circPTPRM	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and their corresponding adjacent non-tumorous liver (ANL) tissue	Expression[Expression[Expression[highly expressed]-expression]-expression]	qRT-PCR//MTT//RNA-seq	The Expression[Expression[up-expression]-expression]regulation of circPTPRM was observed in 73.3% (22/30) of HCC tissues, which was significantly higher than paired ANL tissues (p = 0.023, Fig. 2a, b). circSMAD2 expression in HCC tissues was significantly higher than paired samples (p = 0.0026, Fig. 2a, b). No statistically significant differences in circPTBP3 expression in HCC and ANL tissues were observed (p = 0.107, Fig. 2a, b).		Yes	 In over-confluent cells, circPTPRM expression was significantly reduced (p < 0.01, Fig. 3a). To examine the functional roles of circPTPRM in HCC, we silenced its expression in Huh7 and SMMC-7721 cells using circPTPRM-siRNA-1 and circPTPRM-siRNA-2. circPTPRM silencing was confirmed by qRT-PCR 48 h post-transfection (Fig. 3b). MTT and colony-formation assays were performed to detected proliferation. Compared to control groExpression[Expression[up-expression]-expression]s, cancer cell proliferation was sExpression[Expression[up-expression]-expression]pressed in circPTPRM low-expression groExpression[Expression[up-expression]-expression]s by MTT analysis 72 h and 120 h post-transfection (p < 0.01, Fig. 3c). Consistent with the MTT data, colony-formation assay showed that low-circPTPRM expression led to a significant reduction of colony numbers in HCC cells (p < 0.01, Fig. 3d). These results confirmed that circPTPRM accelerates proliferation in HCC.	31494761
circSMAD2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and their corresponding adjacent non-tumorous liver (ANL) tissue	Expression[Expression[Expression[highly expressed]-expression]-expression]	qRT-PCR//MTT//RNA-seq	The Expression[Expression[up-expression]-expression]regulation of circPTPRM was observed in 73.3% (22/30) of HCC tissues, which was significantly higher than paired ANL tissues (p = 0.023, Fig. 2a, b). circSMAD2 expression in HCC tissues was significantly higher than paired samples (p = 0.0026, Fig. 2a, b). No statistically significant differences in circPTBP3 expression in HCC and ANL tissues were observed (p = 0.107, Fig. 3a, b).		Yes	 In over-confluent cells, circPTPRM expression was significantly reduced (p < 0.01, Fig. 3a). To examine the functional roles of circPTPRM in HCC, we silenced its expression in Huh7 and SMMC-7721 cells using circPTPRM-siRNA-1 and circPTPRM-siRNA-2. circPTPRM silencing was confirmed by qRT-PCR 48 h post-transfection (Fig. 3b). MTT and colony-formation assays were performed to detected proliferation. Compared to control groExpression[Expression[up-expression]-expression]s, cancer cell proliferation was sExpression[Expression[up-expression]-expression]pressed in circPTPRM low-expression groExpression[Expression[up-expression]-expression]s by MTT analysis 72 h and 120 h post-transfection (p < 0.01, Fig. 3c). Consistent with the MTT data, colony-formation assay showed that low-circPTPRM expression led to a significant reduction of colony numbers in HCC cells (p < 0.01, Fig. 4d). These results confirmed that circPTPRM accelerates proliferation in HCC.	31494761
circPTBP3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and their corresponding adjacent non-tumorous liver (ANL) tissue	Expression[No differently]	qRT-PCR//MTT//RNA-seq	The Expression[Expression[up-expression]-expression]regulation of circPTPRM was observed in 73.3% (22/30) of HCC tissues, which was significantly higher than paired ANL tissues (p = 0.023, Fig. 2a, b). circSMAD2 expression in HCC tissues was significantly higher than paired samples (p = 0.0026, Fig. 2a, b). No statistically significant differences in circPTBP3 expression in HCC and ANL tissues were observed (p = 0.107, Fig. 4a, b).		Yes	 In over-confluent cells, circPTPRM expression was significantly reduced (p < 0.01, Fig. 3a). To examine the functional roles of circPTPRM in HCC, we silenced its expression in Huh7 and SMMC-7721 cells using circPTPRM-siRNA-1 and circPTPRM-siRNA-2. circPTPRM silencing was confirmed by qRT-PCR 48 h post-transfection (Fig. 3b). MTT and colony-formation assays were performed to detected proliferation. Compared to control groExpression[Expression[up-expression]-expression]s, cancer cell proliferation was sExpression[Expression[up-expression]-expression]pressed in circPTPRM low-expression groExpression[Expression[up-expression]-expression]s by MTT analysis 72 h and 120 h post-transfection (p < 0.01, Fig. 3c). Consistent with the MTT data, colony-formation assay showed that low-circPTPRM expression led to a significant reduction of colony numbers in HCC cells (p < 0.01, Fig. 5d). These results confirmed that circPTPRM accelerates proliferation in HCC.	31494761
hsa_circ_0079929	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines(SK-Hep-1，SMMC-7721，7702，LM-3,PRL-RF5)	Regulation[PI3K/AKT/mTOR signaling pathway]	Wound Healing Assay//CCK8//qRT-PCR//EdU Staining//Transwell Assay	The expression of hsa_circ_0079299 was lower in HCC tissues.  The inhibitory effect of hsa_circ_0079299 was partly mediated by PI3K/AKT/mTOR signaling pathway.		Yes	Overexpression of hsa_circ_0079299 sExpression[Expression[up-expression]-expression]pressed tumor growth in vitro and in vivo, retarded cell cycle progression while had no effect on cell migration and apoptosis.	30655696
circFOXP9	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues, serum and cell lines	Interaction[miR-875-3p and miR-421]	Other	We found that circ-FOXP1 was significantly Expression[Expression[up-expression]-expression]regulated in HCC tissues, serum and cell lines., which was attributed to the Expression[Expression[up-expression]-expression]regulation of oncogenic transcription factor SOX9. Further mechanismic study revealed that circ-FOXP1 was preferentially located in the cytoplasm and could concurrently sponge miR-875-3p and miR-421, resulting in increasing levels of a cohort of their target oncogenes, including SOX9. 	Clinically, high circ-FOXP1 was closely correlated with larger tumor size, microvascular invasion, advanced TNM stage, and predicted poor prognosis.	Yes	Moreover, knockExpression[down-expression] of circ-FOXP1 evidently retarded tumor growth in vivo, but this effect was significantly abolished after silencing of miR-875-3p or miR-421. 	31698267
circPDE4D	CircRNA	Homo sapiens	Osteoarthritis	OA cartilage tissues	Interaction(miR-103a-3p-FGF18)	FISH//Northern Blot//Luciferase Report Assay//Western Blot	 circPDE4D was significantly downregulated in OA cartilage tissues and during stimulation with inflammatory cytokines. echanistically, we found that circPDE4D exerted its effect by acting as a sponge for miR-103a-3p and thereby regulated FGF18 expression, which is a direct target of miR-103a-3p. 		Yes	The knockdown of circPDE4D predominantly contributed to Aggrecan loss and the upregulation of matrix catabolic enzymes, including MMP3, MMP13, ADAMTS4, and ADAMTS5, but not proliferation or apoptosis. In a murine model of destabilization of the medial meniscus (DMM), the intraarticular injection of circPDE4D alleviated DMM-induced cartilage impairments. 	33125858
hsa_circ_0001598	CircRNA	Homo sapiens	Osteoarthritis	 OA models	Interaction(miR-127-3p)	CCK8//qRT-PCR//Tunel//Western Blot	 In this study, we found that circ_0001598 was significantly upregulated in chondrocytes treated with IL-1β and in cartilage tissue from mice with severed anterior cruciate ligament surgery (ACLT) induced OA models.Mechanistically, knockdown of circ_0001598 affected chondrocyte proliferation, apoptosis, and matrix degradation by regulating miR-127-3p. 		Yes	 Interference with circ_0001598 in vitro restored IL-1β-induced chondrocyte proliferation and apoptosis. Silencing circ_0001598 significantly alleviated ACLT-induced OA in mice.	34917303
circSLC7A2	CircRNA	Homo sapiens	Osteoarthritis	OA model and OA tissues	Interaction(miR-4498/TIMP3 axis)	Other	circSLC7A2 was decreased in OA model and the circularization of circSLC7A2 was regulated by FUS. We further determined that miR-4498 inhibitor reversed circSLC7A2-knockdown-induced OA phenotypes. Intra-articular injection of circSLC7A2 alleviated in vivo OA progression in a mouse model of anterior cruciate ligament transection (ACLT).		Yes	Loss of circSLC7A2 reduced the sponge of miR-4498 and further inhibited the expression of TIMP3, subsequently leading to an inflammatory response. We further determined that miR-4498 inhibitor reversed circSLC7A2-knockdown-induced OA phenotypes. Intra-articular injection of circSLC7A2 alleviated in vivo OA progression in a mouse model of anterior cruciate ligament transection (ACLT).	33960555
hsa_circ_0136474	CircRNA	Homo sapiens	Osteoarthritis	OA cartilage tissue 	Interaction[binding to miR-127-5p]	qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Western Blot	Our findings revealed that the expression levels of both Circ_0136474 and MMP-13 in OA cartilage tissue were significantly higher than that in normal cartilage tissue.  Our study demonstrated that Circ_0136474 and MMP-13 suppressed cell proliferation, while enhanced cell apoptosis by competitive binding to miR-127-5p in OA, which may well provide us with a new therapeutic strategy for osteoarthritis.		Yes	Overexpression of miR-127-5p negatively regulated MMP-13 expression to enhance cell proliferation. Our study demonstrated that Circ_0136474 and MMP-13 suppressed cell proliferation, while enhanced cell apoptosis by competitive binding to miR-127-5p in OA, which may well provide us with a new therapeutic strategy for osteoarthritis.	31402547
circVAMP3	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC patients and cells	Interaction( circVAMP3-LDHA/FGFR1)	In Vivo Experiment//Invasion Assay//Migration Assay//CCK8//qRT-PCR//Bioinformatics Analysis	 Furthermore, circVAMP3 expression was elevated in RCC patients in correspondence with TNM stage.Mechanistically, circVAMP3 was observed to interact directly with lactate dehydrogenase A (LDHA) and modulate its activity. The circVAMP3-LDHA interaction facilitated LDHA phosphorylation at tyrosine 10 (Y10) catalyzed by the upstream kinase fibroblast growth factor receptor type 1 (FGFR1). 	 Furthermore, circVAMP3 expression was elevated in RCC patients in correspondence with TNM stage.	Yes	 Therefore, this study reveals a novel molecular mechanism by which circVAMP3 promotes glycolysis and proliferation through regulating the enzymatic activity of glycolytic enzyme, suggesting that circVAMP3 may represent an RCC biomarker and treatment target.	35525866
circSCNN1A	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction(miR-421/MPP7 axis )	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 The level of circSCNN1A was significantly downregulated in RCC tissues and cells.Interestingly, circSCNN1A could interact with miR-421. Overexpression of miR-421 has reversed the anti-tumor function of circSCNN1A in RCC cells. MPP7 served as a target of miR-421, and MPP7 inhibited the malignant phenotypes of RCC cells. In addition, miR-421 downregulation induced the inhibitory effect on the RCC development via elevating the MPP7 level.		Yes	RCC cell proliferation, invasion and angiogenesis were reduced but apoptosis was promoted by circSCNN1A overexpression. Moreover, RCC tumorigenesis was suppressed by circSCNN1A through the miR-421/MPP7 axis in vivo.	36343886
hsa_circ_0000798	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC patients' tumors and cells	Interaction(miR-589-5p/G3BP1)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 Circ_0000798 is upregulated in RCC patients' tumors and cells, and high circ_0000798 is associated with shorter overall survival.  Proliferation markers Ki67 and Bcl-2 were depressed by inhibiting circ_0000798, accompanied with promoted levels of apoptosis proteins Bax and cleaved caspase-3. Of note, circ_0000798 functions as microRNA (miR) sponge for miR-589-5p and thus controls the expression of miR-589-5p-targeting Ras-GTPase-activating protein-binding protein 1 (G3BP1), a newly identified tumor-promoting gene in RCC. 	 Circ_0000798 is upregulated in RCC patients' tumors and cells, and high circ_0000798 is associated with shorter overall survival. 	Yes	 RNA interference of circ_0000798 impedes cell metabolic viability and abilities of DNA synthesis, colony formation, wound healing, migration, and invasion in RCC cells but also induces cell cycle arrest and apoptosis. Moreover, circ_0000798 interference could delay tumor growth in vivo. 	35857217
hsa_circ_0008717	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction(miR-217/FBXO17 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	Circ_0008717 was upregulated in RCC tissues and cells. MiR-217 was a target of circ_0008717 and bound to the FBXO17 3' untranslated region. The expression of FBXO17 was positively regulated by circ_0008717 but impaired by miR-217 reintroduction. The inhibitory effects of circ_0008717 knockdown on RCC cell malignant behaviors were reversed by miR-217 inhibition or FBXO17 overexpression. Circ_0008717 knockdown inhibited tumor growth in vivo by regulating miR-217 and FBXO17.		Yes	 Silencing circ_0008717 suppressed RCC cell proliferation, migration, invasion and glycolysis but promoted cell apoptosis. 	35357059
hsa_circ_0005875	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC tissues and cells	Interaction(miR-502-5p/ETS1 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Circ_0005875 and ETS1 were upregulated and miR-502-5p was downregulated in RCC tissues and cells. MiR-502-5p was a target of circ_0005875, and miR-502-5p inhibition reversed the inhibitory effects of circ_0005875 knockdown on the malignant behaviors of RCC cells. ETS1 was a direct target of miR-502-5p, and miR-502-5p exerted its anti-tumor role in RCC cells by targeting ETS1. Moreover, circ_0005875 knockdown decreased ETS1 expression by sponging miR-502-5p. Circ_0005875 knockdown suppressed RCC progression by regulating miR-502-5p/ETS1 axis, which might provide a promising therapeutic target for RCC.		Yes	Knockdown of circ_0005875 suppressed RCC cell proliferation, migration and invasion, and induced apoptosis and cell cycle arrest.  Additionally, circ_0005875 depletion suppressed tumor growth in vivo. 	34407050
hsa_circ_000829	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction(SRSF1/SLC39A14)	Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Invasion Assay	Circ_000829 was poorly expressed in RCC tissues and cells, while SRSF1 was highly expressed. Mechanistically, circ_000829 directly bound to SRSF1, and SRSF1 enhanced the expression of SLC39A14B by mediating the alternative splicing of SLC39A14. SLC39A14B upregulation negated the effect of SLC39A14 knockdown on RCC cell proliferation.		Yes	Restoration of circ_000829 reduced the levels of SRSF1 and SLC39A14B, thereby repressing the RCC cell proliferation in vitro and tumor growth in vivo. Meanwhile, overexpression of SRSF1 and SLC39A14B promoted the proliferation and cell cycle entry of RCC cells. 	36062189
hsa_circ_0000274	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cells	Interaction(miR-338-3p/NUCB2/JAK1/STAT3 pathway)	Western Blot//Flow Cytometry//qRT-PCR//RIP//CCK8//ChIP	Compared to normal tissues and cells, circ_0000274 RNA level was elevated in RCC tissues and cells. Circ_0000274 RNA sponged miR-338-3p RNA to positively regulate NUCB2 protein in RCC cells. Inhibition of miR-338-3p reversed the impacts of circ_0000274 knockdown on RCC cell malignant behaviors. MiR-338-3p RNA overexpression repressed the malignant phenotypes of RCC cells, while NUCB2 protein elevation could abrogate the effect. Moreover, circ_0000274 RNA knockdown blocked tumorigenesis in vivo. Besides, circ_0000274 RNA knockdown inactivated the JAK1/STAT3 protein signaling pathway.		Yes	Knockdown of circ_0000274 RNA suppressed cell viability, colony formation, metastasis and tube formation and promoted apoptosis in RCC cells in vitro. 	35569717
circsafb2	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and RCC-derived exosomes	Interaction(miR-620/JAK1/STAT3 axis)	In Vivo Experiment//IHC//Western Blot//Tube Formation Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our data first demonstrated that circSAFB2 leads to immune escape from RCC by mediating M2 macrophage polarization via the miR-620/JAK1/STAT3 axis. These findings indicate a novel molecular mechanism of exosomal circSAFB2 in the progression of RCC and implicate circSAFB2 as a target for exosome-mediated tumor immune evasion.		Yes	Furthermore, we demonstrated that exosomal circSAFB2 mediates the polarization of M2 macrophages through the miR-620/JAK1/STAT3 axis to promote RCC metastasis.	35646637
circSEC24A	CircRNA	Homo sapiens	Osteoarthritis	osteoarthritic cartilage tissues	Interaction(miR-26b-5p/DNMT3A)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ELISA//IF	Circ_SEC24A was upregulated in osteoarthritic cartilage tissues and IL-1β-induced chondrocytes, accompanying with miR-26b-5p downregulation and DNMT3A upregulation.Inhibiting miR-26b-5p counteracted but upregulating miR-26a-5p mimicked the functions of circ_SEC24A silencing. Reinforcing DNMT3A reversed miR-26b-5p overexpression's role in IL-1β-induced chondrocytes. Mechanically, circ_SEC24A and DNMT3A were competitive endogenous RNAs (ceRNAs) for miR-26b-5p.		Yes	Interfering circ_SEC24A abolished IL-1β-induced effects on proliferation inhibition, apoptosis, and ECM degradation in chondrocytes, but overexpressing circ_SEC24A had the opposite effects.	34325283
circHIPK3	CircRNA	Homo sapiens	Osteoarthritis	OA tissues and OA chondrocytes	regulation[as a sponge of miR-124 to regulate SOX8]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	High expressed CircHIPK3 and low expressed miR-124 were found in OA tissues and OA chondrocytes.Low expression of CircHIPK3 promoted the apoptosis of OA chondrocytes by promoting miR-124 to suppress SOX8 expression.		Yes	To our surprise, knocking down CircHIPK3 and transfected miR-124 mimics both inhibited the apoptosis of OA chondrocytes. 	32767319
circPSM3	CircRNA	Homo sapiens	Osteoarthritis	OA cartilage tissue and cells	interaction[ targeting miRNA-296-5p]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	CircPSM3 expression was upregulated in OA cartilage tissue and cells. CircPSM3 participated in the proliferation and differentiation of OA chondrocytes through targeted binding to miRNA-296-5p.		Yes	Low expression of CircPSM3 promoted the proliferation and cell differentiation of OA chondrocytes.	32329819
circANKRD36	CircRNA	Homo sapiens	Osteoarthritis	human chondrocytes	Interaction(miR-599)	qRT-PCR	We performed circRNA sequencing in normal and OA tissues and found the expression of circANKRD36 is decreased in OA tissues. We then found miR-599 to be the target of circANKRD36 and correlate well with circANKRD36 both in vitro and in vivo. 		Yes	knockdown of circANKRD36 promotes the apoptosis and inflammation of chondrocytes in IL-1β stress. 	33205602
hsa_circ_0134111	CircRNA	Homo sapiens	Osteoarthritis	cell lines	Interaction(miR-224-5p/CCL1 axis)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//FISH//CCK8//Luciferase Report Assay//ELISA	In this study, the effects of hsa_circ_0134111 knockdown were evaluated in primary human chondrocytes treated with IL-1β to simulate OA, as well as in a rat model of OA. These results suggest that hsa_circ_0134111 contributes to OA development by binding to miR-224-5p, thereby releasing the inhibition that miR-224-5p exerts over CCL1.		Yes	CCK-8 and flow cytometry assays showed that hsa_circ_0134111 knockdown reversed IL-1β-induced cell decline by inhibiting apoptosis. 	34413269
hsa_circ_0116061	CircRNA	Homo sapiens	Osteoarthritis	OA cartilage tissues	Interaction(miR-200b-3p/SMURF2 axis)	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Cell Viability Assay//ELISA//IHC	Circ_0116061 and SMURF2 were highly expressed, and miR-200b-3p was lowly expressed in OA cartilage tissues. MiR-200b-3p could be sponged by circ_0116061, and its inhibitor could reverse the regulation of circ_0116061 silencing on the biological functions of OA chondrocytes. SMURF2 was a target of miR-200b-3p, and its expression was positively regulated by circ_0116061. 		Yes	Knockdown of circ_0116061 could promote the proliferation and inhibit the apoptosis and inflammation of OA chondrocytes. 	33849596
hsa_circ_0005567	CircRNA	Homo sapiens	Osteoarthritis	 synovial tissues of osteoarthritis patients	Interaction(miR-492/SOCS2 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	The results showed that the hsa_circ_0005567 expression level was downregulated in the synovial tissues of osteoarthritis patients. Hsa_circ_0005567 was proved to be a molecular sponge for miR-492, and SOCS2 was verified as the target of miR-492. 		Yes	Overexpression of hsa_circ_0005567 inhibited M1 macrophage polarization, and promoted M2 macrophage polarization. 	34652255
hsa_circ_0032131	CircRNA	Homo sapiens	Osteoarthritis	CHON-001 cells and an OA rat model.	Interaction(miR-502-5p/PRDX3 axis)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay	 We investigated the functions of hsa_circ_0032131, a circRNA upregulated in OA, using CHON-001 cells and an in vivo OA rat model. 		Yes	 IL-1β-induced inhibition of CHON-001 growth was reversed by silencing hsa_circ_0032131. In addition, hsa_circ_0032131 knockdown reversed IL-1β-induced activation of Trx1, Cyclin D and PRDX3, whereas overexpression of PRDX3, a direct target of miR-502-5p, reversed this effect.	34032607
circCTNNA1	CircRNA	Homo sapiens	Osteoarthritis	OA tissues	Interaction(miR-29a )	CCK8//qRT-PCR//IF//Western Blot	CircCTNNA1 was downregulated in OA, while miR-29a was overexpressed in OA. RNA pull-down assay illustrated the direct interaction between circCTNNA1 and miR-29a. 		Yes	CircCTNNA1 overexpression suppressed the enhancing effects of miR-29a overexpression on cell apoptosis induced by LPS.	34751080
hsa_circ_0003141	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	regulation[miR-1827/UBAP2 axis]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	Using bioinformatics analysis, we have found that the expression of circRNA hsa_circ_0003141 is significantly increased in HCC tissues. Together, our results indicate that hsa_circ_0003141 functions as an oncogene in HCC cells, and suggest that the hsa_circ_0003141/miR-1827/UBAP2 axis might represent a novel therapeutic option for the treatment of HCC.	Ubiquitin-associated protein 2 (UBAP2) is the parent gene for hsa_circ_0003141, and its high expression correlates with poor overall survival rates in HCC patients. 	Yes	 Downregulation of hsa_circ_0003141 suppresses UBAP2 expression, induces apoptosis, and inhibits proliferation and invasion by HCC Huh-7 cells. 	32464601
circZNF609	CircRNA	Homo sapiens	Carcinoma, Hepatocellular		regulation[miR-15a-5p/15b-5p and GLI2 expressions]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Briefly, circZNF609 enhances HCC cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p/15b-5p and GLI2 expressions.		Yes	 Functional tests revealed that decreased expression of circZNF609 suppressed cell proliferation, metastasis and stemness, whereas induced cell apoptosis in HCC. 	32398664
circMAST1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	interaction[miR-1299,CTNND1]	Western Blot//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	CircMAST1 was upregulated in HCC tissues and cell lines; silencing via small interfering RNA inhibited migration, invasion, and proliferation of HCC cell lines in vitro as well as tumor growth in vivo.Moreover, circMAST1 elicits HCC progression by sponging miRNA-1299 and stabilizing CTNND1. 		Yes	CircMAST1 was upregulated in HCC tissues and cell lines; silencing via small interfering RNA inhibited migration, invasion, and proliferation of HCC cell lines in vitro as well as tumor growth in vivo.	32393764
hsa_circ_002136	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-19a-3p/RAB1A pathway)	qRT-PCR	 Circ_002136 was shown for the first time to be differentially upregulated in HCC tissues and cells and transferred by HCC cell-derived exosomes.  Furthermore, a well-established circ_002136 ceRNA regulatory network was constructed, namely circ_002136 blocked miR-19a-3p expression, elevated RAB1A expression activity and stimulated HCC development. 	Finally, high levels of circ_002136 or RAB1A, as well as low levels of miR-19a-3p, negatively affected HCC patient survival.	Yes	 More importantly, selective silencing of circ_002136 depleted the malignant biological behaviors of HCC exosome-activated Huh7 and HA22T cells. Depletion of circ_002136 in vivo effectively retarded the growth of HCC xenograft tumors.	36476239
circSNX27	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-637/FGFR1 axis)	qRT-PCR	The circ_SNX27 and FGFR1 levels were up-regulated, but miR-637 content was reduced in HCC.  Circ_SNX27 served as a sponge of miR-637 to promote FGFR1 expression. MiR-637 reduction abolished the restrained effect of circ_SNX27 absence on HCC cell development. Moreover, miR-637 curbed HCC cell malignant phenotype by regulating FGFR1.		Yes	Circ_SNX27 down-regulation inhibited HCC cell proliferation, motility, and invasion and promoted apoptosis in vitro, as well as weakened tumor growth in vivo. 	36029209
circWDR25	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miRNA-4474-3P-ALOX-15 and EMT axes)	RNA Pull-Down//Luciferase Report Assay//FISH	 We found that overexpressed peritumoral circWDR25 was associated with survival and recurrence in patients with HCC and promoted the progression of HCC cells both in vitro and in vivo. Mechanistically, both exogenous and HSC exosomal-derived circWDR25 regulated the expression of ALOX15 by sponging miR-4474-3p and ultimately inducing an epithelial-to-mesenchymal transition (EMT) in HCC cells. Moreover, exogenous and HSC exosomal-derived circWDR25 promoted the expression of CTLA-4 in HSCs and PD-L1 in HCC cells. 	 We found that overexpressed peritumoral circWDR25 was associated with survival and recurrence in patients with HCC and promoted the progression of HCC cells both in vitro and in vivo. 	Yes	 We found that overexpressed peritumoral circWDR25 was associated with survival and recurrence in patients with HCC and promoted the progression of HCC cells both in vitro and in vivo. 	35934785
circRanGAP1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 cells and clinical tissues	Interaction(miR-27b-3p/NRAS Axis )	qRT-PCR	Here, we found elevated circRanGAP1 in the cells and clinical tissues of patients with HCC. Moreover, circRanGAP1 is mainly located inside the cytoplasm. Mechanistically, circRanGAP1 as an oncogene promotes HCC progression by miR-27b-3p/NRAS/ERK axis, furthermore, affects the infiltration level of tumor-associated macrophages probably by sponging miR-27b-3p. 	Increased circRanGAP1 levels are associated with enlarged tumors and the advanced stage of TNM.	Yes	CircRanGAP1 promotes the growth, migration, and HCC cell invasion, concurrently with the growth and metastasis of tumors in-vivo. 	36348379
hsa_circ_0090049	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(miR-605-5p or miR-548c-3p/UBE2T )	qRT-PCR	 Circ_0090049 and UBE2T were upregulated in liver cancer. MiR-605-5p and miR-548c-3p were identified as targets of circ_0090049, and UBE2T was the target of miR-605-5p and miR-548c-3p. Anti-miR-605-5p, anti-miR-548c-3p or UBE2T overexpression restored the inhibitory effect of circ_0090049 knockdown on HCC cells. 		Yes	Silencing circ_0090049 reduced the proliferation, migration, invasion, and tumor spheroid formation rate of Huh7 and HCCLM3 cells. Animal experiments confirmed the antitumor effect of silence circ_0090049. 	34620742
hsa_circ_0061395	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 liver cancer tissues and cells	Interaction( miR-1182 sponge)	qRT-PCR	Circ_0061395 and SPOCK1 were significantly expressed in liver cancer tissues and cells.  MiR-1182 was a target of circ_0061395. Silencing circ_0061395 inhibited the malignant behavior of HCC cells by releasing miR-1182. In addition, SPOCK1 was the target of miR-1182. Overexpression of SPOCK1 partially restored the inhibitory effect of miR-1182 on cell proliferation.		Yes	 Silencing circ_0061395 reduced the proliferation, migration, invasion, tube formation and tumor spheroid formation rate of Huh-7 and SNU-387 cells.  Animal experiments confirmed the anti-tumor effect of silence circ_0061395. Circ_0061395 induced the changes of the expression of SPOCK1 by regulating miR-1182, thereby mediating the process of HCC, and at least partially promoting the development of HCC cells, providing a novel targeted therapy for HCC.	35775884
circMAP3K4	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Expression(highly expressed)	qRT-PCR	We found circMAP3K4 to be an upregulated circRNA with coding potential in HCC. IGF2BP1 recognized the circMAP3K4 N6-methyladenosine modification and promoted its translation into circMAP3K4-455aa. Functionally, circMAP3K4-455aa prevented cisplatin-induced apoptosis in HCC cells by interacting with AIF, thus protecting AIF from cleavage and decreasing its nuclear distribution. Moreover, circMAP3K4-455aa was degraded through the ubiquitin-proteasome E3 ligase MIB1 pathway. Clinically, a high level of circMAP3K4 is an independent prognostic factor for adverse overall survival and adverse disease-free survival of HCC patients.		Yes	Functionally, circMAP3K4-455aa prevented cisplatin-induced apoptosis in HCC cells by interacting with AIF, thus protecting AIF from cleavage and decreasing its nuclear distribution.	35366894
circTOLLIP	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(miR-516a-5p/PBX3/EMT pathway)	qRT-PCR	 circTOLLIP was significantly upregulated in HCC cells and tissues. Mechanistically, EIF4A3 promoted the biogenesis of circTOLLIP without affecting its stability. Moreover, circTOLLIP sponged miR-516a-5p to elevate the expression of PBX3, thereby activating the epithelial-to-mesenchymal transition (EMT) pathway and facilitating tumor progression in HCC.	High circTOLLIP expression was correlated with poor overall survival (OS) and disease-free survival (DFS) in patients.	Yes	circTOLLIP promoted the proliferation and metastasis of HCC cells in vitro and in vivo. 	35509064
circRASSF5	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-331-3p/PHLPP)	qRT-PCR	CircRASSF5 is obviously downregulated in both HCC tissues and cell lines. Mechanistically, circRASSF5 directly interacts with miR-331-3p as a sponge, and then enhances the expression of PH domain and leucine-rich repeat protein phosphatase (PHLPP), thus restraining the progression of HCC cells.	Low level of circRASSF5 is negatively associated with larger tumor size, severe vascular invasion, more portal vein tumor embolus and unfavorable prognosis.	Yes	Loss-of-function assay reveals that circRASSF5 remarkably impedes the growth and metastasis of HCC cells in vitro and in vivo. 	36217445
circCFH	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(circ-CFH/miR-377-3p/RNF38 axis)	qRT-PCR	circ-CFH was overexpressed in HCC tissues and cells, and the downregulation of circ-CFH inhibited the development of HCC by repressing cell proliferation, migration, invasion, and glycolysis while enhancing apoptosis in vitro, as well as inhibited tumor growth in vivo. miR-377-3p was negatively regulated by circ-CFH, and silencing of miR-377-3p abolished circ-CFH knockdown-mediated effects on HCC cells. Moreover, overexpression of miR-377-3p could impede the HCC process by targeting RNF38. Mechanistically, the circ-CFH/miR-377-3p/RNF38 axis regulated the progression of HCC cells, which might provide new diagnostic markers for HCC.		Yes	circ-CFH was overexpressed in HCC tissues and cells, and the downregulation of circ-CFH inhibited the development of HCC by repressing cell proliferation, migration, invasion, and glycolysis while enhancing apoptosis in vitro, as well as inhibited tumor growth in vivo. 	35415236
hsa_circ_0058051	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Expression(highly expressed)	qRT-PCR	 We found that high circ_0058051 expression was negatively correlated with the prognosis of HCC patients. Circ_0058051 knockdown attenuated the proliferation and colony formation, meanwhile inhibited migration of HCC cells.	 We found that high circ_0058051 expression was negatively correlated with the prognosis of HCC patients. 	Yes	Circ_0058051 knockdown attenuated the proliferation and colony formation, meanwhile inhibited migration of HCC cells.	36114310
hsa_circ_0000285	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines and tumors	Interaction( miR-582-3p/CCNB2 axis)	qRT-PCR	Elevated hsa_circ_0000285 and CCNB2 expressions, and a decreased miR-582-3p expression were observed among the HCC cell lines and tumors. Hsa_circ_0000285 bound to miR-582-3p competitively to improve CCNB2 levels. Inhibiting hsa_circ_0000285 or CCNB2 reversed the miR-582-3p-knockdown-mediated promotion of malignant HCC cell phenotypes.		Yes	Silencing of hsa_circ_0000285 promoted apoptosis and repressed proliferation and migration among HCC cells. Moreover, silencing hsa_circ_0000285 also impeded the growth of HCC tumors in vivo. 	35839486
circSOD2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-497-5p/ANXA11 Axis)	qRT-PCR	CircSOD2 was upregulated in HCC tissues and cells.Mechanically, circSOD2 promoted HCC development by acting as a miR-497-5p sponge and miR-497-5p played a tumor-inhibitory role in HCC cells by targeting ANXA11. Moreover, circSOD2 induced upregulation of ANXA11 expression by interacting with miR-497-5p. Also, the promoting effects of circSOD2 on immune evasion and anti-PD-1 resistance were related to miR-497-5p/ANXA11 axis. 		Yes	Knockdown of circSOD2 resulted in HCC cell growth inhibition, apoptosis promotion, cell cycle arrest and metastasis suppression.	36008700
circLIFR	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(TBK1)	qRT-PCR	Among them, circRNA derived from the LIFR gene, named circLIFR, was significantly downregulated in HCC.  RNA pull-down and mass spectrometry detection revealed circLIFR interacting with TANK binding kinase 1 (TBK1). Anti-TBK1 RIP confirmed the interaction between circLIFR and TBK1. TBK1 is a serine/threonine kinase that regulates several signaling pathways, including the NF-κB pathway. TBK1 inhibitors inhibit NF-κB activation. Overexpression of circLIFR overcame the in-hibitory function of TBK1, resulting in the upregulation of several genes, including MMP13, MMP3, VEGF, and MAPK. 		Yes	 Intriguingly, circLIFR overexpression in SK-Hep-1 cells promoted cell growth and invasion. 	36176304
circGSE1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	(HCC) cells	Interaction( miR-324-5p/TGFBR1/Smad3 axis)	qRT-PCR	Collectively, we revealed that exosomal circGSE1 derived from hepatocellular carcinoma (HCC) cells promotes the progression of HCC by inducing Tregs expansion via regulating the miR-324-5p/TGFBR1/Smad3 axis. 		Yes	In vivo animal metastasis models and bioluminescence imaging were used to verify the effect of exosomal circGSE1 on tumor progression. Collectively, we revealed that exosomal circGSE1 derived from hepatocellular carcinoma (HCC) cells promotes the progression of HCC by inducing Tregs expansion via regulating the miR-324-5p/TGFBR1/Smad3 axis. 	35396771
circTTLL5	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-136-5p/KIAA1522 axis)	qRT-PCR	CircTTLL5 was incorporated into exosomes and highly expressed in HCC tissues and cells. Mechanically, circTTLL5 could sponge miR-136-5p, which controlled its down-stream target KIAA1522. MiR-136-5p inhibition reversed the effects of circTTLL5 knockdown on HCC cells. Besides that, miR-136-5p re-expression inhibited HCC cell growth and metastasis, which was abated by KIAA1522 overexpression.		Yes	CircTTLL5 knockdown suppressed HCC cell proliferation and metastasis in vitro and impeded tumor growth in mice. CircTTLL5 could be delivered to recipient cells via exosomes, and treatment of circTTLL5-elevated exosomes could attenuate the anticancer effects of circTTLL5 knockdown on HCC in vitro and in vivo. 	36528986
circSYPL1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cell lines	Interaction(miR-506-3p/EZH2 )	qRT-PCR	circSYPL1 expression was significantly upregulated in HCC cell lines, in addition to primary and metastatic tumors of patients with HCC. circSYPL1 sponged miR-506-3p to boost EZH2 expression levels, as indicated by luciferase and RNA pull-down assays. Furthermore, circSYPL1 overexpression could upregulate EZH2 expression, while miR-506-3p mimics or EZH2 shRNAs could reverse the circSYPL1-induced malignancy of HCC cells.		Yes	Additionally, it may promote HCC initiation, development as well as progression. By knocking down circSYPL1 siRNA, we were able to drastically decrease the aggressiveness of HCC cells. 	35345511
circTMEM181	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-519a-5p/ARHGAP29 )	qRT-PCR	In this study, we identified a novel circRNA, named circTMEM181, was downregulated in HCC tissues. CircTMEM181 overexpression reduced HCC cell migration and invasion abilities, while circTMEM181 knockdown increased cell motility. Mechanically, circTMEM181 could directly bind to miR-519a-5p and subsequently upregulate ARHGAP29 protein expression.	Decreased expression of circTMEM181 was associated with shorter overall survival of patients with HCC.	Yes	CircTMEM181 overexpression reduced HCC cell migration and invasion abilities, while circTMEM181 knockdown increased cell motility. 	36519254
hsa_circ_0006404	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC specimens and cells	Interaction(miR-624)	qRT-PCR	Our data indicated that circ_0006404 was overexpressed in HCC specimens and cells and ectopic expression of circ_0006404 increased HCC cell growth, cycle, and migration.Moreover, we showed that miR-624 was downregulated in HCC specimens and cells and miR-624 expression was negatively correlated with circ_0006404 expression in HCC specimens. Circ_0006404 sponged miR-624 in HCC cell, and the overexpression of circ_0006404 suppressed miR-624 expression in HCC cell. Furthermore, circ_0006404 induced HCC cell growth, cycle, and migration via regulating miR-624. 		Yes	Our data indicated that circ_0006404 was overexpressed in HCC specimens and cells and ectopic expression of circ_0006404 increased HCC cell growth, cycle, and migration.	35579835
circKIF5B	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	liver cancer cell lines and tissues	Interaction(miR-192 Family/XIAP Axis)	qRT-PCR	 Importantly, we found that circKIF5B circRNA, rather than KIF5B linear mRNA, was notably upregulated in liver cancer cell lines and tissues. Moreover, we found that silencing circKIF5B markedly reduced the proliferation, invasion, and metastasis of liver cancer cells by sponging the miR-192 family, thus decreasing the expression of X-linked inhibitor of apoptosis (XIAP).		Yes	Moreover, we found that silencing circKIF5B markedly reduced the proliferation, invasion, and metastasis of liver cancer cells by sponging the miR-192 family, thus decreasing the expression of X-linked inhibitor of apoptosis (XIAP).	35847962
circEIF3I	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-526b-5p Axis)	qRT-PCR	Expression of circEIF3I was upregulated in HCC tissues. CircEIF3I could sponge miR-526b-5pto regulate downstream HGF. Functionally, circEIF3I regulation in HCC cell progression was associated with miR-526b-5p sponging function and HGF upregulation could attenuate tumor-inhibiting roles of miR-526b-5p. HCC tumor growth was delayed by interfering circEIF3I.		Yes	 Knockdown of circEIF3I suppressed cell proliferation epithelial-mesenchymal transition, migration, invasion and tube formation ability but promoted apoptosis of HCC cells. 	35723810
hsa_circ_0073181	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-548p/ PTPRE axis)	qRT-PCR	 Circ_0073181 and PTPRE were upregulated, and miR-548p was decreased in HCC tissues and cells. Circ_0073181 silencing could inhibit HCC cell growth and metastasis partly by regulating the miR-548p/ PTPRE axis, providing a promising therapeutic target for the HCC treatment.		Yes	 Furthermore, circ_0073181 knockdown could boost proliferation, migration, invasion and repress apoptosis of HCC cells in vitro. The mechanical analysis suggested that circ_0073181 could regulate PTPRE expression by sponging miR-548p. In addition, circ_0073181 knockdown suppressed cell growth of HCC in vivo. 	34657099
hsa_circ_0006789	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-1324 and SOX12)	qRT-PCR	 Circ_0006789 was overexpressed in HCC tissues and cell lines. miR-1324 was confirmed as a target of circ_0006789, and miR-1324 targeted SOX12 to suppress its expression. Circ_0006789 could promote SOX12 expression by sponging miR-1324.		Yes	Circ_0006789 overexpression accelerated the growth, migration and invasion of HCC cells, while knockdown of circ_0006789 exerted the opposite effects.	36017856
hsa_circ_0036412	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(ELAVL1/GLI2 )	qRT-PCR	 Circ_0036412 is overexpressed in HCC cells and features circular structure. Circ_0036412 modulates Hedgehog pathway. GLI2 propels HCC growth in vivo. Circ_0036412 up-regulates GLI2 expression by competitively binding to miR-579-3p, thus promoting the proliferation and inhibiting cell cycle arrest of HCC cells. Circ_0036412 stabilizes GLI2 expression by recruiting ELAVL1. Circ_0036412 propels the proliferation and inhibits cell cycle arrest of HCC cells in vitro through Hedgehog pathway.		Yes	 PRDM1 activates circ_0036412 transcription to regulate the proliferation and cell cycle of HCC cells in vitro.	35382824
hsa_circ_0004658	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	Mφ-Exo	Interaction(miR-499b-5p/JAM3)	qRT-PCR	Our results shown that hsa_circ_0004658 is upregulated in RBPJ+/+ Mφ-Exo compared to WT Mφ-Exo. The effects of RBPJ+/+ Mφ-Exo on HCC cells can be reversed by the hsa_circ_0004658 knockdown. Mechanistic investigations revealed that hsa_circ_0004658 acts as a ceRNA of miR-499b-5p, resulting in the de-repression of JAM3.		Yes	RBPJ+/+ Mφ-Exo and hsa_circ_0004658 inhibits proliferation and promotes apoptosis in HCC cells, whereas hsa_circ_0004658 knockdown stimulated cell proliferation and migration but restrained apoptosis in vitro and promotes tumor growth in vivo. 	35013102
hsa_circ_0064288	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-335-5p/ROCK1 )	qRT-PCR	 Circ_0064288 and ROCK1 expression was up-modulated in HCC, while miR-335-5p was down-modulated. Additionally, circ_0064288 could competitively bind with miR-335-5p thereby up-modulate ROCK1 expression. MiR-335-5p overexpression partly counteracted the effect of circ_0064288 overexpression on HCC cells.	High circ_0064288 expression was associated with shorter survival time of HCC patients. 	Yes	 It was also revealed that circ_0064288 overexpression remarkably enhanced HCC cell growth and migration, while knockdown of circ_0064288 induced opposite effects.	35287604
circRPN2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines and HCC tissues	Interaction(miR-183-5p/FOXO1 axis)	circRNA-seq	CircRPN2 was downregulated in highly metastatic HCC cell lines and HCC tissues with metastasis.These data support a model wherein circRPN2 inhibits HCC aerobic glycolysis and metastasis via acceleration of ENO1 degradation and regulation of the miR-183-5p/FOXO1 axis, suggesting that circRPN2 represents a possible therapeutic target in HCC.	Patients with HCC with lower circRPN2 levels displayed shorter overall survival and higher rates of cumulative recurrence.	Yes	Mechanistic studies in vitro and in vivo revealed that circRPN2 binds to enolase 1 (ENO1) and accelerates its degradation to promote glycolytic reprogramming through the AKT/mTOR pathway, thereby inhibiting HCC metastasis. 	35045986
circCCNB1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and cancer tissues	Interaction(miR-106b-5p/GPM6A )	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 The expression of circCCNB1 and GPM6A were significantly down-regulated in HCC cells and cancer tissues, while miR-106b-5p expression was up-regulated. We demonstrated that circCCNB1 silencing promoted cell proliferation and metastasis of HCC cells by weakening sponging of oncogenic miR-106b-5p to induce GPM6A underexpression. DYNC1I1 gene expression was up-regulated and further led to activation of the AKT/ERK signaling pathway.		Yes	 In addition, circCCNB1 silencing promoted the clone formation ability, the cell cycle G1-S transition, and the growth of xenograft tumors of HCC cells via GPM6A downregulation. 	35002514
hsa_circ_0008194	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 tumor tissues	Interaction(miR-190a/AHNAK )	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 In this study, the abnormal upregulated circ_0008194 in tumor tissues was detected.  The positive correlation between circ_0008194 and AHNAK was also confirmed. Mechanically, circ_0008194 presented the binding ability with miR-190a causing the suppression of miR-190a expression, causing the competitive inhibition of AHNAK, resulting in the promotion of EMT.		Yes	Through knockdown and overexpression of circ_0008194, we conducted in vitro functional studies. We found circ_0008194 could induce the invasion of cells in vitro. 	35199873
hsa_circ_0000098	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction( miR-383/MCUR1 axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//cell invasion assay	 The expression of circ_0000098 was higher in HCC tissues compared to paired adjacent tissues. Furthermore, mechanistic investigation demonstrated that by sequestering miR-383 from the 3'-UTR of MCUR1, circ_0000098 positively regulated MCUR1 expression in HCC cells and finally promoted HCC progression. On the other hand, inhibiting circ_0000098 in HCC cells could diminish doxorubicin (DOX) resistance by decreasing P-glycoprotein (P-gp, MDR1) expression and intracellular ATP levels. 		Yes	 Our experiments indicated that circ_0000098 served as a key oncogenic circRNA to increase HCC cell proliferation and invasion in vitro and HCC progression in vivo. 	36071480
hsa_circ_0005397	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-1283/HEG1)	qRT-PCR	 Circ_0005397 was highly expressed in HCC tissues and cells, in HCC cell lines. 		Yes	 Circ_0005397 silencing inhibited proliferation, migration, invasion and angiogenesis, while induced apoptosis in HCC cells. 	35500803
hsa_circ_0001459	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue and cell lines.	Interaction(miR-6165/IGF1R axis)	qRT-PCR	We found that circ_0001459 expression was significantly elevated in HCC tissue and cell lines. Mechanistically, we revealed that circ_0001459 could sponge miR-6165 and induce the upregulation of its downstream target IGF1R, thus significantly promoting the progression of HCC.		Yes	. Knockdown of circ_0001459 significantly inhibited the proliferation, migration, and invasion of HCC cells, whereas upregulation of circ_0001459 had the opposite effect. 	35199365
circKCNN2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-520c-3p/MBD2 axis)	qRT-PCR	 The expression of circKCNN2 was downregulated in HCC tissues and predicted a favorable overall survival and recurrence-free survival. The expression of circKCNN2 was positively correlated with the parental gene, potassium calcium-activated channel subfamily N member (KCNN2). Nuclear transcription factor Y subunit alpha (NFYA) was proven to inhibit the promoter activity of KCNN2, downregulate the expression of KCNN2 and circKCNN2, and predict an unfavorable recurrence-free survival. miR-520c-3p sponged by circKCNN2 could reverse the inhibitory effect of circKCNN2 on HCC cells and down-regulate the expression of methyl-DNA-binding domain protein 2 (MBD2).	 The expression of circKCNN2 was downregulated in HCC tissues and predicted a favorable overall survival and recurrence-free survival.	Yes	Ectopic expression of circKCNN2 inhibited HCC cell proliferation, colony formation, migration, and tumor formation in a mouse model.	35051313
circPAK1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tumor tissues and cell lines	Interaction( 14-3-3 ζ with YAP)	qRT-PCR	 CircPAK1, a novel circRNA, is highly expressed in HCC tumor tissues and cell lines as well as correlated with poor outcomes in HCC patients. Mechanistically, circPAK1 enhanced HCC progression by inactivating the Hippo signaling pathway, and this kind of inactivation is based on its competitively binding of 14-3-3 ζ with YAP, which weakens the recruitment and cytoplasmic fixation of 14-3-3 ζ to YAP, thus promoting YAP nucleus localization. 	 CircPAK1, a novel circRNA, is highly expressed in HCC tumor tissues and cell lines as well as correlated with poor outcomes in HCC patients.	Yes	 Functionally, circPAK1 knockdown inhibited HCC cell proliferation, migration, invasion and angiogenesis while circPAK1 overexpression promoted HCC progression. The tumor-promoting phenotypes of circPAK1 on HCC were also confirmed by animal experiments. Importantly, the application of CS/si-circPAK1 nanocomplexes showed a better therapeutic effect on tumor growth and metastasis.	36131287
circPTTG1IP	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-16-5p/RNF125/JAK1 axis)	qRT-PCR	CircPTTG1IP expression was decreased in HCC compared to peritumoral tissues. Mechanistically, circPTTG1IP was shown to function as a competing endogenous RNA (ceRNA) of RNF125 by binding miR-16-5p to increase the level of the E3 ubiquitin ligase RNF125, which further ubiquitinated and degraded JAK1 protein. Finally, we demonstrated that administration of filgotinib, a JAK1 inhibitor, restricted HCC progression induced by low circPTTG1IP expression. 	Moreover, low circPTTG1IP expression was revealed to be associated with a poor prognosis of HCC patients. 	Yes	Elevation of circPTTG1IP was revealed to inhibit HCC development both in vitro and in vivo. 	35710093
circCPSF6	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC specimens and cells	Interaction(PCBP2/YAP1)	qRT-PCR	Meanwhile, circCPSF6 was upregulated in HCC specimens, and elevated circCPSF6 expression served as an independent prognostic factor for worse survival of patients with HCC. circCPSF6 triggered expression of YAP1, further activating its downstream cascade. Mechanistically, circCPSF6 competitively bound PCBP2, blunting its binding to YAP1 mRNA, thereby sustaining the stability of YAP1.	Meanwhile, circCPSF6 was upregulated in HCC specimens, and elevated circCPSF6 expression served as an independent prognostic factor for worse survival of patients with HCC. 	Yes	 Loss-of-function assays demonstrated that circCPSF6 maintained cell proliferation and tumorigenicity and reinforced cell motility and tumor metastasis. Functionally, removal of YAP1 reversed the effects of circCPSF6 in vitro and in vivo. 	34916222
hsa_circ_0040705	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and HCC cells	Interaction( miR-557/SOX2 )	Western Blot//CCK8//qRT-PCR//Bioinformatics Analysis//Transwell Assay	 The expression levels of circ_0040705 and SOX2 mRNA were markedly increased in HCC tissues, but miR-557 expression was down-regulated. Circ_0040705 worked as a sponge for miR-557 to down-modulate miR-557 expression, and miR-557 could specifically down-modulate SOX2 expression. 		Yes	 Circ_0040705 overexpression enhanced the growth, migration, invasion, and the expressions of E-cadherin and N-cadherin of HCC cells and promoted lung metastasis in vivo, whereas circ_0040705 knockdown exerted the opposite effects in HCC cells. 	35080329
hsa_circ_0051040	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-569/ITGAV )	qRT-PCR	 In this study, we found that hsa_circ_0051040 was overexpressed in HCC tissues and cell lines and that its expression was correlated with poor prognosis. Moreover, our data demonstrated that hsa_circ_0051040 acted as a sponge for miR-569 to regulate ITGAV expression and induce EMT progression. 	 In this study, we found that hsa_circ_0051040 was overexpressed in HCC tissues and cell lines and that its expression was correlated with poor prognosis. 	Yes	 Knockdown of hsa_circ_0051040 inhibited the migration, invasion, and proliferation of HCC cells in vitro and in vivo, whereas overexpression of hsa_circ_0051040 had the opposite effects. 	36429000
circMDK	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-346/874-3p-ATG16L1 )	Bioinformatics Analysis	Hsa_circ_0095868, derived from exon 5 of the MDK gene (named circMDK), was identified as a new oncogenic circRNA that was significantly upregulated in HCC. Mechanistically, circMDK sponged miR-346 and miR-874-3p to upregulate ATG16L1 (Autophagy Related 16 Like 1), resulting to the activation of PI3K/AKT/mTOR signaling pathway to promote cell proliferation, migration and invasion. 	The upregulation of circMDK was associated with the modification of N6-methyladenosine (m6A) and poor survival in HCC patients.	Yes	Mechanistically, circMDK sponged miR-346 and miR-874-3p to upregulate ATG16L1 (Autophagy Related 16 Like 1), resulting to the activation of PI3K/AKT/mTOR signaling pathway to promote cell proliferation, migration and invasion. 	35524319
hsa_circ_0067835	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues and HCC cell lines	Interaction(miR-1236-3p/Twist2 Axis)	qRT-PCR	In this study, our results of microarray and real-time PCR (RT-PCR) showed that it was obviously elevated in human HCC tumor tissues and HCC cell lines. Inhibition of circ_0067835 restrained cell proliferation and migration in vitro. Furthermore, miR-1236-3p was decreased in tumor samples, and it was indicated to be a target of circ_0067835. Moreover, Twist2 was established to be elevated in HCC tissues, and we identified it as the direct target of miR-1236-3p. Finally, we found that knockdown of miR-1236-3p could reverse the circ_0067835 inhibition effects in HCC cells. In conclusion, our study demonstrated that circ_0067835 contributed to promoting hepatocellular carcinoma cell proliferation and metastasis through downregulating miR-1236-3p expression and then elevating Twist2 expression, which might provide a new vision for HCC patients.		Yes	Inhibition of circ_0067835 restrained cell proliferation and migration in vitro.	36262967
circGPR137B	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC and adjacent normal tissues	Interaction(CircGPR137B/miR-4739/FTO feedback loop)	qRT-PCR	We identified a new dramatically downregulated circGPR137B in HCC tissues, and found that downregulation of circGPR137B or upregulation of miR-4739 was associated with poor prognosis in patients with HCC. Ectopic expression of circGPR137B strikingly repressed the proliferation, colony formation and invasion, whereas knockdown of circGPR137B harbored the opposite effects. Moreover, restored expression of circGPR137B inhibited tumor growth and lung metastasis in vivo. Further investigations showed that circGPR137B, co-localized with miR-4739 in the cytoplasm, acted as a sponge for miR-4739 to upregulate its target FTO, which mediated m6A demethylation of circGPR137B and promoted its expression. Thus, a feedback loop comprising circGPR137B/miR-4739/FTO axis was formed. FTO suppressed cell growth and indicated favorable survival in patients with HCC.	FTO suppressed cell growth and indicated favorable survival in patients with HCC.We identified a new dramatically downregulated circGPR137B in HCC tissues, and found that downregulation of circGPR137B or upregulation of miR-4739 was associated with poor prognosis in patients with HCC.	Yes	Ectopic expression of circGPR137B strikingly repressed the proliferation, colony formation and invasion, whereas knockdown of circGPR137B harbored the opposite effects.	35858900
circSETD2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	liver cancer tissues	Expression(lower expressed)	Bioinformatics Analysis	This study found that circular RNA circ SET domain containing 2 (circSETD2) is abnormally expressed in liver cancer tissues, but the role and molecular mechanismsin the occurrence and development of liver cancer are still unclear. The expression level of circSETD2 was evaluated through Quantitative Real-time Polymerase chain reaction (qRT-PCR) in cancerous liver tissues (30 cases), liver cancer cell lines and para-cancerous tissues. Knockdown and overexpression circSETD2 lentiviral vector was constructed and applied to transfect hepatoma cells. Cell Counting Kit-8 (CCK-8), colony formation assay, flow cytometry and Transwell assay were used to examine the effects of circSETD2 overexpression or knockdown on liver cancer migration, invasion, cell cycle and cell proliferation. The tumourigenicity in vivo was utilized to assess the effect of circSETD2 on the proliferation of liver cancer cells. circSETD2 expression is lower in cell lines and liver cancer tissues. circSETD2 knockdown can considerably increase liver cancer cells' invasion, proliferation and colony formation. While In vitro and in vivo, circSETD2 overexpression shows opposite effect. Western blot showed that circSETD2 knockdown can considerably promote E-cadherin expression and inhibit Vimentin, N-cadherin, matrix metallopeptidase-9 (MMP-9) and MMP-2 expression.		Yes	circSETD2 knockdown can considerably increase liver cancer cells' invasion, proliferation and colony formation. While In vitro and in vivo, circSETD2 overexpression shows opposite effect. 	35260047
hsa_circ_0008583	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-1301-3p/METTL3 pathway)	qRT-PCR	Our data showed that hsa_circ_0008583 was upregulated in HCC tissues and cells.  MiR-1301-3p is directly bound to hsa_circ_0008583 and METTL3. MiR-1301-3p overexpression or METTL3 knockdown could partially counteract hsa_circ_0008583 overexpression-mediated influence on HCC cell behaviors. In addition, hsa_circ_0008583 depletion inhibits HCC tumor growth in vivo. In conclusion, hsa_circ_0008583 promotes HCC progression through the miR-1301-3p/METTL3 axis.		Yes	Hsa_circ_0008583 overexpression promoted Hep3B cell proliferation, migration and invasion, but hsa_circ_0008583 silencing had an opposing influence.	35258395
circACTG1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(miR-940/RIF1 Axis /miR-940/RIF1 Axis )	qRT-PCR	circACTG1 was overexpressed in HCC cells and tissues.  Significantly, circACTG1 was discovered to serve as a miR-940 sponge. miR-940 activation rebated the circACTG1 level, and conversely, miR-940 inhibition boosted the circACTG1 level. However, this effect or relationship was not seen after circACTG1 mutation. Furtherly, miR-940-downregulated expression was also found in HCC patients, and importantly, miR-940 inhibition reversed circACTG1 expression in 97H cells with circACTG1 knockdown. Moreover, the expression of RIF1 was significantly reduced after inhibiting circACTG1 or overexpressing miR-940 but rescued when both circACTG1 and miR-940 were inhibited. Finally, circACTG1 and miR-940 played significant roles of regulating AKT-mTOR signaling.		Yes	Knockdown of circACTG1 restrained 97H and Huh7 cell migration and invasion. 	35769514
circZEB1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-199a-3p/PIK3CA )	qRT-PCR	 Circ-ZEB1 and PIK3CA were upregulated in HCC and predicted a poor prognosis. MiR-199a-3p blocked the effect of circ-ZEB1 on HCC. Circ-ZEB1 served as a biomarker of HCC. Circ-ZEB1 promoted the expression of PIK3CA by silencing miR-199a-3p to affect the progress of HCC.	 Circ-ZEB1 and PIK3CA were upregulated in HCC and predicted a poor prognosis. 	Yes	MiR-199a-3p showed low expression in HCC, whereas downregulation of circ-ZEB1 reduced HCC cell proliferation and promoted cell apoptosis. 	35277182
circSEC24A	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCCLM3 and Hep3B cells	Interaction(miR-421/MMP3 axis)	qRT-PCR	circSEC24A expression was significantly upregulated in HCCLM3 and Hep3B cells. Meanwhile, MMP3 could bind to miR-421 to decrease the functional effects of miR-421 and induce tumor metastasis. circSEC24A interference suppressed HCC cell EMT by sponging miR-421, further regulating MMP3, and inhibiting tumor growth in vivo. 		Yes	Silencing circSEC24A mitigated the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of HCC cells, which was abrogated by downregulation of miR-421.  Knockdown of cicSEC24A suppressed tumor growth in vivo. 	35400271
circUBAP2	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	regulation[ miR-382-5p/PRPF8 axis]	qRT-PCR	 circRNA-UBAP2 was upregulated in ovarian cancer tissues and cell lines. circRNA-UBAP2 acted as a ceRNA to sponged miR-382-5p, increased the expression level of PRPF8, and prompted proliferation and inhibited apoptosis in ovarian cancer cells.		Yes	Knockdown of circRNA-UBAP2 inhibited cell proliferation and promoted cell apoptosis, but circRNA-UBAP2 overexpressed got opposite results. 	32690086
hsa_circ_9119	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	regulation[microRNA-21-5p-PTEN-Akt pathway]	qRT-PCR//Luciferase Report Assay	The expression of circ9119 was clearly reduced in OC tissues and cell lines, whereas the microRNA-21-5p (miR-21) levels were elevated compared with those in normal healthy control tissues and immortalized fallopian epithelial cell line FTE187. Thus, circ9119 could regulate cell proliferation and apoptosis of OC cells via by acting as an miR-21 sponge and targeting the PTEN-Akt pathway.		Yes	Further, circ9119 was overexpressed, causing a notable decrease in the viability and proliferation of OC cells and an increase in apoptosis.	32675386
circFGFR3	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	regulation[miR-29a-3p/E2F1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Our results showed that circFGFR3 expression was higher in OC cells and tissues than in normal ovarian cells and adjacent normal tissues; Therefore, circFGFR3 serves as a promoter of OC by inducing OC cell EMT via the miR-29a-3p/E2F1 axis and circFGFR3 may be a prognostic biomarker for OC patients.	Our results showed that circFGFR3 expression was higher in OC cells and tissues than in normal ovarian cells and adjacent normal tissues; in addition, in OC patients, a high level of CircFGFR3 was related to lower survival rates and higher recurrence rates than a low level of circFGFR3. 	Yes	CircFGFR3 overexpression promotes OC progression by inducing epithelial-mesenchymal transition (EMT) in vitro.	32668414
circCELSR1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cells	regulation[miR-598 ,BRD4 ]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	circCELSR1 and BRD4 were promoted, but miR-598 was suppressed in various ovarian cancer cells. Knockdown of circCELSR1 inhibited BRD4-mediated proliferation/migration related signaling via sponging miR-598, thereby repressing ovarian cancer progression.		Yes	 Knockdown of circCELSR1 suppressed proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), but promoted apoptosis in ovarian cancer cells, and these effects were reversed by miR-598 inhibition or BRD4 overexpression.	32640974
hsa_circ_0009910	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-145 ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Hsa_circ_0009910, representing unfavorable prognosis, induced proliferative and motile phenotypes by suppressing miR-145 in ovarian cancer cells.		Yes	The ovarian cancer cell phenotypes were promoted by hsa_circ_0009910 while repressed by silencing hsa_circ_0009910.	32588730
hsa_circ_102958	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	regulation[miR-1205/SH2D3A Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	hsa_circRNA_102958 was upregulated in OC tissues and cell lines.Our data suggest that hsa_circRNA_102958 promotes OC aggravation through regulation of miR-1205/SH2D3A signaling.	hsa_circRNA_102958 upregulation indicated a poor prognosis in OC patients. 	Yes	Knockdown of hsa_circRNA_102958 significantly suppressed the proliferation, migration and invasion of OC cells and vice versa. 	32547237
hsa_circ_0078607	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-518a-5p/Fas signaling pathway]	qRT-PCR//Luciferase Report Assay	In the present study, we first found that circ_0078607 was downregulated in ovarian cancer. The results of the present study revealed that circ_0078607 suppressed ovarian cancer progression by sponging oncogenic miR-518a-5p to induce Fas expression, which may provide new therapeutic approach for ovarian cancer.		Yes	 Forced circ_0078607 expression significantly suppressed proliferation and promoted apoptosis of ovarian cancer cells.	32503653
circMYLK	CircRNA	Homo sapiens	Ovarian Neoplasms	OC  tissue 	regulation[microRNA-652]	CCK8//qRT-PCR//Luciferase Report Assay	qPCR results indicated that circRNA_MYLK level in OC patients was remarkably higher than that in adjacent ones, and the difference was statistically significant. CircRNA_MYLK may promote the malignant progression of OC via regulating microRNA-652, and its expression was remarkably associated with pathological staging and poor prognosis in patients with OC.	Compared with patients with low expression of circRNA_MYLK, patients with high expression of circRNA_MYLK had a higher pathological staging and a lower overall survival rate.	Yes	 Compared with the control group (sh-NC), the OC cell proliferation ability was remarkably attenuated in the circRNA_MYLK knockdown group (sh-circRNA).	32495861
hsa_circ_0004390	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-198/MET axis]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	We further identified one circRNA derived from the LPAR3 gene and termed Circ0004390, which was frequently upregulated in ovarian cancer tissues. Our findings suggested that Circ0004390 regulated ovarian cancer proliferation by miR-198/MET axis, which might provide a potential target for the treatment of ovarian cancer.		Yes	The knockdown of Circ0004390 can significantly reduce the proliferation of ovarian cancer cells. 	32192774
circPGAM1	CircRNA	Homo sapiens	Ovarian Neoplasms	EOC tissues	regulation[miR-542-3p/CDC5L/PEAK1 pathway]	ChIP//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Circ-PGAM1 was upregulated in EOC tissues, whereas linear PGAM1 was not deregulated in EOC tissues.The circ-PGAM1/miR-542-3p/CDC5L/PEAK1 pathway played an important role in the progression of ovarian cancer and might be a novel therapeutic target for ovarian cancer.		Yes	Silencing of circ-PAGM1 inhibited proliferation, migration, and invasion of ovarian cancer cells and promoted cell apoptosis. 	32167655
hsa_circ_0013958	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cells	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 Hsa_circ_0013958 was highly expressed in ovarian cancer tissues and cells, and its expression was closely related to patient FIGO stage and lymph node metastasis.	 Hsa_circ_0013958 was highly expressed in ovarian cancer tissues and cells, and its expression was closely related to patient FIGO stage and lymph node metastasis.	Yes	Further, in vitro studies showed that knockdown of hsa_circ_0013958 suppressed proliferation, migration, and invasion of ovarian cancer cells but elevated the cell apoptotic rate. 	32157748
hsa_circ_0007874	CircRNA	Homo sapiens	Ovarian Neoplasms	OVA cell lines	regulation[miR-760/SOCS3 pathway]	qRT-PCR//Luciferase Report Assay//FISH	Results verified that hsa_circ_0007874 is downregulated in OVA cell lines. In summary, the data suggest that hsa_circ_0007874 acts as a tumor suppressor by regulating the miR-760/SOCS3 axis, highlighting its potential as an effective therapeutic target for OVA.		Yes	hsa_circ_0007874 overexpression decreased the OVA cell migration and proliferation in vitro and in vivo. 	32023009
hsa_circ_100395	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues 	regulation[miR-1228/p53/EMT axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The expression of circ_100395 was found to be significantly down-regulated in ovarian cancer, while low expression of circ_100395 was highly correlated with the poor outcomes.CircRNA_100395 could inhibit cell growth and metastasis of ovarian cancer cells via regulating the miR-1228/p53/EMT axis.	The expression of circ_100395 was found to be significantly down-regulated in ovarian cancer, while low expression of circ_100395 was highly correlated with the poor outcomes.	Yes	In addition, upregulation of circ_100395 could significantly inhibit tumor growth, metastasis and EMT signaling pathway in ovarian cancer. 	31942183
circLARP4	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian epithelial cells	regulation[miR-513b-5p/LARP4 axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of circ_LARP4 in OC cells was much lower than that in human normal ovarian epithelial cells. Circ_LARP4 could hamper cell proliferation and migration by sponging miR-513b-5p to regulate the expression of LARP4.		Yes	Overexpressing circ_LARP4 impaired cell proliferation, invasion and migration abilities.	31911757
circNFATC3	CircRNA	Homo sapiens	Ovarian Neoplasms	cell lines 	Regulation(up regulation)	Migration Assay//CCK8//qRT-PCR//RNA-seq//Invasion Assay	Breast and ovarian cancer cells showed a greater abundance of circNFATC3 compared to normal breast cell lines, lung fibroblast cells, and LCL cells.		Yes	The knockdown of circNFATC3 induces a reduction in cell proliferation, invasion, migration, and oxidative phosphorylation. Gain-of-function of circNFATC3 in MDA-MB-231 and SK-OV-3 cells show a significant increase in cell proliferation, migration, and respiration. 	33816459
circRAB11FIP1	CircRNA	Homo sapiens	Ovarian Neoplasms	epithelial ovarian cancer (EOC) tissues	Interaction(miR-129/DSC1)	FISH//Co-IP//EdU Staining//Western Blot	 CircRAB11FIP1 expression was elevated in epithelial ovarian cancer (EOC) tissues than in normal ovarian tissues. Also, circRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. 		Yes	 Silencing circRAB11FIP1 inhibited the autophagic flux of ovarian cancer SKOV3 cells. However, circRAB11FIP1 overexpression activated the autophagic flux of ovarian cancer A2780 cells. 	33637694
circLOPD2	CircRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer (OC) tissues	Interaction(miR-378 )	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	The results showed that circ-LOPD2 was highly expressed in ovarian cancer (OC) tissues, circ-LOPD2 expression levels were higher in OVCAR3 and A2780, and circ-LOPD2 expression levels in CAOV3 were lower. We also found that miR-378 is a target of circ-LOPD2. Silencing circ-LOPD2 will increase the expression of miR-378, and overexpression of circ-LOPD2 will decrease the expression of miR-378. 		Yes	After silencing circ-LOPD2, the growth ability of OVCAR3 and A2780 cells decreased, while overexpression of circ-LOPD2 led to the opposite result. 	34759745
hsa_circ_0000554	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian tumor specimens and cells	Interaction( miR-567)	qRT-PCR//Luciferase Report Assay//Invasion Assay	We illustrated that miR-567 was downregulated in ovarian tumor specimens and cells. circ_0000554 was negatively correlated with miR-567 in ovarian tumor specimens.  circ_0000554 sponged miR-567 expression in ovarian tumor. RIP assay showed that elevated expression of miR-567 could be enriched with circ_0000554		Yes	 Elevated expression of circ_0000554 suppressed miR-567 expression in HO8910 cell. circ_0000554 promoted ovarian tumor cell growth, invasion, and EMT via sponging miR-567. 	34709546
hsa_circ_0007841	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Interaction(miR-151-3p/MEX3C axis )	qRT-PCR//Luciferase Report Assay//RIP//Transwell Assay	In the current study, it was found that circ_0007841 expression was upregulated in ovarian cancer tissues and cell lines.  In terms of mechanism, circ_0007841 worked as a competing endogenous RNA (ceRNA) for miR-151-3p to facilitate MEX3C expression. Restoration of MEX3C level recovered the proliferation, migration and invasion of ovarian cancer cells. 	Upregulation of circ_0007841 in patients with ovarian cancer predicts poor prognosis.	Yes	Loss-of-function experiments discovered that circ_0007841 knockdown suppressed the proliferation, migration and invasion of ovarian cancer cells in vitro and in vivo. 	33896797
circRHOBTB3	CircRNA	Homo sapiens	Ovarian Neoplasms		regulation[PI3K/AKT signaling pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	CircRHOBTB3 exerted a suppressor role and inhibited the tumorigenesis by inactivating PI3K/AKT pathway in ovarian cancer.		Yes	 Functionally, circRHOBTB3 overexpression could markedly suppress cell proliferation, metastasis and glycolysis, whereas the opposite results could be observed in the deletion of circRHOBTB3.	32720791
circMTO1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	regulation[ miR-182-5p/KLF15 Axis]	qRT-PCR	We demonstrated that circMTO1 was downregulated in ovarian cancer tissues and cell lines. Mechanistically, we showed that circMTO1 sponged miR-182-5p to support KLF15 expression, eventually leading to inhibition of ovarian cancer progression. 		Yes	 Upregulation of circMTO1 inhibited proliferation and invasion of ovarian cancer cells while downregulation of circMTO1 promoted these processes.	32731816
circEXOC6B	CircRNA	Homo sapiens	Ovarian Neoplasms	cell lines	regulation[ miR-421,RUS1 ]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	As shown in Figure 1A, the level of circEXOC6B was significantly decreased in SKOV3 and OVCAR3 cells, compared with that in IOSE80 cells. In this study, we found that circEXOC6B suppressed the growth of ovarian cancer cells through upregulating RSU1 partially via sponging miR-421. 		Yes	 Downregulation of circEXOC6B markedly promoted the proliferation and invasion in A2780 cells. In contrast, upregulation of circEXOC6B significantly inhibited the proliferation and invasion in SKOV3 cells. Moreover, overexpression of circEXOC6B obviously induced the apoptosis of SKOV3 cells.	32884301
circPLEKHM3	CircRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer tissues 	Regulation[miR-9/BRCA1/DNAJB6/KLF4/AKT1 axis]	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Transwell Assay	CircPLEKHM3 was identified as one of the most significantly down-regulated circRNAs in ovarian cancer tissues compared with normal tissues.  Further analyses showed that circPLEKHM3 sponged miR-9 to regulate the endogenous expression of BRCA1, DNAJB6 and KLF4, and consequently inactivate AKT1 signaling. In addition, AKT inhibitor MK-2206 could block the tumor-promoting effect of circPLEKHM3 depletion, and potentiate Taxol-induced growth inhibition of ovarian cancer cells.		Yes	Functionally, circPLEKHM3 overexpression inhibited cell growth, migration and epithelial-mesenchymal transition, whereas its knockdown exerted an opposite role.	31623606
hsa_circ_0003945	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue and cells	Interaction(miR-34c-5p/LGR4/β-catenin axis activity)	qRT-PCR	In this study, we found that Circ_0003945 was upregulated in HCC tissue, and higher Circ_0003945 expression was positively correlated with tumour size and tumour stage. Furthermore, high plasma levels of circulating Circ_0003945 were confirmed in HCC patients compared with those in non-HCC groups. Mechanistically, Circ_0003945 might exert as a miR-34c-5p sponge to upregulate the expression of leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4), activating the β-catenin pathway, and finally facilitating HCC progression. Additionally, a β-catenin activator could reverse the effect of Circ_0003945 knockdown. 	In this study, we found that Circ_0003945 was upregulated in HCC tissue, and higher Circ_0003945 expression was positively correlated with tumour size and tumour stage. 	Yes	 The functional experiments revealed that overexpression or knockdown of Circ_0003945 promoted or attenuated tumour growth and migration, respectively. 	35170199
circCBFB	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,. HCC cell 	Interaction(miR-424-5p/ATG14 axis)	qRT-PCR	In HCC tissues, circCBFB and ATG14 were highly expressed, and miR-424-5p expression was downregulated.  miR-424-5p was a target gene of circCBFB, and miR-424-5p negatively mediated ATG14. CircCBFB inhibits miR-424-5p and upregulates ATG14, thus promoting HCC cell proliferation and autophagy.		Yes	 Transfection of pcDNA3.1-CircCBFB, miR-424-5p inhibitor, or pcDNA3.1-ATG14 into HCC cells facilitated HCC cell proliferation and autophagy, while suppressing cell apoptosis, evidenced by elevated cell viability, increased protein levels of autophagosome markers (LC3-ΙΙ/LC3-Ι and Beclin1), repressed apoptosis rate, and suppressed protein level of autophagy receptor p62. 	35066780
hsa_circ_0008934	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-1305/TMTC3 axis)	qRT-PCR	 In this study, circ_0008934 expression was found to be significantly upregulated in HCC tissues and cell lines by qRT-PCR. Mechanically, circ_0008934 was a sponge of miR-1305 to facilitate the TMTC3 expression, and the TMTC3 expression in HCC tissues was negatively associated with the survival of HCC patients. Furthermore, rescued assays revealed that the circ_0008934 facilitated HCC proliferation, invasion and migration by regulating miR-1305/ TMTC3 signaling pathways. 	High level of circ_0008934 is closely associated with higher serum AFP (P < 0.001), larger tumor diameter (P = 0.012), microvascular invasion (P = 0.008) and poorer prognosis (P = 0.007) of HCC patients.	Yes	Functionally, knockdown of circ_0008934 inhibited HCC cell proliferation, invasion and migration in vitro and vivo. 	35015267
hsa_circ_0001955	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction( circ_0001955/miR-655-3p/ACER3)	qRT-PCR	Circ_0001955 was highly expression in HCC tissues and cells.Mechanistically, circ_0001955 could competitively sponge miR-655-3p, which targeted ACER3. Besides that, miR-655-3p silencing abolished the anticancer action of circ_0001955 silencing on HCC cells. Moreover, miR-655-3p overexpression inhibited HCC cell oncogenic phenotypes mentioned above, which were attenuated by ACER3 up-regulation. Additionally, circ_0001955 knockdown also impeded HCC growth in a mouse model.		Yes	Functionally, circ_0001955 deletion suppressed HCC tumorigenesis in vitro by suppressing cell growth, metastasis and angiogenesis.	35034572
circRERE	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells	Interaction(miR-1299 or ZC3H13 )	qRT-PCR	The expression of circRERE was significantly upregulated in HCC cells, and its downregulation reduced HCC cell viability and invasion while increasing apoptosis.  Further study showed that circRERE bound directly to miR- 1299. After downregulating the expression of circRERE, miR-1299 expression was significantly enhanced, while the expression of its downstream target gene GBX2 was suppressed, indicating that circRERE promoted the expression of GBX2 through miR-1299.		Yes	The expression of circRERE was significantly upregulated in HCC cells, and its downregulation reduced HCC cell viability and invasion while increasing apoptosis. 	36222159
hsa_circ_0008092	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-502-5p/CCND1 Axis)	qRT-PCR	Circ_0008092 was highly expressed in HCC tissues and cells, which was associated with a shorter survival time in patients with HCC. Circ_0008092 directly targeted miR-502-5p and negatively modulated miR-502-5p expression. CCND1 Conclusion: Our data suggest that circ_0008092 promotes HCC progression by regulating the miR- 502-5p/CCND1 axis.		Yes	 Circ_0008092 overexpression promoted proliferation, migration and invasion, and inhibited apoptosis of HCC cells; circ_0008092 knockdown worked oppositely. 	35899951
hsa_circ_0061140	CircRNA	Homo sapiens	Ovarian Neoplasms	cell lines	Regulation[miR-370/FOXM1 pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	Our results showed that hsa_circ_0061140 was upregulated in ovarian cancer cell lines. Thus, hsa_circ_0061140 appeared to function as a competing endogenous RNA of miR-370 that promoted cell growth and metastasis in ovarian cancer through regulation of the miR-370/FOXM1 pathway mediating EMT.		Yes	 Knockdown of hsa_circ_0061140 suppressed cell proliferation and migration, both in vivo and in vitro, by inhibiting FOXM1 expression through sponging miR-370.	30236833
circWHSC1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Interaction[sponging miR-145 and miR-1182]	RNA Pull-Down//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	We found that circWHSC1 was up-regulated in ovarian cancer tissues.Additionally, circWHSC1 could sponge miR-145 and miR-1182 and up-regulate the expression of downstream targets MUC1 and hTERT. Exosomal circWHSC1 can be transferred to peritoneal mesothelial cells and promotes peritoneal dissemination.	We found that circWHSC1 was up-regulated in ovarian cancer tissues, and circWHSC1 expression was higher in moderate & poor differentiation ovarian cancer tissues than in well differentiation ovarian cancer tissues.	Yes	Overexpression of circWHSC1 increased cell proliferation, migration and invasion, and inhibited cell apoptosis. Silence of circWHSC1 exerted the opposite effects. 	31666098
hsa_circ_0051240	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Regulation[miR-637/KLK4 axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	In this study, we identified hsa_circ_0051240 was significantly increased in ovarian cancer (OC) tissues. In addition, the inhibitory effects by blockage of hsa_circ_0051240 could be attenuated by the miR-637 inhibitor. Furthermore, we also identified that hsa_circ_0051240 act as a sponge of miR-637, and miR-637 directly targeted KLK4 mRNA in OC cells. Altogether, hsa_circ_0051240 promotes OC cell proliferation, migration and invasion through inhibiting the miR-637/KLK4 axis. Therefore, these results demonstrated that the hsa_circ_0051240/miR-637/KLK4 axis might serve as a therapeutic target for OC treatment.		Yes	 Our results indicated that silencing of hsa_circ_0051240 inhibited OC cell proliferation, migration and invasion in vitro, and also prevented OC tumour formation in vivo.	30945557
circKRT7	CircRNA	Homo sapiens	Ovarian Neoplasms	Ovarian cancer tissues,cell lines	regulation[circKRT7-miR-29a-3p-COL1A1 Axis ]	Western Blot//Wound Healing Assay//Colony Formation Assay//qRT-PCR//FISH//Luciferase Report Assay//IHC//Invasion Assay	Our previous research found that KRT7 was abnormally highly expressed in ovarian cancer and plays a role in the progression of ovarian cancer.We found that circKRT7 can promote the proliferation and metastasis of ovarian cancer cells by absorbing miR-29a-3p, which leads to the up-regulation of COL1A1.		Yes	 In vitro, knock-down of circKRT7 can inhibit the migration and invasion of ovarian cancer cells. In vivo experiments, the reduction of circKRT7 expression can also slow tumor growth, and this inhibition was partly counteracted after miR-29a-3p repression.	32982288
circPUM1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Interaction[Sponging miR-615-5p and miR-6753-5p]	qRT-PCR//Luciferase Report Assay	 qRT-PCR analysis showed upregulation of circPUM1 in ovarian cancer tissues compared with normal ovaries.  Bioinformatics analysis and dual-luciferase reporter assays revealed that circPUM1 upregulated the expression of nuclear factor kappa B (NF-κB) and MMP2 by sponging miR-615-5p and miR-6753-5p. Further studies showed that exosomal circPUM1 acted on peritoneal mesothelial cells and increased tumor metastasis. In conclusion, our study indicates that circPUM1 not only promotes ovarian cancer proliferation, migration and invasion, but also acts on the peritoneum and contributes to metastasis of cancer in the form of cancer-derived exosomes.		Yes	Gain- and loss-of-function experiments indicated that circPUM1 increased cell proliferation, migration, and invasion and inhibited cell apoptosis. Intraperitoneal injection of circPUM1-knockout tumor cells in nude mice resulted in a decrease in the metastatic ability of the tumor. 	31751911
hsa-circ-001567	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	Expression[highly expressed]	qRT-PCR	The results showed that VPS13C-has-circ-001567 was expressed at significantly higher levels in OC tumor tissues compared with pericarcinous tissues, and this overexpression was associated with tumor node metastasis stage and lymph node metastasis.	The results showed that VPS13C-has-circ-001567 was expressed at significantly higher levels in OC tumor tissues compared with pericarcinous tissues, and this overexpression was associated with tumor node metastasis stage and lymph node metastasis.	Yes	We found that knockdown of VPS13C-has-circ-001567 significantly promoted apoptosis and inhibited the proliferation of SKOV3 and OV-1063 cells in vitro.Knockdown of VPS13C-has-circ-001567 significantly reduced the tumorigenicity of OC cells.	30376358
circFAM53B	CircRNA	Homo sapiens	Ovarian Neoplasms	OC tissues,cell lines	Regulation[miR‑646/VAMP2 and miR‑647/MDM2 signaling pathways]	qRT-PCR	circ‑FAM53B was overexpressed in OC specimens and cells and correlated with clinical severity and poor prognosis of OC patients.Collectively, the present results indicated that circ‑FAM53B could be a competing endogenous RNA (ceRNA) to competitively sponge miR‑646 and miR‑647 to upregulate VAMP2 and MDM2 expression at the post‑transcriptional level, thus mediating the cellular behaviors of OC cells.	circ‑FAM53B was overexpressed in OC specimens and cells and correlated with clinical severity and poor prognosis of OC patients. 	Yes	Subsequently, the regulatory effects of circ‑FAM53B on the proliferative, apoptotic, migratory, and invasive potential of OC cells were determined by loss/gain‑of‑function experiments.	31638250
circEPSTI1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Interaction[sponging miR-942]	RIP//Luciferase Report Assay//qRT-PCR	qRT-PCR verified that circEPSTI1 was overexpressed in ovarian cancer. In summary, circEPSTI1 regulated EPSTI1 expression and ovarian cancer progression by sponging miR-942. 		Yes	 Inhibition of circEPSTI1 suppressed ovarian cancer cell proliferation, invasion but promoted cell apoptosis.	30887698
circRhoC	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues 	Interaction[VEGFA]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	 Our results showed that circRhoC was significantly up-regulated in ovarian cancer tissues compared to normal ovarian tissues.In conclusion, the oncogenic effect of RhoC in ovarian cancer is at least in part due to circRhoC, which functions not only as a miR-302e sponge to positively regulate VEGFA protein expression, but may also directly bind and modulate VEGFA expression.		Yes	Overexpression of circRhoC in CAOV3 ovarian cancer cell increased cell viability, migration and invasion ability; destroying circRhoC in A2780 had the opposite effects and inhibited ovarian tumour cell A2780 dissemination in the peritoneum in vivo.	31639291
circCSPP1	CircRNA	Homo sapiens	Ovarian Neoplasms	ovarian cance tissues	Interaction[as a miR-1236-3p sponge ]	qRT-PCR	Here, using quantitative reverse transcription (qRT)-PCR, we showed that circ-CSPP1 is highly expressed in ovarian cancer (OC) tissues. Altogether, our findings suggest that by acting as a miR-1236-3p sponge, circ-CSPP1 impairs the inhibitory effect of miR-1236-3p on ZEB1, which subsequently promotes EMT and OC development.		Yes	Subsequent silencing of circ-CSPP1 in OVCAR3 and A2780 cell lines revealed decreased cell growth, migration and invasion, while overexpression of circ-CSPP1 caused opposite results We also found that miR-1236-3p is a target of circ-CSPP1.	30965236
circSFMBT2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	tissues	Interaction(miR-665/TIMP3 axis)	qRT-PCR	 In this study, we identified that a novel circRNA, circSFMBT2, was markedly downregulated by HBx.  The mechanism of circSFMBT2 was to as a sponge of miR-665, which is a negative regulator of tissue inhibitor of metalloproteinases 3 (TIMP3). However, HBx downregulated circSFMBT2 via the interaction with DExH-box helicase 9 (DHX9), which binds to flanking circRNA-forming introns. 	Low expression of circSFMBT2 was correlated with poor prognosis and vascular invasion. 	Yes	Functionally, overexpression of circSFMBT2 significantly inhibited HCC metastasis both in vitro and in vivo. 	36159591
hsa_circ_002178	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation(SRSF1)	qRT-PCR	 GEO2R-based analysis displayed that hsa_circRNA_002178 was upregulated in HCC tissues.echanically, hsa_circRNA_002178 bound to SRSF1 3'-untranslated region (UTR) and stabilized its expression. SRSF1 weakening eliminated the effects of pcDNA-hsa_circRNA_002178 on cell malignant behavior.		Yes	Overexpression or knockdown of hsa_circRNA_002178 encouraged or impeded HCC cell proliferation, migration, invasion, and EMT program.  Finally, the knockdown of hsa_circRNA_002178 was confirmed to prevent xenograft tumor growth.	36065311
hsa_circ_0000711	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissues	interaction[targeting has-miR-103a-3p]	CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	Based on the circRNA expression profile and RT-qPCR results, the expression level of hsa_circ_0000711 was overtly reduced in HCC tissues.  Overexpression of hsa_circ_0000711 promoted the proliferation and inhibited the apoptosis of hepatoma cells via targeting has-miR-103a-3p.		Yes	 The results of CCK-8 and EdU staining assays revealed that the proliferation of hepatoma cells in hsa_circ_0000711 overexpression group was evidently enhanced. 	32373952
circSP3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	50 HCC tissues and matched adjacent nontumorous liver tissues 	Interaction(miR-198)	Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Invasion Assay//Transwell Assay	By analyzing relevant circRNA databases (circBase, TargetScan and CircInteractome), we found that the miR-198-binding circRNA hsa_circSP3 is upregulated in HCC. CircSP3 expression correlated negatively with miR-198 expression in HCC tissues.  Dual luciferase reporter assays indicated that circSP3 bound to miR-198. 		Yes	CircSP3 overexpression in HCC cells induced expression of cyclin-dependent kinase 4, a target gene of miR-198. Silencing circSP3 inhibited HCC cell proliferation and migration by downregulating cyclin-dependent kinase 4, whereas inhibiting miR-198 reversed those effects. In vivo experiments confirmed that circSP3 promoted xenograft tumor growth. 	34314379
circSLC7A11	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	Human tumor samples and The human HCC cell lines HepG2, Hep3B, HCCLM3, Huh7, and MHCC97H, and the immortalized hepatocyte cell line WRL68	Interaction(miR-330-3p/CDK1 axis)	CCK8//qRT-PCR//Western Blot	CircSLC7A11 (hsa_circ_0070975) was conserved and dramatically overexpressed in HCC tissues and cells. Our in vitro and in vivo experiments showed that circSLC7A11 markedly accelerated HCC progression and metastasis through the circSLC7A11/miR-330-3p/CDK1 axis.	HCC patients showing high circSLC7A11 expression had worse prognoses. 	Yes	Our in vitro and in vivo experiments showed that circSLC7A11 markedly accelerated HCC progression and metastasis through the circSLC7A11/miR-330-3p/CDK1 axis.	34844614
hsa_circ_0005397	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-326/PDK2 axis)	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	Hsa_circ_0005397 and PDK2 were up-regulated, whereas miR-326 was down-regulated in HCC tissues and cells. miR-326 was a direct target of hsa_circ_0005397, and inhibition of miR-326 reversed the inhibitory effect of hsa_circ_0005397 silencing on HCC progression. Moreover, PDK2 was a direct target of miR-326 and PDK2 overexpression abated the anti-cancer roles of miR-326 in HCC. Additionally, hsa_circ_0005397 regulated PDK2 expression by sponging miR-326. 		Yes	Hsa_circ_0005397 knockdown inhibited cell proliferation and metastasis, and promoted apoptosis. miR-326 was a direct target of hsa_circ_0005397, and inhibition of miR-326 reversed the inhibitory effect of hsa_circ_0005397 silencing on HCC progression.	33783904
circEPB41L2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cell linesC	Interaction(miR-590-5p)	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 The clinicopathological analysis revealed that down-regulation of circEPB41L2 was negatively associated with tumor size, vascular invasion and alpha-fetoprotein, while positively correlated with HCC prognosis. Bioinformatic analysis and luciferase reporter assay revealed that circEPB41L2 interacts directly with miR-590-5p and the corresponding biological functions were also verified in miRNA rescue experiments.	 The clinicopathological analysis revealed that down-regulation of circEPB41L2 was negatively associated with tumor size, vascular invasion and alpha-fetoprotein, while positively correlated with HCC prognosis. 	Yes	The biological function experiments showed that overexpression of circEPB41L2 could obviously inhibit the proliferation and metastasis of HCC cells in vitro, while knockdown of circEPB41L2 induced opposite results. Moreover, we also found that circEPB41L2 inhibited HCC migration and invasion though EMT signaling pathway. Similarly, overexpression of circEPB41L2 can also significantly inhibit the proliferation of HCC cells in vivo. 	33833580
circGFRA1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction( miR-498/NAP1L3 axis)	qRT-PCR//IHC//Transwell Assay	CircGFRA1 was greatly increased in HCC tissues and cells, and the over-expression of circGFRA1 was intimately related with the advanced clinical stage and poor survival of HCC patients. The expression of circGFRA1 was negatively correlated with the expression of miR-498, but a positive correlation was found between circGFRA1 and NAP1L3 expression in HCC tissues.	CircGFRA1 was greatly increased in HCC tissues and cells, and the over-expression of circGFRA1 was intimately related with the advanced clinical stage and poor survival of HCC patients. 	Yes	Silencing circGFRA1 inhibited the growth and invasion of hepatocellular carcinoma. Moreover, miR-498 over-expression or NAP1L3 inhibition could abrogate the oncogene role of circGFRA1 in HCC in vivo. 	33431945
hsa_circ_0001806	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells 	Interaction(miR-125b/HK2)	qRT-PCR//Luciferase Report Assay//Western Blot	sa_circ_0001806 was up-regulated in HCC tissues and cells and positively associated with the advanced TNM stage, metastasis and poor overall survival. Furthermore, hsa_circ_0001806 acted as a sponge of miR-125b to up-regulate hexokinase II (HK2) expression. In addition, the inhibition of miR-125b and HK2 overexpression partly reversed the inhibitory effect of hsa_circ_0001806 silencing on HCC cell proliferation, migration and glycolysis.	hsa_circ_0001806 was up-regulated in HCC tissues and cells and positively associated with the advanced TNM stage, metastasis and poor overall survival. 	Yes	 The overexpression of hsa_circ_0001806 promoted HCC cell proliferation, migration and glycolysis and inhibited cell apoptosis, while the silence of hsa_circ_0001806 showed an opposite effect. 	34664737
hsa_circ_0001806	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-193a-5p/MMP16 pathway)	CCK8//qRT-PCR//RIP	Circ_0001806 was up-modulated in HCC tissues and cell lines. Circ_0001806 could up-regulate MMP16 expression through repressing miR-193a-5p, thereby facilitating the malignant biological behaviors of HCC. Circ_0001806 promoted HCC progression by regulating miR-193a-5p/MMP16 axis.		Yes	Knockdown of circ_0001806 impeded the multiplication, migration, and invasion of HCC cells.	34730679
circBACH1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-656-3p/SERBP1)	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	CircBAC- H1 and SERBP1 were upregulated in HCC tissues and cells.SERBP1 overexpression partially neutralized the repressive effect of circBACH1 silencing on malignant behaviors of HCC cells.CircBACH1 sponged miR-656-3p to elevate SERBP1 expression, thereby accelerating the progression of HCC.		Yes	Both circBACH1 and SERBP1 knockdown constrained proliferation, migration, invasion, and EMT(epithel-ial-mesenchymal transition), and facilitated apoptosis of HCC cells in vitro.Knockdo-wn of circBACH1 reduced HCC growth in vivo. 	33831787
circZFR	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell	Interaction(miR-375/HMGA2 Axis)	qRT-PCR//Luciferase Report Assay//RIP	 CircZFR and HMGA2 were upregulated while miR-375 was downregulated in HCC tissues and cells. MiR-375 was a direct target of circZFR and its knockdown reversed the inhibitory effect of circZFR silence on the progression of HCC cells. Moreover, HMGA2 was a downstream target of miR-375, and miR-375 suppressed proliferation and glycolysis and induced apoptosis by targeting HMGA2 in HCC cells. Besides, circZFR acted as a molecular sponge of miR-375 to regulate HMGA2 expression.		Yes	CircZFR silence inhibited HCC progression by inhibiting cell proliferation, glycolysis and tumor growth and promoting apoptosis. 	33433801
circUBAP2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-4756/IFIT1/3 axis)	qRT-PCR//MTT//IHC//IF	CXCL11 stimulation upregulated circUBAP2 expression, which was significantly higher in HCC tissues than para-carcinoma tissues. Further downstream, the IFIT1 and IFIT3 levels were significantly upregulated in HCC cells upon CXCL11 stimulation, but downregulated upon circUBAP2 silencing. IFIT1 or IFIT3 silencing reduced the expression of IL-17 and IL-1β, and attenuated the migration capability of HCC cells. Herein, circUBAP2 counteracted miR-4756-mediated inhibition on IFIT1/3 via sponging miR-4756. miR-4756 inhibition reversed the effects induced by circUBAP2 silencing on the IL-17 and IL-1β levels and HCC cell migration. In orthotopic models, miR-4756 inhibition also reversed the effects on metastatic progression induced by silencing circUBAP2.		Yes	Silencing circUBAP2 reversed the effects of CXCL11 on the expression of IL-1β/IL-17 and HCC cell migration. 	33707417
circUBE2J2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(microRNA-370-5P/KLF7)	Western Blot//qRT-PCR//RIP//FISH//IHC	CircUBE2J2 expression in HCC cells was selectively regulated via luciferase reporter assays; circUBE2J2 and KLF7 were observed to directly bind to miR-370-5P. Furthermore, knockdown of circUBE2J2 in HCC could downregulate KLF7, the target of miR-370-5P, thus promoting the proliferation and migration of HCC cells.  Then the related experiment suggested that circUBE2J2 could regulate the expression of KLF7 by sponging miR-370-5p. 		Yes	Furthermore, knockdown of circUBE2J2 in HCC could downregulate KLF7, the target of miR-370-5P, thus promoting the proliferation and migration of HCC cells. 	34686662
hsa_circ_0058493	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC patients	Interaction(METTL3-hsa_circ_0058493-YTHDC1 )	qRT-PCR//Invasion Assay	In this research, a novel circRNA, hsa_circ_0058493, was proven to be upregulated in HCC, which was correlated with the prognosis of HCC patients. Mechanistic experiments revealed that hsa_circ_0058493 contained m6A methylation sites and that methyltransferase-like 3 (METTL3) mediated the degree of methylation modification of hsa_circ_0058493. Taken together, this study explored the oncogenic role of m6A-modified hsa_circ_0058493 and found to accelerate HCC progression via the METTL3-hsa_circ_0058493-YTHDC1 axis.		Yes	Experimentally, hsa_circ_0058493 knockdown suppressed the growth and metastasis of HCC cells in vivo and in vitro. On the contrary, the overexpression of hsa_circ_0058493 in HCC cells had the opposite effect in vitro. 	34888309
hsa_circ_0110102	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cell lines and tissues	Interaction( miR-580-5p/PPARα/CCL2 pathway)	qRT-PCR//ELISA//Western Blot//ChIP	The expression level of hsa_circ_0110102 was significantly downregulated in HCC cell lines and tissues, which was associated with poor prognosis. These results concluded that hsa_circ_0110102 acted as a sponge for miR-580-5p and inhibited CCL2 secretion into tumor microenvironment by decrease the expression of PPARα in HCC cells, then inhibited the pro-inflammatory cytokine release from macrophages by regulating the COX-2/PGE2 pathway. 		Yes	Knockdown hsa_circ_0110102 significantly promoted cell proliferation, migration, and invasion. 	33891564
hsa_circ_0007456	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissue	Interaction(miR-6852-3p/ICAM-1 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	In our previous study, we performed a microarray analysis of circRNAs between the tumor tissues and the adjacent normal tissues of hepatocellular carcinoma (HCC) patients, and found that the circRNA hsa_circ_0007456 is significantly downregulated in the tumor tissues and correlated with the prognosis of HCC. Through a series of screening and validation, we found that hsa_circ_0007456 mainly functioned through sponging miR-6852-3p and regulating the expression of intercellular adhesion molecule-1 (ICAM-1) in HCC. The miR-6852-3p/ICAM-1 axis is essential for the NK cytotoxicity toward HCC mediated by hsa_circ_0007456. 		Yes	We further investigated the relationship between the expression levels of hsa_circ_0007456 in HCC and the susceptibility of NK cells, and found that the expression levels of hsa_circ_0007456 in HCC cell lines significantly influenced their susceptibility to NK cells. 	33462208
hsa_circ_0013290	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines	Expression(highly expressed)	qRT-PCR//Transwell Assay	hsa_circ_0013290 is significantly upregulated in HCC cell lines and mainly located in cytoplasm of HCC cells.		Yes	Hsa_circ_0013290 overexpression promotes cell invasion and migration and inhibits cell apoptosis. In contrast, hsa_circ_0013290 knockdown impedes cell invasion and migration and accelerates cell apoptosis. However, hsa_circ_0013290 did not affect cell proliferation.	34798782
hsa_circ_0000098	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction( miR-1204/ALX4 )	qRT-PCR//Luciferase Report Assay//RIP//Transwell Assay	 Circ_0000098 expression level was markedly declined in HCC tissues and cells, and its underexpression was associated with larger tumor size of HCC patients.  Additionally, circ_0000098 was mainly distributed in the cytoplasm of HCC cells, and up-regulated ALX4 expression through competitively decoying miR-1204.		Yes	 Knocking down circ_0000098 observably promoted the multiplication, migration, invasion, and epithelial-mesenchymal transition (EMT) of Huh7 and SMMC-7721 cells. 	34900665
hsa_circ_0001955	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-646/FZD4 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//IHC//Transwell Assay	Circ_0001955 was a highly expressed circRNA in HCC tissues and cells. Meanwhile, miR-646 could be sponged by circ_0001955, and its inhibitor could reverse the negative regulation of circ_0001955 knockdown on HCC progression. Further, FZD4 was a target of miR-646, and its overexpression could invert the inhibition effect of miR-646 mimic on HCC progression. 		Yes	Circ_0001955 knockdown inhibited the proliferation, metastasis, angiogenesis, and enhanced the apoptosis of HCC cells. 	34021822
hsa_circ_0003006	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	115  tumors and corresponding paracancerous tissue samples	Interaction(miR-542-3p)	qRT-PCR//Luciferase Report Assay//Western Blot	The target miR‑542‑3p and target gene HIF-1A were predicted by bioinformatics analysis, then verified through biotinylated RNA pull-down and dual-luciferase reporter assays. The mechanism, circ-0003006, probably acted as a sponge of miR‑542‑3p and regulated HIF-1A levels in hepatocellular carcinoma cells. 		Yes	Cell account kit 8 (CCK-8) and transwell assay were revealed that circ-0003006 knockdown inhibited the proliferation and metastasis in HCC cells.The subcutaneous tumor formation experiment indicated that circ-0003006 knockdown inhibited the HCC cell growth in vivo.	34675680
circEPS15	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression(lower expressed)	qRT-PCR	The validation of dysregulated circRNAs by qRT-PCR revealed that circEPS15 expression was downregulated in HCC tissues, and the survival curves showed that low circEPS15 levels were associated with poor overall survival in HCC patients. T	The validation of dysregulated circRNAs by qRT-PCR revealed that circEPS15 expression was downregulated in HCC tissues, and the survival curves showed that low circEPS15 levels were associated with poor overall survival in HCC patients. 	Yes	 Then, the overexpression of circEPS15 suppressed tumor cell invasion and migration by inhibiting the TJP1/CDH2/VIM signaling pathway and retarded cell cycle progression, which was confirmed by the Transwell culture system, wound healing assays, flow cytometry and western blot assays. 	35211158
circANTXR1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	peripheral blood, tumor tissues and paracancerous normal tissues	Expression [highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	CircANTXR1 was a stable and highly expressed circRNA in HCC. MiR-532-5p could be sponged by circANTXR1, and its inhibitor could reverse the inhibition of circANTXR1 silencing on HCC cells progression. 		Yes	Silenced circANTXR1 inhibited the proliferation, migration and invasion of HCC cells in vitro, and suppressed HCC tumor growth in vivo. 	34786378
hsa_circ_0001178	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cells	regulation[miR-382/VEGFA axis]	qRT-PCR	 In our current work, we tested circ_0001178 expression in HCC tissues and HCC cells and found it was greatly elevated. To conclude, this research revealed that circ_0001178 induced HCC progression via modulating miR-382 and VEGFA axis.		Yes	Meanwhile, it was shown that HCC cell migration and invasion capacity were markedly inhibited by loss of circ_0001178. Knockdown of circ_0001178 restrained HCC tumor growth in vivo. 	32240747
circMAN2B2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular tissues	regulation[miRNA-217/MAPK1 axis]	CCK8//qRT-PCR	In this study, we investigated differences in the expression of circRNA MAN2B2 (circMAN2B2) in hepatocellular tissues and paired normal tissues. In summary, our study indicated that circMAN2B2 acted as an onco-miRNA in HCC by sponging miRNA-217 to promote MAPK1 expression.		Yes	We found that knockdown of circMAN2B2 expression in the HCC cell lines Hep-G2 and Huh-7 significantly inhibited cell proliferation by sponging (miRNA) miR-217 and inhibiting its function. 	32231737
circABCB10	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-340-5p/miR-452-5p]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	The results revealed that the expression of circ-ABCB10 was downregulated in both HCC tissues and cell lines and was positively correlated with histological grade and tumor size. 	The results revealed that the expression of circ-ABCB10 was downregulated in both HCC tissues and cell lines and was positively correlated with histological grade and tumor size. 	Yes	The overexpression of circ-ABCB10 exerted inhibitory effects on HCC cell proliferation, invasion, and migration.	32196586
hsa_circ_0009910	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-335-5p/ROCK1 axis]	Western Blot//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Circ_0009910 was upregulated in HCC tissues and cell lines.Circ_0009910-silenced suppressed the growth and metastasis of HCC cells through upregulating the inhibitory effect of miR-335-5p on ROCK1.		Yes	Knockdown of circ_0009910 significantly inhibited the proliferation, migration, and invasion of HepG2 cells and suppressed tumor growth and metastasis in vivo. 	32141540
hsa_circ_0091581	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC and adjacent normal tissues	regulation[hsa_circ_0091581/miR-526b/c-Myc/hsa_circ_0091581 ]	qRT-PCR	 Upregulation of hsa_circ_0091581 was identified by RNA-sequencing and validated by quantitative real-time polymerase chain reaction (qRT-PCR).These results revealed that hsa_circ_0091581/miR-526b/c-Myc/hsa_circ_0091581 positive feedback loop plays a vital role in HCC progression and hsa_circ_0091581 may be a potential prognostic biomarker and therapeutic target for HCC.	 Hsa_circ_0091581 expression was correlated with tumor size, disease-free survial and overall survival of HCC patients.	Yes	 Functionally, hsa_circ_0091581 could promote the proliferation of HCC cells in vitro.	32116112
hsa_circ_0011946	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[inducing the EMT process]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	In this research, the expression level of hsa_circ_0011946 was significantly increased in HCC tissues compared to that in adjacent samples.The hsa_circ_0011946 could enhance cell migration and invasion of HCC by inducing the EMT process.	The hsa_circ_0011946 expression was associated with lymphatic metastasis in HCC patients.	Yes	Knockdown of hsa_circ_0011946 led to the inhibition of cell migration and invasion in HCC.	32096173
hsa_circ_0056836	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines and tissues	regulation[miR-766-3p/FOSL2 axis]	qRT-PCR//Luciferase Report Assay//FISH	 The present study showed that hsa_circ_0056836 revealed high expressions in HCC cell lines and tissues compared with corresponding controls. In summary, the hsa_circ_0056836 / miR-766-3p / FOSL2 axis may serve as a promising strategy for HCC treatment.		Yes	Silencing of Hsa_circ_0056836 decreased cell migration, proliferation and invasion. Silencing of hsa_circ_0056836 inhibited the development of HCC in xenograft nude mice.	32048611
circPVT1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[circPVT1/miR-3666/SIRT7]	qRT-PCR	Herein, we found that circPVT1 expression was significantly upregulated in HCC tissues and cell lines. Our study highlights the involvement of circPVT1/miR-3666/SIRT7 in regulating HCC cell growth.		Yes	Knockdown of circPVT1 significantly reduced the growth and colony formation, and increased cell apoptosis, of HCC cells.	32017171
circBACH1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[circBACH1/HuR/p27 axis]	qRT-PCR//RNA Pull-Down//RIP//FISH	Here, we found that circBACH1 was significantly upregulated in HCC tissues and that high circBACH1 levels were closely associated with poor prognosis.In sum, circBACH1 plays a significant role as an oncogene through the circBACH1/HuR/p27 axis in HCC development.		Yes	In addition, circBACH1 could promote HCC growth by accelerating cell cycle progression in vitro and in vivo.	32003018
circTCF4.85	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	regulation[miR-486-5p-targeted inhibition of ABCF2]	qRT-PCR//FISH	Circ-TCF4.85 was detected to be highly expressed in HCC tissues. Taken together, our results reveal that silencing of circ-TCF4.85 suppresses HCC progression via miR-486-5p-targeted inhibition of ABCF2.		Yes	Next, we found that silencing of circ-TCF4.85 repressed HCC cell proliferation, invasion, and migration, while enhancing apoptosis. 	31758671
circIPO11	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues and liver CSCs	Expression [highly expressed]	Northern Blot//ChIP	CircIPO11 is highly expressed in HCC tumor tissues and liver CSCs.CircIPO11 is required for the self-renewal maintenance of liver CSCs to initiate HCC development. Mechanistically, circIPO11 recruits TOP1 to GLI1 promoter to trigger its transcription, leading to the activation of Hedgehog signaling. Additionally, circIPO11 knockout in mice suppresses the progression of chemically induced liver cancer development.		Yes	Additionally, circIPO11 knockout in mice suppresses the progression of chemically induced liver cancer development.	34649567
circCAMSAP1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	GEO(three pairs of HCC tissues and its adjacent normal tissues)	Interaction(miR-1294/GRAMD1A )	In Vivo Experiment//RNA Pull-Down//Bioinformatics Analysis//Wound Healing Assay//Invasion Assay//RIP//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	The expression of circCAMSAP1 was up-regulated in HCC tissues compared with its adjacent normal tissues. 		Yes	Up-regulation of circCAMSAP1 promoted HCC biological functions both in vitro and in vivo. The promotive effects of circCAMSAP1 on HCC progression function through miR-1294/GRAMD1A pathway. 	33484498
hsa-circ_103809	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines	Interaction(miR-1270)	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	CircRNA-103809 was highly expressed in HCC cell lines. 		Yes	After interfering circRNA-103809, the proliferation, migration, invasion and epithelial-to-mesenchymal transition process were all hindered in HCC cells. Significantly, circRNA-103809 competed with PLAG1 like zinc finger 2 (PLAGL2) for binding with microRNA-1270 (miR-1270), which formulated a competing endogenous RNA network in HCC.	32683589
hsa_circ_0021093	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(miR-432/Annexin A2)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Circ_0021093 was highly expressed in HCC tissues and cells, and its level was associated with poor prognosis of HCC patients. 	Circ_0021093 was highly expressed in HCC tissues and cells, and its level was associated with poor prognosis of HCC patients. 	Yes	Functional experiments showed that knockdown of circ_0021093 repressed proliferation, migration and invasion in vitro and tumor growth in vivo by regulating miR-432, while upregulation of circ_0021093 reversed these results.	33675609
hsa_circ_0006602	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 plasma exosomes of primary hepatocellular carcinoma patient and healthy volunteer 	Expression [highly expressed]	CCK8//qRT-PCR//Invasion Assay//Western Blot	Among them, it is further confirmed that exo_circ_0006602 is up-regulated in the large sample cohort. 		Yes	Cell function experiments show that exo_circ_0006602 can significantly improve the proliferation and invasion ability of liver cancer cell lines and also promoted the expression of tumor proliferation-related protein Snail. 	34306340
hsa_circ_NOTCH3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC specimens and cells	Interaction(miR-875-5p)	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	It was confirmed circ_NOTCH3 was highly expressed in HCC specimens and cells. In terms of mechanism, circ_NOTCH3 directly binds to miR-875-5p, regulating its activity by targeting the 3'-UTR of ZNF146.		Yes	 The proliferation, migration, invasion, and oxaliplatin-resistance potential of HCC could be restrained by silencing circ_NOTCH3 or by ectopic expression of miR-875-5p in vitro.	34790400
hsa_circ_0008274	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	The tissues adjacent to cancer and cancer tissues of 55 patients with HCC 	Interaction(microRNA -140-3p)	CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Herein we reported that circ_0008274 was highly expressed in HCC, and its high expression enhanced the proliferation, migration, and invasion of HCC cells, while depleting circ_0008274 inhibited the malignant biological behaviors of HCC cells. Mechanistically, circ_0008274 upregulates GRN expressions via adsorbing miR-140-3p to expedite the progression of HCC.		Yes	 its high expression enhanced the proliferation, migration, and invasion of HCC cells, while depleting circ_0008274 inhibited the malignant biological behaviors of HCC cells.	34002672
circDOCK1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(miR-654-5p/SMAD2 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	As a result, the expression of circRNA DOCK1 and SMAD2 was increased, and miR‑654‑5p was decreased in HCC cells. circRNA DOCK1 directly targeted to miR‑654‑5p and miR‑654‑5p directly targeted to SMAD2. 		Yes	Interference with circRNA DOCK1 inhibited the proliferation, invasion and migration of HCC cells by upregulating miR‑654‑5p expression.	34184075
circSCARB1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC and paired adjacent (within 3 cm around tumors) non-tumor tissues 	Interaction(miR-497)	CCK8//qRT-PCR//Transwell Assay	We found that circRNA SCARB1 was upregulated in HCC. In addition, mature miR-497 and miR-497 were downregulated in HCC. 		Yes	 Analysis of cellular behaviors showed that overexpression of circRNA SCARB1 increased the proliferation and migration of HCC cells, while overexpression of miR-497 decreased cell proliferation and migration. 	34305409
circFAM13B	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue	Interaction(miR-212/E2F5/ P53 pathway)	CCK8//qRT-PCR//RIP//FISH	We found that circFAM13B was the most significantly differentially expressed circRNA in HCC tissue. Further studies revealed that circFAM13B, a sponge of miR-212, is involved in the regulation of E2F5 gene expression by competitively binding to miR-212, inhibits the activation of the P53 signalling pathway, and promotes the proliferation of HCC cells.		Yes	Subsequently, in vitro and in vivo studies also demonstrated that circFAM13B promoted the proliferation of HCC. 	34348712
hsa_circ_0091579	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-624/H3F3B axis)	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	Circ_0091579 was upregulated in HCC tissues and cells. MiR-624 was downregulated, while H3F3B was upregulated in HCC tissues and cells. Circ_0091579 acted as a miR-624 sponge and regulated H3F3B expression by adsorbing miR-624. 		Yes	 Circ_0091579 inhibition decreased xenograft tumor growth in vivo and repressed Warburg effect, migration, invasion, and induced apoptosis of HCC cells in vitro. 	33934291
circGLIS2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(EIF4A3)	RNA Pull-Down//CCK8//qRT-PCR//RIP//IHC//Transwell Assay	Circ_GLIS2 and linear GLIS2 mRNA were reduced in human HCC tissues and cells. GLIS2 promoter region was hypermethylated in HCC cells. EIF4A3 was directly bound with GLIS2 mRNA and promoted circ_GLIS2/GLIS2 expression.	Their low levels correlated with a poor survival rate of HCC patients. 	Yes	Overexpression of circ_GLIS2 and GLIS2 suppressed HCC cell proliferation, migration, and invasion but promoted cell apoptosis. Moreover, overexpression of circ_GLIS2 restrained HCC tumour growth and metastasis in vivo.	34743403
circMRPS35	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	35 pairs of HCC from patients	Interaction(miR-148a/STX3/PTEN)	qRT-PCR//IHC	In this study, we identified a functional RNA, hsa_circ_0000384 (circMRPS35), from public tumor databases using a set of computational analyses, and we further identified that circMRPS35 was highly expressed in 35 pairs of HCC from patients.Mechanically, circMRPS35 sponged microRNA-148a-3p (miR-148a), regulating the expression of Syntaxin 3 (STX3), which modulated the ubiquitination and degradation of phosphatase and tensin homolog (PTEN). Unexpectedly, we detected a peptide encoded by circMRPS35 (circMRPS35-168aa), which was significantly induced by chemotherapeutic drugs and promoted cisplatin resistance in HCC. 		Yes	Moreover, knockdown of the expression of circMRPS35 in Huh-7 and HCC-LM3 cells suppressed their proliferation, migration, invasion, clone formation, and cell cycle in vitro, and it suppressed tumor growth in vivo as well. 	34450251
hsa_circ_0091579	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(miR-1225-5p/PLCB1 Axis)	qRT-PCR	 Expression of circ_0091579 and PLCB1 was increased, while miR-1225-5p expression was decreased in HCC tissues and cells. Circ_0091579 sponged miR-1225-5p to upregulate PLCB1 expression in HCC cells. Silencing of miR-1225-5p contributed to HCC progression, which was mitigated by PLCB1 depletion. 		Yes	Circ_0091579 or PLCB1 depletion had inhibitory effects on HCC cell proliferation and metastasis. Circ_0091579 deficiency could suppress HCC tumor growth in vivo.	33559088
hsa_circ_0074854	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cell lines	Expression(highly expressed)	qRT-PCR	Hsa_circ_0074854 expression was upregulated in HCC tissues and HCC cell lines. Mechanistically, hsa_circ_0074854 knockdown inhibited the migration and invasion of HCC cells via interacting with human antigen R (HuR) to reduce its stability.		Yes	Additionally, hsa_circ_0074854 knockdown was found to inhibit HCC growth in vitro and in vivo. 	33880025
hsa_circ_0003410	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-139-3p/CCL5 axis)	qRT-PCR	Using high-throughput RNA sequencing, we demonstrated that hsa_circ_0003410 was clearly upregulated in HCC. Mechanistically, we identified CCL5 as the target gene of hsa_circ_0003410. RNA-FISH showed the co-expression of hsa_circ_0003410 and CCL5. Western blot and ELISA also verified that hsa_circ_0003410 could upregulate the expression of CCL5 protein.		Yes	5-Ethynyl-2'-deoxyuridine and transwell assays showed that hsa_circ_0003410 facilitated the proliferation and migration of HCC cells in vitro. 	34890089
hsa_circ_0013958	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients	Interaction(miR-532-3p/WEE1 Axis)	qRT-PCR	It revealed that circ0013958 was significantly up-regulated in HCC, which was positively correlated with poor prognosis of HCC patients.  Circ0013958 acted as a miR-532-3p sponge to regulate WEE1 expression, thus promoting the progression of HCC.	It revealed that circ0013958 was significantly up-regulated in HCC, which was positively correlated with poor prognosis of HCC patients. 	Yes	Circ0013958 promoted HCC cell proliferation and invasion, inhibited cell apoptosis in vitro, and promoted tumorigenesis in vivo. 	33937016
circSEC24A	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells 	Interaction(miR-455-3p/PPM1F)	qRT-PCR	circSEC24A acted as a molecular sponge to sequester miR-455-3p, resulting in elevating the expression of PPM1F. miR-455-3p inhibitor reversed the suppressive impact of circSEC24A silencing on malignant behaviors of HCC cells. PPM1F overexpression offsets the inhibitory effect of miR-455-3p mimic on malignant behaviors of HCC cells. circSEC24A sponged miR-455-3p to elevate the PPM1F expression, resulting in accelerating malignant behaviors of HCC cells. The study provided a potential therapeutic target for patients with HCC.		Yes	circSEC24A silencing decreased xenograft tumor growth in vivo and repressed proliferation, metastasis, invasion, epithelial-to-mesenchymal transition (EMT), induced cell cycle arrest, and apoptosis of HCC cells in vitro. The relationship between circSEC24A or PPM1F and miR-455-3p was verified by a dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. 	34459207
circNFIX	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells 	Interaction(miR-3064-5p/HMGA2 axis)	qRT-PCR	Our results showed that circNFIX was remarkably up-regulated in HCC and was associated with a poor survival. Knockdown of circNFIX repressed proliferation, invasion and glutaminolysis of HCC cells. Moreover, circNFIX directly sponged miR-3064-5p to release HMGA2 expression, and thus conferred the malignant development of HCC. 	circNFIX directly sponged miR-3064-5p to release HMGA2 expression, and thus conferred the malignant development of HCC.	Yes	Knockdown of circNFIX repressed proliferation, invasion and glutaminolysis of HCC cells. 	34539988
hsa_circ_0072088	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue and cell lines	Regulation(miR-375/JAK2/STAT3 signaling pathway)	qRT-PCR	Circ_0072088 and JAK2 mRNA expressions were highly expressed in HCC tissues and cell lines while miR-375 expression was remarkably downregulated. Circ_0072088 was resistant to RNase R treatment and mainly located in the cytoplasm of HCC cells. The transfection of circ_0072088 overexpression plasmid or miR-375 inhibitors promoted the proliferation, migration, and invasion, and inhibited the apoptosis of HCC cells, whereas transfection of circ_0072088 siRNA or miR-375 mimics exerted opposite effects. Besides, miR-375 was confirmed as a target of circ_0072088 and miR-375 could further downregulate the expression of JAK2. MiR-375 mimics could reverse the upregulation of JAK2 and p-STAT3 protein induced by circ_0072088 overexpression. Circ_0072088 can enhance the proliferation, migration, and invasion, and impede apoptosis of HCC cells. Mechanistically, circ_0072088 activates JAK2/STAT3 signaling pathway by serving as a molecular sponge of miR-375.		Yes	MiR-375 mimics could reverse the upregulation of JAK2 and p-STAT3 protein induced by circ_0072088 overexpression.	34148288
hsa_circ_0004018	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	THLE-3 & HUVECs	Interaction( FUS/TIMP2 )	qRT-PCR	circ_0004018 was definitely down-regulated in HCC.estrogen receptor 1 (ESR1) mediated circ_0004018 regulated TIMP2 by recruiting FUS. A series of rescue assays verified that circ_0004018 participated in angiogenesis in HCC via modulating TIMP2. In summary, this paper disclosed that ESR1 activated circ_0004018 inhibited angiogenesis in HCC via binding to FUS and stabilizing TIMP2 expression.		Yes	we found that overexpression of circ_0004018 significantly inhibited angiogenesis in HCC. 	34487732
circLRIG3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-449a/LRIG3 axis)	qRT-PCR	circ_LRIG3 expression was upregulated in HCC tissues and cells. Knockdown of circ_LRIG3 suppressed proliferation, migration and invasion and facilitated cell apoptosis in HCC cells in vitro and blocked tumor growth of HCC in vivo. RNF38 overexpression reversed the effects of circ_LRIG3 knockdown on the malignant behaviors of HCC cells. Moreover, circ_LRIG3 could sponge miR-449a to positively modulate RNF38 expression in HCC cells. circ_LRIG3 knockdown inhibited the progression of HCC cells by sponging miR-449a. In addition, circ_LRIG3 silencing might inhibit the Smad2/3 pathway. 		Yes	Knockdown of circ_LRIG3 suppressed proliferation, migration and invasion and facilitated cell apoptosis in HCC cells in vitro and blocked tumor growth of HCC in vivo. RNF38 overexpression reversed the effects of circ_LRIG3 knockdown on the malignant behaviors of HCC cells.	33880997
hsa_circ_0003288	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	L02 and HCC cells	Interaction(hsa_circ_0003288/miR-145/PD-L1 axis)	qRT-PCR	miR-145 directly targeted the PD-L1 3'-untranslated region (UTR) region, and hsa_circ_0003288 acted as a miR-145 sponge to regulate PD-L1 expression. Overexpression of hsa_circ_0003288 increased PD-L1 levels and promoted EMT, migration, and invasiveness of L02 cells. These observations were reversed after knockdown of hsa_circ_0003288 in HepG2 and Huh7 cells. Overexpression of PD-L1 rescued EMT, migration, and invasiveness of HepG2 and Huh7 cells after knockdown of hsa_circ_0003288. Furthermore, hsa_circ_0003288 knockdown reduced EMT in in vivo studies. Hsa_circ_0003288/PD-L1 axis was found to mediate the metastatic phenotypes via the PI3K/Akt pathway in HCC. Additionally, expression levels of hsa_circ_0003288 were increased and positively correlated with PD-L1 expression in HCC tissues.		Yes	Overexpression of hsa_circ_0003288 increased PD-L1 levels and promoted EMT, migration, and invasiveness of L02 cells. These observations were reversed after knockdown of hsa_circ_0003288 in HepG2 and Huh7 cells. Overexpression of PD-L1 rescued EMT, migration, and invasiveness of HepG2 and Huh7 cells after knockdown of hsa_circ_0003288. Furthermore, hsa_circ_0003288 knockdown reduced EMT in in vivo studies.	33858418
circETFA	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues, plasma, and cells	Interaction(miR-612)	qRT-PCR	CircETFA was overexpressed in HCC tissues, plasma, and cells. Clinicopathological data revealed that abnormally high circETFA expression was associated with a poor prognosis. In function, circETFA promotes the malignant phenotype of HCC cells in vivo and in vitro, inhibits cycle arrest, and decreases the proportion of apoptotic cells. In mechanism, it can upregulate C-C motif chemokine ligand 5 (CCL5) in HCC cells, thereby regulating the phosphoinositide 3-kinase (PI3K)/Akt pathway and other key downstream effectors (e.g., FoxO6). Furthermore, circETFA prolonged the half-life of CCL5 mRNA by recruiting the eukaryotic initiation factor 4A3 (EIF4A3) and acted as a sponge of hsa-miR-612 to suppress the silencing effect of hsa-miR-612 on CCL5. In conclusion, CircETFA can increase the expression of CCL5 to promote the progression of HCC by sponging hsa-mir-612 and recruiting EIF4A3, and is promising as a novel biomarker and therapeutic target.	Clinicopathological data revealed that abnormally high circETFA expression was associated with a poor prognosis. 	Yes	In function, circETFA promotes the malignant phenotype of HCC cells in vivo and in vitro, inhibits cycle arrest, and decreases the proportion of apoptotic cells. 	34716323
circCCND1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-497-5p/HMGA2 Axis)	qRT-PCR	Circ-CCND1 and HMGA2 expressions in HCC were significantly up-regulated and miR-497-5p expression was markedly decreased. Mechanistically, miR-497-5p was a direct target of circ-CCND1 and miR-497-5p specifically modulated HMGA2 expression. Furthermore, miR-497-5p inhibitors and or HMGA2 overexpression partially counteracted the suppressing effect induced by si-circ-CCND1 on the malignant phenotype of HCC cells. Circ-CCND1 plays a cancer-promoting role in HCC by modulating the miR-497-5p/HMGA2 axis. 	 High circ-CCND1 expression was associated with relatively large tumor size and lymph node metastasis in HCC patients. I	Yes	 Functionally, knockdown of circ-CCND1 remarkably suppressed HCC cell proliferation, migration, and invasion. 	34564768
hsa_circ_0016788	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-506-3p/PARP14)	qRT-PCR	 The levels of hsa_circ_0016788 and PARP14 were upregulated, and the miR-506-3p level was decreased in HCC tissues in contrast to that in normal tissues. Moreover, miR-506-3p was confirmed to repress the progression of HCC cells by suppressing PARP14. In mechanism, hsa_circ_0016788 acted as a miR-506-3p sponge to regulate the level of PARP14. In addition, hsa_circ_0016788 knockdown also inhibited tumor growth in vivo.		Yes	For functional analysis, hsa_circ_0016788 deficiency inhibited cell glycolysis metabolism, cell vitality, cell proliferation, colony formation, and invasion in HCC cells whereas promoted cell apoptosis.	34340259
hsa_circ_0062682	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients	Interaction(YBX1)	qRT-PCR	 By implementing available transcriptomic analyses of HCC patients, we identified an upregulated circRNA hsa_circ_0062682.  Pathway enrichment analysis and gene set enrichment analysis of the transcriptome data from hsa_circ_0062682 knockdown explained the observed phenotypes and exposed transcription factors E2F1, Sp1, HIF-1α, and NFκB1 as potential downstream targets. Biotinylated oligonucleotide pulldown combined with proteomic analyses identified protein interaction partners of which YBX1, a known oncogene, was confirmed by RNA immunoprecipitation.		Yes	 Stable perturbations of hsa_circ_0062682 in Huh-7 and SNU-449 cell lines influenced colony formation, migration, cell proliferation, sorafenib sensitivity, and additionally induced morphological changes in cell lines, indicating an important role of hsa_circ_0062682 in oncogenesis.	36139684
hsa_circ_0032683	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues 	Interaction(microRNA-338-5p)	qRT-PCR	In GEO (Gene Expression Omnibus) database, hsa_circ_0032683 expression was significantly lower in HCC tissues than in normal liver tissues. Mechanically, hsa_circ_0032683 primarily exists in the cytoplasm and competes with microRNA-338-5p (miR-338-5p) to regulate reticulon 4(RTN4). Our experiments revealed that hsa_circ_0032683 receded the proliferation ability of HCC via ceRNA (competing endogenous RNAs) mechanism, which provided potential biomarkers and therapeutic targets for HCC patients.		Yes	 In vitro and in vivo functional tests revealed that hsa_circ_0032683 could inhibit HCC cells proliferation and promote their apoptosis. 	35030979
circITCH	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(miR-184)	qRT-PCR	CircITCH (hsa_circ_0001141) was a stable circRNA and downregulated in HCC cells.. Mechanistically, miR-184 could be sponged by circITCH, and its overexpression could mitigate the suppressive effects of circITCH overexpression on HCC progression. 		Yes	 Overexpression of circITCH inhibited cell proliferation, migration, invasion, and promoted apoptosis in vitro and in vivo, whereas knockdown of circITCH had the opposite effects. 	35400275
hsa_circ_0008285	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cell lines	Interaction(miR-384/RRM2 axis )	qRT-PCR	 Circ_0008285 expression is elevated to HCC tissues and cell lines.In this study, circ_0008285 could promote the malignant biological behaviors of HCC cells through miR-384/RRM2 axis and has the potential to become a therapeutic target for HCC, providing a new idea for targeted therapy of HCC.                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    		Yes	Silencing of circ_0008285 inhibited the proliferation, migration and invasion of HCC cells but accelerated cell apoptosis in vitro and impeded HCC tumorigenesis in vivo.	35964907
hsa_circ_101555	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-145-5p/CDCA3)	qRT-PCR	hsa_circ_101555 showed greater stability than the linear RNA; while in vitro and in vivo results demonstrated that hsa_circ_101555 silencing significantly suppressed cell proliferation, migration, and invasion of HCC cells.  Rescue experiments further demonstrated that suppression of miR-145-5p significantly attenuated the biological effects of hsa_circ_101555 knockdown in HCC cells. We also identified a putative oncogene CDCA3 as a potential miR-145-5p target. 		Yes	hsa_circ_101555 showed greater stability than the linear RNA; while in vitro and in vivo results demonstrated that hsa_circ_101555 silencing significantly suppressed cell proliferation, migration, and invasion of HCC cells. 	33824281
hsa_circ_0008305	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-660/BAG5 axis)	qRT-PCR	First, it was demonstrated that circ_0008305 was greatly increased in HCC tissues and cells. To sum up, it was illustrated by our study that circ_0008305-mediated miR-660-5p/BAG5 axis triggered HCC progression, which could provide a novel insight on the underlying mechanism of HCC progression.		Yes	Moreover, we observed silencing circ_0008305 markedly repressed HCC cells in vitro growth and reduced tumor growth in vivo. 	33481351
hsa_circ_0046600	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-1258/SERBP1 )	qRT-PCR	Circ_0046600 was highly expressed in HCC tissues and cells. Mechanistically, circ_0046600 could competitively target miR-1258 to prevent the degradation of its target gene SERBP1. 		Yes	 Silencing of circ_0046600 impaired HCC cell growth and metastasis in vitro, as well as impeded HCC tumor growth in vivo.	34784519
circMTO1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC and adjacent nontumor tissue	Interaction( miR-541-5p/ZIC1 axis by regulating Wnt/β-catenin signaling pathway)	CCK8//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC	CircMTO1 is downregulated in HCC as compared to adjacent nontumor tissue, which may suppress the HCC progression by certain signal pathways.These findings indicated that circMTO1 suppressed HCC progression via the circMTO1/ miR-541-5p/ZIC1 axis by regulating Wnt/β-catenin signaling and epithelial-to-mesenchymal transition, making it a novel therapeutic target.		Yes	 The results depicted that silencing circMTO1 or upregulating miR-541-5p expression facilitated HCC cell proliferation, migration, and invasion and inhibited apoptosis. CircMTO1 silencing upregulated the expression of downstream ZIC1 regulators of the Wnt/β-catenin pathway markers, β-catenin, cyclin D1, c-myc, and the mesenchymal markers N-cadherin, Vimentin, and MMP2, while the epithelial marker E-cadherin was downregulated. MiR-541-5p knockdown had the opposite effect and reversed the effect of circMTO1 silencing on the regulation of downstream ZIC1 regulators. 	34930906
circRHOBTB3	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-18a )	qRT-PCR	CircRHOBTB3 was under-expressed in HCC compared to normal tissues.  In HCC cells, circRHOBTB3 overexpression decreased mature miR-18a level but not miR-18a precursor. 		Yes	Cell proliferation analysis showed that circRHOBTB3 overexpression decreased cell proliferation while miR-18a overexpression increased cell proliferation. Moreover, circRHOBTB3 suppressed the role of miR-18a in cell proliferation.	34187598
circWHSC1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(miR-142-3p/HOXA1 )	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	CircWHSC1 was elevated in HCC tissues and cells, and high level of circWHSC1 was associated with worse overall survival of HCC patients.CircWHSC1 functioned as the sponge for miR-142-3p, which directly targeted HOXA1. Inhibition of miR-142-3p ameliorated the effects of circWHSC1 knockdown on HCC cell proliferation and metastasis. Moreover, miR-142-3p overexpression restrained the growth and motility of HCC cells, with HOXA1 elevation reversing the impacts.	CircWHSC1 was elevated in HCC tissues and cells, and high level of circWHSC1 was associated with worse overall survival of HCC patients.	Yes	Knockdown of circWHSC1 suppressed HCC cell proliferation and metastasis in vitro and restrained tumorigenesis in vivo. 	33410156
circC16orf62	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Interaction(miR-138-5p/PTK2/AKT axis)	qRT-PCR//Western Blot//Transwell Assay	Bioinformation analysis and qRT-PCR indicated that CircC16orf62 was prominent upregulated in HCC of which the expression level was positively associated to cancer's malignant progression. The bioinformatic analysis found that miR-138-5p and PTK2 were the downstream target of CircC16or62. Then, the FISH(Fluorescence immunoin situ hybridization) and cell nucleoplasmic separation determined that CircC16orf62 located in the cell cytoplasm. CircC16orf62 functioned as a molecular sponge for miR-138-5p, and a competitive endogenous RNA for PTK2, promoting AKT/mTOR pathway activation.	Bioinformation analysis and qRT-PCR indicated that CircC16orf62 was prominent upregulated in HCC of which the expression level was positively associated to cancer's malignant progression.	Yes	Gain or loss-of-function studies indicated that the reduction of CircC16orf62 expression promotes the proliferation, invasion, and glycolysis of HCC in vitro and in vivo.	34108451
circHPS5	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	CC tissues	Interaction(miR-370/HMGA2 )	In Vivo Experiment//Western Blot//CCK8//Luciferase Report Assay//IHC	The present study identified a circRNA with m6A modification, circHPS5, which was increased in neoplasm HCC tissues and indicated poor patient survival.  Notably, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. In addition, we demonstrated that circHPS5 can act as a miR-370 sponge to regulate the expression of HMGA2 and further accelerate HCC cell tumorigenesis.	The present study identified a circRNA with m6A modification, circHPS5, which was increased in neoplasm HCC tissues and indicated poor patient survival. 	Yes	Silencing of circHPS5 inhibited epithelial-mesenchymal transition (EMT) and cancer stem-like cell (CSC) phenotypes.	34703649
circFOXM1	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells 	Interaction(miR-1179/SPAG5 axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	Luciferase reporter gene activity assay showed that miR-1179 had complementary binding sites with circFOXM1 and SPAG5. CircFOXM1 silencing inhibited malignant phenotypes in HCC cells were partly rescued by either miR-1179 silencing or SPAG5 overexpression. CircFOXM1 promoted HCC cell proliferation and metastasis by regulating miR-1179/SPAG5 axis.		Yes	 CCK8 assay, tumor volume and tumor weight showed that circFOXM1 effectively promoted HCC cell proliferation. Transwell assay showed that circFOXM effectively promoted migration and invasion abilities of HCC cells.	34903799
circUBAP2	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	Interaction( miR-194-3p/MMP9 pathway)	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay	Among 91 HCC patients, circUBAP2 was significantly upregulated in HCC tissues, and negatively correlated with aggressive clinical characteristics and prognosis. Mechanistically, circUBAP2 acts as a competing endogenous RNA (ceRNA) for miR-194-3p, a tumor suppressor in HCC. We confirmed that MMP9 was direct target for miR-194-3p, which was regulated by circUBAP2.	Among 91 HCC patients, circUBAP2 was significantly upregulated in HCC tissues, and negatively correlated with aggressive clinical characteristics and prognosis. 	Yes	 Functional assays demonstrated that circUBAP2 promoted cell proliferation, colony formation, migration, and invasion in vitro. Moreover, circUBAP2 enhanced tumor growth and pulmonary metastasis in vivo.	34239873
circTP63	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cell lines	Interaction(miR-155-5p/ZBTB18 )	In Vivo Experiment//CCK8//qRT-PCR//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	circTP63 was significantly upregulated in HCC tissues and cell lines. Mechanically, circTP63 was a sponge of miR-155-5p to facilitate the ZBTB18 expression, and the ZBTB18 expression in HCC tissues was negatively associated with the survival rate of HCC patients.	 High circTP63 expression is closely associated with the tumor stages, lymph node metastasis, and poor prognosis of HCC patients.	Yes	Functionally, knockdown of circTP63 inhibited cell proliferation, migration, invasion, and promoted cell apoptosis of HCC. Meanwhile, overexpression of circTP63 enhanced HCC progression.	33685441
hsa_circ_0097009	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-1261/SLC7A11 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Microarray analysis and qRT-PCR verified that circRNA, circ0097009, was significantly upregulated in HCC tissues and cell lines. Luciferase reporter assays showed that circ0097009 and SLC7A11 directly bound to miR-1261. Subsequent experiments showed that circ0097009 and SLC7A11 reciprocally regulated their expression via miR-1261 sponging by circ0097009.		Yes	Knockdown of circ0097009 inhibited the proliferation and invasion of HCC cells. 	33987373
circSTIL	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(miR-345-5p/AQP3 Axis)	qRT-PCR	Circ-STIL was upregulated in HCC tissues and cells. MiR-345-5p was a direct target of circ-STIL, and AQP3 was targeted by miR-345-5p in HCC. Circ-STIL knockdown or miR-345-5p overexpression impeded cell malignant behaviors in HCC cells, and the effects could be reversed by miR-345-5p silence or AQP3 enhancement, respectively. Meanwhile, circ-STIL regulated AQP3 expression by sponging miR-345-5p. 		Yes	Circ-STIL knockdown inhibited HCC cell progression by reducing cell proliferation, migration and invasion and promoting cell apoptosis. Besides, circ-STIL downregulation retarded HCC tumor growth in vivo.	34231101
hsa_circ_0061395	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues, serum, cells, and serum-derived exosomes	Interaction(miR-877-5p/PIK3R3 axis)	Flow Cytometry//qRT-PCR//RIP//IHC//Transwell Assay	 Circ_0061395 was upregulated in HCC tissues, serum, cells, and serum-derived exosomes.MiR-877-5p was downregulated while PIK3R3 was upregulated in HCC. Circ_0061395 regulated PIK3R3 expression via competitively binding to miR-877-5p. MiR-877-5p inhibitor overturned circ_0061395 knockdown-mediated influence on malignant behaviors of HCC cells. PIK3R3 overexpression reversed the suppressive influence of miR-877-5p mimic on malignant behaviors of HCC cells.		Yes	Circ_0061395 silencing decreased tumor growth in vivo, and induced cell cycle arrest, apoptosis, repressed proliferation, invasion, and migration of HCC cells in vitro. 	33407443
circZNF83	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(miR-324-5p/CDK16-mediated JAK2/STAT3 signal )	qRT-PCR	GL63 inhibited the circZNF83 expression in HCC cells. CircZNF83 served as a sponge of miR-324-5p and circZNF83/miR-324-5p axis was involved in the functional regulation of GL63 in HCC progression. Moreover, CDK16 was a downstream target of miR-324-5p and circZNF83 could regulate the CDK16 expression by sponging miR-324-5p. In addition, GL63 inactivated the JAK2/STAT3 pathway via downregulating circZNF83 to mediate the miR-324-5p/CDK16 axis. GL63 also repressed tumor growth in vivo through the circZNF83/miR-324-5p/CDK16-mediated JAK2/STAT3 signal inhibition.		Yes	CircZNF83 overexpression attenuated the inhibitory effects of GL63 on HCC cell growth, cell cycle progression, migration, and invasion but the promoting effect on cell apoptosis. 	33982329
circRNF13	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HBV-infected human HCC tissues and HBV-expressing cells (Huh7-HBV and Hep3B-HBV)	Interaction(miR-424-5p/TGIF2)	qRT-PCR	First of all, real-time quantitative PCR (RT-qPCR) was utilized to examine RNA expression, and circ-RNF13 was upregulated in HBV-infected human HCC tissues and HBV-expressing cells (Huh7-HBV and Hep3B-HBV), accompanied with TGFβ-induced factor homeobox 2 (TGIF2) upregulation and microRNA (miR)-424-5p downregulation. In conclusion, circ-RNF13 might sponge miR-424-5p to suppress HBV-associated HCC cells malignant progression and HBV infection by regulating TGIF2, providing a novel insight into the occurrence and treatment of HBV-associated HCC.		Yes	 As a result, blocking circ-RNF13 enhanced the apoptosis rate of Huh7-HBV and Hep3B-HBV cells, but inhibited cell proliferation, colony formation, migration, and invasion in vitro, along with suppressed tumor growth in vivo. 	33714261
hsa_circ_0001588	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction( miR-874/CDK4 Signaling)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Our current study is aimed at investigating the function of circ_0001588 in HCC, which was observed to significantly increase in HCC tissues and cells. Moreover, miR-874 was predicted as a target of circ_0001588. Using luciferase binding assays, we proved that circ_0001588 functions as a molecular ceRNA of miR-874 and that CDK4 acts as a downstream target of miR-874 in HCC. 		Yes	 We demonstrated that the knockdown of circ_0001588 resulted in repressed cell proliferation, migration, and invasion. In vivo studies using a nude mouse model showed that circ_0001588 downregulation reduced tumor size.	34722778
circPRKCI	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cell line	Interaction(miR-1294 and miR-186-5p / FOXK1 )	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results of the present study revealed that miR-1294 and miR-186-5p expression levels were downregulated in the HCC cell line, HCCLM3, and were subsequently downregulated by circ-PRKCI overexpression and upregulated by the knockdown of circ-PRKCI.  In addition, the overexpression of circ-PRKCI upregulated FOXK1 expression levels, while the overexpression of miR-1294 and miR-186-5p downregulated FOXK1 expression levels.		Yes	circ-PRKCI overexpression promoted the viability, invasion and migration of HCCLM3 cells, which was also reversed by the overexpression of miR-1294 and miR-186-5p. 	33880589
hsa_circ_0001306	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-527/FBXW7)	CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay//Transwell Assay	Firstly, the downregulation of hsa_circ_0001306 was identified by high‑throughput RNA sequencing and further verified by qRT-PCR. Mechanistic studies indicated that hsa_circ_0001306 acts as a ceRNA for miR-527, which resulted in the reduction of its endogenous target, FBXW7.		Yes	Knockdown of hsa_circ_0001306 could downregulate F-box and WD repeat domain containing 7(FBXW7), a target of miR-527, thereby promoting HCC cell proliferation and invasion.  Furthermore, hsa_circ_0001306 siRNA increased the multiplication rate of HCC tumors. 	34659544
hsa_circ_0088364	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients' tumors	Interaction(miR-1270-COL4A1 ceRNA pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Expression of circ_0088364 and COL4A1 was upregulated, and miR-1270 was downregulated in HCC patients' tumors; moreover, there were linear correlations among circ_0088364, miR-1270, and COL4A1 expression. Essentially, circ_0088364 and COL4A1 were ceRNAs for miR-1270 via target binding. 		Yes	In function, silencing circ_0088364 or upregulating miR-1270 could suppress cell proliferation, cell cycle entrance, transwell migration and invasion in Huh7 and HCCLM3 cells, as well as promote apoptosis rate. Moreover, above-mentioned effects were accompanied with reduced B-cell lymphoma (Bcl)-2, N-cadherin and Vimentin levels, and elevated Bcl-2-associated X protein (Bax) and E-cadherin levels. Contrarily, exhausting miR-1270 and restoring COL4A1 could severally abrogate the tumor-suppressive roles of circ_0088364 knockdown and miR-1270 overexpression in HCC cells in vitro. In vivo, silencing circ_0088364 retarded xenograft tumor growth in nude mice induced by Huh7 cells by upregulating miR-1270 and downregulating COL4A1.	34951563
circSOX4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues or in cell lines	Interaction(microRNA-432)	Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	CircSOX4 was abnormally highly expressed either in HCC tissues or in cell lines, which was positively correlated with the poor prognosis of HCC patients. Bioinformatics analysis revealed that microRNA-432 contained the binding site pairing to circSOX4 3'UTR, and their binding relationship was confirmed by Luciferase assay. Their expression levels were negatively correlated. In addition, downregulation of microRNA-432 can partially reverse the effect of silenced circSOX4 on regulating apoptosis, proliferation and migration of HCC cells.	CircSOX4 was abnormally highly expressed either in HCC tissues or in cell lines, which was positively correlated with the poor prognosis of HCC patients. 	Yes	 Transfection of small interfering RNA against circSOX4 in HCC cells resulted in inhibited migration and proliferation of HCC cells, while an increase in cell apoptosis. 	33660794
circNOP10	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissue	Interaction(miR-204/SIRT1 pathway)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Cell Apoptosis Assay//Microarray//Cell Cycle Assay//Transwell Assay	The results indicated that increased circNOP10 in GC tissue was involved in tumor stage and prognosis. In addition, circNOP10 sponged microRNA-24 (miR-204)-mediated biological processes through sirtuin 1 (SIRT1), which further confirmed that the circNOP10/miR-204/SIRT1 pathway promoted proliferation and migration as well as epithelial-mesenchymal transition (EMT) through the NF-κβ pathway in GC cell lines.		Yes	 In addition, circNOP10 sponged microRNA-24 (miR-204)-mediated biological processes through sirtuin 1 (SIRT1), which further confirmed that the circNOP10/miR-204/SIRT1 pathway promoted proliferation and migration as well as epithelial-mesenchymal transition (EMT) through the NF-κβ pathway in GC cell lines.	34532100
hsa_circ_0000751	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(microRNA-488)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Invasion Assay//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Colony Formation Assay//EdU Staining//Transwell Assay	The results showed that hsa_circ_0000751 levels were markedly downregulated in GC tissues and cell lines, which were also inversely proportional to the stage of tumor-node-metastasis (TNM) classification, tumor volume, and lymph node metastasis in GC patients. 	which were also inversely proportional to the stage of tumor-node-metastasis (TNM) classification, tumor volume, and lymph node metastasis in GC patients.	Yes	Conversely, hsa_circ_0000751 overexpression suppressed tumor progression, migration, and invasion in vitro and in vivo. From our results, we showed that hsa_circ_0000751 may serve as a miRNA sponge to suppress the activity of miR-488, thereby increasing the expression of the miR-488-target gene, UQCRC2, and limiting GC progression. 	34565283
hsa_circ_0044516	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-149)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay	Upregulated circRNA_0044516 was found in GC tissues and cell lines. 		Yes	Downregulating circRNA_0044516 inhibited the viability and promoted apoptosis of GC cells. CircRNA_0044516 targeted miR-149, and its downregulation elevated miR-149 level in GC cells. 	33140323
CRNDE	LncRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	bone marrow, cell lines	regulation[ miR-345-5p/CREB Axis]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay	In this study, long non-coding RNA colorectal neoplasia differentially expressed (LncRNA CRNDE) was upregulated in the bone marrow of BCP-ALL patients and BCP-ALL cell lines (NALM-6 and RS4;11).In conclusion, LncRNA CRNDE upregulated CREB expression by suppressing miR-345-5p, thus promoting cell proliferation and reducing cell apoptosis in BCP-ALL.		Yes	Functionally, LncRNA CRNDE knockdown restrained cell proliferation and boosted cell apoptosis in NALM-6 and RS4;11 cells. 	32868489
CRNDE	LncRNA	Homo sapiens	Wilms Tumor	 tumor tissues 	regulation[ regulating microRNA-424]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	RT-qPCR results revealed that the expression level of lncRNA CRNDE in tumor tissues of patients with Wilms' tumor was remarkably higher than that of adjacent normal tissues. In addition, CRNDE might accelerate the progression of Wilms' tumor via modulating microRNA-424.	Compared with patients with low expression of CRNDE, the risk of lymph node metastasis was significantly higher in patients with high CRNDE expression (p<0.05).	Yes	 Similarly, compared with control group, the proliferation and metastasis abilities of cells in CRNDE knockdown group were remarkably down-regulated (p<0.05). However, opposite results were observed in CRNDE overexpression group.	32096178
CRNDE	LncRNA	Homo sapiens	Liver Diseases, Alcoholic	ALD tissues	Expression(highly expressed)	In Vivo Experiment	 Three lncRNAs (CRNDE, RBMS3-AS3, and LINC01088) were demonstrated to be potentially useful diagnostic markers in ALD. Among them, the expression of CRNDE is up-regulated.  The result showed ALD tissues in mice had significantly higher CRNDE levels than normal tissues. 		Yes	 In addition, alcohol can induce apoptosis, and knockdown of CRNDE can reduce apoptosis. 	34633988
CRNDE	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cells	Interaction(miR-455-3p/HDAC2 axis)	Western Blot//Transfection//RIP//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The data revealed that the expression of CRNDE was upregulated in NSCLC tissues, while miR-455-3p was downregulated. Moreover, inhibition of miR-455-3p exhibited the opposite effect. CRNDE bound with miR-455-3p, and HDAC2 was found to be targeted by miR-455-3p. Meanwhile, miR-455-3p downregulation reversed the effect of CRNDE knockdown on NSCLC cell function. Furthermore, miR-455-3p notably inhibited the growth and invasion of NSCLC cells via downregulation of HDAC2. Knockdown of CRNDE attenuated NSCLC progression via modulation of the miR-455-3p/HDAC2 axis. 		Yes	CRNDE knockdown inhibited the viability, migration and invasion of NSCLC cells or epidermal growth factor receptor gene (EGFR)-mutant NSCLC cells. 	35611803
Crnde	LncRNA	Mus musculus	Osteosarcoma	Tumor tissues 	Interaction(miR-136-5p/MRP9 axis)	Western Blot//ISH//Wound Healing Assay//CCK8//Luciferase Report Assay//Transwell Assay	The expression of CRNDE in OS tissues was higher than that in normal tissues. High lncRNA CRNDE expression was significantly associated with clinical stage, lung metastasis, and poor prognosis in OS patients. Additionally, overexpression of lncRNA CRNDE promoted proliferation and migration of OS cells. Bioinformatics analysis showed that lncRNA CRNDE competitively inhibited miR-136-5p through acting as a competitive endogenous RNA (ceRNA). It was also revealed that miR-136-5p is a binding target gene of lncRNA CRNDE and that MRP9 is involved in this process as a downstream target gene of miR-136-5p.	High lncRNA CRNDE expression was significantly associated with clinical stage, lung metastasis, and poor prognosis in OS patients. 	Yes	Additionally, overexpression of lncRNA CRNDE promoted proliferation and migration of OS cells.	36034978
Crnde	LncRNA	Mus musculus	Neuralgia	spinal cord tissues	Regulation[miR-136/IL6R axis ]	RNA Pull-Down//Western Blot//RIP//Luciferase Report Assay//PCR//ELISA	" As found, at postoperative days 3, 6, 9 and
12, CRNDE was increased in CCI rats compared to the sham group
(Figure 1a).Overall, it was implied that CRNDE promoted neuropathic pain progression via modulating miR-136/IL6R axis in CCI rat models."		Yes	 Interestingly, overexpression of CRNDE enhanced neuropathic pain behaviors. 	31131445
CRLM1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells and Balb/C nude mice	Regulation	ChIP//Western Blot//qRT-PCR//RIP//FISH//IF	CRLM1 inhibited apoptosis of CRC cells and promoted liver metastasis in Balb/C nude mice.		Yes	CRLM1 inhibited apoptosis of CRC cells and promoted liver metastasis in Balb/C nude mice.	35907898
CREBBP	CircRNA	Homo sapiens	Liver Cirrhosis	epatic stellate cell	Interaction(hsa-miR-1291/LEFTY2 Axis)	Western Blot//qRT-PCR//PCR//Microarray//RNA Network	For example, circCREBBP was significantly down-regulated in primary hepatic stellate cells (HSCs) and liver tissue of HF mice induced by CCl4 compared to those in the vehicle group. Mechanically, circCREBBP acts as a sponge for hsa-miR-1291 and subsequently promotes LEFTY2 expression.		Yes	Overexpression of circCREBBP with AAV8-circCREBBP in vivo prevented CCl4-induced HF worsening by reducing serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) contents, liver hydroxyproline levels, collagen deposition, and levels of pro-fibrosis genes and pro-inflammatory cytokines. Furthermore, in vitro function loss and function gain analysis showed that circCREBBP inhibited HSCs activation and proliferation. 	34887753
CRCAL-3	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Expression[highly expressed]	PCR	As a result, analyses on TCGA datasets showed an upregulated CRCAL-3 expression in 14 solid tumors, including CRC. PCR assay on 253 cases of CRC tissue and 114 cases of normal adjacent tissue confirmed this expression upregulation.	Also, CRCAL-3 expression was exhibited by survival analyses on the 253 CRC patients, to have a negative correlation with patients' overall and progression-free survivals.	Yes	In vitro knockdown of CRCAL-3 resulted in an obvious retardation of proliferation and migration in two CRC cell lines (HCT116 and DLD-1). Moreover, CRCAL-3 knockdown was observed in xenograft models to repress cell proliferation and enhance cisplatin sensitivity. 	31038794
CRART16	LncRNA	Homo sapiens	Stomach Neoplasms	 gastric cancer tissues 	Interaction(miR-122-5p/FOS axis)	IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA//Colony Formation Assay	We found that CRART16 was substantially overexpressed in gastric cancer tissues compared with normal tissues, based on the TCGA database and our clinical samples. CRART16 was found to downregulate miR-122-5p by acting as a sponge, upregulating the target oncogene FOS. Afterward, the increased FOS expression led to the upregulation of VEGFD.	High expression of CRART16 correlated with more advanced tumor stages and poor prognosis.	Yes	Overexpression of CRART16 in gastric cancer cells promoted proliferation, colony formation, angiogenesis, and bevacizumab resistance in vitro, and it promoted tumor growth and angiogenesis in vivo, and vice versa. 	35537818
cRAPGEF5	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC and adjacent nontumor tissues	Interaction[miR-27a-3p/TXNIP pathway  ]	RIP//IP//qPCR//PCR	In this study, we found cRAPGEF5 to be significantly downregulated in RCC tissues.  In conclusion, cRAPGEF5 plays a role in suppressing RCC via the miR-27a-3p/TXNIP pathway and may serve as a promising prognostic biomarker and novel therapeutic target for RCC patients.	Among 245 RCC cases, cRAPGEF5 downregulation correlated positively with aggressive clinical characteristics and independently predicted poor overall survival and recurrence-free survival. 	Yes	Functional assays demonstrated that cRAPGEF5 suppresses RCC proliferation and migration in vitro and in vivo.	31629934
CR594175	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Expression[lower expressed]	CCK8//qRT-PCR//Invasion Assay//Western Blot	We found that lncRNA-CR594175 was lower in adjacent non-cancerous tissues than in primary HCC, and was lower in primary HCC than in its metastasis. 		Yes	Silencing of lncRNA-CR594175 inhibited the proliferation and invasion of HepG2 cells and growth of subcutaneous tumors. 	32983253
CPS1-IT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Expression [lower expressed]	qRT-PCR//Luciferase Report Assay//Western Blot	Expression of CPS1-IT1 were significantly reduced, while HIF-1α and LC3-II were increased in CRC tissues and cell lines. Then, in vitro assays revealed that CPS1-IT1 suppresses EMT and autophagy by inhibiting the activation of HIF-1α in CRC. An in vivo animal model also demonstrated the tumor suppressor mechanism of CPS1- IT1.		Yes	Then, in vitro assays revealed that CPS1-IT1 suppresses EMT and autophagy by inhibiting the activation of HIF-1α in CRC. An in vivo animal model also demonstrated the tumor suppressor mechanism of CPS1- IT1.	29017924
CPS1-IT1	LncRNA	Homo sapiens	Glioma	Glioma tissues	Expression[lower expressed]	CCK8//qRT-PCR//Transwell Assay	In our study, we observed CPS1-IT1 levels were decreased in glioma tissues and cells compared with paired normal brain tissues and human astrocyte cell line, respectively.	Moreover, we analyzed the associations of CPS1-IT1 expression with clinicopathological characteristics, and found low CPS1-IT1 expression was correlated with high World Health Organisation (WHO) grade and large tumor size in glioma patients. Survival analysis showed glioma patients in low CPS1-IT1 expression group had shorter overall survival than those in high CPS1-IT1 expression group, and low CPS1-IT1 expression was an independent prognostic factor for overall survival in glioma patients. 	Yes	The in vitro studies suggested up-regulation of CPS1-IT1 expression resulted in the decrease of proliferation, migration and invasion abilities of glioma cells. In conclusion, CPS1-IT1 plays an anti-oncogenic role in glioma.	31545272
CPA4	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Expression[highly expressed]	qRT-PCR	 Circ-CPA4 and PD-L1 were high-expressed, while let-7 miRNA was low-expressed in NSCLC cells and cancer tissues compared to the human bronchial epithelial (HBE) cells and their paired clinical normal adjacent tissues, respectively.		Yes	 Besides, knock-down of circ-CPA4 inhibited cell growth, mobility and epithelial-mesenchymal transition (EMT), and promoted cell death in NSCLC cells by downregulating PD-L1 through serving as a RNA sponge for let-7 miRNA. 	32746878
CP	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues 	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot//Transwell Assay	Here, the expression of lncRNA AB073614 in CRC tissues was evaluated by quantitative real-time PCR (qRT-PCR).	 A difference analysis in the lncRNA AB073614 expression in CRC patient group suggested that the expression of lncRNA AB073614 was independently associated with higher possibilities of high grade (P = 0.0005), tumor size (> 5 cm) (P = 0.0001), distant metastasis (P = 0.0009), and differentiation level (P = 0.0037).	Yes	"In vitro studies demonstrated that the knockdown of {""type"": ""entrez-nucleotide"", ""attrs"":{""text"": ""AB073614"", ""term_id"": ""51555790"", ""term_text"": ""AB073614""}}AB073614 suppressed SW480 cell proliferation.  Meanwhile, the overexpression of {""type"": ""entrez-nucleotide"", ""attrs"":{""text"": ""AB073614"", ""term_id"": ""51555790"", ""term_text"": ""AB073614""}}AB073614 in SW480 cells accelerated cell growth and invasion, and suppressed cell apoptosis."	31934121
CP	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissue	Expression[Expression[Expression[highly expressed]-expression]-expression]	qRT-PCR	In present study, we demonstrated that lncRNA AB073614 was significantly Expression[Expression[up-expression]-expression]regulated in ovarian cancer tissues compared to adjacent normal tissues in patients.		Yes	Moreover, we demonstrated that lncRNA AB0736141 knockExpression[down-expression] sExpression[Expression[up-expression]-expression]pressed EOC cell proliferation ability and cell colony formation in vitro. In vivo, we showed that AB0736141 knockExpression[down-expression] sExpression[Expression[up-expression]-expression]pressed tumor growth. 	30909184
COX7C-5	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-581/ZEB2 axis)	IHC//Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Here, we show that Lnc-COX7C-5 was significantly upregulated in HCC tissues, which was correlated with poor prognosis in HCC patients. Mechanistically, lnc-COX7C-5 function as a competing endogenous RNA (ceRNA) for miR-581 in HCC cells. Over-expression or knockdown of miR-581 could alter cell phenotypes caused by Lnc-COX7C-5 in HCC. Further investigations indicated that ZEB2 was demonstrated as a downstream target of miR-581. 	Here, we show that Lnc-COX7C-5 was significantly upregulated in HCC tissues, which was correlated with poor prognosis in HCC patients. 	Yes	Lnc-COX7C-5 positively regulated proliferation, migration, and invasion of HCC cells.  In mouse model, over-expression of Lnc-COX7C-5 facilitate lung metastasis of HCC. 	36273755
cox-2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	macrophages	Expression [highly expressed]	qRT-PCR	 The M1 macrophages had higher lncRNA cox-2 expression than that in the non-polarized macrophages and M2 macrophages. These findings indicate that lncRNA cox-2 inhibits HCC immune evasion and tumor growth by inhibiting the polarization of M2 macrophages.		Yes	The lncRNA cox-2 siRNA decreased the expression levels of IL-12, iNOS, and TNF-α in M1 macrophages, increased the expression levels of IL-10, Arg-1, and Fizz-1 in M2 macrophages (all P < 0.05). The lncRNA cox-2 siRNA reduces the ability of M1 macrophages to inhibit HCC cell proliferation, invasion, migration, EMT, angiogenesis and facilitate apoptosis while strengthening the ability of M2 macrophages to promote proliferation HCC cell growth and inhibit apoptosis. 	29131381
CRNDE	LncRNA	Homo sapiens	Leukemia, Promyelocytic, Acute		Expression[highly expressed]	qRT-PCR//Luciferase Report Assay	 We found that CRNDE was highly expressed in the disease state but not in the preleukemic stage of APL, suggesting that CRNDE might be a secondary event coordinating with PML/RARα to promote APL development. 		Yes	 Functional analysis showed that CRNDE knockdown induced differentiation and inhibited proliferation of APL cells, and prolonged survival of APL mice.	33298855
CRNDE	LncRNA	Homo sapiens	Asthma	neutrophils	Regulation(NF-κB)	Western Blot//Wound Healing Assay//Transfection//qRT-PCR//RIP//Luciferase Report Assay//ELISA//EdU Staining//Transwell Assay	CRNDE was upregulated in LPS-EXO and successfully transferred from LPS-treated neutrophils to ASMCs through exosome.  Mechanically, CRNDE loaded in LPS-EXO reinforced TAK1-mediated IKKβ phosphorylation, thereby activating the nuclear factor kappa B (NF-κB) pathway.  In the end, the in vivo experiment demonstrated that CRNDE knockdown in neutrophils effectively reduced the thickness of bronchial smooth muscle in a mouse model for asthma.		Yes	Functionally, silencing CRNDE in LPS-EXO, an IKKβ inhibitor, and an NF-κB inhibitor all removed the upregulation of cell viability, proliferation and migration induced by LPS-EXO in ASMCs. 	34590683
CORO1C	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC samples and cells	Interaction(miR-654-3p/USP7 Axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//PCR//EdU Staining//IF	 Circ_CORO1C expression was elevated in LSCC samples and cells.  USP7 is highly expressed in LSCC tissues and cells, and its expression was suppressed by circ_CORO1C silencing. Besides, the up-regulation of USP7 attenuated the influence of circ_CORO1C silencing on LSCC cell progression. Both circ_CORO1C and USP7 could bind to miR-654-3p. circ_CORO1C regulated USP7 expression by modulating miR-654-3p. miR-654-3p knockdown mitigated the influence of circ_CORO1C silence on LSCC cell progression. 		Yes	 circ_CORO1C silencing constrained cell proliferation and promoted apoptosis via reducing cell proliferation, inducing cell cycle arrest, inhibiting epithelial-mesenchymal transition, and promoting apoptosis, as well as restraining cell migration and invasion. Furthermore, circ_CORO1C silencing reduced tumor growth in vivo.	35064359
CRNDE	LncRNA	Homo sapiens	Leukemia, Lymphocytic, Chronic, B-Cell	 MEC-1 and HG3 cells	Interaction(miR-28/NDRG2 axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay	 Compared with normal B lymphocytes, CRNDE was down-regulated and the methylation level of CRNDE was increased in MEC-1 and HG3 cells.  Moreover, CRNDE functioned as a competing endogenous RNA to repress miR-28, which controlled its down-stream target NDRG2. CRNDE overexpression inhibited cell proliferation and promoted apoptosis via miR-28/NDRG2 axis in CLL. 		Yes	Then, 5-Aza-CdR treatment caused an increase of CRNDE expression in MEC-1 and HG3 cells by demethylation. The overexpression or demethylation of CRNDE inhibited cell proliferation and promoted apoptosis in MEC-1 and HG3 cells by up-regulating CRNDE expression. 	33857783
CRNDE	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	 AML and U937 cells 	Expression [highly expressed]	CCK8//qRT-PCR	 The expression of lncRNA-CRNDE in patients with AML and U937 cells was significantly higher than that in non-malignant hematological controls. Meanwhile, after transfection of pcDNA-CRNDE, the proliferation ability of U937 cells increased significantly, which indicated that the expression of lncRNA-CRNDE might play an essential role in promoting the proliferation of U937 cells.	Results of clinical data showed that the expression of lncRNA-CRNDE was associated with the classification and total survival of myeloid leukemia in clinical patients. 	Yes	After transfection of siRNA-CRNDE, the proliferation and cloning ability of U937 cells decreased, while the apoptosis increased (p < 0.01) and cells were arrested in G0-G1 phase. Meanwhile, after transfection of pcDNA-CRNDE, the proliferation ability of U937 cells increased significantly, which indicated that the expression of lncRNA-CRNDE might play an essential role in promoting the proliferation of U937 cells.	29461608
CRNDE	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	clinical tissues and cell lines	interaction[PI3K/AKT]	qRT-PCR//Western Blot	This study confirmed that CRNDE is markedly up-regulated in clinical tissues and cell lines of cervical cancer. Loss-of-function assays revealed that CRNDE influences proliferation and apoptosis in cervical cancer cells, and Western blot assays revealed that the PI3K/AKT pathway was inactivated in response to CRNDE knockdown.	The high expression of CRNDE positively correlates with advanced FIGO stage and lymph node metastasis. Furthermore, the overall survival rate in the group with highly expressed CRNDE was worse, and the high level of CRNDE may be regarded a prognostic factor because of its results from proportional hazard analysis. 	Yes	 Loss-of-function assays revealed that CRNDE influences proliferation and apoptosis in cervical cancer cells, and Western blot assays revealed that the PI3K/AKT pathway was inactivated in response to CRNDE knockdown. 	30334449
CRNDE	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and adjacent non-cancerous tissues,cell lines(SiHa，HeLa，CaSki，Ms751，C33a,c4-1,Ect1 / E6E7)	Interaction[suppressing PUMA ]	RNA Pull-Down//Western Blot//RIP//qRT-PCR//Cell Viability Assay	 CRNDE expression was markedly increased in cervical cancer tissues compared to the corresponding non-cancerous tissues.Our study demonstrated that CRNDE, combined with PUMA, could be utilized as factor for the clinical diagnosis and prognosis of cervical cancer, and might be potential target for developing effective therapeutic strategy to prevent cervical cancer progression.	 	Yes	Through loss-of-function and gain-of-function approaches, we found that CRNDE knockdown markedly reduced cervical cancer cell proliferation, while CRNDE overexpression significantly promoted cervical cancer cell growth. Consistently, CRNDE decreasing obviously inhibited tumorigenicity of cervical cancer cells in vivo, whereas CRNDE increasing markedly promoted cervical cancer progression.	31202167
CRNDE	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[CRNDE/miR-183/CCNB1-axis]	qRT-PCR//Luciferase Report Assay//Western Blot	Systematic analyses of bioinformatics from several databases predicted that CRNDE, miR-183 and CCNB1 were in the same network path. Their expressions were up-regulated in CC tissues and cells.Our study highlighted a role for the CRNDE/miR-183/CCNB1-axis in CC and offered a promising diagnostic strategy for CC treatment.		Yes	Silencing CRNDE-inhibited cell proliferation, migration and invasion, restricted solid tumor growth and promoted cell apoptosis. 	31605132
CRNDE	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction(miR-4262/ZEB1 Axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CRNDE and ZEB1 were up-regulated, while miR-4262 was down-regulated in cervical cancer tissues and cells. We found that CRNDE sponged miR-4262 and ZEB1 was a target of miR-4262. Furthermore, ZEB1 rescued the effects of miR-4262 overexpression or CRNDE deletion on cervical cancer progression. 		Yes	miR-4262 inhibitor abolished CRNDE silencing-induced repression on cell proliferation, EMT, migration, invasion and promotion on cell apoptosis. 	33469312
CRNDE	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cell lines	Interaction(miR-3163/TWIST1 Axis)	In Vivo Experiment//IHC//Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Here, we discovered that CRNDE level was increased in NPC tissues and cell lines.Mechanically, CRNDE could serve as a molecular sponge of miR-3163 to regulate the expression of TWIST1. 	Additionally, elevated CRNDE positively correlated with large tumor size, advanced TNM stage, distant metastasis, EBV infection and worse prognosis.	Yes	Furthermore, depletion of CRNDE significantly impaired the capacity of proliferation, migration and invasion in NPC cells.	34796452
CRNDE	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues/cell lines	Interaction(miR-545-5p/CCND2 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	This study demonstrated up-regulated expression of CRNDE and CCND2 within NPC tissues/cell lines.  Meanwhile, miR-545-5p was down-regulated.  All inhibiting functions generated by CRNDE down-regulation upon NPC progression could be counterbalanced or synergistically exacerbated, depending on miR-545-5p down-regulation or up-regulation, respectively. Multiple-level investigations revealed CRNDE to serve as a sponge for miR-545-5p, and can target CCND2 within NPCs.		Yes	CRNDE knock-down or miR-545-5p over-expression drastically reduced NPC proliferative, migrative and invasive properties, promoted apoptosis/altered cell cycle, and inhibited CCND2 expression. However, miR-545-5p down-regulation had opposing effects. 	34863152
CRNDE	LncRNA	Homo sapiens	Multiple Myeloma	blood	regulation[IL6 signalling pathway]	qRT-PCR//MTT	 In this study, we have performed CRISPR-mediated deletion of the locus encoding the lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE), a known oncogenic lncRNA that is overexpressed in plasma cells of MM patients and is a marker of poor prognosis.Altogether this study reveals the IL6 signalling pathway as a novel mechanism by which CRNDE impacts upon MM cell growth and disease progression.		Yes	 We found that CRISPR-mediated deletion of the CRNDE locus in MM cells decreases proliferation and adhesion properties, increases sensitivity to Dexamethasone and reduces tumour growth in an in vivo xenograft model.	32879426
CRNDE	LncRNA	Homo sapiens	Pancreatic Neoplasms	 pancreatic cancer tissues and cell lines	Interaction(miR-451a/CDKN2D axis)	In Vivo Experiment//Western Blot//Transfection//Tube Formation Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//ELISA//Colony Formation Assay//Transwell Assay	The results showed that CRNDE was significantly up-regulated in pancreatic cancer tissues as well as cell lines. In addition, CRNDE was found to positively regulate CDKN2D expression and mediate pancreatic cancer cell proliferation and angiogenesis through miR-451a/CDKN2D axis.		Yes	CRNDE overexpression promoted the progression and angiogenesis of pancreatic cancer cells in vitro and in vivo. 	33882369
CRNDE	LncRNA	Homo sapiens	Osteoporosis, Postmenopausal	osteoclast from patients with OP	Expression[highly expressed]	Flow Cytometry//qRT-PCR//MTT//Western Blot	We found that the CRNDE was highly expressed in the osteoclast from patients with OP, compared with OH. 		Yes	We also found that overexpressing CRNDE increased the viability in OH whilst reducing CRNDE in OP decreased the viability. The cell cycle was arrested in G0/G1 phase and the apoptosis rate was improved in OP after transfection with siRNA. 	30280760
CRNDE	LncRNA	Homo sapiens	Prostatic Neoplasms	 Pca tissues and cells 	regulation[miR-101/Rap1A]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	High expression of CRNDE was shown in Pca tissues and cells and predicted poor outcomes of patients. CRNDE contributed to cell proliferation, migration, and invasion by regulating the miR-101/Rap1A axis in Pca, providing a novel strategy for Pca treatment.	High expression of CRNDE was shown in Pca tissues and cells and predicted poor outcomes of patients.	Yes	Overexpression of CRNDE promoted cell proliferation, migration, and invasion but decreased apoptosis in Pca cells, while its knockdown showed an opposite effect. 	32182086
CRNDE	LncRNA	Homo sapiens	Prostatic Neoplasms	PC tissues	Interaction(microRNA-146a-5p)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In PC tissues, the expression level of lncRNA CRNDE was upregulated. miR-146a-5p was verified as a direct target of lncRNA CRNDE. Moreover, the inhibition of miR-146a-5p partially counteracted the effects of lncRNA CRNDE on PC cell proliferation, migration, and invasion.		Yes	Moreover, knockdown of lncRNA CRNDE suppressed PC cell proliferation and migration and induced apoptosis in vitro. 	34232111
CRNDE	LncRNA	Homo sapiens	Colorectal Neoplasms	HCT-116 cells 	Regulation(Akt/mTORC1 pathway)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry	The results demonstrated that CRNDE inhibition decreased the proliferation and increased the apoptosis and cisplatin sensitivity of HCT-116 cells. In addition, CRNDE inhibition attenuated the Warburg effect in HCT-116 cells, as verified by a decrease in ATP production, lactic acid levels, glucose uptake, and the expression of Warburg effect-related enzymes (GLUT1, LDHA, HK2, and PKM2).CRNDE inhibition also suppressed the activity of the Akt/mTORC1 pathway, as demonstrated by the decreased phosphorylation of Akt, S6K, S6, and mTOR and the increased phosphorylation of 4EBP-1 and EIF-4E.		Yes	The results demonstrated that CRNDE inhibition decreased the proliferation and increased the apoptosis and cisplatin sensitivity of HCT-116 cells. In addition, CRNDE inhibition attenuated the Warburg effect in HCT-116 cells, as verified by a decrease in ATP production, lactic acid levels, glucose uptake, and the expression of Warburg effect-related enzymes (GLUT1, LDHA, HK2, and PKM2).	35069879
CRNDE	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cell lines	Regulation[PI3K/AKT/mTOR pathway]	CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 The results showed CRNDE was upregulated in TSCC tissues and cell lines.In conclusion, high levels of CRNDE might promote TSCC progression at least partly through regulating the PI3K/AKT/mTOR pathway.		Yes	CRNDE knockdown repressed the proliferation, colony formation, migration and invasion and promoted apoptosis in TSCC cells.	35521355
CRNDE	LncRNA	Homo sapiens	Inflammatory Bowel Diseases	 colitis tissues,cell lines (HT-29, LOVO, and Caco-2)	Interaction[suppressing miR-495]	qRT-PCR	CRNDE and SOCS1 were highly expressed, but miR-495 was lowly expressed in the DSS-induced colitis tissues and colonic epithelial cell lines.The interaction between CRNDE and miR-495 was confirmed by RNA immunoprecipitation and RNA pull-down assay. The target relationship between miR-495 and SOCS1 was confirmed by the luciferase reporter assay. CRNDE promoted DSS-induced colonic epithelial cell apoptosis via miR-495/SOCS1. CRNDE interference in DSS-induced colitis mouse model alleviated clinical manifestations of IBD.		Yes	Interference of CRNDE inhibited cell apoptosis of DSS-induced colonic epithelial cells.	31251902
CRNDE	LncRNA	Homo sapiens	Sepsis	renal tissues	Interaction[increasing MiR-181a-5p]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ELISA	We demonstrated that CRNDE was markedly down-regulated while miR-181a-5p was significantly up-regulated in sepsis models. For mechanism, miR-181a-5p directly targeted the 3' untranslated region of PPARα, and depressed its protein level, and PPARα was regulated indirectly by CRNDE. We concluded that CRNDE protected renal cell from sepsis-induced injury via miR-181a-5p/PPARα pathway.		Yes	 Knockdown of CRNDE or transfection of miR-181a-5p significantly inhibited proliferation and promoted apoptosis of HK-2 and HEK293 cells, while overexpression of CRNDE and transfection of miR-181a-5p inhibitors had opposite effects. 	31877497
CRNDE	LncRNA	Homo sapiens	Neuroblastoma	SH-SY5Y and SK-N-AS cells, neuroblastoma tissues	Regulation( ERK/MAPK signaling pathway)	Other	 The relative expression of CRNDE was significantly higher in neuroblastoma tissues than in the adjacent normal tissues.  At the mechanistic level, western blotting showed that CRNDE exerted its oncogenic role by affecting the ERK/MAPK signaling pathway. 		Yes	 Moreover, knockdown of CRNDE inhibited tumor cell proliferation and induced apoptosis and cell cycle arrest, whereas elevation of CRNDE promoted cell growth and inhibited apoptosis in neuroblastoma cells. In addition, depletion of CRNDE suppressed migration and invasion, whereas overexpression of CRNDE enhanced the migratory and invasive potential of SH-SY5Y and SK-N-AS cells.  Furthermore, animal experiments confirmed that CRNDE promotes tumor growth and inhibits apoptosis in neuroblastoma in vivo.	36564069
CRNDE	LncRNA	Homo sapiens	Cholangiocarcinoma	IHCC cell lines and tissues	Expression [highly expressed]	Western Blot//Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	Firstly, the relative expression of CRNDE was observed to be upregulated in IHCC cell lines and tissues. Mechanistically, CRNDE was revealed to facilitate the epithelial-mesenchymal transition (EMT) of IHCC cells.	And high CRNDE expression was statistically associated with IHCC differentiation grade, lymph node metastasis, tumor-nodes-metastasis (TNM) stage and size. Survival analysis identified that high CRNDE expression is a predictor of worse overall survival (OS) and progression-free survival (PFS) in patients with IHCC. 	Yes	 Further studies of in vitro assays suggested that CRNDE silencing could suppress the proliferation of HuCCT1 cells following CCK-8 and colony formation assays, while CRNDE ectopic expression in HCCC9810 cells promoted proliferation. Moreover, the migration and invasion of HuCCT1 cells were greatly repressed with CRNDE deficiency following Transwell and Matrigel assays. Accordingly, the motility of HCCC9810 cells was notably accelerated with CRNDE overexpression. 	29556285
COX10-DT	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues 	Interaction(COX10-DT/miR-206/BDNF axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//BrdU//Cell Cycle Assay//Transwell Assay	 Clinically, we found that the lncRNA COX10-DT was commonly overexpressed in breast cancer tissues compared to paired peritumoural tissues. Mechanistically, the lncRNA COX10-DT did not play a role by regulating the expression of its divergent gene COX10 but acted as a competitive endogenous RNA (ceRNA) by directly sponging miR-206, which further regulated the expression of brain-derived neurotrophic factor (BDNF). 		Yes	Functionally, the lncRNA COX10-DT might promote the proliferation and migration of breast cancer cells.	36463760
COMETT	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[miR-339-5p-mediated regulation of CDK14]	Western Blot//ISH//Wound Healing Assay//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//IHC//Transwell Assay	 Here we found that LINC01510 was highly expressed in NSCLC tissues.Furthermore, mechanistic studies revealed that LINC01510 exerted its oncogenic functions in NSCLC through miR-339-5p-mediated regulation of CDK14. 	Besides, Fisher's exact test showed that high expression of LINC01510 was associated with larger tumor size, advanced TNM stage and lymph node metastasis. Kaplan-Meier survival analysis showed that patients with high LINC01510 expression had a much lower overall survival rate.	Yes	Gain- and loss-of-function approaches were employed to investigate the effects of LINC01510 on NSCLC cell phenotypes. Functional studies demonstrated that LINC01510 over-expression promoted NSCLC cell proliferation, cell cycle progression, migration and invasion, but shRNA-mediated LINC01510 depletion inhibited NSCLC cell proliferation, cell cycle progression, migration and invasion. Notably, LINC01510 ablation suppressed tumorigenicity of NSCLC cells in a murine xenograft model. 	30399588
cHP1BP3	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	 BLCA tissue and YTS-1 cells	Interaction( miR-1-3p)	colony Formation Assay//Western Blot//ISH//Proliferation Assay//FISH//IF//Microarray//ELISA//Colony Formation Assay//Transwell Assay	" cHP1BP3 was upregulated in BLCA tissues, and served as an miR-1-3p ""sponge"". "		Yes	cHP1BP3 was shown to modulate migratory ability, proliferation, and colony formation of YTS-1 cells, and displayed tumor-suppressing activity in BLCA. Target glycoproteins of C1GALT1, including integrins and MUC16, were identified.	35864552
ciRS-7	CircRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	regulation[iR-7/EGFR axis]	colony Formation Assay//Western Blot//Wound Healing Assay//qPCR//PCR//Colony Formation Assay//IF	ciRS-7 was highly expressed in PTC tissues and cell lines compared with the corresponding controls. ciRS-7 was significantly upregulated in PTC tissues, and it promoted the progression of PTC by regulating the miR-7/EGFR axis.		Yes	In vitro study showed that ciRS-7 silencing suppressed proliferation, migration, and invasion of TPC-1 and BCPAP. 	32685551
ciRS-7	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LSCC tissues	Interaction(miR-432-5p/DNMT3B axis)	Western Blot//ISH//Transfection//Flow Cytometry//qRT-PCR//RIP//FISH//PCR//IP//Transwell Assay//IF	 Higher ciRS-7 expression in LSCC tissues was closely associated with higher clinical stage, and exacerbated infiltration and lymph node metastasis in LSCC patients. When miR-432-5p was inhibited or DNMT3B was overexpressed, the growth and EMT of LSCC cells were stimulated despite ciRS-7 silencing. Downregulation of ciRS-7 restrained the growth of xenograft tumors in vivo.	 Higher ciRS-7 expression in LSCC tissues was closely associated with higher clinical stage, and exacerbated infiltration and lymph node metastasis in LSCC patients. 	Yes	 Silencing ciRS-7 inhibited LSCC cell viability, epithelial-mesenchymal transition (EMT), and promoted the apoptosis. 	36356335
ciRS-7	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tissues	Expression[highly expressed]	qRT-PCR//Western Blot	ciRS-7 was overexpressed in ccRCC tissues compared with that in matched adjacent normal tissues.	In addition, ciRS-7 up-regulation was closely associated with tumor diameter (P = 0.050), clinical stage (P = 0.009), and distant metastasis (P = 0.007). 	Yes	 ciRS-7 knockdown in 786O and 769P cells markedly inhibited their proliferative and invasive abilities. 	32496306
ciRS-7	CircRNA	Homo sapiens	Arthritis, Rheumatoid	3 patients with RA and 3 healthy participants	Interaction( miR-7)	Transfection//RIP//PCR//IP//Invasion Assay//IF	 We identified distinct miRNA features in RA-FLS, including miR-7, which was significantly lower expressed. Furthermore, we discovered the negative regulatory relationship between ciRS-7 and miR-7 in RA-FLS. Finally, we overexpressed miR-7 in RA-FLS and discovered that miR-7 inhibited RA-FLS hyperproliferation, migration, invasion, and apoptosis, whereas ciRS-7 overexpression reversed these effects.		Yes	 We identified distinct miRNA features in RA-FLS, including miR-7, which was significantly lower expressed. Furthermore, we discovered the negative regulatory relationship between ciRS-7 and miR-7 in RA-FLS. Finally, we overexpressed miR-7 in RA-FLS and discovered that miR-7 inhibited RA-FLS hyperproliferation, migration, invasion, and apoptosis, whereas ciRS-7 overexpression reversed these effects.	35752700
ciRS-7	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells and tissues	Interaction [miR-876-5p/MAGE-A ]	colony Formation Assay//Western Blot//Wound Healing Assay//Colony Formation Assay//qRT-PCR//RIP//MTT//PCR//IP//IHC//Invasion Assay//IF	 Here, we showed that ciRS-7 is up-regulated in esophageal squamous cell carcinoma (ESCC), and is associated with the poor clinicopathological parameters of ESCC patients. Mechanistic studies revealed that ciRS-7 contains nineteen miR-876-5p binding sites and acts as a miR-876-5p sponge. Over-expression of ciRS-7 resulted in the reduced tumor-repressive function of miR-876-5p on its downstream target MAGE-A family.	 Here, we showed that ciRS-7 is up-regulated in esophageal squamous cell carcinoma (ESCC), and is associated with the poor clinicopathological parameters of ESCC patients. 	Yes	Moreover, over-expression of ciRS-7 increased the proliferation, migration and invasion of ESCC cells. In animal experiments, enforced ciRS-7 increased ESCC tumor growth and metastasis through targeting miR-876-5p/MAGE-A family axis. 	29635069
ciRs-6	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction[sponging miR-653 ]	qPCR//CCK8//RNA-seq//PCR//IF	 ciRs-6 is expressed at low levels in cancer tissues and advanced tumor grades and stages, and its expression correlates with better outcomes for bladder cancer patients.In vitro and in vivo, ciRs-6 was shown to suppress bladder cancer growth by sponging miR-653 to elevate March1 levels. 	 ciRs-6 is expressed at low levels in cancer tissues and advanced tumor grades and stages, and its expression correlates with better outcomes for bladder cancer patients.	Yes	 In vitro and in vivo, ciRs-6 was shown to suppress bladder cancer growth by sponging miR-653 to elevate March1 levels.	31819015
CIRPIL	LncRNA	Mus musculus	Myocardial Reperfusion Injury	s I/R injury in mice	Expression(lower expressed)	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//FISH//IF	The microarray screening identifies a down-regulated heart-enriched lncRNA-CIRPIL (Cardiac ischemia reperfusion associated p53 interacting lncRNA, lncCIRPIL) from the hearts of I/R mice. Cardiac-specific transgenic overexpression of lncCIRPIL alleviates I/R injury in mice, while knockout of lncCIRPIL exacerbates cardiac I/R injury. 		Yes	 LncCIRPIL inhibits apoptosis of cultured cardiomyocytes exposed to anoxia/reoxygenation (A/R). 	35851102
CIRKIL	LncRNA	Homo sapiens	Heart Injuries	 I/R myocardium, cardiomyocytes	Interaction(Ku70)	RNA Pull-Down//RIP	The expression of CIRKIL was increased in I/R myocardium and H2O2-treated cardiomyocytes. Mechanistically, CIRKIL directly bound to Ku70 to subsequently decrease nuclear translocation of Ku70 and impair DNA double-strand breaks repair. Concurrent overexpression of Ku70 mitigated CIRKIL overexpression-induced myocardial I/R injury. 		Yes	Overexpression of CIRKIL increased the expression of γH2A.X, a specific marker of DNA double-strand breaks and aggravated cardiomyocyte apoptosis, whereas knockdown of CIRKIL produced the opposite changes. Transgenic overexpression of CIRKIL aggravated cardiac dysfunction, enlarged infarct area, and worsened cardiomyocyte damage in I/R mice. Knockout of CIRKIL alleviated myocardial I/R injury. Furthermore, knockdown of human CIRKIL significantly suppressed cell damage induced by H2O2 in adult human ventricular cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes.	35105170
cir-ITCH	CircRNA	Homo sapiens	Prostatic Neoplasms	PCa tissue,cell lines	regulation[Wnt/β-catenin and PI3K/AKT/mTOR pathways]	Western Blot//qPCR//Proliferation Assay//PCR//Cell Proliferation Assay//IF	We found that cir-ITCH expression was typically downregulated in the tissues and cell lines of PCa compared to that in the peritumoral tissue and in RWPE-1 cells, respectively. Taken together, these data demonstrated that cir-ITCH plays a tumor-suppressive role in human PCa cells, partly through the Wnt/β-catenin and PI3K/AKT/mTOR pathways. 		Yes	The results showed that cir-ITCH overexpression significantly inhibits the proliferation, migration, and invasion of human PCa cells and that reciprocal inhibition of expression occurred between cir-ITCH and miR-17. 	32904490
circMAPK1	LncRNA	Rattus norvegicus	Atherosclerosis	VSMCs	Interaction(miR-22-3p/ methyl-CpG binding protein 2 axis)	In Vivo Experiment//Wound Healing Assay//CCK8//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Transwell Assay//IF	Six circRNAs were up-regulated and 12 circRNAs were down-regulated in the atherosclerotic plaque tissues. Then we focused on circMAPK1, which showed a high level in atherosclerosis. Silencing circMAPK1 suppressed the proliferation and migration of VSMCs. Further study showed that circMAPK1 bound with miR-22-3p. CircMAPK1 silencing increased the level of miR-22-3p and suppressed the level of MECP2, a known target of miR-22-3p. Interestingly, suppression of miR-22-3p rescued the effect of circMAPK1 silencing on the proliferation and migration of VSMCs.		Yes	Silencing circMAPK1 suppressed the proliferation and migration of VSMCs. Further study showed that circMAPK1 bound with miR-22-3p. CircMAPK1 silencing increased the level of miR-22-3p and suppressed the level of MECP2, a known target of miR-22-3p.	34059381
cir-CCDC66	CircRNA	Homo sapiens	Hirschsprung Disease	HSCR tissues	Interaction[sponging miR-488-3p]	qRT-PCR	Thus, we discovered the cir-CCDC66 was downregulated in HSCR compared with the normal gut tissues. In conclusion, this is the first report revealing that cir-CCDC66 modulates DCX expression through sponging miR-488-3p and thus participates in the onset of HSCR.		Yes	The cir-CCDC66 reduction might inhibit cells' proliferation and migration in vitro.	30443988
cicrRNA_105040	CircRNA	Homo sapiens	Stomach Neoplasms	GEO(GC tissues and matched normal tissues)	Interaction(miR-324-5p/HMGA1 axis)	RNA Pull-Down//Western Blot//ISH//qPCR//PCR//IF	Hsa_circ_0091994 (cicrRNA_105040) was identified as a highly upregulated circRNA in GC tissues, whose host gene is negatively associated with the overall survival of patients. Bioinformatics analysis and a luciferase assays revealed that hsa_circ_0091994 knockdown inhibits GC progression by suppressing miR-324-5p and HMGA1 expression. Hsa_circ_0091994 knockdown inhibited the progression of GC by inhibiting the miR-324-5p/HMGA1 axis.	Hsa_circ_0091994 (cicrRNA_105040) was identified as a highly upregulated circRNA in GC tissues, whose host gene is negatively associated with the overall survival of patients. 	Yes	Using cell counting kit-8 and Annexin V assays, we observed that hsa_circ_0091994 knockdown inhibited the viability of AGS and HGC-27 cells by inducing apoptosis. Scratch wound healing assays showed that hsa_circ_0091994 knockdown also inhibited GC cell healing. The antitumor effect of hsa_circ_0091994 knockdown was confirmed in vivo using a mouse xenograft model. 	34483139
cia-MAF	CircRNA	Homo sapiens	Liver Neoplasms	Liver cancer and liver TICs	Expression [highly expressed]	Northern Blot//Microarray	 Here, we have identified a functional circular RNA, termed circRNA activating MAFF (cia-MAF), that is robustly expressed in liver cancer and liver TICs. cia-MAF-KO primary cells and cia-maf-KO liver tumors harbor decreased ratios of TICs, and display impaired liver tumorigenesis, self-renewal, and metastatic capacities. In contrast, cia-MAF overexpression drives liver TIC propagation, self-renewal, and metastasis. Mechanistically, cia-MAF binds to the MAFF promoter, recruits the TIP60 complex to the MAFF promoter, and finally promotes MAFF expression. MAFF is highly expressed in liver tumors and liver TICs, and its antisense oligo (ASO) has therapeutic potential in treating liver cancer without MAFA/MAFG gene copy number alterations (CNAs). 	cia-MAF was highly expressed in liver cancer, and its expression levels were correlated with the clinical severity (Figure 1A), as well as tumor relapse (Figure 1B), patient prognosis (Figure 1C),	Yes	cia-MAF-KO primary cells and cia-maf-KO liver tumors harbor decreased ratios of TICs, and display impaired liver tumorigenesis, self-renewal, and metastatic capacities.	34403373
CHST15	CircRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines 	Interaction(miR-155-5p and miR-194-5p / PD-L1)	colony Formation Assay//RNA Pull-Down//Western Blot//Transfection//qPCR//Flow Cytometry//PCR//ELISA//Colony Formation Assay//Bioinformatics Analysis//IF	CircCHST15 and PD-L1 were high-expressed in lung cancer, and the two was positively correlated. CircCHST15 targeted miR-155-5p and miR-194-5p, the later further targeted PD-L1. 		Yes	Lung cancer cell viability and proliferation were increased by miR-155-5p and inhibited by miR-194-5p.	33777742
Chrnb2	LncRNA	Mus musculus	Dry Eye Syndromes	DED mice	Regulation	In Vivo Experiment//qRT-PCR//RNA-seq//Bioinformatics Analysis	Chrnb2, Gabarapl2, and Usp31 were thereby confirmed as the most significantly altered lncRNAs. Pathway analysis revealed that the neuroactive ligand-receptor interaction signaling pathway was the most enriched, followed by the calcium signaling pathway and cytokine-cytokine receptor interaction. 		Yes	Following treatment of Gabarapl2 siRNA and Chrnb2 siRNA, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were significantly downregulated in the HCECs. 	34957168
CHRF	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue	regulation[EMT ]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	 LncRNA CHRF expression was significantly higher in 103 GC tissue samples compared with the adjacent para-tumor samples.		Yes	Inhibition of lncRNA CHRF reduced the invasion and migration of MKN-7 cells while the over-expression of lncRNA CHRF promoted HGC-27 cells metastasis.	32096147
CHRF	LncRNA	Homo sapiens	Prostatic Neoplasms	cell line	Interaction[microRNA-10b]	qRT-PCR	LncRNA CHRF promoted mesenchymal transition (EMT), showing down-regulation of E-cadherin and up-regulation of N-cadherin, vimentin and ZEB1. Afterwards, we found miR-10b expression was positively correlated with lncRNA CHRF expression, and miR-10b inhibition could reverse the effects of lncRNA CHRF on PC3 and LNCaP cell proliferation and EMT. Finally, lncRNA CHRF was found to activate the GSK3β/AKT and NF-κB pathways via up-regulation of miR-10b. LncRNA CHRF silence repressed proliferation and EMT while promoted apoptosis in PC3 cells via positive regulation of miR-10b. The GSK3β/AKT and NF-κB pathways were activated by lncRNA CHRF, possibly through up-regulation of miR-10b.		Yes	 LncRNA CHRF silence repressed cell number (%), down-regulated expression of cyclinD1, CDK4 and CDK6, and promoted apoptosis along with activation of the casapse-3 and caspase-9. 	30844757
CHRF	LncRNA	Homo sapiens	Myocardial Reperfusion Injury	myocardial I/R injury models	Interaction(miR-182-5p/ATG7 pathway)	RNA Pull-Down//Western Blot//Transfection//Tunel//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//IF	In our current work, we found that the expression of CHRF was upregulated in myocardial I/R injury models.  To sum up, our results suggested that CHRF exacerbated myocardial I/R injury by enhancing autophagy via modulation of the miR-182-5p/ATG7 pathway. 		Yes	 Suppression of CHRF relieved myocardial I/R injury in vivo.  In addition, in vitro silencing of CHRF enhanced cell viability and attenuated lactate dehydrogenase activity (LDH) as well as apoptosis in H9C2 cells treated with hypoxia/reoxygenation injury. Autophagy has been studied to play an important role in myocardial I/R injury. Thus, experiments related to autophagy were done, and the results showed that CHRF knockdown decreased autophagy.	33491285
CHRF	LncRNA	Mus musculus	Cerebral Ischemia/Reperfusion Injury	brain tissue	Regulation[miR-126/SOX6 signaling pathway]	Transfection//Immunoblotting//Tunel//qRT-PCR//Luciferase Report Assay//IF	 In this study, we found that CHRF was significantly correlated with miR-126, and miR-126 expression was decreased in the ischemic core following ischemia, while CHRF expression was increased according to the in vivo and in vitro experiments. Moreover, CHRF played as a competing endogenous RNA (ceRNA) and competed with Sex-determining region Y box 6 (SOX6) to direct binding with miR-126, subsequently regulating ischemic neuronal death. CHRF knockdown in vivo markedly prevented ischemic damage and alleviated neurological dysfunctions. 		Yes	CHRF knockdown in vivo markedly prevented ischemic damage and alleviated neurological dysfunctions.	31060778
ciRS-7	CircRNA	Homo sapiens	Pancreatic Neoplasms	PDAC tissues	Regulation[EGFR/STAT3 signaling pathway]	qRT-PCR//MTT//PCR//Western Blot	 ciRS-7 expression was significantly higher in PDAC tissues than paracancerous tissues (P = 0.002). Furthermore, ciRS-7 knockExpression[down-expression] sExpression[Expression[up-expression]-expression]pressed cell proliferation and invasion of PDAC cells (P < 0.05), and the Expression[down-expression]regulation of ciRS-7 resulted in miR-7 overexpression and subsequent inhibition of epidermal growth factor receptor (EGFR) and signal transducer and activator of transcription 3 (STAT3).		Yes	Furthermore, ciRS-7 knockExpression[down-expression] sExpression[Expression[up-expression]-expression]pressed cell proliferation and invasion of PDAC cells (P < 0.05), and the Expression[down-expression]regulation of ciRS-7 resulted in miR-7 overexpression and subsequent inhibition of epidermal growth factor receptor (EGFR) and signal transducer and activator of transcription 3 (STAT3).	30898507
ciRS-7	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	regulation[MAPK/AKT signaling pathways]	qPCR//Western Blot//PCR//IF	We found that ciRS-7 was highly expressed in OSCC tissues and cell lines compared with normal counterparts. Our results suggested that ciRS-7 can interact directly with miR-7, resulting in upregulation of RAF-1/PIK3CD expression and enhancing metastatic progression of OSCC.		Yes	 Ectopic expression of ciRS-7 significantly promoted OSCC cell proliferation, migration and invasion through in vitro and in vivo. 	32956704
COMETT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation(MET)	Western Blot//ISH//qRT-PCR//MTT//Colony Formation Assay	 In the present study, we found that LINC01510 was significantly upregulated in CRC tissues and cell lines.  Further study indicated that LINC01510 was positively correlated with the expression of MET, and its effects were most likely at the transcriptional level.	 The LINC01510 expression level were associated with the clinicopathological grade and stage. 	Yes	Meanwhile, gain- and loss-of-function assays demonstrated that LINC01510 overexpression increased CRC cell proliferation, and promoted cell cycle progression from the G1 phase to the S phase.	29581707
CiRS-7	CircRNA	Homo sapiens	Ovarian Neoplasms	OC cells and tissues	regulation[ciRS-7/miR-641/ZEB1 or ciRS-7/miR-641/MDM2 axis]	IP//qPCR//PCR	CiRS-7 expression was significantly higher in OC cells and tissues, Targeting ciRS-7/miR-641/ZEB1 or ciRS-7/miR-641/MDM2 axis may be a novel diagnostic, prognostic and therapeutic strategy for OC.	CiRS-7 expression was significantly higher in OC cells and tissues, which was significantly associated with the TNM stages, lymph node metastasis status and overall survival rate in OC patients. 	Yes	CiRS-7 silence inhibited OC cell growth and metastasis.	32667627
COMETT	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cell lines	Interaction[modulating miR-335/SHH and activating Hedgehog pathway]	RNA Pull-Down//ChIP//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	In this study, we firstly reported that LINC01510 was highly expressed in both PTC tissues and cell lines. Moreover, down-regulation of LINC01510 resulted in accelerated apoptosis by promoting the expression of Caspase3/9. In particular, LINC01510 acted as an endogenous sponge by directly binding miR-335, resulting in the suppression of miR-335 expressions. Besides, we confirmed that SHH was a target of miR-335 and miR-335 over-expression distinctly reduced SHH expression in PTC cells. Finally, in the cytoplasm, we provided evidenced that LINC01510 acted as a sponge for miR-335, reducing its ability to promote SHH expression. In addition, the results of Western blot indicated that knockdown of LINC01510 inhibited the expression of SHH and GLI1, suggesting that Hedgehog pathway was suppressed. Taken together, our findings revealed that the newly identified LINC01510/miR-335/SHH axis could be a therapeutic target for PTC.		Yes	Functional assays with a series of cell experiments indicated that knockdown of LINC01510 suppressed the proliferation, migration and invasion of SW1736 and TPC-1 cells. 	31590919
COMETT	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Regulation[Wnt/β-catenin signaling]	qRT-PCR	Moreover, the down-regulated LINC01510 was further confirmed in our fresh tissues and cell lines.Taken together, we found that LINC01510 regulates cell proliferation and invasion by modulating Wnt/β-catenin signaling in RCC.		Yes	Biological functions assays shown that Ectopic expression of LINC01510 not only inhibits RCC cell proliferation both in vitro and in vivo, but also impairs cell invasion ability.	30224058
COL4A2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell line	Interaction(miR-20b-5p/HIF1A axis)	qRT-PCR//RIP	The data revealed an upregulated expression of COL4A2-AS1 in CRC tissues and cell lines than paired adjacent tissues and normal cell line.In CRC cells, miR-20b-5p was sponged by COL4A2-AS1 and hypoxia-inducible factor 1 alpha subunit (HIF1A). Restoration of HIF1A expression reversed the inhibitory effects of silencing COL4A2-AS1 on aerobic glycolysis and proliferation of CRC cells. 		Yes	Silencing COL4A2-AS1 inhibited proliferation, aerobic glycolysis, and promoted apoptosis of CRC cells in vivo and in vitro. However, overexpression of COL4A2-AS1 significantly promoted CRC cell proliferation and aerobic glycolysis.	34477476
COL1A1-014	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Regulation[CXCL12-CXCR4 axis ]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that COL1A1-014 was frequently upregulated in GC tissues as well as cells. Overexpression of COL1A1-014 increased the mRNA expression of chemokine (CXCmotif) ligand (CXCL12) and high levels of CXCL12 and CXCR4 proteins in GC cells. The levels of miR-1273h-5p showed an inverse correlation with COL1A1-014 and CXCL12 in GC cells transfected with miR-1273h-5p. The mRNAs of wild-type COL1A1-014 and CXCL12 showed reduction in HEK293 cells transfected with miR-1273h-5p. This suggested that COL1A1-014 functions as an efficient miR-1273h-5p sponge and as a competing endogenous RNA (ceRNA) to regulate CXCL12. The proliferative activity of COL1A1-014 on GC cells was blocked by CXCL12-CXCR4 axis inhibitor AMD-3100.		Yes	COL1A1-014 increased cell proliferation, colony forming efficiency, migration ability, invasion ability, and weight and volume of grafted tumors, while reduced cell apoptosis.	31650323
COL18A1-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction(miR-1286/KLF12 axis)	In Vivo Experiment//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//IHC//IF	"In this study, we found lncRNA COL18A1-AS1 was downregulated in ccRCC and that higher COL18A1-AS1 expression indicated better prognosis.  Decreased COL18A1-AS1 expression was caused by DNA methylation at the CpG islands within its promoter. Mechanistically, COL18A1-AS1 could competitively bind miR-1286 to increase the expression of Krüppel-like factor 12 (KLF12). Downregulation of COL18A1-AS1 in ccRCC resulted in the low expression of KLF12. COL18A1-AS1/KLF12 positively regulated uncoupling protein 1 (UCP1)-mediated lipid browning, which promotes tumor cell ""slimming"" and inhibits tumor progression. When tumor cell ""slimming"" occurred, lipid droplets turned into tiny pieces, and lipids were consumed without producing ATP energy. "		Yes	Restoring the epigenetically silenced COL18A1-AS1 repressed tumor progression, promoted lipid browning and consumption in vitro and in vivo.	35787628
CNOT2	CircRNA	Homo sapiens	Breast Neoplasms	BC tissues	Interaction(miR-153-3p/ANLN Axis)	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The results assured that circCNOT2 and Twist Family BHLH Transcription Factor (TWIST1) were elevated in BC, while microrNA (miR)-409-3p was reduced. 	CircCNOT2 was positively correlated with TWIST1 and negatively correlated with miR-409-3p. Elevated circCNOT2 is associated with poor prognosis of BC.	Yes	Knockdown circCNOT2 or augmented miR-409-3p could promote apoptosis but repress proliferation, invasion, migration and EMT of BC cells. In addition, overexpression of circCNOT2 or TWIST1 accelerated BC invasion, migration and EMT, which could be reversed by simultaneous transfection of miR-409-3p-mimic. 	34698000
CNALPTC1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-6788-5p/PAK1 pathway)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 The elevated expression level of CNALPTC1 was observed in GC tissues and cell lines. In addition, we observed that CNALPTC1 functions as a molecular sponge for miR-6788-5p, and the level of expression of CNALPTC1 exhibited a negative correlation with miR-6788-5p. Moreover, it was revealed that the miR-6788-5p's direct target was PAK1, which could reverse the inhibitory function of miR-6788-5p.		Yes	 The in vitro analysis indicated that gene silencing of CNALPTC1 resulted in inhibition, whereas upregulation of CNALPTC1 resulted in the promotion of invasion, proliferation, and migration of GC cells, respectively. 	36636079
cMras	CircRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Interaction[miR-567/PTPRG regulatory pathway]	Western Blot//qRT-PCR//PCR//IP//IF	Thirty-six paired LUAD and healthy tissues were collected and cMras resulted significantly downregulated in cancerous tissues. Bioinformatics analysis and experimental evidence confirmed that cMras was a sponge of miRNA-567 and released its direct target, PTPRG. cMras overexpression decreased miR-567 expression and subsequently increased PTPRG expression, while increased miRNA-567 expression blocked the effects induced by cMras. Moreover, PTPRG was downregulated in LUAD and patients with low PTPRG expression exhibited significantly poor prognosis. These results suggested that cMras/miR-567/PTPRG regulatory pathway might be associated to LUAD tumorigenesis and development.	 Thirty-six paired LUAD and healthy tissues were collected and cMras resulted significantly downregulated in cancerous tissues. Its expression was negatively associated with tumour stages.	Yes	cMras overexpression suppressed LUAD growth and metastasis, while endogenous cMras silencing resulted in the opposite effects.	31012177
cMras	CircRNA	Homo sapiens	Adenocarcinoma of Lung	LAC tissues and cells	regulation[ABHD5/ ATGL Axis Using NF-κB Signaling Pathway]	Western Blot//qPCR//Flow Cytometry//MTT//PCR	Low levels of circ_cMras, ABHD5, and ATGL were observed in LAC tissues and cells.Circ_cMras exerted its function through ABHD5/ATGL axis using NF-κB signaling pathway in LAC, which might provide a novel insight for the diagnosis and prognosis of LAC.		Yes	Upregulation of circ_cMras could hamper tumor aggression in vitro and in vivo, exhibiting as the inhibition of cell proliferation, migration, invasion, and promotion of cell apoptosis, as well as the inhibition on tumor growth in vivo. 	32822232
CLSPN	CircRNA	Homo sapiens	Glioblastoma	 GBM tumor tissues and cells	Interaction(miR-370-3p-USP39 pathway)	RNA Pull-Down//Western Blot//Transfection//qPCR//Flow Cytometry//RIP//IF//PCR//IP//Transwell Assay	First, we examined expression of circCLSPN using GSE109569 database and RT-qPCR, and circCLSPN level was upregulated in human GBM tumor tissues and cells (A172 and LN18); moreover, circCLSPN showed a stable structure stability. According to dual-luciferase reporter assay and RNA pull-down assay, miR-370-3p was identified to be targeted and sponged by circCLSPN, and further targeted and negatively regulated USP39. 		Yes	Consequently, circCLSPN silencing suppressed cell viability, colony formation ability, cell cycle progression, migration, and invasion of A172 and LN18 cells in vitro, and promoted apoptosis rate. Allied with those were decreased B cell lymphoma-2 (Bcl-2), matrix metalloproteinase-2 (MMP2) and MMP9 expression, and elevated Bcl-2-associated X protein (Bax) level. 	34269180
CLRN1-AS1	LncRNA	Homo sapiens	Prolactinoma	pituitary prolactinoma tissues	Regulation[Wnt/β-catenin signaling pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Microarray//Colony Formation Assay//EdU Staining//ChIP	LncRNA clarin 1 antisense RNA 1 (CLRN1-AS1) was downregulated in 42 patient samples and inactivated the Wnt/β-catenin signaling pathway. In summary, this study revealed that FOXP1-induced CLRN1-AS1 regulated cellular functions in pituitary prolactinoma by sponging miR-217 to release the DKK1/Wnt/β-catenin signaling pathway.		Yes	Functionally, CLRN1-AS1 suppressed cell proliferation, promoted apoptosis, and inhibited autophagy. 	31235696
CKMT2-AS1	CircRNA	Homo sapiens	Colorectal Neoplasms	Cell lines 	Regulation(AKT/mTOR Signaling Pathway)	qRT-PCR//Western Blot	 We found CKMT2-AS1 was the most significant=0.0105 for SW480 and P=0.0071 for HCT116) difference lncRNA between colorectal cancer treated with autophagy inducer and colorectal cancer without any treatment. Furthermore, we found the phosphorylation of mTOR, AKT was enhanced in SW480, and HCT116 cells treated with autophagy inducer + shRNA-CKMT2-AS1 compared to the cells treated with autophagy inducer of autophagy inducer + shRNA-NC.		Yes	Following, we found the treatment of autophagy inducer and autophagy inducer + shRNA-NC were able to suppress the proliferation of both SW480 and HCT116 cells. In addition, the treatment of autophagy inducer + shRNA-CKMT2-AS1 significantly reduced the apoptosis of SW480 and HCT116 cells induced by autophagy. 	35866106
cis-HOX	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal tumor-initiating cells 	Interaction(HOXC10)	Northern Blot//Western Blot//IF//PCR//IP//Transwell Assay	Here we find that cis-HOX (circular RNA stabilizing HOXC10) is robustly expressed in colorectal tumor-initiating cells (TICs).  Mechanistically, cis-HOX binds to HOXC10 mRNA to attenuate its decay through blocking the K-homology splicing regulatory protein (KSRP)-binding sequence of HOXC10 3' UTR. HOXC10 is highly expressed in colorectal tumors and TICs and triggers Wnt/β-catenin activation by activating FZD3 expression. 		Yes	 cis-HOX knockout decreases colorectal TIC numbers and impairs the self-renewal, tumorigenesis, and metastatic capacities of TICs, whereas cis-HOX overexpression drives colorectal TIC self-renewal and metastasis. 	34320348
CiRS-7	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells 	Interaction( ciRS-7/miR-7/NF-kB axis )	Western Blot//Transfection//qPCR//MTT//PCR//IF	Moreover, remarkably up-regulated ciRS-7 and RELA expressions, as along with down-regulated miR-7 expressions, were found within NSCLC tissues and cells in comparison with normal ones (P < .05).  More than that, ciRS-7 specifically targeted miR-7 to reduce its expressions (P < .05). Ultimately, the NSCLC cells within miR-7 + RELA group were observed with superior proliferative, migratory and invasive capabilities than those within miR-7 group (P < .05), and RELA expression was also significantly modified by both ciRS-7 and miR-7 (P < .05). In conclusion, the ciRS-7/miR-7/NF-kB axis could exert pronounced impacts on the proliferation, migration, invasion and apoptosis of NSCLC cells.		Yes	Besides, overexpressed ciRS-7 and underexpressed miR-7 were correlated with increased proliferation, migration and invasion, yet reduced apoptosis rate of NSCLC cells (P < .05). 	29532994
ciRS-7	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cancer tissues	Regulation[miR-7/HOXB13]	colony Formation Assay//Western Blot//PCR//Colony Formation Assay//IF	 In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival.Mechanistically, ciRS-7 functioned as the sponge of miR-7 and reactivated its downstream HOXB13-mediated NF-κB/p65 pathway. 	 In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival.	Yes	Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell proliferation, migration and invasion in vitro as well as tumor growth and lung metastasis in vivo. 	30082829
ciRS-7	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissue	Interaction[miR-7/KLF4 and NF-κB signals]	qRT-PCR//Western Blot	The expression of ciRS-7 was significantly increased in the ESCC tissues and cells as compared with their corresponding controls.Over expression of miR-7, one of well-known targets of ciRS-7, can attenuate ciRS-7 induced invasion of ESCC cells and over expression of matrix metalloproteinase 2 (MMP2). The expression of stem cell marker KrExpression[Expression[up-expression]-expression]pel-like factor-4 (KLF-4), which has been reported as the target of miR7, increased significantly in ciRS-7 transfected ESCC cells. KnockExpression[down-expression] of KLF-4 also attenuated over expression of ciRS-7 induced cell invasion. In addition, BAY 11-7082, the inhibitor of NF-κB, partially reversed ciRS-7 induced cell invasion. Mechanically studies indicated that ciRS-7 increased the expression of p65 via increasing the phosphorylation of IKK-α. 		Yes	In vitro study showed that ciRS-7 can promote the migration and invasion of ESCC cells.	30207835
ciRS-7	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tumor tissues and cell lines	Interaction(miR-139-3p/TAGLN axis and activating the PI3K/AKT signaling pathway)	PCR	"ciRS-7 was highly expressed in RCC tumor tissues and cell lines, and high ciRS-7 expression correlated with tumor size, high Fuhrman grade and poor survival. Depletion of ciRS-7 significantly inhibited RCC cell proliferation, invasion, tumor growth and metastasis in vivo, while overexpression of ciRS-7 had the opposite effect. Mechanistically, ciRS-7 acts as a ""ceRNA"" for miR-139-3p to prevent TAGLN degradation and promoting RCC progression and metastasis via the PI3K/AKT signaling pathway. In addition, miR-139-3p mimics or inhibitor could reverse the altered malignant tumor behavior caused by ciRS-7 overexpression or silencing. Furthermore, the PBAE/siciRS-7 nanocomplexes could significantly inhibit RCC tumor progression and metastasis in vivo. ciRS-7 acts as a tumor promoter by regulating the miR-139-3p/TAGLN axis and activating the PI3K/AKT signaling pathway to promote RCC progression and metastasis. Drug development of PBAE/si-ciRS-7 nanocomplexes targeting ciRS-7 may represent a promising gene therapeutic strategy for RCC."		Yes	In addition, miR-139-3p mimics or inhibitor could reverse the altered malignant tumor behavior caused by ciRS-7 overexpression or silencing.	34740354
ciRS-7	CircRNA	Homo sapiens	Osteoarthritis	blood	Regulation[ciRS-7/miR-7 axis  ]	Western Blot//qRT-PCR//MTT//PCR//ELISA	Decreased ciRS-7 expression and increased miR-7 expression were observed in OA blood samples. These findings demonstrate that the ciRS-7/miR-7 axis can possibly serve as a regulator in mediating proliferation, apoptosis and inflammation in chondrocytes in the process of OA development.		Yes	Transfection of ciRS-7 siRNA and miR-7 mimic enhanced the impact of IL-1β on inflammatory cytokine release and cell apoptosis as quantified using ELISA and flow cytometry. Conversely, ciRS-7 cDNA and miR-7 inhibitor induced the reverse effect.	30925324
ciRS-7	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	 cells and tissues	Interaction(miR-944/NOX4 Pathway)	RNA Pull-Down//Western Blot//qRT-PCR//PCR//IF	 The results showed that ciRS-7 was highly expressed in both hepatocellular carcinoma cells and tissues.  Further study showed that ciRS-7 regulated the miR-944 level through acting as a microRNA sponge. q-RT-PCR, Western blot, RNA pull-down and dual luciferase activity assays showed that miR-944 targeted and regulated the expression of NOX4. 		Yes	Overexpression of ciRS-7 could promote the proliferation, migration, and invasion of HCC. 	36004692
CRNDE	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Interaction(miR-335-3p)	CCK8//qRT-PCR	lncRNA CRNDE expression was upregulated and miR-355-3p expression was downregulated in OS.  We revealed that miR-335-3p was the target of lncRNA CRNDE. 	In patients with OS, low lncRNA CRNDE expression demonstrated higher overall survival, whereas high lncRNA CRNDE expression was an independent poor prognostic factor.	Yes	It also demonstrated that knockdown of lncRNA CRNDE inhibited OS cell proliferation, migration, and invasion, and inhibition of miR-355-3p promoted this effect. Finally, miR-335-3p partially mediated the stimulatory effects of lncRNA CRNDE in OS.	33522065
CRNDE	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[Wnt/β-catenin signaling pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	The results demonstrated that the expression of CRNDE was high in OS tissues and cell lines, and partly induced by SP1.The mechanistic investigations showed that CRNDE promoted glycogen synthase kinase-3β phosphorylation to activate the Wnt/β-catenin pathway. 		Yes	CRNDE knockdown attenuated OS cell proliferation and invasion and induced apoptosis and G0/G1 arrest.	31898343
CRNDE	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 CD8 + T cells	Interaction(miR-545-5p and TIM-3)	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Here, CRNDE was obviously elevated and negatively correlated with IFN-γ production in tumour-infiltrating CD8 + T cells isolated from OSCC patients. Mechanistically, CRNDE specifically sponged miR-545-5p to induce T-cell immunoglobulin and mucin domain-3 (TIM-3), thus contributing to CD8 + T-cell exhaustion.  TIM-3 is a significant immune checkpoint, and it inhibits cancer immunity. TIM-3 can demonstrate an important role in CD8 + T-cell exhaustion. In summary, loss of CRNDE could induce miR-545-5p and inhibit TIM3 expression, thus significantly activated the anti-tumour effect of CD8 + T cells.		Yes	 TIM-3 is a significant immune checkpoint, and it inhibits cancer immunity. TIM-3 can demonstrate an important role in CD8 + T-cell exhaustion. In summary, loss of CRNDE could induce miR-545-5p and inhibit TIM3 expression, thus significantly activated the anti-tumour effect of CD8 + T cells.	34729919
CYTOR	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Interaction(miRNA-105/PTEN axis)	CCK8//qRT-PCR//Western Blot	Real-time quantitative PCR (qRT-PCR) disclosed that expression of CYTOR was significantly decreased in colon cancer tissues, compared with that of adjacent normal tissues, while miRNA-105 was significantly increased. Correlation study found that CYTOR was negatively correlated with miR-105. The Starbase database predicted the targeting of miR-105 by CYTOR, and qRT-PCR and dual luciferase reporter gene method were used to verify the targeting relationship of CYTOR and miRNA-105/PTEN axis. 		Yes	The proliferation, migration, and invasion rates of the LoVo cells with highly expressed CYTOR were significantly slower. miR-105 mimic could suppress the decrease in proliferation, migration, and invasion rates of colon cancer cells caused by overexpression of CYTOR. 	33936365
CYTOR	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction(miR-136-5p/MAT2B axis)	In Vivo Experiment//RNA Pull-Down//ChIP	LncRNA CYTOR was up-regulated in RCC tissues and cell lines, and miR-136-5p was down-regulated in renal carcinoma cell lines and tissues.miR-136-5p was sponged by lncRNA CYTOR, which negatively regulated the development of RCC. MAT2B was a target gene of miR-136-5p. MAT2B protein interacted directly with BAG3 protein to affect the proliferation, invasion and apoptosis of RCC cells. 		Yes	Downregulation of CYTOR inhibited cell proliferation and invasion and promoted apoptosis. miR-136-5p was sponged by lncRNA CYTOR, which negatively regulated the development of RCC. MAT2B was a target gene of miR-136-5p. MAT2B protein interacted directly with BAG3 protein to affect the proliferation, invasion and apoptosis of RCC cells. 	35597301
CYTOR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Regulation[LINC00152/miR-215/CDK13 axis  ]	qRT-PCR	 In our current investigation, we observed LINC00152 was obviously upregulated in HCC cells.Therefore, it was revealed that LINC00152 contributed to the progression of HCC by the modulation of miR-215 and CDK13.		Yes	Subsequently, the in vivo results demonstrated that silence of LINC00152 restrained HCC development via modulating miR-215 to up-regulate CDK13.	31297882
CYTOR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-125b-5p/KIAA1522 axis]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	 As a result, The Cancer Genome Atlas (TCGA) database indicated that expression of CYTOR and KIAA1522 was increased in HCC tissues and high expression of CYTOR and KIAA1522 was related to worse overall survival.In conclusion, CYTOR interference suppressed the proliferation and cell cycle, and promoted the apoptosis of HCC cells by regulating the miR-125b-5p/KIAA1522 axis.		Yes	The proliferation and cell cycle of HCC cells were suppressed by CYTOR interference while promoted by miR-125b-5p interference and KIAA1522 overexpression.	33318318
CYTOR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-139/PIK3CA]	qRT-PCR	Herein, we identified a significant up-regulation of LINC00152 in both HCC tissues and cell lines.Taken together, our study revealed a crucial regulatory network of LINC00152/miR-139/PIK3CA axis in the tumorigenesis of HCC, implying that LINC00152 may be a biomarker and novel therapeutic target for further clinical therapy of HCC.		Yes	 Functional studies showed that knockdown of LINC00152 inhibited cell proliferation, migration, and invasion, but promoted cell apoptosis, indicating its oncogenic functions in HCC tumorigenesis. 	31954697
CYTOR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-125b/SEMA4C axis)	CCK8//qRT-PCR//EdU Staining//Western Blot	 The results demonstrated that CYTOR was significantly increased in HCC tissues compared with non-tumor tissues and that CYTOR expression was associated with the poor prognosis of patients with HCC.  In addition, CYTOR could directly interact with and negatively regulate miR-125b. Furthermore, semaphorin 4C (SEMA4C) was the target of miR-125b and CYTOR regulated SEMA4C expression by modulating miR-125b.	 The results demonstrated that CYTOR was significantly increased in HCC tissues compared with non-tumor tissues and that CYTOR expression was associated with the poor prognosis of patients with HCC. 	Yes	 Furthermore, CYTOR silencing could inhibit the proliferation and promote the apoptosis of HCC cells. CYTOR overexpression had the opposite effects. The results from in vivo xenograft demonstrated that CYTOR knockdown suppressed tumor growth. 	34584571
CYTOR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction( LINC00152-miR-143a-3p-KLC2 axis )	qRT-PCR	We identified an epigenetic mechanism leading to upregulation of the long intergenic non-coding RNA 152 (LINC00152) expression in human hepatocellular carcinoma (HCC). LINC00152 was confirmed to sponge miR143a-3p in human HCC cell lines, thereby limiting its binding to their respective target genes, like KLC2. KLC2 was identified as a central mediator promoting pro-tumorigenic effects of LINC00152 overexpression in HCC cells. Furthermore, co-expression of LINC00152 and KLC2 was observed in human HCC cohorts and high KLC2 expression was associated with shorter patient survival. The LINC00152-miR-143a-3p-KLC2 axis may represent a therapeutic target in human HCC.	 Furthermore, co-expression of LINC00152 and KLC2 was observed in human HCC cohorts and high KLC2 expression was associated with shorter patient survival. 	Yes	 Functional assays demonstrated that KLC2 promoted cell proliferation, clonogenicity and migration in vitro. 	35563834
CYTOR	LncRNA	Homo sapiens	Ovarian Neoplasms	Ovarian Cancer tissues	Expression[Expression[highly expressed]-expression]	CCK8//qRT-PCR//Microarray	LINC00152 is Expression[up-expression]regulated in epithelial ovarian cancer tissues comparing to normal tissues. To determine the function of LINC00152 in ovarian cancer, we knocked down the expression of LINC00152 in epithelial ovarian cancer cell line SKOV3 with small interference RNAs (siRNAs). The effects of LIN00152 on the proliferation and cell cycle were determined by comparing the cell viability of SKOV3 cells with LIN00152 knockdown and the control cells with negative siRNA. The cell viability was assessed using Cell Counting Kit-8 (CCK-8) and flow cytometry assay. RNA microarray assay was used again in control and LINC00152 knockdown SKOV3 cells to identify downstream signaling pathways.		Yes	Knockdown of LINC00152 expression inhibits cell proliferation and induces cell cycle arrest. 	31799647
CYTOR	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder carcinoma tissues ,cell lines	Regulation[Wnt/β-Catenin Signaling Pathway ]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	We found that Linc00152 was highly expressed in 126 cases of bladder carcinoma tissues (p<0.001) and 4 cell lines (p<0.01), and Linc00152 is more commonly expressed in patients with advanced-stage cancer (p=0.021). This research shows that Linc00152 is highly expressed in patients with bladder cancer and the possible carcinogenic effect of Linc00152 in bladder cancer occurs through activating the Wnt/ß-Catenin signaling pathway, and could be a new biomarker for diagnosis and prevention of this cancer.		Yes	Knockdown of Linc00152 by using siRNAs in bladder cancer cell lines (T24 and HT-1197) suppressed cell viability and growth by causing cell cycle arrest and apoptosis (p<0.001), as well as inhibiting cell migration and invasion (p<0.001).	31042695
CYTOR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 tumor cell	Interaction(LINC00152-USF1/MRPL52 axis)	qRT-PCR//Luciferase Report Assay	NR_024206.2 was the dominant isoform that accounts for 80% of all transcripts of LINC00152. LINC00152 upregulation was associated with unfavorable survival of patients with OSCC. LINC00152 knockdown significantly impaired OSCC cell growth in vitro and in vivo. RNA FISH assay confirmed nuclear and cytoplasmic distribution of LINC00152. It physically interacted with Upstream Transcription Factor 1 (USF1), a common transcription factor in mammalian cells. USF1 could bind to the promoter region of MRPL52 (Mitochondrial Ribosomal Protein L52) and activate its transcription. LINC00152 could enhance the binding, thereby indirectly elevating MRPL52 expression. USF1 or MRPL52 knockdown slowed the proliferation of OSCC cells and partly canceled LINC00152-mediated growth-promoting effects.	LINC00152 upregulation was associated with unfavorable survival of patients with OSCC. 	Yes	LINC00152 knockdown significantly impaired OSCC cell growth in vitro and in vivo. RNA FISH assay confirmed nuclear and cytoplasmic distribution of LINC00152. 	34664331
CYTOR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	oral cancer cells	Regulation(HNRNPC-mediated ZEB1 stabilization)	In Vivo Experiment	Here, we report a survival-related long non-coding RNA, CYTOR, which is highly expressed in the lesions of oral cancer patients. We found that CYTOR can promote both migration and invasion in oral cancer cells as well as the epithelial-mesenchymal transition (EMT). RNA-sequencing of CYTOR-knockdown oral cancer cells revealed that CYTOR can regulate mitochondrial respiration and RNA splicing. Mechanistically, we found that nuclear-localized CYTOR interacts with HNRNPC, resulting in stabilization of ZEB1 mRNAs by inhibiting the nondegradative ubiquitination of HNRNPC. By synthesizing CYTOR-targeting small interfering RNAs (siRNAs) encapsulated in Nanoscale Metal Organic Frameworks (NMOFs), we demonstrate the targeted suppression of CYTOR to inhibit invasion and metastasis of oral cancer cells in a nude mouse model. Cumulatively, this study reveals the potential role of the CYTOR-HNRNPC-ZEB1 axis in regulating mitochondrial metabolism and glycolysis of oral cancer cells, and illustrates the effective use of lncRNA targeting in anti-metastatic cancer therapies.		Yes	RNA-sequencing of CYTOR-knockdown oral cancer cells revealed that CYTOR can regulate mitochondrial respiration and RNA splicing. Mechanistically, we found that nuclear-localized CYTOR interacts with HNRNPC, resulting in stabilization of ZEB1 mRNAs by inhibiting the nondegradative ubiquitination of HNRNPC.	35963855
CYTOR	LncRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction[sponging miR-193b-3p]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	The current study revealed that LINC00152 is overexpressed in osteosarcoma cells, leading to increased cell proliferation, and decreased G0/G1 cell cycle arrest and apoptosis.These results suggested that LINC00152 binds to miR-193b-3p and reduces its expression level, leading to increased cell proliferation and decreased G0/G1 cell cycle arrest and apoptosis in osteosarcoma cells.		Yes	The current study revealed that LINC00152 is overexpressed in osteosarcoma cells, leading to increased cell proliferation, and decreased G0/G1 cell cycle arrest and apoptosis.	31579407
CYTOR	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow	Interaction[Promoting CDK9 Through miR-193a]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	LINC00152 is determined to be upregulated in the AML samples, and the overexpression of LINC00152 is also authenticated in the advanced French-American-British (FAB) AML patients and closely correlated with the poor outcome of AML patients.The mechanical experiments state that LINC00152 and CDK9 were both targeted by miR-193a with the complementary binding sites at 3'-UTR. Moreover, in the rescue experiments, the enhanced LINC00152 expression could regain the suppression of tumor behavior induced by LINC00152 knockdown. In conclusion, this research reveals the important role of lncRNA LINC00152 in the AML leukemogenesis through targeting miR-193a/CDK9 axis. This finding could indicate the important pathogenesis of ncRNA and the vital roles of epigenetic regulation.		Yes	LINC00152 is determined to be upregulated in the AML samples, and the overexpression of LINC00152 is also authenticated in the advanced French-American-British (FAB) AML patients and closely correlated with the poor outcome of AML patients.	30707636
CYTOR	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	 AML patients	Expression(highly expressed)	qRT-PCR//Colony Formation Assay	Importantly, LINC00152 upregulation was correlated with the expression of 16 genes within a 17-gene LSC biomarker panel, which contributed to the accurate prediction of initial therapy resistance in AML. 	 Upregulation of LINC00152 or PARP1 was associated with poor prognosis in AML patients.	Yes	 Knockdown of LINC00152 markedly increased the drug sensitivity of leukemia cells. Furthermore, LINC00152 expression was found to be correlated with poly (ADP-ribose) polymerase 1 (PARP1) expression in AML, whereas LINC00152 knockdown significantly decreased the expression of PARP1.	34295821
CYTOR	LncRNA	Homo sapiens	Glioma		Regulation[miR-612/AKT2/NF-κB pathway]	qRT-PCR//IF//Western Blot	LINC00152 acted as a tumor oncogene with prognostic value for patients with glioblastoma through LINC00152/miR-612/AKT2/NF-κB axis.	LINC00152 was closely associated with glioma WHO classification and poor prognosis, and indicated a poor prognosis in glioblastoma patients. 	Yes	 Tumor growth and invasion were suppressed both in vitro and vivo after LINC00152 was blocked. 	30043319
CYTOR	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[PI3K/AKT signaling pathway]	qRT-PCR//MTT//RIP//Transwell Assay	The levels of LINC00152 and CD164 were obviously increased while miR-613 was especially decreased in glioma tissues and cell lines.Low-expression of LINC00152 modified cell proliferation, apoptosis migration and invasion through LINC00152/miR-613/CD164 axis via PI3K/AKT signaling pathway in glioma, thus providing new therapeutic target in the clinical treatment of glioma.		Yes	The downregulation of LINC00152 and CD164, as well as the upregulation of miR-613 induced cell apoptosis, repressed viability, migration, and invasion. 	32726126
CYTOR	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Interaction[binding to miR-613]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that CYTOR expression was elevated both in NPC tissues and cells. Mechanically, we found that the subcellular localization of CYTOR mostly occurred in the cell cytoplasm. Luciferase reporter and RIP assays confirmed that CYTOR functioned as the molecular sponge of miR-613. Subsequent experiments confirmed that ANXA2 was directly targeted by miR-613.		Yes	Gain- and loss-of-function studies further confirmed that CYTOR induced the upregulation of ANXA2 by competitively binding to miR-613, thus leading to NPC metastasis.	31859457
CYTOR	LncRNA	Homo sapiens	Glioblastoma	U87-MG and LN229 glioblastoma cells	Regulation	FISH//qRT-PCR//migration assay//Cell Viability Assay//Cell Proliferation Assay//Cell Cycle Assay//Invasion Assay	 SiRNA-based knockdown of LINC00152 enhanced malignant tumor behaviors including proliferation, cell cycle entry, migration, and invasion, contradicting previous studies using U87-MG and LN229 glioblastoma cells. Furthermore, LINC00152 knockdown had no influence on survival of A172 glioblastoma cells. 		Yes	 SiRNA-based knockdown of LINC00152 enhanced malignant tumor behaviors including proliferation, cell cycle entry, migration, and invasion, contradicting previous studies using U87-MG and LN229 glioblastoma cells. Furthermore, LINC00152 knockdown had no influence on survival of A172 glioblastoma cells. 	34531451
CYTOR	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	regulation[miR-205-5p/CDK6 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay	The expression of LncRNA CYTOR was significantly elevated in PC. CYTOR can promote PC progression by modulating the miR-205-5p/CDK6 axis, which may be a potential therapeutic target for PC.		Yes	Knockdown of CYTOR significantly inhibited cell proliferation and migration of PC cells. In vivo animal studies showed that CYTOR promoted tumor growth. 	32732173
CYTOR	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues	interaction[miRNA-193b-3p]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	The present study revealed that long intergenic non-coding RNA 00152 (LINC00152) expression was significantly increased in human TSCC tissues compared with in tissues from matched controls using RT-qPCR. Overall, the results of the present study suggested that increased LINC00152 expression in TSCC tissues may act as a sponge of miR-193b-3p to promote cancer progression in vitro.		Yes	In TSCC cell lines, CAL-27 and SCC-9, LINC00152 was revealed to promote TSCC cell proliferation, enhance cell cycle progression and inhibit cell apoptosis.	32194700
CYTOR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC cells	Interaction(E2F1)	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	Both LINC00152 and E2F1 were highly expressed in PTC cells.In addition, E2F1 induced LINC00152 overexpression, which accelerated cell proliferation, migration, and invasion by activating the PI3K/AKT axis, whereas the administration of LY294002, the inhibitor of PI3K, led to reversal of the same.		Yes	 Knockdown of LINC00152 led to reduced cell activity, while LINC00152 overexpression brought about the opposing trends. Likewise, E2F1 knockdown quenched cell proliferation, migration, and invasion. However, the combination of E2F1 knockdown and LINC00152 overexpression resulted in augmented cell growth. Finally, xenograft transplantation validated that E2F1 inhibition could suppress LY294002, thereby discouraging tumor growth.	35592867
CYTOR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[YAP1/LINC00152/FSCN1 Signaling Axis]	RNA Pull-Down//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ChIP	"Here, a YAP1 target gene, long intergenic noncoding RNA 00152 (LINC00152), which is highly expressed in colorectal cancer (CRC), is identified. This finding provides a new regulatory model of the ""YAP1-lncRNA"" in CRC, which gives rise to a new perspective, ""YAP1/LINC00152/miR-632-miR-185-3p/FSCN1,"" to explore the cancer-promoting mechanism of YAP1 involved in CRC."		Yes	 The oncogenic functions of LINC00152 in CRC are demonstrated by a panel of in vitro and in vivo experiments. 	32042551
CRNDE	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines 	Expression[highly expressed]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 CRNDE expression was increased in OSCC tissues and cell lines compared with that in normal tissues and cell lines.  Compared with the control group, the si-CRNDE group displayed a reduction in the expression of CRNDE, in the proliferation, migration and invasion of cells, in the protein expression of N-cadherin, vimentin and Snail, and in the expression of proteins in the Wnt/β-catenin pathway. 		Yes	In conclusion, silencing CRNDE may inhibit EMT, thus decreasing the migration and invasion of human OSCC cells by repressing the activation of the Wnt/β-catenin signaling pathway, thereby restricting cell growth and promoting cell apoptosis.	30867767
CYTOR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Regulation[ miR-107/Rab10 Axis ]	CCK8//qRT-PCR//Transwell Assay//Western Blot	LINC00152, Rab10 was significantly upregulated, and miR-107 was strikingly down-regulated in ESCC tissues and cell lines (TE-1 and KYSE30).In this study, we found that LINC00152 modulated Rab10 to promote cell proliferation, migration and invasion in ESCC by sponging miR-107.		Yes	 LINC00152 depletion decreased cell viability and abilities of migration and invasion by regulating miR-107 in vitro and blocked xenograft tumor growth in vivo. 	31802892
DANCR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[inhibiting p21]	qRT-PCR	DANCR expression level was increased in human NSCLC. DANCR knockdown inhibited EZH-2-mediated epigenetic silencing of p21 promoter and increased p21 expression. Moreover, DANCR knockdown inhibited NSCLC cell proliferation, migration, and invasion in a p21-dependent manner.		Yes	The knockdown of DANCR inhibited NSCLC cell proliferation by inducing cell apoptosis and cell cycle arrest. In addition, DANCR knockdown suppressed NSCLC cell migration and invasion via inhibition of epithelial-mesenchymal transition (EMT).On the contrary, DANCR overexpression had the opposite effects.	30613152
DANCR	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	regulation[ miR-345-5p/Twist1 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	We found that the expression of DANCR was significantly induced in CCA tissues and cells.In this study, we verified that LncRNA DANCR affected cell proliferation, migration, invasion, angiogenesis, epithelial-mesenchymal transition (EMT) and induced apoptosis through modulating miR-345-5p/Twist1 axis in Cholangiocarcinoma.		Yes	 Inhibition of DANCR remarkably suppressed CCA cell proliferation, migration, invasion, EMT and angiogenesis as well as induced cell apoptosis in vitro and in vivo. 	32196584
DANCR	LncRNA	Homo sapiens	Prostatic Neoplasms	 PC patients' serum and cell lines	Interaction(miR-214-5p)	RNA Pull-Down//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay	DANCR was up-regulated in PC patients' serum and cell lines, while miR-214-5p was opposite, showing negative correlation.  We found that DANCR high levels or miR-214-5p low levels were related to PC patients' poor prognosis. DANCR regulates miR-214-5p in a targeted manner, and DANCR over-expression can reduce the cancer inhibitory effect of miR-214-5p on PC cells.	 Besides, DANCR was significantly correlated with PSA, Gleason score and T stage in PC patients. The area under the curve (AUC) of DANCR and miR-214-5p for diagnosing PC was not less than 0.850, while the AUC for predicting poor prognosis was more than 0.800. Cox analysis results also revealed that the two might be prognostic indicators of PC patients.	Yes	 Up-regulating DANCR or down-regulating miR-214-5p could promote PC cells' malignant proliferation and migration, prevent apoptosis, and activate TGF-β signaling pathway, while reverse treatment of DANCR or miR-214-5p can reverse the above results. 	34017385
DANCR	LncRNA	Homo sapiens	tongue squamous cell carcinoma		Regulation[miR-135a-5p/KLF8 axis ]	Western Blot//Wound Healing Assay//qRT-PCR//IF//MTT//Luciferase Report Assay//Transwell Assay	These findings, for the first time, suggest that DANCR plays an oncogenic role in TSCC progression via targeting miR-135a-5p/KLF8 axis, which provides a promising biomarker and treatment approach for preventing TSCC.		Yes	DANCR knockdown reduced the viability and inhibited the migration and invasion of TSCC cells in vitro, while ectopic expression of DANCR induced opposite effects.	31827393
DANCR	LncRNA	Homo sapiens	cervical squamous cell carcinoma		Interaction[HIF‑1α]	CCK8//qRT-PCR//Western Blot	 It was observed that ANCR was downregulated in human papillomavirus (HPV)‑negative patients with CSCC compared with in normal female cases and HPV‑positive patients with CSCC in cervical tissues and in the serum, and the downregulation of ANCR effectively distinguished HPV‑negative patients with CSCC from healthy controls. ANCR overexpression inhibited HIF‑1α expression in HPV‑negative CSCC cells, while HIF‑1α overexpression exhibited no significant effect on ANCR expression. It was therefore concluded that ANCR may inhibit the growth of HPV‑negative cervical squamous cell carcinoma under hypoxic conditions by downregulating HIF‑1α.		Yes	 ANCR overexpression inhibited the proliferation of HPV‑negative CSCC cells under hypoxic conditions, whilst HIF‑1α overexpression reversed this effect.	31746351
DANCR	LncRNA	Homo sapiens	Pre-Eclampsia	 placental tissues of patients 	Interaction(microRNA-214-5p/ PI3K/AKT)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Cell Cycle Assay//Transwell Assay	Studies have shown that lncRNA DANCR is down-regulated in placental tissues of patients with preeclampsia (PE).  Further, the targeted interaction between lncRNA DANCR and miR-214-5p was confirmed by the dual-luciferase reporter gene assay. In addition, the expression of PI3K/AKT signaling pathway-related proteins was analyzed by Western blot. Overexpression of lncRNA DANCR can increase the phosphorylation of PI3K/AKT protein and activate this signaling pathway.		Yes	The results showed that overexpression of lncRNA DANCR significantly increased the proliferation, invasion, migration, and EMT process of trophoblast cells. Interfering with lncRNA DANCR showed the opposite result. 	34652251
DANCR	LncRNA	Homo sapiens	Carcinoma, Basal Cell	BCC tissues 	Interaction(PTCH)	In Vivo Experiment//RNA Pull-Down//cell invasion assay//Western Blot//Wound Healing Assay//Tunel//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay	ANCR and Hedgehog pathway were more highly expressed in BCC tissues than in adjacent normal tissues. An RNA pull-down assay further revealed that ANCR is specifically bound to PTCH. In vivo experiments also showed that ANCR overexpression significantly increased tumor growth and decreased apoptosis, which was reversed by cyclopamine, a specific inhibitor of the Hedgehog signaling pathway.		Yes	ANCR overexpression substantially promoted BCC cell proliferation, invasion, and migration, inhibited apoptosis, and up-regulated BCL2 and decreased the expression of BAX and Cleaved-caspase3 proteins. Additionally, the upregulation of N-cadherin, vimentin, β-catenin, PTCH, GLI1, and SMO expression, and downregulation of E-cadherin expression were observed after ANCR overexpression. Moreover, ANCR knockdown had the opposite effects. 	35642174
DACH1	LncRNA	Homo sapiens	Pulmonary Fibrosis	 lungs of IPF patients, mouse model of lung fibrosis	Interaction(SRSF1/CTNNB1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//FISH//IHC//EdU Staining//IF	Here we report that lncRNA DACH1 (dachshund homolog 1) is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis. Mechanistically, LncDACH1 binding to the serine/arginine-rich splicing factor 1 (SRSF1) protein decreases its activity and inhibits the accumulation of Ctnnb1. Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts. Furthermore, loss of LncDACH1 promoted proliferation, differentiation, and extracellular matrix (ECM) deposition in mouse lung fibroblasts, whereas such effects were abolished by silencing of Ctnnb1. In addition, a conserved fragment of LncDACH1 alleviated hyperproliferation, ECM deposition and differentiation of MRC-5 cells driven by TGF-β1.		Yes	LncDACH1 knockout mice develop spontaneous pulmonary fibrosis, whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation, collagen deposition and differentiation of mouse lung fibroblasts. Similarly, forced expression of LncDACH1 not only prevented bleomycin (BLM)-induced lung fibrosis, but also reversed established lung fibrosis in a BLM model. 	36176913
cZNF532	CircRNA	Homo sapiens	Diabetic Retinopathy	pericytes under diabetic stress, in the retinal vessels of a diabetic murine model, and in the vitreous humor of diabetic patients	Expression[highly expressed]	Microarray			Yes	cZNF532 silencing reduced the viability, proliferation, and differentiation of pericytes and suppressed the recruitment of pericytes toward endothelial cells in vitro.	32343678
CYTOR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues ,cell lines	Regulation[microRNA-193b-3p/ETS1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Linc00152 expression was notably upregulated in GC tissues and cells. Linc00152 upregulation inhibited miR-193b-3p expression by direct interaction and abolished miR-193b-3p-mediated anti-proliferation, anti-migration and anti-invasion effects in GC cells. ETS1 was a target of miR-193b-3p and linc00152 could promote ETS1 expression by downregulating miR-193b-3p.		Yes	 The proliferative, migratory and invasive abilities of GC cells were weakened by linc00152 depletion, miR-193b-3p overexpression or ETS1 knockdown. 	30404587
CYTOR	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines,blood	Interaction[bind with Bcl-2]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Transwell Assay	The results revealed that LINC00152 was overexpressed in tissues, serum, and PBMCs of patients with gastric cancer. LINC00152 could bind with Bcl-2 directly to induce the activation of cell cycle signaling, and this may be a potential target for the therapy of gastric cancer in the future.		Yes	 Moreover, LINC00152 could promote the migration and invasive abilities and suppress the apoptosis, of gastric cancer cells through regulating the Bcl-2 protein family.	30304559
CYTOR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	Interaction(miR-138/SIRT2 axis)	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Transwell Assay	We found that LINC00152, a newly identified lncRNA, was significantly upregulated in GC tissues and affected clinicopathological characteristics in GC patients. Further bioinformatic analysis indicated that LINC00152 competitively bound with miR-138 and regulated the expression of miR-138. Moreover, SIRT2 was further proved to be a downstream target of miR-138. 	We found that LINC00152, a newly identified lncRNA, was significantly upregulated in GC tissues and affected clinicopathological characteristics in GC patients. 	Yes	Furthermore, we observed that LINC00152 knockdown can significantly reduce cell proliferation and promote apoptosis in human gastric cancer cells. 	34697541
CYTOR	LncRNA	Homo sapiens	Stomach Neoplasms	 GC patients	Interaction( EZH2 /CXCL9, 10/CXCR3 axis)	CCK8//qRT-PCR//Western Blot//ChIP	 In this study, we found increased LINC00152 expression levels are positively associated with the poor prognosis of GC patients and negatively associated with the CD8 levels. ChIP assay verified that LINC00152 recruits EZH2 to the promoters of CXCL9 and CXCL10, thus the silencing of LINC00152 promoted the production of CXCL9 and CXCL10.	 In this study, we found increased LINC00152 expression levels are positively associated with the poor prognosis of GC patients and negatively associated with the CD8 levels. 	Yes	Knockdown of LINC00152 suppressed tumor cells growth in vivo and in vitro, increased tumor-infiltrating CD8+ T cells numbers and promoted the expression of CXCL9, CXCL10 and C-X-C Motif Chemokine Receptor 3 (CXCR3) in xenograft tumors.	33709190
CYTOR	LncRNA	Homo sapiens	Stomach Neoplasms	cancer samples and cells	Interaction(miR-103/RAB10)	qRT-PCR	We found that CYTOR expression was increased in metastatic gastric cancer biopsies compared with that in primary samples. CYTOR expression was significantly positively correlated with the invasiveness, lymph node metastasis, and advanced stages of gastric cancer.  Furthermore, CYTOR sponged miR-103 and diminished miR-103 expression, thus rescuing oncogene RAB10 expression. 	We found that CYTOR expression was increased in metastatic gastric cancer biopsies compared with that in primary samples. CYTOR expression was significantly positively correlated with the invasiveness, lymph node metastasis, and advanced stages of gastric cancer. 	Yes	 In addition, downregulation of CYTOR expression hampered cell proliferation and migration but induced cell apoptosis.Knockdown of CYTOR suppressed tumor growth in human BGC823 mouse models. 	34110382
CYTOR	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(HMGA1 )	CCK8//qRT-PCR//Cell Cycle Assay//Western Blot	Treating GC cell lines with LINC00152 siRNAs downregulated the expression of HMGA1. The cell cycle was arrested in the S phase following a reduction in LINC00152 or HMGA1 expression, whereas the expression of the cell cycle inhibitor P27 increased.		Yes	In this study, we showed that acting as a ceRNA of HMGA1, LINC00152 has the same function as HMGA1, considering that it could control the cell cycle and promote GC cell proliferation.	35014092
CYTOR	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot//Transwell Assay	The results showed that Linc00152 was highly expressed in the breast cancer tissues compared to their adjacent normal tissues, and Linc00152 was also up-regulated in the breast cancer cell lines compared to normal cell lines.		Yes	 Knock-down of Linc00152 by using siRNAs in breast cancer cell lines (MDA-MB-231 and MCF-7) significantly suppressed cell viability, cell growth, cell invasion and migration as measured by the CCK-8, colony formation, transwell invasion, and migration assays. 	29863253
CYTOR	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction(KLF5 )	RNA Pull-Down//Western Blot//ISH//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	 Our study found that LINC00152 is significantly upregulated in breast cancer, and that it acts as an indicator of poor survival prognosis. Mechanistic analyses demonstrated that LINC00152 directly binds to KLF5 protein and increases KLF5 stability. Moreover, LINC00152 is also a KLF5-responsive lncRNA, and KLF5 activates LINC00152 transcription by directly binding to its promoter. 	 Our study found that LINC00152 is significantly upregulated in breast cancer, and that it acts as an indicator of poor survival prognosis.	Yes	 Further studies revealed that LINC00152 knockdown suppresses cell proliferation and tumorigenicity in vitro and in vivo.	33842324
CYTOR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	tumor tissue and peripheral blood 	Expression[highly expressed]	qRT-PCR	In NSCLC, the high expression of LINC00152 in tumor tissue and peripheral blood samples has been shown to be associated with worse prognoses of NSCLC patients.	In NSCLC, the high expression of LINC00152 in tumor tissue and peripheral blood samples has been shown to be associated with worse prognoses of NSCLC patients.	Yes	 Overexpression of LINC00152 has been confirmed to promote the proliferation, invasion, and migration of NSCLC cells in vitro, as well as increase tumor growth in vivo.	32133796
CYTOR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tumor tissues	Regulation[miR-153-3p/FYN axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	Our results revealed that LINC00152 expression was up-regulated in ESCC, and correlated with advanced TNM stage, lymph node metastasis, and poor prognosis of ESCC patients.Taken together, LINC00152 contributed to ESCC progression by down-regulating miR-153-3p and promoting FYN expression, uncovering a novel LINC00152/miR-153-3p/FYN regulatory pathway in ESCC.	Our results revealed that LINC00152 expression was up-regulated in ESCC, and correlated with advanced TNM stage, lymph node metastasis, and poor prognosis of ESCC patients.	Yes	 Functionally, LINC00152 knockdown suppressed proliferation, decreased colony forming ability, and induced apoptosis in ESCC cells. 	30784933
CYTOR	LncRNA	Homo sapiens	Cardiomegaly		Regulation[miR-155-mediated IKKi signaling]	Transfection//Immunoblotting//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining	 In the present study, microarray analysis results from GEO database were analyzed, and upregulated lncRNAs in cardiac hypertrophy were identified. Taken together, CYTOR might play a protective role in cardiac hypertrophy through miR-155 and downstream IKKi and NF-κB signaling, most possibly through serving as a ceRNA for miR-155 to counteract miR-155-mediated repression of IKBKE.		Yes	CYTOR knockdown significantly enhanced the inducible effect of AB operation on mice myocardial hypertrophy and Angiotensin II on cardiomyocyte hypertrophy.	30794866
CYTOR	LncRNA	Homo sapiens	Laryngeal Neoplasms	LSCC tissues 	interaction[Sponging MiR-613]	qRT-PCR//Luciferase Report Assay	LINC00152 levels in LSCC tissues were significantly higher than those in adjacent normal tissue, and patients with lymph node metastasis or an advanced clinical stage displayed higher LINC00152 expression.LINC00152 exerts an oncogenic effect on the tumorigenesis of LSCC by sponging miR-613 and may serve as a potential target for treating LSCC.	LINC00152 levels in LSCC tissues were significantly higher than those in adjacent normal tissue, and patients with lymph node metastasis or an advanced clinical stage displayed higher LINC00152 expression.	Yes	 Moreover, siRNA-mediated LINC00152 knockdown significantly inhibited the proliferation, migration and invasion of LSCC cells and induced apoptosis in those cells. 	32266320
CYTOR	LncRNA	Homo sapiens	capillary hemangioma	infantile skin hemangioma tissues	Interaction[miR-139-5p]	Western Blot//ISH//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Linc00152 was overexpressed in the proliferating-phase hemangioma tissues when compared with that in involuting-phase. ubsequent analysis revealed that linc00152 bound with miR-139-5p and linc00152 expression was inversely correlated with the level of miR-139-5p in IH. Same effects of miR-139-5p transfection on HemECs cells were observed as downregulation of linc00152. Moreover, tumor protein D52 (TPD52) was confirmed to be the target of miR-139-5p. Besides, the anti-tumor effect of linc00152 silence on hemangioma cell was reversed by rexpression of TPD52. 		Yes	Downregulation of linc00152 strikingly suppressed the cell viability, migration and invasion of hemangioma cells. Furthermore, silence of linc00152 repressed the growth and lung metastasis of hemangioma cell in vivo. 	31542613
CYTOR	LncRNA	Homo sapiens	capillary hemangioma	IH tissues	Regulation[Akt/mTOR and Notch1 pathways ]	CCK8//qRT-PCR//Western Blot	 The results demonstrated Linc00152 was up-regulated in clinical IH tissues and HemECs.Knockdown of Linc00152 suppressed HemECs proliferation and induced apoptosis via inhibiting Akt/mTOR and Notch1 signaling pathways.		Yes	 Knockdown of Linc00152 in HemECs suppressed the activation of Akt/mTOR and Notch1 signaling pathways and caused reduction in cell proliferation and Ki67 expression in HemECs. Besides, Linc00152 knockdown resulted in a significant increase in apoptotic rate, caspase-3/7 activity, and Bax expression level, as well as a decrease in Bcl-2 expression level. 	30851338
CTBP1-DT	LncRNA	Homo sapiens	Ovarian Neoplasms	a cohort of HGSOC tissues	Interaction(miR-188-5p/MAP3K3 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Bioinformatics Analysis//ChIP	Based on public databases and bioinformatics analyses, the overexpression of lncRNA CTBP1-DT in HGSOC tissues was detected and validated in a cohort of HGSOC tissues. Mechanistically, lncRNA CTBP1-DT could competitively bind to miR-188-5p to protect MAP3K3 from degradation. Moreover, our results revealed that ETV5 could specifically interact with the promoter of lncRNA CTBP1-DT and activate its transcription. 	High expression of lncRNA CTBP1-DT was associated with poor prognosis and was an independent risk factor for survival. 	Yes	Overexpression of lncRNA CTBP1-DT promoted malignant biological behaviour of HGSOC cells, whereas its depletion induced growth arrest of HGSOC cells by vitro and in vivo assays.	34887384
CTBP1-AS2	LncRNA	Mus musculus	Cardiomyocyte Hypertrophy	heart tissues	Regulation[ regulating TLR4]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ChIP	We revealed the up-regulation of CTBP1-AS2 and TLR4 in cardiomyocyte hypertrophy models.  In conclusion, our study uncovered CTBP1-AS2 as a novel regulator of cardiomyocyte hypertrophy through regulating TLR4, providing a new potential treatment target for cardiomyocyte hypertrophy.		Yes	 Loss-of-function assays confirmed that inhibiting CTBP1-AS2 attenuated the Ang II-induced cardiomyocyte hypertrophy.	31220774
CTBP1-AS	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Interaction[microRNA-940]	Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results showed that LncRNA CTBP1-AS was aberrantly overexpressed in breast cancer tissues and breast cancer cells compared to the control group.Bioinformatics analysis and dual-luciferase reporter gene system results validated that microRNA-940 was the downstream target of LncRNA CTBP1-AS. Interestingly, overexpressed microRNA-940 abrogated the effects of LncRNA CTBP1-AS on cell proliferation, apoptosis, and invasion. In conclusion, overexpressed LncRNA CTBP1- AS promoted breast cancer cell proliferation, invasion as well as migration, inhibited cell apoptosis and accelerated breast cancer development by sponging microRNA-940.	Moreover, the expression levels of LncRNA CTBP1-AS were positively related with tumor size, histological grade and the expression levels of Ki-67 and Her2.	Yes	Of note, overexpressed LncRNA CTBP1-AS promoted breast cancer cell proliferation and invasion as well as migration, and decreased cell apoptosis ratio. 	31165609
CTB-193M12.5	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell line	Regulation(WNT10B/Wnt/β-catenin signaling)	qRT-PCR	 CTB-193M12.5 was upregulated in HCC and its high expression was correlated with alpha fetoprotein, large tumor size, aggressive clinical characteristics, and poor survival. Mechanistic investigation demonstrated that CTB-193M12.5 was mainly distributed in nucleus. Histone methyltransferase NSD1 was identified as a CTB-193M12.5 interactor. CTB-193M12.5 bound and recruited NSD1 to the promoter of WNT10B, leading to an increase in di-methylation of histone H3 at lysine 36 (H3K36me2) and the reduction of tri-methylation of histone H3 at lysine 27 (H3K27me3) at WNT10B promoter. Therefore, CTB-193M12.5 epigenetically activated WNT10B transcription. Through upregulating WNT10B, CTB-193M12.5 further activated Wnt/β-catenin signaling. Functional rescue experiments demonstrated that overexpression of WNT10B reversed the tumor suppressive roles of CTB-193M12.5 knockdown, while Wnt/β-catenin signaling inhibitor ICG-001 abolished the oncogenic roles of CTB-193M12.5 overexpression.	 CTB-193M12.5 was upregulated in HCC and its high expression was correlated with alpha fetoprotein, large tumor size, aggressive clinical characteristics, and poor survival. 	Yes	Functional experiments showed that CTB-193M12.5 enhanced HCC cellular proliferation, suppressed HCC cellular apoptosis, and promoted HCC cellular migration and invasion. CTB-193M12.5 knockdown exerted opposite effects in HCC. 	35698644
CTA-217C2.1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
CRYBG3	LncRNA	Homo sapiens	Lung Neoplasms	plasma of NSCLC patients	Interaction(eEF1A1/MDM2/MTBP Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//IP//Transwell Assay	Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.		Yes	In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo.	33809929
CRNDE	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[miR-641/CDK6 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	CRNDE level was upregulated in NSCLC. CRNDE promoted proliferation and inhibited apoptosis of NSCLC cells at least in part by regulating the miR-641/CDK6 axis, suggesting that CRNDE is a potential therapeutic target for NSCLC treatment.		Yes	CRNDE level was upregulated in NSCLC, and its knockdown suppressed NSCLC cells proliferation and enhanced apoptosis, whereas miR-641 antagonized the regulatory effect of CRNDE knockdown by directly binding to CRNDE. 	30982057
CRNDE	LncRNA	Homo sapiens	Colorectal Neoplasms	 Th17 cell	Regulation	RNA Pull-Down//Flow Cytometry//qRT-PCR//FISH//ELISA	CRC exosomes contained abundant CRNDE-h and transmitted them to CD4+ T cells to increase the Th17 cell proportion, RORγt expression, and IL-17 promoter activity. The underlying mechanism is that, CRNDE-h bound to the PPXY motif of RORγt and impeded the ubiquitination and degradation of RORγt by inhibiting its binding with the E3 ubiquitin ligase Itch.		Yes	CRC exosomes contained abundant CRNDE-h and transmitted them to CD4+ T cells to increase the Th17 cell proportion, RORγt expression, and IL-17 promoter activity.  The in vivo experiments confirmed that the targeted silence of CRNDE-h in CD4+ T cells attenuated the CRC tumor growth in mice. 	33495437
CRNDE	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues	regulation[miR-136-5p]	qRT-PCR//Western Blot	 CRNDE was overexpressed and miR-136-5p was low-expressed in RCC. CRNDE can mediate miR-136-5p, promote the development of EMT and RCC cells, showing the potential to serve as a novel biomarker and therapeutic target in RCC treatment.		Yes	Upregulation of CRNDE could promote the viability, migration, invasion of RCC, while downregulation of CRNDE produced the opposite effects.	32808846
CRNDE	LncRNA	Homo sapiens	Osteoarthritis	 bone marrow mesenchymal stem cells	Regulation(SIRT1/SOX9)	RNA Pull-Down//Western Blot//RIP//qRT-PCR//Luciferase Report Assay//Cell Viability Assay	With the prolongation of induction time, the expression of lncRNA-CRNDE, SIRT1, cartilage marker genes Aggrecan and collagen 2 (α1) in BMSC osteogenic differentiation was gradually increased.  lncRNA-CRNDE regulates BMSC chondrogenic differentiation to promote cartilage repair in osteoarthritis through SIRT1/SOX9.		Yes	With the prolongation of induction time, the expression of lncRNA-CRNDE, SIRT1, cartilage marker genes Aggrecan and collagen 2 (α1) in BMSC osteogenic differentiation was gradually increased.	33479807
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[modulating miR-337-3p]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	LncRNA CRNDE was overexpressed in tumor tissues of patients with HCC.Mechanistic investigations demonstrated that lncRNA CRNDE interacted with miR-337-3p and decreased its expression, thereby increasing the protein expression of miR-337-3p's target, SIX1. In addition, in vivo experiments using a xenograft tumor mouse model revealed that lncRNA CRNDE served as an oncogene, partly through sponging miR-337-3p and upregulating SIX1 in HCC.		Yes	LncRNA CRNDE downregulation significantly suppressed cell proliferation and migration.	31099050
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[Wnt/β-catenin signaling pathway ]	Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//IHC//Invasion Assay	CRNDE was significantly upregulated in tumor tissues compared with adjacent normal tissues.Thus, CRNDE could modulate EMT of HCC cells and knockdown of CRNDE impaired the mesenchymal properties. CRNDE increased invasion of HCC cells might be through activating the Wnt/β-catenin signaling pathway.		Yes	 In vitro, we revealed that knockdown of CRNDE inhibited cell proliferation, migration, and cell invasion capacities in HCC. Animal studies indicated that CRNDE knockdown represses both growth and metastasis of HCC tumors in vivo.	30430650
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-33a-5p/CDK6 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	CRNDE and CDK6 were upregulated in HCC tissues and cells, while miR-33a-5p was downregulated.  Overall, the present work indicated that CRNDE plays an oncogenic function in HCC through regulating the miR-33a-5p/CDK6 axis, revealing a potential therapeutic target in HCC.		Yes	Inhibition of CRNDE suppressed the invasion, migration, and proliferation of HCC cells and enhanced apoptosis by modulating proteins associated with mitochondrial apoptosis (caspase 3, Bax, cytochrome-c, Bcl-2), which were the same as the function of miR-33a-5p overexpression. 	32621257
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and HCC tissues	interaction[miR-539-5p]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	lncRNA CRNDE was highly expressed in HCC cells and HCC tissues compared with normal cells and the corresponding adjacent normal tissues.lncRNA CRNDE promotes the expression of POU2F1 by adsorbing miR-539-5p, thus promoting the progression of HCC.		Yes	lncRNA CRNDE promoted the cell viability, migration and invasion of HCC cells, while inhibited the apoptosis and promoted the EMT process of HCC cells. 	32252678
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(miR‑29c‑3p/NASP )	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//IHC//Bioinformatics Analysis//Transwell Assay	 CRNDE was found to be upregulated in HCC tissues and cells, and to be positively associated with the poor prognosis of patients with HCC. Bioinformatics and RT‑qPCR analysis indicated miR‑29c‑3p as a potential target of CRNDE. In line with previous reports, as a tumor suppressor, downregulated expression of miR‑29c‑3p was observed in HCC. In addition, the present study revealed that miR‑29c‑3p directly targeted NASP. 	 CRNDE was found to be upregulated in HCC tissues and cells, and to be positively associated with the poor prognosis of patients with HCC. 	Yes	Furthermore, CRNDE?knockdown suppressed cell proliferation, migration and invasion abilities. 	34633056
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-136-5p/ILF2 )	qRT-PCR//Western Blot	 In addition, we showed that long noncoding RNA colorectal neoplasia differentially expressed-h (lncRNA CRNDE-h) transcript expression was significantly up-regulated in HCC, and a miR-136-5p binding site was newly found in the lncRNA CRNDE-h transcript sequence using IntaRNA tool.  In terms of mechanism, highly-expressed lncRNA CRNDE-h transcript can sponge miR-136-5p, thereby preventing it from interacting with target ILF2 mRNA while promoting the proliferation of HCC cells.		Yes	 In terms of mechanism, highly-expressed lncRNA CRNDE-h transcript can sponge miR-136-5p, thereby preventing it from interacting with target ILF2 mRNA while promoting the proliferation of HCC cells.	34153299
CRNDE	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 clinical specimens of HCC 	Interaction(CRNDE/p300/YY1 axis)	qRT-PCR	In this study, we showed that CRNDE expression is significantly positively correlated with that of epidermal growth factor receptor (EGFR) in clinical specimens of HCC and induces proliferation and sorafenib resistance of HCC via EGFR-mediated signaling. Mechanistically, CRNDE stabilized the p300/YY1 complex at the EGFR promoter and simultaneously enhanced histone H3K9 and H3K27 acetylation, which serve as markers of relaxed chromatin. EGFR was positively upregulated by the epigenetic complex, p300/YY1, in a manner dependent on CRNDE expression, leading to enhanced tumor cell proliferation and sorafenib resistance. Furthermore, C646, a p300 inhibitor, suppressed EGFR transcriptional activity by decreasing chromatin relaxation and YY1 binding, which effectively reduced proliferation/sorafenib resistance and prolonged overall survival.		Yes	In this study, we showed that CRNDE expression is significantly positively correlated with that of epidermal growth factor receptor (EGFR) in clinical specimens of HCC and induces proliferation and sorafenib resistance of HCC via EGFR-mediated signaling. 	35999564
CRNDE	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cells 	Interaction( miR-423-5p/FSCN1 axis)	qRT-PCR//Western Blot	CRNDE and FSCN1 were upregulated in ovarian cancer cells (SKOV3, CAOV-3, IGROV1, A2780 and C13K), while miR-423-5p was downregulated. In addition, CRNDE could sponge miR-423-5p, and FSCN1 was confirmed to be the direct target of miR-423-5p. Furthermore, CRNDE knockdown-induced inhibition of FSCN1 was notably reversed by miR-423-5p downregulation. Knockdown of CRNDE inhibited cell proliferation, migration and invasion of ovarian cancer via miR-423-5p/FSCN1 axis. Thus, CRNDE may serve a new target for ovarian cancer.		Yes	Moreover, silencing of FSCN1/CRNDE significantly decreased proliferation, migration and invasion of ovarian cancer cells (SKOV3 and CI3K) via suppressing MMP-2 and MMP-9. 	35166986
CRNDE	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 bladder cancer tissues and cells	Expression [highly expressed]	qRT-PCR//Cell Apoptosis Assay//Migration Assay	In this work, we have presented evidence that CRNDE was significantly increased in bladder cancer, and overexpressed expression of CRNDE was positively related with advanced TNM stage of bladder cancer patients. 	In this work, we have presented evidence that CRNDE was significantly increased in bladder cancer, and overexpressed expression of CRNDE was positively related with advanced TNM stage of bladder cancer patients. 	Yes	 In addition, in vitro experiments showed that CRNDE strengthened cell migration/proliferation and inhibited cell apoptosis in bladder cancer. 	29710461
CTBP1-DT	LncRNA	Homo sapiens	Pancreatic Carcinoma	 pancreatic carcinoma tissues and cell line	Interaction(miR-141-3p and USP22 )	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 It was demonstrated that CTBP1-AS2 expression was markedly increased in pancreatic carcinoma tissues and cell lines.  In terms of mechanism, it was found that CTBP1‑AS2 adsorbed miR‑141‑3p as a molecular sponge to upregulate the expression level of USP22. 	High CTBP1‑AS2 expression was associated with advanced clinical stage and lymph node metastasis of patients.	Yes	High CTBP1‑AS2 expression was associated with advanced clinical stage and lymph node metastasis of patients.	35039872
CTBP1-DT	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cells	Interaction(miR-140-5p/BMP2 Axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	CTBP1-AS2 was upregulated in NPC cells.cCTBP1-AS2 silencing in SUNE-1 cells raised miR-140-5p expression and repressed BMP2 level. CTBP1-AS2 overexpression in CNE-1 cells suppressed miR- 140-5p expression and elevated BMP2 levels.		Yes	CTBP1-AS2 silencing suppressed NPC cell proliferation and promoted apoptosis.	35894463
CTBP1-DT	LncRNA	Homo sapiens	Glioma	glioma tissues 	regulation[miR-370-3p-Wnt7a axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//migration assay	The lncRNA CTBP1-AS2 had increased expression profiles in tumor tissues, which is associated with poor prognosisThis study provides new insights that a novel lncRNA, CTBP1-AS2, regulates EMT of glioma by modulating the miR-370-3p-Wnt7a axis.	The lncRNA CTBP1-AS2 had increased expression profiles in tumor tissues, which is associated with poor prognosis	Yes	In detail, CTBP1-AS2 knockdown decreased proliferation and migration phenotypes in both U87-MG and LN229 cells.	33150795
CTXND1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	Regulation[Wnt/β-catenin signaling pathway]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Microarray//Transwell Assay	LINC01314 was poorly expressed in GC cells and KLK4 was revealed to be a direct target gene of LINC01314. Overexpressed LINC01314 or silencing of KLK4 led to inhibited GC cell migration and invasion, corresponding to decreased Wnt-1, β-catenin, cyclin D1 and N-cadherin while increased E-cadherin.		Yes	 Overexpressed LINC01314 or silencing of KLK4 led to inhibited GC cell migration and invasion, corresponding to decreased Wnt-1, β-catenin, cyclin D1 and N-cadherin while increased E-cadherin.	31007611
CYTOR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Expression[highly expressed]	CCK8//qRT-PCR	Finally, the potential function of two lncRNAs (CASC9 and LINC00152) that were upregulated in OC tissues and associated with patients' survival time was verified by loss-of-function assays in OC cells. 	Moreover, lots of lncRNAs expression levels are associated with OC patients' overall survival and recurrence-free survival; for example, higher CASC9, LINC01232, and MIR4435-1HG expression levels are related to shorter overall survival and recurrence-free survival in OC patients.	Yes	Next, CCK8 assays showed that knockdown of CASC9 and LINC00152 inhibited SCC4 and SCC25 cells’ proliferation compared with control cells (Fig. 4c–f). 	30543527
CYTOR	LncRNA	Homo sapiens	Glioma	gliomas tissues	Interaction(miR-107/RAB10 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	In this study, we found that LINC00152 was upregulated in gliomas and its expression was significantly associated with high tumor aggressiveness and poor outcomes for glioma patients.Mechanistically, results of the bioinformatics analysis and experimental studies confirmed that LINC00152 and RAB10 as the targets of miR-107, and LINC00152 might act as a sponge for miR-107 to regulate the expression of RAB10 in glioblastoma. Additionally, silencing miR-107 reversed the effects induced by LINC00152 knockdown on glioblastoma cells both in vitro and in vivo.	In this study, we found that LINC00152 was upregulated in gliomas and its expression was significantly associated with high tumor aggressiveness and poor outcomes for glioma patients.	Yes	Functionally, the knockdown of LINC00152 not only inhibited malignant behaviors of glioma, such as proliferation and invasion of glioma cells and induced apoptosis in vitro but also suppressed tumorigenesis in vivo. 	34478013
CYTOR	LncRNA	Homo sapiens	Leukemia, Lymphoid	normal B cells and Chronic Lymphocytic Leukemia B cell clones	Expression(highly expressed)	qRT-PCR	Higher LINC00152 levels were consistently observed in memory B cell populations when compared to naïve B cells in the normal tissues analyzed [peripheral blood (PB), tonsils, and spleen]. In addition, independent stimulation via Immunoglobulins (IG), CD40, or Toll-like Receptor 9 (TLR9) upregulated LINC00152 in PB B cells. The expression of LINC00152 in a cohort of 107 early stage Binet A CLL patients was highly variable and did not correlate with known prognostic markers or clinical evolution. TLR9 stimulation, but not CD40 or IG challenge, was able to upregulate LINC00152 expression in CLL cells. In addition, LINC00152 silencing in CLL cell lines expressing LINC00152 failed to induce significant cell survival or apoptosis changes. These data suggest that, in normal B cells, the expression of LINC00152 is regulated by immunomodulatory signals, which are only partially effective in CLL cells. 	The expression of LINC00152 in a cohort of 107 early stage Binet A CLL patients was highly variable and did not correlate with known prognostic markers or clinical evolution.LINC00152 does not appear to contribute to CLL cell expansion and/or survival in a cohort of newly diagnosed CLL patients.	Yes	LINC00152 silencing in CLL cell lines expressing LINC00152 failed to induce significant cell survival or apoptosis changes.	34679195
CYP24A1	LncRNA	Homo sapiens	Ovarian Neoplasms	Ovarian Cancer tissues	Regulation	qRT-PCR	Moreover, we found that the most upregulated lncBCAS1-4_1 showed 75% same transcripts with CYP24A1 (metabolic enzyme of 1α,25(OH)2D3). Furthermore, lncBCAS1-4_1 could resist the antitumor effect of 1α,25(OH)2D3, which was associated with upregulated ZEB1. 		Yes	 Finally, the lncBCAS1-4_1 gain-of-function cell model was established, which demonstrated that the knockdown of lncBCAS1-4_1 inhibited the proliferation and migration of ovarian cancer cells.	34422647
CYB561-5	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(Bsg)	qRT-PCR//Western Blot	Lnc-CYB561-5 is highly expressed in human NSCLC and is associated with a poor prognosis in lung adenocarcinoma. In addition, RNA pulldown and RNA immunoprecipitation (RIP) assays show that basigin (Bsg) protein interacts with lnc-CYB561-5. Overall, this study demonstrates that lnc-CYB561-5 is an oncogene in NSCLC, which is involved in the regulation of cell proliferation and metastasis. 	Lnc-CYB561-5 is highly expressed in human NSCLC and is associated with a poor prognosis in lung adenocarcinoma. 	Yes	In vivo, downregulation of lnc-CYB561-5 significantly decreases tumour growth and metastasis. In vitro, lnc-CYB561-5 knockdown treatment inhibits cell migration, invasion and proliferation ability, as well as glycolysis rates. 	35064752
CWC27	CircRNA	Homo sapiens	Alzheimer Disease	AD mice and patients	Interaction(Pur-α)	ChIP//Transfection//RIP//PCR//IP//IF	CircCwc27 was a neuronal-enriched circRNA that abundantly expressed in the brain and significantly upregulated in AD mice and patients.  CircCwc27 directly bound to purine-rich element-binding protein A (Pur-α), increased retention of cytoplasmic Pur-α, and suppressed Pur-α recruitment to the promoters of a cluster of AD genes, including amyloid precursor protein (APP), dopamine receptor D1 (Drd1), protein phosphatase 1, regulatory inhibitor subunit1B (Ppp1r1b), neurotrophic tyrosine kinase, receptor, type 1 (Ntrk1), and LIM homeobox 8 (Lhx8). Downregulation of circCwc27 enhanced the affinity of Pur-α binding to these promoters, leading to altered transcription of Pur-α targets. 		Yes	Knockdown of circCwc27 markedly improved AD-related pathological traits and ameliorated cognitive dysfunctions. 	34504314
CUX1	CircRNA	Homo sapiens	Neuroblastoma	NB tissues	regulation[miR-16-5p/DMRT2 Axis]	colony Formation Assay//Flow Cytometry//qRT-PCR//RIP//MTT//PCR//IP//Colony Formation Assay//IF	Circ-CUX1 was highly expressed in NB tissues (n = 50) than that in FAM tissues (n = 50) (Fig. 1a). In conclusion, circ-CUX1 accelerated the proliferation, migration, invasion and glycolysis of NB cells through targeting miR-16-5p/DMRT2 signaling cascade.		Yes	Circ-CUX1 promoted the proliferation, migration, invasion and glycolysis of NB cells. 	33000435
CUL2	CircRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cell lines	Interaction(miR-208a-3p/PPP6C)	Northern Blot//Western Blot//Transfection//Flow Cytometry//PCR//IP//ChIP	 The expression level of circCUL2 was down-regulated in colorectal cancer tissues and cell lines.  Luciferase assay verified that miR-208a-3p could bind with circCUL2/PPP6C. Overexpression of circCUL2 could inhibit cancer progression via targeting the miR-208a-3p/PPP6C signal pathway.		Yes	 Forcing expression of circCUL2 inhibited proliferation ability, induced apoptosis, and autophagy in colorectal cancer cells. 	35027503
cTFRC	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	breast cancer tissues	Interaction[MicroRNA-107]	qRT-PCR//Western Blot//PCR//IF	We detected circular RNA-cTFRC Expression[Expression[up-expression]-expression]-regulated and correlated with tumor grade and poor survival rate of BC patients.  Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, Expression[Expression[up-expression]-expression]-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression.	We detected circular RNA-cTFRC Expression[Expression[up-expression]-expression]-regulated and correlated with tumor grade and poor survival rate of BC patients. 	Yes	Knock Expression[down-expression] of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo.	30782157
CTBP1-DT	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	regulation[miR-3163 ,ZNF217]	RNA Pull-Down//TUNEL//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 CTBP1-AS2 was significantly overexpressed in CC cell lines.CTBP1-AS2 regulates CC progression via sponging miR-3163 to up-regulate ZNF217.		Yes	Knockdown of CTBP1-AS2 curbed cell proliferation, migration and invasion, while stimulated cell apoptosis in vitro. CTBP1-AS2 facilitated xenograft tumor growth in vivo.	32742190
CTD-3252C9.4	LncRNA	Homo sapiens	Pancreatic Neoplasms	 pancreatic cancer cells and tissues	Interaction(IFI/IRF1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Invasion Assay//ChIP	CTD-3252C9.4 was found remarkably decreased in pancreatic cancer cells and tissues. Then, IFI6 was identified as a downstream target that could be down-regulated by CTD-3252C9.4 and IFI6 overexpression could counteract the effects of CTD-3252C9.4 upregulation on the survival and apoptosis of pancreatic cancer cells. Furthermore, mechanism experiments revealed that IRF1 was a transcriptional factor of IFI6 that can be blocked by CTD-3252C9.4 to inhibit IFI6 transcription.		Yes	Overexpression of CTD-3252C9.4 suppressed migration, invasion and proliferation, yet facilitated apoptosis of pancreatic cancer cells both in vitro and in vivo. 	34399768
CTD-2245E15.3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation(ACC1 and PC )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Colony Formation Assay	CTD-2245E15.3 was significantly upregulated in NSCLC and was mainly located in the cytoplasm. CTD-2245E15.3 exerted its oncogenic function by binding ACC1 and PC, which are key anabolic factors for biomolecule synthesis in rapidly proliferating tumor cells. Knockdown of CTD-2245E15.3 increased phosphorylation of ACC1 at an inhibitory site for enzymatic activity and promoted PC degradation via ubiquitination. 		Yes	Knockdown of CTD-2245E15.3 by specific antisense oligonucleotides suppressed cell growth in vitro and in vivo, largely due to cell-cycle arrest and induction of apoptosis.  Overexpression of CTD-2245E15.3 in an orthotopic model of lung cancer led to a significant increase in total tumor burden. 	33941610
CTC-497E21.4	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines	Regulation[RhoA signaling pathway]	qRT-PCR//FISH	CTC-497E21.4 was upregulated in GC tissues and GC cell lines (P < 0.05).Mechanistic investigations indicated that CTC-497E21.4 acted as a ceRNA for miR-22 and regulated NET1 expression. CTC-497E21.4/miR-22-3p/NET1 participated in the RhoA signaling pathway in the GC progression.	 CTC-497E21.4 was upregulated in GC tissues and GC cell lines (P < 0.05), and the expression was associated with depth of invasion, lymph node metastasis, and neurological invasion.	Yes	 Besides, knockdown of CTC-497E21.4 inhibited cell proliferation, invasion and promoted cell cycle arrest in vitro and inhibited tumorigenesis in vivo.	31451992
CTC-338M12.3	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
CTBP1-DT	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues, cell lines	regulation[miR-139-3p/MMP11 Axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	CTBP1-AS2 was highly expressed in GC, and its high expression was strongly associated with increased TNM stage, increased tumor size and low degree of differentiation of the tumor tissues. 	CTBP1-AS2 was highly expressed in GC, and its high expression was strongly associated with increased TNM stage, increased tumor size and low degree of differentiation of the tumor tissues. 	Yes	 Meanwhile, CTBP1-AS2 promoted GC cell proliferation, metastasis and suppressed apoptosis, while miR-139-3p could weaken these effects. 	33204108
CTBP1-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and cells	regulation[SP1/CTBP1-AS2/miR-195-5p/CEP55 axis]	qRT-PCR	We found that CTBP1-AS2 expressions were increased in HCC samples and cells. Overall, an emerging regulatory mechanism of SP1/CTBP1-AS2/miR-195-5p/CEP55 axis was reported in the paper, which possibly served as a new therapeutic HCC treatment target.	As revealed by the clinical assays, high CTBP1-AS2 expression usually related to lymph node metastasis, clinical stage and weaker prognosis specific to HCC patients. 	Yes	 Functionally, CTBP1-AS2 knockdown suppressed HCC cells in terms of the proliferation, migration, invasion, chemotherapy resistance as well as EMT progress, but promoted apoptosis.	32988587
CTBP1-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	regulation[miR-623/Cyclin D1 Axis]	CCK8//qRT-PCR	The downregulation of CTBP1-AS2 in HCC was confirmed by measuring the expression level of CTBP1-AS2 in both HCC and nontumor tissues from HCC patients. Therefore, CTBP1-AS2 promotes cell proliferation in HCC by regulating the miR-623/cyclin D1 axis.		Yes	CCK-8 analysis showed that CTBP1-AS2 and cyclin D1 overexpression promoted the proliferation of HCC cells. 	32522013
CTBP1-DT	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	regulation[miR-216a/ PTEN]	qRT-PCR//Luciferase Report Assay	 We found that CTBP1-AS2 was downregulated in OC and predicted poor survival. CTBP1-AS2 regulates miR-216a/PTEN to suppress OC cell proliferation.	 We found that CTBP1-AS2 was downregulated in OC and predicted poor survival. 	Yes	CTBP1-AS2 and PTEN overexpression resulted in the reduced proliferation rate of OC cells and reduced effects of miR-216a overexpression.	32711584
chr2:206992521|206994966	CircRNA	Homo sapiens	Psoriasis	psoriatic lesions skin	Expression[differently expression]	qRT-PCR//PCR	 To explore potential circRNA-mediated mechanisms of S-MSCs in the pathogenesis of psoriasis, we sequenced mRNAs and circRNAs of MSCs from normal skin and psoriatic lesions, followed by functional prediction and interaction analyses. In total, 129 circRNAs were differentially expressed, including 123 Expression[Expression[up-expression]-expression]-regulated and 6 Expression[down-expression]-regulated circRNAs, in MSCs from psoriatic lesions. 		Yes	KnockExpression[down-expression] of the circRNA gene chr2:206992521|206994966 reduced the capacity of S-MSCs to inhibit T-cell proliferation Expression[Expression[up-expression]-expression]on co-culture in normal as well as lesion-derived S-MSCs. 	30664808
CHEK1	CircRNA	Homo sapiens	Multiple Myeloma	MM cells	Expression(highly expressed)	In Vivo Experiment//Western Blot//Transfection//Co-IP//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//IF	We demonstrated that CHEK1 expression was significantly increased in human MM samples relative to normal plasma cells, and that in MM patients, high CHEK1 expression was associated with poor outcomes. Increased CHEK1 expression induced MM cellular proliferation and evoked drug-resistance in vitro and in vivo. CHEK1-mediated increases in cell proliferation and drug resistance were due in part to CHEK1-induced CIN. CHEK1 activated CIN, partly by phosphorylating CEP170. Interestingly, CHEK1 promoted osteoclast differentiation by upregulating NFATc1 expression. Intriguingly, we discovered that MM cells expressed circCHEK1_246aa, a circular CHEK1 RNA, which encoded and was translated to the CHEK1 kinase catalytic center. Transfection of circCHEK1_246aa increased MM CIN and osteoclast differentiation similarly to CHEK1 overexpression, suggesting that MM cells could secrete circCHEK1_246aa in the BM niche to increase the invasive potential of MM cells and promote osteoclast differentiation.	and that in MM patients, high CHEK1 expression was associated with poor outcomes.	Yes	Increased CHEK1 expression induced MM cellular proliferation and evoked drug-resistance in vitro and in vivo. 	34090465
CBR3-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-145-5p)	qRT-PCR//Western Blot	 High-expression levels of CBR3-AS1 were found in CRC tissues and cell lines. Moreover, we observed that CBR3-AS1 could directly bind to miR-145-5p and negatively regulated its expression in CRC. Further experiments also demonstrated that inhibition of miR-145-5p reverted the effects of CBR3-AS1 knockdown on CRC cells. In addition, compared with the parental cells, CBR3-AS1 expression was strikingly increased in oxaliplatin- (OXA-) resistant CRC cells, and the OXA resistance was notably diminished by CBR3-AS1 knockdown. 	Upregulated CBR3-AS1 was closely associated with poor prognosis and adverse clinicopathological features of CRC patients. 	Yes	. Artificial knockdown of CBR3-AS1 markedly suppressed the proliferation, migration, invasion, and stem-like properties but promoted the apoptosis of CRC cells. 	35466320
CCHE1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	UBC cell and patients	Regulation(ROCK1 )	qRT-PCR	 During the follow-up, plasma CCHE1 levels were significantly increased in UBC patients with DR but slightly decreased in patients with LR and NR. CCHE1 overexpression increased ROCK1 level in UBC cell lines, while ROCK1 overexpression failed to significantly affect CCHE1 expression. Moreover, CCHE1 and ROCK1 overexpression increased UBC cell migration and invasion, and ROCK1 silencing reduced the enhancing effects of CCHE1 overexpression on UBC cell migration and invasion. 	 CCHE1 overexpression on the day of discharge distinguished DR patients from LR and NR patients and healthy controls. Moreover, significant and positive correlations between CCHE1 and ROCK1 on the day of discharge and during the follow-up were found across patients with DR. 	Yes	CCHE1 overexpression increased ROCK1 level in UBC cell lines, while ROCK1 overexpression failed to significantly affect CCHE1 expression. Moreover, CCHE1 and ROCK1 overexpression increased UBC cell migration and invasion, and ROCK1 silencing reduced the enhancing effects of CCHE1 overexpression on UBC cell migration and invasion. 	36017913
CCEPR	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Expression[highly expressed]	Western Blot//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The results demonstrated that CCEPR expression was significantly higher in colorectal cancer tissues when compared with paired adjacent normal tissues.Finally, silencing of CCEPR downregulated matrix metalloproteinase (MMP)-2 and MMP-9 expression and suppressed epithelial-mesenchymal transition in colorectal cancer cells. 	 In addition, CCEPR expression was significantly higher in patients with advanced colorectal cancer (stage III/IV) than those with early-stage colorectal cancer (stage I/II). High CCEPR expression was significantly associated with poor differentiation, advanced clinical stage, positive lymph node metastasis and distant metastasis.	Yes	 In vitro experiments demonstrated that the expression of CCEPR was increased in colorectal cancer cell lines when compared with a normal colon cell line. Knockdown of CCEPR significantly inhibited colorectal cancer cell proliferation, colony formation and cell cycle progression, as well as cell migration and invasion. 	31602230
CCEPR	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues 	regulation[ Wnt/β-catenin signaling pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	CCEPR expression levels were significantly elevated in OC tissues compared with adjacent non?cancer tissues.In conclusion, the present study demonstrated that increased expression levels of CCEPR may predict poor prognosis in patients with OC and contribute to the progression of OC through regulating the Wnt/β‑catenin signaling pathway.	The increased expression levels of CCEPR were associated with increased invasion, higher International Federation of Gynecology and Obstetrics stage and a poorer overall survival rate. 	Yes	 In vitro, the genetic silencing of CCEPR decreased the cell proliferation rate and invasive ability of OC cells, and promoted apoptosis.	32319633
CCDC66	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue	Interaction(miR-370/MDM4 )	qRT-PCR//Luciferase Report Assay//Transwell Assay	 This study showed that circRNA CCDC66 was overexpressed in CRC tissues, and after knockdown, it inhibited the proliferation, migration, and invasion of CRC cells (RKO and HCT-116) in vitro. In addition, the dual-luciferase reporter assay showed that there was a binding site between circCCDC66 and miR-370, as well as between miR-370 and murine double minute 4 (MDM4). That is, circCCDC66 upregulated the expression of MDM4 through competitively binding to miR-370. The expression of circCCDC66 in CRC tissues was positively correlated with MDM4 and negatively correlated with miR-370.		Yes	 This study showed that circRNA CCDC66 was overexpressed in CRC tissues, and after knockdown, it inhibited the proliferation, migration, and invasion of CRC cells (RKO and HCT-116) in vitro. 	35069793
CCDC66	CircRNA	Homo sapiens	Osteoarthritis	OA cartilage tissues 	Interaction(miR-3622b-5p/SIRT3 axis)	Transfection//Western Blot//PCR//IF	It was found that circCCDC66 expression in OA cartilage tissues was upregulated. CircCCDC66 promoted OA chondrocyte apoptosis by regulating the miR-3622b-5p/SIRT3 axis. CircCCDC66 may be a new therapeutic target of OA.		Yes	CircCCDC66 overexpression inhibited proliferation and promoted apoptosis of chondrocytes and increased IL-6 and TNF-α levels in chondrocytes. 	34979511
CCDC26	LncRNA	Homo sapiens	Thyroid Neoplasms	patients' thyroid cancer tissues and thyroid cancer cell lines	Interaction(miR-422a/EZH2/Sirt6 Axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//BrdU//Colony Formation Assay//Transwell Assay	CCDC26 expression was elevated in patients' thyroid cancer tissues and thyroid cancer cell lines. Tumorigenicity analysis in nude mice revealed that CCDC26 contributed to thyroid tumor growth via miR-422a/EZH2/Sirt6 axis in vivo.		Yes	CCDC26 depletion remarkably reduced proliferation, invasion, and migration but induced apoptosis of thyroid cancer cells. 	34007185
CCDC196	LncRNA	Homo sapiens	Liver Neoplasms	cells	Interaction(miR‑522)	In Vivo Experiment//RNA Pull-Down//Transfection//Immunoblotting//Migration Assay//qRT-PCR//Colony Formation Assay//Invasion Assay	LINC00238 was identified as a downregulated molecule in The Cancer Genome Atlas liver hepatocellular carcinoma dataset through Gene Expression Profiling Interactive Analysis software.Mechanistically, RNA pull‑down assays showed that LINC00238 sponged microRNA (miR)‑522 and then reversed the inhibitory effects on two downstream targets, secreted frizzled related protein 2 and dickkopf1.		Yes	Through gain? and loss?of?function experiments, LINC00238 was confirmed as a tumor suppressor that could not only decrease cell viability, migration and invasion in vitro, but also tumorigenesis and tumor metastasis in vivo.	35014686
CCDC183-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-589-5p/SKP1 )	qRT-PCR	Significantly upregulated expression of CCDC183-AS1 was observed in both HCC tissues and cell lines. HCC patients with higher expression of CCDC183-AS1 had a poorer overall survival rate. Mechanistically, CCDC183-AS1 acted as a ceRNA through sponging miR-589-5p to offset its inhibitory effect on the target gene SKP1, then promoted the tumorigenesis of HCC.	Significantly upregulated expression of CCDC183-AS1 was observed in both HCC tissues and cell lines. HCC patients with higher expression of CCDC183-AS1 had a poorer overall survival rate.	Yes	Functionally, overexpression of CCDC183-AS1 markedly promoted HCC cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo, whereas the downregulation of CCDC183-AS1 exerted opposite effects. MiR-589-5p inhibitor counteracted the proliferation, migration and invasion inhibitory effects induced by CCDC183-AS1 silencing.	33541391
CCDC183-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Regulation(TCF7L2)	qRT-PCR//Luciferase Report Assay	Novel molecular mechanisms for developing effective diagnostic and therapeutic strategies are urgently needed; therefore, we screened the lncRNA expression profile in four pairs of BC tissues, showing that CCDC183-AS1 was the most upregulated lncRNA. Subsequently, results of CCK-8, EdU, Transwell, and aerobic glycolysis detection showed that CCDC183-AS1 plays an oncogene role in BC progression.  Furthermore, an investigation of the downstream and upstream factors of CCDC183-AS1 identified a novel MITF/CCDC183-AS1/miR-4731-5p/TCF7L2 axis in BC progression, which might furnish novel insights for developing effective diagnostic and therapeutic strategies for BC.		Yes	Subsequently, results of CCK-8, EdU, Transwell, and aerobic glycolysis detection showed that CCDC183-AS1 plays an oncogene role in BC progression. 	35957803
CCDC144NL-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues	regulation[CCDC144NL-AS1/miR-143-3p/MAP3K7 axis]	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Herein, we report lncRNA CCDC144NL-AS1, which has not been explored in GC, and it is markedly upregulated in GC tissues, which may serve as an independent predictor of poor prognosis.  Taken together, our results elucidate the oncogenic roles of CCDC144NL-AS1/miR-143-3p/MAP3K7 axis in GC progression, providing inspiration for further understanding of the mechanism of GC and making CCDC144NL-AS1 as a potential novel diagnostic and therapeutic target for GC.	 We found that CCDC144NL-AS1 expression was significantly positively associated with a larger tumor size and more pronounced lymph node metastasis.	Yes	Through a series of in vivo and in vitro functional experiments, we observed that CCDC144NL-AS1 could facilitate cell proliferation, invasion and migration and inhibit cell apoptosis in GC.	32647147
CCDC144NL-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells	Expression(highly expressed)	CCK8//qRT-PCR//Wound Healing Assay	 The survival analysis showed that high expression of CCDC144NL antisense RNA 1 (CCDC144NL-AS1) and LINC01614 was positively correlated with the poor prognosis of patients with gastric cancer. The in vitro validation results showed that CCDC144NL-AS1 and LINC01614 were both up-regulated in the gastric cancer cells.	 The survival analysis showed that high expression of CCDC144NL antisense RNA 1 (CCDC144NL-AS1) and LINC01614 was positively correlated with the poor prognosis of patients with gastric cancer. 	Yes	Silence of CCDC144NL-AS1 and LINC01614 both significantly suppressed the cell proliferation and migration of gastric cancer cells, and also promoted the chemosensitivity of gastric cancer cells to 5-fluorouracil.	35083139
CCDC144NL-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-490-3p)	Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	The expression of lncRNA CCDC144NL-AS1 was enhanced in both NSCLC tissues and cell lines.  LncRNA CCDC144NL-AS1 might target miR-490-3p. 	Patients with overexpression of lncRNA CCDC144NL-AS1 have a poor prognosis, and lncRNA CCDC144NL-AS1 is an independent prognostic factor for NSCLC.	Yes	Increased the relative expression level of lncRNA CCDC144NL-AS1 can promote the proliferation, migration, and invasion of NSCLC cells.	34115289
CCDC144NL-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-363-3p/GALNT7)	qRT-PCR//Luciferase Report Assay//IHC//FISH	CCDC144NL-AS1 was up-regulated in CRC tissues and cells. The study demonstrated that the CCDC144NL-AS1/miR-363-3p/GALNT7 axis exerts on key roles in cell proliferation and presents an emerging target for CRC therapy and prognostic biomarker.	 High CCDC144NL-AS1 was connected with the adverse clinicopathological features and worse prognosis of CRC. 	Yes	 Furthermore, knockdown of CCDC144NL-AS inhibited the cell proliferation and led to the cell cycle G0-1/S arrest, whereas upregulated CCDC144NL-AS1 obtained the inverse results. Further study found that CCDC144NL-AS1 functioned as ceRNAs in regulating CRC proliferation.	35154444
CCDC144NL-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue	Interaction(miR-940/WDR5-regulated epigenetic pathway)	CCK8//qRT-PCR//IHC//ChIP	CCDC144NL-AS1 was significantly upregulated in HCC tissue and had a marked relationship with the 5-year prognosis. In vitro study revealed that CCDC144NL-AS1 was highly expressed in HCC cell line MHCC97H but lowly expressed in normal hepatic cell line L02. CCDC144NL-AS1 was found to sponge miR-940 to induce the expression of WD repeat domain 5 (WDR5). ChIP-seq analysis identified that matrix metalloproteinase (MMP) 2, MMP9, and cyclin-dependent kinase (CDK) 1, CDK2, and CDK4 were all targets of WDR5. 		Yes	Overexpression of CCDC144NL-AS1 in L02 enhanced the invasion and proliferation abilities of cells but inhibited the apoptosis rate. Knockdown of CCDC144NL-AS1 in MHCC97H weakened the invasion and proliferation abilities of cells but increased the apoptosis rate. 	33977095
CCDC144NL-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	rOSCC and OSCC-LNM	Regulation(PI3K-AKT-mTOR pathway)	qRT-PCR//Western Blot//Transwell Assay	 The expressions of the lncRNAs, namely MAGI2-AS3 and CCDC144NL-AS1, were significantly upregulated in rOSCC and OSCC-LNM. MAGI2-AS3 was overexpressed in cancer tissue compared to other control groups. MAGI2-AS3 and CCDC144NL-AS1 might promote cell proliferation, invasion, and migration in OSCC cells by regulating the PI3K-AKT-mTOR pathway.		Yes	MAGI2-AS3 and CCDC144NL-AS1 might promote cell proliferation, invasion, and migration in OSCC cells by regulating the PI3K-AKT-mTOR pathway.	36401978
CCDC144NL-AS1	LncRNA	Homo sapiens	Endometriosis	EC tissues	Expression[highly expressed]	qRT-PCR	CCDC144NL-AS1 expression was upregulated in EC tissues compared to EU and normal endometrial (NE) tissues.		Yes	CCDC144NL-AS1 depletion suppressed the migration and invasion of hEM15A cells, but exerted no effects on cell adhesion, proliferation, apoptosis, or cell cycle.	30496345
CCAT2	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction(β-catenin/WISP1 axis)	CCK8//qRT-PCR//Transwell Assay//Western Blot	CCAT2 was overexpressed in ESCC tissues compared with corresponding adjacent tissues. Furthermore, knockdown of CCAT2 could suppress the mRNA and protein levels of β-catenin and Wnt-induced-secreted-protein-1 (WISP1), as well as the mRNA levels of their downstream targets VEGF-A, MMP2, and ICAM-1. High expression of CCAT2 and WISP1 were associated with poor prognosis of ESCC patients.		Yes	CCAT2 knockdown could suppress cell proliferation and invasion in vitro. 	34057837
CCAT2	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells and tissue	Interaction(miR-200b / IGF2BP2/TK1 Axis)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Upregulated CCAT2, IGF2BP2, and TK1 expression and inhibited miR-200b expression were observed in ESCC cells and tissues. CCAT2 bound to miR-200b and reduced its expression, leading to upregulated IGF2BP2 expression. IGF2BP2 improved TK1 mRNA stability to enhance its expression by recognizing its m6A modification. 		Yes	 CCAT2 promoted the migration and invasion of ESCC cells in vitro, and tumorigenesis in vivo by upregulating TK1 expression, while overexpression of miR-200b reversed these effects of CCAT2. 	34386421
CCAT2	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Expression[highly expressed]	Flow Cytometry//qRT-PCR	 It was found through differential expression analysis that the expression of lncRNA CCAT2 showed a significant difference in CRC tissues, and CRC patients with a high expression level of lncRNA CCAT2 had poor prognosis.Based on the results of qRT-PCR assay, lncRNA CCAT2 was significantly highly expressed in CRC tissues. 	 It was found through differential expression analysis that the expression of lncRNA CCAT2 showed a significant difference in CRC tissues, and CRC patients with a high expression level of lncRNA CCAT2 had poor prognosis.	Yes	 LncRNA CCAT2 can promote the growth and proliferation and suppress the apoptosis of CRC cells. 	33099922
CCAT2	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Regulation(RAB14/AKT/GSK3β signaling pathway)	CCK8//qRT-PCR//Western Blot	 Our results showed that CCAT2 was upregulated in CRC tissues and cell lines as com-pared to controls.  Ectopic expression of CCAT2 promoted CRC cell proliferation, migration and invasion, likely through direct interaction with TAF15, transcriptional activation of RAB14, and activation of the AKT/GSK3β signaling pathway. 		Yes	 Ectopic expression of CCAT2 promoted CRC cell proliferation, migration and invasion, likely through direct interaction with TAF15, transcriptional activation of RAB14, and activation of the AKT/GSK3β signaling pathway.  In vivo, CCAT2 promoted CRC cell growth and metastasis in nude mice.	34868956
CCEPR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//migration assay//Colony Formation Assay//Invasion Assay	In the present study, CCEPR mRNA expression level was upregulated in ESCC tissues and cell lines, and overexpression of CCEPR was associated with advanced TNM stage, lymph node metastasis, and poor prognosis in ESCC.	In the present study, CCEPR mRNA expression level was upregulated in ESCC tissues and cell lines, and overexpression of CCEPR was associated with advanced TNM stage, lymph node metastasis, and poor prognosis in ESCC.	Yes	In vitro experiments showed that silencing CCEPR mRNA expression levels significantly suppressed the proliferation, migration, and invasion of ESCC cells, while inducing ESCC cell apoptosis. 	32934710
CCHE1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue and cells	Expression(highly expressed)	CCK8//qRT-PCR//Western Blot	 We found that the CCHE1 was highly expressed in the NSCLC tissue, compared with the adjacent tissue.	We also found that the expression of CCHE1 was closely related to the size and survival time of patients. 	Yes	Moreover, CCHE1 could promote the proliferation, metastasis, and invasion of NSCLC cell line via increasing the expression of ERK/MAPK signaling pathway.	29630113
CCAT2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells and tissue	regulation[CCAT2/miR-145/MDM2 axis ]	qRT-PCR//Luciferase Report Assay	 In the present study, we found that CCAT2 was abnormally upregulated in HCC cells and tissue specimens, exhibiting an inverse correlation with microRNA (miR)-145 expression. Furthermore, a novel CCAT2/miR-145/MDM2 axis was revealed in HCC development and might provide a new target in the molecular treatment of HCC.		Yes	 Both the in vitro and in vivo effects of CCAT2 knockdown on the proliferation and metastasis of HCC cells were reversed by miR-145 inhibitor, indicating that miR-145 modulation accounts for CCAT2-meditated HCC progression. 	32037568
CCHE1	LncRNA	Homo sapiens	Colonic Neoplasms	blood	Interaction[interleukin-17A]	CCK8//qRT-PCR//Western Blot	In the present study, the expression levels of CCHE1 and interleukin (IL)-17A were increased in the plasma of patients with metastatic and non-metastatic colon adenocarcinoma (MC and NMC, respectively) compared with the healthy controls. Transfection of small interfering RNA against IL-17A partially reversed the effects of CCHE1 overexpression on cancer cell proliferation. Upregulation of IL-17A was observed after CCHE1 overexpression, while IL-17A overexpression did not significantly change the expression level of CCHE1. Therefore, CCHE1 may promote growth of colon adenocarcinoma through interactions with IL-17A.	The plasma expression levels of CCHE1 and IL-17A were positively associated with the primary tumor diameter. 	Yes	 CCHE1 and IL-17A overexpression promoted colon adenocarcinoma cell proliferation.	31423215
CDC6	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[target CDC6 by sponging microRNA-215]	qRT-PCR	Clinically, lncRNA-CDC6 was highly expressed in tumor tissues and was positively correlated with clinical stages of breast cancers.Moreover, lncRNA-CDC6 could function as competitive endogenous RNA (ceRNA) via directly sponging of microRNA-215 (miR-215), which further regulating the expression of CDC6. Taken together, our results proved that lncRNA-CDC6 could function as ceRNA and promote the proliferation and metastasis of breast cancer cells, which provided a novel prognostic marker for breast cancers in clinic.	Clinically, lncRNA-CDC6 was highly expressed in tumor tissues and was positively correlated with clinical stages of breast cancers.	Yes	Functionally, the ectopic expression of lncRNA-CDC6 promoted proliferation via regulation of G1 phase checkpoint, and further promoting the migration capability. 	30362551
Cdc14a	CircRNA	Mus musculus	Ischemic Stroke	 plasma and peri-infarct cortex of tMCAO mice	Expression(highly expressed)	In Vivo Experiment//FISH//qPCR	The expression of circCDC14A in plasma and peri-infarct cortex of tMCAO mice significantly increased, and circCDC14A was mainly localized in neutrophils peripherally while in astrocytes in peri-infarct cortex centrally.		Yes	Tail vein injection of lentivirus to interfere with the expression of circCDC14A significantly reduced the infarct volume (P < 0.01) at 72 h after reperfusion and density of activated astrocytes in peri-infarct cortex at 3 days, 5 days and 7 days after tMCAO modeling (all P < 0.0001). Moreover, mNSS (P < 0.0001) and survival rate (P < 0.001) were significantly improved within 7 days in si-circCDC14A group compared to circCon group. Additionally, morphology analysis showed the volume and surface area of each activated astrocytes significantly decreased (P < 0.0001).	34876161
CD82-AS1	LncRNA	Homo sapiens	Diabetic Nephropathies	DKD patients and high-glucose-induced human podocytes	Interaction(HuR)	Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//Transwell Assay	In this study, we found that the expression of lncRNA 254693 was increased in both DKD patients and high-glucose-induced human podocytes. Then, we did bioinformatics analysis via RBPDB and found that lncRNA 254693 can combine with HuR, a RNA binding protein. Meanwhile, immunofluorescence and in situ hybridization double staining was used to prove the existence of colocalization between them. Intriguingly, lncRNA 254693 knockdown decreased HuR levels, while HuR knockdown also decreased the level of lncRNA 254693 and its stability. 		Yes	Downregulation of lncRNA 254693 remarkably reversed the elevation of inflammation, apoptosis, and podocyte injury caused by high glucose. 	35493610
CD27-AS1-208	LncRNA	Homo sapiens	Melanoma	melanoma cell	Regulation(STAT3)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//migration assay//Colony Formation Assay//Invasion Assay	Further, we identified lncRNA CD27-AS1-208 as a novel nuclear-localized factor with prominent facilitative role in melanoma cell proliferation, invasion and migration.  Mechanistically, CD27-AS1-208 could directly interact with STAT3 and contribute to melanoma progression in a STAT3-dependent manner.		Yes	Further, we identified lncRNA CD27-AS1-208 as a novel nuclear-localized factor with prominent facilitative role in melanoma cell proliferation, invasion and migration. Ultimately, the role of CD27-AS1-208 in melanoma progression in vivo was also investigated.	35096622
CD27-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients (N = 40)	Interaction(miR-224-5p/PBX3 signaling)	qRT-PCR//Luciferase Report Assay	In present study, we found that the expression of CD27-AS1 examined by quantitative real-time PCR was markedly increased in the AML patients (N = 40) compared with healthy volunteers (N = 40). Additionally, CD27-AS1 was proved to increase PBX3 expression through sponging miR-224-5p. CD27-AS1 knockdown blocked the MAPK signaling through PBX3 silencing and further inhibited the cell growth of AML cells. 	The overall survival time was significantly shorter in patients with higher CD27-AS1 expression than that in patients with lower CD27-AS1 (P < 0.01).	Yes	Furthermore, downregulation of CD27-AS1 in AML cells suppressed proliferative ability, arrested cell cycle in G0/G1 phase, and induced apoptosis. However, CD27-AS1 overexpression further enhanced the malignant phenotype of AML cells. 	34006845
CD226	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	serum exosomes, tissues and cells of NSCLC	Interaction( miR-1224-3p/HMGA2 axis)	RNA Pull-Down//Western Blot//Transfection//Cell Viability Assay//PCR//IP//Invasion Assay//IF	 The abundance of circCD226 was elevated in serum exosomes, tissues and cells of NSCLC. Mechanistically, circCD226 sponged miR-1224-3p, and miR-1224-3p targeted HMGA2. CircCD226 involved the posttranscriptional regulation of HMGA2 through miR-1224-3p. Moreover, the miR-1224-3p/HMGA2 axis was identified as a functionally downstream effector of circCD226 in regulating NSCLC cell behaviors.		Yes	 NSCLC serum exosomes enhanced NSCLC cell proliferation, migration, invasion and stemness. Loss of circCD226 impeded cell proliferation, migration, invasion and stemness in vitro , as well as tumor growth in vivo . 	35946568
CD209	LncRNA	Homo sapiens	Stomach Neoplasms	cell lines	Regulation[JAK2/STAT3 signaling pathway]	qRT-PCR//MTT//Colony Formation Assay//Western Blot	In this study, the results showed that DC-SIGN was highly expressed in GC cells and significantly correlated with advanced clinical stage and lymphatic metastasis. Mechanistically, knockdown of DC-SIGN inactivated the JAK2/STAT3 signaling pathway, and overexpression of DC-SIGN activated the JAK2/STAT3 signaling pathway. In addition, through LncPath microarray analysis, we identified a lncRNA, RP11-181G12.2, that was significantly upregulated after knockdown of DC-SIGN; this was also confirmed by qRT-PCR. Furthermore, RP11-181G12.2 knockdown enhanced DC-SIGN expression in GC cells, further activating the JAK2/STAT3 signaling pathway. In contrast, DC-SIGN overexpression suppressed RP11-181G12.2 expression.		Yes	Downregulation of DC-SIGN significantly inhibited the proliferation, cell cycle progression, migration and invasion of GC cells in vitro. 	31766099
cCSC1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,colorectal cancer stem cells	Regulation[Hedgehog signaling pathway]	IHC//Western Blot//Wound Healing Assay//qRT-PCR//FISH//Colony Formation Assay	we identified a novel lncRNA (lncRNA-cCSC1) that is highly expressed in CRC and colorectal cancer stem cells (CRCSCs).  Furthermore, aberrant lncRNA-cCSC1 expression resulted in a concomitant alteration of smoothened (SMO) and GLI family zinc finger 1 (Gli1) expression in the Hedgehog (Hh) signaling pathway. Our study is the first to identify a novel lncRNA-cCSC1 in CRC and to indicate that it may regulate CSC-like properties via the Hh signaling pathway. Thus, lncRNA-cCSC1 could be a potential biomarker and promising therapeutic target for CRC.		Yes	The depletion of lncRNA-cCSC1 markedly inhibited the self-renewal capacity of the CRCSCs and reduced their drug resistance to 5-fluorouracil.  In contrast, lncRNA-cCSC1 overexpression increased the self-renewal effect.	31680315
cCSC1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cell lines	Interaction(lncRNA-cCSC1/miR-124-3p axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Our results showed that cell proliferation of CRC was promoted by lncRNA-cCSC1 upregulation and inhibited by lncRNA-cCSC1 downregulation. In addition, miR-124-3p is predicted to be the target of lncRNA-cCSC1 and is negatively correlated with lncRNA-cCSC1. Moreover, the addition of miR-124-3p mimics or inhibitor reversed the effects induced by lncRNA-cCSC1 overexpression or silencing on cell proliferation of CRC. Additionally, lncRNA-cCSC1 regulated the expression level of CD44, a target gene of miR-124-3p. Finally, we studied the effects of the lncRNA-cCSC1/miR-124-3p axis on CD44.		Yes	Our results showed that cell proliferation of CRC was promoted by lncRNA-cCSC1 upregulation and inhibited by lncRNA-cCSC1 downregulation.	33887588
cCNTNAP3	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	esophageal tissue	regulation[p53]	Western Blot//ISH//qRT-PCR//RIP//FISH//PCR//Microarray//IP//IHC//IF	 However, we found that the cCNTNAP3 expression level was significantly downregulated in ESCC tissues. In conclusion, the cCNTNAP3-TP53 positive feedback loop may provide a potential target for the management of ESCC, which also reveals the important role of circRNAs in the regulation of p53.		Yes	In vitro and in vivo studies revealed that cCNTNAP3 inhibited proliferation and increased apoptosis in p53 wild-type ESCC cells, but not in mutant cells.	33239613
CCND2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC epithelial cells	Expression(highly expressed)	Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	CCND2-AS1 expression was significantly over-expressed compared to normal breast epithelial cells. 		Yes	Gain-and loss-of-function experiments were performed in vitro to investigate the role of CCND2-AS1, where we found that CCND2-AS1 knockdown in MDA-MB-231 significantly suppressed cell proliferation, migration, and invasion. In contrast, CCND2-AS1 overexpression in BT-549 had the opposite effects. 	31938243
CCND2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical tissues	Expression[lower expressed]	qRT-PCR	CCND2 AS1 expression was lower in cervical cancer compared with normal cervical tissues, and the level was significantly correlated with the patient age and tumor size.		Yes	CCND2 AS1 overexpression inhibited the proliferation and cell cycle progression of HeLa cells in vitro and/or in vivo, whereas CCND2 AS1 silencing had the opposite effects.	32607313
CCND1	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues and cell lines	interaction[HuR and miR-646]	Western Blot//qPCR//RIP//PCR//IP//IF	 circ-CCND1 was found to be markedly up-regulated in laryngeal squamous cell carcinoma (LSCC) and closely associated with aggressive clinical features and adverse prognosis. Regarding the mechanism, circ-CCND1 physically bound to human antigen R (HuR) protein to enhance CCND1 mRNA stability; on the other hand, circ-CCND1 could act as an effective sponge for miR-646 to alleviate the repression of miR-646 on CCND1 mRNA. 	 circ-CCND1 was found to be markedly up-regulated in laryngeal squamous cell carcinoma (LSCC) and closely associated with aggressive clinical features and adverse prognosis. 	Yes	 Depletion of circ-CCND1 significantly inhibited LSCC cell proliferation in vitro and retarded tumour growth in vivo.	31951319
CCMAlnc	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	interaction[CCMAlnc/miR-5001-5p/HES6 signaling]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Elevated CCMAlnc was detected in CRC cells as well as in clinical CRC tissue samples, and the expression of this lncRNA positively correlated with the poor prognosis of CRC patients.	Elevated CCMAlnc was detected in CRC cells as well as in clinical CRC tissue samples, and the expression of this lncRNA positively correlated with the poor prognosis of CRC patients.	Yes	Functional validation assays revealed that downregulation of CCMAlnc impaired CRC cell proliferation and invasion in vitro, but upregulation of CCMAlnc reversed this effect.	33681178
CCL2	LncRNA	Homo sapiens	Stomach Neoplasms	tumor cell lines (HGC-27 and MKN-45)	Interaction(miR-128/ PARP2 signal pathway)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	CCL2 expression and PARP2 protein levels were up-regulated, while miR-128 expression was obviously lower. All over these results showed lncRNA CCL2 played importance of role in gastric tumor via miR-128/PARP2 axis signal pathway. 		Yes	Meanwhile, CCL2 down-regulating significantly repressed the proliferation, migration, and invasion by regulating miR-128.  PARP2-si obviously suppressed in gastric cancer proliferation, migration, and invasion. Meanwhile, miR-128 mimic and the knockout of CCL2 distinctly decreased PARP2 protein level. 	35000531
CCHE1	LncRNA	Homo sapiens	Stomach Neoplasms	tumor cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	 Expression of lncRNA CCHE1 in the tumor cell lines was increased (p<0.05).		Yes	Up-regulated lncRNA CCHE1 increased proliferative activity and colony formation capacity. 	29771412
CCHE1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells	interaction[PAK2,miR-922]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	qRT-PCR analysis identified the upregulation of CCHE1 in OSCC cells.CCHE1 increases the expression of PAK2 to promote the progression of OSCC by competitively binding to miR-922 in OSCC cells.		Yes	Knockdown of CCHE1 curbed the proliferation, migration, and invasion and hastened the apoptosis in OSCC cell lines.	31981240
CCHE1	LncRNA	Homo sapiens	pancreatic adenocarcinoma	blood	Interaction[ROCK1]	ELISA//Transwell Assay//Western Blot	The results of the present study demonstrated that, compared with healthy controls, CCHE1 and ROCK1 were upregulated in the serum of patients with metastatic pancreatic adenocarcinoma.ROCK1 small interfering RNA-induced silencing partially reversed the enhancing effects of CCHE1 overexpression on cancer cell migration and invasion. Therefore, lncRNA-CCHE1 may be involved in migration and invasion but not in proliferation of pancreatic adenocarcinoma cells, possibly by interacting with ROCK1.		Yes	 CCHE1 overexpression promoted the migration and invasion of human pancreatic adenocarcinoma cell lines, but no significant effects on cell proliferation were identified. 	31423182
CCHE1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cell lines	regulation[MEK/ERK/c-MYC pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	Elevated levels of CCHE1 were verified in NPC cell lines.The present study suggested that downregulation of lncRNA CCHE1 could inhibit cell proliferation, migration and invasion by suppressing MEK/ERK/c-MYC pathway in nasopharyngeal carcinoma.		Yes	Downregulation of CCHE1 significantly inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion. 	32964977
CCAT2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction[up-regulating NDRG1]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this study, we found that CCAT2 were significantly elevated in HCC tissues and cell lines.All these observations demonstrate that CCAT2 acts as an oncogene by up-regulating NDRG1, which may have the potential to be used as a promising prognostic biomarker and therapeutic target for HCC.		Yes	 In this study, we found that CCAT2 were significantly elevated in HCC tissues and cell lines, and it promoted HCC cells proliferation and metastasis both in vitro and in vivo. 	30922920
CCAT2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue	Interaction(miR-4496/Atg5  Axis)	qRT-PCR//Western Blot	In our study, we found that lncRNA CCAT2 expression was significantly increased in HCC tissue and was correlated with advanced stage and venous invasion. Mechanistic investigations found that CCAT2 involved in HCC by regulating miR-4496/Atg5 in cytoplasm.  In nucleus, CCAT2 bound with ELAVL1/HuR to facilitate HCC progression. 	In our study, we found that lncRNA CCAT2 expression was significantly increased in HCC tissue and was correlated with advanced stage and venous invasion. 	Yes	 Further experiments revealed that CCAT2 induced autophagy and promoted migration and invasion in vitro and in vivo. 	34409736
CHASERR	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	regulation[NF-κB/YY1 axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//ChIP	 LINC01578 was upregulated in colon cancer, associated with metastasis, advanced clinical stages, poor overall survival, disease-specific survival, and disease-free survival. Collectively, this study demonstrated that LINC01578 promoted colon cancer metastasis via forming a positive feedback loop with NF-κB/YY1 and suggested that LINC01578 represents a potential prognostic biomarker and therapeutic target for colon cancer metastasis.	 LINC01578 was upregulated in colon cancer, associated with metastasis, advanced clinical stages, poor overall survival, disease-specific survival, and disease-free survival.	Yes	Gain-of-function and loss-of-function assays revealed that LINC01578 enhanced colon cancer cell viability and mobility in vitro and colon cancer liver metastasis in vivo. 	33040438
CCAT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Expression[highly expressed]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 CCAT1 was signifi cantly upregulated in bladder cancer (P < 0.05).	CCAT1 upregulation was positively related to tumor stage (P = 0.004), tumor grade (P = 0.001) and tumor size (P = 0.042). 	Yes	Cell proliferation, migration and invasion were promoted by abnormally expressed CCAT1	31038865
CCAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cell lines	regulation[ERK/AKT pathway]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry	The findings revealed that CCAT1expression was upregulated in OSCC cell lines. Downregulation of CCAT1 suppressed TCA-8113 cell proliferation, invasion, and migration by inactivation of the ERK/AKT pathway via inhibition of DDR2, suggesting the value of CCAT1 in diagnosis and treatment of patients with OSCC.		Yes	Knockdown of CCAT1 repressed cell proliferation, blocked the cell cycle, and suppressed the invasion and migration of TCA-8113 cells. 	32009633
CCAT1	LncRNA	Homo sapiens	Endometrial Neoplasms	cell lines	Interaction[sponge of miR-181a-5p]	CCK8//qRT-PCR//Western Blot//Transwell Assay	The expression level of CCAT1 was significantly upregulated in EC tissue samples compared with matched adjacent healthy tissue samples from patients with endometrial cancer. The results suggest that CCAT1 promotes EC progression by acting as a molecular sponge of miR-181a-5p.		Yes	Cell counting kit-8 and Transwell migration assays demonstrated that CCAT1 knockdown significantly decreased EC cell proliferation and migration.	30988798
CCAT1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Regulation[miR-181a-5p/MMP14 axis]	CCK8//qRT-PCR//Transwell Assay	The expression of CCAT1 in the cervical cancer tissues was higher than in the adjacent normal tissues. Elevated CCAT1 suppressed miR-181a expression, which was accompanied by an increased expression of MMP14 and HB-EGF. In contrast, knocking down CCAT1 resulted in increased expression of miR-181a, along with decreased expression of MMP14 and HB-EGF. Thus, CCAT1 is a key oncogenic lncRNA associated with cervical cancer and plays a role in promoting cervical cancer cell proliferation and invasion by regulating the miR-181a-5p/MMP14 axis.		Yes	 Overexpressing CCAT1 promoted cervical cancer cell proliferation, colony formation, and invasion in vitro.	31084453
CCAT1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Regulation[miR-218/ZFX signaling]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay	Additionally, CCAT1 expression was higher in TNBC patient tumor tissue than adjacent normal breast tissue. Bioinformatics analysis revealed that microRNA-218 (miR-218) is a potential target of CCAT1. Silencing CCAT1 resulted in an increase in miR-218 expression and inhibited TNBC cell proliferation, migration, and invasion. Silencing miR-218 reversed the effects of CCAT1 knockdown on cell proliferation, migration, and invasion, suggesting that CCAT1 promotes TNBC progression by downregulating miR-218 expression. We identified the zinc finger protein ZFX as a putative downstream target of miR-218 through bioinformatics analysis. ZFX expression was higher in TNBC than normal breast cell lines and higher in TNBC tumor tissue than adjacent normal breast tissue. Overexpression of ZFX reversed the tumor-suppressive effects of miR-218 on TNBC cell proliferation, migration, and invasion.		Yes	 Silencing CCAT1 inhibited TNBC cell proliferation, migration, and invasion in vitro, and tumor growth and progression in vivo. 	31310241
CCAT1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung adenocarcinoma tissues	Expression[highly expressed]	qRT-PCR//Transwell Assay//Western Blot	In the current study, the expression of CCAT1 was identified to be increased in lung adenocarcinoma tissues (n=96) by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and its expression level was associated with epidermal growth factor receptor (EGFR) expression (P=0.011), lymphatic metastasis (P=0.003) and tumor node metastasis (TNM) stage (P=0.003). 	In the current study, the expression of CCAT1 was identified to be increased in lung adenocarcinoma tissues (n=96) by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and its expression level was associated with epidermal growth factor receptor (EGFR) expression (P=0.011), lymphatic metastasis (P=0.003) and tumor node metastasis (TNM) stage (P=0.003). 	Yes	In vitro, by using Transwell assays, the overexpression of CCAT1 was demonstrated to promote the migration and invasion of H358 lung adenocarcinoma cells; while downregulation of CCAT1 expression inhibited H1650 cell migration and invasion.	30008869
CCAT1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LAD tissue	regulation[Suppressing miR-219-1]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//cell invasion assay	In this study, we found LAD tissue samples had a higher expression of CCAT1 but a lower expression of miR-219-1 compared to their adjacent non-tumor tissues. In summary, our findings suggested that CCAT1 promotes the progression of LAD via sponging miR-219-1, providing a potential therapeutic target for LAD.		Yes	Knockdown of CCAT1 inhibited the proliferation, migration, and invasion of A549 and H1299 cells, which were reversed by the miR-219-1 inhibitor. 	33193573
CCAT1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and LUAD cells	Regulation(PI3K/AKT/mTOR signalling)	In Vivo Experiment//Western Blot//ISH//Transfection//Co-IP//qRT-PCR//RIP//IF//Luciferase Report Assay//EdU Staining//ChIP	We identified the upregulation of CCAT1 in LUAD tissues and LUAD cells. Moreover, we found that CCAT1 regulated the activity of AKT by promoting the ubiquitination of FKBP51 through binding with USP49. 		Yes	 Subsequently, cell function assays revealed the enhancement of CCAT1 on LUAD cell proliferation and angiogenesis in vitro and in vivo. 	34431227
CCAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	Hep-2 and TU177 cells	Interaction(miR-218-5p/BMI1)	Western Blot//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	Our results depicted that CCAT1 was highly-expressed in Hep-2 and TU177 cells.  Mechanically, CCAT1 regulated the BMI1 expression by competitively binding to miR-218-5p as a competing endogenous RNA (ceRNA), and thus facilitated the growth of Hep-2 and TU177 cells. Downregulation of miR-218-5p or upregulation of BMI1 inhibited the inhibitory effect of silencing CCAT1 on Hep-2 and TU177 cell proliferation, invasion, and migration. 		Yes	Silencing CCAT1 inhibited the proliferation, migration, and invasion of Hep-2 and TU177 cells. 	35261819
CCAT1	LncRNA	Homo sapiens	Prostatic Neoplasms		Expression[highly expressed]	qRT-PCR//MTT//Transwell Assay	Increased CCAT1 was significantly related to lymph node metastasis in prostate cancer. 	Increased CCAT1 was significantly related to lymph node metastasis in prostate cancer. 	Yes	Low-expression of CCAT1 could suppress cell proliferation. Knockdown of CCAT1 inhibited the migration of PC-3 cells. Down-regulation of CCAT1 attenuated the invasion of PC-3 cells.	29863242
CCAT1	LncRNA	Homo sapiens	Prostatic Neoplasms		Interaction[DDX5 and MIR-28-5P]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	 In this study, we found from The Cancer Genome Atlas and Memorial Sloan Kettering Cancer Center database that CCAT1 is highly upregulated in castration-resistant prostate cancer (CRPC) compared with androgen-dependent prostate cancer (ADPC). Mechanistically, in cytoplasm, CCAT1 sponges MIR-28-5P to prevent the anticancer effect. In nucleus, CCAT1 acts as a scaffold for DDX5 (P68) and AR transcriptional complex to facilitate the expression of AR-regulated genes, thus stimulating CRPC progression. Our findings suggest that CCAT1 is an oncogenic factor in the progression of CRPC with different regulatory mechanisms in the nucleus and cytoplasm of cells.		Yes	 In vitro and in vivo studies show that CCAT1 promotes prostate cancer cell proliferation as well as the tumor growth of prostate cancer xenografts.	31387890
CCAT1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC cell line and tissues 	Interaction(miR-130a-3p axis)	qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	CCAT1 was upregulated and miR-130a-3p was downregulated in ccRCC cell line and tissues (all P < 0.05). There was a negative association between CCAT1 and miR-130a-3p expression (r = - 0.373, P = 0.010). MiR-130a-3p mimic and si-CCAT1 inhibited ccRCC cell proliferation and invasion, and induced apoptosis.	 High CCAT1 and low miR-130a-3p expression was correlated with larger tumor size and advanced TNM stage in ccRCC patients. High CCAT1 level suggested a poor survival prognosis.	Yes	There was a negative association between CCAT1 and miR-130a-3p expression (r = - 0.373, P = 0.010). MiR-130a-3p mimic and si-CCAT1 inhibited ccRCC cell proliferation and invasion, and induced apoptosis.	33482824
CCAT1	LncRNA	Homo sapiens	Retinoblastoma	RB cell lines	Interaction(miR-218-5p/MTF2 axis)	Western Blot//Transfection//qPCR//migration assay//Luciferase Report Assay//cell invasion assay	Previously, we have demonstrated that lncRNA colon cancer-associated transcript 1 (CCAT1) in two RB cell lines SO-RB50 and Y79 was obviously overexpressed, and notably, lncRNA CCAT1 attenuated miR-218-5p expressionand induced proliferation, cell migration and invasion.  Functional analysis and rescue analysis showed that lncRNA CCAT1 via competitive binding to miR-218-5p to modulate MTF2 expression thus accelerate EMT, cell migration and invasion of RB.		Yes	Previously, we have demonstrated that lncRNA colon cancer-associated transcript 1 (CCAT1) in two RB cell lines SO-RB50 and Y79 was obviously overexpressed, and notably, lncRNA CCAT1 attenuated miR-218-5p expressionand induced proliferation, cell migration and invasion. 	34265414
CCAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tumor tissues	regulation[suppressing miR-152]	qRT-PCR//MTT//Western Blot//Transwell Assay	CCAT1 expression levels significantly increased in NSCLC tumor tissues and were associated with poor overall survival of NSCLC patients. Long non-coding RNA CCAT1 regulates tumor cell proliferation and invasion in NSCLC through suppressing miR-152.	CCAT1 expression levels significantly increased in NSCLC tumor tissues and were associated with poor overall survival of NSCLC patients. 	Yes	CCAT1 promotes cell proliferation, cell invasion and epithelial-mesenchymal transition of NSCLC cell lines.	32227563
CCAT1	LncRNA	Homo sapiens	Osteoporosis	bone tissues and osteoblasts of ovariectomized rats with osteoporosis	Interaction(miR-34a-5p/SMURF2)	In Vivo Experiment//RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	CCAT1 and SMURF2 were amplified while miR-34a-5p expression was inhibited in bone tissues and osteoblasts of ovariectomized rats with osteoporosis. LncRNA CCAT1 could competitively bind with miR-34a-5p to prevent the degradation of its target gene SMURF2.		Yes	Inhibited CCAT1 improved pathology and restricted osteocyte apoptosis of bone tissues in ovariectomized rats with osteoporosis in vivo, and also enhanced differentiation, mineralization abilities, and proliferation, and suppressed apoptosis of osteoblasts from ovariectomized rats in vitro through upregulating miR-34a-5p expression. 	33402731
CCAL	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation[CCAL/miR-149/FOXM1 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay	We observed that CCAL was upregulated in gastric cancer tissues and was associated with the tumour-node-metastasis stage. These results demonstrated that the CCAL/miR-149/FOXM1 axis functions as a key regulator in gastric cancer metastasis and CCAL potentially represents a biomarker for diagnosis and potential target for therapy in the future.	We observed that CCAL was upregulated in gastric cancer tissues and was associated with the tumour-node-metastasis stage. 	Yes	Functional experiments showed that CCAL promoted gastric cancer cell proliferation and metastasis in vitro and in vivo. 	30250169
CCAL	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	regulation[MiR-29b/ANGPTL4 Axis ]	Western Blot//qRT-PCR//Luciferase Report Assay//ELISA//IHC	Compared with noncancerous tissues, the expression of CCAL was markedly upregulated in osteosarcoma tissues.Our results show that CCAL promotes angiogenesis by regulating the miR-29b/ANGPTL4 axis in osteosarcoma.	Higher CCAL expression levels were closely related to shorter overall survival in patients with osteosarcoma.	Yes	Additionally, functional analysis indicated that CCAL could facilitate tumour angiogenesis in vitro and in vivo in osteosarcoma.	33122950
CBR3-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast tissues	Expression[Expression[highly expressed]-expression]	qRT-PCR//MTT	Our results showed that CBR3-AS1 was overexpressed in breast cancer tissues and cell lines and predicted the prognosis of breast cancer patients.		Yes	We first examined the effect of CBR3-AS1 on cell proliferation in the four breast cancer cell lines. MTT assay revealed that CBR3-AS1 knockdown significantly inhibited cell viability in breast cancer cells at 48 or 72 h after treatment with si-CBR3-AS1 (Fig. 3B–E). At the same time, ectopic expression of CBR3-AS1 in breast cancer cells obviously accelerated the cell proliferation (Fig. 3G–J). Furthermore, stable knockdown of CBR3-AS1 resulted in decreased colony formation (Fig. 4A, P < 0.001), as well as CBR3-AS1 overexpression obviously promoted the colony formation of breast cancer cells (Fig. 4B, P < 0.001). In addition, it was also found that CBR3-AS1 was involved in the regulation of cell apoptosis in breast cancer. Stable knockdown of CBR3-AS1 significantly inducted cell apoptosis (Fig. 4C, P < 0.001), whereas overexpression of CBR3-AS1 possessed an obvious reduction in the proportion of apoptotic cells (Fig. 4D, P < 0.001).	34530987
CBR3-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Expression[highly expressed]	qRT-PCR//MTT	Our results showed that CBR3-AS1 was overexpressed in breast cancer tissues and cell lines and predicted the prognosis of breast cancer patients.		Yes	And CBR3-AS1 exerted biological function as an oncogenic lncRNA, involved in the regulation of cell proliferation, colony formation, apoptosis and tumor growth in breast cancer. 	32550547
CBR3-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	Interaction(miR-409-3p/SOD1 axis)	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	Here, we demonstrate CBR3-AS1 overexpression in NSCLC tissue compared with adjacent normal tissue. CBR3-AS1 may regulate the expression and functions of the miR-409-3p target gene SOD1.CBR3-AS1 downregulation decreased post-irradiation SOD1 expression, increased γH2AX formation, raised levels of reactive oxygen species, and promoted apoptosis. 		Yes	CBR3-AS1 downregulation reduced proliferation, invasion, and migration; inhibited cell cycle progression; and promoted apoptosis of NSCLC cells. CBR3-AS1 also promoted tumor growth in vivo. 	34801596
CCAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[Wnt/β-catenin signaling pathway]	RIP//Western Blot//qRT-PCR	CCAT1 was upregulated in OSCC tissues and cell lines.Luciferase and RIP assays revealed that miR-181a was a direct target of CCAT1. Inhibition of miR-181a partially reversed the efficacy of sh-CCAT1. Moreover, sh-CCAT1 inhibited OSCC tissues growth through inhibiting Wnt signaling in a miR-181a-dependent manner in vivo. lncRNA CCAT1 activated Wnt/β-catenin signaling via inhibiting miR-181a, resulting in the cell proliferation, migration and invasion of OSCC, suggesting that CCAT1 might serve as a potential target of OSCC treatment.		Yes	Knockdown of CCAT1 inhibited the proliferation, migration and invasion of OSCC cells, while the cell apoptosis was enhanced. 	31599709
CCAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[as miR-30c-2-3p sponge]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	 In this study, we demonstrated that CCAT1 was highly expressed in HCC tissues and remarkably associated with metastasis. In general, CCAT1 regulate the expression of CCNE1 by acting as a ceRNA to sponge miR-30c-2-3p in regulating the cell proliferation of HCC.		Yes	". MTT assay in Hep3B
and HepG2 cells showed that overexpressing CCAT1 promoted the
cell proliferation (Figures 2C and S1A in the Supporting Information),
whereas knock down of CCAt1 suppressed the cell proliferation (Fig_x0002_ures 2D and S1B)."	30773676
CCAT2	LncRNA	Homo sapiens	Esophageal Neoplasms	cell lines	Regulation[Wnt signaling pathway]	qRT-PCR//Wound Healing Assay//MTT//Transwell Assay	The expression of CCAT2 was significantly decreased in si-CCAT2 Eca-109 cells.  Treatment with si-CCAT2 and FH535 alone or in combination significantly inhibited the proliferation, migration and invasion of Eca-109 cells. The treatments also promoted apoptosis, upregulated the expression of Bax and APC proteins, and downregulated β-catenin, PCNA, cyclin D1 and c-Myc proteins.		Yes	Treatment with si-CCAT2 and FH535 alone or in combination significantly inhibited the proliferation, migration and invasion of Eca-109 cells.	31423241
CCAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[sponging miR-181]	Luciferase Report Assay//IF	CCAT1 levels were higher in tissue and cell lines of HCC.  Our results show that, mechanistically, CCAT1 promotes autophagy through functioning as a sponge for miR-181a-5p, and then regulating ATG7 expression.		Yes	 In function research, we found that CCAT1 facilitates HCC cell autophagy and cell proliferation. 	31218739
CCAT2	LncRNA	Homo sapiens	Glioma	NHA cells	interaction[sponging miR-424]	Flow Cytometry//qRT-PCR//Colony Formation Assay//Western Blot	LncRNA CCAT2 and VEGFA were highly expressed, while miR-424 was expressed at low levels in NHA cells.The oncogenic lncRNA CCAT2 is highly associated with the development of glioma and exerts its function by upregulating VEGFA via miR-424.		Yes	Furthermore, knockdown of lncRNA CCAT2 decreased cell proliferation, increased cell apoptosis and inhibited endothelial angiogenesis in glioma.	32236863
CCAT2	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tissues and cell lines	regulation[Wnt/β-catenin pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 CCAT2 expression was increased in TC tissue samples and cell lines compared with the controls. In summary, the present study demonstrated that CCAT2 knockdown suppresses TC progression via inactivating the Wnt/β‑catenin cascade, indicating that suppressing CCAT2 and the Wnt/β‑catenin signaling pathway may be a promising therapeutic strategy for treating TC.	Tissue CCAT2 level was associated with T stage and tumor?node?metastasis stage of TC. 	Yes	Silencing CCAT2 inhibited TC cell proliferation, migration and invasion, and promoted TC cell cycle arrest and apoptosis.	33125134
CCAT2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	cell lines	Interaction[binding miR-23b-5p]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 The expression of CCAT2 was upregulated obviously in lung adenocarcinoma cells.These findings indicated that CCAT2 may act as a competitive endogenous RNA (ceRNA) to regulate FOXC1 expression by competitively binding miR-23b-5p in lung adenocarcinoma.		Yes	Cell function analysis showed that upregulation of CCAT2 significantly promoted cell proliferation and migration, and reduction of CCAT2 inhibited cell migration and proliferation. 	30548656
CCAT2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissue and serum samples	Expression [highly expressed]	RNA Pull-Down//IHC//CCK8//qRT-PCR//Flow Cytometry//IF//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CCAT2 was significantly upregulated in human LSCC tissue and serum samples, associated with larger tumor volume, higher clinical stage, and poorer differentiation status. 	CCAT2 was significantly upregulated in human LSCC tissue and serum samples, associated with larger tumor volume, higher clinical stage, and poorer differentiation status. 	Yes	Lentivirus-mediated CCAT2 knockdown notably repressed the cell viability, colony formation, and DNA synthesis rate of LSCC. Screening of transcription factors revealed that YAP/TEAD activity was affected by CCAT2 in LSCC cells. 	34515990
CCAT2	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues, cell lines	regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//Western Blot	In the present study, the reverse transcription-quantitative PCR (RT-qPCR) results indicated that CCAT2 expression was significantly upregulated in PCa tissues, and DU145 and PC3 cell lines compared with normal prostate tissues and the epithelial RWPE-1 cell line, respectively.Overall, the results indicated that CCAT2 regulated PCa via the Wnt/β-catenin signaling pathway; therefore, CCAT2 may exhibit key role during the progression of PCa and may serve as a therapeutic target for the disease.		Yes	Functional assays indicated that CCAT2 downregulation inhibited DU145 and PC3 cell proliferation, cell cycle, migration and invasion.	32831916
CCAT2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells and tissues	Interaction(microRNA-493-5p/CREB1 axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression of CCAT2 was upregulated in CC cells and tissues.Mechanistically, CCAT2 functions as a competing endogenous RNA (ceRNA) to upregulate the expression of CREB1 by binding to miR-493-5p. The overexpression of CREB1 or downregulation of miR-493-5p antagonized the effect of CCAT2 knockdown on the proliferation and EMT of CC cells. 		Yes	However, the knockdown of CCAT2 inhibited the proliferation and epithelial-mesenchymal transition (EMT) of CC cells in vitro and suppressed tumor growth in vivo. 	34499007
CCAT2	LncRNA	Homo sapiens	Neuroblastoma	cancer tissues of children with neuroblastoma 	Expression [highly expressed]	Western Blot//Transfection//qRT-PCR//MTT//Transwell Assay	 lncRNA CCAT2 expression in cancer tissues of children with neuroblastoma was notably higher than that in corresponding paracancerous tissues (P < 0.05), and children with different tissue differentiation, tumor staging, and lymph node metastasis (LNM) showed notably different lncRNA CCAT2 expression (P < 0.05). Compared with HUVEC cells, SH-SY5Y and SK-N-SH cells showed notably up-regulated lncRNA CCAT2, and the expression of it in SH-SY5Y was higher than that in SK-N-SH cells (P < 0.05).	In addition, children with neuroblastoma in the high lncRNA CCAT2 expression group showed lower 3-year survival rate than those in the low expression group (P < 0.05). Multivariate analysis revealed that tissue differentiation, tumor-node-metastasis staging, LNM, and lncRNA CCAT2 expression were all independent risk factors affecting the prognosis of children with neuroblastoma (all P < 0.05).	Yes	Moreover, according to the MTT assay, the si-CCAT2 group showed notably weakened cell viability and proliferation than the CCAT2-NC group (both P < 0.05), and SH-SY5Y cells in the former group were less active than those in the latter group in terms of migration and invasion.  The cell apoptosis rate of SH-SY5Y cells in the si-CCAT2 was higher than that in the CCAT2-NC.	33475889
CCAT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[ targeting miR-219-1 ]	qRT-PCR	The results exhibited the fact that CCAT1 was expressed higher in 57 GC tissue samples than in 57 paired adjacent normal tissue samples. The expression of CCAT1 was also increased in GC cell lines (MKN45, Hs746T, and SGC-7901) compared with the gastric epithelial cell line GES-1.  In conclusion, these results suggested that CAT1 promotes the tumorigenesis and progression of GC by negatively regulating miR-219-1.		Yes	 Finally, in vivo experiment indicated that tumor growth of GC was suppressed through knockdown of CCAT1.	31478245
CCAT1	LncRNA	Homo sapiens	Stomach Neoplasms	 gastric cancer cells	Interaction( miR-140-3p/ATG5)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//H&E Staining//IHC//Invasion Assay//Transwell Assay	 LncRNA CCAT1 was highly expressed in gastric cancer cells. LncRNA CCAT1 can bind to miR-140-3p and regulate its expression, while miR-140-3p further regulates the expression of ATG5. 		Yes	 LncRNA CCAT1 can promote the proliferation, migration, invasion, and autophagy activity of gastric cancer cells.  Overexpression of LncRNA CCAT1 can promote tumor growth in nude mice. After LncRNA CCAT1 silencing, the positive expression rate of ATG5 in nude mice was low.	34417924
CCAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell line	regulation[CCAT1/miR-490 molecular axis]	qRT-PCR//Wound Healing Assay//Transwell Assay	High expression of CCAT1 was observed in NSCLC tissues and cells, with low expression of miR-490.The CCAT1/miR-490 molecular axis has been shown to be important for the treatment of NSCLC.		Yes	CCAT1 promoted the proliferation and metastasis of H1299 and A549 cells, while miR-490 had the opposite effect. CCAT1 could specifically bind to miR-490 and regulate its expression. 	33325119
CCAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-216a-5p/RAP2B axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	The expression of CCAT1 was elevated in NSCLC, and CCAT1 deletion could inhibit NSCLC cell proliferation, migration, and invasion but induce apoptosis in vitro as well as imped tumor growth in vivo.  Taken together, CCAT1 deletion could inhibit cell progression in NSCLC through miR-216a-5p/RAP2B axis, indicating a novel pathway underlying NSCLC cell progression and providing new potential targets for NSCLC treatment.		Yes	The expression of CCAT1 was elevated in NSCLC, and CCAT1 deletion could inhibit NSCLC cell proliferation, migration, and invasion but induce apoptosis in vitro as well as imped tumor growth in vivo. 	33023331
CCAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[ microRNA-218]	CCK8//qRT-PCR//Cell Apoptosis Assay//Western Blot	In the present study, we showed that lncRNA?CCAT1 was upregulated in NSCLC tissues. lncRNA‑CCAT1 enhances tumor growth in NSCLC by directly inhibiting miR‑218 and indirectly increasing BMI‑1 expression.	High expression of lncRNA?CCAT1 was related to tumor growth and reduced survival rate. 	Yes	In vitro and in vivo results demonstrated that lncRNA?CCAT1 knockdown suppressed tumor proliferation and induced apoptosis.	32323859
CCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[miR-181b-5p/TUSC3 Axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	The relative mRNA expression levels of CCAT1 were significantly higher in CRC tissues and cell lines compared with the normal tissues or cells. Bioinformatics and luciferase reporter assays showed that miR-181b-5p was a direct target of CCAT1, and the expression of miR-181b-5p was negatively correlated with the expression of CCAT1 in CRC tissues. Furthermore, CCAT1 positively regulated the level of tumor sExpression[up-expression]pressor candidate 3 (TUSC3) by competing with miR-181b-5p in CRC cells.		Yes	CCAT1 knockdown significantly inhibited CRC cell proliferation in vitro and in vivo. 	31807005
CCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues 	regulation[miR-181a-5p]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Microarray//IHC	 Compared with matched adjacent normal tissues, CCAT1 expression in CRC tissues was significantly increased (P<0.001, Figure 1C).CCAT1 promoted cell proliferation, growth and mobility by targeting miR-181a-5p and the silence of CCAT1 increased the cell apoptosis. 	The CCAT1 expression was positively associated with cancer stage (American Joint Committee on Cancer stage, P<0.05). 	Yes	 Furthermore, Xenograft model was used to show that knockdown of CCAT1 inhibits tumor growth in vivo. 	32380476
CCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	regulation[CCAT1/miR-218 axis ]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The present study revealed that CCAT1 is highly expressed in colorectal cancer tissues.Taken together, the present results identified that the CCAT1/miR-218 axis serves a key role in the regulation of colorectal cancer progression, which may be used as potential therapeutic target for the treatment of colorectal cancer.		Yes	 The results revealed that when compared with the control group, CCAT1-short hairpin (sh)RNA significantly inhibited colorectal cancer cell (SW480) viability and decreased migration and invasiveness. 	32256733
CCAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	 colorectal tissues and cell lines	Interaction(miR-4679/GNG10)	qRT-PCR//Western Blot//H&E Staining	 In this study, we found that in both colorectal tissues and cell lines the level of lncRNA CCAT1 was increased.We then found that hsa-miR-4679 could bind to lncRNA CCAT1 directly, and with further functional analyses, we confirmed that lncRNA CCAT1 sponged hsa-miR-4679 to promote the progression of colorectal cancer. Next, we found that hsa-miR-4679 was directly bound to 3'UTR of GNG10 (guanine nucleotide-binding protein, gamma 10). GNG10 overexpression promoted the progression of colorectal cancer, and this phenotype could be reversed by miR-4679 mimics. 		Yes	Downregulation of lncRNA CCAT1 inhibited the proliferation, migration, and invasion of colorectal cell lines and promoted apoptosis. 	35005034
CCAT1	LncRNA	Homo sapiens	Colonic Neoplasms	 tumour tissues and cells 	Interaction(microRNA-24-3p and FSCN1)	qRT-PCR//Luciferase Report Assay//Tunel//Western Blot	LncRNA-CCAT1 and FSCN1 mRNA/protein were overexpressed, whereas miR-24-3p was down-regulated in the CT-genotyped patients and cells compared with those in the CC-genotyped patients and cells. MiR-24-3p was validated to target lncRNA-CCAT1 and FSCN1 mRNA, and the overexpression of CCAT1 could reduce the expression of miR-24-3p although elevating the expression of FSCN1.		Yes	Knockdown of lncRNA-CCAT1 partly reversed the suppressed growth of CT-genotyped tumours. And the knockdown of lncRNA-CCAT1 partly reversed the dysregulation of lncRNA-CCAT1 and FSCN1 mRNA/protein in rs67085638-CT + NC shRNA mice.	33709519
CDCA3P1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction(CDCA3 mRNA at 1423-1455 region)	qRT-PCR	In this study, we found CDCA3 was a potential oncogenic factor in HCC and characterized the lncCDCA3L, which could inhibit CDCA3. LncCDCA3L is significantly downregulated in HCC and its expression level is associated with tumour size and can act as an independent risk factor affecting postoperative survival time in HCC patients. Mechanistically, lncCDCA3L can repress CDCA3 protein level and inhibit hepatocarcinogenesis by directly binding to CDCA3 mRNA at 1423-1455 region via a novel manner based on a hairpin structure motif.	In this study, we found CDCA3 was a potential oncogenic factor in HCC and characterized the lncCDCA3L, which could inhibit CDCA3. LncCDCA3L is significantly downregulated in HCC and its expression level is associated with tumour size and can act as an independent risk factor affecting postoperative survival time in HCC patients.	Yes	Mechanistically, lncCDCA3L can repress CDCA3 protein level and inhibit hepatocarcinogenesis by directly binding to CDCA3 mRNA at 1423-1455 region via a novel manner based on a hairpin structure motif.	35230745
CDIPTOSP	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues and cells	Interaction(hnRNP K/YAP1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//RIP//RNA-seq//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//ChIP	Here, we discovered a conserved CT-lncRNA, named lnc-CTHCC, which was highly expressed in the testes and HCC. Mechanistically, lnc-CTHCC bound to heterogeneous nuclear ribonucleoprotein K (hnRNP K), which was recruited to the YAP1 promoter for its activation. Additionally, the N6-methyladenosine (m6A) modification was mediated by N6-adenosine-methyltransferase 70-kDa subunit (METTL3) and recognized by insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)/IGF2BP3, which maintained lnc-CTHCC stability and increased its expression in HCC. 		Yes	 A lnc-CTHCC-knockout (KO) mouse model further confirmed that the global loss of lnc-CTHCC inhibited the occurrence and development of HCC. In vitro and in vivo assays also showed that lnc-CTHCC promoted HCC growth and metastasis. 	35122073
CDK6	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	several cervical cancer cells	Interaction( miR-449a)	colony Formation Assay//Western Blot//Flow Cytometry//qRT-PCR//RIP//PCR//IP//Colony Formation Assay//Invasion Assay//IF	Finally, the results showed that circCDK6 level remarkably increased in several cervical cancer cells, especially in Hela and CaSki cells.  The miR-449a was further confirmed to be a potential target of circCDK6, and its expression increased by silencing circCDK6.		Yes	The circCDK6 participated in tumorigenesis and cancer progression and might serve as a tumor suppressive factor in cervical cell progression via Epithelial-MesenchymalTransition (EMT) process by regulating miR-449a.	35152839
CERNA2	LncRNA	Homo sapiens	Glioma	Glioma Tissue,cell lines( U251 and U87)	Interaction[let-7b;PBX3 ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Results showed that HOST2 and PBX3 were highly expressed in glioma tissue whereas let-7b was expressed at much lower levels. The expression of let-7b and PBX3 was detected by RT-qPCR and Western blot analysis after the silencing of lncRNA HOST2. The results showed (Fig. 3E) that the expression of let-7b increased and PBX3 decreased significantly (all P < 0.05) in the si-lncRNA HOST2 groExpression[Expression[up-expression]-expression] compared with the blank groExpression[Expression[up-expression]-expression] and the si-Con groExpression[Expression[up-expression]-expression]. These results suggested that lncRNA HOST2 functioned as a ceRNA and regulated the expression of PBX3 by competitively binding to let-7b.		Yes	Results showed that the high expression of HOST2 in gliomas inhibits the expression of target gene PBX3 induced by let-7b and promotes the development of gliomas. Our results were consistent with recent reports of some related lncRNA RNAs. For instance, knockExpression[down-expression] of lncRNA FOXD3 antisense RNA 1 inhibited the cell growth, migration, and invasion of malignant glioma cells 25. Another study showed that Expression[down-expression]-regulation of lncRNA CCAT2 inhibited cellular proliferation and invasion in glioma cells 26. However, our investigation was the first to demonstrate that knockExpression[down-expression] of lncRNA HOST2 expression may inhibit the growth, migration, and invasion in glioma cells.	30290058
CERNA2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical carcinoma tissues 	Expression[highly expressed]	qRT-PCR	In our study, we found the CERNA2 expression was obviously increased in cervical carcinoma tissues compared with adjacent normal cervical tissues.	 In addition, we observed that metastatic lymph nodes exhibited high levels of CERNA2 expression in contrast to primary cervical carcinoma tissues. Furthermore, high CERNA2 expression was associated with advanced clinical stage, lymph node metastasis, distant metastasis poor histological grade, and short overall survival in cervical carcinoma patients. Moreover, high CERNA2 expression acted as an independent unfavorable predictor for overall survival in cervical carcinoma patients. 	Yes	 The cell migration and invasion assays in vitro suggested that knockdown of CERNA2 remarkably inhibited cell migration and invasion in cervical carcinoma. 	30793356
CERNA2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 HPV-positive CC tissues and cells	Interaction[inhibition of let-7b ]	Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	HOST2 was upregulated in HPV-positive CC tissues and cells, which could promote the proliferation, migration and invasion, but inhibit the apoptosis of HPV-positive CC cells via inhibition of let-7b.		Yes	Over-expressed HOST2 reduced let-7b expression, promoted proliferation migration and invasion and inhibited the apoptosis of CaSki and HeLa cells,silencing HOST2 or overexpressing let-7b enhanced the expression of let-7b, inhibited proliferation migration and invasion, and promoted the apoptosis of CaSki and HeLa cells, and let-7b mimic could reverse the promoting effect of HOST2 on the growth of CC cells.	30964163
CEP85L	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[NFKBIA,miR-942-5p]	ISH//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circ-CEP85L, which has not been studied in GC, was significantly downregulated in GC tissues and that decreased circ-CEP85L expression correlated significantly with a worse prognosis. Therefore, we conclude that circ-CEP85L promotes NFKBIA expression by acting as a sponge of miR-942-5p; thus, inhibiting GC proliferation and invasion. circ-CEP85L is a potential target in the treatment of GC.	We found that circ-CEP85L, which has not been studied in GC, was significantly downregulated in GC tissues and that decreased circ-CEP85L expression correlated significantly with a worse prognosis.	Yes	The knockdown of circ-CEP85L promoted the proliferation and invasion of GC cells, which was reversed by overexpression of circ-CEP85L. 	32026471
CEP128	CircRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Expression[highly expressed]	qRT-PCR	Circular RNA CEP128 was upregulated in glioma tissues and cell lines.		Yes	Knockdown of circular RNA CEP128 inhibited cell proliferation	31599823
Cenpm-202	LncRNA	Rattus norvegicus	Heart Failure	H9c2 cells	Interaction(miR-215-5p/ZEB2 Axis)	RNA Pull-Down//Luciferase Report Assay//Western Blot	We found out that SOX2-OT level was increased by oxygen glucose deprivation/reoxygenation treatment in H9c2 cells. Silencing of SOX2-OT ameliorated cell injury by promoting cell viability, inhibiting cell apoptosis and reducing productions of collagens. Mechanistically, miR-215-5p was confirmed to bind with SOX2-OT after prediction and screening. In addition, we discovered that miR-215-5p negatively regulated zinc finger E-box binding homeobox 2 (ZEB2) protein level by directly binding with ZEB2 3' untranslated region. Finally, we verified that SOX2-OT aggravated cell injury by targeting ZEB2 in H9c2 cells. In conclusion, SOX2-OT aggravated heart failure in vivo and promoted H9c2 cell injury via the miR-215-5p/ZEB2 axis in vitro, implying a novel insight into heart failure treatment.		Yes	Silencing of SOX2-OT ameliorated cell injury by promoting cell viability, inhibiting cell apoptosis and reducing productions of collagens. Finally, we verified that SOX2-OT aggravated cell injury by targeting ZEB2 in H9c2 cells.	34321385
CELF1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 primary cancer tissues 	Interaction(miR-491-5p/EGFR axis)	Western Blot//ISH//Wound Healing Assay//Transfection//CCK8//qRT-PCR//RIP//FISH//PCR//cell invasion assay//IP//Invasion Assay//IF	circ_CELF1 is upregulated in primary cancer tissues from patients with NSCLC, and a high level of circ_CELF1, is associated with malignant characteristics and poor outcomes of patients with NSCLC.  Mechanistically, through directly interacting with miR-491-5p, circ_CELF1 acted as a miRNA sponge that increased the expression of the miR-491-5p target gene EGFR, eventually promoting the progression of NSCLC and increasing cancer resistance to immunotherapy.	 primary cancer tissues 	Yes	Enforced expression of circ_CELF1 exacerbated the malignant transformation of NSCLC cells. 	34788230
C-E-Cad	CircRNA	Homo sapiens	Glioblastoma	GBM tissues	Regulation(EGFR-STAT3 signalling)	Northern Blot//ISH//Transfection//Immunoblotting//RIP//RNA-seq//PCR//IP//Invasion Assay//IF	C-E-Cad is overexpressed in GBM and promotes glioma stem cell tumorigenicity. C-E-Cad activates EGFR independent of EGF through association with the EGFR CR2 domain using a unique 14-amino-acid carboxy terminus, thereby maintaining glioma stem cell tumorigenicity. Notably, inhibition of C-E-Cad markedly enhances the antitumour activity of therapeutic anti-EGFR strategies in GBM.		Yes	C-E-Cad activates EGFR independent of EGF through association with the EGFR CR2 domain using a unique 14-amino-acid carboxy terminus, thereby maintaining glioma stem cell tumorigenicity. Notably, inhibition of C-E-Cad markedly enhances the antitumour activity of therapeutic anti-EGFR strategies in GBM.	33664496
CEBPA-DT	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues	Expression[highly expressed]	qRT-PCR//MTT//Western Blot//Transwell Assay	 The expression of lncRNA CEBPA-AS1 increased significantly in liver cancer tissues (p<0.05).	Meanwhile, CEBPA-AS1 expression was associated with tumor size, portal vein tumor thrombus and invasion and metastasis (p<0.05). 	Yes	 In vitro experiments indicated that downregulation of lncRNA CEBPA-AS1 could effectively reduce cell proliferation, invasion and EMT process.	31646559
CEBPA-DT	LncRNA	Homo sapiens	Liver Neoplasms	human HCC tissues	Interaction(CEBPA-DT-hnRNPC-DDR2/β-catenin axis)	Western Blot//Transfection//qRT-PCR//RNA-seq//Microarray//IHC//IF	Our results suggested that CEBPA-DT promoted HCC metastasis through DDR2/β-catenin mediated activation of Snail1 via interaction with hnRNPC, indicating that the CEBPA-DT-hnRNPC-DDR2/β-catenin axis may be used as a potential therapeutic target for HCC treatment.	CEBPA-DT was upregulated in human HCC tissues with postoperative distant metastasis and intimately related to the worse prognosis of HCC patients. 	Yes	Silencing of CEBPA-DT inhibited the growth, migration and invasion of hepatoma cells in vitro and in vivo, while enhancement of CEBPA-DT played a contrasting role. Mechanistic investigations demonstrated that CEBPA-DT could bind to heterogeneous nuclear ribonucleoprotein C (hnRNPC), which facilitated cytoplasmic translocation of hnRNPC, enhanced the interaction between hnRNPC and DDR2 mRNA, subsequently promoted the expression of DDR2.	36471363
CEBPA-AS1	LncRNA	Rattus norvegicus	Reperfusion Injury	rat model	Interaction(miR-340-5p/APPL1/LKB1/AMPK pathway)	RNA Pull-Down//Tunel//qRT-PCR//RIP//MTT//Luciferase Report Assay	 We found that overexpression of CEBPA-AS1 could attenuate MCAO/IR-induced nerve damage and neuronal apoptosis in the rat model. Upon examining the molecular mechanisms, we found that CEBPA-AS1 stimulated APPL1 expression by combining with miR-340-5p, thereby regulating the APPL1/LKB1/AMPK pathway. In the rescue experiments, CEBPA-AS1 overexpression was found to attenuate OGD/R-induced cell apoptosis and MCAO/IR induced nerve damage, while miR-340-5p reversed these effects of CEBPA-AS1.		Yes	 Knockdown of CEBPA-AS1 aggravated cell apoptosis and enhanced the production of LDH and MDA in the OGD/R cells. 	34919285
CDYL	CircRNA	Homo sapiens	Multiple Myeloma	MM cells and plasma	interaction[sponges miR-1180]	RNA Pull-Down//Western Blot//qPCR//PCR//Cell Apoptosis Assay//IF	Here, we described an important MM-related circular RNA (circRNA), circ-CDYL. It was remarkably increased in both MM cells and plasma.Circ-CDYL could absorb miR-1180 and alleviated the repression of miR-1180 on YAP, leading to increased YAP expression, ultimately triggering MM uncontrolled growth. 		Yes	Depletion of circ-CDYL evidently stunted MM growth.	32321304
CDR1as	CircRNA	Homo sapiens	Stomach Neoplasms	 GC cell	Interaction(miR-876-5p/GNG7 Axis)	Western Blot//qPCR//RIP//PCR//IP//Invasion Assay//IF	In summary, our findings indicate that CDR1as suppresses GC metastasis through the CDR1as/miR-876-5p/GNG7 axis.		Yes	Here, we found that CDR1as knockdown facilitated GC cell migration and invasion while its overexpression inhibited the migration and invasion abilities of GC cells in vitro and in vivo.Moreover, epithelial-mesenchymal transition- (EMT-) associated proteins and MMP2 and MMP9 were downregulated by CDR1as. 	34221006
CDR1as	CircRNA	Homo sapiens	Ovarian Neoplasms	 ovarian cancer tissues	Interaction[as a sponge of miR-135b-5p]	Western Blot//CCK8//qRT-PCR//MTT//PCR	CDR1as expression in ovarian tissues was significantly lower in ovarian cancer patients than in patients without ovarian cancer. CDR1as, acting as a sponge of miR-135b-5p, promotes the expression of HIF1AN and therefore plays a role in tumor inhibition.		Yes	CDR1as overexpression inhibited the proliferation, invasion and migration of ovarian cancer cells.	31190886
Cdr1as	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cells	Regulation	Western Blot//ISH//qRT-PCR//FISH//PCR//IP//IF	Cdr1as was significantly down-regulated in bladder cancer tissues compared with adjacent normal tissues. Cdr1as sponged multiple miRNAs in bladder cancer. Moreover, Cdr1as directly bound to miR-135a and inhibited its activity in bladder cancer.		Yes	Overexpression of Cdr1as inhibited the proliferation, invasion and migration of bladder cancer cells in vitro and slowed down tumour growth in vivo. 	29694981
CDR1as	CircRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues.	Interaction(miR-432-5p/E2F3 axis)	colony Formation Assay//Western Blot//Transfection//Flow Cytometry//IF//PCR//Microarray//Colony Formation Assay//Transwell Assay	We found that circCDR1as was highly expressed in PC tissues.  The levels of circCDR1as in PC tissues and cells were higher than those in controls. CircCDR1as promoted the migration, invasion and proliferation of PC cells in vitro and tumor growth in vivo via mediating E2F3 expression by sponging miR-432-5p.		Yes	CircCDR1as promoted the migration, invasion and proliferation of PC cells in vitro and tumor growth in vivo via mediating E2F3 expression by sponging miR-432-5p.	33593338
CDR1as	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues	interaction[ miR-7]	Flow Cytometry//PCR//Western Blot	 CDR1as levels was robustly increased with the development of NSCLC (P<0.001) and the NSCLC tissues harbored highest expression of CDR1as, which negatively correlated to the expression of miR-7. Mechanistically, CDR1as functioned as miR-7 sponges to up-regulate the key target genes of miR-7 including EGFR, CCNE1 and PIK3CD. 	Patients with high expression of CDR1as had high TNM stage (P=0.004), more lymph nodes metastasis (LNM) (P=0.021) and shorted overall survival time (OS) (P=0.0135). The CDR1as level was an independent prognostic factor for the patients with NSCLC.	Yes	Overexpression of CDR1as induced increased cell vitalities and growth, which could be abrogated by knockdown of CDR1as or overexpressed miR-7 to induce apoptosis and G1/S arrest. 	30022841
CDR1as	CircRNA	Homo sapiens	Cholangiocarcinoma	 CCA cell lines	interaction[MicroRNA 641 ]	colony Formation Assay//qPCR//RIP//PCR//IP//Colony Formation Assay//IF	 In vitro, the CDR1as level was significantly increased in CCA cell lines.In conclusion, our findings indicated that CDR1as might exert oncogenic properties, at least partially, by regulating miR-641 in CCA. CDR1as and miR-641 could be considered therapeutic targets for CCA.		Yes	 The results showed that CDR1as promoted the cell proliferation, migration, invasion, and activation of the AKT3/mTOR pathway in CCA cells.	32423991
CDR1as	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LSCC cells 	Regulation[miR-7 signals]	colony Formation Assay//IHC//Western Blot//Flow Cytometry//PCR//Colony Formation Assay	The CDR1as and miR-7 were overexpressed in LSCC cells to investigate its function and mechanism in vitro and in vivo.CDR1as is an oncogene that promotes LSCC progression by regulating miR-7 signals.	Patients with high TNM stages, poorly differentiated tumours, lymph node metastases and poor prognosis had high CDR1as levels but low miR-7 levels. 	Yes	Overexpression of CDR1as in vitro enhanced cell vitality, and promoted the proliferation, migration, and invasion of two LSCC cell lines (Hep2 and AMC-HN-8.) 	30182381
CDKN2B-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation[NF-kB signaling]	qRT-PCR//Western Blot	TET2 suppressed tumor growth by regulating ANRIL, and ANRIL supported tumor progress as indicated above, but its mechanism was unclear. NF-kB signaling was critical in cancer progression. To identify the relationship between NF-kB and ANRIL, we evaluated p65 protein levels in the nucleus of MG803 cells. Unlike the total protein level in the whole cell, knockdown of ANRIL resulted in a decrease of p65 protein in the nucleus (Figure 4(a)), suggesting that ANRIL could promote p65 to enter nucleus from the cytoplasm. Furthermore, NF-kB inhibitor sc75741 could inhibit migration of gastric cancer cells, and ANRIL could not further suppress migration in the presence of sc75741 (Figure 4(b)). Real-time qPCR indicated knockdown of ANRIL resulted in a decrease in the mRNA levels of NF-kB target genes (Figure 4(c)). All the above results suggested that the function of ANRIL depended on NF-kB signaling.	To confirm the functions of TET2 and ANRIL in human patients, 192 gastric cancer patients were followed up, and the mRNA levels of TET2, ANRIL, and NF-kB target genes in the tumor samples were evaluated with real-time qPCR. There were 125 patients grouped to low TET2 expression and 67 patients arranged to high TET2 expression, and patients with high TET2 expression had significantly longer survival time. For analysis of the relationship between ANRIL and patient survival (Figure 5(a)), 123 patients were grouped to low ANRIL expression, and 69 patients were high ANRIL expression. On the contrary, patients with low ANRIL had a longer survival time (Figure 5(a)). In the tumor samples, expression of TET2 and ANRIL was negatively correlated (Figure 5(b)), and ANRIL was expressed positively related to NF-kB target genes p21, cIAP1, uPA, and MMP2 (Figure 5(c) to (f)). These results further indicated that ANRIL enhanced NF-kB signaling.	Yes	In this study, we found the long non-coding RNA ANRIL was critical for the progression of gastric cancer. Knockdown of ANRIL (also known as CDKN2B-AS) with shRNA increased apoptosis, inhibited tumor growth, and suppressed migration of cancer cells. TET2 (Tet Methylcytosine Dioxygenase 2), a methylcytosine dioxygenase suppressed ANRIL function and prevented cancer progression.	31242038
CERNA2	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tumor tissues and adjacent normal tissues	Interaction[let-7b;CDK6 ]	CCK8//qRT-PCR//Western Blot	The results revealed increased expression levels of HOST2 in tumor tissues from patients with TNBC.The silencing of HOST2 induced cell proliferation inhibition and cell cycle redistribution in MDA‑MB‑231 and MDA‑MB‑468 TNBC cells. In these two cell lines, HOST2 silencing caused a decrease in the phosphorylation of RB1 and CDK6, which was observed at the mRNA and protein levels. However, the silencing of CDK6 did not alter the expression of HOST2. It was hypothesized and confirmed that let‑7b, a previously reported target miRNA of HOST2, was able to directly bind to the 3'UTR of CDK6 and repress its expression. The expression of let‑7b was negatively correlated with the expression of HOST2 and CDK6 in tumor tissues. Overall, the data suggested that lncRNA HOST2 acts as an oncogene in TNBC via the Expression[Expression[up-expression]-expression]regulation of CDK6.		Yes	The silencing of HOST2 induced cell proliferation inhibition and cell cycle redistribution in MDA‑MB‑231 and MDA‑MB‑468 TNBC cells. 	30483747
CERNA2	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	BC tissues and cell lines	Expression[highly expressed]	Western Blot//ISH//qRT-PCR//RIP//FISH//MTT//Colony Formation Assay//Transwell Assay	 The results showed that HOST2 was up-regulated in BC tissues and cell lines.HOST2 could function as a oncogene and promoted STAT3-mediated proliferation and migration through acting as a competing endogenous RNA, which might act as a potential biomarker for TNBC patients.	Clinical outcome analysis demonstrated that high expression of HOST2 was associated with poor prognosis of TNBC patients. 	Yes	 Functional experiments illustrated that knockdown of HOST2 significantly suppressed TNBC cell proliferation and migration. 	32248842
CDK6-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML cells	Regulation	qRT-PCR//Colony Formation Assay	CDK6-AS1 silencing triggered hematopoietic commitment in healthy CD34+ cells, whereas in AML cells the pathological undifferentiated state was rescued. 		Yes	By CDK6-AS1 silencing in vitro, AML mitochondrial mass decreased with augmented pharmacological sensitivity to mitochondria-targeting drugs. In vivo, the combination of tigecycline and cytarabine reduced leukemia progression in the AML-PDX model with high CDK6-AS1 levels, supporting the concept of a mitochondrial vulnerability. 	34816103
CERNA2	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Interaction [ Bcl-2/Bax]	qRT-PCR//MTT	The expression levels of lnc-HOST2 in osteosarcoma tissues were significantly higher than those in corresponding noncancerous bone tissues (p < 0.01). Notably, we confirmed that up-regulation of lnc-HOST2 led to Bcl-2 downregulation and Bax upregulation in osteosarcoma cells.	Statistical assay indicated that the expression level of lnc-HOST2 was positively correlated with tumor stage (p = 0.003) and distant metastasis (p = 0.000). Furthermore, Kaplan-Meier analysis suggested that patients with high lnc-HOST2 showed poorer overall survival than those with low lnc-HOST2 (p = 0.000). The univariate and multivariate analysis further revealed that lnc-HOST2 expression was an independent prognostic factor for overall survival. 	Yes	 Then, functionally, down-regulation of lnc-HOST2 suppressed proliferation and induced cell apoptosis in osteosarcoma cells. 	29509239
CHAER1	LncRNA	Homo sapiens	Atherosclerosis	blood	Regulation[mTOR signaling]	CCK8//qRT-PCR//RIP//ChIP	 We found that the Chaer was highly expressed in serum samples from 28 patients with atherosclerosis, compared with 28 healthy volunteers. Mechanistically, Chaer interacts with Polycomb Repressor Complex 2 (PRC2) through inhibiting histone H3 lysine 27 methylation. Further, this interaction is induced upon mTOR signaling pathway.		Yes	 Through loss- and gain-of-function approaches, we showed that Chaer promotes cell proliferation and induces apoptosis in vitro.	31539156
cFUT8	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissue 	Interaction(miR-548c/FUT8 axis)	qRT-PCR	The results showed that cFUT8 and miR-548c were predominantly co-localized in the HCC cell cytoplasm (Fig. 1o). To determine whether endogenous cFUT8 may serve as a binding platform for miR-548c, we conducted RNA immunoprecipitation (RIP) in HepG2 and Huh7 cells. Strikingly, endogenous miR-548c binding to cFUT8 increased more than 30-fold (Supplementary Fig. S5a). Similarly, endogenous cFUT8, pulled down by miR-548c, was also significantly increased at almost 40-fold in these cells (Supplementary Fig. S5b). With similar processing, expression of FUT8 was significantly enhanced when miR-548c was present (Supplementary Fig. S5c). However, this enrichment was attenuated when coupled with cFUT8 (Fig. 1p). When the free miR-548c level was increased, we identified that FUT8 expression was significantly inhibited at both the mRNA and protein levels (Supplementary Fig. S5d, e). Meanwhile, we performed a dual-luciferase reporter assay to assess whether FUT8 is a direct target of miR-548c. As shown in Fig. 1q, the luciferase activity in both HepG2 and Huh7 cells was significantly reduced by miR-548c mimic transfection, compared with the negative control.		Yes	 Similarly, endogenous cFUT8, pulled down by miR-548c, was also significantly increased at almost 40-fold in these cells (Supplementary Fig. S5b).	33500381
Cfast	LncRNA	Mus musculus	Cardiac Fibrosis	heart tissues	interaction[COTL1 ,TRAP1 ,TGF-β signaling ]	qRT-PCR//RNA Pull-Down//RIP//Western Blot	Using unbiased transcriptome profiling in a mouse model of myocardial infarction (MI), we identified a cardiac fibroblast-enriched lncRNA (AK048087) named cardiac fibroblast-associated transcript (Cfast), which is significantly elevated after MI.Mechanistically, Cfast competitively inhibits the COTL1 interaction with TRAP1 (transforming growth factor-β receptor-associated protein 1), which enhances TGF-β signaling by augmenting SMAD2/SMAD4 complex formation.		Yes	Silencing Cfast expression by small interfering RNAs (siRNAs) or lentiviral short hairpin RNAs (shRNAs) resulted in suppression of fibrosis-related gene expression and transdifferentiation of myofibroblasts into cardiac fibroblasts. Depletion of Cfast by lentiviral shRNAs in mouse hearts significantly attenuated cardiac fibrosis induced by MI or isoproterenol-infusion. Importantly, inhibition of Cfast ameliorated cardiac function following cardiac injury.	33473324
CFAR	LncRNA	Homo sapiens	Cardiac Fibrosis	cardiac fibroblasts and tissues	Interaction(miR-449a-5p/LOXL3/mTOR axis)	Other	 CFAR was upregulated in cardiac fibrosis and its knockdown attenuated the expression of fibrotic marker genes and the proliferation of cardiac fibroblasts, thereby ameliorating cardiac fibrosis. Moreover, CFAR acted as a ceRNA sponge for miR-449a-5p and derepressed the expression of LOXL3, which we experimentally established as a target gene of miR-449a-5p. In contrast to CFAR, miR-449a-5p was found to be significantly downregulated in cardiac fibrosis, and artificial knockdown of miR-449a-5p exacerbated fibrogenesis, whereas overexpression of miR-449a-5p impeded fibrogenesis. Furthermore, we found that LOXL3 mimicked the fibrotic factor TGF-β1 to promote cardiac fibrosis by activating mTOR. 		Yes	CFAR was upregulated in cardiac fibrosis and its knockdown attenuated the expression of fibrotic marker genes and the proliferation of cardiac fibroblasts, thereby ameliorating cardiac fibrosis. 	36334219
CES1P1	LncRNA	Homo sapiens	Diabetic Nephropathies	C57BL/6 mice, HUVECs	Interaction(miR-214-3p/ IL-17)	qRT-PCR//Luciferase Report Assay//Western Blot	 In vitro experiments using high glucose (HG) stimulation of HUVECs cell revealed increased expression of lncRNA-CES1P1, decreased expression of miR-214-3p, and increased expression of the inflammatory factors IL-17, IκB, NF-κB, and IL-6. Luciferase reporter assays showed direct targets of miR-214-3p interaction with lncRNA-CES1P1 and IL-17. 		Yes	Exogenous knockdown of lncRNA-CES1P1 expression decreased renal inflammatory infiltration. 	35834955
CERS6-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	 Interaction(miR-567)	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The expression of lncRNA CERS6-AS1 was elevated in gastric cancer tissues and cells.		Yes	 In addition, the ability of gastric cancer cells to proliferate, migrate and invade could be reduced by knockdown CERS6-AS1. After CERS6-AS1 knockdown, the expression level of miR-567 in gastric cancer tissues decreased, while the expression level of miR-567 increased. 	34852705
CERS6-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction[binding to IGF2BP3]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//FISH//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	 In this study, it was discovered that CERS6-AS1 was overexpressed in BC tissues and cells. Taken together, these evidences suggested that CERS6-AS1 promoted the progression of BC by binding to IGF2BP3 and thus enhancing the stability of CERS6 mRNA, providing a new underlying therapeutic target for BC to improve prognosis.		Yes	CERS6-AS1 accelerated cell proliferation and suppressed cell apoptosis in BC.	31701672
CERS6-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues	regulation[miR-125a-5p,BAP1 ]	qRT-PCR	Then we found CERS6-AS1 was upregulated in BC tissues.Our results indicated CERS6-AS1 promote BC cell proliferation and inhibit cell apoptosis via sponging miR-125a-5p to upregulate BAP1 expression.		Yes	Experimental results of tumor growth in nude mice show that CERS6-AS1 promotes tumor growth.	32808708
CERS6-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(CERS6-AS1/miR-16-5p/UBE2C axis)	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	It was found that CERS6-AS1 and UBE2C were meaningfully upregulated in BC, and knockdown of both CERS6-AS1 and UBE2C inhibited the BC cell proliferation and migration, whereas induced apoptosis. Mechanistically, CERS6-AS1 could facilitate BC progression by sponging miR-16-5p for upregulation of the UBE2C expression.		Yes	It was found that CERS6-AS1 and UBE2C were meaningfully upregulated in BC, and knockdown of both CERS6-AS1 and UBE2C inhibited the BC cell proliferation and migration, whereas induced apoptosis. 	36136991
CERS6-AS1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	Interaction(microRNA-1202 Axis)	qRT-PCR	High expression of IGF2BP3, CERS6-AS1 and GDPD5, and low expression of miR-1202 levels were witnessed in lung cancer tissues. IGF2BP3 positively modulated CERS6-AS1 to regulate miR-1202-targeted GDPD5. Inhibition of CERS6-AS1 or promotion of miR-1202 depressed lung cancer aggravation. CERS6-AS1 silencing or miR-1202 overexpression reversed the impacts induced by IGF2BP3 on lung cancer.		Yes	Suppression of IGF2BP3 restrained lung cancer progression.	35702784
CERS6-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 colorectal cancer tissues and cells	Interaction(miR-15b-5p/SPTBN2)	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	We found that CERS6-AS1 and SPTBN2 were highly expressed in colorectal cancer tissues and cells. Moreover, SPTBN2 levels were positively regulated by CERS6-AS1 and negatively regulated by miR-15b-5p in colorectal cancer cells. Rescue assays revealed that SPTBN2 reversed the inhibitory effect of CERS6-AS1 deficiency on the malignant behaviors of colorectal cancer cells. Overall, the lncRNA CERS6-AS1 facilitates malignant phenotypes of colorectal cancer cells by targeting miR-15b-5p to upregulate SPTBN2.		Yes	CERS6-AS1 depletion inhibited cell viability, proliferation, migration, and invasion; the epithelial-mesenchymal transition process and stemness. It suppressed xenograft tumor growth in colorectal cancer. 	35146902
CERS6-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	papillary thyroid cancer tissues and cells 	Interaction(miR-497-5p/LASP1 Axis)	qRT-PCR//RNA Pull-Down//RIP	High level of CERS6-AS1 and LASP1 was detected in papillary thyroid cancer tissues and cells and predicted poor prognosis.  In contrast, miR-497-5p was decreased in papillary thyroid cancer tissues and cells, which was positively correlated with prognosis.  LASP1 was modulated by CERS6-AS1 through sponging miR-497-5p. Up-regulation of LASP1 or silencing miR-497-5p could weaken the effect of CERS6-AS1 on papillary thyroid cancer cells. 	High level of CERS6-AS1 and LASP1 was detected in papillary thyroid cancer tissues and cells and predicted poor prognosis.  In contrast, miR-497-5p was decreased in papillary thyroid cancer tissues and cells, which was positively correlated with prognosis. 	Yes	Silencing CERS6-AS1 suppressed cell viability and increased ferroptosis in papillary thyroid cancer.  Silencing CERS6-AS1 restrained the growth of xenografted tumors.	35777805
CERS6-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation(MDM2/p53 signaling pathway)	qRT-PCR	 CERS6-AS1 was highly expressed in HCC tissues and cell lines.Bioinformatics analyses combining with PCR analysis identified miR-30b-3p as the potential target of CERS6-AS1, and MDM2 mRNA was verified as the target of miR-30b-3p. The expression of miR-30b-3p was negatively correlated with CERS6-AS1, whereas MDM2 was positively associated with CERS6-AS1. Mechanistic studies showed that CERS6-AS1 may sponge miR-30b-3p to elevate MDM2, thus promoting the MDM2-mediated ubiquitin-dependent degradation of the p53 tumor suppressor. MDM2 overexpression or miR-30b-3p inhibitors blocked the inhibitory effect of CERS6-AS1 knockdown on proliferation, migration and glycolysis. 	Upregulated CERS6-AS1 expression was remarkably correlated with poor prognosis of HCC patients. 	Yes	High CERS6-AS1 expression facilitated cell growth, invasion and glycolysis of HCC cells.  CERS6-AS1 depletion reduced tumor formation in the in vivo mouse model.	35927226
CERS6-AS1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cell lines	Interaction(microRNA-15a-5p/FGFR1 axis)	qRT-PCR//RIP	CERS6-AS1 expression was evidently increased in PDAC tissues and cell lines.  Mechanistically, CERS6-AS1 could competitively bind to microRNA-15a-5p (miR-15a-5p) and effectively work as a molecular sponge in PDAC cells, resulting in the upregulation of fibroblast growth factor receptor 1 (FGFR1), a direct target of miR-15a-5p. Rescue experiments revealed that miR-15a-5p downregulation or FGFR1 restoration rescued the effects of CERS6-AS1 knockdown on the behaviors of PDAC cells.	Patients with PDAC having high CERS6-AS1 expression had shorter overall survival periods than those having low CERS6-AS1 expression.	Yes	Functionally, the knockdown of CERS6-AS1 attenuated the proliferation, migration, and invasion and stimulated apoptosis of PDAC cells in vitro. Additionally, CERS6-AS1 depletion decreased PDAC tumor growth in vivo.	33581689
CERS6-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines 	Interaction(miR-217/YWHAG/RAF1 signaling axis)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//IF	We found that lncRNA CERS6-AS1 was highly expressed in PC tissues and cells. Additionally, high expression of CERS6-AS1 was obviously associated with poor prognosis.	high expression of CERS6-AS1 was obviously associated with poor prognosis.	Yes	Functional assays demonstrated that CERS6-AS1 downregulation significantly inhibited PC cell growth and migration. Moreover, CERS6-AS1 exerted as a molecular sponge for miR-217-5p (miR-217), and miR-217 was confirmed as a potential target of CERS6-AS1.	34168120
CERS6-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	 PC cells and tissues	Interaction(miR-195-5p/WIPI2 axis)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	As shown by RT-qPCR, CERS6-AS1 was significantly upregulated in PC cells and tissues.Mechanistically, CERS6-AS1 interacted with miR-195-5p to elevate the expression level of the WD repeat domain phosphoinositide interacting 2 (WIPI2), which is a downstream target gene of miR-195-5p in PC. Moreover, miR-195-5p expression was negatively associated with CERS6-AS1 expression (or WIPI2 expression) in PC tissues. Rescue assays revealed that WIPI2 overexpression rescued the effects of CERS6-AS1 deficiency on cell viability, proliferation, and apoptosis.		Yes	 Silencing CERS6-AS1 suppressed PC cell viability and proliferation while enhancing cell apoptosis according to colony formation assays, EdU assays, and flow cytometry analyses. 	35199935
CERS6-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	 prostate cancer tissue and cell lines	Interaction(miR-16-5p)	Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	Compared with the adjacent tissues, the relative level of CERS6-AS1 in prostate cancer tissue was increased (P < 0.05), and the relative level of miR-16-5p was decreased (P < 0.05). Compared with RWPE-1 cells, the relative level of CERS6-AS1 in DU145 cells was increased (P < 0.05), and the relative level of miR-16-5p was decreased (P < 0.05).		Yes	Compared with the control group and the si-NC group, the HMGA2 protein expression, the colony formation number, and the scratch healing rate of DU145 cells in the si-CERS6-AS1 group and the miR-16-5p mimic group were reduced (P < 0.05), and the relative level of miR-16-5p and the proliferation inhibition rate and apoptosis were increased (P < 0.05). miR-16-5p is specifically bound to CERS6-AS1 and HMGA2, respectively. Compared with the si-CERS6-AS1 group, the HMGA2 protein expression, the colony formation number, and the scratch healing rate of DU145 cells in the si-CERS6-AS1+miR-16-5p inhibitor group were increased (P < 0.05), and the cell proliferation inhibition rate and apoptosis rate were reduced (P < 0.05).	35706508
CERS6-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines 	Interaction(miR-6838-5p/FOXP2 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Here, we found that the expression of CERS6-AS1 was upregulated in CC tissues and cell lines compared with adjacent tissues and normal human cervical epithelial cells.CERS6-AS1 was verified as a sponge of miR-6838-5p by RNA pull-down and luciferase reporter gene assays.Functional investigations revealed that CERS6-AS1 knockdown inhibited proliferation and invasion, and promoted apoptosis in CC cells, which was reversed by miR-6838-5p inhibitor. Furthermore, forkhead box P2 (FOXP2) was identified as a target for miR-6838-5p, and overexpression of miR-6838-5p decreased the expression level of FOXP2. 		Yes	CERS6-AS1 overexpression promoted proliferation and invasion, and inhibited apoptosis in CC cells, while silencing of CERS6-AS1 led to the opposite results.Besides, CERS6-AS1 was able to sponge miR-6838-5p to accelerate CC cell proliferation and invasion and inhibited cell apoptosis through upregulating FOXP2 expression. 	36444938
CERNA2	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Expression[highly expressed]	qRT-PCR//MTT	In this study, we found that CERNA2 expression was significantly increased in GC tissues and cell lines compared to adjacent non-cancerous tissues and normal gastric epithelial cells, respectively. 	High levels of CERNA2 were correlated with poor clinical parameters and an unfavorable prognosis of GC patients.	Yes	 Moreover, silencing CERNA2 expression effectively inhibited gastric cancer cell growth and induced cell apoptosis in vitro. Collectively, our results demonstrate that the up-regulation of CERNA2 is associated with malignant status and poor prognosis in patients with GC, and silencing CERNA2 expression inhibits gastric cancer cell growth and promotes cell apoptosis, suggesting CERNA2 could possibly be a promising diagnostic and treatment target for GC.	31949664
CDKN2B-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and adjacent normal tissues	Interaction(miR-122-5p/STK39 axis)	Western Blot//Colony Formation Assay//qRT-PCR//Luciferase Report Assay//IHC	As for the results, there is a relative rich expression of CDKN2B-AS1 in breast cancer tissues compared with the corresponding adjacent normal tissues. Compared with the human breast epithelial cell line, the abundant expression of CDKN2B-AS1 in breast cancer cells were revealed as well. In mechanism, CDKN2B-AS1 sponged the miR-122-5p to regulate STK39 expression. Furthermore, the inhibition effect with sh-CDKN2B-AS1 on breast cancer cells was alleviated by miR-122-5p inhibitor. 		Yes	Then, knockdown CDKN2B-AS1 inhibited the malignant biological behaviors of MCF7 and T47D cells. 	34374638
CDKN2B-AS1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	regulation[miR-378b/NR2C2]	qRT-PCR//Transwell Assay//Western Blot	The expression of lncRNA CDKN2B-AS1 was significantly upregulated in lung cancer tissues and cell lines. Taken together, our results comprehensively analyzed the function of CDKN2B-AS1 in lung cancer and provided a possible mechanism that CDKN2B-AS1 facilitates lung cancer development by regulating miR-378b and NR2C2. 		Yes	Overexpression of CDKN2B-AS1 promoted cell proliferation, invasion and reduced cell apoptosis. Knockdown of CDKN2B-AS1 inhibited cell proliferation, invasion and increased cell apoptosis.	33116641
CDKN2B-AS1	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-378b/CAPRIN2 axis)	RNA Pull-Down//Western Blot//Transfection//Migration Assay//Proliferation Assay//qRT-PCR//RIP//migration assay//PCR//Cell Proliferation Assay//IP//IF	We found that the expression of CDKN2B-AS1 and CAPRIN2 was upregulated in CRC and they were linked to the poor differentiation and distant metastasis in CRC patients. Notably, the results of Starbase 2.0 database analysis and in vitro experiments demonstrated that CDKN2B-AS1 could interact with miR-378b and regulate its expression. Furthermore, CAPRIN2 acted as a downstream target of CDKN2B-AS1/miR-378b that involved in modulating β-catenin expression in CRC cells. 	We found that the expression of CDKN2B-AS1 and CAPRIN2 was upregulated in CRC and they were linked to the poor differentiation and distant metastasis in CRC patients.	Yes	CDKN2B-AS1 knockdown attenuated while CDKN2B-AS1 overexpression promoted CRC cell proliferation and migration. 	34511033
CDKN2B-AS1	LncRNA	Homo sapiens	Osteoarthritis	cell lines	Regulation[ miR-122-5p/DUSP4 axis]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	We indicated that the expression of ANRIL was significantly improved in OAS compared to NS. Moreover, ANRIL could regulate the proliferation and apoptosis of OAS via miR-122-5p/DUSP4 axis.		Yes	The expression of ANRIL was decreased and the cell proliferation was reduced in OAS after transfected with siRNA.	31799639
CDKN2B-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	CSCs-derived exosomal 	Interaction(miR-122-5p/P4HA1 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	 Exosomal CDKN2B-AS1 up-regulated P4HA1 expression through miR-122-5p. CDKN2B-AS1 and P4HA1 expressions were up-regulated, and miR-122-5p expression was down-regulated in thyroid cancer. MiR-122-5p inhibitor reversed the function of exosomal CDKN2B-AS1, while P4HA1 silencing attenuated the effect of miR-122-5p inhibitor. Exosomal CDKN2B-AS1 affected the growth and metastasis of thyroid cancer through the miR-122-5p/P4HA1 axis.		Yes	 Silent CDKN2B-AS1 reduced cell viability and stemness. CDKN2B-AS1 was found to be abundant in CSCs and CSCs-derived exosomes. Exosomal CDKN2B-AS1 silencing could transfer to thyroid cancer cells to elevate E-cadherin level, and diminish P4HA1, N-cadherin and Vimentin levels, thus impeding cell migration and invasion. 	36582605
CDKN2B-AS1	LncRNA	Homo sapiens	Multiple Myeloma	 multiple myeloma tissues 	regulation[HIF-1α,miR-411-3p]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//BrdU	 In this study, compared with normal tissues from healthy donors, lncRNA ANRIL and HIF-1α expressions were up-regulated in tumor tissues from multiple myeloma patients. Our results demonstrate that lncRNA ANRIL mediated by miR-411-3p promotes the malignant proliferation and tumor stem cell like property of multiple myeloma through regulating HIF-1α.		Yes	 Further transfection experiments showed that knockdown of ANRIL or overexpression of miR-411-3p significantly inhibited cell proliferation, tumor formation ability and tumor stem cell like property, promoted cell apoptosis in vitro. 	32961145
CDKN2B-AS1	LncRNA	Homo sapiens	Multiple Myeloma	MM patients and cell lines	Interaction(EZH2)	In Vivo Experiment//Western Blot//BrdU//Flow Cytometry//qRT-PCR//RIP//RNA-seq//Cell Proliferation Assay//ChIP	We found that ANRIL was upregulated in MM patients and cell lines, and associated with advanced international staging system (ISS) stage and poor overall survival. Our results indicated that ANRIL exerted oncogenic functions and conferred chemoresistance of MM cells by EZH2-mediated epigenetically silencing of PTEN.	We found that ANRIL was upregulated in MM patients and cell lines, and associated with advanced international staging system (ISS) stage and poor overall survival.	Yes	Enforced ANRIL expression promoted proliferation and tumor xenograft growth of MM cells, while knockdown of ANRIL exhibited opposite effects. Moreover, ANRIL overexpression increased the half-maximal inhibitory concentration (IC50) of bortezomib and reduced bortezomib-induced apoptosis in MM cells.	34034498
CDKN2B-AS1	LncRNA	Homo sapiens	Idiopathic Pulmonary Fibrosis	TGF-β-treated cells and BLM-treated mice	Interaction( CDKN2B-AS1/miR-199a-5p/SESN2 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	We found that the expression of CDKN2B-AS1 was decreased in TGF-β-treated cells and BLM-treated mice. Mechanistically, CDKN2B-AS1 acts as a miR-199a-5p sponge to regulate SESN2 expression. Our results indicate the importance of the CDKN2B-AS1/miR-199a-5p/SESN2 axis.		Yes	Overexpression of CDKN2B-AS1 inhibited cell proliferation and migration, promoted apoptosis, decreased the expression of fibrosis-related proteins and promoted autophagy.  In addition, overexpression of CDKN2B-AS1 alleviated pulmonary fibrosis in BLM-treated mice. 	35291918
CDKN2B-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LSCC tissues	Regulation[miR-181a/Snai2 axis]	CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	ANRIL was up-regulated while miR-181a was down-regulated in LSCC tissues.Dual luciferase reporter assay showed ANRIL could directly sponge miR-181a to counteract its suppression on Snai2, serving as a positive regulator of Snai2. Either knockdown of ANRIL or overexpression of miR-181a significantly inhibited the proliferation, clonogenicity, invasion, migration and epithelial mesenchymal transformation (EMT), as well as promoted the apoptosis of LSCC cells, and knockdown of miR-181a reversed the effects.		Yes	knockdown of ANRIL or overexpression of miR-181a significantly inhibited the proliferation, clonogenicity, invasion, migration and epithelial mesenchymal transformation (EMT), as well as promoted the apoptosis of LSCC cells, and knockdown of miR-181a reversed the effects.	31667207
CDKN2B-AS1	CircRNA	Homo sapiens	Endometrial Neoplasms	 EC tissues and cell lines 	Expression [highly expressed]	In Vivo Experiment//cell invasion assay//Transfection//FISH//qRT-PCR//Cell Proliferation Assay	Real-time quantitative polymerase chain reaction showed that CDKN2B-AS1 was significantly overexpressed in EC, whereas its knockdown inhibited the proliferation and invasion of EC cells and the in vivo growth of transplanted tumors in nude mice. 		Yes	Real-time quantitative polymerase chain reaction showed that CDKN2B-AS1 was significantly overexpressed in EC, whereas its knockdown inhibited the proliferation and invasion of EC cells and the in vivo growth of transplanted tumors in nude mice. 	34712660
CDKN2B-AS1	LncRNA	Homo sapiens	acute myocardial infarction	cell lines	Regulation[miR-7-5p/SIRT1 axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	ANRIL expression was dramatically enhanced in hypoxia-injured H9c2 cells, and silencing ANRIL aggravated hypoxia-induced H9c2 cell injury. Our findings disclosed that ANRIL plays a protective part in hypoxia-induced H9c2 cell injury via modulating the miR-7-5p/SIRT1 axis, suggesting the great potential of ANRIL as a protective target for AMI.		Yes	ANRIL expression was dramatically enhanced in hypoxia-injured H9c2 cells, and silencing ANRIL aggravated hypoxia-induced H9c2 cell injury. 	31264206
CDKN2B-AS1	LncRNA	Homo sapiens	Liver Neoplasms	 LC cases 	Interaction(miR-199a-5p)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	CDKN2B-AS1 in LC cases presented high expression and dropped after therapy (P < 0.05), and the opposite situation of miR-199a-5p was found in the LC cases (P < 0.05). The DLR assay revealed suppressed fluorescence activity of CDKN2B-AS1-WT by miR-199a-5p (P < 0.05). Moreover, according to the rescue assay, the impacts of silencing CDKN2B-AS1 on LC cells could be completely offset by silencing miR-199a-5p (P < 0.05). According to the clone formation and WB assay, the growth and autophagy of LC cells were under the regulation of CDKN2B-AS1 targeting miR-199a-5p (P < 0.05).		Yes	In vitro assays, after silencing of CDKN2B-AS1 and upregulation of miR-199a-5p, LC cells presented weaker viability, invasion and migration activities, and stronger apoptotic activity (all P < 0.05). 	36081669
CDKN2B-AS1	LncRNA	Homo sapiens	Rhinitis, Allergic	AR cell model	Interaction(miR-16-5p/TLR4 Axis)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	Moreover, knockdown of ANRIL reversed the effect of AR on autophagy-related protein and tight junction proteins MiR-16-5p was found to be bound with ANRIL and miR-16-5p inhibitor could reverse ANRIL knockdown-induced downregulation of autophagy-related proteins and epithelial barrier dysfunction. In addition, miR-16-5p directly targeted TLR4. Furthermore, knockdown of ANRIL reversed miR-16-5p and TLR4 expression, autophagy level, and tight junction protein levels in nasal mucosa of AR mice.		Yes	Moreover, knockdown of ANRIL reversed the effect of AR on autophagy-related protein and tight junction proteins MiR-16-5p was found to be bound with ANRIL and miR-16-5p inhibitor could reverse ANRIL knockdown-induced downregulation of autophagy-related proteins and epithelial barrier dysfunction. In addition, miR-16-5p directly targeted TLR4. Furthermore, knockdown of ANRIL reversed miR-16-5p and TLR4 expression, autophagy level, and tight junction protein levels in nasal mucosa of AR mice.	35404176
CDKN2B-AS1	LncRNA	Homo sapiens	Diabetic Nephropathies	SV40-MES13 cells	Regulation(Wnt/β-catenin and MEK/ERK pathways )	qRT-PCR//Transfection	Lnc-ANRIL expression was significantly higher in HG-treated SV40-MES13 cells compared with normal glucose-treated SV40-MES13 cells and osmotic control-treated SV40-MES13 cells. Lnc-ANRIL knock-down suppressed cell proliferation and promoted cell apoptosis in HG-treated SV40-MES13 cells. As for fibrosis, lnc-ANRIL knock-down reduced fibronectin and collagen I expressions in HG-treated SV40-MES13 cells. Besides, the expressions of supernatant tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), interleukin (IL)-1β, IL-6, IL-8 and IL-18 were reduced in Sh-ANRIL group compared with Sh-NC group. Furthermore, Wnt3, β-catenin, p-MEK1 and p-ERK1 expressions were suppressed in Sh-ANRIL group compared with Sh-NC group, which suggested that lnc-ANRIL knock-down inhibited Wnt/β-catenin and MEK/ERK pathways in HG-treated SV40-MES13 cells.		Yes	Lnc-ANRIL knock-down suppressed cell proliferation and promoted cell apoptosis in HG-treated SV40-MES13 cells. As for fibrosis, lnc-ANRIL knock-down reduced fibronectin and collagen I expressions in HG-treated SV40-MES13 cells. Besides, the expressions of supernatant tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), interleukin (IL)-1β, IL-6, IL-8 and IL-18 were reduced in Sh-ANRIL group compared with Sh-NC group. Furthermore, Wnt3, β-catenin, p-MEK1 and p-ERK1 expressions were suppressed in Sh-ANRIL group compared with Sh-NC group, which suggested that lnc-ANRIL knock-down inhibited Wnt/β-catenin and MEK/ERK pathways in HG-treated SV40-MES13 cells.	32726814
CDKN2B-AS1	LncRNA	Homo sapiens	endometriosis of ovary	endometrial stromal cells and Ishikawa cells	Interaction(miR-424-5p)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	The relative expression level of CDKN2B-AS1 was up-regulated in eutopic and ectopic endometria. In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin. miR-424-5p was confirmed the target of CDKN2B-AS1 through bioinformatics tools and luciferase reporter assays. In addition, the enhanced effect of cellular phenotype of CDKN2B-AS1 overexpression was significantly attenuated by miR-424-5p overexpression. Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay. Mechanistically, CDKN2B-AS1 acts as a ceRNA by sponging miR-424-5p and targets AKT3.		Yes	In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin.Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay.	33820740
CDKN2B-AS1	LncRNA	Homo sapiens	laryngeal squamous cell carcinoma	LSCC tissues	Interaction[miR-497/CDK6 Pathway]	qRT-PCR//Luciferase Report Assay	The expression of CDKN2B-AS1 was significantly higher in LSCC tissues than in adjacent normal tissues. Mechanically, CDKN2B functions as an oncogenic lncRNA in LSCC via regulating miR-497/CDK6 axis.	Higher CDKN2B-AS1 was closely associated with lymph node metastasis and advanced clinical stage. 	Yes	Moreover, CDKN2B-AS1 knockdown by siRNA significantly inhibited the proliferation, induced cell apoptosis, and suppressed migration and invasion in LSCC cells. 	31754305
CDKN2B-AS1	LncRNA	Homo sapiens	laryngeal squamous cell carcinoma	LSCC tissues	regulation[CDKN2B-AS1/miR-324-5p/ROCK1 axis ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay	CDKN2B-AS1 was upregulated in LSCC tissues, and the upregulation of CDKN2B-AS1 was correlated with overall survival, advanced clinical stage, and lymph node metastasis. The upregulation of CDKN2B-AS1 was correlated with overall survival, advanced clinical stage, and lymph node metastasis and promoted LSCC cell growth via miR-324-5p/ROCK1 axis.	CDKN2B-AS1 was upregulated in LSCC tissues, and the upregulation of CDKN2B-AS1 was correlated with overall survival, advanced clinical stage, and lymph node metastasis. 	Yes	 In AMC-HN-8 cells, the knockdown of CDKN2B-AS1 by siRNA inhibited cell viability, blocked cell cycle in G1 phase, and increased the expression levels of cyclin-dependent kinase inhibitor 1A (p21), cleaved caspase3, and cleaved PPoly (ADP-Ribose) polymerase 1.	31960744
CDKN2B-AS1	LncRNA	Homo sapiens	Burkitt Lymphoma		regulation[TGF-β1 signaling pathway]	qRT-PCR	In conclusion, the findings of the present study suggested that the knockdown of ANRIL may inhibit cell proliferation and promote cell apoptosis in BL by regulating the TGF?β1 signaling pathway, which may provide a novel target for the treatment of BL.		Yes	The results revealed that ANRIL silencing inhibited the proliferation and promoted the apoptosis of BL cells. 	33325535
CDKN2B-AS1	LncRNA	Homo sapiens	T-cell acute lymphoblastic leukemia	blood	regulation[LncRNA ANRIL/miR-7-5p/TCF4 axis ]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	ANRIL was significantly up-regulated in T-ALL samples. LncRNA ANRIL can modulate malignant phenotypes of T-ALL cells, possibly by regulating miR-7-5p/TCF4 axis, and it serves as a potential therapeutic target for T-ALL.		Yes	Its knockdown markedly inhibited viability, migration and invasion of T-ALL cells, but its overexpression exerted the opposite effects. 	32714094
CDKN2B-AS1	LncRNA	Homo sapiens	clear cell renal cell carcinoma	KIRC tissues	Interaction(IGF2BP3/CDKN2B-AS1/NUF2 axis)	In Vivo Experiment//IHC//Western Blot//Transwell Assay//Wound Healing Assay//Colony Formation Assay//qRT-PCR//RIP//ChIP-seq//ChIP	Here, according to the integrated analysis of RNA sequencing and survival data in TCGA-KIRC datasets, cyclin-dependent kinase inhibitor 2B antisense lncRNA (CDKN2B-AS1) was discovered to be the most upregulated among the 14 lncRNAs that were significantly overexpressed in KIRC and related to shorter survival. Thus, we conclude that the stabilization of CDKN2B-AS1 by IGF2BP3 drives the malignancy of KIRC through epigenetically activating NUF2 transcription and that the IGF2BP3/CDKN2B-AS1/NUF2 axis may be an ideal prognostic and diagnostic biomarker and therapeutic target for KIRC.	Here, according to the integrated analysis of RNA sequencing and survival data in TCGA-KIRC datasets, cyclin-dependent kinase inhibitor 2B antisense lncRNA (CDKN2B-AS1) was discovered to be the most upregulated among the 14 lncRNAs that were significantly overexpressed in KIRC and related to shorter survival. 	Yes	Functionally, CDKN2B-AS1 depletion suppressed cell proliferation, migration, and invasion both in vitro and in vivo.	33608495
CDKN2B-AS1	LncRNA	Homo sapiens	Renal Insufficiency, Chronic	plasma of patients with CKD	Interaction(EZH2/BDNF )	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Transfection//qRT-PCR//RIP//FISH//ELISA//IHC//IF	 In this study, we found that the circulating ANRIL level was increased and correlated with vascular endothelial dysfunction in patients with CKD, also negatively correlated with plasma brain-derived neurotrophic factor (BDNF) concentration. We constructed the ANRIL knockout mice model, and found that ANRIL deficiency reversed the abnormal expression of BDNF, along with endothelial nitric oxide synthase (eNOS), vascular adhesion molecule 1 (VCAM-1) and Von Willebrand factor (vWF). To explore the specific mechanism, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) were used to explore the binding of ANRIL to histone methyltransferase Enhancer of zeste homolog 2 (EZH2). Further experiments found increased EZH2 and histone H3 lysine 27 trimethylation (H3K27me3) levels at the BDNF promoter region. 		Yes	We constructed the ANRIL knockout mice model, and found that ANRIL deficiency reversed the abnormal expression of BDNF, along with endothelial nitric oxide synthase (eNOS), vascular adhesion molecule 1 (VCAM-1) and Von Willebrand factor (vWF).  Meanwhile, mitochondrial dynamics-related proteins, Dynamin-related protein 1 (Drp1) and mitofusins (Mfn2) level were also recovered. In addition, in vitro, serum derived from CKD patients and uremia toxins induced abnormal expression of ANRIL. By making use of the gain- and loss-of-function approaches, we observed that ANRIL mediated endothelial dysfunction through BDNF downregulation. 	35906216
CDKN2A-DT	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cells	Interaction(SOSTDC1 axis)	qRT-PCR//Luciferase Report Assay//Western Blot//FISH	Herein, we unearthed that CDKN2A-AS1, BMP2/4/7, SMAD1/5/9 and phosphorylation of SMAD1/5/9 (p-SMAD1/5/9) were upregulated in EOC tissues and cells, whereas SOSTDC1 was downregulated in EOC tissues and cells. We firstly demonstrated that CDKN2A-AS1 bound directly with the SOSTDC1. CDKN2A-AS1 downregulated the expression of SOSTDC1, but upregulated the expression of BMP2/4/7, SMAD1/5/9, and p-SMAD1/5/9. 		Yes	CDKN2A-AS1 downregulated the expression of SOSTDC1, but upregulated the expression of BMP2/4/7, SMAD1/5/9, and p-SMAD1/5/9. CDKN2A-AS1 promoted the proliferation, migration, invasion of EOC cells and tumor growth in vivo, whereas SOSTDC1 inhibited the proliferation, migration, invasion of EOC cells. Knockdown SOSTDC1 rescued the inhibitory effect of si-lncRNA CDKN2A-AS1 on the EOC cells proliferation, migration and invasion. 	34110955
CDKN2B-AS1	LncRNA	Homo sapiens	Atherosclerosis	blood plasma	Interaction(let-7b/TGF-βR1 signalling pathway)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//ELISA	ANRIL levels were increased in patients with acute coronary syndrome. The expression of ANRIL is associated with the inflammatory cytokines monocyte chemoattractant protein-1 and interleukin-10, which are secreted in response to endothelial dysfunction. Knockdown of ANRIL significantly promoted cell proliferation and tubule formation and inhibited inflammatory activation and apoptosis of human umbilical vein endothelial cells (HUVEC). ANRIL-mediated inhibition of let-7b regulates HUVEC dysfunction by targeting the TGF-βR1/Smad signalling pathway.		Yes	Knockdown of ANRIL significantly promoted cell proliferation and tubule formation and inhibited inflammatory activation and apoptosis of human umbilical vein endothelial cells (HUVEC). 	32783191
CDKN2B-AS1	LncRNA	Homo sapiens	Glioma	 glioma cells	Interaction(miR-34a/Sirt1/PI3K/AKT and mTOR pathways)	Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Invasion Assay	ANRIL was upregulated in glioma cells and its suppression inhibited cell proliferation, migration and invasion but promoted cell apoptosis. ANRIL acted as a sponge of miR-34a, and Sirt1 is a target of miR-34a. Then, Sirt1 was proved to function through activation of the PI3K/AKT and mTOR signaling pathways. 		Yes	ANRIL was upregulated in glioma cells and its suppression inhibited cell proliferation, migration and invasion but promoted cell apoptosis. 	29057547
CDKN2B-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-199a-5p/DDR1 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	 CDKN2B-AS1 is significantly upregulated in glioma tissues and cell lines.Further, a miR-199a-5p inhibitor attenuates the inhibitory effects of sh-CDKN2B-AS1 on these cell phenotypes. CDKN2B-AS1 positively regulates DDR1 expression by directly sponging miR-199a-5p. 		Yes	CDKN2B-AS1 knockdown significantly inhibits cell proliferation, invasion, and migration, while promoting apoptosis of glioma cell lines U251 and U87. Moreover, CDKN2B-AS1 knockdown efficiently inhibits U87 tumor xenograft growth in mice.	34559933
CDKN2B-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	interaction[GAS6]	CCK8//qRT-PCR//RIP//Transwell Assay	CDKN2BAS was upregulated in ovarian cancer tissues, especially those with advanced FIGO stage and high pathological grade. LncRNA CDKN2BAS is upregulated in ovarian cancer. By positively interacting with GAS6, CDKN2BAS triggers the progression of ovarian cancer.	CDKN2BAS was upregulated in ovarian cancer tissues, especially those with advanced FIGO stage and high pathological grade.	Yes	The overexpression of CDKN2BAS enhanced proliferative and migratory potentials in HEY and SKOV-3 cells. 	32572907
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Regulation[miR-153-5p/ARHGAP18 signaling axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	CDKN2BAS was remarkably up-regulated in metastatic HCC tissues compared with the adjacent non-tumor tissues. Our study revealed that lncRNA CDKN2BAS promotes HCC metastasis by regulating the miR-153-5p/ARHGAP18 signaling.		Yes	CDKN2BAS promotes HCC cell growth and migration in vitro and in vivo. 	30510148
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Regulation[NF-κB and Wnt/β-catenin pathways,miR-191]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	These data demonstrated that ANRIL knockdown suppressed proliferation, migration, invasion, and promoted apoptosis in HepG2 cells by down-regulating miR-191 and inactivating NF-κB and Wnt/β-catenin signaling pathways.		Yes	Knockdown of ANRIL inhibited proliferation, induced apoptosis, meanwhile suppressed migration and invasion of HepG2 cells.	30249208
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[let-7c-5p/NAP1L1 axis]	qRT-PCR	Here, we identified a novel oncogenic lncRNA CDKN2B-AS1, which was highly expressed in HCC and positively associated with large tumor size, microvascular invasion, high tumor grade, advanced tumor stage and reduced survival of HCC patients.CDKN2B-AS1, an oncogenic lncRNA of HCC, promoted NAP1L1-mediated PI3K/AKT/mTOR signaling by acting as a molecular sponge of let-7c-5p.	Here, we identified a novel oncogenic lncRNA CDKN2B-AS1, which was highly expressed in HCC and positively associated with large tumor size, microvascular invasion, high tumor grade, advanced tumor stage and reduced survival of HCC patients.	Yes	CDKN2B-AS1 knockdown inhibited cell proliferation, migration and invasion, and induced G1 arrest and apoptosis of HCC cells in vitro, and CDKN2B-AS1 silencing suppressed tumor growth and metastasis of HCC in vivo.	30165194
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[MiR-199a-5p/ARL2 axis]	qRT-PCR	First, we found that lncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells.  Mechanistically, lncRNA ANRIL acted as a competing endogenous RNA to increase ARL2 (ADP-ribosylationfactor-like 2) expression via sponging miR-199a-5p. Notably, the miR-199a-5p/ARL2 axis is necessary for ANRIL-mediated promoting effects on HCC cell mitochondrial function. This work reveals a novel ANRIL-miR-199a-5p-ARL2 axis in HCC cell progression, which might provide potential targets for HCC treatment.		Yes	 Functional experiment showed that overexpression of lncRNA ANRIL promoted mitochondrial function in HCC cells, evident by the increased mitochondrial DNA copy numbers, ATP (Adenosine triphosphate) level, mitochondrial membrane potential, and the expression levels of mitochondrial markers, while ANRIL knockdown exerted the opposite effects. 	31670868
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 cell lines	Interaction[targeting of miR-384 and STAT3]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	ANRIL expression was upregulated in HCC cells, including SMCC7721, HepG2, MHCC-97H, SNU449 and HUH-7 cells, in comparison to the normal human liver cells LO2. ANRIL is involved in HCC progression by direct targeting of miR-384 and STAT3. Also, ANRIL could act as a potential candidate for HCC diagnosis, prognosis, and therapy.		Yes	Knockdown of ANRIL suppressed HCC cell proliferation and induced cell cycle arrest and apoptosis. HCC cell migration and invasion capacity were inhibited by inhibition of ANRIL.	31679275
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Interaction[sponging miR-144]	qRT-PCR	 ANRIL was highly expressed in MHCC97 and Li-7 cells when compared to THLE-3 cells. One of the possible mechanisms responsible for the tumour-promoting actions is that ANRIL sponging miR-144 to derepress PBX3.		Yes	ANRIL overexpression promoted cell viability, migration, invasion and suppressed apoptosis of MHCC97 and Li-7 cells. 	31609763
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[Sponging miR-424-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	CDKN2B-AS1 expression was increased in HCC tissues and cells.The present study revealed that high-expressed CDKN2B-AS1 may associate with the progression of HCC by affecting the cell viability, migration, invasion, and EMT of HCC cells by negatively regulating miR-424-5p.		Yes	Silencing of CDKN2B-AS1 suppressed cell viability, migration, invasion, and EMT, while overexpression of CDKN2B-AS1 produced the opposite results. 	32801906
CDKN2B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HepG2 cells	Regulation(Wnt/β-catenin pathway)	qRT-PCR	Knocking down of ANRIL led to alleviated cell growth and increased cell apoptosis of HepG2 cells through markedly increased expression levels of Bax and Bad. In contrast, dramatically diminished the expressions of anti-apoptotic factors including Bid and Bcl-2 in comparison to the scrambled control group (si-NC). Furthermore, ANRIL silencing resulted in an inactivated Wnt/β-catenin pathway by suppressing key genes associated with this pathway.		Yes	Knocking down of ANRIL led to alleviated cell growth and increased cell apoptosis of HepG2 cells through markedly increased expression levels of Bax and Bad.	34111289
CDKN2B-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	regulation[miR-143-3p/SMAD3 axis ]	CCK8//qRT-PCR//Transwell Assay//Western Blot	CDKN2B-AS1 was upregulated in OC and correlated with clinicopathologic features.  In conclusion, CDKN2B-AS1 promoted tumor growth, invasion, and migration of OC by regulation of miR-143-3p/SMAD3 axis, hinting that CDKN2B-AS1 might be a potential biomarker for OC diagnosis and treatment.		Yes	The knockdown of CDKN2B-AS1 hampered the development of OC, as reflected by the suppression of cell proliferation, migration, and invasion, and the enhancement of cell apoptosis, whereas the effects could be rescued by the overexpression of SMAD3. 	32305052
CDKN2B-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cell lines	Regulation[miR-181a-5p/TGFβI axis]	Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//IHC//Invasion Assay//Transwell Assay	In the present study, RT-PCR showed that the mRNA level of CDKN2B-AS1 was significantly upregulated while the miR-181a-5p was downregulated in cervical cancer cell lines. In summary, our study demonstrated that the CDKN2B-AS1/miR-181a-5p/TGFβI axis might play a vital role in cervical cancer development.		Yes	 In addition, the interference of CDKN2B-AS1 by shRNA resulted in the suppression of cell proliferation, invasion, migration and promotion of apoptosis and senescence, and either CDKN2B-AS1 overexpression or miR-181a-5p showed reversed results.	30884187
CDKN2B-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OVCAR-3 cell lines	Interaction(Wnt/β-catenin)	CCK8//qRT-PCR//Western Blot	ANRIL down-regulating in OVCAR-3 cell lines resulted in significant inhibition of cellular proliferation, apoptosis induction, as well as suppression of cellular invasion. More importantly, we observed that ANRIL inhibition suppressed the vital components expression of the Wnt/β-catenin cascade.		Yes	ANRIL down-regulating in OVCAR-3 cell lines resulted in significant inhibition of cellular proliferation, apoptosis induction, as well as suppression of cellular invasion. Besides, knockdown of ANRIL led to pro-apoptotic genes up-regulation, Bad and Bax and anti-apoptotic genes down-regulation, Bid and Bcl-2. 	33772549
CDKN2B-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and blood	Interaction[TGF-β/Smad pathway]	Flow Cytometry//MTT//Western Blot	The lncRNA ANRIL was highly expressed in the tissues and serum of patients.The lncRNA ANRIL regulates the TGF-β/Smad signaling pathway to promote the proliferation and suppress the apoptosis of OSCC cells.		Yes	The proliferation ability of the cells transfected with si-ANRIL was significantly reduced, while that of the cells transfected with ANRIL-OE was overtly increased.	31364119
CDKN2B-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues 	Regulation[miR-125a-3p/FGFR1/MAPK signaling]	IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	In this study, we found that ANRIL expression was upregulated in HNSCC and correlated with tumor progression. Thus, it could be concluded that ANRIL promoted the progression of HNSCC via miR-125a-3p/FGFR1/MAPK signaling, which might provide a new target for the diagnosis and treatment of HNSCC.		Yes	 Further functional analysis showed that knockdown of ANRIL significantly inhibited proliferation in vivo and in vitro.	30555745
CDKN2B-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	CDKN2B-AS1 was found to be markedly up-regulated in OS tissues and cell lines. 	 Clinical data further demonstrated highly expressed CDKN2B-AS1 tended to be strongly positively correlated with tumor size, distant metastasis and TNM stage.	Yes	 Loss-of-function of CDKN2B-AS1 leaded to inhibited cell proliferation and induced cell cycle G0/G1 phase arrest. In addition, CDKN2B-AS1 knockdown significantly suppressed OS cells migration and invasion.	31724892
CDKN2B-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS samples and cells	regulation[microRNA-122/CCNG1 axis]	CCK8//qRT-PCR//EdU Staining//Transwell Assay	In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells.We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. 		Yes	 Those in vitro investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. 	33283575
CDKN2B-AS1	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cells	interaction[MAP3K3,miR-4458]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	 In this study, we firstly assessed the expression of CDKN2B-AS1 in OS tissues and cells, showing that CDKN2B-AS1 expression were remarkably upregulated in OS tissues and cells.Our results suggested that CDKN2B-AS1 facilitated OS progression by sponging miR-4458 to enhance MAP3K3 expression, which provides a novel insight into improving diagnostic and therapeutic strategies for patients with OS.		Yes	Moreover, CDKN2B-AS1 knockdown suppressed cell proliferation, migration, and EMT progress in OS. 	31950433
CDKN2B-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow 	Regulation[regulating miR-34a]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	ANRIL was up-regulated both in the BM samples from AML patients and cell lines (HL-60 and THP-1), of which expression was negatively correlated with miR-34a expression.ANRIL promotes AML development through HDAC1-mediated epigenetic suppression of ASPP2 via negatively regulating miR-34a, which might serve as a therapeutic target for AML treatment.		Yes	ANRIL knockdown inhibited cell proliferation, migration and invasion but promoted apoptosis of AML cells, while overexpression of miR-34a exerted opposite effects. miR-34a was verified as a downstream gene targeted by ANRIL. 	31830533
CDKN2B-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues 	Expression[highly expressed]	qRT-PCR	Then further verification was obtained by means of RT-qPCR that ANRIL was highly expressed in CC tissues. 		Yes	In addition, high expression of ANRIL was related to increased E-cadherin expression, high migration of CC as well as decreased cell apoptosis rate.	30198868
DANCR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung adenocarcinoma tissues and cells	Interaction( miR-496/mTOR)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//IHC	 In this study, we demonstrated that differentiation antagonizing non-protein coding RNA (DANCR) was up-regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR inhibited tumour cell proliferation, migration and invasion and restored cell apoptosis rescued; cotransfection with a miR-496 inhibitor reversed these effects. Luciferase reporter assays showed that miR-496 directly modulated DANCR; additionally, we used RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays to further confirm that the suppression of DANCR by miR-496 was RISC-dependent. Our study also indicated that mTOR was a target of miR-496 and that DANCR could modulate the expression levels of mTOR by working as a competing endogenous RNA (ceRNA). 		Yes	 In this study, we demonstrated that differentiation antagonizing non-protein coding RNA (DANCR) was up-regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR inhibited tumour cell proliferation, migration and invasion and restored cell apoptosis rescued; cotransfection with a miR-496 inhibitor reversed these effects. Furthermore, the knockdown of DANCR reduced tumour volumes in vivo compared with those of the control group. 	29266795
DANCR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LAD tissue and cell lines	Regulation[DANCR/HMGA2 axis ]	qRT-PCR//IHC//Western Blot//Transwell Assay	In the present study, it was revealed that the lncRNA DANCR was upregulated in LAD tissue and cell lines, compared with para‑tumor tissue and a normal lung cell line. Furthermore, HMGA2 was overexpressed in LAD tissue and in SPCA1 and A549 cells, compared with para‑tumor tissue and a normal lung cell line. Inhibition of HMGA2 suppressed the invasive ability of SPCA1 and A549 cells, and DANCR promoted the invasive ability via regulation of HMGA2 in SPCA1 and A549 cells. The findings of the present study revealed that DANCR promoted the invasion of LAD cells by positively regulating HMGA2. Thus, a DANCR/HMGA2 axis may be a novel potential target in the molecular treatment of LAD.		Yes	 Functionally, the study revealed that knockdown of DANCR inhibited invasion and HMGA2 expression in the LAD cell lines, SPCA1 and A549. 	30535487
DANCR	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Interaction[miR-33b/MMP16]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the current study, we demonstrate that DANCR was increased in PC tissues and cell lines. In addition, we identified direct binding to the predicted miR-33b binding site on DANCR. We also showed that there is reciprocal repression between DANCR and miR-33b. Furthermore, a miR-33b inhibitor partially abrogated knockdown of DANCR and caused inhibitory effects. We also demonstrated that DANCR functions as a miR-33b sponge to positively regulate MMP16 expression in PC cells. Collectively, the data reveal that DANCR exerts its function by regulating miR-33b/MMP16 expression, implying an important role for a lncRNA-miRNA-mRNA functional network and suggesting a novel potential therapeutic target for PC.		Yes	Knockdown of DANCR significantly suppressed cell proliferation, migration, and invasion and influenced the levels of epithelial-to-mesenchymal transition-associated proteins, as demonstrated by the observation of enhanced E-cadherin levels and reduced N-cadherin levels in PC cells. 	31515968
DSCAM-AS1	LncRNA	Homo sapiens	stomach carcinoma	GC tissues and cell lines	Interaction(miR-204/TPT1 axis)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	In this study, we found that DSCAM-AS1 was significantly overexpressed in GC tissues and cell lines. We identified miR-204 as a target of DSCAM-AS1 and found that it targeted TPT1 in GC cells, which further led to decreased expression of miR-204 in GC tissues and cell lines. A rescue assay revealed that knocked-down DSCAM-AS1 hindered GC progression, which was reversed upon miR-204 downregulation or TPT1 overexpression. 		Yes	Functional experiments indicated that GC cells with DSCAM-AS1 silencing exhibited a dynamic reduction in proliferation and migration. 	34372727
DSCAM-AS1	LncRNA	Homo sapiens	endometrial adenocarcinoma	endometrial cancer	Expression(highly expressed)	Western Blot//Transfection//qRT-PCR//Cell Apoptosis Assay//Microarray	Initial analysis of open-source data revealed DSCAM-AS1 overexpression in endometrial cancer (EC) (p < 0.01) and a significant association with shorter overall survival of EC patients (HR = 1.78, p < 0.01). 		Yes	 DSCAM-AS1 knockdown triggered an anti-tumoral transcriptome response as revealed by Affymetrix microarray analysis, emerging from down-regulation of tumor-promoting genes and induction of tumor-suppressive networks.  Finally, several genes regulated upon DSCAM-AS1 silencing in vitro were found to be inversely correlated with this lncRNA in EC tissues.	35885035
DRHC	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[miR-8075 ]	CCK8//qRT-PCR	The present study revealed that lncRNA DRHC was Expression[down-expression]regulated and lncRNA Hox transcript antisense RNA (HOTAIR) was Expression[Expression[up-expression]-expression]regulated in tumor tissues compared with adjacent healthy tissues in patients with triple negative breast cancer (TNBC).The results obtained in the current study suggested that lncRNA DRHC may inhibit the proliferation of TNBC cells by Expression[down-expression]regulating the expression of lncRNA HOTAIR.		Yes	 In vitro overexpression of lncRNA DRHC in TNBC cell lines resulted in decreased expression of lncRNA HOTAIR; however, lncRNA HOTAIR overexpression did not affect the expression level of lncRNA DRHC. Overexpression of lncRNA DRHC inhibited, while overexpression of lncRNA HOTAIR promoted the proliferation of the TNBC cell lines. In addition, lncRNA HOTAIR overexpression attenuated the inhibitory effects of lncRNA DRHC overexpression on cancer cell proliferation.	31516593
DRHC	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[MEK/ERK signaling]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH	 Here, we reported a novel lncRNA, CTC-505O3 (lncRNA DRHC), that was downregulated in HCC and its low expression was associated with dismal survival. oreover, we found that lncRNA DRHC interacted with MYBBP1A and modulated MEK/ERK signaling via c-Myb.	 Here, we reported a novel lncRNA, CTC-505O3 (lncRNA DRHC), that was downregulated in HCC and its low expression was associated with dismal survival. 	Yes	Gain-of-function studies indicated that it inhibited proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in HCC cell lines in vitro. lncRNA DRHC also inhibited tumorigenicity in vivo. 	30362626
DRAIC	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	interaction[UCHL5 and NFRKB ]	Western Blot//Co-IP//CCK8//qRT-PCR//Transwell Assay	 DRAIC is down-regulated in GC tissues and cell lines while its potential interacting molecules UCHL5 and NFRKB are up-regulated, and DRAIC is positively correlated with NFRKB protein instead of mRNA.  DRAIC suppresses GC proliferation and metastasis via interfering with the combination of UCHL5 and NFRKB and mediating ubiquitination degradation.	Lower DRAIC and higher UCHL5 and NFRKB indicated advanced progression of GC patients. 	Yes	 DRAIC combined with UCHL5 and attenuated binding of UCHL5 and NFRKB, meanwhile promoting the degradation of NFRKB via ubiquitination, and then inhibited the proliferation and metastasis of GC cells, which can be rescued by oeNFRKB.	32351584
DRAIC	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC cells	regulation[miR-149-5p/NFIB]	qRT-PCR//RNA Pull-Down	DRAIC and NFIB showed high expression in EC cells, while miR-149-5p showed low expression.  Moreover, DRAIC has an effect on the autophagy of EC cells through miR-149-5p/NFIB.		Yes	 Down-regulating DRAIC, NFIB and over-expressing miR-149-5p can inhibit EC cells' proliferation and invasion, and improve apoptosis and autophagy. 	32659236
DRAIC	LncRNA	Homo sapiens	Glioma	glioma tissues,cell lines	interaction[ targeting miR-18a-3p]	ChIP//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Compared with adjacent non-cancerous normal tissues, SET7/9 and DRAIC were both downregulated and miR-18a-3p was upregulated in glioma cells.  In this research, we discovered that the expression of SET7/9 was low in glioma cells and SET7/9-mediated H3K4me3 enrichment on the DRAIC promoter regulated the growth and metastasis of glioma cells by targeting miR-18a-3p.		Yes	In U251 cells, SET7/9 and DRAIC overexpression inhibited cell proliferation, migration and invasion.  The inhibition of DRAIC promoted the growth and metastasis of U251 cells, while the co-transfection of si- DRAIC and miR-18a-3p further promoted the growth and metastasis of U251 cells.	33336743
DRAIC	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	Regulation[DRAIC-miR-122-SATB1 axis ]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	In this study, we found that DRAIC was significantly increased in NPC tissues.  In conclusion, these findings revealed the important roles of DRAIC-miR-122-SATB1 axis in NPC and suggested that DRAIC may be a potential therapeutic target for NPC.		Yes	Functional assays revealed that ectopic expression of DRAIC enhances NPC cell growth, migration and invasion. DRAIC knockdown represses NPC cell growth, migration and invasion.	31497998
DRAIC	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(miR-3940-3p axis)	Transfection//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 lnc DRAIC was upregulated in LUAD tissues and cells, but miR-3940-3p was downregulated. Lnc-DRAIC and miR-3940-3p have the potential as independent prognostic factors for LUAD. Furthermore, the inhibition of lnc DRAIC can inhibit cell proliferation, migration, and invasion of LUAD partly as a ceRNA of miR-3940-3p.	Both of them showed significant associations with and TNM stage, lymph node metastasis, and a poor prognosis. 	Yes	Lnc-DRAIC and miR-3940-3p have the potential as independent prognostic factors for LUAD. Furthermore, the inhibition of lnc DRAIC can inhibit cell proliferation, migration, and invasion of LUAD partly as a ceRNA of miR-3940-3p.	34764698
DRAIC	LncRNA	Homo sapiens	Hirschsprung Disease	 colon tissue	Interaction(miR-34a-5p/ITGA6 signal axis)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The lncRNA DRAIC was significantly increased in colon tissue from HSCR patients. The RNA pull-down and dual-luciferase reporter assays have proven the competitive relationship between DRAIC and ITGA6 through their association with miR-34a-5p. 		Yes	The overexpression of DRAIC inhibited SH-SY5Y cell and human 293T cell proliferation and migration. Knockdown of DRAIC, however, promoted cell proliferation and migration. 	34471485
DQ786243	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	liver cancer and HCC cell	Interaction(miR‑15b‑5p/Wnt3A axis)	qRT-PCR	lncDQ and Wnt3A expression were significantly increased in HCC tissues, whereas miR‑15b‑5p was downregulated in HCC tissues. Low expression of miR‑15b‑5p was also associated with poor prognoses for patients with HCC. lncDQ was able to bind with miR‑15b‑5p and served as a competing endogenous RNA. As the target gene of miR‑15b‑5p, Wnt3A was correlated with poor prognoses for patients with HCC. lncDQ inhibited miR‑15b‑5p so as to promote HCC cell invasion and proliferation through activation of the Wnt3A/β‑catenin/EMT pathway. 	 Low expression of miR‑15b‑5p was also associated with poor prognoses for patients with HCC.	Yes	Silencing of lncDQ expression significantly attenuated proliferation and invasion of liver cancer and HCC cells, however the inhibition of miR‑15b‑5p was able to reverse this effect. However, silencing of lncDQ and miR‑15b‑5p expression simultaneously resulted in the partial rescue of the inhibitory effect in the liver cancer and HCC cells. 	33760109
DPP10-AS1	LncRNA	Homo sapiens	Lung Neoplasms	cancer tissues	Interaction(DPP10)	In Vivo Experiment//qRT-PCR//MTT//Cell Cycle Assay//Colony Formation Assay	The novel antisense lncRNA DPP10-AS1 was found to be highly expressed in cancer tissues (P < 0.0001), and its upregulation predicted poor prognosis in patients with lung cancer (P = 0.0025).Importantly, DPP10-AS1 positively regulated DPP10 gene expression, and both were coordinately upregulated in lung cancer tissues. Mechanically, DPP10-AS1 was found to associate with DPP10 mRNA but did not enhance DPP10 mRNA stability. 	The novel antisense lncRNA DPP10-AS1 was found to be highly expressed in cancer tissues (P < 0.0001), and its upregulation predicted poor prognosis in patients with lung cancer (P = 0.0025).	Yes	Notably, DPP10-AS1 promoted lung cancer cell growth, colony formation, and cell cycle progression, and repressed apoptosis in lung cancer cells by upregulating DPP10 expression. Additionally, DPP10-AS1 facilitated lung tumor growth via upregulation of DPP10 protein in a xenograft mouse model.	34106559
DPP10-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CCSCs	Interaction(miR-127-3p and ADCY1)	CCK8//qRT-PCR//Western Blot//Transwell Assay	Poorly expressed DPP10-AS1 and ADCY1, while highly expressed miR-127-3p were found in CCSCs. Taken together, this study demonstrates that DPP10-AS1 inhibits CCSC proliferation by regulating miR-127-3p and ADCY1, providing fresh insight into a promising novel treatment strategy for colon cancer.	Low expression of DPP10-AS1 was correlated with TNM stage, lymphatic node metastasis, and tumor differentiation. 	Yes	Upregulation of DPP10-AS1 increased ADCY1 protein expression, decreased the protein expression of CCSC-related factors, inhibited sphere formation, colony formation, proliferation, invasion and migration, and accelerated apoptosis of HT-29 and SW480 cells by suppressing the expression of miR-127-3p. Further, the above in vitro findings were also confirmed by in vivo assays. 	33744851
DOCK9-DT	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	exosomes 	regulation[ Wnt/β-catenin pathway]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Based on the result of differentially expressed lncRNAs in PTC via bioinformatics databases, we discovered that DOCK9-AS2 was upregulated in PTC, and presented elevation in plasma exosomes of PTC patients. In conclusion, PTC-CSCs-derived exosomal lncRNA DOCK9-AS2 activated Wnt/β-catenin pathway to aggravate PTC progression, indicating that DOCK9-AS2 was a potential target for therapies in PTC.		Yes	Functionally, DOCK9-AS2 knockdown reduced proliferation, migration, invasion, epithelial-to-mesenchymal (EMT) and stemness in PTC cells.	32917852
DOCK1	CircRNA	Homo sapiens	bladder carcinoma	BC tissues,cell lines	Interaction[circDOCK1/hsa-miR-132-3p/Sox5 pathway]	Western Blot//qPCR//Luciferase Report Assay//Microarray//EdU Staining//Transwell Assay	 CircDOCK1 was Expression[Expression[up-expression]-expression]regulated in BC tissues and cell lines. CircDOCK1 played its role via regulation of circDOCK1/hsa-miR-132-3p/Sox5 pathway in BC cells. 		Yes	 Repression of circDOCK1 reduced cell viability, inhibited cell proliferation and curbed the cell migration potential of BC cell. SExpression[Expression[up-expression]-expression]pression circDOCK1 inhibited the tumour growth in vivo.	30983072
DNM3OS	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines	Expression[Expression[highly expressed]-expression]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH	We observed that DNM3OS was Expression[Expression[up-expression]-expression]regulated in GC tissues and cell lines, and high DNM3OS expression was correlated with malignant features and served as an indicator of a poor prognosis for GC patients.	We observed that DNM3OS was Expression[Expression[up-expression]-expression]regulated in GC tissues and cell lines, and high DNM3OS expression was correlated with malignant features and served as an indicator of a poor prognosis for GC patients	Yes	DNM3OS knockExpression[down-expression] inhibited the proliferation of GC cells, and reduced DNM3OS sExpression[Expression[up-expression]-expression]pressed tumor growth in vivo. 	30770102
DNM3OS	LncRNA	Homo sapiens	Osteoarthritis	OA tissues	Interaction[sponging miR-126]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	The expression of DNM3OS was down-regulated in OA patients. Our results showed that DNM3OS could affect the CHON-001 cell proliferation and apoptosis by regulating IGF1 by sponging miR-126.		Yes	Functional assays demonstrated that ectopic expression of DNM3OS promoted the proliferation and inhibited apoptosis of CHON-001 cells, and that knocking down DNM3OS suppressed cell proliferation and induced apoptosis. 	31526393
DNM3OS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	Interaction(KDM6B/TIAM1 axis)	qRT-PCR	DNM3OS was significantly upregulated in HCC compared to adjacent liver tissues. Biochemically, DNM3OS was mainly localized in the nucleus and physically interacted with KDM6B. The association of DNM3OS with KDM6B induced the expression of TIAM1 through reduction of H3K27me3 at the TIAM1 promoter. 	High DNM3OS expression was associated with TNM stage, vascular invasion, and poor prognosis of HCC patients.	Yes	 Silencing of DNM3OS inhibited HCC cell proliferation and invasion in vitro and tumorigenesis and metastasis in vivo. Overexpression of DNM3OS enhanced HCC cell proliferation, invasion, and metastasis. 	33472090
DNM3OS	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines	Interaction( miR-193a-3p/MAP3K3 Axis)	qRT-PCR//Bioinformatics Analysis//RIP//Western Blot	DNM3OS expression was remarkably increased in OC tissues and cell lines, which was associated with the unfavorable prognosis of the patients. DNM3OS directly interacted with miR-193a-3p, and miR-193a-3p targeted MAP3K3 by directly binding to 3'UTR. DNM3OS could up-regulate the expression of MAP3K3 via repressing miR-193a-3p expression.	DNM3OS expression was remarkably increased in OC tissues and cell lines, which was associated with the unfavorable prognosis of the patients. 	Yes	DNM3OS overexpression enhanced OC cell proliferation, migration, and invasion; suppressed E-cadherin protein expression; and facilitated N-cadherin protein expression, while the transfection of miR-193a-3p mimics had the opposite effects.	34027641
DNM3OS	LncRNA	Homo sapiens	Mouth Neoplasms	oral cancer tissues and cells	regulation[DNM3OS/miR-204-5p/HIP1 axis ]	RNA-seq//Microarray	DNM3OS was upregulated in oral cancer tissues and cells.Within oral carcinoma tissue samples, expression of DNM3OS and HIP1 was increased whereas the miR-204-5p expression was downregulated; miR-204-5p had a negative correlation with DNM3OS and HIP1, respectively, while DNM3OS and HIP1 were positively correlated with each other.		Yes	DNM3OS knockdown in CAL27 and SCC-9 cells inhibited cell viability and migration. 	32463958
DSCAM-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical carcinoma specimens 	Interaction(miR-338-3p)	Cell Proliferation Assay//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay	DSCAM-AS1 was upregulated in cervical carcinoma specimens compared to control no-tumor specimens.Moreover, our data revealed that miR-338-3p expression was downregulated in cervical carcinoma cells and specimens. There was a negative correlation between miR-338-3p expression and DSCAM-AS1 expression in cervical carcinoma specimens. Elevated expression of miR-338-3p decreased cervical carcinoma cell growth and cycle and invasion. 		Yes	Overexpression of DSCAM-AS1 induced cervical carcinoma cell growth and cycle. 	35378649
DSCAM-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	 EC tissues and cells	Interaction(miR-136-5p)	In Vivo Experiment//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	It was revealed that DSCAM-AS1 was expressed at a high level in EC tissues and cells after analyzing patient data and data obtained from The Cancer Genome Atlas. Furthermore, it was revealed that DSCAM-AS1 acted as a microRNA (miR)-136-5p sponge to exert its oncogenic roles in EC. 	 Notably, it was also revealed that high DSCAM-AS1 expression was associated with a less favorable overall survival in patients with EC. 	Yes	 Knockdown of DSCAM-AS1 was able to suppress EC cell proliferation by upregulating cell apoptosis in vitro.	34691252
DNAJC3-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[receptor/phosphatidylinositol 3-kinase/protein kinase B/nuclear factor κB signaling pathway]	Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay	By constructing a differential lncRNA expression profile, we screened gene chips and found that DNAJC3-AS1 was highly expressed in CRC tissues and was associated with poor prognosis in patients with CRC. Mechanically, we found that DNAJC3-AS1 regulates fatty acid synthase to promote the progression of CRC via the epidermal growth factor receptor/phosphatidylinositol 3-kinase/protein kinase B/nuclear factor κB signaling pathway. 	By constructing a differential lncRNA expression profile, we screened gene chips and found that DNAJC3-AS1 was highly expressed in CRC tissues and was associated with poor prognosis in patients with CRC. 	Yes	Further, we proved through assays such as wound healing, colony formation, and Cell Counting Kit-8 (CCK8) that interfering with DNAJC3-AS1 could reduce the proliferation, migration, and invasion of CRC cells. 	33604287
DSCAM-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cell lines	Interaction[sponging miR-136]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In this research, we showed that the expression of DSCAM-AS1 was significantly upregulated in melanoma samples and cell lines.  Furthermore, mechanistic investigations indicated that DSCAM-AS1 could interact with miR-136 and negatively influence the expression of miR-136.	 Clinical investigation indicated that higher expression of DSCAM-AS1 was associated with ulceration and advanced stage and led to significantly poorer survival time. High DSCAM-AS1 expression in melanoma was confirmed to be an independent predictor of poor survival of patients using univariate and multivariate analysis. 	Yes	 Functional investigations revealed that knockdown of DSCAM-AS1 inhibited the ability of cell proliferation, colony formation, migration, invasion, whereas promoted cell apoptosis.	31002140
DUXAP10	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[HuR/Sox12 axis]	qRT-PCR//RIP//IF	Here, we show that DUXAP10 is overexpressed in glioma tissues and cells. Further rescuing experiments show that the HuR/Sox12 axis is responsible for DUXAP10-mediated effects on glioma cell stemness.		Yes	Loss of function experiments reveal that DUXAP10 knockdown has little effects on glioma cell viability, but significantly reduces the stemness of glioma cells, which is characterized as the decrease of stemness marker expression, tumor sphere-forming ability, and ALDH activity. 	33340249
DUXAP10	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cells	Interaction( EZH2 and LSD1)	In Vivo Experiment//Transfection//Invasion Assay//Migration Assay//Flow Cytometry//qRT-PCR//RIP//Microarray//Colony Formation Assay//Bioinformatics Analysis	In this study, we found that DUXAP10 was overexpressed in PC tissues compared with normal tissues. Mechanistic studies revealed that DUXAP10 has a crucial role in G2/M arrest. We further showed that DUXAP10 regulated PC cell proliferation through interact with RNA-binding protein EZH2 and LSD1. 	DUXAP10 expression was significantly higher in patients with an advanced TNM stage and positive lymph node metastasis. 	Yes	Bioinformatic analysis showed that cell cycle progression was increased in patients with high DUXAP10 expression. In vitro and in vivo assays of DUXAP10 alterations revealed a complex integrated phenotype affecting cell growth, apoptosis, migration, and invasion. 	29286182
DUXAP10	LncRNA	Homo sapiens	Prostatic Neoplasms	cell lines	Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	Results showed that the expression of DUXAP10 was higher in PC3 and DU145 cell lines than that in the 22RV1 cell line.		Yes	Additionally, the knockdown of DUXAP10 could remarkably inhibit the proliferation, migration, and induce apoptosis of prostate cancer cells, and significantly increase the number of G0/G1 cells in PC3 and DU145 cell lines.	31114994
DUXAP10	LncRNA	Homo sapiens	Melanoma	MM tissues and cells	Interaction[Suppressing CADM1 ]	RIP//Wound Healing Assay//qRT-PCR//Transwell Assay	Here, we found that LNMAT1 was upregulated in MM tissues and cells, and its expression levels were further enhanced in MM patients with lymph node metastasis and metastatic MM cells.Lastly, rescue assays demonstrated that LNMAT1 promoted cell migration and invasion of MM by suppressing CADM1 expression. 	Here, we found that LNMAT1 was upregulated in MM tissues and cells, and its expression levels were further enhanced in MM patients with lymph node metastasis and metastatic MM cells.	Yes	Using loss-of-function assays, we found that LNMAT1 promoted cell migration and invasion and lung metastasis in MM in vitro and in vivo.	31334110
DUSP5P1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(ARHGAP5 )	FISH	We demonstrated that gastric cancer (GC) patients with high DUSP5P1 expression had shortened survival in two independent cohorts. Mechanistically, DUSP5P1 activated ARHGAP5 transcription by directly binding to the promoter of ARHGAP5 with a binding motif of TATGTG. RNA-seq revealed that ARHGAP5 activated focal adhesion and MAPK signaling pathways to promote GC metastasis. 		Yes	DUSP5P1 promoted GC cell migration and invasion in vitro and metastasis in vivo.	36307394
DUSP16	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-432-5p/E2F6 Axis)	Western Blot//Transfection//qPCR//Flow Cytometry//RIP//IF//PCR//IP//Bioinformatics Analysis//Transwell Assay	CircDUSP16 expression was upregulated in CRC tissues and cell lines. CircDUSP16 caused a negative regulation in miR-432-5p expression. In addition, E2F6 expression was elevated in CRC tissues.Inhibition of miR-432-5p promoted the proliferative and metastatic activity of CRC cells and inhibited the induction of apoptosis. Inhibition of E2F6 expression partially abolished the effects caused by miR-432-5p depletion. Moreover, circDUSP16 upregulated E2F6 expression by reducing miR-432-5p expression.	 High circDUSP16 expression was correlated with low survival rate. 	Yes	Furthermore, circDUSP16 silencing repressed CRC tumor growth in vivo. Furthermore, circDUSP16 knockdown repressed cell proliferation, migration, and invasion and induced apoptosis in CRC. 	34456589
DUBR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cell lines (H1975, A549)	Regulation(c-Myc/DUBR/ZBTB11 axis)	Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay//ChIP	Analysis of mRNA expression in The Cancer Genome Atlas (TCGA) LUAD database and in-house LUAD cohort (n = 94) showed that DUBR was significantly downregulated in LUAD, and was associated with poor prognosis. In LUAD cell lines (H1975, A549), overexpression of DUBR significantly suppressed the migration and invasion of the LUAD cells. We demonstrated that c-Myc could bind to the promoter of DUBR, and transcriptionally suppressed its expression. Knockdown of c-Myc almost completely blocked the invasion and migration of LUAD cells, whereas knockdown of DUBR partially rescued c-Myc-knockdown suppressed cell migration and invasion. Furthermore, DUBR overexpression significantly increased the expression of a downstream protein of DUBR, zinc finger, and BTB domain containing 11 (ZBTB11), in H1975 and A549 cells; knockdown of ZBTB11 partially rescued the DUBR-overexpression suppressed cell migration and invasion; knockdown of c-Myc significantly upregulated the expression of ZBTB11 in LUAD cells. Finally, we revealed that DUBR/ZBTB11 axis suppressed oxidative phosphorylation in LUAD cells. In short, we demonstrate that c-Myc/DUBR/ZBTB11 axis suppresses migration and invasion of LUAD by attenuating cell oxidative phosphorylation, which provides new insights into the regulatory mechanism of DUBR.	Analysis of mRNA expression in The Cancer Genome Atlas (TCGA) LUAD database and in-house LUAD cohort (n = 94) showed that DUBR was significantly downregulated in LUAD, and was associated with poor prognosis. 	Yes	Knockdown of c-Myc almost completely blocked the invasion and migration of LUAD cells, whereas knockdown of DUBR partially rescued c-Myc-knockdown suppressed cell migration and invasion. Furthermore, DUBR overexpression significantly increased the expression of a downstream protein of DUBR, zinc finger, and BTB domain containing 11 (ZBTB11), in H1975 and A549 cells; knockdown of ZBTB11 partially rescued the DUBR-overexpression suppressed cell migration and invasion; knockdown of c-Myc significantly upregulated the expression of ZBTB11 in LUAD cells. 	33758355
DSCR8	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-137/Cdc42)	In Vivo Experiment//RNA Pull-Down//Western Blot//Invasion Assay//Tunel//qRT-PCR//RIP//FISH//MTT//Luciferase Report Assay//Cell Cycle Assay//IHC//Bioinformatics Analysis//Transwell Assay	Here, qRT-PCR detected upregulated expression of DSCR8 and Cdc42 and downregulated expression of miR-137 in GC.  Dual-luciferase reporter gene, RNA immunoprecipitation, and biotin pull-down assays showed that DSCR8 could bind to miR-137 could bind to Cdc42.	 Statistical analysis showed that DSCR8 was closely associated with some malignant clinicopathological features (such as tumor size, metastasis, and stage) in GC patients. 	Yes	In vitro and in vivo assays showed that DSCR8 could promote proliferation, invasion, and the cycle of GC cells and inhibit cell apoptosis. In addition, a rescue experiment showed that DSCR8 regulated progression of GC cells via miR-137. 	34553033
DSCR8	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues 	regulation[DSCR8/miR-98-5p/STAT3/HIF-α axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	DSCR8 was remarkedly increased in OC tissues and associated with poorer survival of OC patients.  The present results suggested a positive feedback loop of lncRNA DSCR8/miR-98-5p/STAT3/HIF-α axis in the progression of OC.	DSCR8 was remarkedly increased in OC tissues and associated with poorer survival of OC patients. 	Yes	Overexpressing DSCR8 promoted cell proliferation, invasion, and EMT but inhibited apoptosis. 	32984052
DSCAM-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-577/HMGB1 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 DSCAM-AS1 and HMGB1 were upregulated, while miR-577 was downregulated in NSCLC tissues and cells. In conclusion, DSCAM-AS1 facilitated NSCLC progression by regulating the HMGB1-mediated Wnt/β-catenin pathway, providing a promising therapeutic target for NSCLC.		Yes	DSCAM-AS1 promoted cell proliferation, migration and invasion, and restrained cell apoptosis in NSCLC cells.	32386483
DSCAM-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC samples	regulation[DSCAM-AS1/miR-122-5p Axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	FSTL3 and DSCAM-AS1 were remarkably up-regulated in NSCLC samples, and miR-122-5p was down-regulated. Taken together, our study identified that FSTL3 was a new oncogene of NSCLC, which was regulated by DSCAM-AS1 and miR-122-5p. 	FSTL3 was associated with worse prognosis of NSCLC patients. 	Yes	FSTL3 knockdown markedly inhibited the viability, migration and invasion of NSCLCs in vitro and in vivo.	32280246
DSCAM-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines 	interaction[miR-384,AKT3]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//Transwell Assay	Here, we discovered that the expression of DSCAM-AS1 exhibited a significant upregulation in CRC tissues and cell lines in comparison with the corresponding control. In summary, DSCAM-AS1 exerted an oncogenic role in CRC by functioning as a competing endogenous RNA of miR-384 to bring about regulation of AKT3 expression.	Increased DSCAM-AS1 expression was associated with poor prognosis for those diagnosed with CRC.	Yes	Loss-of function assay illustrated that knockdown of DSCAM-AS1 resulted in significant inhibition of cell proliferation, invasion and migration in vitro, and impaired tumor growth in vivo.	32453706
DSCAM-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues	regulation[ miR-204/SOX4 Axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	DSCAM-AS1 was significantly upregulated in CC and high expression of DSCAM-AS1 was associated with poor prognosis in patients with colon cancer. The present study demonstrated that DSCAM-AS1 acted as an oncogenic lncRNA in CC progression by regulating miR-204/SOX4 axis and DSCAM-AS1 may serve as a novel therapeutic target in the treatment of colon cancer.		Yes	Knockdown of DSCAM-AS1 significantly suppressed CC cells proliferation and migration.	32606930
DSCAM-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-124 )	Other	DSCAM-AS1 was upregulated, while miR-124 was downregulated in HCC tissues. DSCAM-AS1 and miR-124 were inversely correlated across HCC tissues but not normal tissues. miR-124 overexpression increased DSCAM-AS1 level while DSCAM-AS1 overexpression decreased miR-124 level.	DSCAM-AS1 level increased, while miR-124 level decreased along with the clinical stage increasing. 	Yes	In addition, miR-124 overexpression decreased HCC cell proliferation, while DSCAM-AS1 increased HCC cell proliferation.	35695605
DSCAM-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-138-5p/EZH2 axis.)	qRT-PCR//MTT//Transwell Assay//Western Blot	DSCAM-AS1 expression was remarkably increased in OSCC tissues and cell lines, and DSCAM-AS1 knockdown could significantly restrain OSCC cell proliferation, migration, and invasion.MiR-138-5p was identified as a target of DSCAM-AS1, and its inhibitor could reverse the suppressive effects of DSCAM-AS1 knockdown on OSCC progression. EZH2 was verified as a target of miR-138-5p, and EZH2 knockdown could counteract the promotional impact of miR-138-5p inhibitor on OSCC progression. Additionally, DSCAM-AS1, as a ceRNA, could regulate EZH2 expression via miR-138-5p.		Yes	DSCAM-AS1 expression was remarkably increased in OSCC tissues and cell lines, and DSCAM-AS1 knockdown could significantly restrain OSCC cell proliferation, migration, and invasion.	35717565
DSCAM-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells 	interaction[sponging miR-101]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 In the present study, it was demonstrated that DSCAM-AS1 expression was significantly upregulated in OS tissues and cells and high expression of DSCAM-AS1 predicted poor prognosis in OS patients.  The present study demonstrated that DSCAM-AS1 accelerated OS cell progression by sponging miR-101, which might provide a new sight in the treatment of OS.	 In the present study, it was demonstrated that DSCAM-AS1 expression was significantly upregulated in OS tissues and cells and high expression of DSCAM-AS1 predicted poor prognosis in OS patients. 	Yes	 In addition, the silencing of DSCAM-AS1 suppressed the viability and invasion of OS cells, while DSCAM-AS1 overexpression promoted cell viability and invasion. 	32744697
DSCAM-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	regulation[miR-877-5p/ATXN7L3 axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 In this research, our findings presented that DSCAM-AS1 expression was up-regulated in CC cells. Our findings clarified that DSCAM-AS1 played as an oncogenic lncRNA by targeting miR-877-5p/ATXN7L3 axis to promote CC progression, which may provide insights into the prevention of CC.		Yes	DSCAM-AS1 led to the development of CC by enhancing cell proliferation, migration and invasion ability.	31737900
DSCAM-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	 tumor tissues and cell lines	Interaction(miR-136-5p/PBX3 axis)	In Vivo Experiment//Western Blot//ISH//Transfection//qRT-PCR//Luciferase Report Assay//IF	 Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. 		Yes	knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. 	35142595
DNM3OS	LncRNA	Homo sapiens	Huntington Disease	HD PC12 cells	Interaction(miR-196b-5p/GAPDH pathway )	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	Our results show that GAPDH and DNM3OS were upregulated in HD PC12 cells, downregulation of which lead to inhibition of aggregate formation accompanied by a decreased apoptosis rate and increased relative ROS levels and cell viability. Moreover, upregulated DNM3OS decreased the expression of miR-196b-5p by sponging, and GAPDH was a direct target of miR-196b-5p, playing an important pathogenic role in the formation of aggregates in the HD cell model. 		Yes	Our results show that GAPDH and DNM3OS were upregulated in HD PC12 cells, downregulation of which lead to inhibition of aggregate formation accompanied by a decreased apoptosis rate and increased relative ROS levels and cell viability.	34369082
DANCR	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues,cell lines	Regulation[miR-135a/NLRP37 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In pancreatic cancer, DANCR was up-regulated while miR-135a was down-regulated.  A negative relationship was found between DANCR and miR-135a expression. Moreover, we found that miR-135a reversed the effects of DANCR in the promoting of pancreatic cancer cells, which was achieved by regulating the downstream protein of NLRP3. The correlations among DANCR, miR-135a and NLRP3 were confirmed in animal experiments. Conclusion DANCR promoted proliferation and invasion through the regulating of miR-135a / NLRP3 axis in pancreatic cancer cell. Our results suggest that DANCR may be a potential target for the therapy of pancreatic cancer.		Yes	The over-expression of DANCR promoted the proliferation and invasion of pancreatic cancer cells. 	31267381
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[miR-513c/Cul4A/ANXA10 axis]	qRT-PCR	Our data show that lncRNA DLX6-AS1 and Cul4A were highly expressed, while miR-513c and ANXA10 were poorly expressed in HCC tissues and cells.In vivo experiments verified that lncRNA DLX6-AS1 promoted the progression of HCC through the miR-513c/Cul4A/ANXA10 axis.		Yes	Moreover, the silencing of lncRNA DLX6-AS1 impeded the viability, invasion, and migration of HCC cells, while stimulating cell apoptosis. 	33277615
DLX6-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	regulation[FHL2 ,miR-195-5p]	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	DLX6-AS1 and FHL2 were up-regulated in OC tissues and cells, DLX6-AS1, as an oncogene in OC, accelerated tumor progression by up-regulating FHL2 via mediating miR-195-5p, suggesting that DLX6-AS1 was a hopeful target for the lncRNA-targeted therapy in OC.		Yes	DLX6-AS1 knockdown inhibited proliferation, migration, and invasion but induced apoptosis of OC cells. 	32774164
DLX6-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and bladder cell lines	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//Western Blot	 Our results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis.The results from in vitro and in vivo assays implied that DLX6-AS1 exerted enhanced effects on bladder cancer cell proliferation, invasion and migration partly via modulating EMT and the activity of Wnt/β-catenin signaling pathway.	 Our results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis.	Yes	The in vitro experimental data showed that DLX6-AS1 overexpression promoted bladder cancer cell growth, proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT); while DLX6-AS1 inhibition exerted tumor suppressive actions on bladder cancer cells.	31787849
DLX6-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	regulation[miR-195-5p/VEGFA signaling pathway]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	DLX6-AS1 was highly expressed in BC tissues and significant negative correlation with the 5-year survival in the BC patients. Our study demonstrated that DLX6-AS1 played an oncogenic role in BC through miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK pathway.	DLX6-AS1 was highly expressed in BC tissues and significant negative correlation with the 5-year survival in the BC patients. 	Yes	The results showed that the proliferation, migration and invasion activities of BC cells were promoted by DLX6-AS1 overexpression, while cell apoptosis was repressed.	32756011
DLX6-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cell lines	Regulation[miR-641/HOXA9 signaling pathway]	qRT-PCR	DLX6-AS1 was found to be significantly upregulated in OS tissues and OS cell lines. Our results suggested that DLX6-AS1 functions as a ceRNA by targeting miR-641/HOXA9 signal pathway to suppress OS cell proliferation and metastasis.	High expression of DLX6-AS1 was significantly correlated with advanced TNM stage, high tumor grade, and distant metastasis of patients with OS. 	Yes	 Knockdown of DLX6-AS1 suppressed OS cell proliferation, invasion, and migration, and induced cell apoptosis. Knockdown of DLX6-AS1 also suppressed in vivo tumor growth.	30838699
DLX6-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Regulation[DLX6-AS1/miR-141-3p axis]	RNA Pull-Down//Western Blot//RIP//qRT-PCR//Luciferase Report Assay	 In conclusion, the knockdown of DLX6-AS1 might suppress OS progression via sponging miR-141-3p and downregulating Rab10, suggesting a novel DLX6-AS1/miR-141-3p/Rab10 pathway in OS progression.		Yes	Functionally, cell proliferation, migration and invasion were evaluated by utilizing the MTT assay and transwell assays. Xenograft experiments depicted that DLX6-AS1 knockdown restrained the tumor growth of MG-63 cells in vivo. 	35528911
DLX6-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues ,cell lines	Interaction[targeting miR‑199a]	CCK8//qRT-PCR//Luciferase Report Assay	In the present study, DLX6‑AS1 expression was identified to be significantly upregulated in cervical cancer tissues and cell lines by reverse transcription‑quantitative polymerase chain reactions.Bioinformatics analysis predicted that micro RNA (miR)‑199a was a direct target of DLX6‑AS1. 		Yes	Knockdown of DLX6‑AS1 inhibited cell proliferation and induced cell apoptosis. Overexpression of miR‑199a counteracted the role of DLX6‑AS1 in facilitating proliferation and inhibiting apoptosis in in vitro rescue assays. 	30535431
DLX6-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	regulation[miR-16-5p/ARPP19 Axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Elevated DLX6-AS1 expression was disclosed in CC cells. DLX6-AS1 accelerates the progression of CC through sponging miR-16-5p and upregulates ARPP19, which offers a novel insight into prognosis and remedy of CC.		Yes	DLX6-AS1 silence attenuated proliferation, migration, and epithelial-mesenchymal transition program as well as enhanced CC cell apoptosis. 	32077747
DLX6-AS1	LncRNA	Homo sapiens	Glioma	 glioma cells and tissue	Interaction[sponging miR-197-5p ]	qRT-PCR	Here, we demonstrated that DLX6-AS1 expression was both high-expressed in the glioma cells and tissue, and the overexpression of DLX6-AS1 was clinically correlated with the poor outcome of glioma patients. Overall, our finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1, acting as a novel therapeutic target for glioma.	Here, we demonstrated that DLX6-AS1 expression was both high-expressed in the glioma cells and tissue, and the overexpression of DLX6-AS1 was clinically correlated with the poor outcome of glioma patients. 	Yes	In the cellular functional assays, silenced DLX6-AS1 expression by siRNAs inhibited the proliferation, invasion and tumor growth in vitro and in vivo, while the enhanced DLX6-AS1 expression by plasmids promotes them.	30366080
DLX6-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC tissues and cells	Interaction[targeting MiR-199a-5p]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The expression of lncRNA DLX6-AS1 was up-regulated in NPC tissues and cells.We found that DLX6-AS1 was a cancer-promoting lncRNA to facilitate the progression of NPC, and its underlying mechanism was suppressing miR-199a-5p expression. This study can provide novel clues for the treatment of NPC.		Yes	The proliferation, migration, and invasion of NPC were enhanced by overexpressed DLX6-AS1 but inhibited by DLX6-AS1 knockdown.	31782911
DLX6-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	interaction[miR-181b]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The high expression of DLX6-AS1 was observed in pancreatic cancer tissues, and high expression of DLX6-AS1 was positively correlated with larger tumor size, advanced TNM stage and lymph node metastasis.Collectively, our data suggested that DLX6-AS1 promotes cancer cell proliferation and invasion by attenuating the endogenous function of miR-181b in pancreatic cancer.	The high expression of DLX6-AS1 was observed in pancreatic cancer tissues, and high expression of DLX6-AS1 was positively correlated with larger tumor size, advanced TNM stage and lymph node metastasis.	Yes	 Knockdown of DLX6-AS1 dramatically impaired cancer cell proliferation, migration and invasion.	30250401
DLX6-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and PC cell lines	Interaction[miR-497-5p/FZD4/FZD6/Wnt/β-catenin pathway]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	We observed that DLX6-AS1 was highly expressed in PC tissues and PC cell lines, and was negatively correlated with the survival of PC patients. Collectively, these findings suggested that DLX6-AS1/miR-497-5p/FZD4/FZD6/Wnt/β-catenin signaling pathway is involved in the pathogenesis of PC, and DLX6-AS1 could be a potential biomarker and target for PC treatment.	We observed that DLX6-AS1 was highly expressed in PC tissues and PC cell lines, and was negatively correlated with the survival of PC patients. 	Yes	We found that overexpression of DLX6-AS1 promoted proliferation, migration, and invasion of PC cells, inhibited apoptosis, increased Bcl-2, cyclin D1, and MMP-2 expression, and decreased cleaved caspase 3, p27, and E-cadherin expression in PC cells. In addition, overexpression of DLX6-AS1 promoted PC growth by increasing tumor volume and weight and increasing the number of liver and lung metastatic foci. Knockdown of DLX6-AS1 showed an opposite effect in all the experiments. 	31118816
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	non-small-cell lung cancer (NSCLC) cell 	Regulation(wnt/β-catenin pathway)	Other	In conclusion, the exogenous overexpression of a DLX6-AS1-encoded peptide could facilitate NSCLC cell growth by activating wnt/β-catenin pathway.		Yes	The exogenous overexpression of this ORF-encoded peptide promoted NSCLC cell proliferation, migration, and invasion. 	36017915
DLX6-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tissues	Interaction(miR-193b-3p/HOXA1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	DLX6-AS1 and HOXA1 were up-regulated, and miR-193b-3p was down-regulated in TC.DLX6-AS1 targeted miR-193b-3p and positively regulated HOXA1. miR-193b-3p inhibition mitigated the impaired tumorigenesis induced by down-regulated DLX6-AS1. 		Yes	Depleted DLX6-AS1 or restored miR-193b-3p disturbed cell growth and promoted autophagy. 	34514705
DLX6-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial cancer tissues and cells	interaction[ p300/E2F1]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//CHIP//EdU Staining//Transwell Assay	DLX6-AS1 and DLX6 were highly expressed in endometrial cancer tissues and cells, and their silencing weakened the proliferative and invasive abilities of endometrial cancer cells and tumours, while promoting apoptosis.  Mechanistic investigations indicated that DLX6-AS1 formed a triplex structure with DLX6 via interaction with p300/E2F1 acetyltransferase. 		Yes	DLX6-AS1 and DLX6 were highly expressed in endometrial cancer tissues and cells, and their silencing weakened the proliferative and invasive abilities of endometrial cancer cells and tumours, while promoting apoptosis. 	32951317
DLX6-AS1	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues and cell lines	Interaction[targeting miR-424-5p]	RNA Pull-Down//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	In this study, we first demonstrated that lncRNA DLX6 antisense RNA 1 (DLX6-AS1) was upregulated in cancer tissues and cells lines compared with normal adjacent and cell line. Taken together, these results suggested that upregulated DLX6-AS1 promoted cell proliferation, migration, and invasion of HCC through increasing expression of WEE1 via targeting miR-424-5p.		Yes	Knock-down DLX6-AS1 by transfection with small interfering RNA (siRNA) suppressed cell proliferation, migration, and invasion of HCC cells.	30805988
DLX6-AS1	LncRNA	Homo sapiens	Laryngeal Neoplasms	 tumor tissues	regulation[miR-26a/TRPC3 Pathway]	qRT-PCR//Luciferase Report Assay//Western Blot	lncRNA DLX6-AS1 had increased expression in tumor tissues compared with adjacent normal tissues and in higher clinical stages compared with lower stages, which was associated with poor prognosis.This study provides new evidence that a novel lncRNA, DLX6-AS1, regulates mitochondrial calcium homeostasis, respiration and tumor proliferation via modulating the miR-26a/TRPC3 axis in laryngeal cancer.	ncRNA DLX6-AS1 had increased expression in tumor tissues compared with adjacent normal tissues and in higher clinical stages compared with lower stages, which was associated with poor prognosis.	Yes	 In detail, DLX6-AS1 knockdown decreased cell proliferation and affected key mitochondrial metabolic parameters in both HEp-2 and Tu-177 cells. 	32368147
DLX6-AS1	LncRNA	Homo sapiens	Neuroblastoma	 NB tissues and cell lines	Interaction[miR-107/BDNF pathway]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	 The expression of DLX6-AS1 was increased in NB tissues and derived cell lines, and high expression of DLX6-AS1 was positively correlated with advanced TNM stage and poor differentiation.Overall, our finding supports that DLX6-AS1 promotes NB progression by regulating miR-107/BDNF pathway, acting as a novel therapeutic target for NB.	 The expression of DLX6-AS1 was increased in NB tissues and derived cell lines, and high expression of DLX6-AS1 was positively correlated with advanced TNM stage and poor differentiation.	Yes	Knockdown of DLX6-AS1 induced neuronal differentiation, apoptosis and inhibited the growth, invasion, and metastasis of NB cells in vitro and impaired tumor growth in vivo. 	31787850
DLX6-AS1	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	regulation[miR-513c-5p/PLK4 axis]	qRT-PCR	Our data showed that DLX6-AS1 was significantly overexpressed in NB tissues and cells. Our findings identified a novel regulatory mechanism, the DLX6-AS1/miR-513c-5p/PLK4 axis, in NB progression, highlighting a strong rationale for developing DLX6-AS1 as a new target for NB management.		Yes	Moreover, DLX6-AS1 silencing repressed NB cell viability, colony formation, migration, and invasion, and promoted cell cycle arrest and apoptosis in vitro, as well as decreased tumor growth in vivo. 	33031637
DLX6-AS1	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	regulation[STAT2,miR-506-3p]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	DLX6-AS1 expression was highly elevated in NB tissues and cells.DLX6-AS1 regulated cell proliferation, cell cycle and glycolysis in vitro and tumor growth in vivo to promote the development of NB by upregulating STAT2 via targeting miR-506-3p.		Yes	DLX6-AS1 deficiency inhibited NB cell proliferation, cell cycle and glycolysis in vitro.Moreover, DLX6-AS1 deficiency weakened tumor growth in vivo.	32904436
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cells	Regulation[Notch signaling pathway]	qRT-PCR//Western Blot	We first verified the increased expression of DLX6-AS1 in EOC patient samples and cell lines.Mechanistic studies revealed that the knockdown of DLX6-AS1 down-regulated Notch1, p21, and Hes1, indicating that the activity of the Notch signaling pathway was inhibited.	 Clinical assays indicated that high DLX6-AS1 was significantly associated with FIGO stage, lymph node metastasis and poor prognosis. Furthermore, multivariate Cox regression analysis confirmed DLX6-AS1 as an independent prognostic factor in EOC patients.	Yes	Functionally, the down-regulation of DLX6-AS1 decreased EOC cells proliferation, migration, invasion and induced cell cycle G1/S phase arrest and cell apoptosis. 	31081076
DNAJC3-DT	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer cells	regulation[miR-214-3p/LIVIN axis]	Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The highest level of DNAJC3-AS1 was found in LoVo cells, followed by Caco-2 cells (Figure 1(a)). These findings suggested that DNAJC3-AS1 may promote colon cancer progression by regulating the miR-214-3p/LIVIN axis.		Yes	We found that the down-regulation of DNAJC3-AS1 inhibited the proliferation of colon cancer cells and induced growth arrest. Down-regulation of DNAJC3-AS1 also inhibited the migration, invasion, and epithelial-mesenchymal transition (EMT) of colon cancer cells. 	32352854
DLX6-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[PI3K/AKT/mTOR pathway]	CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	DLX6-AS1 was up-regulated in 60 CRC tissues when compared to normal adjacent colorectal tissues.In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation, invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.	DLX6-AS1 was up-regulated in 60 CRC tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. 	Yes	The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion, and migration, but inhibited cell apoptosis; while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. 	31646562
DNAJC3-DT	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tissues and cell lines	Interaction(miR-27a-3p/PRDM14 axis)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	The expression of DNAJC3-AS1 was upregulated in ccRCC tissues and cell lines compared to their normal counterparts. Moreover, we also found that DNAJC3-AS1 acted as a sponge of miR-27a-3p and identified PRDM14 as a target of miR-27a-3p.		Yes	 In vitro, silencing DNAJC3-AS1 reduced the proliferation, migration and invasion of ccRCC cells. Downregulation of DNAJC3-AS1 also led to the apoptosis of ccRCC cells.	33629299
DNAJC3-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-27b )	BrdU//qRT-PCR//RNA Pull-Down	DNAJC3-AS1 was overexpressed in HCC and predicts the poor survival. MiR-27b was downregulated at mature miRNA level, but upregulated at premature level. DNAJC3-AS1 directly interacted with premature miR-27b and was localized to both nuclear and cytoplasm. DNAJC3-AS1 overexpression upregulated premature miR-27b and downregulated mature miR-27b, while DNAJC3-AS1 knockdown led to the opposite results. 		Yes	 DNAJC3-AS1 suppressed the role of miR-27b in inhibiting cell proliferation.	34815712
DNAH17-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC specimens and cell lines	regulation[miR-877-5p/CCNA2 pathway]	qRT-PCR	We observed that the expression of DNAH17-AS1 and CCNA2 mRNA was distinctly upregulated in NSCLC specimens and cell lines, while miR-877-5p expression was significantly decreased.Overall, we identified a novel NSCLC-related lncRNA, DNAH17-AS1 which may exert an oncogenic function via serving as a sponge for miR-877-5p to upregulate CCNA2.	Clinical assays revealed that high DNAH17-AS1 was associated with TNM stage, distant metastasis and shorter overall survival and disease-free survival.	Yes	 Functional assays indicated that knockdown of DNAH17-AS1 suppressed the proliferation, migration and invasion of H1299 and 95D cells, and promoted apoptosis. 	32981678
DNAH17-AS1	LncRNA	Homo sapiens	Pancreatic Carcinoma	PC cells 	regulation[ miR-432-5p/PPME1 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	DNAH17-AS1 was upregulated in PC cells and was associated with aggressive tumor behavior and poor prognosis for patients. 	DNAH17-AS1 was upregulated in PC cells and was associated with aggressive tumor behavior and poor prognosis for patients.  DNAH17-AS1 functions in PC as a tumor promoter by regulating the miR-432-5p/PPME1 axis. 	Yes	 Silencing DNAH17-AS1 promoted the apoptosis and reduced the viability, invasion, and migration of PC cells.	32351291
DNACR	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue and cell lines	Interaction[regulating miR-216a-5p]	Flow Cytometry//qRT-PCR//Western Blot//Transwell Assay	We found that a significantly elevated of DNACR was detected in osteosarcoma tissue and cell lines.DANCR was a sponge of miR-216a-5p activity. DANCR regulated survival of osteosarcoma through targeting miR-216a-5p. Additionally, SOX5 was a direct target of miR-216a-5p, overexpression miR-216a-5p exerted inhibition effects via down-regulating SOX5 expression. Furthermore, DANCR regulated SOX5 expression by sponging to miR-216a-5p. In conclusion, LncRNA DANCR silence inhibits SOX5-medicated progression and autophagy in osteosarcoma via regulating miR-216a-5p which indicating DANCR may act as a potential prognostic biomarker and therapeutic target for osteosarcoma.		Yes	Functional experiments suggested that down-regulation of DANCR inhibited cells proliferation, migration, invasion and autophagy but induced apoptosis in osteosarcoma in vitro.Additionally, we also determined knockdown of DANCR inhibited the growth and autophagy of osteosarcoma in vivo.	31918278
DMTF1v4	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissue	Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	Compared with para-carcinoma tissue, lncRNA DMTF1v4 in colon cancer tissue was highly expressed (p<0.001). 		Yes	Downregulating lncRNA DMTF1v4 in HT-29 cells showed that lncRNA DMTF1v4 promotes cell proliferation and migration, and suppresses apoptosis (p<0.05).	29949153
DMTF1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-17-5p/SRSF2 Axis]	qRT-PCR	The results showed that MRUL was overexpressed in NSCLC samples and correlated with the poor prognosis of patients who had NSCLC. By combining bioinformatics analysis and experimental validation, we found that MRUL regulated NSCLC progression through promoting SRSF2 by sponging miR-17 in NSCLC cells. 	The results showed that MRUL was overexpressed in NSCLC samples and correlated with the poor prognosis of patients who had NSCLC. 	Yes	Knockdown of MRUL considerably repressed NSCLC cell proliferation, invasion, and migration. 	33123591
DMTF1	LncRNA	Homo sapiens	Osteosarcoma	cancer tissues and cell lines	regulation[ miR-125a-5p/FUT4 Axis]	qRT-PCR	We found that lncRNA MRUL was up-regulated in cancer tissues and cell lines. In conclusion, these results demonstrated that OS-upregulated lncRNA MRUL promoted cell proliferation, and metastasis via negatively regulating miR-125a-5p, and imply that lncRNA MRUL may be a potential biomarker for OS.		Yes	Functional experiments showed that knockdown of lncRNA MRUL inhibited OS cell proliferation, and metastasis. 	32670359
DLX6-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	The data revealed that the expression of DLX6-AS1 was significantly upregulated in GC tissues compared with adjacent paired noncancerous tissues.	Furthermore, the expression of DLX6-AS1 was higher in advanced GC tissue samples (III/IV) compared with the expression in early-stage samples (I/II). Furthermore, the current study demonstrated that a high expression of DLX6-AS1 was significantly associated with advanced clinical stage, lymph node metastasis and distant metastasis.	Yes	 In vitro experimental data indicated that DLX6-AS1 was upregulated in GC cell lines and that the inhibition of DLX6-AS1 markedly reduced GC cell proliferation, colony formation, cell cycle progression, migration and invasion. Further investigation revealed that knockdown of DLX6-AS1 inhibited EMT in GC cells.	31105791
DLX6-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 cell lines	Interaction[FUS-regulated MAP4K1]	Western Blot//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	Firstly, we measured DLX6-AS1 expression in GC and then found the elevated level of DLX6-AS1.In summary, DLX6-AS1 modulated GC progression through FUS-regulated MAP4K1.		Yes	The silencing of DLX6-AS1 suppressed cell proliferation, migration and EMT process of GC cells. 	31591939
DLX6-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Regulation[ miR-204-5p/OCT1 axis ]	qRT-PCR//ChIP//Luciferase Report Assay//Western Blot	We first demonstrated that DLX6-AS1 was upregulated in GC tissues and cell lines and was associated with T3/T4 invasion, distant metastasis and poor clinical prognosis.This study revealed that OCT1-induced DLX6-AS1 promoted GC progression and the EMT via the miR-204-5p/OCT1 axis, suggesting that this lncRNA might be a promising prognostic biomarker and therapeutic target for GC.	We first demonstrated that DLX6-AS1 was upregulated in GC tissues and cell lines and was associated with T3/T4 invasion, distant metastasis and poor clinical prognosis.	Yes	 Further functional analysis showed that downregulation of DLX6-AS1 inhibited GC cell proliferation, migration, invasion and EMT in vitro. 	31463827
DLX6-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	interaction[Targeting microRNA-4290]	qRT-PCR	DLX6-AS1 was overexpressed in GC tissues and cell lines. LncRNA DLX6-AS1 regulated tumor growth and aerobic glycolysis in GC by targeting miR-4290 and PDK1, suggesting DLX6-AS1 might serve as a novel potential therapeutic target for GC treatment from bench to clinic.		Yes	 DLX6-AS1 knockdown by short hairpin RNA (shRNA) significantly inhibited cell viability and colony formation, and induced apoptosis. DLX6-AS1 silencing impaired aerobic glycolysis but stimulated mitochondrial respiration in GC cells.	32239379
DLX6-AS1	LncRNA	Homo sapiens	Breast Neoplasms	bladder cancer tissues	Regulation[miR-505-3p/RUNX2 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay	 In the current study, the expression of DLX6-AS1 in the BC tissue samples was evaluated and the correlation between DLX6-AS1 expression and clinicopathological parameters were also analyzed. Moreover, luciferase reporter assay validated that DLX6-AS1 acted as an endogenous sponge to miR-505-3p and negatively regulated its expression. Additionally, miR-505-3p inhibited runt-related transcription factor 2 (RUNX2) expression by directly bind to its 3'- untranslated region (3'-UTR) and overexpression of RUNX2 partially reversed the effect of miR-505-3p mimics on BC cell proliferation and invasion. Furthermore, in BC tissues, miR-505-3p expression level was inversely associated with DLX6-AS1 and RUNX2, respectively. In conclusion, these findings demonstrated that DLX6-AS1 functioned as an oncogenic role that promoted BC proliferation and invasion through miR-505-3p/RUNX2 axis, which might serve as a potential therapeutic target for BC treatment.	We found that DLX6-AS1 expression was much higher in tumor tissues than that in adjacent normal tissues and was positively associated with poor prognosis in BC patients.	Yes	DLX6-AS1 knockdown significantly suppressed BC cell proliferation, invasion, migration, and promoted apoptosis.	31705901
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Interaction[downregulating PRR11 expression and upregulating miR-144]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	 DLX6-AS1 and PRR11 were elevated in NSCLC tissues and cells. In addition, DLX6-AS1 and PRR11 were demonstrated to interact with microRNA-144 (miR-144) and DLX6-AS1 upregulated PRR11 expression by acting as a competing endogenous RNA (ceRNA) of miR-144 in NSCLC cells. Furthermore, DLX6-AS1 knockdown suppressed tumor growth in NSCLC in vivo by upregulating miR-144 and downregulating PRR11.		Yes	Knockdown of DLX6-AS1 and PRR11 significantly suppressed cell proliferation, migration and invasion and induced apoptosis in NSCLC cells, which was reversed by PRR11 overexpression. 	30551440
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[miR-27b-3p/ GSPT1 axis]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	DLX6-AS1 was over-expressed in NSCLC tumor tissues and cell lines and its level of expression was found to be associated with tumor size and advanced clinical stage in patients with NSCLC.DLX6-AS1 was found to interact with miR-27b-3p/GSPT1. DLX6-AS1 expression was negatively correlated with miR-27b-3p expression, but positively correlated with GSPT1 expression in NSCLC samples. DLX6-AS1 knockdown also effectively suppressed tumor growth in an in vivo xenograft model. Conclusion: DLX6-AS1 regulated NSCLC progression by targeting the miR-27b-3p/GSPT1 axis, which may provide novel insights for NSCLC prognosis and therapy.	DLX6-AS1 was over-expressed in NSCLC tumor tissues and cell lines and its level of expression was found to be associated with tumor size and advanced clinical stage in patients with NSCLC.	Yes	Downregulation of DLX6-AS1 inhibited cell proliferation, cell clone formation, migration, and invasion of NSCLC cells.	31190891
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,blood,cell lines	Expression[highly expressed]	qRT-PCR	First, it was revealed that the expression levels of DLX6-AS1 were significantly increased in tumor tissues compared with in adjacent normal tissues. In addition, DLX6-AS1 was highly expressed in NSCLC cell lines compared with in BEAS-2B cells. It was subsequently demonstrated that the serum DLX6-AS1 level was significantly higher in patients with NSCLC compared with in healthy controls.	Additionally, the higher DLX6-AS1 expression was associated with advanced disease stage, positive lymph node metastasis and poor tumor differentiation of NSCLC. ROC analysis demonstrated that the sensitivity and specificity of DLX6-AS1 were higher than those of CYFRA21-1, which is a serum marker for NSCLC.	Yes	DLX6-AS1-knockdown inhibited cell proliferation and migration in vitro. 	31612030
DLX6-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	 Interaction(miR-16-5p/BMI1 axis)	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	DLX6-AS1 was overexpressed in NSCLC tissues and cells, and was inextricably linked with the poor prognosis of NSCLC patients. 		Yes	Depletion of DLX6-AS1 oppressed cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) but promoted apoptosis in NSCLC.	35116677
DLX6-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Expression[highly expressed]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	Compared with the paired adjacent noncancerous tissues, DLX6‑AS1 expression was upregulated in the ESCC tissues and significantly associated with differentiation status, Tumor‑Node‑Metastasis stage, distant metastasis, and lymph node metastasis. 	Compared with the paired adjacent noncancerous tissues, DLX6‑AS1 expression was upregulated in the ESCC tissues and significantly associated with differentiation status, Tumor‑Node‑Metastasis stage, distant metastasis, and lymph node metastasis. 	Yes	Knockdown of DLX6‑AS1 significantly suppressed cell proliferation, invasion and migration abilities, and enhanced the apoptotic rate in the two ESCC cell lines.	30592268
DUXAP10	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction(SOX18)	Invasion Assay//Migration Assay//qRT-PCR//MTT//Colony Formation Assay//EdU Staining	 In this study, we identified an lncRNA called DUXAP10 by analysis of GEO data, which was significantly up-regulated in OS tissues and cell lines. Mechanistically, DUXAP10 mainly localized in cytoplasm and could specifically bind to HuR to increase the stability of SOX18 mRNA. Meanwhile, SOX18 knockdown largely reversed increased proliferation of OS cells induced by DUXAP10 overexpression.		Yes	 Experiments in vitro revealed that lncRNA DUXAP10 promoted proliferation, migration, and invasion of OS cells and inhibited their apoptosis. We also demonstrated that DUXAP10 promoted the formation and growth of OS by tumor formation assay.	36053455
DUXAP10	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[ Wnt/β-catenin and PI3K/Akt signaling pathways ]	Western Blot//CCK8//qRT-PCR//MTT//Transwell Assay	The results showed that DUXAP10 is dramatically elevated in HCC tumor tissues and cell lines. Collectively, DUXAP10 plays a critical role in regulating HCC development, potentially by regulating EMT and cell proliferation through the PI3K/Akt and Wnt/β-catenin signaling.		Yes	Knockdown of DUXAP10 by DUXAP10 si-RNA significantly inhibited the cell viability, proliferation and induce the apoptosis of HCC cell line.	30996112
DUXAP10	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Expression[highly expressed]	qRT-PCR//Western Blot	The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues.	Moreover, ONCOMINE database analysis indicated that high DUXAP10 levels were correlated with high clinical stages, inferior TNM classification, and poor overall survival.	Yes	Furthermore, the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin.	33215419
EIF1AX-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC cell 	Interaction(EIF1AX/PCBP1)	In Vivo Experiment//Western Blot//Flow Cytometry//FISH//qRT-PCR//RNA-seq//IHC	Here, using RNA sequencing analysis, we systemically screened and identified the lncRNA eukaryotic translation initiation factor 1A, X-linked (EIF1AX)-AS1, which is aberrantly downregulated in clinical EC tissues and closely correlated with tumor type.Mechanistically, EIF1AX-AS1 interacts with EIF1AX mRNA and poly C binding protein 1 (PCBP1), which promote EIF1AX mRNA degradation. Intriguingly, by interacting with internal ribosome entry site-related protein Y-box binding protein 1 (YBX-1), EIF1AX promotes c-Myc translation through the internal ribosome entry site pathway. c-Myc promotes EIF1AX transcription and thus forms a feed-forward loop to regulate EC cell proliferation. 		Yes	EIF1AX-AS1 markedly inhibited EC cell proliferation and promoted apoptosis in vitro and in vivo.	35080085
EGOT	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	regulation[Hedgehog pathway]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	We observed that EGOT is significantly down-regulated in breast cancer tissues and cell lines, and EGOT expression is negatively correlated with the Ki67 expression.  We conclude that lncRNA EGOT may inhibit breast cancer cell viability and migration via inactivation of the Hh pathway.		Yes	Overexpression of EGOT in BT549 cells decreased cell viability and migration.	32150666
EGOT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-33b-5p/CROT axis]	qRT-PCR	Data from this study revealed that EGOT expression was obviously upregulated in CRC tissues and cell lines, and high EGOT expression indicated poor overall survival of CRC patients. In conclusion, lncRNA EGOT mediates the tumor-facilitating part in CRC via miR-33b-5p/CROT pathway.	Data from this study revealed that EGOT expression was obviously upregulated in CRC tissues and cell lines, and high EGOT expression indicated poor overall survival of CRC patients.	Yes	 Besides, functional assays proved that EGOT knockdown inhibited cell proliferation and promoted cell apoptosis in CRC. 	32373939
EGOT	LncRNA	Homo sapiens	Colonic Neoplasms	Colon Cancer tissues,blood	interaction[microRNA-33a-5p and microRNA-33b-5p]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	The online database and qRT-PCR detection showed that EGOT was highly expression in patients with CC and had good diagnostic value. However, the tumor in nude mice was significantly lessened after knockout of EGOT. Bioinformatic analysis showed that microRNA-33a-5p and microRNA-33b-5p had targeted binding sites with EGOT.	The five-year survival rate of patients with high expression of EGOT decreased. EGOT and TNM staging were independent prognostic factors of patients with CC. 	Yes	Functional analysis revealed that the growth and invasion abilities of cells increased, and the apoptosis rate decreased after overexpression. Upregulation of EGOT inhibited autophagy of CC cells and promoted cell growth.	33408522
EGLN3	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	interaction[IRF7 ,miR-1299]	qPCR//PCR	 The results indicated that circ-EGLN3 was elevated in RCC tissues and cell lines and predicted unfavorable prognosis for the patients with RCC.Collectively, our study suggested that circ-EGLN3 knockdown suppressed RCC progression through acting as a ceRNA to regulate the IRF7 expression by targeting miR-1299. 		Yes	Silenced circ-EGLN3 hindered cell proliferation, migration, and invasion but facilitated apoptosis of RCC cells.	31904147
EGLN3	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC cells and tissues	Interaction(miR-1224-3p/HMGXB3 axis)	Western Blot//Transfection//qRT-PCR//PCR//IF	circ-EGNL3 acts as a sponge for miR-1224-3p, which targeted HMGXB3. Circ-EGNL3 indirectly upregulated HMGXB3 by targeting miR-1224-3p, and overexpression of circ-EGLN3 reversed the repressive effects of miR-1224-3p on RCC.	Circ-EGLN3 was upregulated in RCC cells and tissues and correlated with poor overall survival.	Yes	"Silencing of circ-EGNL3 decreased RCC cell proliferation, migration, and invasion. Mechanistic studies indicated that circ-EGNL3 acts as a sponge for miR-1224-3p, which targeted HMGXB3. Circ-EGNL3 indirectly upregulated HMGXB3 by targeting miR-1224-3p, and overexpression of circ-EGLN3 reversed the repressive effects of miR-1224-3p on RCC.

"	34274607
EGFR-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[EGFR expression]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//EdU Staining	In our study, EGFR-AS1 significantly up-regulated in GC tissues and correlated with tumor size.  Mechanismly, depletion of EGFR-AS1 was found to decrease EGFR expression by reduction of EGFR mRNA stability.	In our study, EGFR-AS1 significantly up-regulated in GC tissues and correlated with tumor size. 	Yes	 Moreover, knock-down of EGFR-AS1 inhibited the proliferation of GC cells via suppressing EGFR-dependent PI3K/AKT pathway in vitro and in vivo. 	30138934
EGFR-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction[Sponging miR-145 ]	Transwell Assay//qRT-PCR//Luciferase Report Assay//Western Blot	Their data showed that EGFR-AS1 and ROCK1 were upregulated in ESCC and positively correlated. Therefore, EGFR-AS1 may upregulate ROCK1 by sponging miR-145 to promote ESCC cell invasion and migration.	Survival analysis showed that high EGFR-AS1 and ROCK1 expression levels predicted poor survival. 	Yes	In esophageal squamous cell carcinoma (ESCC) cells, EGFR-AS1 and ROCK1 overexpression mediated the increased rates of ECSS cell invasion and migration.	31702393
EGFR-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC  tissues	interaction[micorRNA-381,ROCK2 ]	qRT-PCR//Transwell Assay//Western Blot	It was revealed that epidermal growth factor receptor-antisense RNA 1 (EGFR-AS1) was upregulated in BC and positively associated with rho associated coiled-coil containing protein kinase 2 (ROCK2). Therefore, EGFR-AS1 may sponge miR-381 to upregulate ROCK2 in BC, thereby promoting cell invasion and migration.	Analysis of data collected in follow-ups indicated that EGFR-AS1 expression was significantly associated with poorer overall survival of patients with BC. 	Yes	In addition, EGFR-AS1 and ROCK2 overexpression resulted in the promotion of cell invasiveness and migration of HT-1197 BC cells.	32194685
EGFR-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cell lines	Interaction(miR-2355-5p/ACTN4-mediated WNT pathway)	RNA Pull-Down//Western Blot//Transfection//Invasion Assay//Tunel//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	EGFR-AS1 was notably overexpressed in CC cell lines. Mechanistically, up-regulation of EGFR-AS1 was attributed to the activation of H3K27 acetylation (H3K27ac). Further, EGFR-AS1 was revealed to function as miR-2355-5p sponge. Additionally, miR-2355-5p was down-regulated in CC cells and ACTN4 was identified as a target gene of miR-2355-5p. Ultimately, overexpressed ACTN4 could reserve the suppressive role of EGFR-AS1 silencing in CC cell growth. Last but not least, EGFR-AS1 facilitated CC cell growth via ACTN4-mediated WNT pathway.		Yes	 Loss-of-functional experiments revealed that EGFR-AS1 promoted CC cell proliferation, migration and invasion, and suppressed cell apoptosis. Ultimately, overexpressed ACTN4 could reserve the suppressive role of EGFR-AS1 silencing in CC cell growth. Last but not least, EGFR-AS1 facilitated CC cell growth via ACTN4-mediated WNT pathway.	34998421
EGFR-AS1	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	Interaction[miR-133b/RACK1 ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC	 The results indicated that lnc-EGFR-AS1 expression was increased in glioma cells and tissues.These findings elucidated that EGFR-AS1 accelerated cell proliferation, migration, invasion and prevented apoptosis in glioma cells by regulating miR-133b/RACK1, providing new insights for the diagnosis and molecular therapy of GBM.		Yes	EGFR-AS1 knockdown suppressed proliferation, migration and invasion of glioma cells, but induced apoptosis. Additionally, lnc-EGFR-AS1 functioned as a sponge for miR-133b.	31545240
EGFR-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Expression[highly expressed]	qRT-PCR	 It was found that EGFR?AS1 was abnormally upregulated in NSCLC tissues compared with adjacent normal lung tissues. 	 Furthermore, patients with NSCLC with increased expression of EGFR?AS1 had a poor prognosis.	Yes	EGFR?AS1 knockdown significantly inhibited NSCLC malignancy in vitro, including cell proliferation and chemoresistance. 	30431074
EGFR-AS1	LncRNA	Homo sapiens	Kidney Neoplasms	 RCC tissues	Expression[highly expressed]	qRT-PCR//RNA Pull-Down	In our validation cohort (n = 204), EGFR-AS1 was significantly upregulated in RCC tissues (P < 0.001).	Multivariate analysis suggested that higher EGFR-AS1 expression predicted a poor prognosis in RCC patients (high vs low: P = 0.018, HR = 2.204, 95% CI: 1.145-4.241).	Yes	Gain-of-function and loss-of-function studies showed that EGFR-AS1 promoted cell proliferation and invasion in vitro and in vivo.	30770799
EGFEM1P	LncRNA	Homo sapiens	Thyroid Neoplasms	papillary thyroid tumors and thyroid cancer cells 	Interaction(miR-369-3p/TCF4 axis)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Bioinformatics Analysis	The results demonstrated that EGFEM1P was upregulated in papillary thyroid tumors and thyroid cancer cells compared with normal adjacent tissues and human normal thyroid epithelial Nthy-ori 3-1 cell line. In the examined thyroid cancer cells, EGFEM1P was demonstrated to interact with miR-369-3p and decreased miR-369-3p expression levels. Thereafter, TCF4 was determined to be a target gene of miR-369-3p and EGFEM1P promoted TCF4 expression via regulating miR-369-3p expression levels.		Yes	 At last, it was found that EGFEM1P expression promoted rapid cell proliferation and inhibited cell apoptosis in thyroid cancer cells via acting as a miR-369-3p sponge. 	36380872
EFNA1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[ eIF4B]	qRT-PCR	We found that lncRNA-GMAN was significantly overexpressed in HCC tissues.The results demonstrated the stability of p-eIF4B and the elevation of mRNA translation and anti-apoptosis-related protein expression, which further induced proliferation and metastasis of HCC. 	GMAN expression is associated with vascular invasion, histological grade, tumor, node, metastasis (TNM) stage, short overall survival, and disease-free survival. 	Yes	Knockdown of GMAN induced apoptosis and suppressed invasive and migration potential in vitro and vivo, whereas ectopic GMAN expression produced the opposite effect. 	31875526
EBLN3P	LncRNA	Homo sapiens	Colorectal Neoplasms	Ninety-five paired CRC tissue samples 	Interaction( miR-323a-3p)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	 EBLN3P was highly expressed in CRC, and its high expression was distinctly associated with increased tumor size, histology/differentiation and advanced TNM stage, and poor clinical outcome of CRC patients.  Mechanistically, overexpression of EBLN3P exhibited tumorigenic effects through downregulating the inhibitory effects of miR-323a-3p on UHMK1 expression. 	 EBLN3P was highly expressed in CRC, and its high expression was distinctly associated with increased tumor size, histology/differentiation and advanced TNM stage, and poor clinical outcome of CRC patients	Yes	EBLN3P silencing significantly inhibited the proliferation and metastasis and induced the apoptosis of CRC cells.	34109193
EBLN3P	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction(miR-224-5p/Rab10 signaling axis)	CCK8//qRT-PCR	 The increased expression of EBLN3P and Rab10 and decreased expression of miR-224-5p were observed in osteosarcoma tissues and cell lines.Bioinformatics analysis and luciferase assay revealed that EBLN3P could directly interacted with miR-224-5p to attenuate miR-224-5p binding to the Rab10 3'-untranslated region. Furthermore, the mechanistic investigations revealed activation of the miR-224-5p/Rab10 regulatory loop by knockdown of miR-372-3p or overexpression of Rab10, thereby confirming the in vitro role of EBLN3P in promoting osteosarcoma cell proliferation, migration and invasion. 		Yes	Besides, the overexpression of EBLN3P or knockdown of miR-224-5p were revealed to promote the proliferation, migration and invasion of osteosarcoma cells.	33479458
EBLN3P	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cell lines	Interaction( miR-655-3p/Bcl-2 axis)	Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Bioinformatics Analysis	The results revealed that EBLN3P was upregulated, whereas miR-655-3p was downregulated in LUAD cell lines (A549 and NCI-H23).Bioinformatics analysis and dual-luciferase reporter assays indicated that EBLN3P interacted with miR-655-3p. Mechanistically, miR-655-3p inhibits cell viability and induces apoptosis by inhibiting Bcl-2 expression. The high expression of Bcl-2 reversed the impact of miR-655-3p on the inhibition of cell bioactivity and induction of apoptosis in A549 cells.		Yes	Knockdown of EBLN3P notably inhibited the bioactivity and induced apoptosis in A549 cells by upregulating miR-655-3p.	35473552
EBLN3P	LncRNA	Homo sapiens	Liver Neoplasms		regulation[microRNA-144-3p/DOCK4 Signal]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The present study is the first to demonstrate that EBLN3P may act as a ceRNA to modulate DOCK4 expression by competitively sponging miR-144-3p, leading to the regulation of liver cancer progression, which provides new insights for liver cancer diagnosis and treatment.		Yes	The present results revealed that overexpression of EBLN3P or knockdown of miR-144-3p promoted liver cancer cell proliferation, migration and invasion.	33061623
EBLN3P	LncRNA	Homo sapiens	T-cell acute lymphoblastic leukemia	human T-ALL cell lines	Interaction(miR-655-3p)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	The expression of lncRNA EBLN3P was upregulated while that of miR-655-3p was downregulated in human T-ALL cell lines and lncRNA EBLN3P negatively regulated miR-655-3p.		Yes	LncRNA EBLN3P knockdown significantly inhibited proliferation, invasion, and migration of Jurkat cells and induced their apoptosis. Downregulating miR-655-3p reversed the effects of lncRNA EBLN3P knockdown on Jurkat cells. 	35220878
EGOT	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue,cell lines	Interaction[Hedgehog Pathway ]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	The expression of EGOT was observably elevated in GC. Moreover, EGOT mediated cyclin D1 expression in GC cells which was regulated by Hedgehog pathway. Further, loss of EGOT downregulated Hedgehog signaling pathway in GC cells. EGOT functions as an oncogene in GC, and may be useful as a conceivable diagnostic and prognostic biomarker for GC tumorigenesis.	Upregulation of EGOT was related with lymphatic metastasis and TNM stage.	Yes	In addition, knockdown of EGOT by siRNA could significantly inhibit GC cell proliferation and arrest cycle progression in G1 phase. 	29209988
EIF3J-DT	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cells	Interaction(EIF3J-AS1/MAFG)	qRT-PCR//Western Blot//Invasion Assay//Migration Assay	In this study, we investigated the high level of EIF3J-AS1 in PCa tissues and cells, and used functional assays to show that knocking down EIF3J-AS1 inhibited PCa cell proliferation and metastatic ability. A preliminary mechanistic investigation also showed that EIF3J-AS1 may increase the expression of MAF bZIP transcription Factor G (MAFG) in PCa. The expression correlation between EIF3J-AS1 and MAFG was found to be positive in PCa tissues. 		Yes	In this study, we investigated the high level of EIF3J-AS1 in PCa tissues and cells, and used functional assays to show that knocking down EIF3J-AS1 inhibited PCa cell proliferation and metastatic ability. 	34976178
DUXAP10	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	interaction[p21]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//ChIP	In this study, DUXAP10 was certified to be upregulated in ESCC tissues and cells.Results of mechanism experiments suggested that DUXAP10 motivated ESCC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21. 	 Besides, it was positively correlated with short survival time. 	Yes	 Moreover, down-expression of DUXAP10 contributed to decreased cell proliferation and metastasis. Silenced DUXAP10 led to increased apoptosis rate and stagnation of cell cycle.	30215547
EIF3J-DT	LncRNA	Homo sapiens	Esophageal Neoplasms	 Eca tissues	interaction[sponging miR-373-3p]	CCK8//qRT-PCR//RIP//Transwell Assay	Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients.	Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. 	Yes	Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments.	32811869
ELFN1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CC cells and tissues	Interaction( ELFN1-AS1/miR-4270/AURKB axis)	qRT-PCR//RIP//Western Blot	It was found that AURKB and ELFN1-AS1 expression was upregulated, whereas miR-4270 was downregulated in CC cells and tissues.  MiR-4270 was predicted to be a target of ELFN1-AS1 and AURKB as a target of miR-4270. Their interactions were further elucidated using luciferase reporter and RNA RIP assays. More importantly, treatment with a miR-4270 inhibitor not only rescued the tumor-suppressing effect of ELFN1-AS1 silencing but also abrogated the tumor suppressor functions of AURKB silencing in CC cells. Taken together, the ELFN1-AS1/miR-4270/AURKB axis facilitates CC tumorigenesis; therefore, targeting this axis might be a promising intervention in preventing CC progression.		Yes	ELFN1-AS1 silencing exhibited anti-proliferative, anti-migratory, and pro-apoptotic effects in CC cells. The tumor-suppressive effect of ELFN1-AS1 silencing was verified using in vivo assays. 	36561847
ELFN1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer cells	Interaction(miR-191-5p/TRIM14 )	Western Blot//Invasion Assay//CCK8//FISH//Luciferase Report Assay//Bioinformatics Analysis	MiR-191-5p contains a binding sequence with ELFN1-AS1 and is downregulated by ELFN1-AS1 in colon cancer cells.  The expression of TRIM14 is inhibited by ELFN1-AS1 siRNA or miR-191-5p mimics in LoVo and HT29 cells. The treatment of the miR-191-5p inhibitor in ELFN1-AS1 knockdown cells can significantly increase cell proliferation and invasion ability. Overexpression of TRIM14 in miR-191-5p-mimic-treated cells can rescue the inhibition of proliferation and invasion caused by miR-191-5p mimics. 		Yes	 The expression of TRIM14 is inhibited by ELFN1-AS1 siRNA or miR-191-5p mimics in LoVo and HT29 cells. The treatment of the miR-191-5p inhibitor in ELFN1-AS1 knockdown cells can significantly increase cell proliferation and invasion ability. Overexpression of TRIM14 in miR-191-5p-mimic-treated cells can rescue the inhibition of proliferation and invasion caused by miR-191-5p mimics. 	35652045
ELFN1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	 OV tissues and cell lines	regulation[miR-497-3p/CLDN4 axis ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that ELFN1-AS1 was significantly upregulated in OV tissues and cell lines. Taken together, our findings indicated that ELFN1-AS1 acted as an oncogene in ovarian cancer through regulating the expression of CLDN4 by directly interacting with miR-497-3p.	High expression of ELFN1-AS1 was associated with poor prognosis in OV patients. 	Yes	 Knockdown of ELFN1-AS1 inhibited the proliferation, migration and invasion of SKOV3 cell lines and repressed tumor growth in xenografted ovarian models. 	32779991
ELFN1-AS1	LncRNA	Homo sapiens	Osteosarcoma	 OS and in OS cells	Interaction(miR-138-5p and miR-1291)	qRT-PCR	The level of ELFN1-AS1 was markedly upregulated in patients with advanced OS and in OS cells. Exosomal ELFN1-AS1 from 143B cells was able to promote macrophage M2 polarization, and M2 macrophage in return facilitated OS progression. Mechanistically, overexpression of ELFN1-AS1 upregulated CREB1 level via sponging miR-138-5p and miR-1291 in macrophage via.		Yes	 In addition, overexpression of ELFN1-AS1 significantly promoted the proliferation, migration and invasion of OS cells, while knockdown of ELFN1-AS1 exhibited the opposite effects. 	35785218
ELFN1-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	ESCA tissues and cell lines	regulation[GFPT1 ,miR-183-3p]	qRT-PCR	The lncRNA ELFN1-AS1 was significantly up-regulated in ESCA tissues and cell lines when compared with the counterparts.  In summary, the results of this study suggest that the lncRNA ELFN1-AS1 facilitates the progression of ESCA by acting as a competing endogenous RNA (ceRNA) to promote GFPT1 expression via sponging miR-183-3p.		Yes	 Down-regulation of ELFN1-AS1 restrained cell proliferation, migration, and invasion of ESCA in vitro. 	32229685
ELFN1-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	 The Cancer Genome Atlas (TCGA)-Pancreatic Adenocarcinoma (PAAD) data set	Expression [highly expressed]	In Vivo Experiment//Western Blot//Wound Healing Assay//Transfection//Flow Cytometry//CCK8//qRT-PCR//IF//IHC//Transwell Assay	Through bio-information analysis and in vitro and in vivo experiments, we found that LncRNA ELFN1-AS1 was highly enriched in pancreatic cancer data sets and highly expressed in pancreatic cancer cell lines and tissues. 		Yes	The knocking down of lncRNA ELFN1-AS1 significantly increased cancer cell death and growth arrest. Xenografts in nude mice showed that the growth of SW1990 cells in the mice group with a stable knock down of lncRNA ELFN1-AS1 was significantly slower than that in the control group.	34164511
ELFN1-AS1	LncRNA	Homo sapiens	Retinoblastoma	retinoblastoma tissues and cell lines	Interaction(miR-4270/SBK1 Axis)	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	ELFN1-AS1 was highly expressed in retinoblastoma tissues and cell lines. ELFN1-AS1 was the competing endogenous RNA for miR-4270 and promoted SBK1expression.	ELFN1-AS1 was positively correlated with retinoblastoma progression and prognosis. 	Yes	ELFN1-AS1 knockdown curtailed retinoblastoma proliferation, migration and invasion. 	33574704
ELF3-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(hnRNPK)	In Vivo Experiment//ChIP//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Transwell Assay	We observed that ELF3-AS1 was highly expressed in GC tissues, and high ELF3-AS1 expression predicted poor prognosis. Mechanistic investigations revealed that ELF3-AS1 may regulate the downstream target gene, C-C motif chemokine 20, by binding with the RNA-binding protein hnRNPK. 	We observed that ELF3-AS1 was highly expressed in GC tissues, and high ELF3-AS1 expression predicted poor prognosis. T	Yes	 The knockdown of ELF3-AS1 significantly inhibited cell proliferation, migration, and epithelial-mesenchymal transition and promoted apoptosis. 	34418240
ELF3-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell and tissues	Interaction(SNAI2-ELF3-AS1 feedback loop )	RNA Pull-Down//Western Blot//FISH//RIP//RNA-seq	The ELF3 gene and antisense lncRNA ELF3-AS1 were both transcriptionally repressed by SNAI2 or SNAI1. Down-regulation of ELF3-AS1 and ELF3 predicted poor prognosis in GC. ELF3-AS1 mainly inhibited GC metastasis by repressing SNAI2 signaling. Additionally, ELF3-AS1 modulated ELF3 mRNA stability by RNA-RNA interaction. The RNA duplexes formed by ELF3 mRNA and lncRNA ELF3-AS1 directly interacted with the double-stranded RNA (dsRNA) binding protein complex ILF2/ILF3 (NF45/NF90). In turn, the ILF2/ILF3 complex dynamically regulated the expression of ELF3-AS1 and ELF3 by affecting the dsRNA stability.	Down-regulation of ELF3-AS1 and ELF3 predicted poor prognosis in GC. 	Yes	lncRNA ELF3-AS1 negatively regulated GC cell cycle progression via suppressing G1/S transition and histone synthesis. 	36457025
ELF3-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[Downregulating miR-212]	qRT-PCR//Colony Formation Assay//Transwell Assay	In this study, the authors observed that ELF3-AS1 was upregulated in NSCLC tissues in comparison with that in paired nontumor tissues collected from 68 NSCLC patients.Therefore, ELF3-AS1 is upregulated in NSCLC and promotes cancer cell invasion and migration by downregulating miR-212 through methylation.		Yes	In addition, overexpression of ELF3-AS1 inhibited the role of miR-212 in suppressing cancer cell invasion and migration.	32598181
ELF3-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissue 	Regulation[ELF3-AS1/KLF8 signaling]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Microarray	ELF3-AS1 was highly expressed in bladder cancer and correlated with poor prognosis.Furthermore, ELF3-AS1 could interact with KLF8 to stabilize KLF8 by protecting it from proteasome-mediated degradation. KLF8 in turn could bind ELF3-AS1 promoter and transactivate ELF3-AS1 expression. The positive feedback loop between ELF3-AS1 and KLF8 enhanced KLF8 signaling by increasing MMP9 expression. Collectively, our study has unraveled a novel mechanism of ELF3-AS1-mediated oncogenesis in bladder cancer by reinforcement of ELF3-AS1/KLF8 signaling with potential implications for therapeutic intervention.		Yes	 ELF3-AS1 could increase viability and migration of bladder cancer cells in vitro and promoted xenograft tumor growth in vivo. 	30528231
ELF3-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[KLF12,miR-205 ]	CCK8//qRT-PCR//Western Blot	It was found that ELF3-AS1 was upregulated in OS tissues, and ELF3-AS1 expression level increased with increasing clinical stage.	It was found that ELF3-AS1 was upregulated in OS tissues, and ELF3-AS1 expression level increased with increasing clinical stage.	Yes	 ELF3-AS1 and KLF12 overexpression resulted in an increased proliferation rate in OS cells, while miR-205 played an opposite role and attenuated the effects of ELF3-AS1 overexpression.	32194747
ELF3-AS1	LncRNA	Homo sapiens	Glioma	glioma specimens	Expression[highly expressed]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The ELF3-AS1 expression level was significantly higher in glioma specimens compared with adjacent nontumor specimens (p < 0.01). 	A high expression of ELF3-AS1 was shown to be associated with the WHO grade (p = 0.023) and KPS score (p = 0.012). ROC assays revealed that high ELF3-AS1 expression had an AUC value of 0.8073 (95% CI: 0.7610 to 0.8535) for glioma. Using the Kaplan-Meier analysis, we found that patients with a high ELF3-AS1 expression had significantly poor OS (p = 0.006) and DFS (p = 0.0002). In a multivariate Cox model, we confirmed that ELF3-AS1 expression was an independent poor prognostic factor for glioma patients. 	Yes	The functional assay revealed that knockdown of ELF3-AS1 suppressed the proliferation and invasion of glioma cells.	33014189
ELF209	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Interaction[HNRNPAB]	Western Blot//ISH//Migration Assay//qRT-PCR//FISH//RIP//Microarray//Invasion Assay//ChIP	Furthermore, we found lnc-ELF209 could stabilize TPI protein expression. We also found that lnc-ELF209 overexpression in HCCLM3 cell resulted in a lower rate of lung metastatic, which suggested a less aggressive HCC phenotype. Collectively, these findings offer new insights into the regulatory mechanisms that underlie HNRNPAB cancer-promoting activities and demonstrate that lnc-ELF209 is a HNRNPAB-regulated lncRNA that may play an important role in the inhibition of HCC progression.		Yes	 Up/downregulation assays and rescue assays indicate that lnc-ELF209 inhibits cell migration, invasion and epithelial-mesenchymal transition regulated by HNRNPAB. 	31090062
ELDR	LncRNA	Homo sapiens	Mouth Neoplasms	OSCC samples and cell lines	regulation[ILF3-cyclin E1 signaling]	Flow Cytometry//qRT-PCR//RNA Pull-Down//FISH	Here, we show that ELDR is highly expressed in OSCC patient samples and in cell lines.  We further show that the ELDR-ILF3 axis regulates Cyclin E1 expression and phosphorylation of the retinoblastoma (RB) protein.		Yes	Overexpression of ELDR in normal non-tumorigenic oral keratinocytes induces cell proliferation, colony formation, and PCNA expression. We also show that ELDR depletion reduces OSCC cell proliferation and PCNA expression. 	33043604
EIF4G3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction( miR-4449/SIK1 axis)	Transfection//Co-IP//RIP//IP//IHC//IF	Downregulated expression of circular RNA EIF4G3 (circEIF4G3; hsa_circ_0007991) was found in GC and was associated with poor clinical outcomes.  Mechanistic studies revealed that circEIF4G3 bound to δ-catenin protein to promote its TRIM25-mediated ubiquitin degradation and interacted with miR-4449 to upregulate SIK1 expression.	Downregulated expression of circular RNA EIF4G3 (circEIF4G3; hsa_circ_0007991) was found in GC and was associated with poor clinical outcomes. 	Yes	Overexpression of circEIF4G3 suppressed GC growth and metastasis through the inhibition of β-catenin signaling, whereas knockdown of circEIF4G3 showed the opposite effects. 	35780119
EIF3J-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Regulation[miR-3163/YAP1 axis]	Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	Results showed that EIF3J-AS1 was upregulated in CRC tissues and cell lines. In conclusion, we first found that H3K27 acetylation-induced lncRNA EIF3J-AS1 improved proliferation and impeded apoptosis of colorectal cancer through the miR-3163/YAP1 axis, which might potentially provide a novel molecular-targeted strategy for CRC treatment.		Yes	 The silence of EIF3J-AS1 led to reduced proliferation and facilitated apoptosis of CRC cells.	31709617
EIF3J-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[miR-122-5p/CTNND2 axis]	qRT-PCR	 In the current study, we demonstrated that EIF3J-AS1 expression was obviously upregulated in HCC tissues compared to adjacent noncancerous tissues. Mechanistically, EIF3J-AS1 inversely regulated miR-122-5p expression via acting as a competing endogenous RNA (ceRNA) in HCC cells. Furthermore, catenin delta 2 (CTNND2) was recognized as a novel target of miR-122-5p. CTNND2 restoration partially reversed EIF3J-AS1 knockdown-induced inhibitory effects on HCC cell proliferation, migration and invasion. Importantly, we found that hypoxia induced EIF3J-AS1 and CTNND2 expression, and led to miR-122-5p downregulation in HCC cells. 	Notably, the expression of EIF3J-AS1 was correlated with prognostic features including tumor size, vascular invasion and tumor stage. 	Yes	 EIF3J-AS1 knockdown remarkably suppressed the proliferation, migration and invasion of HCC cells.	31421822
E2F4as	LncRNA	Homo sapiens	Ovarian Neoplasms	blood	Expression[highly expressed]	qRT-PCR	Results: The expression of E2F4as was significantly higher in the serum of OC patients than in that of control patients (p < 0.05).		Yes	The knockdown of E2F4as in ovarian cancer cells led to a decrease in cell proliferation, invasion and migration and an increase in apoptosis. 	33287341
E2F	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[RUNX2]	CCK8//qRT-PCR//IHC//Western Blot	We found that lncRNA EPEL and Runt-related transcription factor 2 (RUNX2) were both Expression[Expression[up-expression]-expression]regulated in gastric cancer. EPEL and RUNX2 were positively correlated in tumor.  Consistently, EPEL overexpression resulted in Expression[Expression[up-expression]-expression]regulated RUNX2 expression, while RUNX2 overexpression did not affect lncRNA EPEL expression.	 Patients with high expression level of lncRNA EPEL showed poor survival.	Yes	LncRNA EPEL and RUNX2 overexpression promoted, while lncRNA EPEL siRNA silencing inhibited the migration, proliferation, and invasion of gastric cancers.	31584135
DXL6-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Regulation[miR-223-HSP90B1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 Moreover, lncRNA DXL6-AS1 was upregulated in BC tissues and functioned as a sponge for miR-223 and reduced its expression in BC cells, thereby enhancing cell proliferation and invasion.		Yes	 Moreover, lncRNA DXL6-AS1 was upregulated in BC tissues and functioned as a sponge for miR-223 and reduced its expression in BC cells, thereby enhancing cell proliferation and invasion.	31615303
DUXAP9	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	Interaction[ LINC01296/miR-598/Twist1 ]	qRT-PCR	"The results illustrated that the elevated LINC01296 expression in NSCLC tissue specimens and cell lines were closely correlated with the poor prognosis of patients with NSCLC.Mechanical studies showed that INC01296 harbored miR-598, acting as a microRNA ""sponge."" Besides, miR-598 targeted the 3'-UTR of Twist1. Interestingly, transcription factor Twist1 could bind with the promoter of INC01296 and activate its transcriptional level. In summary, we conclude that INC01296/miR-598/Twist1 constitutes a positive feedback loop to promote the tumorigenesis of NSCLC, providing a novel insight and a valuable therapeutic strategy."		Yes	Functional studies revealed that LINC01296 knockdown silenced by small interfering RNAs inhibited proliferation, accelerated apoptosis in vitro, and impaired tumor growth in vivo.	30240003
DUXAP8	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	interaction[EZH2 and H3K27me3]	RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//EdU Staining//Transwell Assay	The levels of lncRNA DUXAP8 were significantly increased in CRC tissues and CRC cell lines. Our data indicated that lncRNA DUXAP8 could induce the progression of CRC by negatively regulating E-cadherin via interaction with EZH2 and H3K27me3.		Yes	Knockdown of lncRNA DUXAP8 inhibited cell proliferation and the EMT process, and increased cell apoptosis, and overexpression of lncRNA DUXAP8 had an opposite effect. 	33149618
DUXAP8	LncRNA	Homo sapiens	Colorectal Neoplasms	human colorectal cancer tissues and cell lines	Interaction(miR-519b/ZNF277 Axis)	CCK8//qRT-PCR//Western Blot	We found that the expression level of Duxap8 in colorectal cancer was closely correlated with tumor size (P = 0.024), tumor depth (P = 0.035) and lymphatic invasion (P =0.067) among 50 colorectal cancer patients. Then, we proved that the expression level of Duxap8 was significantly increased in human colorectal cancer tissues and cell lines. Mechanically, we found that Duxap8 was principally located in the cytoplasm. Furthermore, Duxap8 functioned as a competing endogenous RNA to induce the development and progression of colorectal cancer through sponging miR-519b-3p to upregulate ZNF277.	We found that the expression level of Duxap8 in colorectal cancer was closely correlated with tumor size (P = 0.024), tumor depth (P = 0.035) and lymphatic invasion (P =0.067) among 50 colorectal cancer patients. Then, we proved that the expression level of Duxap8 was significantly increased in human colorectal cancer tissues and cell lines. 	Yes	 Functionally, Duxap8 knockdown inhibited the proliferation and induced the apoptosis of colorectal cancer cells, while Duxap8 overexpression facilitated the proliferation and suppressed the apoptosis in colorectal cancer in vitro. Moreover, knockdown of Duxap8 inhibited the size and weight of tumors in mice injected with colorectal cancer cells, overexpression of Duxap8 promoted the growth of colorectal cancer cells in vivo. 	34511937
DUXAP8	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cells	Interaction(miR-223-3p/CXCR4 axis)	CCK8//qRT-PCR//Wound Healing Assay	We found that knockdown of DUXAP8 inhibited the proliferation, migration, and invasion of PTC cells. DUXAP8 could sponge miR-223-3p through the specific binding site. CXCR4 was a target of miR-223-3p. 		Yes	We found that knockdown of DUXAP8 inhibited the proliferation, migration, and invasion of PTC cells. DUXAP8 could sponge miR-223-3p through the specific binding site. CXCR4 was a target of miR-223-3p. 	33522355
DUXAP8	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 tissues	Interaction(miR‑20b‑5p/SOS1 axis)	qRT-PCR//Luciferase Report Assay//RIP	 The analysis of the TCGA‑THCA data revealed that DUXAP8 was one of the most significantly upregulated lncRNAs in PTC. This finding was further confirmed in tissues from patients with PTC.  The results of the present study also revealed that miR‑20b‑5p could directly target DUXAP8. 	Increased DUXAP8 expression was associated with higher grade and poorer prognosis in patients with PTC.	Yes	In PTC cell lines, silencing of DUXAP8 expression with small interfering RNA‑DUXAP8 (si‑DUXAP8) induced cell apoptosis and attenuated cell proliferation. Additionally, transfection of PTC cells with si‑DUXAP8 decreased the phosphorylation levels of MEK1/2 and ERK1/2, as well as downregulated the expression of son of sevenless 1 (SOS1), cyclin D1 (CCND1) and c‑Myc. 	33760128
DUXAP8	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	interaction[Sponging MiR-490-5p]	Flow Cytometry//qRT-PCR//Western Blot	In this study, we found that lncRNA DUXAP8 was upregulated in tumor samples and served as an oncogene in HCC.Mechanically, the present study showed that DUXAP8 serves as a sponge of MiR-490-5p to promote the expression of BUB1 in HCC.		Yes	The knockdown of DUXAP8 significantly suppresses cell proliferation and the cell cycle but induces cell apoptosis in HCC.	32849765
DUXAP8	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC clinical samples	regulation[miR-422a/PDK2 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 DUXAP8 expression HCC clinical samples was significantly increased and this was correlated with unfavorable pathological indexes.DUXAP8 was a sponge of tumor suppressor miR-422a in HCC, enhanced the expression of PDK2 indirectly, and functioned as an oncogenic lncRNA.	High expression of DUXAP8 was associated with shorter overall survival time of patients.	Yes	Its overexpression remarkably facilitated the proliferation, metastasis, and epithelial-mesenchymal transition of HCC cells. Accordingly, knockdown of it suppressed the malignant phenotypes of HCC cells.	32022476
DUXAP8	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-9-3p/IGF1R axis)	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	DUXAP8 and IGF1R were upregulated and miR-9-3p was downregulated in HCC tissues and cells compared with adjacent healthy tissues and a normal liver cell line, respectively. In addition, compared with the corresponding control groups, DUXAP8 knockdown and miR-9-3p overexpression suppressed proliferation, migration and invasion, which was reversed by miR-9-3p inhibitor and IGF1R overexpression, respectively. 		Yes	In addition, compared with the corresponding control groups, DUXAP8 knockdown and miR-9-3p overexpression suppressed proliferation, migration and invasion, which was reversed by miR-9-3p inhibitor and IGF1R overexpression, respectively. 	34035852
DUXAP8	LncRNA	Homo sapiens	Ovarian Neoplasms	cells 	interaction[targeting miR-590-5p]	qRT-PCR//Luciferase Report Assay//Western Blot	Compared with normal ovarian cells, the expression of DUXAP8 in ovarian cancer cells was significantly increased, while the expression of miR-590-5p was decreased (p < 0.05).Taken together, lncRNA DUXAP8 can regulate the proliferation and apoptosis of ovarian cancer cells, and its mechanism may be related to the regulation of YAP1 gene by targeting miR-590-5p.		Yes	After DUXAP8 interference, cell proliferation and colony formation were decreased, and apoptosis was increased. The results of in vivo experiment are consistent with the in vitro experiments. 	32749665
DUXAP8	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Regulation[PTEN]	CCK8//qRT-PCR//Colony Formation Assay	LncRNA DUXAP8 expression was higher in bladder cancer tissues; it was in a positive correlation with the TNM stage and tumor size, but negatively correlated with the total survival time.Our results pointed out that lncRNA DUXAP8 was overexpressed in bladder cancer tissues, which can promote the progression of bladder cancer through inhibiting PTEN.	LncRNA DUXAP8 expression was higher in bladder cancer tissues; it was in a positive correlation with the TNM stage and tumor size, but negatively correlated with the total survival time.	Yes	Knockdown of DUXAP8 decreased cell viability and cellular proliferation.	29917188
DUXAP8	LncRNA	Homo sapiens	Osteosarcoma	 OS samples and OS cell lines 	Interaction(miR‑635/TOP2A axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The expression of lnc‑DUXAP8 was significantly upregulated in OS samples and OS cell lines compared with normal tissues.		Yes	 Knockdown of lncRNA DUXAP8 inhibited proliferation, migration and invasion in OS cells. Notably, mechanistic investigation revealed that lncRNA DUXAP8 predominantly acted as a competing endogenous RNA in OS by regulating the miR‑635/topoisomerase alpha 2 (TOP2A) axis.	33982765
DUXAP8	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	Interaction( miR-1297/RCN2)	In Vivo Experiment//RNA Pull-Down//Transfection//Tube Formation Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	DUXAP8 was notably upregulated in CC cells. Mechanically, DUXAP8 boosted the expression of reticulocalbin-2 (RCN2) through relieving the binding of miR-1297 to RCN2 3'-UTR. Moreover, miR-1297 inhibition and RCN2 overexpression could counteract the inhibitory effects of DUXAP8 knockdown on the malignant phenotypes of CC cells. 		Yes	 Downregulation of DUXAP8 repressed cell malignant behaviors and angiogenesis in CC. 	34774078
DUXAP8	LncRNA	Homo sapiens	Glioma	glioma tissues	Expression[highly expressed]	CCK8//qRT-PCR//Colony Formation Assay	 In the present study, it was revealed that pseudogene DUXAP8 is significantly upregulated in glioma tissues, compared with adjacent normal tissues.	Patients with increased DUXAP8 expression were associated with higher Karnofsky Performance Status, advanced World Health Organization grade, poor disease-free survival and overall survival rates of patients with glioma. 	Yes	 Furthermore, in vitro assays, Cell-Counting Kit-8 cell viability and cell colony forming assays demonstrated that reduced DUXAP8 expression significantly suppressed proliferation capacity.	30867791
DUXAP8	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cells	Interaction(miR-26b-5p)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	our results elucidated that that DUXAP8 promoted tumor progression in LUAD by targeting miR-26b-5p, which provide a novel therapeutic target for diagnosis and therapy of LUAD.		Yes	Loss-of-function experiments were performed to assess the function of DUXAP8 proliferation and apoptosis of H1975 and A549 cells. Functionally, silencing DUXAP8 inhibited proliferation and induced apoptosis of LUAD cells. 	33269379
DUXAP8	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-409-3p/HK2/LDHA axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	DUXAP8 was highly expressed in NSCLC, while miR-409-3p was downregulated. DUXAP8 promoted cell viability, migration and glycolysis by regulating miR-409-3p/HK2/LDHA axis. 	High expression of DUXAP8 was positively related to the grade division and negatively associated with the 5-year survival rate of NSCLC patients.	Yes	Downregulated DUXAP8 significantly suppressed cell growth, metastasis and glycolysis.	32801745
DUXAP8	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[TRIM44-mediated AKT/mTOR pathway]	qRT-PCR//MTT//RNA Pull-Down//Transwell Assay	DUXAP8 and TRIM44 were upregulated in NSCLC tissues and cell lines, while miR-498 was downregulated.Our results identified that LncRNA DUXAP8 could regulate cell proliferation, metastasis and EMT in NSCLC cells by inhibiting miR-498 through the activation of TRIM44-mediated AKT/mTOR pathway.		Yes	 Functionally, knockdown of DUXAP8 could repress proliferation, migration, invasion, Epithelial-Mesenchymal Transition (EMT) and phosphorylation of AKT/mTOR in NSCLC cells.	32271433
DUXAP8	LncRNA	Homo sapiens	Melanoma	melanoma tissue and cells 	Interaction( miR-3182/NUPR1 pathway)	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	lncRNA DUXAP8 was upregulated in melanoma tissue and cells compared with normal tissues and cells.  lncRNA DUXAP8 targeted miR-3182, while miR-3182 targeted NUPR1. The overexpression of NUPR1 reversed the effects of DUXAP8 knockdown or miR-3182 mimic on melanoma progression. 	The levels of DUXAP8 inversely correlated with survival time of patients with melanoma. 	Yes	Knockdown of lncRNA DUXAP8 inhibited proliferation, migration and invasion of melanoma cells.	33981357
DUXAP8	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	DUXAP8 was overexpressed in ESCC tissues than that of normal adjacent tissues.	 DUXAP8 expression was positively correlated to tumor stage and lymph node metastasis, whereas negatively correlated to the survival rate of ESCC patients.	Yes	Cell proliferation, colony formation and invasion abilities were significantly decreased after knockdown of DUXAP8 in ESCC cells. 	29771416
DUXAP8	LncRNA	Homo sapiens	Neuroblastoma	NB tissues	regulation[miR-29 ,NOL4L ]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Collectively, DUXAP8 deteriorated NB through serving as a sponge for miR-29 to up-regulate the expression of NOL4L in vitro and in vivo.	We found the expression of DUXAP8 was positively related to the stage of NB tumors, and it was negatively associated with the survival rate of NB patients. 	Yes	DUXAP8 knockdown inhibited the proliferation, colony formation, cycle and motility of NB cells.	32522628
DUXAP8	LncRNA	Homo sapiens	Sinonasal Squamous Cell Carcinoma	 SNSCC cells	Interaction(miR-584-5p/FNDC3B Pathway)	RNA Pull-Down//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	DUXAP8 is overexpressed in SNSCC cells. Furthermore, DUXAP8 up-regulates the expression of FNDC3B via sponging miR-584-5p. Rescue experiments demonstrated that DUXAP8 mediates the progression of SNSCC via up-regulating FNDC3B expression. 		Yes	 Functionally, DUXAP8 silencing suppresses the malignant progression of SNSCC. 	35695194
DUXAP8	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal tissues	Interaction[DUXAP8 ]	CCK8//qRT-PCR//Luciferase Report Assay//ChIP	In this study, we first provided evidence that DUXAP8 was overexpressed in CRC and increasing expression of DUXAP8 indicates advanced clinical progression and poor survival of CRC patients.  Furthermore, an inverse relationship between DUXAP8 and miR-577 was found. In addition, we confirmed that DUXAP8 served as competing endogenous RNA to modulate miR-577, which can modulate RAB14, a well-studied oncogene.		Yes	 Functional assays via in vitro assays revealed that DUXAP8 knockdown through shRNA in HCT116 and LOVO cells inhibited cell proliferation, migration and invasion, and promoted apoptosis. 	31364111
DUXAP8	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[EZH2/LSD1]	CCK8//qRT-PCR//RIP//EdU Staining//Transwell Assay	LncRNA DUXAP8 was Expression[Expression[up-expression]-expression]regulated in CRC tissues and cell lines. Its level remained higher in CRC with larger tumor size or higher tumor grade.RIP assay further demonstrated the interaction between DUXAP8 and LSD1, EZH2. 		Yes	KnockExpression[down-expression] of DUXAP8 sExpression[Expression[up-expression]-expression]pressed the proliferative, migratory and invasive abilities of DLD-1 and SW480 cells. 	31786844
DUXAP8	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung cancer tissues and the normal tissue,cell lines(A549，SPC-A1，SK-MES-1,NCI-H1299)	Expression[highly expressed]	CCK8//qRT-PCR//Invasion Assay//Transwell Assay	The expression of LncRNA DUXAP8 in tumor tissues was significantly higher than that of the normal tissue (P<0.001).Among 4 lung cancer cell lines, LncRNA DUXAP8 in A549 cells was the highest (P<0.001).	 	Yes	 The results indicated that LncRNA DUXAP8 overexpression significantly promoted the A549 cells' proliferation, enhanced invasion and induced tumor growth. Conversely, LncRNA DUXAP8 knockout significantly suppressed A549 cells' proliferation, weakened invasion and inhibited tumor growth.	33817152
DUXAP9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Regulation[miR-485-5p/PAK4 axis ]	Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Our study showed that LINC01296 was over-expressed in OSCC tissues and cell lines. Knockdown of LINC01296 effectively inhibits cell viability, migration and invasion but promotes cell apoptosis in vitro. The in vivo experiment showed that LINC01296 knockdown inhibited OSCC tumor growth. 	The level of LINC01296 was positively correlated with the patient's tumor node metastasis (TNM) stage and nodal invasion.	Yes	 Knockdown of LINC01296 effectively inhibits cell viability, migration and invasion but promotes cell apoptosis in vitro. The in vivo experiment showed that LINC01296 knockdown inhibited OSCC tumor growth. 	35591837
DUXAP9	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[sponging miR-5095]	CCK8//qRT-PCR//Wound Healing Assay//Luciferase Report Assay	In our study, we indicate that the expression of LINC01296 was overexpressed in NSCLC samples compared to adjacent non-tumor tissues. 		Yes	 Ectopic expression of LINC01296 promoted NSCLC cell proliferation and migration.	30899389
DUXAP9	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Regulation[KLF2]	qRT-PCR//RIP//ChIP	In the current study we showed that LINC01296 expression is significantly higher in ESCC tissues when compared with corresponding adjacent normal tissues.Moreover, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays demonstrated that LINC01296 promotes cell proliferation and invasion by epigenetic suppression of KLF2 expression via an interaction with EZH2 in ESCC cells.	Higher LINC01296 expression was associated with lymph node metastasis, TNM stage, and worse overall survival rate in ESCC patients. 	Yes	 Furthermore, functional assays in vitro demonstrated that knockdown of LINC01296 inhibited ESCC cell proliferation, colony formation, migration, and invasiveness. 	30416853
DUXAP9	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cell lines and cancerous tissues	Expression[highly expressed]	qRT-PCR//MTT//Transwell Assay	We found that LINC01296 was upregulated in ESCC cell lines and cancerous tissues, as compared with normal esophagus cells and adjacent normal tissue samples.	High LINC01296 expression was significantly correlated with differentiation grade (p=0.000), lymph nodes metastasis (p=0.002), distant metastasis (p=0.002), and TNM stage (p = 0.015). Moreover, ESCC patients with high LINC01296 expression experienced shorter OS and DFS (p=0.0009 and p=0.0005, respectively). 	Yes	Functionally, the results of in vitro assay indicated that down-regulation of LINC01296 significantly suppressed ESCC cells proliferation, migration, and invasion, suggesting that LINC01296 contributed to tumorigenesis of ESCC.	30058683
DUXAP9	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	LCa tissues	Regulation[regulating microRNA-760 ]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	LINC01296 expression was remarkably higher in LCa tissues than that of normal liver tissues. LINC01296 could promote the proliferative ability and invasiveness of hepatoma cells by inhibiting the expression of microRNA-760. 	 Meanwhile, LINC01296 expression was associated with poor prognosis of LCa. Patients with high LINC01296 expression were more likely to have lymph node metastasis. 	Yes	In vitro experiments showed that the knockdown of LINC01296 significantly inhibited the proliferation and migration of HCC cells. 	31799652
DUXAP9	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue samples and cell lines	regulation[miR-26a/PTEN axis]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Transwell Assay	 Linc01296 expression was increased in both HCC tissue samples and cell lines. These findings indicated that Linc01296 is involved in HCC progression via regulating miR-26a/PTEN.		Yes	Knockdown of Linc01296 suppressed HCC cell processes, such as proliferation, migration and invasion, and enhanced apoptosis in vitro; these effects were reversed by a miR-26a mimic or PTEN overexpression. 	31318685
DUXAP9	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Interaction(3' untranslated region (UTR) of sox9)	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay	 We found that DUXAP9 positively regulated HCC cell stemness, as characterized by the change of sphere-formation ability, ALDH activity and stemness marker expression. 		Yes	We found that DUXAP9 overexpression increased the expression of stemness markers(Nanog, Oct4, ABCG2) (Figure 1(B)–(D)), while DUXAP9 knockdown decreased it.	34086387
DUXAP9	LncRNA	Homo sapiens	Ovarian Neoplasms		Interaction[regulating EMT]	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	We found that LINC01296 was over-expressed in ovarian cancer tissues and cell lines, when comparing with adjacent normal tissue samples and normal cells. Moreover, western blotting analysis displayed that knockdown of LINC01296 significantly increased E-cadherin, but reduced N-cadherin and vimentin expressions in SKOV3 and OVCAR3 cells, compared with no-transfection cells.	Higher LINC01296 expression was significantly correlated with shorter progression-free survival and overall survival. 	Yes	For the functional experiments, knockdown of LINC01296 suppressed cell proliferation, inhibited colony formation ability, abrogated cell migration and invasion potential, and enhanced cell apoptosis. 	31176022
DUXAP9	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues 	Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Microarray//Colony Formation Assay//Transwell Assay	The expression of LINC01296 was significantly higher in most cancer tissues than that in adjacent normal tissues,	The expression of LINC01296 was significantly higher in most cancer tissues than that in adjacent normal tissues, and was positively correlated with clinical stages of the cancer (P=0.016), lymph node metastasis (P=0.034), and pathologic grades (P=0.012). The increased level of LINC01296 was associated with a poorer prognosis and shorter survival of the patients. Multivariate analysis showed that the LINC01296 expression was an independent predictor of overall survival in bladder cancer.	Yes	Additionally, LINC01296 knockdown inhibited the proliferation, migration and progression of cell cycle of bladder cancer cells, and was involved in the regulation of epithelial-mesenchymal transition.	30588032
DUXAP9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	clinical samples and cell lines	Interaction(SRSF1)	qRT-PCR//FISH	LINC01296 was highly expressed in clinical samples and cell lines of oral squamous cell carcinoma. In mechanism, LINC01296 plays a tumor-promoting role by binding to SRSF1 protein.		Yes	Overexpression of LINC01296 promoted the proliferation, invasion, and migration of oral squamous cell carcinoma cells and accelerated the formation of xenografts, while silencing LINC01296 inhibited tumor progression. 	34195277
DUXAP9	LncRNA	Homo sapiens	Neoplasm Metastasis	The matched lung cancer tissue (n=40) and the matched normal lung tissue, Paired colorectal cancer tissue (n=40) and matched normal bowel tissue (n=40) 	Interaction(miR-141-3p/ZEB1-ZEB2 axis)	Transfection//Luciferase Report Assay//Western Blot	 In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis.  We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. 	 In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis.  	Yes	 We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. 	33854632
DUXAP9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell line	Regulation(Wnt and MAPK signaling)	qRT-PCR//Wound Healing Assay	LINC01296 was overexpressed in the TCGA-OSCC datasets.  LINC01296 was overexpressed in OSCC tissues compared with para-carcinoma tissues. Moreover, the expression of linc01296 was higher in CAL-27, HSC-2, and SCC-25 cells than in normal human oral keratinocytes (NHOKs). Functional analysis suggested that LINC01296might be involved in the regulation of the Wnt and MAPK signaling pathways. 	High LINC01296expression was strongly correlated with poor outcomes of OSCC patients. 	Yes	Additionally, LINC01296 deficiency suppressed the growth, migration, and invasion of OSCC cells, whereas overexpression of TFAP2A-AS1 cause opposite results.	35154446
DUXAP9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues	Expression(highly expressed)	qRT-PCR//Transwell Assay	 LINC01296 expression was notably up-regulated in HNSCC, which was associated with promoter hypomethylation. A	Also, it was positively correlated with the HNSCC pathological stage and patients with higher LINC01296 expression levels had a poor prognosis. 	Yes	 LINC01296 silencing inhibits HNSCC cell migration and invasion. LINC01296 also participate in the HNSCC progression mainly through protein phosphorylation and microtubule-based process regulation. 	34515611
DUXAP9	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissue,cell lines	Interaction[Bcl-2/caspase-3 pathway]	qRT-PCR	 LINC01296 was enhanced in PDAC tissues and cell lines. Moreover, silencing of LINC01296 followed by treatment with small interfering RNAs suppressed cell proliferation and promoted cell apoptosis by affecting the Bcl-2/caspase-3 pathway. Importantly, LINC01296 attenuation impaired the migratory and invasive potential partly by reversing EMT.	 LINC01296 was enhanced in PDAC tissues and cell lines, and this overexpression was correlated with advanced tumor stages and positive lymph node metastasis in patients with PDAC. In addition, upregulation of LINC01296 was an independent prognostic predictor for patients with PDAC after surgery.	Yes	Moreover, silencing of LINC01296 followed by treatment with small interfering RNAs suppressed cell proliferation and promoted cell apoptosis by affecting the Bcl-2/caspase-3 pathway.	30203487
DUXAP9	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells and patient tissues	Interaction(miR-143-3p/ATG2B)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Colony Formation Assay	 LINC01296 is the one with the most significant overexpression.  LINC01296 also acts as the sponge of miR-143-3p. Lowering the expression of LINC01296 leads to decreased expression of autophagy-related 2B (ATG2B), a target gene of miR-143-3p. These results demonstrated that the LINC01296/miR-143-3p/ATG2B axis is crucial in promoting the development of NSCLC and paclitaxel resistance. 		Yes	Knockdown of LINC01296 inhibits the growth and migration, arrests the cell cycle, and promotes the apoptosis of NSCLC cells. Knocking down LINC01296 in vivo suppresses tumor growth and metastasis. 	34695177
DUXAP9	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	Interaction(LINC01296/miR-5095/MYCN )	In Vivo Experiment//Western Blot//ISH//Transfection//Migration Assay//FISH//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Invasion Assay	Microarray data analysis and reverse transcription-quantitative polymerase chain reaction analysis demonstrated that LINC01296 was significantly upregulated in human CCA compared with nontumor tissues.Mechanistically, LINC01296 was demonstrated to sponge microRNA-5095 (miR-5095), which targets MYCN proto-oncogene bHLH transcription factor (MYCN) mRNA in human CCA. By inhibition of miR-5095, LINC01296 overexpression upregulated the expression of MYCN and promoted cell viability, migration and invasion in CCA cells. 	Furthermore, the expression of LINC01296 in human CCA was positively associated with tumor severity and clinical stage. 	Yes	Knockdown of LINC01296 dramatically suppressed the viability, migration and invasion of RBE and CCLP1 cells, and promoted cell apoptosis in vitro. Furthermore, LINC01296 knockdown inhibited tumor growth in a xenograft model. 	29620172
DUXAP9	LncRNA	Homo sapiens	Kidney Neoplasms	112 pairs of localized ccRCC tumor tissues	Regulation(IGF2BP2/PI3K/AKT )	RNA Pull-Down//Wound Healing Assay//Flow Cytometry//FISH//CCK8//Colony Formation Assay	In this study, we characterized a lncRNA DUXAP9 and the upregulation of DUXAP9 was analyzed by quantitative real-time PCR in 112 pairs of localized ccRCC tumor tissues compared with adjacent normal tissues. Pull-down, RNA immunoprecipitation and RNA stability assays (involving actinomycin D) showed that DUXAP9 was methylated at N6-adenosine and binds to IGF2BP2, which increases its stability. DUXAP9 activate PI3K/AKT pathway and Snail expression in renal cancer cells.	DUXAP9 expression was an independent risk factor for poor prognosis in localized ccRCC (p<0.05).	Yes	DUXAP9 knockdown in renal cancer cells inhibited renal cancer cells proliferation and motility capacities in vitro and reversed epithelial-mesenchymal transition (EMT), whereas overexpression of DUXAP9 promoted renal cancer cells proliferation and motility capacities in vitro and induced EMT.	34168980
DUXAP9	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cell line	Interaction( miR-584-5p, miR-34a-5p/TRIM59 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The level of LINC01296 and TRIM59 were increased, whereas miR-584-5p and miR-34a-5p levels were reduced in NB tissues in contrast to that in normal tissues. Moreover, miR-584-5p and miR-34a-5p were validated to act as a tumor repressive effect in NB cells by restraining TRIM59. The results also showed that LINC01296 could regulate the development of NB. In mechanism, LINC01296 acted as a miR-584-5p and miR-34a-5p sponge to modulate TRIM59 expression. In addition, LINC01296 knockdown also attenuated tumor growth in vivo. LINC01296 promotes the progression of NB by increasing TRIM59 expression via regulating miR-584-5p and miR-34a-5p, which also offered an underlying targeted therapy for NB treatment.		Yes	For functional analysis, LINC01296 deficiency inhibited the cell vitality, cell proliferation, migration and invasion in NB cells, whereas promoted cell apoptosis. 	35305236
DLX6-AS1	LncRNA	Homo sapiens	Pre-Eclampsia	PE placenta tissues	regulation[ DLX6-AS1/miR-149-5p/ERP44]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 Higher levels of DLX6-AS1 and ERP44, lower level of miR-149-5p were observed in PE placenta tissues.DLX6-AS1 inhibited proliferation and invasion of trophoblast cells, and suppressed angiogenesis of HUVEC cells by miR-149-5p/ERP44 pathway.		Yes	The inhibitory impact of DLX6-AS1 overexpression or ERP44 overexpression on proliferation and invasion of trophoblast cells as well as angiogenesis of HUVEC cells was reversed by up-regulating miR-149-5p.	32250737
DLX6-AS1	LncRNA	Mus musculus	Parkinson Disease	 PD mice	Interaction(miR-223-3p/NRP1 axis)	Flow Cytometry//qRT-PCR//MTT//Western Blot	DLX6-AS1 was overexpressed in PD mice. DLX6-AS1 acted as the ceRNA of miR-223-3p to promote NRP1. Down-regulation of miR-223-3p or overexpression of NRP1 partially annulled the effect of silencing DLX6-AS1 on BV2 microglial inflammation. Overall, DLX6-AS1 promotes the microglial inflammatory response in PD through the ceRNA mechanism of miR-223-3p/NRP1.		Yes	Silencing DLX6-AS1 improved neurological function and alleviated microglial inflammation in PD mice.  Silencing DLX6-AS1 inhibited LPS-induced inflammation of BV2 microglia. 	35550840
DLX6-AS1	LncRNA	Mus musculus	Reperfusion Injury	brain tissues	regulation[miR-149-3p]	qRT-PCR//Luciferase Report Assay//Tunel//Western Blot	 DLX6-AS1 levels were upregulated during ischemia/reperfusion (I/R) and downregulation of DLX6-AS1 reduced acute injury and ameliorated long-term neurological impairments induced by cerebral I/R in mice.Therefore, this suggests that miR-149-3p sponging by DLX6-AS1 may lead to cerebral neuron I/R-induced impairments through upregulation of apoptotic BOK activity, which offers a new approach to the treatment of stroke impairment.		Yes	Additionally, silencing of DLX6-AS1 significantly decreased the neuronal apoptosis in vivo and in vitro.	33216728
DCST1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[AKT/mTOR signaling pathways]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 LncRNA DCST1-AS1 was confirmed hyper-expression both in HCC tissues and HCC cells. Our results suggested that lncRNA DCST1-AS1, as a carcinogenic factor in HCC, promoted cell proliferation, and invasion, inhibited apoptosis and autophagy by modulating the AKT/mTOR signaling cascade.	High expression of lncRNA DCST1-AS1 was significantly correlated with inferior prognosis. 	Yes	 Moreover, lncRNA DCST1-AS1 depletion suppressed proliferation and accelerated apoptosis, activated cycle arrest, restrained cell migration, and stimulated autophagy in HCC cells. 	31364110
DCST1-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissue	interaction[Sponge miR-92a-3p]	qRT-PCR//Transwell Assay//Western Blot	 We in this study found that DCST1-AS1 was upregulated in EC. DCST1-AS1 is downregulated in EC and may sponge miR-92a-3p, thereby promoting cancer cell invasion and migration.	 Survival analysis revealed that high levels of DCST1-AS1 expression predicted poor survival of EC patients.	Yes	Moreover, DCST1-AS1 overexpression led to upregulated Notch1 and increased cancer cell invasion and migration rates.	32110096
DCST1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	regulation[miR-874-3p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 DCST1-AS1 expression was increased in cervical cancer tissues and cells. Inhibition of DCST1-AS1 suppressed the proliferation, migration and invasion of cervical cancer cells by increasing miR-874-3p expression, which could be alleviated by the inhibition of miR-874-3p.		Yes	Inhibition of DCST1-AS1 suppressed the proliferation, invasion and migration of cervical cancer cells and decreased the expression of KI67, proliferating cell nuclear antigen, matrix metalloproteinase (MMP)-2 and MMP-9.	33025624
DCST1-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM tissues	regulation[miR-29b]	qRT-PCR	 It was observed that the upregulation of DCST1-AS1 in GBM predicted poor survival. 		Yes	Overexpression of DCST1-AS1 resulted in increased cell proliferation.	32418155
DCST1-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC patients	Interaction(MiR-665/HOXB5 and MiR-873-5p/CADM1 Pathways)	In Vivo Experiment//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	In this work, we identified a novel lncRNA DC-STAMP domain-containing 1-antisense 1 (DCST1-AS1), which is highly upregulated and correlated with poor survival in EC patients.  Mechanistically, DCST1-AS1 mediated EC progression by inducing the expression of homeobox B5 (HOXB5) and cell adhesion molecule 1 (CADM1), via acting as a competing endogenous RNA for microRNA-665 (miR-665) and microRNA-873-5p (miR-873-5p), respectively. In addition, we found that the expression of miR-665 and miR-873-5p was significantly downregulated, while HOXB5 and CADM1 expression levels were increased in EC tissues. 		Yes	Overexpression of DCST1-AS1 significantly enhanced EC cell proliferation, colony formation, migration, and invasion in vitro and promoted tumor growth of EC in vivo. 	34497766
DCST1-AS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	 CSCC tissues	regulation[ miR-107,CDK6 ]	Western Blot//CCK8//qRT-PCR//MTT//Luciferase Report Assay	We found that DCST1-AS1 was upregulated in CSCC and predicted poor survival.DCST1-AS1 may sponge miR-107 to upregulate CDK6 in CSCC.	 We found that DCST1-AS1 was upregulated in CSCC and predicted poor survival.	Yes	Moreover, overexpression of DCST1-AS1 led to upregulate CDK6 and increase cell proliferation rate, while overexpression of miR-107 played an opposite role and attenuate the effects of overexpression of DCST1-AS1.	32943926
DCAF1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction(miR-93-5p/FRMD6 axis)	colony Formation Assay//RNA Pull-Down//IHC//Western Blot//Transfection//qPCR//Colony Formation Assay//Flow Cytometry//RIP//MTT//PCR//IP//Transwell Assay//IF	 Circ_VPRBP was down-regulated in cervical cancer tissues and cells, and overexpression of circ_VPRBP inhibited proliferation and promoted apoptosis of Caski and C33A cells. MiR-93-5p was a target of circ_VPRBP, and miR-93-5p mimic reversed the effect of circ_VPRBP on cell behavior. FRMD6 was a downstream target of miR-93-5p, and down-regulated FRMD6 reversed the cell viability, migration and invasion of cervical cancer cells inhibited by anti-miR-93-5p. Circ_VPRBP inhibited tumor growth by regulating miR-93-5p and FRMD6 in vivo.		Yes	Circ_VPRBP was down-regulated in cervical cancer tissues and cells, and overexpression of circ_VPRBP inhibited proliferation and promoted apoptosis of Caski and C33A cells. 	35501594
DBH-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Regulation[miR-138/FAK/Src/ERK pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	DBH-AS1 expression was upregulated and miR-138 expression was downregulated in HCC tissues and cells.  DBH-AS1 facilitated the development of HCC via miR-138/FAK/Src/ERK pathway, establishing the molecular basis of DBH-AS1 in clinical application for HCC.		Yes	DBH-AS1 silencing and miR-138 overexpression reduced cell viability, inhibited colony formation, and induced apoptosis. 	30142544
DBH-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue and cell lines	Regulation[PI3K-AKT signaling pathways]	CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//EdU Staining	We observed that DBH-AS1 was distinctly overexpressed in osteosarcoma tissue and cells, and associated with lymph node status and metastasis status.Moreover, suppression of DBH-AS1 could inhibit the activation of the PI3K/Akt pathway, which was demonstrated by examining the expression levels of p-PI3K and p-Akt.	Osteosarcoma patients with a higher DBH-AS1 expression showed significantly poorer overall survival than those with lower DBH-AS1 expression. 	Yes	Functional assays revealed that knockdown of DBH-AS1 inhibited cell proliferation, migration and invasion, while promoted apoptosis in osteosarcoma.	30840262
DBH-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cells	Interaction(miR-3163/USP44 axis)	In Vivo Experiment//MeRIP//qPCR//Luciferase Report Assay//Colony Formation Assay	 We found that PC tissues exhibited DBH-AS1 downregulation that was particularly pronounced in gemcitabine-resistant PC tissues and cells. Mechanistically, DBH-AS1 was able to increase PC cell sensitivity to gemcitabine by sequestering miR-3163 and thus upregulating USP44 in these tumor cells. Clinically, patient-derived PC tumor xenografts exhibiting high levels of DBH-AS1 expression were found to be responsive to gemcitabine treatment.	This DBH-AS1 downregulation was negatively correlated with the malignancy of PC tumors and with patient survival outcomes.	Yes	Additionally, decreased DBH-AS1 expression in PC was found to be linked to the METTL3-dependent m6A methylation of the lncRNA, with functional analyses revealing that DBH-AS1 was able to suppress the growth of PC cells. 	35433957
DBH-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tumor tissues and cell lines	regulation[miR-223-3p/EGFR/AKT axis]	colony Formation Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Herein, we observed significant reductions in DBH-AS1 expression in melanoma tumor tissues and cell lines. These findings therefore suggest that DBH-AS1 can enhance glycolytic activity in melanoma cells, thereby disrupting melanoma progression via miR-223-3p/EGFR/AKT axis.		Yes	Knockdown DBH-AS1 in melanoma cells impaired their proliferative, migratory, and invasive potential. 	32744696
DBH-AS1	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBC tissues and cells	regulation[DBH-AS1/BUD13/FN1 axis]	qRT-PCR	In this research, long non-coding RNA dopamine β hydroxylase antisense RNA 1 (DBH-AS1) was found to be upregulated in DLBC tissues and cells. In this way, DBH-AS1/BUD13/FN1 axis was confirmed.		Yes	Knockdown of DBH-AS1 suppressed the proliferation, migration, and invasion of cancer cells.	32091157
DATOC-1	LncRNA	Mus musculus	Carcinoma, Ovarian Epithelial	 EOC tissues	Interaction( miR7)	qRT-PCR	We identified the lncRNA RP5-1120P11.1 as DATOC-1, which highly expressed in EOC tissues than in adjacent. Furthermore, knockdown of DATOC-1 increased the expression of miR7. The evidence showed that miR7 functioning as a tumor suppressor gene in EOC.	And Kaplan-Meier analysis indicated that the patients with EOC that expressed high levels of DATOC-1 had a worse prognosis and shorter disease OS compared with DATOC-1 low-expressed patients. 	Yes	 In addition, DATOC-1 were further identified participating in EOC cell proliferation, cell cycle regulation and cell invasion. And knockdown of DATOC-1 inhibits tumor progression in vivo.	35116553
DARS1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(miR-3200-5p/CKAP2 and FAK-ERK pathway)	qRT-PCR	 DARS-AS1 was overexpressed in HCC tissues (vs. that in non-tumor tissues) and was closely correlated with the patients' tumor stage. DARS-AS1 up-regulated CKAP2, which aggravated HCC. Further investigation illustrated that either DARS-AS1 or CKAP2 activated FAK-ERK pathway, and miR-3200-5p was competitively restrained by DARS-AS1. miR-3200-5p exerted tumor-suppressive effects in HCC and inactivated CKAP2 and FAK-ERK pathway.	 DARS-AS1 was overexpressed in HCC tissues (vs. that in non-tumor tissues) and was closely correlated with the patients' tumor stage. 	Yes	 DARS-AS1 facilitated HCC cell proliferation and hampered apoptosis. HCC cell migration and EMT were enhanced by DARS-AS1. 	34596006
DARS1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC cell model 	Interaction(miR-194-5p/TSPAN1 and ITGA2 )	qRT-PCR//ChIP//Western Blot	 The OC cell model exhibited overexpressed lncRNA DARS-AS1 compared to normal cells. lncRNA DARS-AS1 positively regulated TSPAN1 expression by binding with miR-194-5p and TSPAN1-mediated ITGA2 hypomethylation in OC cells. Further rescue function studies demonstrated that lncRNA DARS-AS1 affected OC cell viability, migration, invasion, and apoptosis ability by modulating miR-194-5p and TSPAN1 expressions.		Yes	lncRNA DARS-AS1 knockdown led to reduced OC cell growth and metastasis while inducing the apoptosis in the OC cell model. 	36187230
DARS1-AS1	LncRNA	Homo sapiens	Osteosarcoma	 osteosarcoma specimens, osteosarcoma cell lines (Saos-2, SOSP-9607, U2OS, and MG-63)	Interaction(miR-532-3p/CCR7)	qRT-PCR//Luciferase Report Assay	We firstly showed that DARS-AS1 expression is upregulated in 73.5% (25/34) of cases with osteosarcoma. Moreover, DARS-AS1 expression is overexpressed in osteosarcoma specimens than in nontumor samples. The DARS-AS1 is overexpressed in the osteosarcoma cell lines (Saos-2, SOSP-9607, U2OS, and MG-63) compared to hFOB. These data firstly suggested that DARS-AS1 exerted as one oncogene in osteosarcoma partly via regulating miR-532-3p/CCR7.		Yes	Overexpression of DARS-AS1 promotes cell growth and invasion in MG-63 osteosarcoma cell. 	35422889
DARS1-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow tissues	interaction[Binding to microRNA-425]	qRT-PCR//Western Blot	DARS-AS1 was overexpressed in bone marrow tissues of AML patients and cells, and DARS-AS1 knockdown suppressed the proliferation of AML cells and induced apoptosis.All in all, we highlighted here that DARS-AS1 enhanced the expression of TGFB1 through binding to miR-425 to modulate AML progression via the Smad2/3 pathway, which might perform as a therapeutic target for AML.		Yes	DARS-AS1 was overexpressed in bone marrow tissues of AML patients and cells, and DARS-AS1 knockdown suppressed the proliferation of AML cells and induced apoptosis.	33073700
DARS1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cell lines	regulation[Downregulating HMGB1 via Sponging miR-188-5p]	Flow Cytometry//qRT-PCR//IF//Luciferase Report Assay//Transwell Assay	Downregulation of DARS-AS1 markedly inhibited the proliferation and invasion of cervical cancer cells.In this study, we found that DARS-AS1 knockdown suppressed the growth of cervical cancer cells via downregulating HMGB1 via sponging miR-188-5p.		Yes	Downregulation of DARS-AS1 markedly inhibited the proliferation and invasion of cervical cancer cells. Moreover, DARS-AS1 knockdown obviously induced the apoptosis of SiHa and HeLa cells. 	33176595
DARS1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells	Regulation(IGF2BP3)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transwell Assay//Transfection//CCK8//qRT-PCR//FISH//Flow Cytometry//Colony Formation Assay//Invasion Assay//IF	 Downregulation of DARS-AS1 significantly induced apoptosis and cell cycle arrest in cervical cancer cells. Meanwhile, the invasion ability of cervical cancer cells was inhibited by DARS-AS1 knockdown as well. RNA pull-down and FISH results showed that DARS-AS1 interacted with IGF2BP3. Mechanistically, DARS-AS1 positively regulated IGF2BP3 expression via stabilization of IGF2BP3 mRNA. 		Yes	 Downregulation of DARS-AS1 significantly induced apoptosis and cell cycle arrest in cervical cancer cells. Meanwhile, the invasion ability of cervical cancer cells was inhibited by DARS-AS1 knockdown as well.  In addition, in vivo experiments revealed that downregulation of DARS-AS1 inhibited tumor growth in SiHa xenograft model.	33658798
DCST1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cell	Regulation(NF-κB signaling)	CCK8//qRT-PCR//IHC//Western Blot	Here, we reported that DCST1-AS1 was significantly increased in OSCC cells. Then, we observed that loss of DCST1-AS1 suppressed OSCC progression via inactivating NF-κB signaling. As well established, NF-κB signaling exerts critical roles in tumor progression, and our study proved that DCST1-AS1 could regulate NF-κB signaling. 		Yes	 We found that loss of DCST1-AS1 obviously inhibited the proliferation, migration, and invasion of OSCC cells and xenograft tumor growth. Meanwhile, silencing of DCST1-AS1 also repressed the percentage of macrophages expressing M2 markers CD206 and CD11b. DCST1-AS1 shRNA enhanced the percentage of macrophages expressing M1 markers CD80 and CD11c. T	34414241
DCST1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[sponging miR-1254]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	LncRNA DCST1-AS1 was highly expressed in HCC tissues.DCST1-AS1 up-regulates the expression of FAIM2 by up-regulating the expression of miR-1254, ultimately promoting the proliferation of HCC cells.  Dual‑luciferase reporter assays demonstrated that SPRY4‑IT1 may have regulated the expression of ZEB1 and ZEB2 by sponging miR‑101. In conclusion, SPRY4‑IT1 inhibition increased miR‑101 levels, resulting in downregulation of ZEB1/2 expression and thus exerting anti‑tumour effects in OS.	LncRNA DCST1-AS1 was highly expressed in HCC tissues, and the high expression of DCST1-AS1 was significantly correlated with larger tumours and shorter survival time.	Yes	Moreover, DCST1-AS1 knockout significantly inhibited proliferation, promoted apoptosis and cycle arrest of HCC cells, and inhibited tumour growth in vivo	30617187
DGCR5	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tissues	Interaction(miR-211-5p/Snail Signal Axis)	Western Blot//qPCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//EdU Staining//Transwell Assay	Quantitative polymerase chain reaction further demonstrated that the expression level of DGCR5 major isoform (isoform-1) was higher in ccRCC tissues than that in papillary/chromophobe RCC and other multiple solid malignant tumors. Thus, our study indicates that DGCR5 isoform-1 could contribute to ccRCC progression by sponging miR-211-5p through regulating the expression of Snail protein and could serve as a reliable diagnostic biomarker in ccRCC.		Yes	Thus, our study indicates that DGCR5 isoform-1 could contribute to ccRCC progression by sponging miR-211-5p through regulating the expression of Snail protein and could serve as a reliable diagnostic biomarker in ccRCC.	34322486
DCST1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(hsa-miR-582-5p/HMGB1 axis )	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//cell invasion assay//Colony Formation Assay	 We found that the expression of lncRNA DCST1-AS1 was up-regulated in CRC tissues and cell lines, and CRC patients with high lncRNA DCST1-AS1 expression were associated with a poor prognosis. Functional assay further confirmed the crucial role of lncRNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis in modulating the malignant phenotype of CRC cells. 	 We found that the expression of lncRNA DCST1-AS1 was up-regulated in CRC tissues and cell lines, and CRC patients with high lncRNA DCST1-AS1 expression were associated with a poor prognosis.	Yes	. Loss-of-function and gain-of-function experiment in CRC cell lines confirmed that lncRNA DCST1-AS1 promoted the malignant phenotype of CRC cells, including cell proliferation, colony formation, migration, and invasion.	34967274
DEPDC1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(F11R)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//IF//Colony Formation Assay//Transwell Assay	DEPDC1-AS1 was overexpressed in GC tissues and cell lines, and associated with a worse prognosis in GC patients. Mechanistically, DEPDC1-AS1 served as a scaffold by combining with HuR to target the specific mRNA F11R.	DEPDC1-AS1 was overexpressed in GC tissues and cell lines, and associated with a worse prognosis in GC patients. 	Yes	In vitro and in vivo assays showed that DEPDC1-AS1 promoted HGC-27 cell proliferation and migration. 	35466755
DENND1B	CircRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC cells	Interaction(miR-122-5p/TIMP2 axis)	colony Formation Assay//Western Blot//Transfection//Colony Formation Assay//Flow Cytometry//qRT-PCR//IF//MTT//PCR//IP//IHC//Transwell Assay	circ_DENND1B was downregulated in ccRCC and circ_DENND1B overexpression suppressed the malignant behaviors of ccRCC cells.  circ_DENND1B acted as a sponge of miR-122-5p. miR-122-5p upregulation reversed the effects of circ_DENND1B on cell proliferation, migration, invasion and apoptosis.TIMP2 was a target of miR-122-5p. Overexpression of circ_DENND1B regulated TIMP2 level by inhibiting miR-122-5p expression in ccRCC cells. 		Yes	 circ_DENND1B acted as a sponge of miR-122-5p. miR-122-5p upregulation reversed the effects of circ_DENND1B on cell proliferation, migration, invasion and apoptosis. circ_DENND1B overexpression inhibited the tumor growth of ccRCC in vivo.	36578555
DDX3ILA1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[DDX3/YY1/MMP1/PI3K-AKT axis ]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	 Elevated expression of TCONS_00012883 was confirmed in CRC and positively associated with a poor prognosis. TCONS_00012883 significantly promoted CRC progression via the DDX3/YY1/MMP1 axis, and thus, may act as a major role in diagnosis and therapy of CRC.	 Elevated expression of TCONS_00012883 was confirmed in CRC and positively associated with a poor prognosis. 	Yes	Functionally, gain- and loss-of-function assays indicated that TCONS_00012883 promoted proliferation and metastasis of CRC cell lines in vitro and in vivo. 	33135346
DDX21	LncRNA	Homo sapiens	Breast Neoplasms	BC cell lines	Interaction(miR‐1264/QKI axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Wound Healing Assay//qRT-PCR//FISH//IF//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircDDX21 expression was downregulated in the normal mammary gland cell line MCF10A compared with other BC cell lines 	 Interestingly, low expression of circDDX21 indicated prolonged survival in TNBC patients	Yes	 Overexpression of circDDX21 repressed the proliferation, migration, invasion and clone formation abilities of the two TNBC cell lines, whereas circDDX21 knockdown promoted these abilities	35522944
DDX11‑AS1	LncRNA	Homo sapiens	Breast Neoplasms	MCF‑7 and MDA‑MB‑231 cells	Regulation(microRNA‑497)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//IF//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The present study demonstrated that the expression levels of lncRNA DDX11‑AS1 were markedly increased in paclitaxel (PTX)‑resistant breast cancer cell lines. By contrast, knockdown of DDX11‑AS1 expression inhibited PTX resistance of breast cancer cells, and suppressed the proliferation, invasion and migration of breast cancer cells, which was achieved via upregulation of miR‑497 expression. In conclusion, knockdown of lncRNA DDX11‑AS1 could inhibit the proliferation, migration and PTX resistance of breast cancer cells by upregulating miR‑497 expression.		Yes	By contrast, knockdown of DDX11‑AS1 expression inhibited PTX resistance of breast cancer cells, and suppressed the proliferation, invasion and migration of breast cancer cells, which was achieved via upregulation of miR‑497 expression.	35169864
DDX11-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tumour tissues and cells	regulation[miR-873-5p/SPC18 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	In this study, we found that DDX11-AS1 expression was up-regulated in GC tumour tissues and cells. In conclusion, DDX11-AS1 may serve as an oncogene in GC progression by sponging miR-873-5p and promoting SPC18 expression, providing a new insight into the mechanisms of DDX11-AS1 and elucidating a promising therapy target in GC.	Increased DDX11-AS1 expression was associated with advanced TNM stage and lymph node metastasis. 	Yes	 Functionally, knockdown of DDX11-AS1 repressed cell proliferation and clone formation, while induced cell cycle arrest and apoptosis.	32054332
DDX11-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumour tissues and cells	regulation[PI3K/AKT signalling]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	The level of lncRNA DDX11-AS1 was up-regulated in NSCLC tumour tissues and cells. All in all, DDX11-AS1 promotes NSCLC development via regulating PI3K/AKT signalling.		Yes	In function aspect, knockdown of DDX11-AS1 caused an apparent inhibitive effect on cell proliferation in vitro and in vivo. DDX11-AS1 inhibition promoted cell apoptosis in vitro.	32298476
DDX11-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[miR-873/CLDN7 axis]	qRT-PCR//ChIP	 We identified DDX11-AS1 as a new CRC-related lncRNA whose levels were distinctly up-regulated in CRC specimens and cell lines, partly induced by YY1.  Mechanistic studies showed that the up-regulation of DDX11-AS1 competitively bound to miR-873 prevented CLDN7 from miRNAs-mediated degradations, thus facilitated the CRC progress. Further rescue assays were carried out to achieve confirmation.	Clinical explorations suggested that increased expressions of DDX11-AS1 in CRC were positively associated with lymph nodes metastasis and TNM stage and had a distinct influence on the overall survival. Further multivariate assays indicated that DDX11-AS1 was an independent prognostic parameter implying a poorer clinical outcome for patients with CRC. 	Yes	 Functional assays revealed that the knockdown of DDX11-AS1 suppressed the proliferation, migration, and invasion of CRC cells, and stimulate apoptosis. 	31298324
DDX11-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[ miR-195-5p/MACC1 pathway]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	DDX11-AS1 was upregulated in HCC tissues and cells,In addition, MACC1 was a target of miR-195-5p, and its overexpression reversed the suppression effect of miR-195-5p on HCC cell progression.		Yes	DDX11-AS1 was upregulated in HCC tissues and cells, and its silencing could inhibit HCC cell proliferation, migration, invasion and glucose metabolism, and promote apoptosis in vitro. Also, DDX11-AS1 knockdown reduced HCC tumor growth in vivo.	32961346
DDX11-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell line	Interaction(miR-34a-3p/TRAF5 )	qRT-PCR	Elevated DDX11-AS1 and TRAF5 and reduced miR-34a-3p exhibited in HCC. In addition, DDX11-AS1 bound to miR-34a-3p to target TRAF5. Silencing TRAF5 or elevating miR-34a-3p expression mitigated up-regulated DDX11-AS1-mediated promotion of tumor growth.		Yes	Silenced DDX11-AS1 or up-regulated miR-34a-3p inhibited the proliferation, migration, invasion, promoted apoptosis of HCC cells and repressed the tumor growth in nude mice. 	33752668
DDX11-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells	regulation[DDX11]	RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 In this research, a dramatically upregulated expression of DDX11-AS1 was detected in osteosarcoma cells.To sum up, DDX11-AS1 contributes to osteosarcoma progression via stabilizing DDX11.		Yes	Loss-of-function assays revealed that decreased expression of DDX11-AS1 impaired osteosarcoma cell proliferation, metastasis as well as epithelial-mesenchymal transition (EMT) process. 	32014424
DDX11-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction(HNRNPC axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//Cell Apoptosis Assay//IHC//Bioinformatics Analysis	 In this study, we found that the expression of DDX11-AS1 was elevated in glioma tissues, and patients with high expression of DDX11-AS1 had poor prognosis.Mechanistically, DDX11-AS1 interacted with RNA-binding protein heterogeneous nuclear ribonucleoprotein C (HNRNPC) to promote Wnt/β-catenin and AKT pathways and the epithelial-mesenchymal transition process. 	 In this study, we found that the expression of DDX11-AS1 was elevated in glioma tissues, and patients with high expression of DDX11-AS1 had poor prognosis.DDX11-AS1 was a potential prognostic marker. 	Yes	 Functionally, DDX11-AS1 promoted glioma cell proliferation and migration.	35614994
DDX11-AS1	LncRNA	Homo sapiens	esophageal carcinoma	ESCA tissues and cell lines	Interaction(miR-514b-3p/RBX1 axis)	Bioinformatics Analysis	We found that the expression of lncRNA DDX11-AS1 in ESCA tissues and cell lines was significantly upregulated.  In terms of mechanism, our data showed that miR-514b-3p/RING box protein 1 (RBX1) axis played a crucial role in the oncogenic function of lncRNA DDX11-AS1. LncRNA DDX11-AS1 expression impaired the inhibitory function of miR-514b-3p on RBX1 through sponging effect. 		Yes	Subsequently, silencing lncRNA DDX11-AS1 significantly inhibited the proliferation, migration and invasion of ESCA cells, and induced the level of cell apoptosis. 	34281459
DDX11-AS1	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues and cells	Interaction(PARP1/p53 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Co-IP//Migration Assay//qRT-PCR//FISH//RIP//RNA-seq//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//IHC	Upregulation of DDX11-AS1 expression through demethylation was significantly associated with a poor prognosis. Further mechanistic studies revealed that DDX11-AS1 promoted the growth of HCC by interacting with PARP1 through attenuating its binding to p53, leading to downregulated expression of p53 for inhibiting the transcription of downstream genes such as p21.	Upregulation of DDX11-AS1 expression through demethylation was significantly associated with a poor prognosis	Yes	 Knockdown of DDX11-AS1 expression in xenograft mice using anti-DDX11-AS1 oligonucleotide suppressed liver tumor proliferation. These findings indicate that DDX11-AS1 plays a role in the development of liver cancer by affecting the cell cycle.	34371129
DDX11	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	Interaction(miR-30d-5p/SNAI1/ZEB2 )	qRT-PCR//Bioinformatics Analysis//RIP	In this research, high DDX11-AS1 expression was detected in ESCC cells as well as tissues and was linked to the poor prognosis of patients with ESCC. Mechanistic analysis depicted that DDX11-AS1 may function as a ceRNA through sponging miR-30d-5p to upregulate the expression of SNAI1 and ZEB2. Meanwhile, overexpression of DDX11-AS1 might cause the activation of the Wnt/β-catenin signaling pathway via targeting miR-30d-5p. 	In this research, high DDX11-AS1 expression was detected in ESCC cells as well as tissues and was linked to the poor prognosis of patients with ESCC. 	Yes	DDX11-AS1 promoted cell proliferation, migration, invasion ability and epithelial mesenchymal transition (EMT) process in vitro. 	34866524
DDN-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction[DDN-AS1-miR-15a/16-TCF3 ]	qRT-PCR	On the basis of the data of The Cancer Genome Atlas, lncRNA DDN and PRKAG1 antisense RNA 1 ( DDN-AS1) that is overexpressed in CC tissues predicted poor prognosis for patients with CC. Moreover, quantitative reverse transcription PCR analysis further identified the upregulation of DDN-AS1 in CC tissues and cell lines.Mechanism investigations revealed that DDN-AS1 was upregulated by its upstream transcription activator transcription factor 3 ( TCF3). Moreover, DDN-AS1 increased the expression of TCF3 by competitively binding miR-15a and miR-16. In conclusion, DDN-AS1-miR-15a/16-TCF3 feedback loop contributes to cell proliferation, migration, and invasion in CC.		Yes	 Loss-of-function assays revealed that knockdown of DDN-AS1 suppressed CC progression by efficiently inhibiting cell proliferation, migration, and invasion.	30582201
DDGC	LncRNA	Homo sapiens	primary ovarian insufficiency	GCs from patients with biochemical premature ovarian insufficiency 	Interaction(RAD51 and WT1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Co-IP//CCK8//qRT-PCR//FISH//RIP//RNA-seq//Luciferase Report Assay//Cell Cycle Assay//EdU Staining//IF	Here, we recognized a minimally expressed lncRNA RP4-545C24.1 (which we named DDGC) in GCs from patients with biochemical premature ovarian insufficiency (bPOI). Mechanistically, silencing DDGC downregulated RAD51 by competitively binding with miR-589-5p, and this resulted in significant inhibition of DNA damage repair capacity.In addition, decreased expression of DDGC promoted ubiquitin-mediated degradation of Wilms tumor 1 (WT1) protein through interactions with heat shock protein 90 (HSP90), which led to aberrant differentiation of GCs.		Yes	Mechanistically, silencing DDGC downregulated RAD51 by competitively binding with miR-589-5p, and this resulted in significant inhibition of DNA damage repair capacity. In addition, decreased expression of DDGC promoted ubiquitin-mediated degradation of Wilms tumor 1 (WT1) protein through interactions with heat shock protein 90 (HSP90), which led to aberrant differentiation of GCs. Moreover, DDGC was able to ameliorate the etoposide-induced DNA damage and apoptosis in vivo.	34786213
DCST1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissue samples and cell lines	interaction[miR-873-5p,MYC]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Colony Formation Assay//Transwell Assay	Consistent with the microarray results, we found that DCST1-AS1 was up-regulated in both TNBC tissue samples and cell lines.MYC, DCST1-AS1 and miR-873-5p form a positive regulatory loop to promote TNBC cell proliferation and metastasis.		Yes	 Knockdown of DCST1-AS1 inhibits TNBC cell proliferation and metastasis, while overexpression of DCST1-AS1 promotes TNBC cell proliferation and metastasis. 	31897227
DARS1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cell lines	Interaction(ATP1B2/cGMP-PKG pathway)	Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	DARS-AS1 was expressed at high levels in CC tissues and cell lines, and high expression of DARS-AS1 indicated a lower survival rate.Then, biological function experiments exhibited that the promotion of cell proliferation, invasion, and migration resulted due to the upregulation of DARS-AS1 could be canceled by ATP1B2 overexpression. Finally, Western blot revealed that upregulation of DARS-AS1 could activate the cGMP-PKG pathway, while overexpression of ATP1B2 reversed this activation. 	DARS-AS1 was expressed at high levels in CC tissues and cell lines, and high expression of DARS-AS1 indicated a lower survival rate.	Yes	Then, biological function experiments exhibited that the promotion of cell proliferation, invasion, and migration resulted due to the upregulation of DARS-AS1 could be canceled by ATP1B2 overexpression. Finally, Western blot revealed that upregulation of DARS-AS1 could activate the cGMP-PKG pathway, while overexpression of ATP1B2 reversed this activation. 	33634536
DARS1-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC clinical tumors and cells 	Interaction(miR-129-2-3p/CDK1/ NF-κB/STAT3 signaling pathway)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Tunel//qRT-PCR//Luciferase Report Assay//H&E Staining//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	In this study, DARS-AS1, a newly reported CUMS-responsive lncRNA, was found to be enriched in TNBC clinical tumors and cells and positively correlated with late clinical stage in patients with TNBC.  DARS-AS1 overexpression significantly enhanced the migration and invasion of TNBC tumors by inhibiting miR-129-2-3p and upregulated CDK1 to activate the NF-κB/STAT3 signaling pathway both in vitro and in vivo.	In this study, DARS-AS1, a newly reported CUMS-responsive lncRNA, was found to be enriched in TNBC clinical tumors and cells and positively correlated with late clinical stage in patients with TNBC. 	Yes	 DARS-AS1 overexpression significantly enhanced the migration and invasion of TNBC tumors by inhibiting miR-129-2-3p and upregulated CDK1 to activate the NF-κB/STAT3 signaling pathway both in vitro and in vivo.	35688263
DARS1-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues	Interaction[microRNA-129]	CCK8//qPCR//Transwell Assay	qPCR results revealed that the level of DARS-AS1 in tumor tissues of thyroid cancer patients was remarkably higher than that in adjacent tissues, and the difference was statistically significant.qPCR results indicated that there was a negative correlation between the level of microRNA-129 and DARS-AS1 in thyroid cancer tissues. In addition, cell proliferation and migration ability in the microRNA-129 overexpression group were remarkably decreased. The recovery experiment also found that there was a mutual regulation between DARS-AS1 and microRNA-129, which together affected the malignant progression of thyroid cancer.	Compared with patients with low expression of DARS-AS1, patients with high DARS-AS1 expression had a higher incidence of high tumor stage, distant metastasis, and a lower overall survival rate.	Yes	Besides, compared with NC group, the proliferation and migration ability of shRNA-AS1 expression knockdown group sh-DARS-AS1 was remarkably decreased. 	31841198
DARS1-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	regulation[miR-194-5p/DARS signaling]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining	However, Gene Expression Profiling Interactive Analysis (GEPIA) and starBase databases revealed the up-regulation of DARS-AS1 in ccRCC. Moreover, DARS was testified as the oncogene in ccRCC and DARS-AS1 worked as a tumor-facilitator in ccRCC through miR-194-5p/DARS signaling.		Yes	Functional assays including colony formation assay, EdU assay, caspase-3 activity detection, flow cytometry analysis and JC-1 assay were implemented to identify the role of DARS-AS1 in ccRCC. 	32526457
DANCR	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian malignant tissues,cell lines	Regulation[miR-145/VEGF axis]	qRT-PCR	DANCR was upregulated in ovarian malignant tissues and ovarian cancer cells.Collectively, DANCR plays a promotional role in tumor angiogenesis in ovarian cancer through regulation of miR-145/VEGF axis. 		Yes	Knockdown of DANCR efficiently impaired ovarian tumor growth through inhibition of tumor angiogenesis. Furthermore, the conditional culture medium from DANCR-knockdown ovarian cells significantly inhibited tube formation and invasion of HUVEC in vitro. 	31545000
DANCR	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer cell lines	Interaction(miR-335/VEGF-C axis)	qRT-PCR//Luciferase Report Assay	 In this study, DANCR was highly expressed in bladder cancer cell lines. Dual luciferase assay confirmed that DANCR targets miR-335/VEGF-C. Transfection of miR-335 mimic promotes the proliferation, migration, invasion and lymphatic metastasis of bladder cancer cells, overexpression of DANCR eliminates the promotion of miR-335 mimic on bladder cancer cells. 		Yes	Transfection of si-DANCR significantly inhibits the proliferation, migration, invasion and lymphatic metastasis of bladder cancer cells. 	33968662
DANCR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	interaction[ sponging miR-216a-5p]	qRT-PCR//Luciferase Report Assay	 Up-regulated DANCR expression and down-regulated miR-216a-5p expression were observed in both OSCC tissues and cells,We concluded that DANCR may promote the growth and metastasis of OSCC cells and suppress OSCC cell apoptosis by sponging miR-216a-5p.	Up-regulated DANCR expression and down-regulated miR-216a-5p expression were observed in both OSCC tissues and cells, and they were proven strongly correlated to the histological grade, clinical staging and lymph node metastasis of OSCC patients.	Yes	 Both DANCR shRNA and miR-216a-5p mimic decreased proliferative, migration and invasive abilities of OSCC cells with increased cell apoptosis. However, DANCR group showed completely opposite trends. 	32860589
DANCR	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Interaction[sponging miR-214]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	DANCR expression was up-regulated in EC tissues as compared to the normal control tissues.DANCR played an important role in promoting tumorigenesis of EC via sponging miR-214.		Yes	Knockdown of DANCR in AN3CA and HEC-1B cells markedly suppressed cell proliferation and induced cell apoptosis.	31161373
DANCR	LncRNA	Homo sapiens	Osteosarcoma	OS tissues,cell lines	Interaction[p38MAPK signalling pathway]	CCK8//qRT-PCR//EdU Staining//Transwell Assay	ANCR was up-regulated in OS cells and tissues.Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCR-induced inhibition of cell migration and invasion.		Yes	ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells.	31727012
DANCR	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissue and cells	regulation[miR-149/MSI2 axis]	qRT-PCR//Western Blot//Transwell Assay	DANCR was significantly up-regulated in both osteosarcoma tissue and cells.It may be used as a potential target in the treatment of osteosarcoma in the future, by targeting the miR-149/MSI2 axis to regulate the occurrence and development of osteosarcoma.	The high expression of DANCR was significantly positively correlated with tissue typing and advanced TNM stage. 	Yes	DANCR can significantly reduce the migration and invasion of osteosarcoma cells. 	32633342
DANCR	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC cells and tissues	Regulation[microRNA-33a-5p/AXL signaling pathway ]	CCK8//qRT-PCR//Colony Formation Assay	 DANCR was revealed to promote PDAC progression, with relatively higher expression levels in PDAC cell lines and tissues.Besides, microRNA-33a-5p/AXL signaling pathway may be involved in mediating the function of DANCR.	Correlation analysis of the clinicopathological features and DANCR expression found that high DANCR expression was statistically correlated with vascular invasion (P=0.013), advanced T stage (P=0.005), lymph node metastasis (P<0.001) and advanced TNM stage (P<0.001). Notably, survival analysis discovered that high DANCR expression predicted lower OS rate and shorter PFS period. In addition, high DANCR expression was identified as an independent risk factor for poor OS (HR=1.199, 95% CI=1.113-1.290, P<0.001) and PFS (HR=1.199, 95% CI=1.114-1.290, P<0.001) of PDAC.	Yes	Moreover, in vitro assays detected that the migration and invasion of Panc1 cells with DANCR deficiency were significantly suppressed in the Transwell assay and the Matrigel assay. However, the motility of BxPC3 cells with DANCR overexpression was obviously increased. In addition, the loss of DANCR suppressed the proliferation of Panc1 cells in the CCK-8 assay and the colony formation assay, while ectopic expression of DANCR in BxPC3 cells promoted the proliferation.	30519037
DANCR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction[sponging miR-335-5p]	qRT-PCR	In this study, we discovered that DANCR was significantly elevated in cervical cancer tissues and cells, and was closely correlated with poor prognosis of cervical cancer patients. In summary, this study demonstrated that DANCR promoted cervical cancer progression by functioning as a competing endogenous RNA (ceRNA) to regulate ROCK1 expression via sponging miR-335-5p, suggesting a novel potential therapeutic target for cervical cancer.	In this study, we discovered that DANCR was significantly elevated in cervical cancer tissues and cells, and was closely correlated with poor prognosis of cervical cancer patients. 	Yes	In addition, knockdown of DANCR inhibited proliferation, migration, and invasion of cervical cancer cells in vitro, indicating that DANCR functioned as an oncogene in cervical cancer.	30362591
DANCR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	regulation[Wnt/β-catenin signaling pathway]	CCK8//qRT-PCR//EdU Staining//Western Blot	DANCR is increased in cervical cancer tissues and cell lines.Our findings suggest DANCR as an oncogenic lncRNA in cervical cancer through activating the Wnt/β-catenin signaling pathway, and imply that DANCR may be a promising prognostic biomarker and therapeutic target for cervical cancer.	 Increased expression of DANCR is associated with large tumor size, advanced FIGO stage, and poor overall survival of cervical cancer patients. 	Yes	Functional experiments showed that enhanced expression of DANCR promotes cervical cancer cell proliferation in vitro and xenograft growth in vivo. Conversely, DANCR knockdown inhibits cervical cancer cell proliferation in vitro and xenograft growth in vivo.	32123519
DANCR	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	112 cases of CC tissues 	Interaction(microRNA-145-3p/ZEB1 axis)	In Vivo Experiment//ChIP//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	KLF5, DANCR, and ZEB1 were upregulated but miR-145-3p was downregulated in CC tissues. KLF5 activated DANCR expression and the high DANCR expression was related to tumor staging, infiltrating muscle depth and lymphatic metastasis of CC patients. MiR-145-3p was targeted by DANCR and ZEB1 was targeted by miR-145-3p.	KLF5 activated DANCR expression and the high DANCR expression was related to tumor staging, infiltrating muscle depth and lymphatic metastasis of CC patients. 	Yes	Reduced DANCR or elevated miR-145-3p repressed malignant behaviors of CC cells. The tumor diameter and weight were also repressed by DANCR silencing or miR-145-3p elevation. 	34233586
DANCR	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and breast cancer cells	Interaction[targetting miR-216a-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay	Our results showed that DANCR was up-regulated in TNBC tissues and breast cancer cells compared with normal breast tissues and cells. To deeply understand its molecular mechanism, miRNA-216a-5p was identified as a target of DANCR by bioinformatic analysis. Experiments demonstrated that miRNA-216a-5p interacted with DANCR and its inhibitor could weaken the influences induced by DANCR knockdown for cancer cells, including cell proliferation and invasion, and the expression of Nanog, SOX2, and OCT4. Therefore, DANCR might act as a tumor promoter by targetting miRNA-216a-5p, which might provide a potential therapy target for breast cancer treatment.		Yes	 Further study indicated that DANCR overexpression significantly promoted cell proliferation and invasion in vitro and contributed to tumor growth in vivo	30910842
DANCR	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	interaction[miR-33a-5p]	qRT-PCR	The results showed that LncRNA DANCR was increased in glioma tissues and cells compared with normal brain tissues and cells.In tumor tissues, knockdown of DANCR increased the expression of miR-33a-5p, reduced EMT and increased apoptosis.	DANCR expression was positively correlated with the malignancy and poor prognosis of glioma patients.	Yes	Knockdown of DANCR remarkably reduced the increase of tumor volumes in xenograft mouse models.	29940760
DANCR	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	interaction[EZH2,PTEN]	qRT-PCR//RNA Pull-Down//RIP	Our results indicated that ANCR and EZH2 were upregulated and PTEN was downregulated in glioma tissues and cell lines. In conclusion, we have found that restrained ANCR could repress invasion, migration, and proliferation, as well as promote apoptosis of glioma cells through interacting with EZH2 and regulating the expression of PTEN, offering an effective therapeutic target for patients with glioma.		Yes	 Inhibited ANCR, reduced EZH2, or elevated PTEN could reduce the ability of invasion, migration, and proliferation, and promote apoptosis of glioma cells. 	33293663
DANCR	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines (U251, U118, LN229, and U87MG)	Interaction(miR-634/RAB1A )	Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay	Our results showed that DANCR was significantly up-regulated in glioma tissues and cell lines (U251, U118, LN229, and U87MG). In addition, we verified that DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression. The present study demonstrated that DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma, and DANCR might potentially serve as a therapeutic target for the treatment of glioma patients.	 High DANCR expression was correlated with advanced tumor grade. 	Yes	Inhibition of DANCR suppressed the glioma cells proliferation and induced cells arrested in the G0/G1 phase. 	29301870
DANCR	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Wound Healing Assay//Colony Formation Assay	Reverse transcription‑quantitative polymerase chain reaction results suggested that DANCR was significantly upregulated in NPC cells. 		Yes	Overexpression of DANCR promoted 5‑8F cell proliferation and migration, as detected by Cell Counting Kit‑8, colony formation and wound healing assays. DANCR knockdown suppressed cell proliferation and migration, and promoted cell apoptosis in SUNE‑1 cell.  Knockdown of DANCR decreased tumor growth in a xenograft model following subcutaneous injection of SUNE‑1 cells.	30720067
DANCR	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	cell lines	Regulation[IL-6/JAK1/STAT3 signaling]	RNA Pull-Down//Western Blot//Co-IP//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Invasion Assay//ChIP	 In the current study, we investigated the expression and biological functions of DANCR in NPC cells and found that DANCR is highly expressed in NPC cells and IL-6 stimulation upregulates DANCR expression through an STAT3-dependent manner. Taken together, the present study for the first time demonstrates that DANCR, acting as an oncogene in NPC, promotes NPC progression by interacting with STAT3 and enhancing JAK1 binding to STAT3 to strengthen IL-6/JAK1/STAT3 signaling, suggesting that it may be a potential target to be used as a novel strategy to develop NPC therapeutics.		Yes	 Besides, DANCR knockdown attenuates IL-6-induced proliferation and invasion of NPC cells.	30849642
DANCR	LncRNA	Homo sapiens	Atherosclerosis	 blood samples of AS patients, VSMCs and HUVECs	Interaction(miR-214-5p/COX20 signaling pathway)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//ELISA	DANCR was significantly increased in the blood samples of AS patients and ox-LDL treated VSMCs and HUVECs. DANCR regulated COX20 expression by acting as a competing endogenous RNA (ceRNA) of miR-214-5p. Rescue experiments demonstrated that miR-214-5p downregulation obviously attenuated si-DANCR-induced protective effects on ox-LDL-caused endothelial injury.		Yes	DANCR downregulation obviously increased viability and reduced apoptosis of ox-LDL-treated VSMCs and HUVECs. Meanwhile, DANCR downregulation reduced the levels of inflammatory cytokines, including interleukin (IL)-6 (IL-6), IL-1beta (IL-1β), IL-6 and tumor necrosis factor (TNF)-alpha (TNF-α) and MDA while increasing the SOD level in ox-LDL-treated VSMCs and HUVECs. 	35177003
DANCR	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Interaction[Sponging miR-214-5p]	CCK8//qRT-PCR//Western Blot//Transwell Assay	DANCR was markedly upregulated in clinical tissues and cell lines of PC.  Furthermore, DANCR acted as sponge to regulate miR-214-5p, and miR-214-5p inhibitor reversed the effects of DANCR knockdown on PC cells. Moreover, DANCR positively modulated E2F2 expression through miR-214-5p in PC cells.	High DANCR expression exhibited a significant correlation with poor prognosis. 	Yes	 DANCR knockdown inhibited growth and metastasis of PC cells. 	31213582
DANCR	LncRNA	Homo sapiens	Ovarian Neoplasms	Ovarian Cancer tissues	Interaction[Expression[Expression[highly expressed]-expression]F1]	qRT-PCR//RIP	DANCR was Expression[Expression[up-expression]-expression]regulated in OC tissues and cell lines.Expression[Expression[up-expression]-expression]F1 was found to be Expression[down-expression]regulated in OC tissues and negatively correlated to DANCR. DANCR was mainly distributed in the cytoplasm and interacted with Expression[Expression[up-expression]-expression]F1. 		Yes	Overexpression of DANCR accelerated HO8910 and HEY cells to proliferate and migrate. 	31858532
DANCR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell	Interaction(miR-125b-5p)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	In HCC cells, DANCR was highly expressed and miR-125b-5p was decreased. evels of p-p38/p38, p-ERK1/2/ERK1/2, and p-JNK/JNK were suppressed by sh-DANCR and miR-125b-5p mimic. LncRNA DANCR negatively targeted and directly bound to miR-125b-5p. Knockdown of miR-125b-5p could reverse the inhibitory effects of sh-DANCR on HCC cells.		Yes	 sh-DANCR or miR-125b-5p mimic stimulation reduced HepG2 or Huh-7 cell progression while promoted cell apoptosis evidenced by increased apoptotic rate, elevated levels of Bax and cleaved-caspase-3, and decreased Bcl-2. Moreover, the migration rate and invasiveness of HCC cells were also inhibited by sh-DANCR and miR-125b-5p mimic.	33272103
DANCR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[HNRNPA1 ]	RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay//ChIP	The results indicated that ANCR was highly expressed in HCC tissues and cells, which promoted the proliferation and migration/invasion of HCC cells. In conclusion, ANCR promoted HCC metastasis by upregulating HNRNPA1, inhibiting HNRNPA1 degradation and sponging miR-140-3p.		Yes	The results indicated that ANCR was highly expressed in HCC tissues and cells, which promoted the proliferation and migration/invasion of HCC cells.	31868085
DANCR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[DANCR/miR-138/Sox4]	ChIP//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Transwell Assay	Here, we demonstrated that differentiation antagonizing noncoding RNA (DANCR) was overexpressed in NSCLC tissues. In addition, we found that Sox4 bound to the promoter regions of DANCR gene to activate DANCR expression, suggesting a positive feedback loop of DANCR/miR-138/Sox4 in NSCLC. 	Upregulation of DANCR expression was significantly associated with larger tumor size, advanced TNM stage and lymph node metastasis, and also predicted poor prognoses of patients with NSCLC. 	Yes	Functional experiments showed that DANCR enhanced NSCLC growth and metastasis both in vitro and in vivo.	30906628
DARS1-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cell lines	Interaction(miR-188-5p/ KLF12 axis)	Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//BrdU//Colony Formation Assay//Invasion Assay	Cell functional experiments revealed that lncRNA DARS-AS1 participated in enhancing LUAD proliferation, invasion, and migration by inhibiting miR-188-5p. The investigation on DARS-AS1/miR-188-5p led to the discovery of KLF12 as a downstream target of miR-188-5p, and the regulatory pathway was established as DARS-AS1/miR-188-5p/KLF12. 		Yes	Cell functional experiments revealed that lncRNA DARS-AS1 participated in enhancing LUAD proliferation, invasion, and migration by inhibiting miR-188-5p. The investigation on DARS-AS1/miR-188-5p led to the discovery of KLF12 as a downstream target of miR-188-5p, and the regulatory pathway was established as DARS-AS1/miR-188-5p/KLF12. 	34644678
DANCR	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer Tissue 	regulation[FoxO1 ]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//ELISA//Transwell Assay	 LncRNA ANCR was highly expressed in GC.  Based on these results, the overexpression of LncRNA ANCR promoted the invasion and metastasis of GC cells via down-regulating FoxO1 to inhibit macrophage polarization to M1.		Yes	The overexpression of LncRNA ANCR in macrophages reduced the concentrations of M1 macrophage polarized marker molecules IL-1β and IL-6 in the supernatant of cells, and inhibited the polarization of macrophages to M1, while the knockdown of LncRNA ANCR produced the opposite effect.	31894487
DANCR	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	regulation[miR-4319/VAPB axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	DANCR and VAPB were upregulated, while miR-4319 was downregulated in breast cancer tissues and cells. DANCR facilitated breast cancer cell progression through regulating the miR-4319/VAPB axis, indicating that DANCR might be a potential biomarker and therapeutic target for breast cancer treatment.		Yes	Knockdown of DANCR hindered proliferation, migration, and invasion and promoted apoptosis of breast cancer cells.	32818383
DANCR	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	regulation[DANCR-miR-758-3p-PAX6]	qRT-PCR	 DANCR and PAX6 were up-regulated in BC tissues and cell lines, while miR-758-3p was opposite. DANCR-miR-758-3p-PAX6 molecular network plays a key regulatory role in BC cell apoptosis and autophagy, which may provide reference for treating patients.		Yes	Down-regulating DANCR inhibited the malignant proliferation of BC cells and also promoted apoptosis and autophagy, which showed that caspase-3, caspase-9, Bax/Bcl-2, LC3B, Atg5 transcription and protein levels increased, while Beclin-1 transcription and protein levels decreased. 	32581581
DANCR	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue,cell lines	regulation[SOCS3 ]	qRT-PCR//MTT//ELISA//Transwell Assay//ChIP	DANCR was significantly up-regulated in tissue samples from patients with breast cancer, as well as in breast cancer cell lines, as compared with normal tissues and breast epithelial cells, respectively. Mechanistically, DANCR promoted the binding of enhancer of zeste homolog 2 (EZH2) to the promoter of SOCS3, thereby epigenetically inhibiting SOCS3 expression.	The highest DANCR expression levels were associated with advanced tumor grades or lymph node metastasis. 	Yes	DANCR was necessary and sufficient to control multiple malignant phenotypes of breast cancer cells in vitro and xenograft growth in vivo. 	31860165
DANCR	LncRNA	Homo sapiens	Breast Neoplasms	Forty-eight breast cancer and paracancerous tissue samples, cell lines	Interaction(miR-331)	Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression of lncRNA ANCR in breast cancer tissue was significantly lower than that in adjacent normal tissue (p < 0.05). LncRNA ANCR was lowly expressed in various human breast cancer cell lines, being lowest in high-metastatic cell line (MDA-MB-231HM) (p < 0.05).  ANCR bound miR-331 targetedly, and the former negatively regulated the expression of the latter. 		Yes	Silencing lncRNA ANCR significantly enhanced the proliferation and invasion capacities of breast cancer cells, and promoted their tumor formation abilities in nude mice (p < 0.05). 	34783641
DANCR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung biopsies and plasma	Regulation[ TGF-β Pathway]	qRT-PCR//Western Blot//Transwell Assay	ANCR was significantly downregulated in NSCLC patients compared with healthy controls in lung biopsies and plasma. ANCR can inhibit NSCLC cell migration and invasion by downregulating TGF-β1 expression.	Downregulated expression of ANCR distinguishes NSCLC patients from healthy controls and low NSCLC expression level indicates shorter postoperative survival time of NSCLC patients. 	Yes	ANCR overexpression inhibited NSCLC cell migration and invasion and downregulated TGF-β1 expression, while TGF-β1 treatment showed no significant effects on ANCR expression but promoted NSCLC cell migration and invasion. 	30154397
DANCR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	A549 and NCI-H1299 cells	Regulation	qRT-PCR//Western Blot	 Over 90% DANCR silencing was observed along with inhibition of cell migration, invasion, and spheroid formation relative to transfection with negative control siRNA in RGD-PEG-ECO nanoparticles. DANCR knockdown further showed efficacy in reducing migration and invasion of epidermal growth factor receptor (EGFR)-inhibitor resistant NSCLC along with resensitization to the inhibitor. 		Yes	 Over 90% DANCR silencing was observed along with inhibition of cell migration, invasion, and spheroid formation relative to transfection with negative control siRNA in RGD-PEG-ECO nanoparticles. DANCR knockdown further showed efficacy in reducing migration and invasion of epidermal growth factor receptor (EGFR)-inhibitor resistant NSCLC along with resensitization to the inhibitor. 	35811871
DANCR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cells	regulation[Wnt/β-Catenin Signaling Pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	Our results showed that ANCR was lowly expressed in both HCC tissues and HCC cells.Our study demonstrated that ANCR can suppress cell proliferation, migration and invasion, as well as promote apoptosis of HCC cells via modulation of the Wnt/β-catenin signaling pathway.	 ANCR expression was closely associated with tumor size, tumor-node-metastasis (TNM) stages and vascular invasion in HCC.	Yes	ANCR could dramatically inhibit cell proliferation, migration and invasion, as well as promote apoptosis in MHCC97H and HCCLM3 cells.	32982283
DANCR	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissue	Expression[highly expressed]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP	Compared with paracancerous tissue, ANCR expression in lung cancer tissue significantly increased, and FOXO1 significantly decreased (P<0.01), being negatively correlated (P<0.01). 	The patients with higher TNM stage, lower differentiation degree and lymph node metastasis had higher relative expression of ANCR lncRNA. 	Yes	Compared with the NC group, sh-ANCR lncRNA and FOXO1 groups had fewer proliferative cells, more significant arrest in the G0/G1 phase, more apoptotic cells, increased expressions of Bax and P27, and reduced expressions of Bcl-2 and cyclin D1 (P<0.05). Compared with the sh-ANCR lncRNA group, the above results of the sh-ANCR lncRNA + sh-FOXO1 group were reversed (P<0.05).	35117833
DANCR	LncRNA	Homo sapiens	Lung Neoplasms	 high-grade lung cancer tissues and aggressive cancer cells	Interaction(miR-216a)	qRT-PCR//RNA Pull-Down//Colony Formation Assay	 DANCR upregulation was seen in lung cancer, particularly in high-grade lung cancer tissues and aggressive cancer cells. The miR-216a level in cancer cells was negatively correlated with DANCR expression. 		Yes	 Ectopic DANCR expression induced lung cancer cell proliferation and colony formation, whereas DANCR silencing induced opposing effects. The miR-216a level in cancer cells was negatively correlated with DANCR expression. 	29651883
DANCR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-185-5p/HMGA2 axis)	Western Blot//Wound Healing Assay//qRT-PCR//RIP//Transwell Assay	In this study, we demonstrated that the expression of DANCR was elevated in CRC tissues and cell lines, and its high expression was significantly associated with increased TNM stage and positive lymph node metastasis. DANCR was further identified as a molecular sponge for miR-185-5p, and DANCR could indirectly increase the expression of HMGA2 via repressing miR-185-5p. In conclusion, DANCR/miR-185-5p/HMGA2 axis participated in the progression of CRC.	In this study, we demonstrated that the expression of DANCR was elevated in CRC tissues and cell lines, and its high expression was significantly associated with increased TNM stage and positive lymph node metastasis. 	Yes	 DANCR overexpression promoted CRC cell proliferation, migration, invasion and cell cycle progression, but inhibited apoptosis; while knocking down DANCR caused the opposite effects. 	33481014
DANCR	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues and cell lines	regulation[DANCR/microRNA-518a-3p/MDMA]	qRT-PCR	DANCR was highly-expressed in CC tissues and cell lines, and higher levels of DANCR were linked with worse prognosis and less survival time of CC patients.This study provided evidence that silencing of DANCR might inhibit the growth and metastasis of CC cells through the DANCR/miR-518a-3p/MDM2 ceRNA network and the defect of Smad2/3 while activation of the p53 signaling pathways. 	DANCR was highly-expressed in CC tissues and cell lines, and higher levels of DANCR were linked with worse prognosis and less survival time of CC patients.	Yes	Silencing of DANCR inhibited proliferation, viability, metastasis and resistance to death of CC cells.	32423468
DANCR	LncRNA	Homo sapiens	Osteoarthritis	OA tissues and cells	Interaction(miR-577/SphK2 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 The present study found that DANCR was significantly upregulated in patients with OA. The study also showed that DANCR acted as a competitive endogenous RNA to sponge miR-577, which targeted the mRNA of SphK2 to regulate the survival of OA chondrocytes.		Yes	 Functional assays demonstrated that DANCR inhibition suppressed the proliferation of OA chondrocytes and induced cell apoptosis. 	29678573
DANCR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Interaction[ROCK1/LIMK1/COFILIN1 pathway]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	 The results of qRT-PCR and bioinformatic analysis revealed the high expression of DANCR in HCC. Next, the antineoplastic effect of miR-27a-3p on cell growth and motility of HCC was confirmed. In addition, we clarified that DANCR acted as a ceRNA to decoy miR-27a-3p via mediating ROCK1/LIMK1/COFILIN1 pathway. In the end, we validated that DANCR/miR-27a-3p axis regulates EMT progression by cell immunofluorescence and Western blot.		Yes	DANCR accelerated proliferation and metastasis of HCC cells and the knockdown of DANCR had the opposite effect. Meanwhile, xenograft tumours in sh-DANCR group grow slower and have smaller volumes compared with negative control group. 	31038266
DANCR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Interaction[targeting miR-216a-5p and KLF12]	qRT-PCR	We found that DANCR was significantly upregulated in HCC cell lines in comparison to LO2 cells.Here, the correlation between miR-216a-5p and DANCR was confirmed using dual-luciferase reporter assay and radioimmunoprecipitation assay. Subsequently, Kruppel-like factor 12 (KLF12) exerts an important role in different tumor types. KLF12 can function as a downstream target of miR-216a-5p.		Yes	Then, we observed that knockdown of DANCR could greatly inhibit Huh7 and HepG2 cell proliferation. In addition, HCC cell apoptosis was increased by silence of DANCR and meanwhile, cell cycle progression was blocked in G1 phase. Apart from these, downregulation of DANCR repressed HCC cell migration and invasion ability obviously.Finally, the in vivo experiments were used and the data proved that DANCR also strongly suppressed HCC tumor growth in vivo via targeting miR-216a-5p and KLF12. 	30430564
DGCR5	LncRNA	Mus musculus	Chronic Sciatic Nerve Injury	dorsal spinal cord	Regulation[DGCR5/miR-330-3p/PDCD4 axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ELISA	Here, it was observed that DGCR5 was significantly decreased in chronic sciatic nerve injury (CCI) rat models. Taken these together, it was implied that DGCR5/miR-330-3p/PDCD4 axis participated in neuropathic pain treatment.		Yes	DGCR5 overexpression was able to alleviate neuropathic pain development including mechanical and thermal hyperalgesia.	30317600
DGCR5	LncRNA	Homo sapiens	Prostatic Neoplasms	PC Tissues	Interaction[TGF-β1]	qRT-PCR//Western Blot	we found that DGCR5 was Expression[down-expression]-regulated in tumor tissues than in adjacent healthy tissues of PC patients.DGCR5 and TGF-β1 were inversely correlated in tumor tissues but not in adjacent healthy tissues.	DGCR5 expression was not affected by clinical stages, but low DGCR5 level in the tumor was correlated with poor survival. 	Yes	DGCR5 over-expression resulted in Expression[down-expression]-regulation of TGF-β1, while TGF-β1 treatment did not significantly affect DGCR5 expression. DGCR5 over-expression led to decreased stemness of PC cells, but TGF-β1 treatment played a reverse role and attenuated the effects of DGCR5 over-expression. 	31920375
DLGAP1-AS2	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(Six3/Wnt1/β-catenin signaling axis)	IHC//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//ChIP	In agreement with previous studies, our findings demonstrated that DLGAP1-AS2 was significantly up-regulated in GC and its high expression was associated with poor prognosis, suggesting that DLGAP1-AS2 might be a putative oncogenic lncRNA of GC.Taken together, our results suggest that DLGAP1-AS2 functions as an oncogenic factor by directly interacting with Six3 to relieve its suppression on Wnt1 expression, thereby driving the malignancy of GC. DLGAP1-AS2/Six3/Wnt1/β-catenin signaling axis might serve as a promising diagnostic and therapeutic target for GC.	In agreement with previous studies, our findings demonstrated that DLGAP1-AS2 was significantly up-regulated in GC and its high expression was associated with poor prognosis, suggesting that DLGAP1-AS2 might be a putative oncogenic lncRNA of GC.	Yes	 Loss of DLGAP1-AS2 restricted cell proliferation, migration, and invasion in GC cell lines. 	34545072
DLEU2	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells 	Interaction(RARB /MAPK)	qRT-PCR//Transwell Assay//RIP//ChIP	DLEU2 was highly expressed in CRC according to the bioinformatic analysis and its high expression was detected in CRC cells compared to the normal colon epithelial cells (FHC). Retinoic acid receptor beta (RARB) expression was elevated in cells after DLEU2 downregulation. The promoter methylation of RARB was enhanced in CRC cells compared to normal FHC cells. DLEU2 induced promoter methylation of RARB to downregulate its expression. Further silencing of RARB restored proliferation and invasiveness of cells blocked by sh-DLEU2. Upregulation of DLEU2 activated the mitogen activated kinase-like protein (MAPK) signaling pathway to trigger CRC progression. 		Yes	Downregulation of DLEU2 in CRC SW480 and HT29 cells suppressed viability, migration, invasiveness, and resistance to apoptosis of cells. 	35611845
DLEU2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue samples and cell line	Interaction(miR-30a-5p/PTP4A1 axis)	qRT-PCR	 As a consequence, we found that lncRNA DLEU2 was upregulated in HCC tissue samples and associated with distant metastasis and poor survival in patients with HCC. Furthermore, lncRNA DLEU2 harbored a negative correlation and specific binding with miR-30a-5p in HCC cells. Knockdown of lncRNA DLEU2 upregulated miR-30a-5p, but downregulated its target PTP4A1, and miR-30a-5p abrogated lncRNA DLEU2-induced tumor-promoting effects and PTP4A1 upregulation. 	 As a consequence, we found that lncRNA DLEU2 was upregulated in HCC tissue samples and associated with distant metastasis and poor survival in patients with HCC.	Yes	Knockdown of lncRNA DLEU2 impaired HCC cell proliferation, colony formation and invasion, but ectopic expression of lncRNA DLEU2 abolished these effects. 	36049439
DLEU2	LncRNA	Homo sapiens	Osteosarcoma	 osteosarcoma tissues and cells	interaction[miR-337-3p]	qRT-PCR//Luciferase Report Assay//RIP	 In osteosarcoma tissues and cells, DLEU2 expression level was raised remarkably in comparison with that in para-carcinoma normal tissues, and DLEU2 high expression had associations with poor prognosis, tumour stages, and TS of osteosarcoma cases.This study is the first to demonstrate the roles of DLEU2 in osteosarcoma and revealed that DLEU2 may serve as a ceRNA to sponge miR-337-3p and then promote the progression of osteosarcoma, providing a potential therapeutic target for osteosarcoma.	 In osteosarcoma tissues and cells, DLEU2 expression level was raised remarkably in comparison with that in para-carcinoma normal tissues, and DLEU2 high expression had associations with poor prognosis, tumour stages, and TS of osteosarcoma cases.	Yes	Cell migration ability and viability were blocked by DLEU2 knockdown but enhanced by ectopic DLEU2 expression in vitro and in vivo. 	32196715
DLEU2	LncRNA	Homo sapiens	Esophageal Neoplasms	EC tissues	Regulation[miR-30e-5p/E2F7 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	With the help of GEPIA analysis, we observed that lncRNA DLEU2 was up-regulated in EC tissues and associated with poor prognosis. 		Yes	Loss-of-function assay showed that silencing lncRNA DLEU2 inhibited the proliferation, migration and invasion of EC cells, and induced apoptosis by regulating the Bcl-2/Bax axis and Caspase cascade. Overexpression of lncRNA DLEU2 increased the proliferation, migration and invasion abilities of TE-1 cells, as well as decreased cell apoptosis.	31884338
DLEU2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tumor tissues	interaction[Targeting miR-128-3p]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay	We demonstrated that DLEU2 was upregulated in cervical cancer tumor tissues. Taken together, these results suggested knockdown of DLEU2 inhibited cervical cancer progression via targeting miR-128-3p.		Yes	Downregulation of DLEU2 inhibited cell proliferation, induced apoptosis and cell cycle arrest at G2/M phase of cervical cancer cells in vitro, and suppressed tumor growth in vivo. 	33116599
DLEU2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction(ZFP36)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//migration assay//RNA-seq//Cell Proliferation Assay//Colony Formation Assay	Here, the results of RNA microarray and RNA-sequencing dataset analysis showed that lncRNA DLEU2 was significantly upregulated in CC tissues. Mechanistically, lncRNA DLEU2 promoted the progression of the cell cycle and inhibited the activity of the Notch signaling pathway by inhibiting p53 expression. Additionally, lncRNA DLEU2 probably interacted with ZFP36 Ring Finger Protein (ZFP36) to inhibit the expression of p53. 		Yes	Functional experiments and bioinformatics analysis revealed that lncRNA DLEU2 promoted CC cell proliferation and accelerated the cell cycle. 	33675808
DLEU2	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues and cell lines	Interaction(miR-205-5p/TNFAIP8 axis)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Bioinformatics Analysis//Transwell Assay	DLEU2 and tumor necrosis factor-α-induced protein 8 (TNFAIP8) were highly expressed in thyroid cancer tissues and cell lines.  DLEU2/miR-205-5p/TNFAIP8 signaling axis was identified in thyroid cancer cells. 		Yes	DLEU2 and TNRAIP8 promoted the proliferation, migration and aerobic glycolysis and restrained the apoptosis of thyroid cancer cells. 	33764889
DLEU2	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and PC cell lines	Interaction[upregulating microRNA-455]	CCK8//qRT-PCR//Western Blot	 In this study, we found that the DLEU2 level was substantially upregulated in PC tissues and PC cell lines, and significantly associated with poor clinical outcomes in PC patients. Furthermore, bioinformatics analysis, luciferase reporter assay, and RNA immunoprecipitation assay revealed that DLEU2 directly bond to microRNA-455 (miR-455) and functioned as an endogenous sponge for miR-455, which could remarkably suppress cell growth and invasion. We also determined that SMAD2 was a direct target of miR-455, and the restoration of SMAD2 rescued cell growth and invasion that were reduced by DLEU2 knockdown or miR-455 overexpression. In addition, low miR-455 expression and high SMAD2 expression was correlated with poor patient survival. These results indicate that DLEU2 is an important promoter of PC development, and targeting the DLEU2/miR-455/SMAD2 pathway could be a promising therapeutic approach in the treatment of PC.		Yes	Overexpression of DLEU2 significantly induced PC cell proliferation and invasion, whereas knockdown of DLEU2 impaired cell proliferation and invasion in vitro. 	30838724
DLEU2	LncRNA	Homo sapiens	Idiopathic Pulmonary Fibrosis	IPF tissues	Interaction(miR‑369‑3p / TRIM2)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//IHC//IF	As a result, DLEU2 expression was found to be upregulated in IPF and in transforming growth factor (TGF)‑β1‑stimulated A549 cells.  DLEU2 directly targeted miR‑369‑3p. The effect of the silencing of DLEU2 on TGF‑β1‑stimulated A549 cells was suppressed by the silencing of miR‑369‑3p. TRIM2 was the target protein of miR‑369‑3p.		Yes	The silencing of DLEU2 inhibited the TGF‑β1‑induced proliferation, migration and epithelial‑mesenchymal transition (EMT) of A549 cells and bleomycin (BLM)‑induced pulmonary fibrosis in mice. 	33760118
DLEU2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCCs tissues	regulation[miR-30c-5p/PIK3CD/Akt axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//EdU Staining	We found that DLEU2 was significantly upregulated and predicted poor clinical outcomes in LSCC patients.DLEU2 and its targeted miR-30c-5p/PIK3CD/Akt axis may represent valuable prognostic biomarkers and therapeutic targets for LSCCs.		Yes	In addition, ectopic overexpression of DLEU2 promoted the proliferation and migration of LSCC cells both in vivo and in vitro.	32555190
DLEU2	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Interaction(miR-582-5p/SGK1 axis)	In Vivo Experiment//ChIP//Western Blot//Transfection//qRT-PCR//FISH//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	Our results showed that DLEU2 was upregulated in advanced prostate cancer tissues. Mechanistically, DLEU2 promoted serum and glucocorticoid-induced protein kinase 1 (SGK1) expression by acting as an miR-582-5p sponge, and the transcription of DLEU2 was activated by the dysregulation of E2F transcription factor 2 (E2F2) expression in prostate cancer. Furthermore, knockdown of DLEU2 attenuated prostate cancer tumorigenesis in vivo. 	Patients with prostate cancer displaying high expression of DLEU2 had a poor prognosis. 	Yes	Moreover, we demonstrated that overexpression of DLEU2 facilitated the proliferation, migration, and invasion of prostate cancer in vitro. 	35075115
DLEU2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[sponging miR-30a-5p]	Western Blot//FISH//RIP//qRT-PCR//Transwell Assay	 Herein, the expression of lncRNA DLEU2 was elevated in NSCLC tissues.Furthermore, lncRNA DLEU2 harboured a negative correlation with miR-30a-5p expression in NSCLC tissues and acted as a sponge of miR-30a-5p, which reversed the tumour-promoting effects of lncRNA DLEU2 by targeting putative homeodomain transcription factor 2 in NSCLC. Altogether, lncRNA DLEU2 promoted the tumorigenesis and invasion of NSCLC by sponging miR-30a-5p.		Yes	Silencing of lncRNA DLEU2 repressed the tumorigenesis and invasive potential of NSCLC, whereas re-expression of lncRNA DLEU2 showed the opposite effects. 	31721438
DLEU2	LncRNA	Homo sapiens	Mouth Neoplasms	 OC cells	Interaction(miR-30a-5p/RAP1B Axis)	Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Microarray//Invasion Assay//Transwell Assay	Our research shows that, in contrast to miR-30a-5p, DLEU2 or RAP1B was upregulated in OC cells, and high expression of DLEU2 or RAP1B was associated with poorer overall survival.miR-30a-5p was predicted to interact with DLEU2 or RAP1B by bioinformatics, and dual-luciferase analysis confirmed this interaction. Notably, si-DLEU2 suppressed RAP1B expression and protein level, and after overexpression of RAP1B in OC cells, reversal of suppressed DLEU2 expression was observed. 	Our research shows that, in contrast to miR-30a-5p, DLEU2 or RAP1B was upregulated in OC cells, and high expression of DLEU2 or RAP1B was associated with poorer overall survival.	Yes	Inhibiting the expression of DLEU2 slowed the proliferation and reduced the ability of migration and invasion of Tca8113 and CAL-27 cells. 	36277988
DLEU2	LncRNA	Homo sapiens	Wilms Tumor	Wilm's tumor tissues and in vitro cell lines	Interaction(miR-539-3p/HOXB2 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Transwell Assay	DLEU2 and HOXB2 were significantly highly expressed in primary Wilm's tumor tissues and in vitro cell lines.MiR-539-3p was confirmed to be a target of DLEU2. DLEU2 silencing inhibited the malignant behaviors of Wilm's tumor cells by releasing miR-539-3p. In addition, HOXB2 was a target of miR-539-3p. Overexpression of HOXB2 partially restored the inhibitory effects of miR-539-3p on Wilm's tumor cell malignant behaviors.		Yes	Silencing of DLEU2 reduced the proliferation, migration and invasion of Wilm's tumor cells, and promoted cell apoptosis. Animal experiments also confirmed the anti-tumor effects of DLEU2 silencing in vivo.	36209036
DLEU1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[DLEU1/microRNA-300/RAB22A axis]	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	DLEU1 expression remains higher in breast cancer tissues than in normal adjacent tissues, and has a certain diagnostic value. Dual-luciferase reporter gene assay confirmed that DLEU1 and RAB22A could bind to microRNA-300. Further verification showed that RAB22A expression was positively regulated by DLEU1, but negatively regulated by microRNA-300. Finally, we found that DLEU1 overexpression could reverse the inhibitory effects of microRNA-300 on proliferation, migration, and EMT of breast cancer cells.	The overall survival of breast cancer patients was negatively correlated with DLEU1 expression. 	Yes	Overexpression of DLEU1 or RAB22A, or microRNA-300 knockdown could enhance the migratory and invasive capacities, as well as increase EMT ofBT549 cells. On the contrary, knockdown of DLEU1 or RAB22A, or microRNA-300 overexpression in MCF-7 cells obtained the opposite trends of cellular behaviors.	31841195
DLEU1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Regulation(HIF-1α/CKAP2 )	In Vivo Experiment//RNA Pull-Down//Transwell Assay//RIP//Colony Formation Assay//ChIP	We demonstrated that up-regulation of DLEU1 was detected in breast cancer tissues and cells, particularly in tumors of higher malignancy. Mechanistically, DLEU1 interacted with HIF-1α to collectively activate the transcription of CKAP2. By activating ERK and STAT3 signaling, CKAP2 essentially mediated the pro-tumor activities of DLEU1.		Yes	DLEU1 knockdown inhibited the growth and the motility of breast cancer cells. 	35853854
DLEU1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tumor tissues	Expression[highly expressed]	Western Blot//Wound Healing Assay//EdU Staining//qRT-PCR//RIP//Invasion Assay	The expression of DLEU1 was up-regulated in NSCLC tumor tissues.DLEU1 overexpression promoted the proliferation, migration, and invasion, but inhibited the apoptosis of NSCLC cells by upregulating CDK1 expression, binding with SRC and altering the expression of P70(S6K), MMP2 and E-cadherin. 		Yes	DLEU1 overexpression promoted the proliferation, migration, and invasion, but inhibited the apoptosis of NSCLC cells by upregulating CDK1 expression, binding with SRC and altering the expression of P70(S6K), MMP2 and E-cadherin. Besides, xenograft tumors in nude mice demonstrated that DLEU1 overexpression accelerated tumor growth.	30551552
DLEU1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissue and cells	Interaction(DLEU1/DYNLL1 axis )	RNA Pull-Down//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay	 In a screen for differentially expressed lncRNAs in ESCC, we determined that DLEU1 was one of the most overexpressed lncRNAs in ESCC tissues and that upregulated DLEU1 expression was associated with a worse prognosis. Mechanistically, DLEU1 could bind and stabilize DYNLL1 by interfering with RNF114-mediated ubiquitination and proteasomal degradation. The DLEU1/DYNLL1 axis subsequently upregulated antiapoptotic BCL2 and promoted cell survival. Furthermore, DLEU1 upregulation was at least partly facilitated by promoter hypomethylation. 	 In a screen for differentially expressed lncRNAs in ESCC, we determined that DLEU1 was one of the most overexpressed lncRNAs in ESCC tissues and that upregulated DLEU1 expression was associated with a worse prognosis.	Yes	Functional assays showed that DLEU1 promoted tumor growth by inhibiting cell apoptosis. 	35619131
DLEU1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction( miR-320b/PRPS1)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Transwell Assay	In our study, the level of DLEU1 in CRC tissues is investigated by qRT-PCR. Our data exhibited that DLEU1 level was observably increased in CRC tissues and CRC cell lines and was closely associated with bad prognosis of CRC patients.Mechanistically, through interacting with miR-320b in CRC, DLEU1 promoted the level of PRPS1 which was a target of miR-320b. The rescue experiment confirmed that knockdown of DLEU1 repressed cell proliferation, migration and invasion while stimulated cell apoptosis via miR-320b/phosphoribosyl pyrophosphate synthetase 1 (PRPS1) axis. 	In our study, the level of DLEU1 in CRC tissues is investigated by qRT-PCR. Our data exhibited that DLEU1 level was observably increased in CRC tissues and CRC cell lines and was closely associated with bad prognosis of CRC patients.	Yes	CRC cell proliferation was repressed by sh-LncRNA DLEU1, whereas cell apoptosis was markedly stimulated. Moreover, knockdown of DLEU1 inhibited cell migration and invasion. 	34113562
DLEU1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines 	Regulation[DLEU1/miR-133a/IGF-1R axis]	qRT-PCR//Luciferase Report Assay//RIP	 In this study, real-time quantitative polymerase chain reaction (qRT-PCR) in HCC tissues and cell lines revealed that DLEU1 expression was up-regulated, and the increased DLEU1 was closely associated with advanced tumour-node-metastasis stage, vascular metastasis and poor overall survival. Luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay demonstrated that DLEU1 could sponge miR-133a. Moreover, miR-133a inhibition significantly reversed the suppression effects of DLEU1 knockdown on HCC cells. Besides, we found that silenced DLEU1 significantly decreased insulin-like growth factor 1 receptor (IGF-1R) expression (a target of miR-133a) and its downstream signal PI3K/AKT pathway in HCC cells, while miR-133a inhibitor partially reversed this trend. Furthermore, DLEU1 knockdown impaired tumour growth in vivo by regulating miR-133a/IGF-1R axis. Collectively, these findings indicate that DLEU1 promoted HCC progression by sponging miR-133a to regulate IGF-1R expression. Deleted in lymphocytic leukaemia 1/miR-133a/IGF-1R axis may be a novel target for treatment of HCC.	 In this study, real-time quantitative polymerase chain reaction (qRT-PCR) in HCC tissues and cell lines revealed that DLEU1 expression was up-regulated, and the increased DLEU1 was closely associated with advanced tumour-node-metastasis stage, vascular metastasis and poor overall survival.	Yes	Function experiments showed that knockdown of DLEU1 significantly inhibited HCC cell proliferation, colony formation, migration and invasion, and suppressed epithelial to mesenchymal transition (EMT) process via increasing the expression of E-cadherin and decreasing the expression of N-cadherin and Vimentin.	31207081
DLEU2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[binding to EZH2]	Western Blot//CCK8//qRT-PCR//RIP//Colony Formation Assay//EdU Staining//Transwell Assay	DLEU2 was upregulated in HCC tissues.DLEU2 accelerates the proliferative, migratory and invasive abilities of HCC cells via binding to EZH2, thus aggravating the progression of HCC.	DLEU2 was upregulated in HCC tissues, especially in those larger than 5 cm in tumor size, accompanied with vascular invasion and in worse tumor stage.	Yes	Knockdown of DLEU2 attenuated proliferative, migratory and invasive abilities of SMMC7721 and HCLM3 cells.Knockdown of EZH2 attenuated the inhibited proliferation in HCC cells with DLEU2 knockdown.	31376657
DLEU2	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-375-3p/FOXF1 )	CCK8//qRT-PCR//Transwell Assay//Western Blot	LINC00022 was highly expressed in CRC tissues compared with paired para-carcinoma tissues (n = 41).  Conversely, LINC00022 overexpression showed that opposite effect. We further demonsrtaed that LINC00022 could upregulate FOXF1 expression through sponging miR-375-3p. Moreover, miR-375-3p knockdown reversed the effects of LINC00022 down-regulation.		Yes	 CRC cells with LINC00022 knockdown exhibited decreased cell proliferation, migration, and invasion abilities but increased apoptosis accompanied by decreased protein levels of c-Myc, cyclin D1, cleaved caspase 3, cleaved poly(ADP-ribose) polymerase, matrix metalloproteinase (MMP) 2, and MMP9. Additionally, LINC00022 downregulation in CRC cells suppressed the tube formation of human umbilical vein endothelial cells (HUVECs) as evidenced by decreased vascular endothelial growth factor A levels in LINC00022-silenced cells. The inhibitory effect of LINC00022 knockdown on tumor growth was also observed in an in vivo model. 	35468741
DGCR5	LncRNA	Homo sapiens	Gallbladder Neoplasms	GBC tissues and cell lines	regulation[MEK/ERK1/2 and JNK/p38 MAPK Pathways]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Here, we found that DGCR5 was upregulated in GBC tissues and cell lines.Taken together, it was uncovered in our study that DGCR5 exerts an oncogenic role by sponging miR-3619-5p and activating MEK/ERK1/2 and JNK/p38 MAPK pathways in GBC progression.		Yes	Through functional experiments, it was demonstrated that silence of DGCR5 significantly suppressed the cell proliferation, migration, invasion, and induced apoptosis and cell cycle arrest in GBC cells. 	32742494
DLEU2	LncRNA	Homo sapiens	Colorectal Neoplasms	45 pairs of CRC tissues	Interaction(CDK6/CDKN1A)	CCK8//qRT-PCR//Transwell Assay//Western Blot	 This study sought to investigate the effects of DLEU2 on CRC pathogenesis, and the underlying mechanism involved. Using a quantitative real-time polymerase chain reaction (qRT-PCR) assay, we demonstrated that the expression levels of DLEU2 in 45 pairs of CRC tissues were higher than those in the corresponding normal colon mucosal tissues.  When DLEU2 was silenced using short interfering RNA (siRNA) in CRC cell line, the results demonstrated that DLEU2 silencing suppressed CRC cell tumorigenesis in vitro, which was associated with decreased expression of cyclin dependent kinase 6(CDK6), ZEB1, and ZEB2 as well as enhancing the expression of Cyclin-dependent kinase inhibitor 1A (CDKN1A). 	In addition, CRC patients with high DLEU2 expression levels exhibited poor overall survival (OS) and recurrence-free survival (RFS), as determined by analyses and measurements from the GEO and GEPIA databases. 	Yes	 When DLEU2 was silenced using short interfering RNA (siRNA) in CRC cell line, the results demonstrated that DLEU2 silencing suppressed CRC cell tumorigenesis in vitro, which was associated with decreased expression of cyclin dependent kinase 6(CDK6), ZEB1, and ZEB2 as well as enhancing the expression of Cyclin-dependent kinase inhibitor 1A (CDKN1A). 	33391439
DLGAP1-AS2	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells 	Interaction(AFF3/ER)	RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay	Our results showed that DLGAP1-AS2 is significantly upregulated in breast cancer and that tamoxifen can induce DLGAP1-AS2 expression. Mechanistically, DLGAP1-AS2 can bind to the AFF3 protein to inhibit its degradation, which further promotes ER signalling.		Yes	Further investigation suggested that upregulation of DLGAP1-AS2 can increase cell viability and inhibit apoptosis, while downregulation of DLGAP1-AS2 results in the opposite effects. 	35449318
DLGAP1-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC and paired non-tumor tissues from 64 NSCLC patients	Interaction(miR-503/cyclin D1)	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	DLGAP1-AS2 was upregulated in NSCLC and predicted poor survival.Interaction between DLGAP1-AS2 and miR-503 was confirmed by dual luciferase activity assay. Overexpression experiments showed that DLGAP1-AS2 and miR-503 overexpression failed to significantly affect the expression of each other. Interestingly, DLGAP1-AS2 overexpression upregulated cyclin D1, a target of miR-503, increased cell proliferation and reduced the effects of miR-503 overexpression on cyclin D1 expression and cell proliferation.	DLGAP1-AS2 was upregulated in NSCLC and predicted poor survival.	Yes	Overexpression experiments showed that DLGAP1-AS2 and miR-503 overexpression failed to significantly affect the expression of each other. Interestingly, DLGAP1-AS2 overexpression upregulated cyclin D1, a target of miR-503, increased cell proliferation and reduced the effects of miR-503 overexpression on cyclin D1 expression and cell proliferation.	34454450
DLGAP1-AS2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC cells.	Epigenetics(m6A-modified)	qRT-PCR//MeRIP//RIP//Western Blot	 Clinical data showed that DLGAP1-AS2 high-expression was correlated with advanced pathological stage and poor prognosis. Mechanistically, m6A methyltransferase METTL3 enhanced the stability of DLGAP1-AS2 via m6A site binding. Moreover, DLGAP1-AS2 interacted with YTHDF1 to enhance the stability of c-Myc mRNA through DLGAP1-AS2/YTHDF1/m6A/c-Myc mRNA.	 Clinical data showed that DLGAP1-AS2 high-expression was correlated with advanced pathological stage and poor prognosis. 	Yes	Functionally, DLGAP1-AS2 overexpression promoted the aerobic glycolysis and DLGAP1-AS2 knockdown suppressed the tumor growth of NSCLC cells. 	35972892
DLGAP1-AS2	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(CTCF/Myc)	MeRIP//qRT-PCR//RIP//Luciferase Report Assay//IHC//ChIP	 DLGAP1-AS2 was significantly increased in CRC tissues and cell lines.  Mechanistically, DLGAP1-AS2 directly bound CTCF, a well-known transcriptional repressor of Myc, resulting in reduced binding of CTCF on Myc promoter and activating Myc transcription. The second hairpin structure of DLGAP1-AS2 was critical for the interaction between DLGAP1-AS2 and CTCF in the nucleus. 		Yes	 Knockdown of DLGAP1-AS2 inhibited CRC cell proliferation, migration, invasion in vitro, and tumor growth in vivo.	36222892
DLGAP1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-515-5p/MARK4 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	DLGAP1-AS1 was up-regulated in GC tissues and cell lines,  and its high expression was closely associated with larger tumor size, higher TNM  stage, and lymph node metastasis. 		Yes	Furthermore, DLGAP1-AS1 overexpression enhanced cell proliferation, migration, and invasion, and miR-515-5p could reverse these effects. DLGAP1-AS1 participated in the regulation of the MARK4 signaling pathway by targeting miR-515-5p. 	34037089
DLGAP1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells 	Interaction(miR-149-5p/TGFB2 axis)	CCK8//qRT-PCR//Western Blot	These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC.		Yes	Functional assays showed that silencing DLGAP1-AS1 expression remarkably inhibited cell proliferation and aggressiveness ability and enhanced apoptosis rate and cell chemosensitivity to 5-FU. 	33816780
DLGAP1-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction( miR-1297/EZH2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 This study seeks to characterize the expression of DLGAP1-AS1 in glioma tissues, which we found to be raised in both glioma samples and cell lines.DLGAP1-AS1 was found to function as a miR-1297 sponge, based on information from luciferase reporter assays, RNA pull-down assays and publicly available online databases. miR-1297 was in turn found to functionally target EZH2. DLGAP1-AS1 modulated EZH2 expressions through miR-1297 sponging.		Yes	Functional experiments revealed that DLGAP1-AS1 promoted in vitro glioma cell invasion, migration and proliferation. 	33901010
DLGAP1-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(DLGAP1-AS1/miR-628-5p/DDX59 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	The authors observed increased DLGAP1-AS1 expression in glioma tissues and cell lines with higher WHO grades and shorter survival time. The authors identified DLGAP1-AS1 as a molecular sponge of miR-628-5p in glioma cells as the biological functions of DLGAP1-AS1 are partially mediated via miR-628-5p. In addition, DLGAP1-AS1 upregulated DDX59 expression by inhibiting miR-628-5p expression.	The authors observed increased DLGAP1-AS1 expression in glioma tissues and cell lines with higher WHO grades and shorter survival time.	Yes	DLGAP1-AS1 promoted the proliferation, migration, invasion, and EMT of glioma cells, while miR-628-5p counteracted these effects. 	35113786
DLGAP1-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM cells	Interaction(miR-515-5p/ROCK1/NFE2L1 axis )	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	DLGAP1-AS1 was distinctly upregulated in GBM cells. MiR-515-5p could be sponged by DLGAP1-AS1 in GBM cells and to repress cell proliferation in GBM. Further, Rho-associated coiled-coil containing protein kinase 1 (ROCK1) and Nuclear factor erythroid-2 like 1 (NFE2L1) were confirmed as the target gene of miR-515-5p. Wnt signaling pathway could be activated by DLGAP1-AS1 via regulating ROCK1 and NFE2L1 expression. 		Yes	 DLGAP1-AS1 depletion inhibited cell proliferation, but induced apoptosis.	34536977
DLGAP1-AS1	LncRNA	Homo sapiens	Glioblastoma	glioma samples, U87 cell and U251 cell 	Regulation(ATG4A)	CCK8//qRT-PCR//Transfection//Bioinformatics Analysis	The results demonstrated that DLGAP1-AS1 was higher in WHO IV glioma than in WHO II and WHO III gliomas, higher in WHO III glioma than in WHO II glioma samples, higher in IDH1 wildtype glioma than in IDH1-mutant glioma samples, and higher in 1p/19q noncodeletion glioma than in 1p/19q codeletion glioma samples. Our conclusion suggested that DLGAP1-AS1 may be a potential prognosis biomarker and facilitated the occurrence and development of glioma via ATG4A in GBM.	Moreover, we observed that higher expression levels of DLGAP1-AS1 were correlated to shorter OS time in both low-grade and high-grade gliomas. 	Yes	 The data revealed that DLGAP1-AS1 knockdown greatly hindered U87 cell and U251 cell proliferation.	35341001
DLGAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cancerous tissues	Interaction(microRNA-193a-5p/DTL axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//RIP//Flow Cytometry//Luciferase Report Assay//IHC//Bioinformatics Analysis//Transwell Assay	The lncRNA DLGAP1-AS1 and denticleless protein homolog (DTL) presented upregulated expression, but microRNA-193a-5p (miR-193a-5p) showed downregulated expression in cancerous tissues of human lung samples from 48 patients with NSCLC. In conclusion, our study highlights a novel regulatory network of the lncRNA DLGAP1-AS1/miR-193a-5p/DTL axis in NSCLC, providing a potential therapeutic strategy for NSCLC.		Yes	 Partial loss of lncRNA DLGAP1-AS1 reduced malignant cell viability, migration, and invasion but induced apoptosis.	36183046
DLG1-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	regulation[ DLG1-AS1/miR-497/YAP1 axis ]	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	The long non-coding RNA (lncRNA), DLG1-AS1, is upregulated in papillary thyroid cancer (PTC) tissues and cell lines. These findings demonstrate that the DLG1-AS1-miR-497-YAP1 axis promotes the growth and metastasis of PTC by forming a ceRNA network.	Here, we found that increased expression of DLG1-AS1 caused lymph node metastasis and advanced tumor-node-metastasis (TNM) stage.	Yes	DLG1-AS1 knockdown inhibited proliferation, invasion, and migration of PTC cells, and impaired tumorigenesis in vivo in mouse xenografts.	33197895
DLG1-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells 	regulation[Downregulating miR-203]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 We found that DLG1-AS1 was upregulated whereas miR-203 was downregulated in tumor tissues of patients and in TNBC cells compared to the adjacent healthy tissues of patients with TNBC and in normal breast MCF-10A cells, respectively.These results indicate that DLG1-AS1 may promote cancer cell proliferation in TNBC by downregulating the tumor suppressor miR-203.		Yes	TNBC cell migration was promoted by DLG1-AS1 overexpression and inhibited by miR-203 overexpression or DLG1-AS1 knockdown.	32908786
DLG1-AS1	LncRNA	Homo sapiens	Thyroid Nodule	blood	Expression[highly expressed]	qRT-PCR	In this study, upregulation of DLG1-AS1 distinguished PTC patients from BTN patients and healthy controls		Yes	In addition, DLG1-AS1 overexpression promoted the proliferation of PTC cells. 	31718630
DLEUI	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues ,cell lines	regulation[miR-421,ROCK1 ]	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//IF	DLEU1 levels were higher in PTC cell lines (BHP5-16, TPC-1,8505C, and SW1736) and patient tissues (n=54) than in a human thyroid follicular epithelial cell line (Nthy-ori3-1) or adjacent normal thyroid tissues.These findings demonstrate that DLEU1 promotes PTC progression by sponging miR-421 and increasing ROCK1 expression.	 High DLEU1 expression correlated positively with lymph node metastasis and advanced clinical stages in PTC patients.	Yes	 CCK-8, flow cytometry, wound healing, and Transwell invasion assays demonstrated that DLEU1 silencing decreases TPC-1 cell proliferation, survival and progression, but they can be rescued by miR-421 knockdown or ROCK1 overexpression. DLEU1 knockdown in TPC-1 cells decreased in vivo xenograft tumor size and weight compared to controls in nude mice. 	32910787
DLEU2	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	 Interaction(miR-23b-3p/NOTCH2 axis and Notch signaling pathway)	RNA Pull-Down//ChIP//Western Blot//Tunel//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	The expression of long non-coding RNA (lncRNA) DLEU2 was observably high in GC cells and tissues. Moreover, DLEU2 was activated by signal transducer and activator of transcription 1 (STAT1) and sequestered microRNA-23b-3p (miR-23b-3p) to modulate the expression of notch receptor 2 (NOTCH2), thereby stimulating Notch signaling pathway. More importantly, DLEU2 contributed to GC progression via targeting miR-23b-3p/NOTCH2 axis.		Yes	DLEU2 silence depressed the capacities of proliferation, migration and invasion but promoted apoptosis in GC cells. 	33785336
DLEU2	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-30a-5p)	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 DLEU2 was significantly up-regulated in GC tissues and cell lines. The expression of DLEU2 was significantly associated with pathological grading and TNM stage of GC patients. Furthermore, knockdown of DLEU2 inhibited the proliferation, migration, and invasion of AGS and MKN-45 cells, while overexpression of DLEU2 promoted the proliferation, migration, and invasion of HGC-27 cells. MiR-30a-5p could directly bind to the 3' UTR region of ETS2. Moreover, DLEU2 bound to miR-30a-5p through the same binding site, which facilitated the expression of ETS2. Knockdown of DLEU2 reduced the protein level of intracellular ETS2 and inhibited AKT phosphorylation, while overexpression of DLEU2 induced the expression of ETS2 and the phosphorylation of AKT. ETS2 was highly expressed in GC tissues. The expression of ETS2 was significantly associated with age, pathological grading, and TNM stage. ETS2 overexpression promoted cell proliferation and migration of AGS and MKN-45 cells. Furthermore, ETS2 overexpression rescued cell proliferation and migration inhibition induced by DLEU2 down-regulation and miR-30a-5p up-regulation in AGS and MKN-45 cells.	The expression of DLEU2 was significantly associated with pathological grading and TNM stage of GC patients. 	Yes	 Furthermore, knockdown of DLEU2 inhibited the proliferation, migration, and invasion of AGS and MKN-45 cells, while overexpression of DLEU2 promoted the proliferation, migration, and invasion of HGC-27 cells. 	34261460
DLEU2	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(DLEU2/PI3K/Akt axis)	CCK8//qRT-PCR//Western Blot//Transwell Assay	The expression of DLEU2 was aberrantly up-regulated in GC tissues and cells, which was correlated with the degree of tumor differentiation, cancer antigen 19-9 (CA19-9) and Lauren histologic classification of patients with GC. Mechanistically, the DLEU2/PI3K/Akt axis promoted the progression of GC and the EMT by down-regulating the expression of E-Cadherin and up-regulating those of N-Cadherin and Vimentin.	The expression of DLEU2 was aberrantly up-regulated in GC tissues and cells, which was correlated with the degree of tumor differentiation, cancer antigen 19-9 (CA19-9) and Lauren histologic classification of patients with GC. 	Yes	Silencing of DLEU2 induced apoptosis, attenuated viability, migration and invasion as well as inhibited the PI3K/Akt signaling pathway in GC cells.	35736813
DLEU2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[miR-30c-5p/SOX9 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our studies confirmed that lncRNA DLEU2 was highly expressed in NSCLC tissues and cell lines. lncRNA DLEU2 directly interacted with miR-30c-5p, which further targeted SOX9 and exerted oncogenic functions in NSCLC. Mechanistically, overexpression of lncRNA DLEU2 exhibits tumorigenic effects through downregulating the inhibitory effect of miR-30c-5p on SOX9 expression. In conclusion, Our finding confirmed that lncRNA DLEU2 as a novel oncogenic in NSCLC, which provide a potential novel diagnostic and therapeutic target for NSCLC.	Our studies confirmed that lncRNA DLEU2 was highly expressed in NSCLC tissues and cell lines, which was correlated with shorter overall survival in NSCLC patients.	Yes	In vitro, knockdown of lncRNA DLEU2 inhibited proliferation, invasion, migration and induced apoptosis of both A549 and LLC cells; In vivo, it suppressed tumor growth and metastasis. 	31541993
DLEU1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	regulation[miR-429/TFAP2A axis]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	 The expression of lncRNA DLEU1 and TFAP2A were upregulated, and miR-429 was downregulated in OC tissues.Silencing of DLEU1 inhibited the proliferation, migration, and invasion of OC cells by regulating miR-429/TFAP2A axis, indicating a potential therapeutic target for OC.		Yes	 Silencing of DLEU1 inhibited the proliferation, migration, and invasion of OC cells.	33170430
DLEU1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BLCA tissues	Regulation[Regulating the miR-99b/HS3ST3B1 Axis]	qRT-PCR//Western Blot	Here, we found that DLEU1 was Expression[up-expression]regulated in BLCA tissues and BCA patients with high DLEU1 expression exhibited a shorter survival time.Furthermore, mechanistic analysis and functional assays validated that DLEU1 induced cell proliferation, invasion, and cisplatin resistance of BCA cells by de-repressing the expression of HS3ST3B1 through sponging miR-99b. Low miR-99b and high HS3ST3B1 levels were correlated with worse prognosis in patients with BCA.	Here, we found that DLEU1 was Expression[up-expression]regulated in BLCA tissues and BCA patients with high DLEU1 expression exhibited a shorter survival time	Yes	Ectopic expression of HS3ST3B1 or inhibition of miR-99b reversed DLEU1 knockdown-mediated sExpression[up-expression]pression of cell proliferation, invasion, and cisplatin resistance.	30984249
DLEU1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 OSCC cells	Interaction(miR‑149‑5p/CDK6 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 Meanwhile, DLEU1 directly bound to miR‑149‑5p, and CDK6 was found to be the direct target of miR‑149‑5p. Furthermore, DLEU1 knockdown‑induced inhibition of OSCC cell proliferation was significantly reversed by the miR‑149‑5p antagomir. Knockdown of lncRNA DLEU1 reversed the proliferation of OSCC cells via regulation of the miR‑149‑5p/CDK6 axis. 	DLEU1 expression was negatively associated with the survival rate of patients with OSCC. 	Yes	In addition, silencing of DLEU1 notably inhibited the proliferation of OSCC cells by inducing apoptosis.	33880596
DIAPH1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cells and tissues 	Epigenetics(m6A methylation)	ChIP//Western Blot//Transfection//Migration Assay//qRT-PCR//Invasion Assay//Transwell Assay	Mechanistically, lncRNA DIAPH1-AS1 was identified as a bona fide m6A target of WTAP. WTAP-mediated m6A modification of DIAPH1-AS1 enhanced its stability relying on the m6A reader IGF2BP2-dependent pathway. Furthermore, DIAPH1-AS1 acted as a molecular adaptor that promoted MTDH-LASP1 complex formation and upregulated LASP1 expression, ultimately facilitating NPC growth and metastasis.		Yes	 Furthermore, DIAPH1-AS1 acted as a molecular adaptor that promoted MTDH-LASP1 complex formation and upregulated LASP1 expression, ultimately facilitating NPC growth and metastasis.	34999731
DHRS4-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[ TP53- and TET1-associated DHRS4-AS1/miR-224-3p axis]	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//RIP	Real-time PCR showed that DHRS4-AS1 was downregulated in cancerous tissues, and bioinformatics analysis revealed that high DHRS4-AS1 expression indicated a good prognosis for NSCLC patients.In conclusion, TP53- and TET1-associated DHRS4-AS1/miR-224-3p axis is an essential mechanism by which NSCLC modulates cancer cell stemness.	Real-time PCR showed that DHRS4-AS1 was downregulated in cancerous tissues, and bioinformatics analysis revealed that high DHRS4-AS1 expression indicated a good prognosis for NSCLC patients.	Yes	DHRS4-AS1 partially reversed the miR-224-3p-decreased TP53 and TET1, resulting in the inhibition of tumor growth in vivo. 	33425890
DHRS4-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells	Interaction(miR-522-3p/SOCS5 axis)	CCK8//qRT-PCR//BrdU//Western Blot	Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues based on the database TCGA. It was also detected in a lower-than-usual expression quantity in HCC tissues we collected and HCC cell lines.Our study subsequently lucubrated that miR-522-3p was a negative target of DHRS4-AS1. Increased expression level of miR-522-3p was examined in HCC tissues and cell lines. Similarly, miR-522-3p mimics could reverse the inhibitory effect on HCC brought by DHRS4-AS1. SOCS5 was then discovered as a down-stream target of miR-522-3p, which suggested that SOCS5 participated in DHRS4-AS1/miR-522-3p axis to collectively mediate the development of HCC. 	Kaplan-Meier survival analysis revealed that high expression of DHRS4-AS1 contributed to higher overall survival rate of HCC patients.	Yes	CCK-8, BrdU and colony-forming assays collectively demonstrated that overexpression of DHRS4-AS1 significantly restrained HCC cell proliferation. In vivo xenograft animal experiment showed that DHRS4-AS1 could efficiently preclude the tumor growth of HCC. Further investigation performed using flow cytometry and western blot showed that DHRS4-AS1 exerted its effects by accelerating cell apoptosis and capturing cell cycle in G0/G1 phase. 	34666613
DHRS4	LncRNA	Homo sapiens	Endometriosis	EC-ESCs and tissues 	Interaction(DHRS4-AS1/miR-139-5p/ARRDC3 axis )	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Compared with the EN group, DHRS4-AS1 levels were lower and miR-139-5p levels were higher in EC-ESCs and tissues obtained from patients with endometriosis. Functional assays validated that DHRS4-AS1 targets miR-139-5p, with ARRDC3 being a downstream target of miR-139-5p.Rescue experiments demonstrated that DHRS4-AS1 inhibited EC-ESC proliferation, migration, and invasion, but promoted apoptosis, by targeting miR-139-5p in endometriosis. cleaved-Caspase3 expression level and the cleaved-Caspase 3/Caspase 3 ratio increased, while the expression levels of MMP-9 decreased, after transfection with DHRS4-AS1 overexpression plasmids; however, the effects induced by DHRS4-AS1 overexpression could be partially reversed by co-transfection with the miR-139-5p mimic. 		Yes	Rescue experiments demonstrated that DHRS4-AS1 inhibited EC-ESC proliferation, migration, and invasion, but promoted apoptosis, by targeting miR-139-5p in endometriosis. cleaved-Caspase3 expression level and the cleaved-Caspase 3/Caspase 3 ratio increased, while the expression levels of MMP-9 decreased, after transfection with DHRS4-AS1 overexpression plasmids; however, the effects induced by DHRS4-AS1 overexpression could be partially reversed by co-transfection with the miR-139-5p mimic. 	35414313
DGUOK-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC cell lines	interaction[miR-653-5p]	qRT-PCR//RIP	We found that DGUOK-AS1 was aberrantly upregulated in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) tissues through TCGA database. Real-time quantitative polymerase chain reaction (RT-qPCR) also verified the high expression of DGUOK-AS1 in CC cell lines. DGUOK-AS1 sequesters miR-653-5p to elevate EMSY in CC. 		Yes	Loss-of-function assays indicated that DGUOK-AS1 silence repressed CC cell growth.	32283566
DGUOK-AS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CESC tissues and cells	Interaction(miR-499a-5p/ SPRR1B )	Western Blot//Transfection//CCK8//qRT-PCR//RIP//migration assay//Luciferase Report Assay//BrdU	DGUOK-AS1 and SPRR1B expressions were obviously elevated, whereas the expression of miR-499a-5p was reduced in both CESC tissues and cells. Notably, DGUOK-AS1 inhibited miR-499a-5p to release SPRR1B, which significantly accelerated the development of CESC.		Yes	Silencing of DGUOK-AS1 attenuated cell growth and boosted apoptosis of CESC cells. Notably, DGUOK-AS1 inhibited miR-499a-5p to release SPRR1B, which significantly accelerated the development of CESC.	34808501
DGCR5	LncRNA	Homo sapiens	Stomach Neoplasms	blood	Interaction[binding to miR-23b]	qRT-PCR	In this study, we demonstrated that DGCR5 was downregulated in cancerous tissues and plasma samples from patients with GC. In conclusion, our results show that DGCR5 is a tumor-suppressive lncRNA that regulates PTEN and BTG1 expression through directly binding to miR-23b. This mechanism may contribute to a better understanding of GC pathogenesis and provide a potential therapeutic strategy for GC.	 In this study, we demonstrated that DGCR5 was downregulated in cancerous tissues and plasma samples from patients with GC, and its downregulation was associated with advanced TNM stage and positive lymphatic metastasis.	Yes	Gain- and loss-of-function of DGCR5 revealed that DGCR5 functioned as a competing endogenous RNA for miR-23b to suppress GC cell proliferation, invasion and migration, and facilitate apoptosis by regulating PTEN and BTG1 in vitro. Furthermore, the overexpression of DGCR5 suppressed tumor growth, and inhibited the expression of miR-23b and proliferation antigen Ki-67, but increased the expression of PTEN and BTG1 in vivo. 	30515803
DGCR5	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	Regulation[miR-211-5p/EPHB6 axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	RT-qPCR revealed that DGCR5 expression in NSCLC cells was significantly lower than in normal cell.  These findings collectively identified DGCR5/miR-211-5p/EPHB6 triple axis in NSCLC, which may novel understanding regarding the tumorigenesis of NSCLC.		Yes	DGCR5 overexpression suppresses NSCLC cell growth, migration, and invasion. 	31241800
DGCR5	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC clinical samples	Interaction(SRSF1)	CCK8//qRT-PCR//Western Blot	In this study, we found that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) was upregulated in ESCC clinical samples, which associated with poor prognosis. Mechanistically, DGCR5 could directly bind with SRSF1 to increase its stability and thus stimulate alternative splicing events. Furthermore, we clarified that SRSF1 regulated the aberrant splicing of myeloid cell leukemia-1 (Mcl-1) and initiated a significant Mcl-1L (antiapoptotic) isoform switch, which contributed to the expression of the full length of Mcl-1. 	In this study, we found that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) was upregulated in ESCC clinical samples, which associated with poor prognosis. 	Yes	 Through RNA interference and overexpression approaches, we confirmed that DGCR5 contributed to promote ESCC cell proliferation, migration, and invasion while inhibited apoptosis in vitro. Moreover, the cell-derived xenograft (CDX) model was validated that DGCR5 could facilitate the tumorigenesis of ESCC in vivo.	34099633
DGCR5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[miR-21]	CCK8//qRT-PCR	It was revealed that the expression of DGCR5 was Expression[down-expression]regulated, while microRNA (miR)-21 was Expression[Expression[up-expression]-expression]regulated in CRC. The expression level of DGCR5 in tumor tissue decreased, while expression levels of miR-21 increased, with advancing stages of the disease. miR-21 overexpression increased cancer cell proliferation and attenuated the effects of DGCR5 overexpression. 		Yes	DGCR5 overexpression showed no significant effects on cancer cell migration and invasion, but sExpression[Expression[up-expression]-expression]pressed cancer cell proliferation in vitro. 	31452812
DGCR5	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction[sequestering miR-2861]	qPCR//PCR//IF	In the present study, it was revealed that DGCR5 was significantly downregulated in PTC tissues compared with that in adjacent normal tissues. Taken together, the present results demonstrated that DGCR5 inhibits PTC progression via sponging miR-2861, indicating DGCR5 may serve as a therapeutic target.		Yes	Through functional experiments, it was demonstrated that ectopic overexpression of DGCR5 markedly suppressed PTC cell growth and invasion.	30651878
DGCR5	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC cells	Regulation [EGFR]	Western Blot//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay	We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro.  LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR.		Yes	We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. 	29393141
DGCR5	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cells	Regulation[Wnt signaling pathway]	qRT-PCR	 It was indicated that DGCR5 was decreased in HCC tissues and HCC cells including HepG2, Hep3B, MHCC-97L, SNU-449, and SNU-182 cells compared with the normal human liver cell line LO2. Taken these together, it was uncovered in our research that DGCR5 could play tumor suppressive role by targeting Wnt signaling in HCC progression.		Yes	Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU-449 cells. 	30230592
DGCR5	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BCa tissues 	Interaction[ promotes P21]	qRT-PCR	 Here, we found that DGCR5 expression was significantly downregulated in BCa tissues compared with adjacent normal tissues. In summary, our study demonstrated that DGCR5 transcriptionally promotes P21 expression to suppress BCa progression.	Higher expression of DGCR5 predicted higher survival rate in BCa patients.	Yes	Functional experiments indicated that DGCR5 overexpression markedly inhibited that proliferation, colony formation, and cell-cycle progression in BCa cells. 	30238982
DGCR5	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	RegulationWnt signaling pathway]	qRT-PCR	Here, in our current study, we observed that DGCR5 was downregulated in human cervical cancer cell lines (MS751, SiHa, HeLa, and HT-3) compared with the primary normal cervical squamous cells (NCSC1 and NCSC2).  In conclusion, we reported that DGCR5 was involved in cervical cancer progression via modulating the Wnt pathway.		Yes	Silence of DGCR5 obviously induced cervical cancer cell viability and cell proliferation. Reversely, upregulation of DGCR5 inhibited HeLa and C33A cell survival and proliferation. Furthermore, silencing of DGCR5 increased cervical cancer cell colony formation ability and decreased cell apoptosis, whereas its overexpression exhibited an opposite process.	30552671
DGCR5	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//Transwell Assay	 In this study, DGCR5 expression was obviously higher in TNBC tissues when compared with that in adjacent non-tumor samples.Our study suggests that DGCR5 enhances TNBC cell proliferation and metastasis via inducing Wnt/β-catenin signaling pathway in vitro and in vivo.		Yes	Cell proliferation, migration and invasion in TNBC were inhibited after knockdown of DGCR5 in vitro.	32521856
DGCR5	LncRNA	Homo sapiens	Glioma	glioma tissues	regulation[miR-21/Smad7 and miR-23a/PTEN axes]	Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Herein, we identified lncRNA DGCR5 as a downregulated lncRNA in glioma that was negatively regulated by NF-κB1 in an NF-κB1 RE-dependent manner.  In conclusion, lncRNA DGCR5 suppresses the capacity of glioma cells to migrate and invade via miR-21/Smad7, whereas it inhibits the proliferation and enhances the apoptosis of glioma cells through miR-23a/PTEN.		Yes	LncRNA DGCR5 overexpression significantly inhibited the capacity of glioma cells to proliferate, migrate, and invade, whereas promoted the apoptosis of glioma cells. 	33085646
DGCR5	LncRNA	Homo sapiens	Glioblastoma	Glioblastoma Tissues	Expression[lower expressed]	Immunoblotting//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	LncRNA DGCR5 was down expressed in glioblastoma. 		Yes	Transfection of DGCR5 markedly repressed cell viability and colony formation ability of U87 and U251 cells. Additional, DGCR5 overexpression caused cell cycle arrest and increased cell apoptosis.Moreover, upregulation of DGCR5 suppressed the growth and promoted cell apoptosis of U87 cell in vivo.Finally, overexpression of DGCR5 impaired the migration, invasiveness, and reversed epithelial-to-mesenchymal transition (EMT) process of glioblastoma cell.	31799672
DGCR5	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and LUAD cell lines	Interaction(hsa-mir-22-3p)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Bioinformatics Analysis	It was observed that DGCR5 was upregulated in LUAD tissues and LUAD cell lines.Both mRNA expression and protein levels of BCL-2 were increased by DGCR5 downregulation while reversely BAX was increased. Additionally, a novel microRNA target of DGCR5, hsa-mir-22-3p was identified through bioinformatics search and confirmed by dual-luciferase reporter system. Gain and loss-of-function studies were performed to verify whether DGCR5 exerts its biological functions through regulating hsa-mir-22-3p in vitro. Overexpression of DGCR5 was able to reverse the tumor inhibitory effect of hsa-mir-22-3p mimics.	Downregulated DGCR5 expression was greatly associated with smaller tumor size, implying a favorable prognosis of LUAD patients. 	Yes	Inhibition of DGCR5 can prevent LUAD progression via playing anti-apoptosis roles. Furthermore, in vivo tests tumor xenografts were established to detect the function of DGCR5 in LUAD tumorigenesis. 	29030962
DICER1-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cells 	Interaction(miR-5586-5p/YTHDF3 )	RNA Pull-Down//MeRIP	Bio-information analysis indicated that DICER1-AS1 was downregulated in PC and negatively correlated with glycolytic genes expression. Mechanistically, DICER1-AS1 promoted transcription of its sense gene DICER1 by recruiting transcriptional factor YY1 to the DICER1 promoter. Meanwhile, DICER1 promoted maturation of miR-5586-5p which consequently inhibited glycolytic gene expression including LDHA, HK2, PGK1, and SLC2A1. Notably, enhanced interaction between N6-methyladenosine (m6A) reader YTHDF3 and DICER1-AS1 led to degradation of DICER1-AS1 in response to glucose depletion. Moreover, our data revealed that YTHDF3 was a critical target for miR-5586-5p, by which forming a negative feedback with DICER1-AS1 to regulate glycolysis of PC.		Yes	 Meanwhile, overexpression of DICER1-AS1 inhibited glycolysis, proliferation, and metastasis of PC cells both in vitro and in vivo. 	35183226
DICER1-AS1	LncRNA	Homo sapiens	Osteosarcoma	 osteosarcoma cells	Regulation[miR-30b/ATG5]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Results showed that lncRNA DICER1-AS1 was up-regulated in osteosarcoma cells using microarray analysis and RT-PCR. In summary, all the results conclude that DICER1-AS1 regulates the proliferation, invasion and autophagy of osteosarcoma via miR-30b/ATG5 axis, providing a novel insight for osteosarcoma tumorigenesis.		Yes	Cellular functional experiments revealed that DICER1-AS1 knockdown suppressed the proliferation, migration, invasion and autophagy of osteosarcoma cells in vitro.	29772430
DICER1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-296-5p/STAT3 Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The expressions of DICER1-AS1 and STAT3 mRNA were significantly up-regulated while miR-296-5p expression was remarkably down-regulated in CRC tissues and cell lines.DICER1-AS1 acts as an oncogenic lncRNA in CRC via modulating miR-296-5p/STAT3 axis. 		Yes	Over-expression of DICER1-AS1 or transfection of miR-296-5p inhibitors could promote the proliferation, migration and invasion and inhibit apoptosis of CRC cells, whereas knockdown of DICER1-AS1 or transfection of miR-296-5p mimics had the opposite effects. 	33116860
DLEU1	LncRNA	Homo sapiens	Premature Ovarian Failure 7	POF and control ovary tissues 	Interaction( MiR-146b-5p)	qRT-PCR//Transfection//RNA Pull-Down//Cell Apoptosis Assay	Increased DLEU1 expression and decreased miR-146b-5p expression were observed in POF.DLEU1 directly interacted with MiR-146b-5p and was expressed in both nuclear and cytoplasm samples of KGN cells. 		Yes	In KGN cells, DLEU1 and miR-146b-5p failed to regulate the expression of each other. However, DLEU1 promoted cell apoptosis and reduced the inhibitory effects of miR-146b-5p on cell apoptosis.	34740384
DLEU1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 oral squamous cell carcinoma (OSCC) cells	Regulation( JAK-STAT signaling)	qRT-PCR//ChIP//Western Blot	 We previously reported that DLEU1 (deleted in lymphocytic leukemia 1) is one of the lncRNAs overexpressed in oral squamous cell carcinoma (OSCC) cells, where it exhibits oncogenic activity.  Chromatin immunoprecipitation-sequencing (ChIP-seq) analysis revealed that DLEU1 knockdown induced significant changes in the levels of histone H3 lysine 4 trimethylation (H3K4me3) and H3K27 acetylation (H3K27ac) in OSCC cells. Notably, DLEU1 knockdown suppressed levels of H3K4me3/ H3K27ac and expression of a number of interferon-stimulated genes (ISGs), including IFIT1, IFI6 and OAS1, while ectopic DLEU1 expression activated these genes. Western blot analysis and reporter assays suggested that DLEU1 upregulates ISGs through activation of JAK-STAT signaling in OSCC cells.		Yes	Notably, DLEU1 knockdown suppressed levels of H3K4me3/ H3K27ac and expression of a number of interferon-stimulated genes (ISGs), including IFIT1, IFI6 and OAS1, while ectopic DLEU1 expression activated these genes. Moreover, IFITM1, one of the ISGs induced by DLUE1, was frequently overexpressed in primary OSCC tumors, and its knockdown inhibited OSCC cell proliferation, migration and invasion. 	34650128
DLEU1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	Interaction(miR-126-5p/GAB1 axis)	qRT-PCR//MTT//Western Blot	Our results indicated that DLEU1 and GAB1 were upregulated, while miR-126-5p was downregulated in OSCC cells. DLEU1 mediated biological effects in OSCC through binding to miR-126-5p, which directly targeted GAB1. miR-126-5p knockdown rescued the inhibitory function of DLEU1 depletion on proliferation, migration and invasion. Meanwhile, the miR-126-5p mimic exerted suppressive functions in the progression of OSCC, which were neutralized after GAB1 overexpression. 		Yes	 Silencing DLEU1 reduced OSCC cell proliferation, migration, and invasion, while DLEU1 overexpression had the opposite effects. 	36039933
DLEU1	LncRNA	Homo sapiens	Endometrial Neoplasms		interaction[mTOR]	qRT-PCR//RIP//Western Blot	 In order to focus on the role and mechanism of lncRNA DLEU1 in endometrial carcinoma, we used qRT-PCR to detect the expression of lncRNA DLEU1 and found that lncRNA DLEU1 was highly expressed in endometrial carcinoma compared to normal endometrium.RiP confirmed that lncRNA DLEU1 could bind to mTOR. 		Yes	In addition, up-regulation of lncRNA DLEU1 promoted cell viability, migration, invasion, and reduced the proportion of apoptosis. Otherwise, down-regulation of lncRNA DLEU1 produced opposite results. Xenograft nude mice model assay showed that lncRNA DLEU1 can promote tumorigenesis in vivo.	29745433
DLEU1	LncRNA	Homo sapiens	Osteosarcoma	 osteosarcoma tissue, cell line	Regulation[regulating the miR-671-5p/DDX5 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our results showed that DLEU1 was highly expressed in osteosarcoma tissue specimens and cells. In conclusion, DLEU1 acted as an oncogene in osteosarcoma by directly sponging miR-671-5p and regulating the expression of DDX5. 		Yes	Downregulation of DLEU1 in osteosarcoma cells inhibited the cell proliferation, migration and invasion. 	31379208
DLEU1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissue	Regulation[miR-381/CXCR4 axis]	qRT-PCR	Our studies indicated that the DLEU1 expression level was upregulated in PDAC tissue samples compared with adjacent normal tissue.Bioinformatics analysis predicted that miR-381 potentially targeted the DLEU1 3'-untranslated region (UTR), suggesting an interaction between miR-381 and DLEU1. Furthermore, miR-381 also targeted the chemokine receptor-4 (CXCR4) messenger RNA 3'-UTR, which was validated by luciferase reporter assay. Taken together, our study demonstrated the oncogenic role of DLEU1 in clinical PDAC specimens and cellular experiments, showing the potential involvement of DLEU1/miR-381/CXCR4 pathway. These results provide novel insight into PDAC tumorigenesis.	Moreover, the aberrant overexpression of DLEU1 indicated poor prognosis of patients with PDAC. 	Yes	Loss-of-function experiments revealed that DLEU1 knockdown inhibited the proliferation, migration, and invasion of PDAC cells in vitro and decreased tumor growth in vivo.	30382579
DLEU1	LncRNA	Homo sapiens	Glioblastoma		Interaction[SP1-DLEU1-miR-4429 ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//ChIP	We found that DLEU1 was up-regulated in GBM and DLEU1 knockdown significantly inhibited GBM cell proliferation and induced apoptosis. As predicted by bioinformatics analysis and validated in mechanistic assays, SP1 could bind to the promoter region of DLEU1 to activate DLEU1 transcription. Additionally, miR-4429 was verified as a target gene of DLEU1 and negatively modulated by DLEU1. More importantly, miR-4429 overexpression repressed the mRNA and protein levels of SP1 via binding to the 3'UTR of SP1. Overexpression of SP1 or miR-4429 inhibitor could partly abolish the effect of DLEU1 knockdown on cell viability and apoptosis in GBM. Accordingly, our experimental data revealed that SP1-DLEU1-miR-4429 formed a feedback loop to promote GBM development, providing a new evidence for the role of DLEU1 in GBM.		Yes	We found that DLEU1 was up-regulated in GBM and DLEU1 knockdown significantly inhibited GBM cell proliferation and induced apoptosis. 	31713587
DLEU1	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	Interaction(miR-149-5p/YAP1/TEAD2/SOX2 axis)	Cell Proliferation Assay//qRT-PCR//In Vivo Experiment//Western Blot	 In this study, TCGA data analysis showed upregulation of DLEU1 expression in CCA. Furthermore, we confirmed that DLEU1 expression was increased in CCA tissues and cells compared with corresponding controls.  Mechanistically, DLEU1 expression was transcriptionally facilitated by transcription factor YY1. Moreover, DLEU1 promoted oncogene YAP1 expression by functioning as a sponge to competitively bind to miR-149-5p. YAP1 promoted CCA proliferation, invasion and stemness maintenance, whereas miR-149-5p inhibited malignant biological behavior of CCA. Rescue experiments confirmed that the cancer-promoting effect of DLEU1 was saved by interfering miR-149-5p or YAP1. Furthermore, YAP1 promoted tumor stemness maintenance partly by acting as a transcriptional coactivator to promote TEAD2-induced SOX2 expression. 	Upregulated DLEU1 was related to poor clinicopathological characteristics. 	Yes	Functionally, silencing DLEU1 inhibited CCA proliferation, invasion, stemness maintenance and chemo-resistance, whereas amplifying DLEU1 promoted malignant biological behavior of CCA cells. 	35864972
DLEU1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues and cells 	interaction[miR-490 ]	qRT-PCR	 DLEU1 was upregulated in EC tissues and cells. Our findings indicate that DLEU1 contributes to EC development by sponging miR-490 to regulate SP1 expression.		Yes	Suppression of DLEU1 significantly inhibited Ishikawa cell viability, promoted cell apoptosis, decreased BCL-2 expression and increased the expression of Bax, cleaved-caspase-3 and cleaved-caspase-3, suppressed cell migration and invasion, and inhibited EMT via increasing the expression of E-cadherin and decreasing the expression of N-cadherin, Snail and Vimentin.	30001771
DKFZp434J0226	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	clinical specimens	Interaction(SF3B6)	In Vivo Experiment//RNA Pull-Down//Western Blot//Co-IP//Migration Assay//qRT-PCR//RIP//Microarray//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//IF	Clinical analyses revealed that overexpression of DKFZp434J0226 was associated with worse tumor grading, frequent perineural invasion, advanced tumor-node-metastasis stage, and decreased overall survival and time to progression.  Mechanistically, DKFZp434J0226 interacted with the splicing factor SF3B6 and promoted its phosphorylation, which further regulated the alternative splicing of pre-mRNA.	Clinical analyses revealed that overexpression of DKFZp434J0226 was associated with worse tumor grading, frequent perineural invasion, advanced tumor-node-metastasis stage, and decreased overall survival and time to progression. 	Yes	 Functional assays demonstrated that DKFZp434J0226 promoted PDAC cell migration, invasion, and growth in vitro and accelerated tumor proliferation in vivo. 	34470609
DICER-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues 	Interaction(microRNA-650/CSR1 )	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay	DICER-AS1 and CSR1 expression levels were significantly decreased in gastric cancer tissues compared with normal tissues, and qPCR analysis showed that miR-650 was upregulated in gastric cancer tissues. Bioinformatic analysis and dual luciferase reporter assays revealed that DICER-AS1 functioned as a competing endogenous RNA that sponged miR-650, which in turn regulated CSR1 expression. 		Yes	. Importantly, ectopic DICER-AS1 and CSR1 expression inhibited cell proliferation and migration in vitro and suppressed xenograft tumorgenicity in vivo.	34586953
DIRC1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[AKT/mTOR signaling]	CCK8//qRT-PCR//Western Blot//Transwell Assay	The results showed that high expression of DIRC1 was found in GC tissues compared with normal gastric tissues.Mechanically, the activity of AKT/mTOR signaling was suppressed by the knockdown of DIRC1.	High expression of DIRC1 was associated with more cases of severer tumor malignancy and shorter OS; besides, high-level of DIRC1 was suggested to be an independent prognostic factor for GC. 	Yes	 Furthermore, the knockdown of DIRC1 inhibited SGC-7901 GC cells proliferation, migration and invasion.	30575946
DIRC1	LncRNA	Homo sapiens	gastric adenocarcinoma	 macrophages, dendritic cells, and Th1 cells	Regulation	qRT-PCR//RNA-seq//Bioinformatics Analysis	 Increased DIRC1 expression in STAD was associated with T stage (P = .004), race (P = .045), histologic grade (P = .029) and anatomic neoplasm subdivision (P = .034). 	 Increased DIRC1 expression in STAD was associated with T stage (P = .004), race (P = .045), histologic grade (P = .029) and anatomic neoplasm subdivision (P = .034). 	Yes	DIRC1 is related to epidermis, collagen-containing extracellular matrix, receptor-ligand activity, protein digestion and absorption, etc. 	36401393
DIO3OS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Regulation(hnRNPK-MYC-CDC25A axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis//ChIP	 DIO3OS is downregulated in NSCLC, and its low expression is related to poor prognosis. DIO3OS competitively bound heterogeneous nuclear ribonucleoprotein K (hnRNPK), repressed the binding of hnRNPK to MYC DNA and MYC mRNA, reduced the promoting roles of hnRNPK on MYC transcription and translation, led to the repression of MYC transcription and translation, and therefore remarkably decreased the expression of MYC and CDC25A, a downstream target of MYC. 	 DIO3OS is downregulated in NSCLC, and its low expression is related to poor prognosis. 	Yes	Ectopic expression of DIO3OS repressed NSCLC cell growth and motility and promoted NSCLC cell apoptosis in vitro. DIO3OS also repressed NSCLC tumorigenesis and metastasis in vivo. 	34761103
DIO3OS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[microRNA-328/Hhip Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	DIO3OS was lower in HCC tissues and cells, while upregulation of DIO3OS repressed malignant biological behavior both in vitro and in vivo. All in all, the obtained data suggested that DIO3OS interacted with Hhip-dependent Hh signaling pathway to inhibit HCC progression through binding to miR-328, which may be a potent therapeutic target for HCC.		Yes	DIO3OS was lower in HCC tissues and cells, while upregulation of DIO3OS repressed malignant biological behavior both in vitro and in vivo.	32547226
DIO3OS	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissue samples and cells	regulation[ DIO3OS/let-7d/NF-κB2 axis]	Wound Healing Assay//Immunoblotting//CCK8//qRT-PCR//Luciferase Report Assay//ELISA//IHC//Transwell Assay	DIO3OS showed to be considerably increased within thyroid cancer tissue samples and cells.  In conclusion, DIO3OS/let-7d/NF-κB2 axis regulates the viability, DNA synthesis capacity, invasion, and migration of thyroid cancer cells.		Yes	Knocking down DIO3OS within thyroid carcinoma cells suppressed cancer cell viability, the capacity of DNA synthesis, cell invasion, as well as cell migration; besides, proliferating markers, ki-67 and PCNA, were decreased by DIO3OS knockdown.	33058043
DIO3OS	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and PC cell lines	Interaction[upregulating ALDOA]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 Our results showed that DIO3OS was highly expressed in human PC tissues and PC cell lines. Through online predictive tools and functional experiments, we found that DIO3OS could bind directly to microRNA-122 (miR-122) and inhibited its expression, which functioned as a tumor suppressor in PC cells. We also verified that ALDOA was the direct target of miR-122, and the tumor suppressive effects caused by DIO3OS knockdown or miR-122 overexpression could be rescued by re-expression of ALDOA in PC cells.		Yes	DIO3OS exhibited oncogenic properties in stimulating PC cell proliferation and invasion in vitro and promoting cancer growth in vivo. 	31384177
DINOL	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[modulating p21 and Bax]	qRT-PCR	 It was manifested that DINO was significantly downregulated in GC tissues. Taken these, DINO might exert a tumor inhibitory role in the progression of GC through modulating p21 and Bax.		Yes	 Moreover, it was displayed that GC cell proliferation was suppressed by DINO overexpression, whereas silencing DINO increased cell proliferation significantly.	30775800
CBR3-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction(miR-29a)	qRT-PCR//RNA Pull-Down//Transwell Assay	 CBR3-AS1 was downregulated, and miR-29a was upregulated in CRC.  CBR3-AS1 and miR-29a directly interacted with each other. CBR3-AS1 was localized in both nucleus and cytoplasm fractions. CBR3-AS1 is downregulated in CRC and inhibits miR-29a-mediated cell migration and invasion by sponging miR-29a.		Yes	 CBR3-AS1 overexpression failed to alter miR-29a expression but reduced its enhancing effects on cell invasion and migration. 	35107754
CBR3-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	regulation[ miR-136-5p/Smad3 axis]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//IHC	PlncRNA-1 was found to be overexpressed in 71.43% of bladder cancer tissues. 	Moreover, the expression level correlated with tumor invasion, T stage, age, and number of tumors, but not with gender, recurrent status, preoperative treatment, pathological grade, and tumor size. 	Yes	Inhibiting PlncRNA-1 expression impaired the proliferation, migration, and invasion of T24 and 5637 bladder cancer cells in vitro and in vivo.	33288752
circRAB31	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and gastric cancer cell lines	Interaction(miR-885-5p)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Wound Healing Assay//Invasion Assay//Tunel//Migration Assay//CCK8//Flow Cytometry//FISH//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	circRAB31 was downregulated in gastric cancer tissues and gastric cancer cell lines compared with normal tissues and a human gastric epithelial cell line (GES-1). 		Yes	Overexpression of circRAB31 suppressed gastric cancer proliferation and metastasis in vitro and in vivo, whereas silencing of circRAB31 had the opposite effects. Bioinformatic analysis as well as pull-down and luciferase assays revealed that circRAB31 exerted tumor-suppressive functions by binding directly to miR-885-5p. 	34901392
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	blood	Regulation[ IRF7 and the RIG-I-like receptor signaling pathway]	Flow Cytometry//qRT-PCR//MTT//EdU Staining//Transwell Assay	A high expression of AFAP1-AS1 was identified in NSCLC, alongside with a reduced level of IL-12 and increased levels of IL-10 and interferon (IFN)-γ.lncRNA AFAP1-AS1 promotes migration and invasion of non-small cell lung cancer via up-regulating IRF7 and the RIG-I-like receptor signaling pathway.	Aberrant expressions of AFAP1-AS1 were associated with pathological grade, TNM staging and metastatic potential of NSCLC.	Yes	Over-expression of AFAP1-AS1 promoted NSCLC cell proliferation, invasion and migration while inhibiting cell apoptosis.	30278439
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Expression[highly expressed]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	It was found that AFAP1-AS1 expression was upregulated in NSCLC tissues and cells. 		Yes	Knockdown of AFAP1-AS1 and overexpression of miR-139-5p inhibited NSCLC cell proliferation, colony formation and chemotherapy resistance and increased cell apoptosis.	31696057
AFAP1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	regulation[miR-498/VEGFA Axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The expression levels of lncRNA AFAP1-AS1 and VEGFA mRNA were upregulated, but miR-498 was downregulated in ESCC tissues and cells.Downregulation of AFAP1-AS1 impeded the proliferation and migration and induced apoptosis of ESCC cells by regulating miR-498/VEGFA axis, which might serve as a novel biomarker for the diagnosis and treatment of ESCC.		Yes	Functionally, AFAP1-AS1 silencing inhibited the proliferation and migration and induced apoptosis of ESCC cells. 	32801880
AFAP1-AS1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer clinical tissues	Interaction(SNIP1/c-Myc)	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//FISH//qRT-PCR//H&E Staining//IP//Transwell Assay	AFAP1-AS1 was highly expressed in lung cancer clinical tissues and its expression was positively correlated with lung cancer patients' poor prognosis.AFAP1-AS1 promoted lung cancer cells migration and invasion through interacting with Smad nuclear interacting protein 1 (named SNIP1), which inhibited ubiquitination and degradation of c-Myc protein.	AFAP1-AS1 was highly expressed in lung cancer clinical tissues and its expression was positively correlated with lung cancer patients' poor prognosis.In vivo experiments confirmed that AFAP1-AS1 could promote lung cancer metastasis.	Yes	In vivo experiments confirmed that AFAP1-AS1 could promote lung cancer metastasis.	34168109
AFAP1-AS1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cells	Interaction(miR-545-3p/HDGF axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//migration assay//Invasion Assay	The expression levels of AFAP1-AS1 and HDGF were increased, while miR-545-3p was decreased in lung cancer tissues and cells.  Furthermore, AFAP1-AS1 mediated cell progression through regulating miR-545-3p expression. In addition, miR-545-3p negatively regulated the expression level of HDGF via binding 3'-untranslated region of HDGF. As expected, AFAP1-AS1 knockdown inhibited lung cancer progression via affecting miR-545-3p/HDGF axis. 		Yes	 AFAP1-AS1 knockdown suppressed lung cancer cell proliferation, migration, and invasion and induced apoptosis. 	33290312
AFAP1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	blood	Interaction[LncRNA GAS8-AS ]	CCK8//qRT-PCR	LncRNA AFAP1-AS1 was upregulated in CRC patients and was inversely correlated with GAS8-AS1 only in CRC patients but not in healthy controls.GAS8-AS1 overexpression mediated the downregulation of AFAP1-AS1 in colon cancer cells, while AFAP1-AS1 overexpression did not significantly affect GAS8-AS1 expression. Expression level of GAS8-AS1 decreased, while expression level of AFAP1-AS1 increased with the increase of primary tumor diameters.		Yes	 GAS8-AS1 overexpression led to inhibited, while AFAP1-AS1 overexpression led to promoted proliferation of CRC cells, and AFAP1-AS1 overexpression reduced the inhibitory effects of GAS8-AS1 overexpression on cancer cell proliferation. 	31132513
AFAP1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-195-5p and WISP1)	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 AFAP1-AS1 and WISP1 expressions were notably increased, and miR-195-5p expression was markedly reduced in CRC. The dual-luciferase assay verified that AFAP1-AS1 could bind to miR-195-5p. miR-195-5p could target and regulate WISP1 expression. Overexpression of WISP1 or miR-195-5p inhibition reversed the inhibition effect of AFAP1-AS1 knockdown on the biological activity of CRC cells.		Yes	AFAP1-AS1 knockdown could inhibit the malignant behavior of CRC cells.	34335760
AFAP1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues	Expression[highly expressed]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	We analyzed the lncRNA expression patterns in Gene Expression Omnibus (GEO) datasets and the Cancer Genome Atlas (TCGA) RNA-seq datasets, and found that the expression level of AFAP1-AS1 was significantly elevated in CC tissues. 	High levels of AFAP1-AS1 were associated with poor disease-free survival and overall survival in CC patients.	Yes	In vitro experiments demonstrated that AFAP1-AS1 knockdown significantly inhibited the cell invasive and migration capability in CC cell line HT-29.	30588252
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tumorous tissues,cell line	Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	AFAP1-AS1 was upregulated in surgical tumorous tissues from hepatocarcinoma patients compared with the paired paracancerous non-tumor liver tissues, and in hepatocarcinoma Huh7, HCCLM3 and HepG2 cell lines compared with LO2, a normal liver cell line. 		Yes	AFAP1-AS1 knockdown noticeably suppressed the proliferative, migratory and invasive properties, and the epithelial-mesenchymal transition (EMT) process of HepG2 and HCCLM3 through upregulating E-cadherin and downregulating N-cadherin and vimentin. 	32280542
AFAP1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC cells and tissues 	Interaction(miR-107/PDK4 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The present study revealed that AFAP1-AS1 expression was elevated in OC cells and tissues. AFAP1-AS1 functioned as a sponge of miR-107, and miR-107 reversed the effects of AFAP1-AS1 on OC cells. It was validated that miR-107 was able to bind to PDK4, and AFAP1-AS1 regulated PDK4 expression by competitively binding with miR-107.	AFAP1-AS1 expression and FIGO stage were positively correlated. 	Yes	AFAP1-AS1 knockdown repressed OC cell proliferation, migration and invasion.	33926489
AFAP1-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissues,cell 	Expression[highly expressed]	CCK8//qRT-PCR//EdU Staining//Transwell Assay	 No matter in BCa tissues or in cell samples, compared to the corresponding normal controls, AFAP1-AS1 was found highly expressed; at the same time, in invasive bladder cancer tissues, the expression level of AFAP1-AS1 was also higher than that in non-invasive tissues. 	 Meanwhile, survival analysis revealed that patients with BCa with high expression of AFAP1-AS1 owned a shorter overall survival rate than those with low expression, indicating a negative interplay between AFAP1-AS1 expression and patients' prognosis.	Yes	 In addition, in BCa cell lines, according to the results of CCK-8, EDU, and transwell assays, the proliferative capacity, as well as the invasive ability of BCa cells, were found weakened after downregulation of AFAP1-AS1. 	32964963
AFAP1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues,cell lines	Regulation[up-regulated]	CCK8//qRT-PCR//Western Blot	 The expression of AFAP1-AS1 was higher in the OSCC tissues than in the NOK cells, and the relative expression of AFAP1-AS1 was higher in the SCC25 cells than in the NOK cells (P<0.001). 	AFAP1-AS1 expression was associated with the degree of diffe-rentiation, TNM stage, lymphatic metastasis, and poor prognosis of OSCC (P<0.05). Patients with a high expression of AFAP1-AS1 had lower survival rates than those with a low expression of AFAP1-AS1 (P<0.05).	Yes	The inhibition of AFAP1-AS1 expression consequently suppressed the proliferation, invasion, and migration of SCC25.	31875436
AFAP1-AS1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	regulation[miR-545-3p/VEGFA pathway]	qRT-PCR	Herein, we found the high expression of AFAP1-AS1 in human EC tissues, and AFAP1-AS1 was correlated with EC patients' prognosis and clinical features. We further showed that AFAP-AS1 could promote the expression of VEGFA through the adsorption of miR-545-3p, thus promoting the angiogenesis and invasion of EC, and contribute to tumor growth and metastasis in vivo. 	Herein, we found the high expression of AFAP1-AS1 in human EC tissues, and AFAP1-AS1 was correlated with EC patients' prognosis and clinical features. 	Yes	AFAP-AS1 could affect EC cell proliferation, migration, and invasion, and contributed to endothelial cell angiogenesis.	32504788
AFAP1-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Regulation[RhoC/ROCK1/p38MAPK/Twist1 signaling pathway]	qRT-PCR//Western Blot	AFAP1-AS1 expression is upregulated in human OS tissues and cell lines.AFAP1-AS1 knockdown elicits a signaling inhibition including decreased levels of RhoC, ROCK1, p38MAPK and Twist1. Moreover, AFAP1-AS1 interacts with RhoC. Overexpression of RhoC can partly reverse AFAP1-AS1 downregulation-induced cell EMT inhibition.		Yes	AFAP1-AS1 knockdown induces OS cell apoptosis and cell cycle G0/G1 arrest, suppresses OS cells growth, migration, invasion, vasculogenic mimicry formation and epithelial-mesenchymal transition (EMT), and affects actin filament integrity. AFAP1-AS1 knockdown suppresses OS tumor formation and growth in nude mice. 	31443665
AFAP1-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	regulation[ miR-497/IGF1R axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 In this study, quantitative real time polymerase chain reaction (qRT-PCR) revealed that AFAP1-AS1 was upregulated in OS tissues and cell lines. Taken together, these findings indicate that AFAP1-AS1 promotes OS progression by regulating miR-497/IGF1R axis, providing a therapeutic target for OS.	Increased AFAP1-AS1 was associated with poor prognosis.	Yes	 Loss-of-function experiments demonstrated that knockdown of AFAP1-AS1 inhibited the proliferation, colony formation, migration, invasion and induced cell apoptosis.	32509208
AFAP1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms		Expression[highly expressed]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Cell Cycle Assay//Transwell Assay	 In the present study, we found that AFAP1‑AS1 was elevated and hypomethylated in cervical cancer and was associated with a poor prognosis of patients with cervical cancer by analyzing the Cancer RNA‑Seq Nexus (CRN), MethCH and UCSC XENA databases.		Yes	Wound healing experiments and matrigel invasion experiments revealed that the downregulation of AFAP1‑AS1 suppressed the migration and invasion of cervical cancer cells. 	30816545
AFAP1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CD44v6(+) CC cells 	Interaction(miR-27b-3p/VEGF-C axis)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Microarray//Cell Cycle Assay	CD44v6(+) CC cells had remarkable stemness and a high level of AFAP1-AS1. In the mechanism study, miR-27b-3p/VEGF-C signaling was demonstrated to be a key downstream of AFAP1-AS1 in the CD44v6(+) CC cells.		Yes	However, AFAP1-AS1 knockdown with siAFAP1-AS1 suppressed the cell cycle transition of G(1)/S phase and inhibited self-renewal of CD44v6(+) CC cells, the levels of the stemness markers octamer-binding transcription factor 4 (OCT4), osteopontin (OPN), and cluster of differentiation 133 (CD133), and the epithelial-mesenchymal transition (EMT)-related proteins Twist1, matrix metalloprotease (MMP)-9, and VEGF-C. 	34334630
AFAP1-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Regulation[Wnt/β-Catenin Signaling Pathway ]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay	We found that AFAP1-AS1 was overexpressed in TNBC tissues and cells.Our results also revealed that upregulation of AFAP1-AS1 activated Wnt/β-catenin pathway to promote tumorigenesis and cell invasion by increasing the expression of C-myc and epithelial-mesenchymal transition-related molecules in TNBC.	Overexpression of LncRNA AFAP1-AS1 was associated with poor prognosis in TNBC patients.	Yes	Moreover, we demonstrated that upregulation of AFAP1-AS1 promoted cell proliferation and invasion, and inhibited cell apoptosis in vitro, while overexpression of AFAP1-AS1 promoted tumor growth in vivo.	30505272
AFAP1-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues	Expression[highly expressed]	qRT-PCR	AFAP1-AS1 was upregulated in the glioma tissues compared with that in the control tissues, and the expression level was correlated with glioma grading and KPS scores.		Yes	 After knockdown of AFAP1-AS1, the invasion capacities of the glioma cells declined significantly, and the expressions of invasion-related proteins MMP2 and MMP9 also decreased significantly.	30178845
AFAP1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	interaction[binds to KAT2B]	RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay//ChIP	AFAP1-AS1 is upregulated in NPC and is a poor prognostic indicator for survival in NPC patients. Mechanistic investigations suggested that AFAP1-AS1 binds to KAT2B and promotes acetyltransferase activation at two residues (E570/D610). KAT2B further promotes H3K14 acetylation and protein binding to the bromo domain of TIF1α. Consequently, TIF1α acts as a nuclear transcriptional coactivator of RBM3 transcription, leading to YAP mRNA stabilization and enhanced NPC tumorigenicity.	AFAP1-AS1 is upregulated in NPC and is a poor prognostic indicator for survival in NPC patients. 	Yes	AFAP1-AS1 was required for NPC proliferation in vitro and tumorigenicity in vivo.	33330099
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Regulation[p21 ]	qRT-PCR//RIP//ChIP	AFAP1-AS1 expression was increased in NSCLC tissues and was correlated with clinical outcomes of NSCLC.Mechanistic investigations found that AFAP1-AS1 could interact with EZH2 and recruit EZH2 to the promoter regions of p21, thus epigenetically repressing p21 expression.		Yes	 Further experiments revealed that inhibition of its expression in NSCLC cells resulted in diminished cell growth in vitro and in vivo.	29793547
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Regulation[AFAP1 ]	qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	In this study, we conducted global lncRNA profiling and identified that AFAP1-AS1 is significantly upregulated in NSCLC, suggesting that AFAP1-AS1 may be important for lung cancer development.Mechanistically, AFAP1-AS1 functions through positively regulating the expression of AFAP1 protein.		Yes	Through gain- and loss-of-function studies, AFAP1-AS1 was demonstrated to promote cell migration and invasion. 	30293090
AFAP1-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	TC tissues and cells	Interaction(miR-204-3p/DUSP4 axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	Highly expressed AFAP1-AS1 was in association with advanced TNM stage and positive lymph node metastasis. MiR-204-3p was targetedly repressed by AFAP1-AS1, and miR-204-3p could negatively regulate DUSP4 expression. AFAP1-AS1 augmented the expression of DUSP4 via repressing miR-204-3p, and the effects of AFAP1-AS1 overexpression on thyroid cancer cells were also partly abolished by miR-204-3p restoration.	Highly expressed AFAP1-AS1 was in association with advanced TNM stage and positive lymph node metastasis. 	Yes	Knockdown of AFAP1-AS1 suppressed the proliferation, migration and invasion of thyroid cancer cells, and overexpression of AFAP1-AS1 induced a reversed effect. 	34652441
AFAP1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(miR-497-5p)	In Vivo Experiment//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	AFAP1-AS1 was upregulated in breast cancer tissues and cells, and AFAP1-AS1 knockdown could hinder proliferation and migration of breast cancer cells, and contribute to cell apoptosis. MiR-497-5p, which was downregulated in breast cancer, was verified to be a target of AFAP1-AS1 and inversely correlated with AFAP1-AS1 expression. SEPT2, as a target gene of miR-497-5p, was negatively regulated by miR-497-5p and positively correlated with AFAP1-AS1 expression. Importantly, AFAP1-AS1 could upregulate SEPT2 expression by sponging miR-497-5p, and modulate cell progression by regulation of the miR-497-5p/SEPT2 axis in breast cancer. 		Yes	AFAP1-AS1 was upregulated in breast cancer tissues and cells, and AFAP1-AS1 knockdown could hinder proliferation and migration of breast cancer cells, and contribute to cell apoptosis. 	32955920
AGAP2-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	interaction[binding to miRNA-425-5p]	Western Blot//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Transwell Assay	We found that AGAP2-AS1 expression was significantly higher in human PTC tissues than adjacent noncancerous tissues (n=110; p<0.01) and correlated with lymph node metastasis (p=0.01) and tumor-node-metastasis stage (p=0.006). These results demonstrate that AGAP2-AS1 expression is significantly elevated in PTC tissues and that, by binding to miRNA-425-5p, it upregulates the MMP2 expression, thereby increasing the invasiveness and migration capacity of PTC cells.	We found that AGAP2-AS1 expression was significantly higher in human PTC tissues than adjacent noncancerous tissues (n=110; p<0.01) and correlated with lymph node metastasis (p=0.01) and tumor-node-metastasis stage (p=0.006). 	Yes	AGAP2-AS1 downregulation decreased migration and invasion by PTC cells, and reduced expression of matrix metalloproteinase-2 (MMP2).	32960785
AGAP2-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues	Interaction[suppressing ANKRD1 and ANGPTL4]	ChIP//Flow Cytometry//qRT-PCR//RIP//MTT//Colony Formation Assay//EdU Staining//Transwell Assay	Increased expression of AGAP2-AS1 was associated with tumor size and pathological stage progression in patients with PC.Furthermore, AGAP2-AS1 epigenetically inhibited the expression of ANKRD1 and ANGPTL4 by recruiting zeste homolog 2 (EZH2), thereby promoting PC proliferation and metastasis. In summary, our data show that RREB1-induced upregulation of AGAP2-AS1 regulates cell proliferation and migration in PC partly through suppressing ANKRD1 and ANGPTL4 by recruiting EZH2. AGAP2-AS1 represents a potential target for the diagnosis and treatment of PC in the future.	Increased expression of AGAP2-AS1 was associated with tumor size and pathological stage progression in patients with PC.	Yes	AGAP2-AS1 affected proliferation, apoptosis, cycle arrest, invasion, and metastasis of PC cells in vitro, and AGAP2-AS1 regulated PC proliferation in vivo. 	30814490
AGAP2-AS1	LncRNA	Homo sapiens	Cholangiocarcinoma	32 intrahepatic tumor tissues	Expression [highly expressed]	Western Blot//qPCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//IHC//ChIP	AGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. 		Yes	AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. 	33522895
AGAP2-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues and cell lines	Interaction(miR-193a-3p/LOXL4 axis)	cell invasion assay//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	Our results showed that AGAP2-AS1 expression was remarkably increased in human LSCC tissues and cell lines. In addition, AGAP2-AS1 sponged miR-193a-3p and regulated its expression in LSCC cells. Inhibition of miR-193a-3p reversed the effects of AGAP2-AS1 knockdown on LSCC cells. Furthermore, Lysyl oxidase-like 4 (LOXL4) was a target gene of miR-193a-3p and the role of miR-193a-3p was mediated by LOXL4.		Yes	 Knockdown of AGAP2-AS1 significantly inhibited the proliferation and invasion of LSCC cells.	35113007
AGAP2-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	Prostate cancer tissues	regulation[AGAP2-AS1/miR-195-5p/PDLIM5]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//IHC//Transwell Assay	 LncRNA AGAP2-AS1 was found to be highly expressed in prostate cancer.Taken together, the key findings of our study demonstrated that lncRNA AGAP2-AS1 silencing exerted suppressive effects on the development of prostate cancer via the miR-195-5p-dependent downregulation of PDLIM5.		Yes	Silencing of lncRNA AGAP2-AS1 contributed to the suppression of proliferation, migration and invasion of cancer cells in vitro.	33101368
AGAP2-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa cells	Interaction(miR-628-5p/FOXP2 feedback loop)	In Vivo Experiment//Western Blot//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	AGAP2-AS1 was confirmed to be highly expressed in PCa cells. According to mechanism assays, AGAP2-AS1 sponged miR-628-5p, which was found to restrain PCa cell growth. Besides, FOXP2 was identified as a target gene of miR-628-5p, and its expression was negatively regulated by miR-628-5p and positively modulated by AGAP2-AS1.		Yes	Functionally, AGAP2-AS1 silencing inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition process and induced apoptosis.	34255057
AGAP2-AS1	LncRNA	Homo sapiens	ovarian carcinoma	tumors and adjacent healthy tissues	Interaction[ lncRNA MEG3]	qRT-PCR	Compared with adjacent healthy tissues, AGAP2-AS1 was significantly upregulated in tumor tissues.lncRNA AGAP2-AS1 is upregulated in ovarian carcinoma and negatively regulates lncRNA MEG3 to participate in the regulation of cancer cell proliferation.	 	Yes	AGAP2-AS1 overexpression led to downregulation of MEG3, while MEG3 overexpression failed to affect AGAP2-AS1. AGAP2-AS1 overexpression promoted proliferation of OC cells, while MEG3 overexpression inhibited proliferation of OC cells.	31233485
AGAP2-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction(IGF2BP2/SLC7A11)	CCK8//qRT-PCR//Flow Cytometry//Western Blot	In the current study, the findings revealed that AGAP2-AS1 was considerably greater in melanoma than in healthy tissues and that the level of AGAP2-AS1 in cancer tissue was significantly linked to the cancerous TNM stage of patients. The mechanistic results suggest AGAP2-AS1 increases SLC7A11 mRNA stability through the IGF2BP2 pathway. 	In the current study, the findings revealed that AGAP2-AS1 was considerably greater in melanoma than in healthy tissues and that the level of AGAP2-AS1 in cancer tissue was significantly linked to the cancerous TNM stage of patients. Individuals with high AGAP2-AS1 had a considerably shorter survival duration than patients with low AGAP2-AS1, regardless of progression-free survival or overall survival.	Yes	 Functionally, downregulating the expression of AGAP2-AS1 can inhibit the growth of melanocytes. Compared with the control group, AGAP2-AS1 knockdown increased Erastin-mediated iron death in melanoma cells. However, iron death inhibitor FERSINT-1 restored this effect, while Erastin induced melanoma cell death. Besides, intracellular iron and Fe2+ levels increased after AGAP2-AS1 knockdown in melanoma cells treated with Erastin compared with the si-NC group. In addition, AGAP2-AS1 silencing resulted in a significant decrease in glutathione (GSH) content in Erastin-treated melanoma cells. 	35707044
AGAP2-AS1	LncRNA	Homo sapiens	Coronary Artery Disease	EV recipient cells	Regulation(VEGFA-dependent mechanism)	qRT-PCR	A human lncRNA array revealed that certain EV-lncRNAs are significantly dysregulated in CAD patients. Circulating small EVs (sEVs) from patients with (n = 30) or without (n = 30) CAD were used to quantify PUNISHER (also known as AGAP2-antisense RNA 1 [AS1]), GAS5, MALAT1, and H19 RNA levels. PUNISHER (p = 0.002) and GAS5 (p = 0.02) were significantly increased in patients with CAD, compared to non-CAD patients. Fluorescent labeling and quantitative real-time PCR of sEVs demonstrated that functional PUNISHER was transported into the recipient cells. Mechanistically, the RNA-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNPK), interacts with PUNISHER, regulating its loading into sEVs. Knockdown of PUNISHER abrogated the EV-mediated effects on endothelial cell (EC) migration, proliferation, tube formation, and sprouting. Angiogenesis-related gene profiling showed that the expression of vascular endothelial growth factor A (VEGFA) RNA was significantly increased in EV recipient cells. Protein stability and RNA immunoprecipitation indicated that the PUNISHER-hnRNPK axis regulates the stability and binding of VEGFA mRNA to hnRNPK. Loss of PUNISHER in EVs abolished the EV-mediated promotion of VEGFA gene and protein expression. Intercellular transfer of EV-incorporated PUNISHER promotes a pro-angiogenic phenotype via a VEGFA-dependent mechanism.		Yes	Knockdown of PUNISHER abrogated the EV-mediated effects on endothelial cell (EC) migration, proliferation, tube formation, and sprouting.	34484864
AGAP2-AS1	LncRNA	Homo sapiens	Psoriasis	skin tissue of psoriasis patients 	Interaction(miR-424-5p/AKT3 axis)	Western Blot//Transfection//MeRIP//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay	We found that AGAP2-AS1 level was upregulated in the skin tissue of psoriasis patients than that of healthy controls and AGAP2-AS1 could promote proliferation and inhibit apoptosis of keratinocytes. Methyltransferase like 3(METTL3)-mediated m6A modification suppressed the expression of AGAP2-AS1 via YTHDF2-dependent AGAP2-AS1 stability. Thus, downregulation of METTL3 resulted in the upregulation of AGAP2-AS1 in psoriasis. AGAP2-AS1 functioned as a competitive endogenous RNA by sponging miR-424-5p to upregulate AKT3, activate AKT/mTOR pathway, as well as promote cell proliferation in keratinocytes.		Yes	We found that AGAP2-AS1 level was upregulated in the skin tissue of psoriasis patients than that of healthy controls and AGAP2-AS1 could promote proliferation and inhibit apoptosis of keratinocytes. 	34930676
AGAP2-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Interaction(MiR-628-5p)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	Our results showed that AGAP2-AS1 was significantly upregulated in PTC tissues.  MiR-628-5p was found to act as a target miRNA of AGAP2-AS1 in PTC. The expression level of miR-628-5p in PTC  tissues was negatively associated with that of AGAP2-AS1. 		Yes	Knockdown of AGAP2-AS1 inhibited the proliferation,  migration and invasion of PTC cells. In vivo experiment showed that AGAP2-AS1 knockdown inhibited the tumorigenesis of PTC.	33604734
AFAP-AS1	LncRNA	Homo sapiens	Thyroid Carcinoma, Anaplastic	cell lines	Interaction(miR-155-5p/ ETS1/ERK pathway)	In Vivo Experiment//IHC//Western Blot//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay	 Firstly, we showed that relative RNA expression of AFAP-AS1 in ATC cells was higher than in immortalized thyroid cells. miR-155-5p was negatively regulated by AFAP-AS1. Moreover, AFAP-AS1 regulated ETS1/ERK pathway by sponging miR-155-5p. 		Yes	 Next, AFAP-AS1 was verified as an oncogene in ATC since knock-down of AFAP-AS1 inhibited cell proliferation and accelerated apoptosis. Finally, we confirmed knock-down of AFAP-AS1 significantly suppressed tumor proliferation in vivo. 	33999777
AFAP1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Expression[highly expressed]	Flow Cytometry//qRT-PCR//Wound Healing Assay//MTT	The results indicated that AFAP1-AS1 expression levels were significantly increased in GC tissues and cell lines compared with the corresponding noncancerous tissues and normal gastric cells. 	In addition, the patients with GC with increased AFAP1-AS1 expression exhibited an advanced clinical stage and an association with the occurrence of lymph node metastasis compared with those with decreased AFAP1-AS1 expression.	Yes	In vitro assays demonstrated that knockdown of AFAP1-AS1 decreased levels of cell proliferation and migration.	31452798
AFAP1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue and cell lines	regulation[miR-155-5p/FGF7 Axis]	qPCR//RIP//PCR//IP//IF	 AFAP1-AS1 was upregulated in GC tissues and cell lines and was closely correlated with poor prognosis of GC patients.AFAP1-AS1 might be an oncogenic lncRNA that promoted GC progression by acting as a competing endogenous RNA (ceRNA) that regulates the expression of FGF7 through sponging miR-155-5p, suggesting that AFAP1-AS1 may be a novel potential therapeutic target for GC.	 AFAP1-AS1 was upregulated in GC tissues and cell lines and was closely correlated with poor prognosis of GC patients.	Yes	AFAP1-AS1 knockdown inhibited proliferation, migration, and invasion of GC cells, indicating that AFAP1-AS1 acts as an oncogene in GC. 	32051698
AFAP1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[KLF2]	qRT-PCR//ChIP//Western Blot	AFAP1-AS1 was upregulated in GC tissues, and its expression in lymph node metastasis and progressive gastric cancer tissues were much higher. LncRNA AFAP1-AS1 accelerates the proliferative and migratory abilities of GC cells by downregulating the expression of KLF2, thus promoting the progression of GC.	AFAP1-AS1 was upregulated in GC tissues, and its expression in lymph node metastasis and progressive gastric cancer tissues were much higher. 	Yes	 Knockdown of AFAP1-AS1 reduced the viability, proliferative and migratory abilities, but induced apoptosis of GC cells.	32016968
AFAP1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tumor tissues and also GC cell lines	Interaction(miR-205-5p/AFAP1)	Western Blot//EdU Staining//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Microarray//Colony Formation Assay//Invasion Assay	qPCR results showed that AFAP1-AS1 was significantly overexpressed in GC tumor tissues and also GC cell lines, comparing to their paired non-GC tissues. Mechanical analysis suggested that AFAP1-AS1 is involved in regulation of its maternal gene, AFAP1, at both mRNA level and protein level. Luciferase reporter gene assay indicated that lncRNA AFAP1-AS1, as a ceRNA, is able to sponge miR-205-5p. Moreover, miR-205-5p has been well demonstrated to participate in the regulation of AFAP1 expression and the phenotypes of GC cells, including proliferation, migration and invasion.	Furthermore, statistical analysis revealed that the overexpression of AFAP1-AS1 was significantly correlated with tumor size (p=0.018) and grade of differentiation (p=0.042). 	Yes	Subsequently, artificially decreasing the expression of AFAP1-AS1 with its specific siRNA dramatically inhibited the proliferation, migration and invasion of GC cell lines (SGC-7901 and BGC-823 cells). 	34234560
AFAP1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue,cell lines (MCF-7, SK-RB-3, MDA-MB-231and MDA-MB-468)	Expression[highly expressed]	qRT-PCR//Wound Healing Assay	The expression of AFAP1-AS1 was up-regulated in human breast cancer tissue and associated with malignancy status, high expression of AFAP1-AS1 had a poor prognosis in breast cancer patients.	The expression of AFAP1-AS1 was up-regulated in human breast cancer tissue and associated with malignancy status, high expression of AFAP1-AS1 had a poor prognosis in breast cancer patients.	Yes	AFAP1-AS1 knockdown can inhibit the proliferation, metastasis and promote apoptosis of MCF-7.	29974352
AFAP1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues	Interaction(miR-2110/Sp1 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 Expression of the lncRNA actin filament-associated protein 1 antisense RNA1 (AFAP1-AS1) has been found to be significantly higher in TNBC than in other subtypes or in normal tissue samples. Mechanistically, the dual-LRA highlighted that miR-2110 was an inhibitory target of AFAP1-AS1, and that AFAP1-AS1 functioned as a miR-2110 sponge to increase Sp1 expression. 		Yes	We found that silencing AFAP1-AS1 and Sp1 or upregulating miR-2110 suppressed the proliferation, migration, and invasion of MDA-MB-231 and MDA-MB-468 cells in vitro as well as tumor growth in vivo. 	34145213
AFAP1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 nasopharyngeal carcinoma tissues and cells	Interaction(miR-497-5p/CELF1 pathway)	Western Blot//Transfection//Wound Healing Assay//qPCR//CCK8//RIP//Luciferase Report Assay//Transwell Assay//ChIP	In current study, AFAP1-AS1 was found to be up-regulated in nasopharyngeal carcinoma tissues and cells. The interaction between AFAP1-AS1 and miR-497-5p was confirmed. AFAP1-AS1 was demonstrated to regulate CELF1, a target gene of miR-497-5p. Further functional analysis revealed that AFAP1-AS1 knockdown attenuated SP1-induced nasopharyngeal carcinoma progression. 		Yes	AFAP1-AS1 overexpression and knockdown were conducted in nasopharyngeal carcinoma cells. The results proved that AFAP1-AS1 promoted the survival and migration of nasopharyngeal carcinoma cells. Additionally, specificity protein 1 (SP1) was enhanced in nasopharyngeal carcinoma tissues and cells, and induced AFAP1-AS1 expression. 	33400247
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	Regulation[AFAP1-AS1/LSD1/HBP1 axis]	qRT-PCR//RIP//ChIP	 Here we reported that AFAP1-AS1, recruiting and binding to lysine-specific demethylase 1 (LSD1), was generally overexpressed in human non-small-cell lung cancer (NSCLC) tissues using quantitative real-time PCR. In conclusion, our results indicate that AFAP1-AS1 is carcinogenic and that the AFAP1-AS1/LSD1/HBP1 axis could constitute a new therapeutic direction for NSCLC.	 Higher AFAP1-AS1 expression was significantly correlated with larger tumor size (P = .008), lymph node metastasis (P = .025), higher TNM stage (P = .024), and worse overall survival in NSCLC patients.	Yes	In vitro experiments revealed that AFAP1-AS1 downregulation inhibited cell migration and induced apoptosis; AFAP1-AS1 knockdown also hindered tumorigenesis in vivo.	31069893
ADAMTS9-AS1	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	Regulation(Wnt1, β-catenin, c-myc and PCNA)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Invasion Assay//Transwell Assay	Using quantitative real-time PCR analysis, we found that ADAMTS9-AS1 was upregulated in glioma tissues and cells in comparison to corresponding controls.  Furthermore, we demonstrated that knockdown of ADAMTS9-AS1 suppressed Wnt1, β-catenin, c-myc and PCNA, while upregulating E-cadherin expression.	. ADAMTS9-AS1 expression level was correlated to tumor size (p=0.005) and WHO grade (p=0.002). Kaplan-Meier analysis and Cox multivariate analysis showed that ADAMTS9-AS1 could serve as an independent prognostic factor affecting the overall survival of glioma patients.	Yes	Functionally, depletion of ADAMTS9-AS1 significantly suppressed the proliferation, migration and invasion in glioma cell lines (U251 and U87), as shown via CCK-8 assay, Edu corporation assay, wound healing assay and transwell assay. 	34923953
ADORA2A-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction(FSCN1/AKT Axis)	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Invasion Assay	ADORA2A-AS1 was identified as an HCC-related lncRNA, whose low expression was correlated with advanced stage and poor outcome in HCC.Mechanistically, ADORA2A-AS1 competitively bound HuR (Hu Antigen R), repressed the binding of HuR to FSCN1 transcript, decreased FSCN1 transcript stability, and downregulated FSCN1 expression. The expression of FSCN1 was negatively correlated with ADORA2A-AS1 in HCC tissues. Through downregulating FSCN1, ADORA2A-AS1 repressed AKT pathway activation. Functional rescue assays showed that blocking of FSCN1/AKT axis abrogated the roles of ADORA2A-AS1 in HCC.	ADORA2A-AS1 was identified as an HCC-related lncRNA, whose low expression was correlated with advanced stage and poor outcome in HCC.	Yes	 Gain- and loss-of functional experiments demonstrated that ADORA2A-AS1 inhibited HCC cell proliferation, induced cell apoptosis, repressed cell migration and invasion, and repressed xenograft growth and metastasis in vivo. 	34733789
ADIRF-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction(miR-761/IRS1 axis.)	CCK8//qRT-PCR	 ADIRF-AS1 was found to be overexpressed in OS, and the overall survival of patients with OS who had high ADIRF-AS1 levels was shorter than that of those with low levels. Mechanistically, ADIRF-AS1 acted as a competitive endogenous RNA for microRNA-761 (miR-761) that siphoned miR-761 away from its target, namely insulin receptor substrate 1 (IRS1), leading to IRS1 overexpression. Rescue experiments showed that low levels of miR-761 or restoration of IRS1 could neutralize the effects of ADIRF-AS1 ablation in OS cells.	 ADIRF-AS1 was found to be overexpressed in OS, and the overall survival of patients with OS who had high ADIRF-AS1 levels was shorter than that of those with low levels. 	Yes	ADIRF-AS1 knockdown led to restricted proliferation, migration, and invasiveness of OS cells and increased apoptosis. Additionally, ADIRF-AS1 downregulation impeded tumor growth in vivo.	35030964
ADIRF-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction(PBAF)	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	 ADIRF-AS1 expression correlates with survival in human ccRCC, particularly in PBRM1 wild-type, but not mutant, tumors. Our findings suggest that ADIRF-AS1 functions partly through PBAF to regulate specific genes as a BMAL1-CLOCK-regulated, oncogenic lncRNA.		Yes	 Loss of ADIRF-AS1 eliminates in vivo tumorigenesis, partially rescued by concurrent loss of PBRM1 only when co-injected with Matrigel, suggesting a PBRM1-independent function of ADIRF-AS1. 	36261012
ADIPOQ	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and Caco-2 cells	regulation[miR-219c-3p/TP53 pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results suggested that the expression of ADIPOQ and TP53 was downregulated in human colorectal cancer tissues and Caco-2 cells.  For the first time, we found that lncRNA-ADIPOQ was downregulated in human colorectal cancer cells, which could facilitate tumor proliferation, migration and invasion as a ceRNA by sponging with miR-219c-3p.		Yes	qRT-PCR and CCK-8 assay showed that ADIPOQ expression is correlated with the proliferation of colorectal cancer cells. Transwell assay showed that ADIPOQ regulated the migration ability of colorectal cancer cells.	32744690
ADAMTS9-AS2	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cells	Interaction(miR-223-3p and TGFBR3)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Microarray//Cell Cycle Assay//Invasion Assay//Transwell Assay	qRT-PCR results demonstrated that lncADAMTS9-AS2 was lowly expressed in lung cancer tissues. In vivo assay found that ADAMTS9-AS2 suppressed the lung tumor growth. Bioinformatics predicted that miR-223-3p bound directly to the ADAMTS9-AS2 and TGFBR3, which was later confirmed by luciferase reporter system. ADAMTS9-AS2 transfection increased TGFBR3 mRNA and protein expressions in lung cancer cells, but miR-223-3p transfection significantly decreased them. Besides, our results showed that miR-223-3p induced cellular apoptosis while TGFBR3 group showed the complete opposite effect. It was proved that ADAMTS9-AS2 and TGFBR3 were the direct genes of miR-223-3p. MiR-223-3p promotes proliferation, migration and invasion of lung cancer cells by targeting TGFBR3. 		Yes	High expression of ADAMTS9-AS2 in lung cancer cells significantly reduced proliferation ability and inhibited migration, as well as elevating their apoptosis rate. 	29707897
ADAMTS9-AS2	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues,cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	ADAMTS9-AS2 was down-regulated in CRC patients according to the gene microarray analysis, which was confirmed in CRC tissues and cells.	High expression of ADAMTS9-AS2 was associated with a higher 5-year RFS rate (83.8% vs 73.5%, P=0.041) and it was an independent prognostic factor for RFS [hazard ratio (HR)=0.528; 95% CI 0.299 to 0.932; P=0.028] at the early stage of CRC. 	Yes	ADAMTS9-AS2 overexpression in CRC cells inhibited cell proliferation, migration, and invasion, while suppression of ADAMTS9-AS2 showed opposite effects. 	31413211
ADAMTS9-AS2	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues and cells	Interaction[CDH3 ]	qRT-PCR//RNA Pull-Down//RIP//ChIP	Esophageal cancers expressed low levels of ADAMTS9-AS2 and high levels of CDH3.Overexpressed ADAMTS9-AS2 aids in the suppression of esophageal cancer development, which is achieved via inducing CDH3 promoter methylation.		Yes	Furthermore, proliferation, invasion, and migration of esophageal cancer cells were inhibited by ADAMTS9-AS2 via downregulation of CDH3. Suppressed esophageal cancer development in vivo was also detected after ADAMTS9-AS2 overexpression.	31621118
ADAMTS9-AS2	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC tissue and cells	Interaction(miR-196b-5p/PPP1R12B )	qRT-PCR//Western Blot	ADAMTS9-AS2 was significantly lowly expressed while miR-196b-5p was increased in EC tissue and cells. ADAMTS9-AS2 bound to miR-196b-5p and constrained its expression. Overexpressed ADAMTS9-AS2 inhibited EC cell malignant progression via downregulating miR-196b-5p, while overexpressed miR-196b-5p reversed this inhibitory effect. ADAMTS9-AS2 modulated PPP1R12B level by competitively inhibiting miR-196b-5p. PPP1R12B played a modulatory role in EC by inhibiting cell cycle pathway. Overexpressed ADAMTS9-AS2 regulated the tumor-forming ability of EC cells in vivo through miR-196b-5p/PPP1R12B/cell cycle signaling pathway axis. ADAMTS9-AS2 downregulated PPP1R12B by adsorbing miR-196b-5p, so as to regulate the cell cycle signaling pathway to inhibit EC malignant progression.		Yes	Overexpressed ADAMTS9-AS2 inhibited EC cell malignant progression via downregulating miR-196b-5p, while overexpressed miR-196b-5p reversed this inhibitory effect. ADAMTS9-AS2 modulated PPP1R12B level by competitively inhibiting miR-196b-5p. PPP1R12B played a modulatory role in EC by inhibiting cell cycle pathway. 	35503407
ADAMTS9-AS2	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tumor samples	Regulation(RPL22/ TGF-β signaling)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Wound Healing Assay//Invasion Assay//Migration Assay//CCK8//qRT-PCR//Microarray//Colony Formation Assay//EdU Staining	The expression of ADAMTS9-AS2 was decreased in TNBC tumor samples (P < 0.05), with such downregulation being correlated with TNM stage, age, and tumor size.  From a mechanistic perspective, ADAMTS9-AS2 was found to control the expression of RPL22 and to thereby modulate TGF-β signaling to control TNBC progression.	The expression ofADAMTS9-AS2 was decreased in TNBC tumor samples (P < 0.05), with such downregulation being correlated with TNM stage, age, and tumor size. 	Yes	Overexpressing ADAMTS9-AS2 promoted the apoptotic death and cell cycle arrest of tumor cells in vitro and inhibited tumor growth in vivo. 	34178640
ADAMTS9-AS2	LncRNA	Homo sapiens	Carcinoma, Adenoid Cystic	cells	Regulation[PI3K/Akt and MEK/Erk Signaling]	RNA Pull-Down//Western Blot//ISH//qRT-PCR//Luciferase Report Assay//ChIP	In our study, we found that ADAM metallopeptidase with thrombospondin type 1 motif, 9 (ADAMTS9) antisense RNA 2 (ADAMTS9-AS2) was significantly upregulated in SACC patients with metastasis and SACC-lung metastasis (LM) cells.Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, and thus it activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis.	Moreover, ADAMTS9-AS2 expression was closely associated with the prognosis and distant metastasis in SACC patients. 	Yes	 Knockdown of ADAMTS9-AS2 significantly inhibited migration and invasion of SACC cells in vitro and distant lung metastasis in vivo.	30217729
ADAMTS9-AS2	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues 	Regulation[miR-600/EZH2 axis]	Western Blot//ISH//qRT-PCR//RIP//Luciferase Report Assay	Our results indicate that the lncRNA ADAMTS9-AS2 is most significantly upregulated in TSCC tissues from patients with lymph node metastasis and is closely associated with poor prognosis. In summary, our results demonstrate an explicit oncogenic role of ADAMTS9-AS2 in TSCC tumorigenesis via competition with miR-600, suggesting a new regulatory mechanism of ADAMTS9-AS2 and providing a potential therapeutic target for TSCC patients.		Yes	 Furthermore, ADAMTS9-AS2 knockdown in TSCC cells leads to a inhibition of cell migration and invasion and reverses TGF-β1 induced EMT. ADAMTS9-AS2 knockdown also inhibits TSCC cell growth in vitro and in vivo. 	30970517
ADAMTS9-AS2	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer cell 	Regulation	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	The results suggested that ADAMTS9-AS2 downregulated the phosphorylation of AKT and mTOR, the protein expression level of PIK3CB, as well as the expression levels of autophagy protein SQSTM1 and antiapoptotic protein Bcl-2. 		Yes	The results demonstrated that ADAMTS9-AS2 inhibited liver cancer cell proliferation, migration and invasion. Finally, the effect of ADAMTS9 on PI3K/AKT/mTOR signaling pathway-associated proteins [AKT, phosphorylated-AKT, phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit β (PIK3CB), mTOR and phosphorylated-mTOR], several key autophagy-related proteins [light chain 3-I/II (LC3-I/II), beclin 1 (BECN1) and sequestosome 1 (SQSTM1)] and apoptosis-related proteins (Bax and Bcl-2) was detected via western blotting. 	33850531
ADAMTS9-AS2	LncRNA	Homo sapiens	Oral Submucous Fibrosis	OSCC tissues	regulation[AKT signalling pathway]	Western Blot//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	lncRNA ADAMTS9-AS2 is down-regulated in OSCC tissues compared with OSF and normal mucous tissues. Through profiling miRNA expression profile regulated by exosomal ADAMTS9-AS2, significantly enriched pathways include metabolic pathway, PI3K-Akt signalling pathway and pathways in cancer, indicating that exosomal ADAMTS9-AS2 exerts its functions through interacting with miRNAs during OSF progression. 	 Low ADAMTS9-AS2 expression is associated with poor overall survival. 	Yes	 Functional studies reveal that exosomal ADAMTS9-AS2 suppresses OSCC cell growth, migration and invasion in vitro. 	33345447
ADAMTS9-AS2	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder tumor cells	regulation[PI3K/AKT/mTOR signal pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	 First, ADAMTS9-AS2 downregulation in bladder tumor cells was identified.Third, ADAMTS9-AS2 was linked with PI3K/AKT/mTOR pathway related-molecules, several key autophagy, and apoptotic proteins.		Yes	Second, ADAMTS9-AS2 contributed to the inhibition of proliferation, migration, and invasion in bladder tumor cells.	32801743
ADAMTS9-AS2	LncRNA	Mus musculus	Ischemic Stroke	MCAO mice	Interaction(miR-185-5p/IGFBP-2 Axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Transfection//qRT-PCR//RIP//Luciferase Report Assay//IF	The results showed that ADAMTS9-AS2 was decreased in the plasma of acute ischemic stroke (AIS) patients and in the brain tissue and plasma of MCAO mice, and the low expression of ADAMTS9-AS2 was associated with the increase in infarct size.Molecular mechanism results indicated that ADAMTS9-AS2 and miR-185-5p affected the pathological process of ischemic stroke through ceRNA mechanism, and IGFBP-2 was a downstream target gene of miR-185-5p. These findings demonstrated that ADAMTS9-AS2 promoted angiogenesis through regulating miR-185-5p/IGFBP-2 axis, suggesting that ADAMTS9-AS2 may be a potential marker for the diagnosis and treatment of neurological diseases.		Yes	Besides, compared with the control group, MCAO treatment slightly promoted angiogenesis, which was enhanced by the overexpression of ADAMTS9-AS2. 	35098480
ADAMTS9-AS1-202	LncRNA	Homo sapiens	Mouth Neoplasms	oral cancer tissues	Expression[lower expressed]	qRT-PCR	LncRNAs were aberrantly expressed in oral cancer tissues. The expression levels of ENST00000470447.1 and ENST00000412353.1 in oral cancer tissues were significantly lower than those in matched adjacent noncancerous tissues (P < .001). 	 Furthermore, ENST00000470447.1 expression was significantly correlated with tumor differentiation (P = .030). Cox regression analyses demonstrated that high ENST00000470447.1 expression was associated with better disease-free survival for patients with oral cancer (hazard ratio: 0.25, 95% CI: 0.06-0.95; P = .041).	Yes	in vitro assays indicated that overexpression of ENST00000470447.1 significantly inhibited the proliferation, migration, and invasion ability of Tca-8113 cells, whereas promoted the apoptosis of Tca-8113 cells.	30969450
ADAMTS9-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction( miR-301b-3p/TGFBR2/JAK STAT pathway)	Luciferase Report Assay//Transwell Assay//EdU Staining//Western Blot	Markedly inactivated ADAMTS9-AS1 in breast cancer pertained to patient's prognosis. MiR-301b-3p was capable of binding TGFBR2/ADAMTS9-AS1. However, overexpression of ADAMTS9-AS1 stimulated miR-301b-3p binding ADAMTS9-AS1 and repressed miR-301b-3p binding TGFBR2 mRNA. ADAMTS9-AS1 could sequester miR-301b-3p to inhibit progression of breast cancer via TGFBR2/JAK STAT pathway. 	Markedly inactivated ADAMTS9-AS1 in breast cancer pertained to patient's prognosis.	Yes	ADAMTS9-AS1 interference enhanced cancer proliferation and invasion, facilitated levels of KI67, PCNA, MMP-9 and MMP-2, and activated the JAK STAT signaling pathway. While silencing miR-301b-3p reversed the effect of ADAMTS9-AS1 interference. 	34900984
ADAMTS9-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	Our data showed that ADAMTS9-AS1 expression level was significantly up-regulated in CRC tissues and cell lines compared with corresponding controls. 	High ADAMTS9-AS1 level was associated with TNM stage, lymph node invasion and worse survival prognosis.	Yes	 Depletion of ADAMTS9-AS1 significantly suppressed cell proliferation, G1/S transition, migration and invasion, as well as suppressed CDK4/Cyclin D1 and epithelial-mesenchymal transition (EMT).	32918700
ADAMTS9-AS1	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC cells	Interaction( miR-587/SLC7A11 axis )	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting results showed that ADAMTS9-AS1 expression was elevated in EOC cells; microRNA-587 expression was up-regulated and SLC7A11 expression was down-regulated after knocking down ADAMTS9-AS1 by transfection with siRNAs; however, microRNA-587 inhibitor reversed SLC7A11 expression in ADAMTS9-AS1 knocking down cells. Additionally, micoRNA-587 inhibitor reversed the effect of ADAMTS9-AS1 silence on the ferroptosis and cell function. Moreover, dual-luciferase reporter gene assay and RNA immunoprecipitation assay confirmed that miR-587 was as a sponge for ADAMTS9-AS1 and SLC7A11.		Yes	Ferroptosis related marker detection and cell function assay confirmed that knocking down ADAMTS9-AS1 inhibited EOC cells proliferation and migration by promoting ferroptosis. Overexpression of micoRNA-587 also promoted ferroptosis while inhibited cells proliferation and migration in EOC cells. 	35311457
ADORA2A-AS1	LncRNA	Homo sapiens	Leukemia, Myelogenous, Chronic, BCR-ABL Positive	CML tissues and cells	Interaction(TGFBR1/ABCC2)	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay	We found that the expression of ADORA2A-AS1 was upregulated in CML. Besides, ADORA2A-AS1 promoted the expression of transforming growth factor-beta receptor 1 (TGFBR1) and ATP binding cassette subfamily C member 2 (ABCC2) via sponging miR-665, thereby exerting a tumor-promoting activity. 		Yes	Further, knockdown of ADORA2A-AS1 inhibited the proliferation, induced apoptosis, arrested cell cycle, and enhanced imatinib sensitivity in CML cells. 	35034552
ADPGK-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	 PC tissues and cells 	Interaction(miR-205-5p/ZEB1)	In Vivo Experiment//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//IHC//Transwell Assay	 MiR-205-5p was low-expressed while ZEB1 and ADPGK-AS1 were high-expressed in PC tissues and cells compared with the normal. Dual-luciferase reporter gene assay proved that ADPGK-AS1 could directly target miR-205-5p and miR-205-5p could directly target ZEB1 3'UTR. 		Yes	The expression of MiR-205-5p was negatively correlated with proliferation, migration and invasion, and positively correlated with apoptosis rate of PC cells, while ZEB1 and ADPGK-AS1 had an inversed effect. Further in vitro and in vivo investigation indicated that epithelial-mesenchymal transition (EMT) could be restrained by miR-205-5p through targeting ZEB1. ADPGK-AS1 strongly promoted the tumorigenesis via downregulating miR-205-5p expression and induced the EMT process in vivo.	29667486
AFAP1-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC cells	interaction[ targeting miR-145 ]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results showed that miR-145 expression was low, whereas AFAP1-AS1 and MTH1 expression was high in TNBC cells and that miR-145 mimics reduced TNBC cell proliferation and invasion, whereas miR-145 knockdown exerted the opposite activity in TNBC cells.This study revealed that AFAP1-AS1 could promote TNBC cell proliferation and invasion via regulation of MTH1 expression through targeting of miR-145.		Yes	Moreover, knockdown of AFAP1-AS1 reduced tumor cell proliferation and invasion, but miR-145 co-transfection rescued tumor cell viability and colony formation ability.	32376943
ADPGK-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction[targeting miR-542-3p ]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	LncRNA ADPGK-AS1 expression was induced while miR-542-3p expression was reduced in OS tissues and cells.ADPGK-AS1 affected cell proliferation, invasion, migration, and apoptosis via targeting miR-542-3p in OS, providing a theoretical basis and a new therapeutic target for the diagnosis and treatment of OS.		Yes	Functional experiments showed that inhibition of ADPGK-AS1 could decrease cell proliferation, migration, and invasion, as well as promoted cell apoptosis in OS cells. 	31696461
AFAP1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissue and cells	Interaction[suppressing RBM5 ]	qRT-PCR//Transwell Assay//Western Blot	The expression level of AFAP1-AS1 was significantly higher in prostate cancer samples than that in corresponding ones. AFAP1-AS1 acts as an oncogene in prostate cancer by enhancing cell metastasis and proliferation via suppressing RBM5, which might be a novel therapeutic strategy in treatment for prostate cancer.		Yes	Additionally, the cell proliferation, migration, and invasion capacities were inhibited after AFAP1-AS1 was knocked down in prostate cancer cells.	31081081
AFAP1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues and cell lines	Interaction[targeting miR-512-3p]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay	AFAP1-AS1 is highly expressed in prostate cancer tissues and cell lines. AFAP1-AS1 regulates miR-512-3p, so as to realize the regulation effect on the proliferation, invasion and migration of prostate cancer cells, and thereby promote the occurrence and development of prostate cancer, so as to provide the corresponding program for the treatment of prostate cancer. 	The expression level of AFAP1-AS1 is correlated with histological grade and distant metastasis.The overall level of patients with high expression of AFAP1-AS1 is low, and their survival rate is relatively low. 	Yes	Silencing AFAP1-AS1 can significantly increase the proliferation and migration of prostate cancer cells. AFAP1-AS1 silencing induces cell cycle arrest at G0/G1 phase. 	31669642
AFAP1-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	castration-resistant C4-2 cells and NE-like cells	Interaction(miR-15b/IGF1R Axis)	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	AFAP1-AS1 level was markedly increased in castration-resistant C4-2 cells and NE-like cells (PC3, DU145, and NCI-H660), compared with androgen-sensitive LNCaP cells. Mechanistically, AFAP1-AS1 functioned as an oncogene in PCa through binding to miR-15b and destroying its tumor suppressor function. 		Yes	Functionally, AFAP1-AS1 knockdown repressed tumor cell proliferation and invasion. 	34126893
AFAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	Regulation[PTEN-dependent signaling]	CCK8//qRT-PCR//Western Blot//Transwell Assay	We observed that AFAP1-AS1 expression was significantly upregulated in ccRCC tissues and that patients with high-level expression of AFAP1-AS1 had a shorter overall survival. Downregulation of AFAP1-AS1 resulted in an increase in E-cadherin and a decrease in vimentin. Noticeably, we found that PTEN has a negative correlation with the lncRNA AFAP1-AS1 expression. Further studies verified that PTEN deficiency effectively attenuated the ability of AFAP1-AS1 in promoting ccRCC cell proliferation, invasion, migration, and EMT. Moreover, the similar biological response of silencing AFAP1-AS1 was observed in our ccRCC mice model. Knockdown of AFAP1-AS1 evidently suppressed tumor growth. Taken together, our results provide the evidences that silencing of AFAP1-AS1 inhibits cell proliferation, EMT, and metastasis through PTEN-dependent signaling, and our findings elucidate a novel potential therapeutic target or biomarker for the treatment of ccRCC.	We observed that AFAP1-AS1 expression was significantly upregulated in ccRCC tissues and that patients with high-level expression of AFAP1-AS1 had a shorter overall survival. 	Yes	Knockdown of AFAP1-AS1 markedly suppressed the progression of proliferation, invasion, migration, and EMT in ccRCC cells.	30832752
AFAP1-AS1	LncRNA	Homo sapiens	Retinoblastoma	RB tissues and cells	Interaction(miR-545-3p/GNB1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Increased AFAP1-AS1 and GNB1 expression in RB tissues and cells was confirmed by RT-qPCR;conversely, miR-545-3p was found to be downregulated in RB tissues and cells.Moreover, AFAP1-AS1 was found to target miR-545-3p. The anti-miR-545-3p treatment phenocopied the effect of AFAP1-AS1 overexpression and promoted RB cell growth in vivo. miR-545-3p was found to directly target GNB1. GNB1 silencing resulted in reduced proliferation and migration of RB cells and attenuated the oncogenic effect of the miR-545-3p inhibitor. 		Yes	AFAP1-AS1 overexpression resulted in increased proliferation and migration of RB cells, whereas AFAP1-AS1 silencing resulted in decreased proliferation and migration of RB cells. 	35193469
AFAP1-AS1	LncRNA	Homo sapiens	Melanoma	melanoma cell lines	regulation[miR-653-5p/RAI14 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	AFAP1-AS1 was highly expressed in melanoma cell lines. AFAP1-AS1 exerts its oncogenic function in melanoma by targeting miR-653-5p/RAI14 axis.		Yes	 Suppression of AFAP1-AS1 impaired cell proliferation, migration, invasion and EMT in melanoma.	32228518
AFAP1-AS1	LncRNA	Homo sapiens	Pituitary Neoplasms	pituitary adenoma tissues 	Regulation	Western Blot//Transfection//qRT-PCR//Cell Proliferation Assay//Cell Cycle Assay	We observed that the expression of AFAP1-AS1 was considerably higher in the pituitary adenoma tissues as compared to its expression in the adjacent tissues. Finally, knockdown of AFAP1-AS1 also promoted the expression of PTEN and inhibited the expression of PI3K and p-AKT. 		Yes	 Additionally, knockdown of AFAP1-AS1 inhibited the proliferation, arrested the cell cycle in the G1-to-S transition phase, and promoted apoptosis in GH3 and MMQ cells. 	31938218
AFAP1-AS1	LncRNA	Homo sapiens	laryngeal carcinoma	 LC patients	Expression(highly expressed)	Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	Herein, a remarkable elevation of lncRNA AFAP1-AS1 was observed in LC patients. 	 And higher lncRNA AFAP1-AS1 level was correlated to worse clinical pathological characteristics.	Yes	Moreover, lncRNA AFAP1-AS1 silencing was revealed to repress TU212 malignant phenotypes.	35968243
AFAP1-AS1	LncRNA	Homo sapiens	Endometriosis	ectopic endometrial tissues 	Interaction[ZEB1]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//ELISA//IHC//EdU Staining//Transwell Assay	 AFAP1-AS1 levels were much higher in ectopic endometrial tissues than that in eutopic tissues.The knockdown of AFAP1-AS1 significantly inhibited expression from promoter site pGL3-P886 of the EMT-related transcription factor ZEB1. The size of subcutaneous tumours in nude mice was significantly reduced after down-regulation of AFAP1-AS1 expression.		Yes	After knockdown of AFAP1-AS1, the morphology of endometrial epithelial cells varied from spindle fiber shaped to polygon epithelioid and proliferation, migration, and invasion were each inhibited.	30506548
AFAP1-AS1	LncRNA	Homo sapiens	Endometriosis	ESCs	Interaction(miR-424-5p/ STAT3/TGF-β/Smad signaling pathway)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-β1 (TGF-β1)/Smad2 axis via directly targeting miR-424-5p. 		Yes	In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail.	33949053
AFAP1-AS1	LncRNA	Homo sapiens	Endometriosis	Exo of ESCs	Interaction(miR-15a-5p/BCL9)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//Bioinformatics Analysis//IF	The Exo was successfully isolated from ESCs and we observed high expression of AFAP1-AS1 and BCL9 but low expression of miR-15a-5p in EMS. AFAP1-AS1 bound to BCL9, which was targeted by miR-15a-5p in EMS. In vivo experiments in nude mice revealed that inhibition of Exosomal AFAP1-AS1 suppressed migration and invasion of EcESCs through miR-15a-5p/BCL9.		Yes	Moreover, Exo derived from EcESCs could deliver AFAP1-AS1 to EcESCs and thus promoting proliferation, migration, and invasion of ESCs. 	35513844
AFAP1-AS1	LncRNA	Homo sapiens	gallbladder carcinoma	GBC cell	Interaction(AFAP1-AS1/hsa-miR-15a-5p/bcl-2 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In SGC-996 and NOZ cells, AFAP1-AS1 was significantly expressed and hsa-miR-15a-5p was modestly expressed. In addition, AFAP1-AS1 bound hsa-miR-15a-5p and hsa-miR-15a-5p targeted bcl-2. Increased bcl-2 expression was observed in the GBC cells. AFAP1-AS1 may regulate GBC cell proliferation and apoptosis via has-miR-15a-5p to mediate bcl-2 expression.		Yes	Transfection of the hsa-miR-15a-5p inhibitor elevated proliferation of SGC-996 and NOZ cells and decreased apoptosis, whereas transfection of si-AFAP1-AS1 reduced the proliferation rate and increased apoptosis. 	35404727
AFAP1-AS1	LncRNA	Homo sapiens	Hirschsprung Disease	intestinal tissue	regulation[AFAP1-AS1/microRNA-195/E2F3 axis ]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 AFAP1-AS1 was reduced in HSCR patients.  Altogether, AFAP1-AS1 silencing acts as an endogenous RNA by interacting with miR-195 to alter E2F3 expression, thus conferring repressive effects on ENCSC activity and promoting HSCR progression.		Yes	 Meanwhile, knockdown of AFAP1-AS1 reduced the cell migratory and proliferative capacities and facilitated cell apoptosis along with G0/G1 phase arrest.	32959905
AFAP1-AS1	CircRNA	Homo sapiens	Thyroid Cancer, Papillary		Expression [highly expressed]	qRT-PCR//Wound Healing Assay//Colony Formation Assay//Transwell Assay	Results Compared with the paracancerous tissue, the expression level of AFAP1-AS1 mRNA in the papillary thyroid carcinoma tissue significantly increased. 		Yes	Knockdown of AFAP1-AS1 significantly reduced the colony-forming ability, invasion and migration ability of TPC-1 cells. Compared with shNC group and control group, knockdown of AFAP1-AS1 significantly reduced the mRNA and protein expression of snail2, vimentin and β-catenin.	33441229
AFAP1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissuses	Interaction(CCNA2)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RNA-seq//Cell Cycle Assay	Bioinformatics analyses indicated that AFAP1-AS1 was upregulated in OSCC. Further research indicated that AFAP1-AS1 regulated OSCC cell proliferation by targeting CCNA2.	Overexpression of AFAP1-AS1 was positively correlated with lymph node metastasis, tumor stage, and pathological grade. 	Yes	 Down-regulation of AFAP1-AS1 in OSCC led to decreased proliferation in vitro and, notably, inhibition of tumor growth in vivo. 	34703311
AFAP1-AS1	LncRNA	Mus musculus	Pancreatic Neoplasms	PC tissues	Interaction[binding to miR-384]	RNA Pull-Down//Western Blot//ISH//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	High expression of AFAP1-AS1 and ACVR1 with low expression of miR-384 were detected in PC tissues. Taken together, AFAP1-AS1 functions as an endogenous RNA by competitively binding to miR-384 to regulate ACVR1, thus conferring inhibitory effects on PC cell stemness and tumorigenicity.		Yes	 The knockdown of AFAP1-AS1 or overexpression of miR-384 was confirmed to impair PC cell self-renewal ability, tumorigenicity, invasion, migration and stemness.	30819221
ADPGK-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[sponging miR-3196]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	ADPGK-AS1 was increased in GC tissues and cell lines. GC patients with an increased expression of ADPGK-AS1 had a poor prognosis compared to those with a reduced expression. We unveiled that ADPGK-AS1 could promote GC progression via sponging miR-3196 and therefore upregulating KDM1B, providing a novel prognostic biomarker and therapeutic target for GC patients.		Yes	ADPGK-AS1 knockdown led to inhibition of GC cell proliferation and migration. 	30944080
ADPGK-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cell lines	Regulation[miR-3196/OTX1 axis ]	qRT-PCR//Luciferase Report Assay//RIP	 ADPGK-AS1 expression level was upregulated in BC tissues and cell lines. Currently, ADPGK-AS1 acted as a competing endogenous RNA (ceRNA) via modulating miR-3196/OTX1 axis in BC.	High expression of ADPGK-AS1 predicted poor prognosis for BC patients.	Yes	Functionally, ADPGK-AS1 promoted cell proliferation, migration, induced epithelial-mesenchymal transition (EMT) process, and suppressed cell apoptosis.	31264061
ADPGK-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cells	regulation[ADPGK-AS1/miR-525/FUT1]	qRT-PCR//Luciferase Report Assay	ADPGK-AS1 was upregulated in CRC tissues and cells.ADPGK-AS1 is upregulated in CRC. The regulatory loop ADPGK-AS1/miR-525/FUT1 exacerbates the progression of CRC by promoting the proliferation, migration, and invasion of tumor cells.		Yes	Knockdown of ADPGK-AS1 attenuated the proliferative, migratory, and invasive abilities of CRC cells.	32196589
AGAP2-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cells	Interaction(miR-9-5p-MMP2/MMP9)	Bioinformatics Analysis	Herein, based on a variety of bioinformatics tools for the reverse prediction of target genes associated with the prognosis of GBM, a ceRNA network of AGAP2-AS1-miR-9-5p-MMP2/MMP9 was constructed, and a potential therapeutic target for GBM was identified. 		Yes	Enrichment analysis predicted that the ceRNA regulatory network participates in the processes of cell proliferation, differentiation, and migration.	33889541
AGAP2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissue and cell lines	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	In this study, we found that lncRNA AGAP2-AS1 was differentially expressed in glioma tissue samples and cell lines.Higher expression of AGAP2-AS1 was correlated with the lower overall survival of glioma patients.  Mechanistically, AGAP2-AS1 upregulated HDGF by sponging miR-15a/b-5p. The function of AGAP2-AS1-miR-15a/b-5p-HDGF axis was confirmed by performing rescue assays. Experimental results suggested that miR-15a/b-5p and HDGF involved in AGAP2-AS1-mediated glioma cell proliferation. Moreover, AGAP2-AS1 and HDGF were found to activate Wnt/β-catenin signaling pathway in glioma cell lines. In summary, this study demonstrated that AGAP2-AS1 promoted glioma cell proliferation by sponging miR-15a/b-5p to upregulate the expression of HDGF.	Higher expression of AGAP2-AS1 was correlated with the lower overall survival of glioma patients. 	Yes	Functionally, AGAP2-AS1 knockdown inhibited glioma cell proliferation and accelerated glioma cell apoptosis.	30684575
AGAP2-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues 	Expression[Expression[Expression[highly expressed]-expression]-expression]	CCK8//qRT-PCR	In our results, we found AGAP2-AS1 expression was increased in GBM compared with adjacent normal brain tissues or low-grade glioma tissues, and there was no significantly different between low-grade glioma tissues and normal tissues. 	Kaplan-Meier survival analysis indicated patients with GBM having high-expression of AGAP2-AS1 had shorter overall survival time than those with low expression of AGAP2-AS1. 	Yes	The loss-of-function studies showed that Expression[down-expression]regulation of AGAP2-AS1 depressed cell proliferation, migration, and invasion, and promoted cell apoptosis in GBM. 	30525219
APCDD1L-DT	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	Epigenetics(hypermethylation)	In Vivo Experiment//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay	 The expression of APCDD1L-AS1 was downregulated in ccRCC.  APCDD1L-AS1 was able to inhibit the progression of ccRCC, and its decreased expression could be caused by DNA hypermethylation and loss of VHL protein expression.	 Decreased APCDD1L-AS1 expression was related to higher tumor stage and histological grade and shorter RFS (Relapse-free survival). 	Yes	Besides, APCDD1L-AS1 overexpression restrained the growth and metastasis of ccRCC cells in vitro and in vivo. 	35414787
AP000695.2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 lung adenocarcinoma tissues and cell lines	Expression(highly expressed)	Cell Proliferation Assay//qRT-PCR	Here, we discovered that AP000695.2 was significantly upregulated in lung adenocarcinoma tissues compared with healthy adjacent lung tissue and higher in LUAD cell lines than in normal human bronchial epithelial cell lines.	A higher expression of AP000695.2 was positively correlated with aggressive clinicopathological characteristics, and AP000695.2 served as an independent prognostic indicator for the overall survival, disease-free survival, and progression-free survival in patients with LUAD.	Yes	Our in vivo data confirmed that AP000695.2 promotes the proliferation, migration, and invasion of LUAD cells. GSEA results suggested that AP000695.2 co-expressed genes were mainly enriched in immune-related biological processes such as JAK-STAT signaling pathway and toll-like receptor signaling pathway.	35685240
AP000439.2	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC-exo	Interaction(STAT3 /TGF-β and IL-10 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//migration assay//RNA-seq	LncRNA AP000439.2 was highly enriched in the ccRCC-exo. Nuclear-localized AP000439.2 directly interacted with signal transducer and activator of transcription 3 (STAT3) proteins and phosphorylated STAT3 in macrophages. RNA-Seq results showed overexpression of AP000439.2 activated NF-κB signaling pathway. Silencing of STAT3 suppressed overexpression of AP000439.2-induced up-regulation of TGF-β and IL-10 expression, and p65 phosphorylation. 		Yes	Overexpression of exosomal AP000439.2 promoted M2 macrophage polarization whereas AP000439.2-deficient exosome had the opposite effects. AP000439.2-deleted exosome inhibited tumor growth in vivo.	36153596
AOC4P	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation[MAPK signaling pathway]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	The expression of lncRNA AOC4P in gastric cancer tissues was higher than that in adjacent tissues.Inhibition of lncRNA AOC4P expression can inhibit cell proliferation, migration and invasion, promoting cell apoptosis to some extent. Inhibition of lncRNA AOC4P expression also can result in the decreased expression levels of extracellular-signal-regulated kinase 1 (ERK1), c-Jun N-terminal kinases (JNK) and p38 proteins.	OS or DFS time were significantly shortened in patients with gastric cancer with high expression of lncRNA AOC4P.	Yes	 Inhibition of lncRNA AOC4P expression can inhibit cell proliferation, migration and invasion, promoting cell apoptosis to some extent. 	31696472
AOC4P	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue and cell lines	Interaction(UHRF1)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	 UPAT was overexpressed in GC tissue and cell lines.  UPAT expression in GC was positively correlated with UHRF1 expression. UHRF1 overexpression offset the inhibitory effects of UPAT down-regulation on cell proliferation, migration, invasion and cell cycle, and partially reversed the positive effect of UPAT down-regulation on apoptosis.	Decreased UPAT level was associated with higher overall survival. 	Yes	Down-regulation of UPAT diminished cell proliferation, Cyclin D1 expression, and migration and invasion rates, increased apoptosis rate and cleaved caspase-3 expression, and blocked cell cycle in AGS and NCI-N87 cells. 	35294719
AOC4P	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC samples and cells	regulation[Wnt/β-catenin pathway]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	AOC4P was lowly expressed in NSCLC samples and cells.  In conclusion, AOC4P overexpression suppresses viability and invasion and induces apoptosis in NSCLC cells via inhibition of the Wnt/β-catenin pathway.		Yes	Overexpression of AOC4P inhibited viability, the expression of MMP-2 and MMP-9, and invasion of NSCLC cells. Apoptosis and caspase-3/7 activity were suppressed in response to AOC4P overexpression in NSCLC cells. AOC4P overexpression suppressed tumor growth in a xenograft mouse model.	32325081
AOC4P	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cell lines	Expression[lower expressed]	qRT-PCR//Western Blot//Transwell Assay	The results showed that AOC4P expression levels were decreased in EOC tissues and cell lines, and that the under-expression of AOC4P was positively correlated with FIGO stage and lymph node metastasis. 	The results showed that AOC4P expression levels were decreased in EOC tissues and cell lines, and that the under-expression of AOC4P was positively correlated with FIGO stage and lymph node metastasis. 	Yes	Furthermore, the knockdown of AOC4P expression in poorly metastatic EOC cell lines remarkably facilitated cell migration/invasion while the overexpression of AOC4P in highly metastatic EOC cell lines reduced the metastatic ability of these cells in vitro. 	32334623
ANXA2P2	LncRNA	Homo sapiens	Glioblastoma	glioma tissue samples and cells	regulation[ANXA2P2/miR-9/LDHA axis ]	qRT-PCR//MTT//Luciferase Report Assay	 The expression of ANXA2P2 showed to be dramatically upregulated within glioma tissue samples and cells. In conclusion, ANXA2P2/miR-9/LDHA axis modulates the aerobic glycolysis progression in glioma cells, therefore affecting glioma cell proliferation.		Yes	 Knocking down ANXA2P2 within glioma cells significantly inhibited cell proliferation and aerobic glycolysis, as manifested as decreased lactate and increased glucose in culture medium, and downregulated protein levels of glycolysis markers, GLUT1, HK2, PFK, as well as LDHA. miR-9 was predicted to target both lncRNA ANXA2P2 and LDHA. 	32707073
ANXA2	CircRNA	Homo sapiens	Lung Neoplasms	 lung cancer cell lines and tissues	Interaction(miR-33a-5p/PDPK1 )	TUNEL//Western Blot//Transfection//Tunel//qRT-PCR//PCR//IF	The expression abundance of circANXA2 is high in lung cancer cell lines and tissues. circANXA2 further affects downstream PDPK1 expression by regulating miR-33a-5p and thereby affecting the malignancy of the lung cancer cells. circANXA2 inhibits miR-33a-5p activity by directly interacting with miR-33a-5p. circANXA2 regulates the transcription of the miR-33a-5p downstream target gene PDPK1 and affects the malignant progression of lung cancer.		Yes	 Knocking down of circANXA2 inhibits the proliferation and clonogenesis of the lung cancer cells. Knocking down circANXA2 promotes apoptosis. 	34992655
ANKRD40CL	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	interaction[sponging miR-490-3p]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	LINC00483 and MAPK1 levels were increased in gastric cancer tissues and cells.Besides, inhibition of LINC00483 decreased xenograft tumor growth by regulating miR-490-3p/MAPK1 axis.		Yes	 Knockdown of LINC00483 or MAPK1 inhibited cells viability, migration and invasion but promoted apoptosis in gastric cancer cells. Moreover, MAPK1 overexpression attenuated the effect of LINC00483 knockdown on gastric cancer development.	32293550
ANKRD40CL	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[LINC00483/miR-204-3p/FMNL2 axial]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	 In the present study, we found a novel lncRNA, long intergenic non-protein coding RNA 483 (LINC00483), which was upregulated in CRC. LINC00483/miR-204-3p/FMNL2 axial might be a novel target in molecular treatment of CRC.	We also illustrated that upregulated LINC00483 was correlated with poor clinicopathological features of patients with CRC. 	Yes	Functionally, we displayed that a knockdown of LINC00483 suppressed LOVO and HT29 cells proliferation and metastatic ability. 	30594388
ANKRD40CL	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC biopsies 	Regulation(HNF4α)	qRT-PCR	LINC00483 was downregulated in CRC biopsies and metastases and its decreased levels were associated with severe clinical features.Moreover, we found that LINC00483 is potentially under negative control of transcription factor HNF4α. In conclusion, we propose that LINC00483 is a tumor suppressor in CRC that, through an RNA-RNA network, may control cell migration and participate in proliferation signaling.		Yes	 Inhibition of the MAPK pathway and cell cycle arrest by starvation induced an upregulation of LINC00483, while the epithelial to mesenchymal transition activation by TGFβ-1 and IL-6 caused its down-modulation.Moreover, enforced expression of LINC00483 provoked a slowing down of cell migration rate without affecting cell proliferation. 	33552987
ANKRD40CL	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues and cells	Interaction(miR-19a-3p/TBK1/MAPK axis)	qRT-PCR//Luciferase Report Assay//IHC//EdU Staining	Our data showed that LINC00483 was significantly upregulated in PDAC compared to normal tissue. Subsequently, we found that miR-19a-3p binds to TBK1 in PDAC and LINC00483 could regulate PDAC cell progression by regulating miR-19a-3p via the TBK1/MAPK pathway.	High level of LINC00483 was correlated with advanced clinical stage, tumor invasion and metastasis, and adverse prognosis in PDAC patients.	Yes	 LINC00483 suppression inhibited proliferation and invasion in vitro and tumor development in vivo via modulation of miR-19a-3p expression.	35433983
ANKRD40CL	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	Regulation[miR-508-3p/RGS17 axis]	Wound Healing Assay//Tunel//qRT-PCR//Luciferase Report Assay//Transwell Assay	Linc00483 aberrantly overexpressed in both cervical cancer tissues and cell lines comparing to the Control groups. Knock-down of Linc00483 inhibited the development of cervical cancer by regulating miR-508-3p/RGS17 axis.		Yes	Knock-down of Linc00483 inhibited cervical cancer cell proliferation, invasion as well as migration, and promoted cell apoptosis.	31454494
ANKRD12	CircRNA	Homo sapiens	Neoplasms	cell line	Expression[Expression[Expression[highly expressed]-expression]-expression]	PCR//Invasion Assay//Western Blot	We performed Real-time PCR analysis on 12 different cell lines from breast, ovarian and lung cancer and normal breast and lung to assess the cell-type specific expression of circANKRD12 (Additional file 1: Figure S1:Fig. ​S1:Fig.2c).2c). Most of these cell lines show a high abundance of both ANKRD12 circRNA and mRNA. Ovarian cancer cell lines show a higher abundance of ANKRD12 circRNA compared to breast and lung cancer cell lines.		Yes	Silencing of circANKRD12 induces a strong phenotypic change by significantly regulating cell cycle, increasing invasion and migration and altering the metabolism in cancer cells.	31185953
ANAPC7	CircRNA	Homo sapiens	Pancreatic Neoplasms	human pancreatic cancer cells, 3-dimensional spheroids and organoids, mouse models, and clinical specimens	Interaction(CREB-miR-373-PHLPP2 axis)	In Vivo Experiment//RNA Pull-Down//Luciferase Report Assay//RIP	 We identified circANAPC7 as a sponge for miR-373, which inhibited tumor growth and muscle wasting in vitro and in vivo.  This study identified circANAPC7 as a novel tumor suppressor, which functions through the CREB-miR-373-PHLPP2 axis, leading to AKT dephosphorylation, and cyclin D1 and transforming growth factor-β down-regulation to suppress tumor growth and muscle wasting in pancreatic cancer.		Yes	 We identified circANAPC7 as a sponge for miR-373, which inhibited tumor growth and muscle wasting in vitro and in vivo. 	35176309
ALOX12-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer cells and tissues	Interaction(miR-3171/AGO2)	Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	ALOX12-AS1 expression is downregulated in cervical cancer, and over-expression of ALOX12-AS1 could inhibit cervical cancer cells proliferation in vitro.  Further, mechanistically investigation revealed that ALOX12-AS1 could interact with AGO2 and sponge miR-3171, thereby antagonizing its' repression of tumor suppressor phosphatase and tensin homolog expression in cervical cancer cell.		Yes	ALOX12-AS1 expression is downregulated in cervical cancer, and over-expression of ALOX12-AS1 could inhibit cervical cancer cells proliferation in vitro. 	34407056
ALMS1-IT1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD patients	Regulation(AVL9)	Western Blot//Bioinformatics Analysis//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	 We report that ALMS1-IT1 and AVL9 were both highly expressed in LUAD and correlated with poor outcomes in LUAD patients. In summary, ALMS1-IT1/AVL9 may promote the malignant progression of LUAD, at least in part by regulating the cyclin-dependent kinase pathway.	Of note, the prognosis of LUAD patients with low expression of both ALMS1-IT1 and AVL9 was superior to that of other patients. 	Yes	 Furthermore, the proliferation, migration and invasion of LUAD cells were decreased in cells lacking ALMS1-IT1, and this decrease could be almost completely reversed through overexpression of AVL9.  Gene set enrichment analysis revealed that expression of genes related to the cell cycle pathway is closely related to both the high expression of ALMS1-IT1 and AVL9 in LUAD. 	33683834
ALKBH3-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients, Huh7 cells	Interaction(HIF-1α/ALKBH3-AS1/ALKBH3 )	qRT-PCR	The high ALKBH3-AS1 expression was markedly associated with a decreased survival rate of HCC patients. A significant positive correlation between ALKBH3-AS1 and ALKBH3 mRNA levels was confirmed in HCC specimens. ALKBH3-AS1 silencing reduced ALKBH3 expression by stabilizing its mRNA stability in HCC cells. Notably, the impact of ALKBH3 silencing on HCC cells was similar to that of ALKBH3-AS1 knockdown. ALKBH3 restoration prominently attenuated the suppressive effects resulting from ALKBH3-AS1 silencing in HCCLM3 cells. Hypoxia-inducible factor-1α (HIF-1α) transcriptionally activated ALKBH3-AS1 expression in hypoxic HCC cells. ALKBH3-AS1 knockdown markedly attenuated cell proliferation and invasion in hypoxic Huh7 cells. 	The high ALKBH3-AS1 expression was markedly associated with a decreased survival rate of HCC patients.	Yes	ALKBH3-AS1 knockdown repressed and ALKBH3-AS1 overexpression enhanced HCC cell invasion and proliferation. ALKBH3-AS1 silencing restricted HCC growth in vivo. 	36098205
ALAHM	LncRNA	Homo sapiens	Adenocarcinoma of Lung	serum EVs	Interaction(AUF1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transwell Assay//Wound Healing Assay//qRT-PCR//FISH//RIP//ELISA//Colony Formation Assay//IF	 Highly enriched lncRNA-ALAHM was identified from serum EVs of lung adenocarcinoma (LUAD) patients with liver metastasis by high-throughput sequencing. As results, ALAHM expression in LUAD cell EVs was significantly increased.  LUAD-cell-derived EVs overexpressing ALAHM significantly promoted lung cancer liver metastasis in model mice. ALAHM of LUAD cell EVs also promotes hepatocyte parasecretion of HGF by binding with AUF1 and increases the proliferation, invasion, and migration of LUAD cells. 		Yes	The effects of ALAHM on hepatocyte paracrine HGF as well as proliferation, invasion, and migration of LUAD cells were observed in vitro. 	35281743
AP001625.6	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
APOA1-AS	LncRNA	Homo sapiens	Pre-Eclampsia	placental tissues of EOSPE patients and cells	Expression(highly expressed)	qRT-PCR//ELISA	Increased APOA1-AS was found in the placental tissues of EOSPE patients. Furthermore, APOA1-AS siRNA improved pregnancy outcomes in PE rats with increased expression of vascular endothelial growth factor, placental growth factor, and fms-like tyrosine kinase receptor (Flt-1) but decreased expression of E-cadherin, intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).		Yes	Furthermore, APOA1-AS siRNA improved pregnancy outcomes in PE rats with increased expression of vascular endothelial growth factor, placental growth factor, and fms-like tyrosine kinase receptor (Flt-1) but decreased expression of E-cadherin, intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).	35130745
AGAP2-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	tumor tissues	regulation[miR-195-5p]	qRT-PCR	The expression of AGAP2-AS1, miR-195-5p, and FOSL1 in tumor tissues isolated from EC patients and EC cell lines was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), the results of which illustrated that AGAP2-AS1 and FOSL1 were increased while miR-195-5p was reduced in EC.		Yes	Next, the ectopic expression, knockdown, and reporter assay experiments were all employed to elucidate the mechanism of AGAP2-AS1/miR-195-5p/FOSL1 in the processes of EC cell proliferation, cell cycle, apoptosis, invasion, and migration as well as tumor growth. Knockdown of AGAP2-AS1 or overexpression of miR-195-5p reduced EC cell proliferation, migration, and invasion, blocked cell cycle entry, and elevated apoptosis. 	32199129
APOC1P1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	Expression[highly expressed]	Cell Proliferation Assay//qRT-PCR	LncRNA APOC1P1 expression was increased in ccRCC tissues compared with normal kidney tissues (P < 0.001).	Its expression was higher in the Fuhrman grade III and IV group than in the Fuhrman grade I and II group (P < 0.05) and significantly upregulated in the advanced stage group (P < 0.05). Kaplan-Meier analyses revealed that elevated LncRNA APOC1P1 expression was significantly associated with poor overall survival (P < 0.05) but may not be an independent prognostic factor.	Yes	Knockdown of LncRNA APOC1P1 inhibited cell proliferation, induced apoptosis, and arrested cells at the G1/S phase (P < 0.05). Silencing of LncRNA APOC1P1 also led to decreased cell migration and invasion (P < 0.05). 	31871500
ARHGAP10	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues ,cell lines	Regulation[miR-150-5p/GLUT-1 Axis ]	CCK8//FISH//qRT-PCR//Luciferase Report Assay//RNA-seq//Transwell Assay	Thus, the present study aims at investigating the role of circARHGAP10 in NSCLC progression, which has been observed to be significantly upregulated in both NSCLC tissues and cell lines with profile analysis.Silencing circARHGAP10 also suppressed proliferation and metastasis by targeting the miR-150-5p/GLUT1 axis in NSCLC, which was confirmed with a luciferase reporter assay. Overexpression of GLUT1 or downregulation miR-150-5p will recover NSCLC cell proliferation and metastasis after a knockdown of circARHGAP10. 	A higher expression of circARHGAP10 also leads to a poor prognosis in NSCLC patients with fluorescence in situ hybridization (FISH). 	Yes	Silencing circARHGAP10 also suppressed proliferation and metastasis by targeting the miR-150-5p/GLUT1 axis in NSCLC, which was confirmed with a luciferase reporter assay. Overexpression of GLUT1 or downregulation miR-150-5p will recover NSCLC cell proliferation and metastasis after a knockdown of circARHGAP10. 	31561126
ARFRP1	LncRNA	Homo sapiens	Osteoarthritis	OA cartilage tissues	regulation[miR-15a-5p/TLR4 axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	 ARFRP1 and TLR4 levels were increased and miR-15a-5p level was decreased in OA cartilage tissues and lipopolysaccharides (LPS)-induced chondrocytes. ARFRP1 knockdown inhibited LPS-induced the injury of chondrocytes. Our findings confirmed that ARFRP1 mediated LPS-induced the injury of chondrocytes through regulating NF-κB pathway by modulation of miR-15a-5p/TLR4 axis, providing theoretical basis for the treatment of OA patients.		Yes	ARFRP1 knockdown inhibited LPS-induced the injury of chondrocytes. 	32931797
ARAP1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC cell lines	regulation[miR-2110/HDAC2/PLIN1 axis]	RNA Pull-Down//ChIP//Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	First of all, the GEPIA data suggested that ARAP1-AS1 was highly expressed in breast invasive carcinoma (BRAC) tissues compared with the normal breast tissues. Meanwhile, the expression of ARAP1-AS1 was greatly up-regulated in BC cell lines.To sum up, ARAP1-AS1 serves a tumor-promoter in BC development through modulating miR-2110/HDAC2/PLIN1 axis, which may help to develop novel effective targets for BC treatment.		Yes	ARAP1-AS1 knockdown led to repressed proliferation, strengthened apoptosis and blocked migration of BC cells. 	32110804
ARAP1-AS1	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	Expression[highly expressed]	Flow Cytometry//MTT//Western Blot	 LncRNA ARAP1-AS1 is highly expressed in lung cancer tissues and cells.		Yes	Knockdown of LncRNA ARAP1-AS1 can significantly inhibit the proliferation and clonal formation of lung cancer cells and induce G0/G1 cell cycle arrest.Furthermore, knockdown of ARAP1-AS1 can also notably inhibit the growth of lung cancer cells and substantially reduce the expression of Ki-67 in tumor-bearing tissues in nude mice.	33447422
ARAP1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Regulation[Wnt/β-Catenin Signaling Pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	ARAP1-AS1 was highly expressed in CRC tissues and cell lines.  YY1 transcription factor (YY1) enhanced the transcription activity of ARAP1-AS1. The YY1/ARAP1-AS1 axis promoted CRC cell migration and invasion. YY1/ARAP1-AS1 could regulate the Wnt/β-catenin signaling pathway.		Yes	ARAP1-AS1 knockdown suppressed cell migration, invasion, and epithelial-mesenchymal transition (EMT).	31173500
ARAP1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	 tissues and cells	Interaction(miR-4735-3p /PLAGL2)	qRT-PCR//MTT//RIP	Compared to normal samples and cells, upregulation of ARAP1-AS1 was observed in tissues and cells of ovarian cancer. Of note, ARAP1-AS1 contributed to the malignant phenotypes of ovarian cancer cells through modulation of miR-4735-3p/PLAGL2 axis, revealing ARAP1-AS1 as a promising therapeutic target for ovarian cancer patients.		Yes	Therewith, it was disclosed that knockdown of ARAP1-AS1 alleviated the carcinogenicity of ovarian cancer cells.	34149172
ARAP1-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cells	Interaction(miR-3918/KIF20A Axis)	qRT-PCR//RIP	ARAP1-AS1 and KIF20A were overexpressed in bladder cancer, while miR-3918 was underexpressed. miR-3918 was sponged by ARAP1-AS1, and targeted KIF20A. In addition, miR-3918 expression was inversely correlated with ARAP1-AS1 and KIF20a expression levels in bladder cancer tissues. In addition, the rescue experiment showed that interference with miR-3918 could reverse the effect of low ARAP1-AS1 or KIF20A expression on bladder cancer cell malignancy. 		Yes	 The downregulation of ARAP1-AS1 or KIF20A expression significantly inhibited the viability and proliferation of cancer cells and promoted apoptosis, whereas low expression of miR-3918 or high expression of ARAP1-AS1/KIF20A showed the opposite effect.	35556220
ARAP1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer cells	regulation[ARAP1-AS1/EZH2/DUSP5 axis ]	CCK8//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	 In the current research, ARAP1-AS1 was discovered to exhibit a high level in cervical cancer cells. Finally, rescue assays certified the oncogenic function of ARAP1-AS1/EZH2/DUSP5 axis in cervical cancer.		Yes	Besides, the knockdown of ARAP1-AS1 repressed cell proliferative and migratory capacities in cervical cancer, as detected by loss-of-function assays including CCK-8, EdU, colony formation, and transwell assays.	32985327
ARAP1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer (CC) tissues, cell lines and serum	Expression[highly expressed]	RNA Pull-Down//ChIP//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Here, we focused on an oncogenic lncRNA, ARAP1 antisense RNA 1 (ARAP1-AS1), which was notably upregulated in cervical cancer (CC) tissues, cell lines and serum. 	 High ARAP1-AS1 expression was closely associated with larger tumor size, advanced FIGO stage as well as lymph node metastasis.	Yes	In vitro and in vivo assays showed that knockdown of ARAP1-AS1 inhibited, while overexpression of ARAP1-AS1 promoted CC cell growth and dissemination.	31953923
ARAP1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC samples	Interaction(miR-149-3p and POU2F2)	In Vivo Experiment//IHC//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression of ARAP1-AS1 was enhanced in CC samples, while miR-149-3p was markedly suppressed. ARAP1-AS1 downregulated miR-149-3p via sponging it. ARAP1-AS1 and miR-149-3p exhibited a negative correlation in CC samples. On the other hand, ARAP1-AS1 enhanced the expression of POU2F2, which was validated as a target gene of miR-149-3p.		Yes	Additionally, ARAP1-AS1 overexpression enhanced the viability, migration, and invasion of CC cells. 	33965958
ARAP1-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	 TC cell lines and tissues	Interaction(miR-516b-5p/PDE5A axis)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	 ARAP1-AS1 and PDE5A were evidently upregulated in the TC cell lines and tissues whereas miR-516b-5p was poorly expressed. ARAP1-AS1 had been revealed to be correlated negatively to miR-516b-5p. Finally, we demonstrated that the miR-516b-5p inhibitor was capable of reversing ARAP1-AS1-knockdown's repressive effects on TC cell development by means of regulating PDE5A expression.		Yes	ARAP1-AS1 silencing in TC cells hampered cell proliferation, reduced their viability and boosted apoptosis. Moreover, it inhibited tumor growth in vivo. 	36730555
ARAP1-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC cells	Interaction(miR-361-3p/placental growth factor axis)	RNA Pull-Down//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay	The results showed that the levels of ARAP1-AS1 and PGF increased in ccRCC cells, while miR-361-3p expression decreased. Moreover, ARAP1-AS1 sponges miR-361-3p to increase PGF expression. In conclusion, our study revealed that ARAP1-AS1 enhanced the malignancy of ccRCC cells by regulating the miR-361-3p/PGF axis.		Yes	 Cell functional experiments showed that cell proliferation and migration were inhibited by silencing ARAP1-AS1 or PGF, while miR-361-3p inhibitor or PGF overexpression could relieve the inhibitory effect of silencing ARAP1-AS1 on ccRCC cells.	34516333
AQP4-AS1	LncRNA	Homo sapiens	Diabetes Mellitus	clinical samples, Müller cells	Regulation(AQP4)	In Vivo Experiment//Transfection	AQP4-AS1 was significantly increased in the clinical samples of diabetic retinopathy patients, high glucose-treated Müller cells, and diabetic retinas of a murine model. Mechanistically, AQP4-AS1 regulated retinal neurovascular dysfunction through affecting AQP4 levels.		Yes	 AQP4-AS1 silencing in vivo alleviated retinal neurodegeneration and vascular dysfunction as shown by improved retinal capillary degeneration, decreased reactive gliosis, and reduced RGC loss. AQP4-AS1 directly regulated Müller cell function and indirectly affected endothelial cell and RGC function in vitro.	35172268
APTR	LncRNA	Homo sapiens	Stomach Neoplasms	gastric tumor samples 	Expression(lower expressed)	Bioinformatics Analysis	 LncRNA APTR is lower expressed in gastric tumor samples and low expression of APTR predicts a poor diagnosis and outcome in GC patients.  Silencing APTR promotes gastric cancer proliferation and invasiveness. APTR expression is negatively correlated with inflammatory signaling in the gastric tumor microenvironment.	 LncRNA APTR is lower expressed in gastric tumor samples and low expression of APTR predicts a poor diagnosis and outcome in GC patients. 	Yes	 Silencing APTR promotes gastric cancer proliferation and invasiveness. APTR expression is negatively correlated with inflammatory signaling in the gastric tumor microenvironment.	36075114
APTR	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and OS cell lines	Regulation[APTR/miR-132-3p/YAP1 axis]	qRT-PCR	Herein, APTR expression was demonstrated to be significantly upregulated in OS tumor tissues and four OS cell lines (including MG63, 143B, Saos-2, and HOS) compared with the adjacent tissues and human osteoblast cell line hFOB1.19, respectively. Also, Yes-associated protein 1 (YAP1) was determined as an inhibitory target of miR-132-3p. Moreover, our findings demonstrated that the repression of YAP1 protein expression and the suppression of Ki-67, MMP9, and Bcl2 expression induced by APTR knockdown required increased miR-132-3p. Thus, APTR contributed to OS progression through repression of miR-132-3p and upregulation of YAP1 expression. Therefore, we have uncovered a novel regulatory mechanism by which the APTR/miR-132-3p/YAP1 axis can regulate OS progression.		Yes	In functional terms, knockdown of APTR and overexpression of miR-132-3p both, remarkably repressed human OS cell proliferation, invasion and migration, and induced apoptosis.	30317613
APTR	LncRNA	Homo sapiens	uterine fibroid	 UL tumor tissues	Interaction(Erα/Wnt pathway )	In Vivo Experiment//Western Blot//RIP//FISH//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay	 We found that lncRNA Alu-mediated p21 transcriptional regulator (APTR) showed higher expression in UL tumor tissues compared with that in normal uterine tissues. The results showed that APTR function was suppressed. APTR increased the expressions of the proteins in the Wnt pathway, and inhibiting ERα eliminated these responses. In conclusion, our data suggest that APTR promoted leiomyoma cell proliferation through the Wnt pathway by targeting ERα, suggesting a new role of APTR in the Wnt signaling pathway in UL.		Yes	APTR induced cell proliferation and colony formation both in vitro and in vivo. 	33777725
APPAT	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	regulation[ miR-328a/Pkp1 signal pathway ]	qRT-PCR//Luciferase Report Assay//Western Blot	The expressions of lncRNA APPAT, Pkp1 protein levels and miR-328a were commonly expressed in breast cancer cells. LncRNA APPAT regulated the proliferation, migration, invasion of breast cancer by regulating miR-328a/Pkp1 signaling pathway, providing a novel possible strategy for the treatment of breast cancer.		Yes	 The inhibition of lncRNA APPAT expression repressed cell proliferation, migration and invasion in breast cancer and reverse results were found after lncRNA APPAT overexpressing. 	32495884
APPAT	LncRNA	Homo sapiens	Atherosclerosis	HASMCs	Interaction(miR-647)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	APPAT and miR-647 have inverse effects on human aortic smooth muscle cells' (HASMCs) proliferation and migration. APPAT negatively regulated the cell activity, whereas miR-647 did it in a positive way (p<0.05). Three pairs of molecular interplay were found: mutual negative regulation between APPAT and miR-647, APPAT downregulated FGF5, miR-647 regulation on FGF5 (p<0.05). Subcellular location assay confirmed the molecular interaction of APPAT and miR-647.		Yes	APPAT and miR-647 have inverse effects on human aortic smooth muscle cells' (HASMCs) proliferation and migration. APPAT negatively regulated the cell activity, whereas miR-647 did it in a positive way (p<0.05). 	35880306
APP	LncRNA	Homo sapiens	Prostatic Neoplasms		Regulation[ lncAPP/miR218 axis]	RIP//Luciferase Report Assay	The underlying mechanism of lncRNA was investigated by RNA immunoprecipitation, dual-luciferase reporter system assay, etc. Upregulation of lncAPP promoted cell migration and invasion via competitively binding miR218 to facilitate ZEB2/CDH2 expression. In addition, in vivo subcutaneous tumor xenograft models and tail intravenously injection metastatic models were constructed to evaluate lncRNA function. Targeting lncAPP/miR218 axis in cell lines and tumor xenografts restrained tumor progression properties both in vitro and in vivo. These results establish that lncAPP/miR218 axis plays a critical role in PCa progression, and they also suggest new strategies to prevent tumor progression for therapeutic purposes.		Yes	 In vitro and in vivo studies demonstrated that lncAPP enhanced cell proliferation and promoted migration and invasion.	31107971
AL592284.1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction(miR-30a-5p/Vimentin/EMT axis)	In Vivo Experiment//IHC//Western Blot//ISH//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	We observed that the levels of AL592284.1 in CC were distinctly increased. Luciferase reporter assay confirmed that miR-30a-5p/Vimentin regulatory axis is the direct downstream of AL592284.1. Rescue experiments indicated that AL592284.1 induced overexpression of Vimentin via sponging miR-30a-5p, resulting in the promotion of CC progression.		Yes	Functional assays revealed that knockdown of AL592284.1 suppressed the proliferation, migration, invasion and EMT progress of CC cells. 	34509725
AL355338	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction( ENO1/EGFR)	RNA Pull-Down//Co-IP//Flow Cytometry//qRT-PCR//FISH//RIP//IHC//IF	AL355338 was an upregulated glycolysis-associated lncRNA in NSCLC. Mechanistic investigations showed that AL355338 directly bound with alpha-enolase (ENO1) and enhanced the protein's stability by modulating its degradation and ubiquitination. A positive correlation was observed between AL355338 and ENO1 in NSCLC, and ENO1 was subsequently confirmed to be responsible for the oncogenic role of AL355338. 		Yes	Functional assays revealed that AL355338 was critical for promoting aerobic glycolysis and NSCLC progression.	34627260
AL161431.1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC patients, tissues, and cells	interaction[targets miR-1252-5p ]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay	High expression levels of AL161431.1 were observed in EC patients, tissues, and cells. Our novel results indicate that AL161431.1 targets and binds to miR-1252-5p, resulting in the de-repression of MAPK signaling in EC cells. 		Yes	 Loss-of-function experiments validated the carcinogenic role of AL161431.1.	32196580
AL161431.1	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer cells and tissues	Expression(highly expressed)	In Vivo Experiment//Western Blot//Transwell Assay//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//IHC//IF	We found that lncRNA AL161431.1 was highly expressed in pancreatic cancer cells and tissues. 		Yes	 Knock down of lncRNA AL161431.1 led to increased cancer cell death and cell cycle arrest. Xenograft growth of SW1990 cells with stable knockdown of lncRNA AL161431.1 in mice was significantly slower than that of SW1990 cells with scrambled control shRNA. 	34395245
AK001058	LncRNA	Mus musculus	Colorectal Neoplasms	colorectal cancer tissues	Interaction[ADAMTS12]	qRT-PCR//Western Blot	The results showed that AK001058 overexpression notably accelerated tumor growth. AK001058 overexpression also decreased cell apoptosis, worsened microvessel morphology and increased the expression of VEGFA and angiopoietin II. Moreover, AK001058 decreased the expression of ADAMTS12 by increasing its methylation level. Nevertheless, AK001058 knockdown exerted the opposite function. Therefore, AK001058 knockdown could effectively inhibit tumor growth mostly accounting for decreased cell apoptosis and tumor angiogenesis, which was partly dependent on the high methylation level of ADATS12. 		Yes	The results showed that AK001058 overexpression notably accelerated tumor growth. AK001058 overexpression also decreased cell apoptosis, worsened microvessel morphology and increased the expression of VEGFA and angiopoietin II. Moreover, AK001058 decreased the expression of ADAMTS12 by increasing its methylation level. Nevertheless, AK001058 knockdown exerted the opposite function. Therefore, AK001058 knockdown could effectively inhibit tumor growth mostly accounting for decreased cell apoptosis and tumor angiogenesis, which was partly dependent on the high methylation level of ADATS12. 	31632580
AIVR	CircRNA	Homo sapiens	Orthomyxoviridae	A549 cells 	Interaction(CREBBP)	Western Blot//ISH//qRT-PCR//FISH//PCR//IP//IF	 We characterized a novel intronic circRNA, AIVR, that was upregulated in influenza virus-infected A549 cells and found that silencing of AIVR significantly promoted influenza virus replication in A549 cells. We further found that AIVR predominantly localizes in the cytoplasm and works as a microRNA (miRNA) sponge. One of the miRNAs absorbed by AIVR binds the mRNA of CREBBP, which is an important component of the large nucleoprotein complex interferon beta (IFN-β) enhanceosome that accelerates IFN-β production. 		Yes	We characterized a novel intronic circRNA, AIVR, that was upregulated in influenza virus-infected A549 cells and found that silencing of AIVR significantly promoted influenza virus replication in A549 cells.	34281396
AIRN	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Regulation(CUL4A/AIRN )	qRT-PCR	Using a quantitative real-time polymerase chain reaction, we corroborated that LncRNA AIRN expression was raised in the HCC tissues and cells.  In the cycloheximide-chase assay, the knockdown of LncRNA AIRN enhanced the stability of STAT1 protein. In the immunoprecipitation assay, the knockdown of LncRNA AIRN restrained the cullin 4A (CUL4A)-mediated ubiquitination of STAT1 protein. 		Yes	 The cell transfection, MTT and flow cytometry assays expounded that the LncRNA AIRN/STAT1 axis was bound up with the regulation of the proliferation and apoptosis of HCC cells. The in vivo experiments corroborated that the knockdown of LncRNA AIRN restrained the tumor growth of HCC. 	33759138
AIRN	LncRNA	Homo sapiens	Diabetic Cardiac Fibrosis	diabetic hearts and high glucose (HG)-treated cardiac fibroblasts (CFs)	Regulation(m6A-IMP2-p53 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Cell Cycle Assay//EdU Staining//IF	Diabetic hearts showed a significant impairment in cardiac function, accompanied by obviously increased cardiac fibrosis. Interestingly, lncRNA Airn expression was significantly decreased in both diabetic hearts and high glucose (HG)-treated cardiac fibroblasts (CFs). AAV-mediated Airn reconstitution prevented cardiac fibrosis and the development of DCM, while Airn knockdown induced cardiac fibrosis phenotyping DCM. As in vitro, Airn reversed HG-induced fibroblast-myofibroblast transition, aberrant CFs proliferation and section of collagen I. In contrast, Airn knockdown mimicked a HG-induced CFs phenotype. Mechanistically, we identified that Airn exerts anti-fibrotic effects by directly binding to insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) and further prevents its ubiquitination-dependent degradation. Moreover, we revealed that Airn/IMP2 protected p53 mRNA from degradation in m6A manner, leading to CF cell cycle arrest and reduced cardiac fibrosis. As a result, ablation of p53 blunted the inhibitory effects of Airn on fibroblast activation and cardiac fibrosis.		Yes	AAV-mediated Airn reconstitution prevented cardiac fibrosis and the development of DCM, while Airn knockdown induced cardiac fibrosis phenotyping DCM. As in vitro, Airn reversed HG-induced fibroblast-myofibroblast transition, aberrant CFs proliferation and section of collagen I.	36384975
Airn	LncRNA	Mus musculus	Fatty Liver, Alcoholic	 liver tissues of AFL C57BL/6mice 	Regulation( mTOR ubiquitination)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Co-IP//qRT-PCR//RIP//MTT//ELISA	 LncRNA-AIRN was highly expressed in the liver tissues of AFL C57BL/6mice and oleic acid+alcohol (O+A)treated AML-12cells by using quantitative real-timePCR.Furthermore, the knockdown of lncRNA-AIRN reducedmTOR protein level by promoting the E3 ubiquitin ligase FBXW7-mediated ubiquitination.The lncRNA-AIRN/mTORaxis was involved in the regulation of the mitophagy of O+A treated hepatocytes, which was confirmed by the cell transfection and the MTT assay.		Yes	Furthermore, the knockdown of lncRNA-AIRN reducedmTOR protein level by promoting the E3 ubiquitin ligase FBXW7-mediated ubiquitination.The lncRNA-AIRN/mTORaxis was involved in the regulation of the mitophagy of O+A treated hepatocytes, which was confirmed by the cell transfection and the MTT assay.	33676386
AIM1-3	LncRNA	Homo sapiens	Diabetes Mellitus, Type 2	peripheral blood mononuclear cells	Regulation(lower expressed)	qRT-PCR	The microarray analysis revealed that there were 55 lncRNAs and 36 mRNAs differentially expressed in patients with T2DM compared with healthy controls. Notably, lnc-HIST1H2AG-6 was significantly upregulated and lnc-AIM1-3 was significantly downregulated in patients with T2DM, which was validated in a large-scale qRT-PCR examination (90 controls and 100 patients with T2DM). Spearman's rank correlation coefficient revealed that both lncRNAs were correlated with 36 differentially expressed mRNAs. Furthermore, functional enrichment (KEGG and GO) analysis demonstrated that the two lncRNA-related mRNAs might be involved in multiple biological functions, including cell programmed death, negative regulation of insulin receptor signal, and starch and sucrose metabolism. Multivariate logistic regression analysis revealed that lnc-HIST1H2AG-6 and lnc-AIM1-3 were significantly correlated with T2DM (OR = 5.791 and 0.071, respectively, both P = 0.000). Furthermore, the ROC curve showed that the expression of lnc-HIST1H2AG-6 and lnc-AIM1-3 might be used to differentiate patients with T2DM from healthy controls (area under the ROC curve = 0.664 and 0.769, respectively).		Yes	Notably, lnc-HIST1H2AG-6 was significantly upregulated and lnc-AIM1-3 was significantly downregulated in patients with T2DM, which was validated in a large-scale qRT-PCR examination (90 controls and 100 patients with T2DM). Spearman's rank correlation coefficient revealed that both lncRNAs were correlated with 36 differentially expressed mRNAs. Furthermore, functional enrichment (KEGG and GO) analysis demonstrated that the two lncRNA-related mRNAs might be involved in multiple biological functions, including cell programmed death, negative regulation of insulin receptor signal, and starch and sucrose metabolism. 	34092238
AGO2	LncRNA	Homo sapiens	Breast Neoplasms	26 female breast cancer patients’ tumor tissues and paired paracancerous tissues 	Interaction(miR-21-5p/FASLG axis)	In Vivo Experiment//IHC//Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	By analyzing the CASC7 expression in breast cancer cell lines, both the expression levels of CASC7 in cancer tissues and cell lines were obviously downregulated compared to those in paired paracancerous tissues and normal human epithelial MCF10A cells.  We further confirmed that CASC7 functions by regulating miR-21-5p/FASLG axis. 		Yes	A series of functional experiments were conducted to show that the cell proliferation, migration, and invasion were inhibited when CASC7 overexpressed in breast cancer cells. 	34889164
AGO2	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues	Regulation( PI3K/Akt signaling pathway )	qRT-PCR//Transwell Assay//Western Blot	 The LncRNA-CASC7 expression in colon cancer was considerably decreased than in nearby healthy tissues (P<0.01).Similarly, the expression of lncRNA-CASC7 was decreased in 5 colon cancer cell lines.  Overexpression of lncRNA-CASC7 significantly inhibited the expression of proteins Ki-67 and PNCA (associated with proliferation) and proteins N-cadherin, E-cadherin, and vimentin (linked with metastasis). Further studies showed that overexpression of LncRNA-CASC7 could significantly inhibit the PI3K/Akt signaling pathway in colon cancer cells.	Its expression level was linked to survival rate, lymph node metastasis, and tumor node metastasis (TNM) stage. 	Yes	The proliferative, invasive, and migratory potential of cells was considerably decreased by lncRNA-CASC7 overexpression. 	35070408
AGO2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(miR-30a-5p/ KLF10/TGF-β/SMAD3 pathway)	RNA Pull-Down//IHC//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression levels of CASC7 were increased and the expression levels of miR-30a-5p were reduced in HCC cells and tissues.  In HCC tumor tissues, the expression of miR-30a-5p was negatively correlated with the expression of CASC7. Moreover, as a target of miR-30a-5p, KLF10 was regulated by CASC7 and miR-30a-5p, and CASC7 regulated the KLF10/TGF-β/SMAD3 pathway via binding to miR-30a-5p, thereby promoting HCC cell progression.		Yes	Knockdown of CASC7 and overexpression of miR-30a-5p reduced tumor growth as well as HCC cell proliferation, invasion and migration. 	35484972
AGO2	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation[Wnt/β-catenin signaling pathway]	Western Blot//qPCR//CCK8//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	We found that CASC7 was downregulated in glioma tissues and cell liens and predicted poor prognosis for patients with glioma. Taken together, all research findings suggested that CASC7 inhibited the progression of glioma via regulating Wnt/β-catenin signaling pathway.	We found that CASC7 was downregulated in glioma tissues and cell liens and predicted poor prognosis for patients with glioma. 	Yes	 To determine the involvement of CASC7 in the biological processes of glioma, we conducted gain or loss-of function assays in two glioma patients. We found that CASC7 suppressed glioma cell proliferation and induced glioma cell apoptosis.	30661904
AGO2	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	interaction[sponging miR-92a]	Western Blot//ISH//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Marked downregulation of CASC7 was observed in NSCLC tissues and cell lines, and this downregulation of CASC7 was closely associated with distant metastasis, lymph node involvement and poor overall survival in NSCLC patients.  Collectively, the results of the present study indicated that CASC7 may act as a tumor‑suppressive lncRNA that inhibits NSCLC progression by sponging miR‑92a. 	Marked downregulation of CASC7 was observed in NSCLC tissues and cell lines, and this downregulation of CASC7 was closely associated with distant metastasis, lymph node involvement and poor overall survival in NSCLC patients. 	Yes	 Furthermore, overexpression of CASC7 significantly suppressed the proliferation, invasion and migration of the NSCLC cells A549 and H358, and promoted cell apoptosis in vitro. 	32626930
AGO2	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues 	Interaction(miR-34a-5p/TP73)	Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	CASC7 and TP73 expression were significantly lower, whereas miR-34a-5p expression was higher in PTC tissues than the adjacent normal tissues.  Mechanistically, CASC7 acted as a sponge of miR-34a-5p to upregulate TP73 expression. Moreover, miR-34a-5p mimic transfection could abate the CASC7-regulated PTC cell proliferation, migration, and apoptosis.		Yes	Furthermore, CASC7 overexpression inhibited cell proliferation and migration, whereas facilitated cell apoptosis in human PTC cell lines (K1 and TPC-1). 	33706708
AGO2	LncRNA	Homo sapiens	Neuroblastoma	neuroblastoma tissues	regulation[downregulating miR-10a]	qRT-PCR	We observed the downregulation of CASC7 in neuroblastoma tissues compared to non-cancer tissues of neuroblastoma patients. We therefore concluded that lncRNA CASC7 may upregulate phosphatase and tensin homolog by downregulating miR-10a to inhibit neuroblastoma cell proliferation.		Yes	CASC7 overexpression resulted in inhibition, while miR-10a overexpression resulted in increased proliferation rate of neuroblastoma cells.	32101951
AGAP2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	Interaction(HuR/MTA1 )	RNA Pull-Down//IHC//Western Blot//Tunel//CCK8//RIP//Flow Cytometry//qRT-PCR//Colony Formation Assay//ChIP	AGAP2-AS1 was overexpressed in BC tissues and cells, and AGAP2-AS1 silencing inhibited cell proliferation but facilitated apoptosis.Physiologically, AGAP2-AS1 bound to HuR to stabilize its own expression, and AGAP2-AS1-HuR complex upregulated H3K27ac levels in the MTA1 promoter region to elevate MTA1 promoter activity and MTA1 expression. H3K27ac upregulation partially-annulled the promotive effect of si-AGAP2-AS1 on BC apoptosis by upregulating MTA1.		Yes	AGAP2-AS1 was overexpressed in BC tissues and cells, and AGAP2-AS1 silencing inhibited cell proliferation but facilitated apoptosis. si-AGAP2-AS1 in vivo inhibited MTA1 expression to enhance apoptosis and suppress tumor growth.	35369814
AGAP2-AS1	LncRNA	Homo sapiens	Lung Neoplasms	MRC-5 cells	Interaction(MyD88/NF-κb signaling)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	We demonstrated that exosomes from the LC patients (cancer-exo) notably increased the metastatic ability of MRC-5 cells, promoting the expressions of the CAF biomarkers and lncRNA AGAP2-AS1. Overexpression of lncRNA AGAP2-AS1 prominently activated MRC-5 cells. Moreover, EIF4A3 was upregulated in the cancer-exo-treated MRC-5 cells, and EIF4A3 was verified to bind with lncRNA AGAP2-AS1 to improve its stability. The MyD88/NF-κB signaling pathway was subsequently proved to be positively regulated by lncRNA AGAP2-AS1, and the promotive role of lncRNA AGAP2-AS1 in LC and activating CAFs was confirmed in vivo.		Yes	We demonstrated that exosomes from the LC patients (cancer-exo) notably increased the metastatic ability of MRC-5 cells, promoting the expressions of the CAF biomarkers and lncRNA AGAP2-AS1. 	36541122
AGAP2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	regulation[miR-4,668-3p/SRSF1 axis]	RNA Pull-Down//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	In the present study, AGAP2-AS1 was unveiled as highly expressed in CRC cell lines compared to normal cells.AGAP2-AS1 facilitates cell proliferation, motility and EMT in CRC via targeting the miR-4,668-3p/SRSF1 axis. 		Yes	AGAP2-AS1 knockdown suppressed cell proliferation, migration, invasion and the epithelial-to-mesenchymal transition process. 	32639657
AGAP2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell	Interaction(miR-182-5p/CFL1 axis)	qRT-PCR//FISH//RIP//Colony Formation Assay//ChIP	AGAP2-AS1 expression was significantly elevated in CRC cells and could be transcriptionally activated by E2F Transcription Factor 4 (E2F4). MicroRNA-182-5p (miR-182-5p) was the target downstream molecule of AGAP2-AS1. Furthermore, Cofilin 1 (CFL1) was proved as the target of miR-182-5p. Mechanically, AGAP2-AS1 could boost the CFL1 expression via competitively binding to miR-182-5p in CRC. 		Yes	Down-regulated AGAP2-AS1 could weaken CRC cell growth, migration, invasion, and epithelial-mesenchymal transition (EMT). 	34838479
AGAP2-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissues	Regulation(LINC-PINT)	qRT-PCR//Transwell Assay	The expression of AGAP2-AS1 was upregulated in colon cancer tissues compared with that in adjacent normal tissues, and the expression of AGAP2-AS1 in colon cancer tissues was not significantly affected by tumor stages.  In addition, we found that the expression of LINC-PINT was downregulated in colon cancer tissues compared with that in adjacent normal tissues and had a reverse correlation with the expression of AGAP2-AS1 in colon cancer tissues. 		Yes	 Furthermore, overexpression of AGAP2-AS1 could increase the proliferation, invasion and migration of colon cancer cells, while overexpression of LINC-PINT could attenuate the effects of overexpression of AGAP2-AS1 on the proliferation, migration and invasion of colon cancer cells. We also found that AGAP2-AS1 promoted colon cancer cell proliferation, migration and invasion through the Hippo signaling.	33688258
AGAP2-AS1	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues	Expression[lower expressed]	qRT-PCR	Clinically, AGAP2-AS1 expression was decreased in EOC tissues compared to that in the controls. 	Low expression of AGAP2-AS1 was associated with advanced FIGO stage, high histological grade, serous subtype and lymph node metastasis in patients with EOC.	Yes	AGAP2-AS1 inhibited cell migration, invasion and proliferation in vitro. AGAP2-AS1 suppressed tumor growth in vivo.	32742478
AK001058	LncRNA	Homo sapiens	Colorectal Neoplasms	cell lines	Interaction[ ADAMTS12]	CCK8//qRT-PCR//Western Blot	The results indicated that the expression of AK001058 was significantly increased in CRC. In conclusion, AK001058 promotes the proliferation, invasion, migration, and prolonged S stage of CRC by regulating methylation of ADAMTS12.		Yes	AK001058 also significantly promoted cell proliferation, migration and invasion, and prolonged S stage of CRC, while silencing the expression of AK001058 showed contrary effects.	31632555
AK001903	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Expression[highly expressed]	CCK8//qRT-PCR//ISH	The findings of the study confirmed that lncRNA-AK001903 was upregulated in CC cells and tissues compared with normal cell line H8 and peritumoral tissues. 		Yes	Knockdown of lncRNA-AK001903 inhibited cell proliferation, invasion and migration in Ca Ski cells. 	33363614
AK002107	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[AK002107/miR-140-5p/TGFBR1/EMT ]	Western Blot//ISH//qRT-PCR//MTT//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	The expression of lncRNA AK002107 is frequently upregulated in HCC samples and cell lines. In summary, lncRNA AK002107 functions as an oncogene in tumors by inhibiting miR-140-5p, targeting TGFBR1, and then inducing EMT. The lncRNA AK002107/miR-140-5p/TGFBR1/EMT regulatory network may be a valuable target for the development of novel diagnostic and treatment methods for HCC.	 Patients with HCC who have elevated lncRNA AK002107 expression exhibit poorer overall survival and disease-free survival. 	Yes	Silencing lncRNA AK002107 expression significantly inhibited HCC cell proliferation, colony formation, and invasion both in vitro and in vivo.	30943320
AK12348	LncRNA	Rattus norvegicus	Myocardial Reperfusion Injury	 A/R cardiomyocytes	Regulation( PARP and Caspase-3)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//IHC	The relative level of lncRNA AK12348, LDH release and cell apoptotic rate in A/R cardiomyocytes was significantly higher than that in normal cardiomyocytes. After transfection with siRNA-lncRNA AK12348, LDH release and cell apoptotic rates in A/R cardiomyocytes were reduced, while the values in normal cardiomyocytes had almost no change. The protein expression values of PARP and Caspase-3 in A/R cardiomyocytes were much higher than the Control. After knockdown of lncRNA AK12348, the values decreased.		Yes	After transfection with siRNA-lncRNA AK12348, LDH release and cell apoptotic rates in A/R cardiomyocytes were reduced, while the values in normal cardiomyocytes had almost no change. The protein expression values of PARP and Caspase-3 in A/R cardiomyocytes were much higher than the Control. After knockdown of lncRNA AK12348, the values decreased.	29398472
AL139385.1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cancer tissues and cell lines.	Interaction(hsa-miR-532-5p)	Transfection//CCK8//qRT-PCR//migration assay//BrdU	In this study, we investigated the role of AL139385.1 in LUAD and found that DNA hypomethylation was positively correlated with AL139385.1 expression in LUAD. Moreover, we uncover that the expression of AL139385.1 in LUAD tissues was significantly higher than that of AL139385.1 expression in adjacent normal tissues.We also found that AL139385.1 was upregulated in LUAD cancer tissues and cell lines.  Finally, we constructed a ceRNA network that includes hsa-miR-532-5p and four mRNAs (GALNT3, CYCS, EIF5A, and ITGB4) specific to AL139385.1 in LUAD.		Yes	Knockdown of AL139385.1 significantly inhibited cell proliferation and migration abilities of LUAD.	35651789
AL110200	LncRNA	Homo sapiens	Ischemic Stroke	 THP-1 cells and peripheral blood of coronary heart disease group 	Mutation(rs901681)	qRT-PCR//Transfection//ELISA//Genotyping	 Increased expression of AL110200 was observed in THP-1 cells under oxidized low-density lipoprotein treatment. AL110200 expression in peripheral blood was significantly higher in the coronary heart disease group than in the controls. Patients carrying rs901681 GG had a lower risk for stroke recurrence at age ≥60 years (p = 0.001), cardiovascular stroke death (p = 0.022) and all-cause mortality (p = 0.034) in the all-age group.	 Patients carrying rs901681 GG had a lower risk for stroke recurrence at age ≥60 years (p = 0.001), cardiovascular stroke death (p = 0.022) and all-cause mortality (p = 0.034) in the all-age group.	Yes	Knockdown of AL110200 reduced the adhesive and invasive ability of THP-1 cells. 	33934454
AL033381.2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation(PRKRA )	qRT-PCR	qRT-PCR analysis revealed that AL033381.2 is upregulated in HCC tissues.Mechanistically, RNA pull-down experiments, mass spectrometry, PathArray™, and RIP were used to determine that AL033381.2 binds to PRKRA and may be involved in AL033381.2-mediated oncogenic functions in HCC cells. Moreover, rescue experiments demonstrated that PRKRA overexpression rescues the abilities of HCC cell proliferation, migration, and invasion that were affected by AL033381.2 knockdown. 		Yes	 Through in vitro and in vivo experiments, we found that AL033381.2 dramatically facilitates the growth and metastasis of HCC.	35035655
AKT3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Microarray	We found that CASC15 was upregulated in NSCLC tissues and cell lines.	High expression levels of CASC15 were correlated with malignancies and poor survival rate in NSCLC patients.	Yes	 In addition, we demonstrated that CASC15 knockdown inhibited NSCLC cell proliferation, migration and invasion in vitro. Xenograft model showed CASC15 knockdown significantly suppressed NSCLC tumor growth. 	31396336
AKT3	CircRNA	Homo sapiens	Esophageal Neoplasms	 esophageal cancer cell and  Clinical samples	Interaction( miR-17-5p/ RHOC and STAT3)	qRT-PCR//Luciferase Report Assay//Western Blot	Furthermore, miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p.		Yes	 In vitro assays showed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer.	33519139
AKT1	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	CC samples and cell lines	regulation[circ-AKT1/miR-942-5p/AKT1 axis]	colony Formation Assay//RNA Pull-Down//Northern Blot//Western Blot//ISH//qPCR//FISH//RIP//PCR//IP//Colony Formation Assay//IF	We discovered the new circRNA, circ-0033550, upregulated in CC. Its associated gene was AKT (also known as protein kinase B) serine/threonine kinase 1 (AKT1), so we renamed circ-0033550 as circ-AKT1.Mechanically, we illustrated that circ-AKT1 upregulated AKT1 by sponging miR-942-5p. Rescue assays confirmed the role of the circ-AKT1/miR-942-5p/AKT1 axis in CC progression.		Yes	Functionally, gain- and loss-of-function experiments indicated that circ-AKT1 and AKT1 promoted CC cell proliferation and invasion.	32193155
AK137033	LncRNA	Rattus norvegicus	Diabetic Osteoporosis	ASCs	Interaction(Wnt signaling pathway via DNA methylation)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//IF	Compared with CON-ASCs, AK137033 expression, the DNA methylation level of the sFrp2 promoter region, Wnt signaling pathway markers, and the osteogenic differentiation potential were decreased in DOP-ASCs. In vitro experiments showed that AK137033 silencing inhibited the Wnt signaling pathway and osteogenic ability of CON-ASCs by reducing the DNA methylation level in the sFrp2 promoter region. Additionally, overexpression of AK137033 in DOP-ASCs rescued these changes caused by DOP. Moreover, the same results were obtained in vivo.		Yes	AK137033 small interfering RNA (SiRNA) and an AK137033 overexpression plasmid were used to regulate the expression of AK137033 in CON-ASCs and DOP-ASCs in vitro. Lentiviruses that carried shRNA-AK137033 or AK137033 cDNA were used to knockdown or overexpress AK137033, respectively, in CON-ASCs and DOP-ASCs in vivo.Compared with CON-ASCs, AK137033 expression, the DNA methylation level of the sFrp2 promoter region, Wnt signaling pathway markers, and the osteogenic differentiation potential were decreased in DOP-ASCs. 	34953002
AK136714	LncRNA	Homo sapiens	Atherosclerosis	the plaque and plasma of the atherosclerosis patients 	Interaction(HuR/ TNF-α, IL-1β and IL-6 )	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//PCR//H&E Staining	Compared with the healthy group, lncRNA AK136714 expression was elevated in the plaque and plasma of the atherosclerosis patients in a GEO dataset. Moreover, AK136714 was found to bind directly to HuR to increase the mRNA stability of TNF-α, IL-1β and IL-6 mRNAs. In addition, AK136714 promoted the transcription of Bim. 		Yes	AK136714 silencing inhibited atherosclerosis formation in ApoE-/- mice. AK136714 silencing also protected the endothelial barrier and inhibited endothelial cell inflammation. In vitro assays showed that knockdown of AK136714 suppressed the inflammatory response and apoptosis in human umbilical vein endothelial cells (HUVECs). 	34015766
AK093407	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissue and cells	Expression(highly expressed)	Flow Cytometry//qRT-PCR//MTT//Western Blot	 The results showed that the expression of AK093407 in human colon cancer tissue was higher than in para-carcinoma tissue. The amount of AK093407 in HCT-15 and HCT-116 cells was higher than that in normal colorectal epithelial NM460 cells. 		Yes	When AK093407 was silenced, the proliferation of HCT-15 and HCT-116 cells decreased, the apoptosis rate increased, the cell cycle was arrested in the G1/S phase, the expression of caspase-3, caspase-8, caspase-9, bax, cyclin-A1, cyclin- B1, p21, p27 increased, and the expression of bcl-2, cyclin-D1, cyclin-E1, p-Stat3 decreased.	35400339
AK006774	LncRNA	Homo sapiens	Myocardial Reperfusion	infarct area 	Interaction(miR-448/bcl-2 signaling axis)	In Vivo Experiment//RNA Pull-Down//Tunel//Flow Cytometry//qRT-PCR//Luciferase Report Assay	  We first found that AK006774 overexpression reduced I/R-induced infarct area and cardiomyocyte apoptosis in vivo. Accordingly, AK006774 inhibited apoptosis and oxidative stress in cardiomyocytes subjected to H/R treatment in vitro. Mechanistically, AK006774 modulated the expression of bcl-2 by sponging miR-448. Overexpression of miR-448 antagonized the effects of AK006774 on cardiomyocyte apoptosis. 		Yes	  We first found that AK006774 overexpression reduced I/R-induced infarct area and cardiomyocyte apoptosis in vivo. Accordingly, AK006774 inhibited apoptosis and oxidative stress in cardiomyocytes subjected to H/R treatment in vitro. 	34369259
AK087124	LncRNA	Mus musculus	Atherosclerosis	 plasma and plaque from atherosclerotic mice	Interaction(miR-224-5p/PTEN axis)	RNA Pull-Down//Western Blot//Transfection//qPCR//Luciferase Report Assay//ELISA	We investigated the roles of lncRNA AK087124 and miR-224-5p in atherosclerotic pathogenesis and found that AK087124 was up-regulated while miR-224-5p was down-regulated in in the plasma and plaque from atherosclerotic mice compared with normal mice.  Bioinformatic prediction combining with luciferase assays indicated that AK087124 could sponge miR-224-5p and enhance the PTEN expression which is a target of miR-224-5p.RNA pull down assays also showed that biotin-miR-224-5p probe could interacted directly with AK087124 and PTEN. 		Yes	The function study indicated that knockdown of AK087124 inhibited ox-LDL induced endothelial apoptosis and inflammatory response. 	33974917
AK077216	LncRNA	Homo sapiens	colorectal adenocarcinoma	CRA tissues	Interaction(miR-34a)	qRT-PCR//Transwell Assay	 AK077216 was downregulated in CRA tissues compared to that in non-tumor tissues of CRA patients. MiR-34a was upregulated in CRA tissues and inversely correlated with AK077216. Overexpression of AK077216 decreased the expression levels of miR-34a, while overexpression of miR-34a did not affect the expression of AK077216.	 During a 5-year follow-up, patients with lower expression levels of AK077216 in CRA tissues showed significantly lower overall survival.	Yes	 Overexpression of AK077216 inhibited CRA cell migration and invasion, while overexpression of miR-34a accelerated cancer cell migration and invasion and attenuated the effects of overexpression on AK077216 on cell behaviors.	35484046
AK058003	LncRNA	Homo sapiens	esophageal carcinoma	EC tissues	Expression[highly expressed]	qRT-PCR//Wound Healing Assay	LncRNA AK058003 was highly expressed EC tissues compared with para-carcinoma tissues (p<0.01).		Yes	LncRNA AK058003 is highly expressed in EC patients, which promotes proliferation, migration, invasion, and metastasis of EC cells. 	32495875
AK035396	LncRNA	Homo sapiens	Myocardial Reperfusion Injury	MIRI models	Interaction(Mterf1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Tunel//qRT-PCR//Cell Apoptosis Assay	 In vivo and in vitro MIRI models, AK035396 was up-regulated after myocardial infarction.  AK035396 directly interacts with Mterf1 and inhibits the level of Mterf1. Further experiments have shown that inhibiting Mterf1 will promote the expression of mitochondrial genes COXII and CYTb and cause cell apoptosis. 		Yes	Functional studies have shown that knockdown of AK035396 reduces the apoptosis of primary cardiomyocytes and mouse myocardial tissue. 	34820386
AK027294	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue,cell lines	Interaction[upregulating PCNA]	qRT-PCR//MTT//EdU Staining	AK027294 expression level was significantly higher in GC tissue samples and cell lines.Furthermore, the expression of PCNA was downregulated via silence of AK027294 in GC cells, while the expression of PCNA was upregulated via overexpression of AK027294 in GC cells. The correlation analysis showed that PCNA expression was positively correlated with AK027294 expression in GC tissues.		Yes	 Results of MTT assay, colony formation assay, and EdU incorporation assay showed that cell proliferation was inhibited through the silence of AK027294 in GC cells, while cell proliferation was promoted through overexpression of AK027294 in GC cells.	31298327
AK025387	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues 	Expression[highly expressed]	qRT-PCR	 In this research, we identify one kind of lncRNA, called AK025387, which is highly expressed in metastatic gastric cancer samples compared with non-metastatic gastric cancer samples.	The expression of AK025387 is significantly positively correlated with lymph node metastasis. 	Yes	 The in situ hybridization demonstrates that AK025387 is located in both nucleus and cytoplasm, but mostly in cytoplasm. AK025387 promotes gastric cancer cells migratory and invasive ability, but it inhibits apoptosis in vitro.	32509569
AK024094	LncRNA	Homo sapiens	Breast Neoplasms	BCa tissues and cell lines	regulation[miRNA-181a]	qRT-PCR//Luciferase Report Assay	 AK024094 was significantly upregulated in BCa tissues and cell lines. In addition, AK024094 accelerates the proliferation and metastasis of BCa cells by targeting miRNA-181a.	Meanwhile, the rate of distant metastasis was significantly higher, and the overall survival was shorter in BCa patients with high expression of AK024094. 	Yes	The knockdown of AK024094 significantly attenuated the proliferative, migratory, and invasive abilities of MDA-MB-468 and MCF-7 cells.	32141560
AK021443	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Expression [highly expressed]	qRT-PCR	AK021443 expression was increased in HCC tissues and cell lines. However, these functions could be reversed by overexpression of AK021443. AK021443 significantly controlled HepG2 and Bel-7402 cell proliferation, colony formation, invasion, and migration by repressing EMT, which might provide a potential therapeutic target for HCC diagnosis.		Yes	 Knockdown of AK021443 significantly reduced HepG2 and Bel-7402 cell proliferation, invasion, and migration.  Furthermore, inhibition of AK021443 in HepG2 and Bel-7402 cells significantly repressed EMT ability. Knockdown of AK021443 in vivo also significantly inhibited tumor growth with decreased Ki-67 levels and EMT phenotype in tumor tissues.	29638164
ADAMTS9-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction(PI3K/AKT/mTOR signaling pathway)	Flow Cytometry//qRT-PCR	In this study, we detected that ADAMTS9-AS1 is highly expressed in bladder cancer. Interestingly, the up-regulation of ADAMTS9-AS1 was accompanied by the activation of PI3K/AKT/mTOR signaling pathway, while the down-regulation of ADAMTS9-AS1 lead to an opposite effect. 		Yes	We observed that the up-regulation of ADAMTS9-AS1 promoted cell proliferation, migration and invasion, and reduced the apoptosis and autophagy of 5637 and T42 cell lines.  Meanwhile, the down-regulation of ADAMTS9-AS1 increased the apoptosis and autophagy, and suppressed their proliferation, migration and invasion.	34428588
ADAMTS9-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-128 and miR-150/Ras/MAPK and Wnt pathways)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	Then, RT-qPCR verified the upregulation of ADAMTS9-AS1 in glioma tissues and cell lines.  Furthermore, dual-luciferase assay supported that cytoplasmic ADAMTS9-AS1 is capable of sponging miR-128 and miR-150, which are known as regulators of Ras/MAPK, PI3K, and Wnt pathways. Overall, these results introduced ADAMTS9-AS1 as an oncogene that upregulates Ras/MAPK and Wnt pathways through sponging of the miR-128 and miR-150 in glioma cells. 		Yes	Finally following the ADAMTS9-AS1 overexpression, upregulation of Ras/MAPK and Wnt signaling pathways was verified through western blotting and Top/Fop flash assay, respectively. At the cellular level, ADAMTS9-AS1 overexpression brought about reduced sub-G1 cell population, increased proliferation rate, reduced apoptosis level, increased migration rate, shortened Bax/Bcl2 ratio, induced EMT, and stemness characteristics of transfected cells, detected by flow cytometry, MTT assay, scratch test, and RT-qPCR. 	36449154
CBR3-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cells and tissues	Interaction(miR-140-5p/DDX54-NUCKS1-mTOR signaling pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Co-IP//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay	The obtained data showed that CBR3-AS1 demonstrated a high expression in osteosarcoma cells. Mechanically, CBR3-AS1 sponged miR-140-5p and recruited DDX54 to upregulate NUCKS1, thus activating the mTOR signaling pathway.		Yes	CBR3-AS1 could promote stemness and EMT of osteosarcoma cells as well as osteosarcoma tumor growth. 	35592388
circEIF4G3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[sponging miR-335 ]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//FISH	A total of 3 hepatocellular carcinoma (HCC) tissues and their matched non-cancerous tissues were collected and screened for dysregulated circRNA using human circRNA microarray and the result showed circ-EIF4G3 was significantly up-regulated in hepatocellular carcinoma. Our study demonstrates that circ-EIF4G3 promotes the proliferation, invasion and migration of gastric cancer via sponging miR-335.	An increase level in the circ-EIF4G3 expression was associated with higher TNM stage and lymphatic metastasis. 	Yes	 In vitro assays of the GC cell lines AGS and BGC-823 demonstrated that knockdown of circ-EIF4G3 inhibited cell proliferation, invasion and migration significantly. 	31257089
hsa_circ_0001829	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-155-5p/SMAD2 axis]	ISH//qRT-PCR	We found that hsa_circ_0001829 was significantly upregulated in GC tissues and cell lines. Taken together, our findings firstly demonstrated a novel oncogenic role of hsa_circ_0001829 in GC progression through miR-155-5p-SMAD2 axis, and our study may offer novel biomarkers and therapeutic targets for GC.		Yes	 Loss- and gain-of- function assays showed that hsa_circ_0001829 promotes GC cells proliferation, migration and invasion, and the affected cell cycle progression and apoptosis rates may account for the effect of hsa_circ_0001829 on GC proliferation.	33308284
circB3GNTL1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	regulation[miR-598]	Flow Cytometry//qRT-PCR	The results showed that CircB3GNTL1 expression was up-regulated and miR-598 expression was up-regulated in gastric cancer tissues and cell lines;It was concluded that CirB3GNTL1 prevents decomposition of glutamines and induces apoptosis by controlling miR-598 in gastric cancer cells.		Yes	Knockdown circB3GNTL1 prevented proliferation and glutamine decomposition of the gastric cancer cells and induced apoptosis compared with normal para-cancers and gastric cancer cell lines. 	33287917
circASAP2	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	regulation[miR-770-5p/CDK6 axis]	qRT-PCR//MTT//Transwell Assay	The expression levels of circ_ASAP2 and CDK6 were increased, and miR-770-5p level was decreased in GC tissues and cells.Circ_ASAP2 knockdown can repress the development of GC cells partly through regulating the miR-770-5p/CDK6 axis, suggesting an underlying circRNA-targeted therapy for GC treatment.		Yes	 Furthermore, circ_ASAP2 knockdown inhibited cell viability, migration, and invasion of GC cells.	33284890
hsa_circ_100876	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	regulation[miR-665/YAP1 Signaling]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	Our study confirmed that circRNA_100876 was highly expressed in GC lesions compared with the adjacent normal tissues (P < 0.001).Therefore, we demonstrated that circRNA_100876 over-expression in GC could promote GC tumor growth, migration and invasion and exert its effects through miR-665/YAP1 signaling.	High circRNA_100876 expression was negatively associated with survival outcome (P = 0.000).	Yes	 Furthermore, the down-regulation of circRNA_100876 could inhibit GC cell proliferation, invasion, and migration by suppressing the EMT pathway. 	33262782
circCUL3	CircRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues,cell lines	regulation[STAT3/HK2 Axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	High-regulated expression of circCUL3 was observed in both GC tissues and cell lines. In summary, the present findings provide mechanistic insights into circCUL3/miR-515-5p/STAT3/HK2 axis regulation on the GC Warburg effect, providing a novel possibility for an understanding of GC pathogenesis.	Clinically, the high expression of circCUL3 was closely correlated with advanced clinical stage and overall survival in GC patients.	Yes	Functionally, cellular experimental investigations demonstrated that circCUL3 promoted the proliferation, glucose consumption, lactate production, ATP quantity, and extracellular acidification rate (ECAR) of GC cells. In vivo, circCUL3 knockdown repressed tumor growth.	33230436
circPRRX1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues, cell lines	regulation[MicroRNA-665/YWHAZ Axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Compared with normal tissues and cells, circ-PRRX1 and YWHAZ levels were upregulated, and miR-665 was downregulated in GC tissues and cells.  Circ-PRRX1 knockdown suppressed GC development by targeting miR-665 to inhibit YWHAZ expression, and the potential molecular mechanism may provide a theoretical basis for GC therapy.		Yes	Functionally, circ-PRRX1 knockdown inhibited the viability, migration, and invasion and promoted apoptosis in GC cells, whereas anti-miR-665 abolished these effects.	33201331
hsa_circ_0004872	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[hsa_circ_0004872/miR-224/Smad4/ADAR1]	ChIP//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//FISH//Luciferase Report Assay//EdU Staining//Transwell Assay	 In this study, we found that hsa_circ_0004872 was dramatically downregulated in GC tissues compared with adjacent noncancerous tissues. Our findings showed that hsa_circ_0004872 acted as a tumor suppressor in GC by forming a negative regulatory loop consisting of hsa_circ_0004872/miR-224/Smad4/ADAR1. Thus, hsa_circ_0004872 may serve as a potential biomarker and therapeutic target for GC.	The expression level of hsa_circ_0004872 was associated with tumor size and local lymph node metastasis.	Yes	Enforced expression of hsa_circ_0004872 inhibited the proliferation, invasion and migration of GC cells, whereas knockdown of hsa_circ_0004872 had the opposite effects. Nude mice experiments showed that ectopic expression of hsa_circ_0004872 dramatically inhibited tumor growth and metastasis in vivo.	33172486
circPDZD8	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	interaction[ sponging miR-197-5p]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	CircPDZD8 was up-regulated in gastric cancer tissues and cells, Kaplan-Meier survival analysis indicated that gastric patients had a poor overall survival when circPDZD8 levels were high. Importantly, circPDZD8 could up-regulate CHD9 expression by sponging miR-197-5p, and modulate cell progression by regulation of the miR-197-5p/CHD9 axis in gastric cancer. 	CircPDZD8 was up-regulated in gastric cancer tissues and cells, Kaplan-Meier survival analysis indicated that gastric patients had a poor overall survival when circPDZD8 levels were high. 	Yes	CircPDZD8 knockdown could hinder proliferation and migration of gastric cancer cells.	33049714
hsa_circ_0005556	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	regulation[ hsa_circ_0005556/miR-4270/MMP19 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The expression of hsa_circ_0005556 in gastric cancer tissues and gastric cancer cell lines was higher compared to normal controls.  Our study shows that the hsa_circ_0005556/miR-4270/MMP19 axis is involved in proliferation, migration, and invasion of gastric cancer cells through the competing endogenous RNA (ceRNA) mechanism.		Yes	In vitro, the downregulation of hsa_circ_0005556 significantly inhibited proliferation, migration, and invasion of gastric cancer cells. In vivo, the downregulation of hsa_circ_0005556 suppressed tumor growth in nude mice.	33024586
circC16orf62	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	regulation[ miR-421/TUBB2A axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	"Circ_C16orf62 andTUBB2A were downregulated in GC tissues and cells.These findings demonstrate that circ_C16orf62 impeded proliferation, migration, and invasion in vitro and retarded tumor growth in vivo by the miR-421/TUBB2A axis in GC, providing a potential therapeutic strategy for patients with GC.
"		Yes	 Circ_C16orf62 was predominantly located in the cytoplasm of GC cells, and repressed proliferation, migration, and invasion of GC cells. 	33006960
hsa_circ_001653	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	interaction[binding to microRNA-377]	qRT-PCR//Luciferase Report Assay//Western Blot	hsa_circ_001653 was found to be an up-regulated circRNA in GC tissues and cells. Collectively, the demonstration that hsa_circ_001653 exerts its anticancer effects by regulating the miR-377-NR6A1 axis increases our understanding of gastric cancer pathophysiology.		Yes	Down-regulation of hsa_circ_001653 inhibited GC cell proliferation, migration and invasion, while stimulating cell apoptosis.	33006200
circFLNA	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	interaction[as a Sponge of miR-646]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Transwell Assay	 Our results found that circFLNA was upregulated in GC tissues and cells. Further experiments revealed that circFLNA could sponge miR-646, and miR-646 could target PFKFB2. 		Yes	Silencing of circFLNA could suppress the proliferation, migration, invasion, glycolysis, and enhance the apoptosis of GC cells. Also, circFLNA knockdown reduced GC tumor volume and weight in vivo.	32982406
hsa_circ_100782	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cells	interaction[miR-574-3p]	CCK8//qRT-PCR//Luciferase Report Assay	 In the current study, compared with adjacent non-cancerous normal tissues, the expressions of circRNA_100782 and Rb were both downregulated in human gastric cancer cells.In this research, we discovered that circRNA_100782 was downregulated in gastric cancer cells and is associated with cell proliferation and invasion by inhibiting tumor suppressor gene Rb by interacting with miR-574-3p.		Yes	Through qRT-PCR and CCK-8 assay, we found that the expression of circRNA_100782 is related to the proliferation of gastric cancer cells. Besides, we also found that circRNA_100782 regulated the migration ability of gastric cancer cells through transwell assay.	32964973
circRIMS	CircRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues 	interaction[hsa-miR-148a-5p and hsa-miR-218-5p]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	 We observed that circRIMS expression was markedly upregulated in T3N3M0 GC tissues and significantly correlated with clinical stage in the RNA sequencing data.  CircRIMS remarkably promoted GC cell metastasis in vitro, functioning as a sponge for hsa-miR-148a-5p and hsa-miR-218-5p.		Yes	CircRIMS remarkably promoted GC cell metastasis in vitro, functioning as a sponge for hsa-miR-148a-5p and hsa-miR-218-5p.	32954174
circNHSL1	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues, and cells,exosomes	regulation[miR-149-5p/YWHAZ Axis]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay	CircNHSL1 was highly expressed in GC cell-derived exosomes, GC tissues, and cells. Our studies disclosed that circNHSL1 knockdown repressed migration, invasion, and glutaminolysis in vitro and inhibited tumor growth in vivo by miR-149-5p/YWHAZ axis in GC, implying an underlying circRNA-targeted therapy for GC treatment.		Yes	 Its knockdown impeded GC cell migration, invasion, and glutaminolysis.	32848466
circHIPK3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[CircHIPK3/miR-876-5p/PIK3R1 axis ]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	CircHIPK3 was upregulated in GC tissues and cells compared with controls, and circHIPK3 was more resistance to RNase R than linear homeodomain interacting protein kinase 3 (HIPK3) mRNA.The circHIPK3 mediated the proliferation, migration, invasion, and glutaminolysis of GC cells partly through regulation of miR-876-5p/PIK3R1 axis by the mechanism of competing endogenous RNAs (ceRNA), indicating circHIPK3 was a GC-associated circRNA that promoted GC development.		Yes	Silencing of circHIPK3 inhibited GC cells proliferation, migration, invasion, and glutaminolysis as well as tumor tumorigenic ability. 	32817745
hsa_circ_0000144	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	regulation[GPRC5A ,miR-623]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our data indicated that circ_0000144 was up-regulated and miR-623 was down-regulated in GC tissues and cells.Our study indicated that circ-0000144 knockdown repressed GC progression at least partly by regulating GPRC5A expression via sponging miR-623, illumining a novel therapeutic target for GC treatment.		Yes	 Moreover, the knockdown of circ_0000144 weakened GC cell proliferation, colony formation, migration, invasion and glutaminolysis and accelerated cell apoptosis by up-regulating miR-623. Additionally, circ_0000144 depletion inhibited tumor growth in vivo.	32766708
circMRPS35	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	interaction[circMRPS35/KAT7/FOXO1/3a pathway ]	RNA Pull-Down//CCK8//qRT-PCR//RNA-seq//Invasion Assay//ChIP	Our findings not only reveal the pivotal roles of circMRPS35 in governing histone modification in anticancer treatment, but also advocate for triggering circMRPS35/KAT7/FOXO1/3a pathway to combat gastric cancer.		Yes	 Biologically, circMRPS35 suppresses the proliferation and invasion of gastric cancer cells in vitro and in vivo. 	32164722
circDLST	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[NRAS/MEK1/ERK1/2 signaling]	Western Blot//FISH//RIP//qRT-PCR//Luciferase Report Assay	The expression levels of circDLST were dramatically elevated in GC tissues as compared with the adjacent normal tissues, and acted as an independent prognostic factor of poor survival in patients with GC. CircDLST promotes the tumorigenesis and metastasis of GC cells by sponging miR-502-5p to activate the NRAS/MEK1/ERK1/2 signaling.	The expression levels of circDLST were dramatically elevated in GC tissues as compared with the adjacent normal tissues, and acted as an independent prognostic factor of poor survival in patients with GC. 	Yes	 Knockdown of circDLST inhibited the cell viability, colony formation, DNA synthesis, cell invasion and liver metastasis in vitro and in vivo, whereas overexpression of circDLST had the opposite effects. 	30953514
circNHSL1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[miR-1306-3p/SIX1/vimentin axis]	ISH//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We found that the level of circNHSL1 was significantly up-regulated in gastric cancer, and positively correlated with clinicopathological features and poor prognosis of patients with gastric cancer. CircNHSL1 promotes gastric cancer progression through miR-1306-3p/SIX1/Vimentin axis, and may serve as a novel diagnostic marker and target for treatment of gastric cancer patients.	We found that the level of circNHSL1 was significantly up-regulated in gastric cancer, and positively correlated with clinicopathological features and poor prognosis of patients with gastric cancer. 	Yes	Functionally, circNHSL1 promoted cell mobility and invasion, as well as in vivo tumorgenesis and metastasis.	31438963
circSPECC1	CircRNA	Homo sapiens	Stomach Neoplasms	cell lines	Interaction[KDM4A/YAP1 pathway]	RNA Pull-Down//Luciferase Report Assay//RIP	This study showed that circ_SPECC1 was down-regulated in various GC cell lines, significantly inhibited GC cell proliferation and invasion, and promote apoptosis, which might play an anti-oncogene role.  Circ_SPECC1 was mainly located in the cytoplasm, and its sequence contained multiple potential binding sites of miR-526b. Pull-down experiments with biotinylated miR-526b mimics and circ_SPECC1 probe showed that they could enrich each other. RIP experiments found hat anti-AGO2 antibody could significantly enrich circ_SPECC1. Further dual luciferase reporter gene assay also confirmed that miR-526b could bind directly to circ_SPECC1. miR-526b was also down-regulated in GC cells, and one of its important target genes was KDM4A. Both circ_SPECC1 and miR-526b inhibited the expression of KDM4A and its downstream effector YAP1, but miR-526b inhibitors terminated the above-mentioned inhibition of circ_SPECC1, and KDM4A overexpression reversed the inhibition of circ_SPECC1 and miR-526b on YAP1 expression. Both miR-526b and KDM4A siRNA inhibited GC cell proliferation and invasion, and promote apoptosis; KDM4A overexpression had the opposite effects, and significantly blocked the regulation of miR-526b on cell growth and invasion. Therefore, circ_SPECC1 can enhance miR-526b inhibitory effect on downstream KDM4A/YAP1 pathway by adsorbing it, thus inhibiting GC cell growth and invasion. These findings enrich the mechanism of circRNAs in GC and will provide more new targets for the prevention and treatment of GC.		Yes	This study showed that circ_SPECC1 was down-regulated in various GC cell lines, significantly inhibited GC cell proliferation and invasion, and promote apoptosis, which might play an anti-oncogene role. 	31349968
circHECTD1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[targeting miR-1256 and activating β-catenin/c-Myc signaling]	Western Blot//CCK8//qRT-PCR//FISH//RIP//RNA-seq//Luciferase Report Assay//Transwell Assay	 In this study, we showed that circHECTD1 expression was markedly upregulated in gastric cancer (GC) and was associated with lymph node metastasis and American Joint Committee on Cancer stage.Dual-luciferase and RNA immunoprecipitation assays demonstrated that miR-1256 was a direct downstream target of circHECTD1. circHECTD1 targeted miR-1256 and subsequently increased the expression level of USP5. The circHECTD1/miR-1256/USP5 axis exerted its tumor-promoting effects by activating the downstream β-catenin/c-Myc signaling pathway. In vivo mouse models further verified the oncogenic roles of circHECTD1 in GC. 	In this study, we showed that circHECTD1 expression was markedly upregulated in gastric cancer (GC) and was associated with lymph node metastasis and American Joint Committee on Cancer stage. The circHECTD1 expression level was found to be an independent prognostic factor for GC patients. 	Yes	circHECTD1 knockdown inhibited GC cell glutaminolysis, proliferation, migration, and invasion, whereas circHECTD1 overexpression promoted GC progression.	31371702
hsa_circ_0000144	CircRNA	Homo sapiens	Stomach Neoplasms	cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay	Hsa_circ_0000144 was highly expressed in GSE78902 samples from the GEO database (Fig. 5a). To further verify the results, we chose two cell lines and found that the expression of hsa_circ_0000144 was upregulated in MGC-803 GC cancer cells lines compared to GES-1 normal cells (Fig. 5b).		Yes	Hsa_circ_0000144 knockdown suppressed tumor growth in vitro.	31636511
circERBB2	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Interaction[miR-503/CACUL1 and miR-637/MMP-19 signaling]	CCK8//qRT-PCR//Invasion Assay//Transwell Assay	We found circ-ERBB2 was strikingly increased in GC tissues and cells. We further predicted and identified circ-ERBB2 sponged miR-503 and miR-637 by bioinformatics analysis and luciferase reporter system. CACUL1 and MMP-19 were then predicted and confirmed as the target of miR-503 and miR-637, respectively. Furthermore, rescue assays indicated that circ-ERBB2 promoted tumor growth and invasion via miR-503/CACUL1 and miR-637/MMP-19 pathways, respectively.	Noticeably, circ-ERBB2 upregulation in tumorous tissues was linked to patients' tumor size, depth of invasion, and overall survival.	Yes	 A series of gain and loss-of-function assays indicated its oncogenic role in GC cells, including cell proliferation, apoptosis, migration and invasion. 	30853181
circCOL6A3	CircRNA	Homo sapiens	Stomach Neoplasms	cell lines	Interaction[miR-3064-5p]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Both circCOL6A3 and COL6A3 were highly expressed in GC cells, while miR-3064-5p was down-regulated.  CircCOL6A3 regulated the expression of miR-3064-5p, and the effect of si-circCOL6A3 on cell biological behaviors was abolished by miR-3064-5p inhibitor. MicroRNA-3064-5p targets COL6A3 to regulate its expression. 		Yes	Depleted circCOL6A3 significantly decreased cell viability and mobility, and increased cell apoptosis.. Taken together, the present study indicated that overexpressed circCOL6A3 promoted cell proliferation, migration and apoptosis of gastric cancer through rescission of miR-3064-5p-induced inhibitory effect on COL6A3. 	31122696
hsa_circ_0000467	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines,blood	Expression[highly expressed]	qRT-PCR	 Hsa_circ_0000467 was significantly upregulated in GC tissue compared to adjacent nontumor tissue (n = 51, P < 0.05). Similar results were detected in the HGC-27, MGC-803, AGS, NUGC-3, GES-1 cell lines (n = 15, P < 0.001), and in the plasma samples from GC patients (n = 20, P < 0.05). 	Moreover, the hsa_circ_0000467 expression level is closely associated with TNM stage. Additionally, Cox multivariate analysis showed that hsa_circ_0000467 is a novel independent prognostic factor.	Yes	Furthermore, in vitro experiments demonstrated that knockdown of hsa_circ_0000467 markedly inhibited the proliferation, migration, and invasion of GC cells. Moreover, hsa_circ_0000467 silencing increased tumor apoptosis in vitro.	30461077
hsa_circ_006100	CircRNA	Homo sapiens	Stomach Neoplasms	cell lines	Interaction[miR-195/GPRC5A signalling]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	 An upregulated hsa_circ_006100 level and downregulated miR‐195 level were found in all four GC cell lines (Figure ​(Figure3A).3A). Forced hsa_circ_006100 expression promoted the migration and invasion of MGC-803 and AGS cells, while those activities were inhibited by miR-195. Mechanistically, GPRC5A was predicted as a target of miR-195 and was upregulated in gastric cancer. A miR-195 inhibitor restored cell viability, proliferation, migration and invasion, and repressed apoptosis via GPRC5A. In vivo studies showed that knockdown of hsa_circ_006100 delayed tumour growth, reduced PCNA expression and upregulated miR-195 and BCL-2 expression which was restored by miR-195 inhibition due to GPRC5A/EGFR signalling, and changed the EMT phenotype in vivo.	Patients with a high hsa_circ_006100 level or low miR-195 level had tumours with a high TNM stage, poor cellular differentiation and lymph node metastasis. miR-195 was targeted and inhibited by hsa_circ_006100. 	Yes	 Overexpression of hsa_circ_006100 enhanced cellular viability and proliferation, while miR-195 suppressed hsa_circ_006100-enhanced cell growth and induced apoptosis in MGC-803 and AGS cells. In vivo studies showed that knockdown of hsa_circ_006100 delayed tumour growth	31318114
circHIPK3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines	Interaction[Wnt/β-catenin pathway]	CCK8//qRT-PCR//Wound Healing Assay//Colony Formation Assay	 CircHIPK3 level was higher in GC tissues relative to paracancerous tissues.Identically, its level was higher in GC cells compared with that of GES cells.CircHIPK3 promotes GC cells to proliferate and migrate by regulating the Wnt/β-catenin pathway. Upregulation of circHIPK3 indicates poor prognosis of GC patients.	 The expression level of circHIPK3 was negatively correlated to the overall survival of GC patients.	Yes	 Silence of circHIPK3 weakened proliferative and migratory abilities of GC cells.	31599413
hsa_circ_101882	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Regulation[EMT signaling pathway]	Migration Assay//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Invasion Assay	Hsa_circ_101882 expression levels were significantly increased in GC tissue and GC cell lines. Mechanically, the dysregulated expression of hsa_circ_101882 affects EMT signaling pathway, which was examined by detecting E-cadherin, N-cadherin, vimentin, and Snail expression levels.		Yes	Functionally, low expression of hsa_circ_101882 revealed anti-tumor effects via inhibiting cell growth, migration, and invasion and promoting cell apoptosis.	31420917
hsa_circ_0000291	CircRNA	Homo sapiens	Stomach Neoplasms	cell lines	Regulation[ miR-183/ITGB1 Axis]	qRT-PCR//Luciferase Report Assay//Western Blot	Our data showed that hsa_circ_0000291 was upregulated in GC cell lines.Taken together, hsa_circ_0000291 knockdown inhibited GC cell metastasis and growth by regulating the miR-183/ITGB1 axis. 		Yes	Our data showed that hsa_circ_0000291 was upregulated in GC cell lines, whereas hsa_circ_0000291 silencing suppressed cell metastasis and proliferation in in vivo and in vitro studies. 	31814763
circSMARCA5	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Transwell Assay	 The circSMARCA5 level was decreased in GC tissues and cell lines. 	The low expression level of circSMARCA5 was correlated to poorer overall survival and disease-free survival. Low circSMARCA5 expression was revealed as an independent unfavorable predictive factor for GC. 	Yes	Upregulation of circSMARCA5 dampened the proliferation, migration, and invasion of GC cells, whereas circSMARCA5 knockdown promoted GC progression.	30956729
circPRKCI	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines	Interaction[binding to microRNA-545]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ-PRKCI was significantly highly expressed in GC tissues, as well as cell lines. These results indicated that circ-PRKCI might promote the development of GC by adsorbing microRNA-545 in a sponge manner.	High expression of circ-PRKCI was positively associated with a poor prognosis of GC patients. 	Yes	Overexpression of circ-PRKCI significantly promoted the proliferation and invasion of GC cells, whereas reduced the proportion of apoptotic GC cells. 	31773680
circPRMT5	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	Regulation[circ-PRMT5/miR-145/miR-1304/MYC axis]	qRT-PCR//Luciferase Report Assay	Circ-PRMT5 expression was significantly higher in GC than in adjacent normal tissues, and GC patients with circ-PRMT5 high expression had shorter survival times. High circ-PRMT5 expression may provide a poor prognostic indicator of survival in GC patients and targeting circ-PRMT5/miR-145/miR-1304/MYC axis may be a novel therapeutic strategy for GC.	Circ-PRMT5 expression was significantly higher in GC than in adjacent normal tissues, and GC patients with circ-PRMT5 high expression had shorter survival times. 	Yes	Functionally, circ-PRMT5 silence inhibited GC cell growth and invasion. 	31701767
circZNF609	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[inhibiting miRNA-145-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	QRT-PCR data revealed a higher level of circ-ZNF609 in GC tissues relative to ANT.  Circ-ZNF609 promotes proliferative and invasive abilities of gastric cancer cells by inhibiting miRNA-145-5p expression as a ceRNA, thus accelerating gastric cancer progression.		Yes	The knockdown of circ-ZNF609 in BGC823 and MGC803 cells suppressed proliferative and invasive abilities. 	31773689
circLMTK2	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[miR-150-5p/c-Myc axis]	qRT-PCR//Luciferase Report Assay//Western Blot	circLMTK2 was frequently upregulated in GC tissues.Our findings demonstrate that circLMTK2 functions as a tumour promoter in GC through the miR-150-5p/c-Myc axis and could thus be a prognostic predictor and therapeutic target for GC.	circLMTK2 was frequently upregulated in GC tissues, and high circLMTK2 expression was associated with poor prognosis, lymph node metastasis and poor TNM stage in GC patients. 	Yes	Functionally, circLMTK2 overexpression promoted GC cell proliferation and tumourigenicity in vitro and in vivo.	31722712
circRBMS3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[miR-153-SNAI1 axis]	qRT-PCR//Microarray	In the current study, high throughput microarray assay showed that circRBMS3 was upregulated in GC tissues, which was further confirmed by quantitative reverse transcription polymerase chain reaction.  Collectively, these results suggested that circRBMS3 promoted GC cells proliferation and invasion via regulating miR-153/SNAI1 axis.	Correlation analysis revealed that high circRBMS3 expression was associated with advanced TNM stage, depth of invasion, and lymph-node metastasis. Kaplan-Meier analysis indicated that GC patients with high circRBMS3 expression have a poor overall survival (OS). 	Yes	Function assays showed that circRBMS3 silencing reduced GC cells proliferation and invasion in vitro, and inhibited the tumor growth in vivo.	30132886
circDB	CircRNA	Homo sapiens	Stomach Neoplasms	GCa tissues	Interaction[binding microRNA-34a]	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	The expression of circ-DB and MET in GCa tissues was significantly higher than that in the corresponding adjacent tissues. Circ-DB may regulate MET level through microRNA-34a and affect the proliferative ability and migration of GCa cells.		Yes	 In vitro cell experiments showed that low expression of circ-DB inhibited cell migration, which could be recovered by the co-transfection with microRNA-34a inhibitor.	31799656
circDUSP16	CircRNA	Homo sapiens	Stomach Neoplasms		Interaction[sponging miR-145-5p]	Western Blot//FISH//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression levels of circDUSP16 were markedly increased in GC tissue samples and acted as an independent prognostic factor of poor survival in patients with GC. CircDUSP16 facilitates the tumorigenesis and invasion of GC cells by sponging miR-145-5p, and may provide a novel therapeutic target for GC.	The expression levels of circDUSP16 were markedly increased in GC tissue samples and acted as an independent prognostic factor of poor survival in patients with GC. 	Yes	 Knockdown of circDUSP16 repressed the cell viability, colony formation, and invasive potential in vitro and in vivo, but ectopic expression of circDUSP16 reversed these effects. 	31776711
hsa_circ_0000190	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cells	regulation[miR-1252/PAK3 pathway]	qRT-PCR//Luciferase Report Assay//FISH	Circ_0000190 was down-regulated in gastric cancer tissues and cells, with a major location in cytoplasm.Circ_0000190 suppresses gastric cancer progression potentially via inhibiting miR-1252/PAK3 pathway, employing circ_0000190 might be a promising therapeutic strategy for the treatment of gastric cancer.		Yes	 Circ_0000190 inhibited gastric cancer cell viability, proliferation and migration, and induced apoptosis and cell cycle arrest by regulating the expression of capase-3, p27 and cyclin D. 	32742198
hsa_circ_0005556	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[miR-767-5p]	circRIP//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The upregulation of circ_0005556 was validated by qRT-PCR in GC tissues and cells, and a higher circ_0005556 level indicated a poorer prognosis.The in vitro knockdown of circ_0005556 remarkably repressed GC cell progression by increasing the expression of miR-767-5p.	The upregulation of circ_0005556 was validated by qRT-PCR in GC tissues and cells, and a higher circ_0005556 level indicated a poorer prognosis.	Yes	Knockdown of circ_0005556 was revealed to repress GC cell viability, invasion, and migration and to promote GC cell apoptosis. 	32728015
ADAMTS9-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	 Pca tissues	Interaction(miR-142-5p/CCND1 axis)	qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Bioinformatics Analysis	 ADAMTS9-AS1 expression is down-regulated in PCa. Importantly, microRNA-142-5p (miR-142-5p) mimic and small-interfering RNA targeting cyclin D1 (CCND1, si-CCND1) could attenuate the inhibitory effects of ADAMTS9-AS1 overexpression on PCa cell growth.		Yes	Forcing ADAMTS9-AS1 expression impedes PCa cell proliferation via initiating cell apoptosis.	33704879
circPIP5K1A	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[CircPIP5K1A/miR-671-5p/KRT80 axis]	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircPIP5K1A was up-regulated in GC tissues and cells with a circular structure.CircPIP5K1A/miR-671-5p/KRT80 axis contributes to GC progression through PI3K/AKT pathway, implying this axis may be a potential therapeutic target for the treatment of GC patients.		Yes	Functionally, circPIP5K1A silence limited cell proliferation, invasion, migration and EMT process. 	32169757
hsa_circ_0005075	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues,GC cell lines	regulation[miR-431/p53/epithelial-mesenchymal transition axis ]	Western Blot//CCK8//qRT-PCR//EdU Staining//Transwell Assay	Then, our data revealed that CircRNA_0005075 was found to be significantly up-regulated in GC tissues as well as GC cell lines, and the GC patients with higher CircRNA_0005075 expression were more likely to have poor outcomes. Briefly, circRNA_0005075 could directly inhibit the expression level of miR-431, then regulate the p53/Epithelial-mesenchymal transition axis, and finally inhibit cell growth and metastasis in GC.	Then, our data revealed that CircRNA_0005075 was found to be significantly up-regulated in GC tissues as well as GC cell lines, and the GC patients with higher CircRNA_0005075 expression were more likely to have poor outcomes. 	Yes	Down-regulation of CircRNA_0005075 could significantly suppress the GC cell proliferation and cell metastasis ability, while the addition of miR-431 inhibitors could counteract this effect. 	32133664
circHIPK3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	interaction[Sponging miR-107,Regulating BDNF]	CCK8//qRT-PCR//Colony Formation Assay//EdU Staining//Transwell Assay	circHIPK3 was further confirmed to be upregulated in all GC tissues and cells tested.	Furthermore, circHIPK3 levels were associated with Tumor & Lymph Node & Metastasis(TNM) stage (P = 0.032). The area under the receiver operating characteristic curve (ROC) was 0.743 (95% confidence interval 0.615-0.872; P = 0.001). 	Yes	CCK-8, colony formation, Transwell and EdU assays were performed to evaluate the effects of circHIPK3 on cell proliferation and migration in GC. 	32110057
hsa_circ_0006282	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[miR-155,FBXO22]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The expression of circ_0006282 in GC tissues was significantly higher than its adjacent non-cancer tissues and over-expression of circ_0006282 was associated with tumor size, lymph nodes metastasis and TNM stage, but no obvious links with other pathological parameters.Our findings indicated that over-expression of circ_0006282 down‑regulated miR-155 to activate the expression of FBXO22, thus promoting proliferation and metastasis of GC cells, which provides a promising therapeutic target for GC treatment.	The expression of circ_0006282 in GC tissues was significantly higher than its adjacent non-cancer tissues and over-expression of circ_0006282 was associated with tumor size, lymph nodes metastasis and TNM stage, but no obvious links with other pathological parameters.	Yes	Knockdown of circ_0006282 inhibited the proliferation and metastasis ability of GC cells in vitro and suppressed the tumor growth in vivo.	32099403
hsa_circ_0010882	CircRNA	Homo sapiens	Stomach Neoplasms	plasma of GC patients and GC cell lines	regulation[PI3K/Akt/mTOR signaling pathway]	qRT-PCR//Western Blot	We found that hsa_circ_0010882 expression was significantly upregulated in the plasma of GC patients and GC cell lines.  It plays an important role in proliferation, migration, and invasive genotypes of GC cell lines via regulation of the PI3K/Akt/mTOR signaling pathway.	 In addition, GC patients with higher expression of hsa_circ_0010882 had significantly lower overall survival than patients with lower expression of hsa_circ_0010882.	Yes	The proliferation, migration, and invasiveness of GC cell lines were inhibited following hsa_circ_0010882 knock-down, while GC cellular apoptosis increased.	32096170
circSMAD7	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[EMT process]	qRT-PCR//Wound Healing Assay//Transwell Assay	In this study, RT-qPCR results showed that circ-SMAD7 expression was significantly lower in GC tissues compared to that in adjacent ones.These results indicate that upregulation of circ-SMAD7 inhibits GC cell migration and invasion via reversing the EMT process.		Yes	Cell migration and invasion of GC were inhibited via upregulation of circ-SMAD7.	32096163
hsa_circ_0000467	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	interaction[Binding to MicroRNA miR-326-3p]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Invasion Assay	This study showed that hsa_circ_0000467 expression was higher in gastric cancer tissues than in corresponding adjacent tissues (P < 0.050) and that hsa_circ_0000467 expression levels were correlated with gastric cancer histological grade (P < 0.050). In conclusion, hsa_circ_0000467 plays a regulatory role in the development and progression of gastric cancer by regulating miR-326-3p, and this circRNA may be a potential diagnostic marker and therapeutic target of gastric cancer.		Yes	 Cell function experiments indicated that hsa_circ_0000467 downregulation decreased the proliferation and invasion ability of BGC-823 and SGC-7901 cells and the number of cells entering the G2/M phase.	32090087
circRBM33	CircRNA	Homo sapiens	Stomach Neoplasms	GC specimens and cell lines	interaction[targeting miR-149]	qRT-PCR//Luciferase Report Assay//RIP	CircRBM33 was distinctly upregulated in GC specimens and cell lines and a close correlation between circRBM33 expression and clinical characteristics of GC was observed.Rescue experiments indicated that circRBM33 manipulates biological function in GC cells through the circRBM33/miR-149/IL-6 axis. 		Yes	After silencing circRBM33, the apoptosis of GC cells increased, while proliferation, migration, and invasion decreased. 	32044717
hsa_circ_104433	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	interaction[miR-497-5p]	qRT-PCR//Luciferase Report Assay	The level of circRNA_104433 showed upregulation in GC tissues, and the expression of it showed a positive correlation with the degree of differentiation and the size of the tumor.CircRNA_104433 directly binds to miR-497-5p, which directly regulates CDC25A.	The level of circRNA_104433 showed upregulation in GC tissues, and the expression of it showed a positive correlation with the degree of differentiation and the size of the tumor.	Yes	Knockdown of circRNA_104433 inhibited cell cycle transition, and cell proliferation, while promoted cell apoptosis in GC.	32021419
circHIAT1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[ miR-21]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	Our findings demonstrated that circHIAT1 was lowly expressed in GC tissues.CircHIAT1 functioned as a tumor inhibitor in GC cells through downregulating miR-21, and could be a novel target for GC treatment.		Yes	After transfection with PLCDH-circHIAT1 in MKN28 and MKN45 cells, cell viability was decreased, while the expression levels of p53 and p21 were raised, as well as apoptosis.	32020707
circMAN2B2	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[miR-145,PI3K/AKT and JNK pathways]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	As relative to paracancerous tissues, circMAN2B2 was high-expressed in GC tissues. CircMAN2B2 exerted its function possibly through regulating miR-145 as well as PI3K/AKT and JNK pathways.		Yes	Silence of circMAN2B2 clearly declined SNU-16 and AGS cells viability, survival, migration but enhanced apoptosis. 	32020674
circATXN7	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	interaction[miR-4319,ENTPD4]	RNA Pull-Down//Tunel//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//EdU Staining//Transwell Assay	The results showed an upregulated circATXN7 expression in GC tissues and cell lines.CircATXN7 promoted GC development through sponging miR-4319 and regulating ENTPD4, which identified circATXN7 as a new biomarker in GC.		Yes	Besides, silenced circATXN7 hampered the proliferation and invasion as well as promoted the apoptosis in GC cells. 	31997941
circRHOBTB3	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	interaction[ miR-654-3p]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	The expression of circRHOBTB3 was lower in GC tissues and cell lines. Taken together, this study revealed that circRHOBTB3 might function as competing endogenous RNA (ceRNA) for miR-654-3p, which could contribute to growth inhibition of GC through activating p21 signaling pathway. 	Downregulation of circRHOBTB3 was significantly correlated with poor differentiation and unfavorable prognosis in patients with GC.	Yes	Overexpression of circRHOBTB3 in GC cells led to decreased proliferation and induced G1/S arrest in vitro, accompanied with inhibited xenograft tumor growth in vivo, while the opposite effects were achieved in circRHOBTB3-silenced cells.	31928527
hsa_circ_102231	CircRNA	Homo sapiens	Stomach Neoplasms	Gastric cancer tissues and plasma	Expression [highly expressed]	qRT-PCR	 CircRNA_102231 expression was significantly upregulated in GC tissue and plasma samples, which can be used as a biomarker for GC diagnosis and prognosis. The function assays showed that circRNA_102231 knockdown inhibited GC cell proliferation and invasion both in vitro and in vivo. CircRNA_102231 was able to bind to IRTKS, increasing IRTKS protein stability, leading to GC progression.  In sum, our data demonstrate that circRNA_102231 is a novel oncogene in GC and acts as a potential biomarker and therapeutic target for GC patients.	high expression of circRNA_102231 was observed more often in patients with larger tumor volume, lymph node metastasis and higher clinical stage. Moreover, Kaplan–Meier plotter showed that GC patients with high circRNA_102231 had shorter survival time than those with low circRNA_102231	Yes	The function assays showed that circRNA_102231 knockdown inhibited GC cell proliferation and invasion both in vitro and in vivo. 	34374630
circAXIN1	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tumor	Expression [highly expressed]	Western Blot//Co-IP//Migration Assay//Colony Formation Assay//qRT-PCR//RNA-seq//IHC//Invasion Assay//ChIP	"CircAXIN1 is highly expressed in GC tissues compared with its expression in paired adjacent normal gastric tissues. CircAXIN1 overexpression enhances the cell proliferation, migration, and invasion of GC cells, while the knockdown of circAXIN1 inhibits the malignant behaviors of GC cells in vitro and in vivo. Mechanistically, AXIN1-295aa competitively interacts with APC, leading to dysfunction of the ""destruction complex"" of the Wnt pathway."	The expression of circAXIN1 is positively associated with lymph node metastasis.	Yes	CircAXIN1 overexpression enhances the cell proliferation, migration, and invasion of GC cells, while the knockdown of circAXIN1 inhibits the malignant behaviors of GC cells in vitro and in vivo. 	34863211
hsa_circ_101996	CircRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines 	Interaction( miR-143)	In Vivo Experiment//qRT-PCR//Invasion Assay//ChIP	The result showed that hsa_circRNA_101996 expression was significantly upregulated in GC tissues compared to that in the adjacent tissues, and its level in cancer tissue was correlated with tumor size, lymphatic metastasis, and distant metastasis. Compared with the low hsa_circRNA_101996 expression group, the three-year survival rate of patients in the high hsa_circRNA_101996 expression group was significantly lower. 	and its level in cancer tissue was correlated with tumor size, lymphatic metastasis, and distant metastasis. Compared with the low hsa_circRNA_101996 expression group, the three-year survival rate of patients in the high hsa_circRNA_101996 expression group was significantly lower. 	Yes	The knockdown of hsa_circRNA_101996 dramatically suppressed the cell migration, invasion, and proliferation of GC cells by sponging to absorb miR-143 and elevated the expression of TET2. 	34659556
hsa_circ_0009172	CircRNA	Homo sapiens	Stomach Neoplasms	 tissues and cell lines	Interaction(miR-485-3p/NTRK3 axis)	RNA Pull-Down//Luciferase Report Assay	The hsa_circRNA_0009172 expression was downregulated in gastric cancer tissues and cell lines, indicating a positive association with patient prognosis.	The hsa_circRNA_0009172 expression was downregulated in gastric cancer tissues and cell lines, indicating a positive association with patient prognosis.	Yes	 Functionally, hsa_circ_0009172 overexpression inhibited proliferative, invasive and migrative potential of gastric cancer cells as well as epithelial-mesenchymal transition (EMT)-related proteins by sponging miR-485-3p to inhibit NTRK3, while miR-485-3p overexpression could reverse the inhibitory effect of hsa_circ_0009172 on gastric cancer. Furthermore, either up-regulation of hsa_circ_0009172 or down-regulation of miR-485-3p led to the suppression of xenograft tumor growth in nude mice.	33531648
hsa_circ_0081146	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(miR-144)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//Transwell Assay	Circ_0081146 was upregulated in GC tissues and cells.  	Patients with high expression of circ_0081146 had a significantly reduced 5-year overall survival rate.	Yes	Circ_0081146 knockdown restrained the growth, migration and invasion of GC cells in vitro as well as tumorigenesis in vivo. Circ_0081146 targeted miR-144 and HMGB1 was targeted by miR-144. Circ_0081146 was negatively correlated with miR-144 expression, while positively correlated with HMGB1 expression in GC tissues.	33496921
hsa_circ_0000039	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-1292-5p)	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	Circ_0000039 expression was up-regulated in GC tissues and cell lines, and it was significantly related with poor differentiation of tumor tissues.	Circ_0000039 expression was up-regulated in GC tissues and cell lines, and it was significantly related with poor differentiation of tumor tissues.	Yes	 In addition, circ_0000039 overexpression enhanced the proliferation, migration and invasion of GC cells, while circ_0000039 depletion inhibited these malignant biological behaviors. In terms of mechanism, it was found that circ_0000039 promoted the proliferation and progression of GC cells by adsorbing miR-1292-5p and up-regulating the expression of DEK.	33104023
hsa_circ_100269	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer (GC) samples and cells	Interaction(PI3K/Akt axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Cell Cycle Assay//Transwell Assay	Our findings revealed downregulation of hsa_circRNA_100269 in GC tissues compared to non-cancerous control. Additionally, the levels of PI3K were remarkably elevated in GC tissues, where hsa_circRNA_100269 and PI3K was negatively correlated. 	Moreover, the expression of hsa_circRNA_100269 was associated with histology grade and occurrence of metastasis in GC patients.	Yes	In addition, hsa_circRNA_100269 was downregulated in GC cells compared to normal gastric epithelial cells. Overexpressed hsa_circRNA_100269 notably inhibited the proliferation, migration, invasion and EMT of GC cells, whereas cell cycle arrest at G0/G1 phase was promoted and cell apoptosis was enhanced. 	33901239
hsa_circ_0032821	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[MEK1/ERK1/2 signaling pathway]	CCK8//qRT-PCR//Transwell Assay//Western Blot	 Circ_0032821 was significantly upregulated in human GC tumors and cells.Circ_0032821 expression induced cell proliferation, EMT, migration, invasion, and autophagy inhibition in human GC cells in vitro and in vivo through activating MEK1/ERK1/2 signaling pathway, suggesting circ_0032821 as an oncogenic role in GC.	Moreover, circ_0032821 might be a biomarker for the advanced Tumor node metastasis (TNM) stage, lymphoid node metastasis and poor prognosis in gastric cancer.	Yes	Knockdown of circ_0032821 by transfection induced decrease of cell proliferation, EMT, migration and invasion, but increase of autophagy of AGS and HGC-27 cells in vitro, as well as induced tumor growth inhibition in vivo. 	32165864
hsa_circ_0001649	CircRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	regulation[miR-20a,ERK and Wnt/β-catenin pathways]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Hsa_circ_0001649 was downregulated in GC cells and tissues.Upregulation of hsa_circ_0001649 restrained GC cell growth and metastasis by downregulating miR-20a and thereby inactivated ERK and Wnt/β-catenin pathways.		Yes	Upregulation of hsa_circ_0001649 restrained viability, proliferation, migration, and invasion, while promoted apoptosis. 	32212290
circKIAA0907	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissue	regulation[miR-452-5p/KAT6B Axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	CircKIAA0907 was downregulated in GC and had higher stability than its linear isoform. This work demonstrated that circKIAA0907 has diagnostic and therapeutic value in GC by acting as an oncogenic molecule via the miR-452-5p/KAT6B axis.		Yes	Functionally, circKIAA0907 upregulation resulted in the repression of proliferation, cell cycle, and autophagy and promotion of apoptosis in GC cells.	32722658
circCCDC66	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[c-Myc and TGF-β signaling pathways]	Wound Healing Assay//Flow Cytometry//qRT-PCR//CCK8//Colony Formation Assay//Transwell Assay	CircCCDC66 expression was elevated in both GC tissues and cell lines compared to adjacent normal tissues and normal gastric epithelial cell line.CircCCDC66 promotes GC growth and metastasis by activating c-Myc and TGF-β signaling pathways, suggesting that it may serve as a potential biomarker for GC.	The upregulation of circCCDC66 in GC tissues was related to tumor stage and lymphatic metastasis.	Yes	CircCCDC66 knockdown significantly inhibited GC cell proliferation, migration and invasion and induced cell apoptosis in GC cells.	32226494
circREPS2	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[RUNX3/β-catenin Signaling]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	In the present study, we found that circREPS2 was downregulated in GC tissues and cell lines.  In conclusion, circREPS2 suppresses the progression of GC via miR-558/RUNX3/β-catenin signaling and is a novel promising biomarker and target for GC treatment.	 Low expression of circREPS2 was associated with a higher tumor-node-metastasis (TNM) stage, poor tumor differentiation, and larger tumor size in GC patients. 	Yes	 Functionally, circREPS2 significantly inhibited GC cell proliferation, migration, invasion, and epithelial-mesenchymal transformation (EMT) in vitro and tumorigenesis in vivo. 	32721878
hsa_circ_0081143	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[miR-497-5p/EGFR Axis]	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	These data indicated that circ_0081143 expression was increased in GC tissues and cells.The present work suggested that circ_0081143 knockdown ameliorated hypoxia-induced migration, invasion, and EMT in GC cells at least partly by the miR-497-5p/EGFR axis, illuminating a novel molecular target for GC treatment.		Yes	The knockdown of circ_0081143 relieved hypoxia-induced GC cell migration, invasion, and epithelial/mesenchymal transition (EMT).	32678674
circNRIP1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-182/ROCK1 Axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 circNRIP1 expression was enhanced in gastric cancer tissues and cells and high expression of circNRIP1 indicated poor survival of patients.Knockdown of circNRIP1 suppressed cell migration and invasion, arrested cell cycle at G0-G1 phase and promoted apoptosis in gastric cancer cells. 	 circNRIP1 expression was enhanced in gastric cancer tissues and cells and high expression of circNRIP1 indicated poor survival of patients.	Yes	Silence of circNRIP1 inhibited progression of gastric cancer by increasing miR-182 and decreasing ROCK1, providing a novel target for the treatment of gastric cancer.	32636647
hsa_circ_0032627	CircRNA	Homo sapiens	Stomach Neoplasms	cell lines	regulation[ miR-502-5p expression]	qRT-PCR//Luciferase Report Assay//MTT//Colony Formation Assay	 Compared with that in gastric mucosal cell lines, the expression level of circ_0032627 was upregulated in the selected four GC cell lines,  The expression level of circ_0032627 is raised in GC cells, and circ_0032627 affects the proliferation and apoptosis of GC cells by sponging miR-502-5p.		Yes	 Compared with that in gastric mucosal cell lines, the expression level of circ_0032627 was upregulated in the selected four GC cell lines, and circ_0032627 knockdown substantially inhibited the proliferation of GC cells, but promoted their apoptosis. 	32633357
circFGD4	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-532-3p/APC/β-catenin signalling pathway]	RNA Pull-Down//ISH//qRT-PCR//RIP//Luciferase Report Assay	circFGD4 expression was down-regulated the most in human GC tissues and cell lines. circFGD4 suppressed GC progression through sponging miR-532-3p and enhancing APC expression to inactivate the β-catenin signalling. 	 Low expression of circFGD4 was correlated with poor tumour differentiation, lymphatic metastasis, and poor prognosis of GC patients. 	Yes	circFGD4 suppressed GC cell viability, colony formation, migration, induced epithelial-mesenchymal transition (EMT), and tumorigenesis and metastasis in vivo.	32633323
circHN1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Expression[highly expressed]	qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circHN1 was upregulated in GC tissues and cell lines compared to adjacent non-tumor tissues and normal gastric epithelial cells. 		Yes	 Additionally, circHN1 silencing significantly promoted GC cell growth, colony formation, migration, and invasion, whereas circHN1 overexpression had the opposite effects.CircHN1 overexpression also suppressed gastric cancer growth in the mouse xenograft tumor model. 	32608539
circSHKBP1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and serum 	regulation[miR-582-3p/HUR/VEGF pathway]	RNA Pull-Down//Western Blot//ISH//qRT-PCR//RIP//Luciferase Report Assay	Increased expression of circSHKBP1(hsa_circ_0000936) was revealed in GC tissues and serum and was related to advanced TNM stage and poor survival.  Our findings demonstrate that exosomal circSHKBP1 regulates the miR-582-3p/HUR/VEGF pathway, suppresses HSP90 degradation, and promotes GC progression. 	Increased expression of circSHKBP1(hsa_circ_0000936) was revealed in GC tissues and serum and was related to advanced TNM stage and poor survival. 	Yes	Overexpression of circSHKBP1 promoted GC cell proliferation, migration, invasion and angiogenesis in vitro and in vivo, while suppression of circSHKBP1 plays the opposite role.	32600329
hsa_circ_103809	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells 	interaction[binding to microRNA-101-3p]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	Hsa_circ_103809 showed an increased expression both in GCa tissues and cell lines, predicting a poor prognosis of GCa patients. Hsa_circ_103809, highly expressed in GCa, may promote the migration capacity of GCa cells by adsorbing microRNA-101-3p and thus become a new therapeutic target for GCa.	Hsa_circ_103809 showed an increased expression both in GCa tissues and cell lines, predicting a poor prognosis of GCa patients.	Yes	Meanwhile, the invasive and migration capacities of GCa cells were remarkably reduced after the knockdown of hsa_circ_103809. 	32572921
hsa_circ_0023642	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	interaction[sponging microRNA-223]	qRT-PCR//RNA Pull-Down	The current study showed that hsa_circ_0023642 was upregulated in GC and presented a high positive correlation with the malignant progression of GC. We confirmed that hsa_circ_0023642 could serve as a sponge of miR-223, subsequently promoting GC progression.		Yes	In addition, in vitro experiments showed that the silencing of hsa_circ_0023642 in GC cell lines MKN-45 and SGC-7901 significantly reduced the proliferation, invasion, and migration of GC cells. 	32562304
circRPL15	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-502-3p/OLFM4/STAT3 pathway]	qRT-PCR//Luciferase Report Assay//FISH	circ-RPL15 was upregulated in GC tissues and cell lines, and the overexpressed circ-RPL15 was correlated with poorer survival of GC patients.circ-RPL15 promotes GC progression and predicts poor prognosis of GC patients, and regulates the malignant phenotypes of GC cells by mediating the miR-502-3p/OLFM4/STAT3 axis.	circ-RPL15 was upregulated in GC tissues and cell lines, and the overexpressed circ-RPL15 was correlated with poorer survival of GC patients.	Yes	Functionally, circ-RPL15 upregulation distinctly promoted the proliferation, migration and invasion of GC cells and inhibited apoptosis.	32559850
hsa-circ-0000670	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell line	regulation[microRNA-384/SIX4 axis]	Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The expression of hsa-circ-0000670 was determined by RT-qPCR to be highly expressed in gastric cancer tissues relative to corresponding adjacent normal tissues, as well as in gastric cancer cell lines relative to normal gastric mucosal epithelial cell line. Dual-luciferase reporter gene and RIP assays identified the binding of hsa-circ-0000670 to microRNA-384 (miR-384) and the binding of miR-384 to sine oculis-related homeobox 4 (SIX4).		Yes	Additionally, silencing of SIX4 delayed tumor growth and progression, which were reversed by overexpression of hsa-circ-0000670.	32535033
circCYFIP2	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[miR-1205/E2F1 axis]	qRT-PCR	circCYFIP2 was found to be significantly upregulated in GC tissues and cell lines. Collectively, our findings suggested that circCYFIP2 might serve as an oncogenic circRNA to promote GC progression via the miR-1205/E2F1 axis, which provided a potential therapeutic target for the treatment of GC.	High expression of circCYFIP2 was associated with metastasis and poor prognosis of GC patients.	Yes	Function assays revealed that overexpression or knockdown of circCYFIP2 significantly enhanced or reduced GC cell proliferation and invasion abilities. 	32526476
circMAT2B	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues 	regulation[miR-515-5p/HIF-1α axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//ChIP	Circ-MAT2B was notably increased in GC and could be used as a sensitive and specific indicator of GC diagnosis and prognosis. 	Circ-MAT2B was notably increased in GC and could be used as a sensitive and specific indicator of GC diagnosis and prognosis. 	Yes	 Stable knockdown of circ-MAT2B dramatically inhibited GC cell viability, colony formation, DNA synthesis, glucose uptake and lactate production in vitro, and retarded tumor growth in vivo.	32467667
hsa_circ_000684	CircRNA	Homo sapiens	Stomach Neoplasms	GC cell lines and clinical tissues	interaction[microRNA-186 ]	qRT-PCR	Expression of hsa-circ-000684 and that of ZEB1 mRNA were elevated while microRNA-186 (miR-186) expression was downregulated in GC cell lines and clinical tissues.Collectively, our data show that hsa-circ-000684 reduces the miR-186 expression which leads to an increase in the ZEB1 expression and, consequently, promotion of GC progression.		Yes	 In addition, the effects of hsa-circ-000684 on the proliferation, migration, invasion, and tube formation of GC cells were examined through gain-and loss-of-function experiments. Furthermore, we introduced tumor xenografts into nude mice to better understand these effects in vivo. Either knockdown of hsa-circ-000684 or upregulation of miR-186 inhibited GC cell proliferation, migration, invasion, and tube formation in vitro, and reduced the xenograft tumor growth in nude mice.	32388910
circCCDC9	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-6792-3p/CAV1 axis]	RNA Pull-Down//qRT-PCR//RIP//FISH//Luciferase Report Assay	Evidently down-regulated expression of circCCDC9 was observed in both GC tissues and cell lines.CircCCDC9 functions as a tumor suppressor in inhibiting the progression of GC through miR-6792-3p/CAV1 axis, which has provided an exploitable biomarker and therapeutic target for patients with GC.	Expression of circCCDC9 was negatively correlated with tumor size, lymph node invasion, advanced clinical stage and overall survival in GC patients.	Yes	Functionally, overexpression of circCCDC9 significantly inhibited the proliferation, migration and invasion of GC cell lines in vitro and tumor growth and metastasis in vivo, whereas miR-6792-3p mimics counteracted these effects.	32386516
hsa_circ_0017639	CircRNA	Homo sapiens	Stomach Neoplasms	GC cell	regulation[miR-224-5p/USP3 axis]	qRT-PCR//RNA Pull-Down//FISH	The data illustrated that in hsa_circ_assays, expression was enhanced in GC cell. Our collective findings advised that hsa_circ_0017639 takes part in GC progression through regulating the miR-224-5p/USP3 axis, highlighting its potential as an effective GC therapeutic target.		Yes	Downregulation of hsa_circ_0017639 decreased GC cell proliferation and migration in in vitro and in vivo experiments. 	32376451
circSMC3	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	regulation[miR-4720-3p/TJP1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay	Using circRNAs microarray, we detected the dysregulated circRNAs and identified an upregulated circRNA, circSMC3 (hsa_circ_0000260), in gastric cancer tissues.Thus, our results indicate that circSMC3 promotes gastric cancer cell proliferation and motility through miR-4720-3p/TJP1.	Patients with high circSMC3 expression levels had a poor overall survival via Kaplan-Meier survival analysis implied that gastric cancer. 	Yes	Functionally, loss of circSMC3 abolished the proliferation and motility of gastric cancer cells. 	32314520
hsa_circ_100876	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	interaction[miR-136 and MIEN1]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our data indicated that the expression of circRNA_100876 was raised in GC tissues.Collectively, our data identified that the promotion of GC growth and metastasis induced by circRNA_100876 interacted with miR-136 and MIEN1, indicating an emerging announcement for uncovering the potential mechanism of GC progression.		Yes	 In vitro, functional experiments confirmed that cell proliferation, invasion along with migration was promoted by circRNA_100876 in GC tissues. 	32305633
circDONSON	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[up-regulated]	Northern Blot//ChIP//Transwell Assay//ISH//CCK8//qRT-PCR//Colony Formation Assay//EdU Staining//IF	Elevated expression of circ-DONSON was observed in GC tissues and positively associated with advanced TNM stage and unfavorable prognosis.circ-DONSON was localized in the nucleus, recruited the NURF complex to SOX4 promoter and initiated its transcription. Silencing of the NURF complex subunit SNF2L, BPTF or RBBP4 similarly attenuated GC cell growth and increased apoptosis. circ-DONSON knockdown inhibited GC growth in vivo.		Yes	Silencing of circ-DONSON significantly suppressed the proliferation, migration and invasion of GC cells while promoting apoptosis. 	30922402
hsa_circ_0067997	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[inhibition of miR-515-5p]	qRT-PCR	qRT-PCR was used to validate the expression of circ_0067997 in GC tissues and cell lines. The results revealed that circ_0067997 was upregulated in GC, and high circ_0067997 expression was associated with the poor overall survival rate of GC patients.	qRT-PCR was used to validate the expression of circ_0067997 in GC tissues and cell lines. The results revealed that circ_0067997 was upregulated in GC, and high circ_0067997 expression was associated with the poor overall survival rate of GC patients.	Yes	 Knockdown of circ_0067997 significantly reduced cell viability, inhibited colony formation, and attenuated invasive ability, whereas overexpression of circ_0067997 exhibited opposed effects. Circ_0067997 was identified to be a sponge for miR-515-5p directly.	30688097
circHuR	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	Interaction[inhibiting CNBP]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot	Circ-HuR (hsa_circ_0049027) was predominantly detected in the nucleus, and was down-regulated in gastric cancer tissues and cell lines. Mechanistically, circ-HuR interacted with CCHC-type zinc finger nucleic acid binding protein (CNBP), and subsequently restrained its binding to HuR promoter, resulting in down-regulation of HuR and repression of tumor progression.		Yes	 Ectopic expression of circ-HuR suppressed the growth, invasion, and metastasis of gastric cancer cells in vitro and in vivo. 	31718709
AC118344.1	LncRNA	Homo sapiens	Stomach Neoplasms		regulation[AC118344.1-AKT2-HK2/MMP2 axis]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 Therefore, our findings provide a novel mechanism of the AC118344.1-AKT2-HK2/MMP2 axis in regulating the development of gastric cancer cells.		Yes	Upregulating the expression of AC118344.1 induces cell proliferation, invasion in vitro, and lung metastasis in vivo whereas downregulating the expression of AC118344.1 inhibits these effects. 	33324106
AC104958.2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 65 HCC samples and 30 paired adjacent non-tumor liver tissue	Interaction(PCBP2 )	RNA Pull-Down//Western Blot//qRT-PCR//RIP//RNA-seq//Transwell Assay	By RNA sequencing (RNA-seq) in a series of 65 HCC samples and 30 paired adjacent non-tumor liver tissue, we identified a novel lncRNA AC104958.2 that was significantly upregulated in HCC tissues and associated with MVI.  In addition, the interaction between AC104958.2 and Poly (rC) binding protein 2 (PCBP2) was identified by RNA pull down and mass spectrometry (MS), which was further validated by RNA immunoprecipitation (RIP). PCBP2 was also upregulated in HCC and associated with MVI. 	High expression of both AC104958.2 and PCBP2 was correlated with tumor size, TNM stage and MVI in HCC. 	Yes	Overexpression of AC104958.2 obviously elevated cell viability, metastasis, invasion and epithelial-mesenchymal transition (EMT), while knockout of AC104958.2 mediated by CRISPR/Cas9 technique showed the opposite effects. 	34418457
AC104041.1	LncRNA	Homo sapiens	head and neck squamous cell carcinoma		regulation[Wnt2B/β-catenin pathway]	qRT-PCR//Luciferase Report Assay//RIP//FISH	In this work, we identified a novel lncRNA AC104041.1 which is highly upregulated and correlated with poor survival in HNSCC patients.Moreover, we demonstrate that salinomycin, which as a highly effective antibiotic in the elimination of cancer stem cells through the Wnt/β-catenin signaling, could enhance the inhibition of tumor growth by antisense oligonucleotides (ASO) targeting AC104041.1 in HNSCC cells and PDXs (patient-derived xenograft) model. 	In this work, we identified a novel lncRNA AC104041.1 which is highly upregulated and correlated with poor survival in HNSCC patients.	Yes	 Moreover, AC104041.1 overexpression significantly promoted tumor growth and metastasis of HNSCC in vitro and in vivo. 	32826863
AC098934	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues and cells	Interaction(METTL3)	In Vivo Experiment//Wound Healing Assay//Invasion Assay//CCK8//qRT-PCR//Bioinformatics Analysis//Transwell Assay	 Compared to the normal tissues, AC098934 was more highly expressed in LUAD tissues.Mechanistically, AC098934 could bind to the m6A antibody and METTL3 protein. METTL3 overexpression promoted the m6A modification on AC098934, thereby increasing the interaction of m6A modification.		Yes	After AC098934 was knocked down by siRNA, the proliferation, invasion, migration as well as tumorigenesis abilities of both A549 and H1299 cells were reduced. 	35711823
AC092839.1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
AC092718.4	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Regulation( PI3K-Akt signaling)	BrdU//qRT-PCR	 In this study, we found that AC092718.4 was highly expressed in LUAD and high expression of AC092718.4 was correlated with poor overall survival (OS) and disease-specific survival (DSS) in LUAD.Kyoto Encyclopedia of Genes and Genomes (KEGG) results showed that AC092718.4 was involved in the PI3K-Akt signaling pathway, Th17 cell differentiation, and cell apoptosis. AC092718.4 expression was correlated with immune cell infiltration. 	 In this study, we found that AC092718.4 was highly expressed in LUAD and high expression of AC092718.4 was correlated with poor overall survival (OS) and disease-specific survival (DSS) in LUAD.	Yes	Finally, we found that the knockdown of AC092718.4 inhibited lung adenocarcinoma (LUAD) cell growth and promote cell apoptosis. 	36490353
AC092171.4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues	regulation[microRNA-1271,GRB2]	qRT-PCR	AC092171.4 was significantly upregulated in HCC tumor tissues compared to normal liver tissues. These findings demonstrate that AC092171.4 promotes growth and progression of HCC by sponging miR-1271 and upregulating GRB2. 		Yes	In vitro cell proliferation, migration and invasiveness were all higher in AC092171.4-overexpressing HCC cells, but lower in AC092171.4-silenced HCC cells, than in controls. Balb/c nude mice injected with AC092171.4-silenced HCC cells had smaller xenograft tumors, which showed less growth and pulmonary metastasis than control tumors.	32692718
AC092127.1	LncRNA	Homo sapiens	Breast Neoplasms	BC cells	Interaction(AC092127.1/miR-451a/AEBP2 axis)	RNA Pull-Down//Western Blot//In Vitro Experiment//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	MiR-451a was expressed at a low level in BC cells. Overexpression of miR-451a repressed BC cells proliferation, migration and invasion. Moreover, long non-coding RNA AC092127.1 acted as a sponge of miR-451a to enhance the expression level of AE binding protein 2 (AEBP2) that was demonstrated to be the target gene of miR-451a in BC cells. Finally, rescue experiments validated that miR-451a and AEBP2 involved in AC092127.1-mediated BC cell growth, migration and invasion.		Yes	rescue experiments validated that miR-451a and AEBP2 involved in AC092127.1-mediated BC cell growth, migration and invasion.	34352938
AC087588.2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cells	Interaction(hsa-miR-30a-5p)	CCK8//qRT-PCR//migration assay	In this study, we found that AC087588.2 was upregulated and associated with a poor prognosis in LUAD.  Finally, we constructed a ceRNA network that included hsa-miR-30a-5p and four mRNAs (ANLN, POLR3G, EHBP1, and ERO1A) specific to AC087588.2 in LUAD. The Kaplan-Meier survival analysis showed that lower expression of hsa-miR-30a-5p and higher expression of ANLN, POLR3G, EHBP1, and ERO1A were associated with adverse clinical outcomes in patients with LUAD. 		Yes	 Functionally, the knockdown of AC087588.2 restrained LUAD cell proliferation and migration in vitro.	35769906
AC087388.1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression(highly expressed)	qRT-PCR//Wound Healing Assay//Colony Formation Assay//Invasion Assay	The results demonstrated that the lncRNA SLC16A1-AS1, AC087388.1, and ELFN1-AS1 were significantly overexpressed in the CRC tissues in comparison to their normal counterpart margins. 		Yes	Downregulation of lncRNA AC087388.1 remarkably decreased the cell proliferation and viability of the CRC cells. In addition, the data demonstrated that the downregulation of lncRNA AC087388.1 significantly suppressed cell growth and colony formation capability in the cells. Also, downregulation of lncRNA AC087388.1 attenuated motility and invasion of CRC cells, and significantly decreased the expression of invasion genes. 	35193569
AC083843.1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
AC079630.4	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues	Expression(lower expressed)	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	AC079630.4 was significantly down-regulated in lung cancer tissues, including in its subtypes. 	 Samples with low AC079630.4 expression had a more advanced pathological stage and a worse prognosis than those with high expression. 	Yes	 In experimental validation, AC079630.4 over-expression could significantly inhibit the proliferation and clonality, and up-regulated the receptors of TRAIL (TRAIL-R1 and TRAIL-R2) in lung cancer cells. 	34282054
AC079061.1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells	Interaction(VIPR1 axis)	qRT-PCR	Experimental results suggested that lncRNA-AC079061.1 and VIPR1 were frequently downregulated in HCC cells, while hsa-miR-765 was significantly upregulated. Moreover, the lncRNA-AC079061.1/VIPR1 axis suppressed the proliferation and invasion of HCC cells.		Yes	Experimental results suggested that lncRNA-AC079061.1 and VIPR1 were frequently downregulated in HCC cells, while hsa-miR-765 was significantly upregulated. Moreover, the lncRNA-AC079061.1/VIPR1 axis suppressed the proliferation and invasion of HCC cells.	36038907
AC073352.1	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues 	Interaction(YBX1)	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//EdU Staining//Migration Assay//qRT-PCR//FISH//RIP//Cell Viability Assay//Invasion Assay	Here we identified a novel lncRNA AC073352.1 that was significantly upregulated in breast cancer tissues and was associated with advanced TNM stages and poor prognosis in breast cancer patients.  Collectively, our results demonstrated that AC073352.1 promoted breast cancer metastasis and angiogenesis via binding YBX1, and it could serve as a promising, novel biomarker for prognosis and a therapeutic target in breast cancer.	Here we identified a novel lncRNA AC073352.1 that was significantly upregulated in breast cancer tissues and was associated with advanced TNM stages and poor prognosis in breast cancer patients. 	Yes	 In addition, AC073352.1 was found to promote the migration and invasion of breast cancer cells in vitro and enhance breast cancer metastasis in vivo. 	34218256
AC068039.4	LncRNA	Homo sapiens	Pulmonary Arterial Hypertension	PASMCs	Interaction(miR-26a-5p/TRPC6)	Western Blot//Transfection//qRT-PCR//migration assay//Luciferase Report Assay//Microarray//Cell Proliferation Assay//Cell Cycle Assay	Consistent with microarray analysis, quantitative PCR verified that AC068039.4 was obviously up-regulated in hypoxia-induced PASMCs. Further experiment indicated AC068039.4 promoted hypoxic PASMCs proliferation via sponging miR-26-5p. In addition, transient receptor potential canonical 6 (TRPC6) was confirmed to be a target gene of miR-26a-5p.		Yes	 Knocking down AC068039.4 alleviated proliferation and migration of PASMCs and regulated cell cycle progression through inhibiting cells entering the G0/G1 cell cycle phase. 	33026218
AC025180.1	LncRNA	Homo sapiens	Breast Neoplasms	 breast tumours	Interaction(ITGA2/CCND1 and ACLY)	RNA-seq	 A novel lncRNA (AC025180.1;ENSG00000249899), named herein I2ALR, was identified at the ITGA2 gene locus, and was variably expressed in breast tumours and breast cancer cell subtypes. I2LAR knockdown resulted in upregulation of ITGA2 gene expression, whilst over-expression of I2ALR resulted in downregulation of ITGA2 mRNA. Further, examination of two downstream targets of ITGA2 associated with breast tumor stemness and metastasis (CCND1 and ACLY), revealed concomitant gene expression changes in response to I2ALR modulation.		Yes	I2LAR knockdown resulted in upregulation of ITGA2 gene expression, whilst over-expression of I2ALR resulted in downregulation of ITGA2 mRNA. Further, examination of two downstream targets of ITGA2 associated with breast tumor stemness and metastasis (CCND1 and ACLY), revealed concomitant gene expression changes in response to I2ALR modulation.	35098437
AC023794.4-201	LncRNA	Homo sapiens	laryngeal squamous cell carcinoma		Expression[lower expressed]	Flow Cytometry//qRT-PCR//Transwell Assay	 In our previous study, it was demonstrated that the expression level of the long non-coding RNA (lncRNA) AC023794.4-201 were decreased in laryngeal squamous cell carcinoma, particularly in cases of LSCC with lymphatic metastasis. In conclusion, the findings of the present study suggested that AC023794.4-201 may exert tumor-suppressive functions in the progression of LSCC and may serve as a potential prognostic biomarker for LSCC.	 Moreover, low expression levels of AC023794.4-201 were revealed to be an adverse prognostic factor for patients with LSCC.	Yes	AC023794.4-201 inhibited the proliferation and the cloning capacity of LSCC cells compared with the negative control group as indicated by real-time cell analysis and the plate colony formation assay. 	32566004
AC020978	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[PKM2/HIF-1α axis]	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//FISH//RIP//Luciferase Report Assay//ChIP	The present study indicated that AC020978 was upregulated in NSCLC, significantly correlated with advanced TNM stage and poor clinical outcomes, representing as an independent prognostic predictor. 	The present study indicated that AC020978 was upregulated in NSCLC, significantly correlated with advanced TNM stage and poor clinical outcomes, representing as an independent prognostic predictor. 	Yes	Functional assays revealed AC020978's role in promoting cell growth and metabolic reprogramming.	32308748
AC020978	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(MDH2 stability)	In Vivo Experiment//RNA Pull-Down//Wound Healing Assay//RIP//FISH//IF//IHC//Transwell Assay	In this study, we evaluated the expression levels of AC020978 in a series of NSCLC tissues using FISH assays and found that higher AC020978 expression levels were closely associated with metastasis and unfavorable prognosis. Further investigation demonstrated that AC020978 interacted with malate dehydrogenase 2 (MDH2) and maintained MDH2 stability. Knockdown of MDH2 weakened the facilitating effect on cell metastasis and 2-hydroxyglutarate (2-HG) metabolism in AC020978-overexpressed NSCLC cells. 		Yes	Functional studies showed that AC020978 promoted NSCLC migration and invasion both in vitro and in vivo. 	34424600
AC016405.3	LncRNA	Homo sapiens	Breast Neoplasms	BRCA tissues and cells 	Interaction(miR-22-3p/ERBB3 )	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The results showed that AC016405.3 is highly expressed in BRCA tissues as well as cells and positively correlated with poor prognosis in BRCA patients.  Mechanistically, AC016405.3 functioned as a competing endogenous RNA (ceRNA) for miR-22-3p in the cytoplasm and sponged miR-22-3p to release its suppression of ERBB3. 	The results showed that AC016405.3 is highly expressed in BRCA tissues as well as cells and positively correlated with poor prognosis in BRCA patients	Yes	Silencing AC016405.3 obviously repressed the malignant behaviors of BRCA cells. 	34403532
AC114812.8	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	cell lines(T24，UM-UC-3，J82)	Regulation[miR-371b-5p/FUT4 axis]	CCK8//Wound Healing Assay//Luciferase Report Assay//Transwell Assay	 Our findings revealed that AC114812.8 was significantly upregulated in BC and could markedly facilitate the proliferation, migration, and invasion of bladder cancer cells both in vitro and in vivo. Furthermore, duel-luciferase reporter assay revealed that AC114812.8 could regulate the FUT4 expression level by sponging miR-371b-5p to facilitate BC progression. We detected the levels of EMT-related biomarkers in AC114812.8-overexpressing BC cells by western blot analysis and found that AC114812.8 could promote EMT process. Rescue experiments showed that miR-371b-5p could rescue the effect of AC114812.8 on proliferation and metastasis of BC. Our results suggest that AC114812.8 could be a novel prognostic biomarker and therapeutic target for bladder cancer.		Yes	 Our findings revealed that AC114812.8 was significantly upregulated in BC and could markedly facilitate the proliferation, migration, and invasion of bladder cancer cells both in vitro and in vivo.	31706102
AC136007.2	LncRNA	Homo sapiens	Cerebral Ischaemia/Reperfusion Injury	SH-SY5Y cells	Regulation(AMPK/mTOR)	Western Blot//Tunel//qRT-PCR//Cell Apoptosis Assay//EdU Staining//IF	OGD/R downregulated AC136007.2 expression in SH-SY5Y cells, decreased viability by inducing apoptosis, and stimulated secretion of TNF-α, IL-6, and IL-1β. We conclude that AC136007.2 alleviates cerebral I/R injury by suppressing AMPK/mTOR-dependent autophagy.		Yes	OGD/R downregulated AC136007.2 expression in SH-SY5Y cells, decreased viability by inducing apoptosis, and stimulated secretion of TNF-α, IL-6, and IL-1β. 	34419936
circCACTIN	CircRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues	Interaction[Sponging MiR-331-3p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//IHC//Invasion Assay	CircCACTIN expression was obviously up-regulated in GC tissues and cell lines.Binding interactions were detected between circCACTIN and miR-331-3p, and between miR-331-3p and TGFBR1 by Dual-luciferase reporter assays. Mechanistically, we demonstrated that circCACTIN promoted gastric cancer progression by sponging miRNA-331-3p and regulating TGFBR1 mRNA expression. 		Yes	Knockdown of circCACTIN inhibited GC cells proliferation, migration, invasion and EMT. Enforced-expression of circCACTIN promoted GC cells migration, invasion and EMT, but had no effect on GC cells proliferation. Moreover, in vivo experiments, circCACTIN up-regulation promoted GC tumor growth and EMT, and circCACTIN down-regulation inhibited GC tumor growth and EMT. 	31182928
AC245100.4	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa cells	Regulation	qRT-PCR//migration assay//Western Blot	 The AC245100.4 or PAR2 knockdown resulted in a decrease in Vimentin but an increase in E-cadherin protein levels, while the AC245100.4 or PAR2 overexpression got the opposite results. Moreover, we discovered that AC245100.4 activated the p38-MAPK via regulating PAR2. In brief, these results have suggested that AC245100.4 and PAR2 served as oncogenic factors in cellular migration in PCa cells.		Yes	We found that AC245100.4 promoted the migration of prostate cancer cells via regulating PAR2. 	35570225
ADAMTS9-AS1	LncRNA	Homo sapiens	Endometriosis	murine model of EMs	Interaction(miR-6516-5p/GPX4-dependent ferroptosis)	RNA Pull-Down//Western Blot//Tunel//Migration Assay//qRT-PCR//FISH//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	The current data showed that ADAMTS9-AS1 expression was significantly upregulated in ecEM compared with eutopic endometrium (euEM) in patients with EMs and in a murine model of EMs. Taken together, these results demonstrate that upregulated ADAMTS9-AS1 accelerates ESC proliferation and migration by regulating miR-6516-5p/GPX4-dependent ferroptosis and may be a potential target for the treatment of EMs.		Yes	Functionally, ADAMTS9-AS1 knockdown in ectopic ESCs (EESCs) decreased cell viability and migration, whereas ADAMTS9-AS1 overexpression in normal ESCs (NESCs) enhanced cell viability and migration. More importantly, the effect of ADAMTS9-AS1 inhibition on decreasing ESC viability was significantly blocked by ferrostatin-1 (Fer-1, a ferroptosis inhibitor), and ADAMTS9-AS1 overexpression repressed erastin (a ferroptosis activator)-induced cell death. 	35173188
ADAMTS9-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	interaction[Sponging miR-513a-5p]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	ADAMTS9-AS1 was downregulated in breast cancer tissues as well as cell lines. In conclusion, lncRNA ADAMTS9-AS1 inhibited the aggressive phenotypes of breast carcinoma cells via sponging miR-513a-5p and regulating ZFP36.		Yes	Upregulation of ADAMTS9-AS1 suppressed the growth and invasiveness of breast carcinoma cells in vitro as well as inhibiting cellgrowth in vivo.	33149676
ADAMTS14	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues,cell lines	Interaction[miR-572/ RCAN1]	Microarray//PCR//IF	CircADAMTS14 and RCAN1 were lowly expressed in HCC clinical specimens and cell lines using microarrays and qRT-PCR, but miR-572 inversely.		Yes	Overexpressed circADAMTS14 and RCAN1 induced apoptosis of HCC cells and inhibited cell proliferation and invasion. But overexpressed miR-572 could decrease apoptosis of HCC cells and promote proliferation and invasion. In vivo, circADAMTS14 inhibited the tumor growth, correlated positively with the protein expression levels of RCAN1	30317540
ADAM9	CircRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Interaction[ADAM9/miR-217/PRSS3]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	In this research, low miR-217 and high circ-ADAM9 expression were found in PC tissues and cell lines, which was closely associated with advanced clinical stage and lymph node metastasis.Stepwise mechanism studies indicated that circ-ADAM9 alleviated the inhibitory effect of miR-217 on PRSS3 by directly sponging miR-217 to increase the expression level of PRSS3, resulting in the activation of ERK/VEGF signalling pathway. In vivo, circ-ADAM9 silencing or miR-217 overexpression evidently retarded the growth of tumour, and the combination of them exhibited an additive inhibitory effect on tumourigenicity. Briefly, the ceRNA regulatory network of circ-ADAM9/miR-217/PRSS3 plays a pivotal role in PC progression by the regulation of ERK/VEGF signalling pathway.	In this research, low miR-217 and high circ-ADAM9 expression were found in PC tissues and cell lines, which was closely associated with advanced clinical stage and lymph node metastasis. Patients with low miR-217 or high circ-ADAM9 expression had shorter survival time than those with high miR-217 or low circ-ADAM9 expression.	Yes	Functionally, manipulation of miR-217 and circ-ADAM9 expression showed opposite effects on cell proliferation, migration and invasion. 	31810373
ACVR2A	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-1290 )	colony Formation Assay//RNA Pull-Down//Transfection//Colony Formation Assay//CCK8//qRT-PCR//RIP//PCR//IP//Transwell Assay//IF	The relative level of circACVR2A in GC tissues and cell lines is remarkably upregulated. The downregulation of circACVR2A promotes GC cell proliferation and metastasis and suppressed the expression level of E-cadherin and Vimentin. The miR-1290 inhibitor reversed the effect of circACVR2A on cell progression in GC cell.		Yes	 The downregulation of circACVR2A promotes GC cell proliferation and metastasis and suppressed the expression level of E-cadherin and Vimentin. 	35186081
acv3UTR	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue	regulation[miR-590-5p/YAP1 axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	Here, we found that acvr1b gene 3'UTR (acv3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients.Mechanistically, our results suggested that acv3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. 	Here, we found that acvr1b gene 3'UTR (acv3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients.	Yes	Forced expression of acv3UTR promoted GC cells growth in vitro and in vivo.	32066878
ACTA2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells 	Interaction(miR-378a-3p/PLCXD2 axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Reverse transcription-quantitative polymerase chain reaction analyses and subcellular fractionation assays showed that ACTA2-AS1 was lowly expressed in GC cells and was mainly distributed in the cytoplasm. Mechanistically, ACTA2-AS1 served as a competing endogenous RNA (ceRNA) to bind with miR-378a-3p and thereby, antagonized the inhibitory effect of miR-378a-3p on the expression of messenger RNA phosphatidylinositol specific phospholipase C X domain containing 2 (PLCXD2). The binding capacity between miR-378a-3p and ACTA2-AS1 (or PLCXD2) was detected by RNA pulldown assays, luciferase reporter assays and RNA immunoprecipitation assays. Moreover, PLCXD2 knockdown rescued the inhibitory effect of ACTA2-AS1 overexpression on malignant behaviors of GC cells. Overall, ACTA2-AS1 inhibits malignant phenotypes of GC cells by acting as a ceRNA to target miR-378a-3p/PLCXD2 axis.		Yes	Overexpressed ACTA2-AS1 inhibited GC cell viability, proliferation, migration, invasion, and epithelial-mesenchymal transition process, as suggested by cell counting kit-8 assays, colony formation assays, wound healing assays, Transwell assays and Western blot analyses. 	35274046
ACTA2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Expression(lower expressed)	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//FISH//Colony Formation Assay//Transwell Assay	ACTA2-AS1 expression was downregulated in CRC. Collectively, ACTA2-AS1 inhibits the viability, proliferation, migration and invasion of CRC cells to effectively suppress the progression of CRC.		Yes	Overexpressed ACTA2-AS1 repressed the cell viability, proliferation, migration and invasion, increased cleaved caspase-3 level yet decreased PCNA, Bcl-2, MMP-2 and MMP-9 levels. ACTA2-AS1 silencing, however, did oppositely.	35325674
ACTA2-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells 	Interaction(miR-532-5p /CXCL2)	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Compared with paracancerous tissues and HOSEpiC cells, OC tissues and cells showed increased ACTA2-AS1 and CXCL2 expression and decreased miR-532-5p expression (all P<0.05). ACTA2-AS1 acted as ceRNA in OC by negatively regulating miR-532-5p. Moreover, CXCL2, positively correlated with ACTA2-AS1 in expression (P<0.0001, r=0.7385), was the target of miR-532-5p, and its overexpression could partially offset the influence of miR-532-5p on OC cells.		Yes	Additionally, upregulating ACTA2-AS1 intensified the proliferation and invasion of cancer cells and suppressed their apoptosis (all P<0.05), and inhibition of it resulted in opposite results. In contrast, overexpressing miR-532-5p suppressed the proliferation, invasion, and clone formation of the cells and promoted their apoptosis (all P<0.05). The effect of ACTA2-AS1 on OC cells can be partially reversed by overexpressing miR-532-5p. 	34093945
ACTA2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells 	regulation[ ACTA2-AS1/miR-143-3p/SMAD3 axis ]	CCK8//qRT-PCR//Flow Cytometry//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	ACTA2-AS1 was significantly increased in CC tissues and cells and miR-143-3p was down-regulated.  The ACTA2-AS1/miR-143-3p/SMAD3 axis can play a crucial role in cervical carcinogenesis, providing new clues for the early diagnosis and treatment of CC.	Clinically, the higher expression of ACTA2-AS1 was significantly correlated with higher FIGO stage.	Yes	Loss-of-function assay revealed that silencing of ACTA2-AS1 inhibited cell proliferation, colony formation, migration and promoted apoptosis in CC. 	32774166
ACTA2-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	119 patients and cell lines	Interaction(miR-532-5p)	Cell Proliferation Assay//qRT-PCR//Transfection//Luciferase Report Assay	The TNBC tissues were collected from 119 patients, where the reduced level of ACTA2-AS1 and increased level of miR-532-5p were observed by PCR and showed a significantly negative correlation (P < 0.001). Moreover, in TNBC cell, overexpressing ACTA2-AS1 was found to suppress cell proliferation and metastasis, which was reversed by the upregulation of miR-532-5p.	 Both ACTA2-AS1 and miR-532-5p were closely associated with the malignant development and poor prognosis of TNBC patients.	Yes	Moreover, in TNBC cell, overexpressing ACTA2-AS1 was found to suppress cell proliferation and metastasis, which was reversed by the upregulation of miR-532-5p.	35896973
ACTA2-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD samples and cells	regulation[miR-378a-3p and miR-4428,SOX7 ]	qRT-PCR	 In this paper, ACTA2-AS1 was identified as a downregulated lncRNA in LUAD samples and cells.  To summarize, ACTA2-AS1 suppresses the malignant processes of LUAD cells through sequestering miR-378a-3p and miR-4428 to augment SOX7 expression.		Yes	 Functionally, ACTA2-AS1 overexpression restrained cell proliferation but accelerated cell apoptosis in LUAD. In addition, we determined the suppressive effect of ACTA2-AS1 on LUAD cell invasion, migration, and epithelial-mesenchymal transition progress. 	32808728
ACTA2-AS1	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues and cell lines	Expression[lower expressed]	Flow Cytometry//qRT-PCR//Western Blot//Transwell Assay	 As demonstrated in Fig. 1, the expression level of ACTA2-AS1:4 in cancerous tissues collected from 17 patients with liver cancer was significantly downregulated compared with the corresponding adjacent non-cancerous tissues (P<0.05; Fig. 1A). 		Yes	 This inhibition of ACTA2‑AS1:4 expression significantly promoted the proliferation, cell cycle progression, migration and invasion of LM3 cells.	30664183
ACTA2-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	human colon adenocarcinoma tissues and colon adenocarcinoma cell lines	Interaction(miR-4428/BCL2L11)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3' untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone.		Yes	 Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. 	33845844
ACAP2	CircRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissue and colon cancer SW480 cells	Regulation[ACAP2/Hsa-miR-21-5p/ Tiam1]	Western Blot//PCR//IF	CircRNA-ACAP2 and Tiam1 were shown to be highly expressed in colon cancer tissue and colon cancer SW480 cells, but miR-21-5p was expressed at a low level.The present study shows that the circRNA-ACAP2/hsa-miR-21-5p/Tiam1 regulatory feedback circuit could affect the proliferation, migration, and invasion of colon cancer SW480 cells. 		Yes	SW480 cell proliferation was suppressed when the expression of circRNA-ACAP2 and Tiam1 was decreased and the expression of miR-21-5p was increased in vivo and in vitro. 	30212824
ACACA	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-1183 and PI3K/PKB pathway]	Western Blot//qPCR//PCR//IP//IF	The level of circ?ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR?1183.Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.		Yes	Knockdown of circ?ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate.	32236577
AC245100.4	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines	regulation[microRNA-145-5p/RBBP5 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The present study identified that AC245100.4 expression was significantly upregulated in PCa tissues and cell lines.Overall, the present study proposed a novel model in which the AC245100.4/miR‑145‑5p/RBBP5 ceRNA network induced the development of PCa, providing novel insights for PCa treatment.		Yes	Knockdown of AC245100.4 impaired tumor growth in an animal model. Biological function analysis indicated that AC245100.4 overexpression notably promoted cell proliferation and migration, while knockdown of AC245100.4 suppressed cell proliferation and migration. 	33416179
AC245100.4	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate tissues	interaction[binds HSP90 ]	CCK8//qRT-PCR//RIP//FISH	AC245100.4 expression was upregulated in prostate cancer and mainly located in the cytoplasm. AC245100.4 promotes the proliferation of prostate cancer via binding of HSP90.		Yes	 Knockdown of AC245100.4 inhibited proliferation of prostate cancer. 	32811161
AC016405.3	LncRNA	Homo sapiens	Glioblastoma	GBM tissue,cell lines	Interaction[modulation of TET2 by microRNA-19a-5p sponging ]	Western Blot//ISH//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//Transwell Assay	It showed that AC016405.3 was downregulated in GBM tissue specimens and cell lines, and it also illustrated that the downregulated AC016405.3 was closely correlated with several aggressive features of patients with GBM. In summary, the findings of the current study identified a novel lncRNA and illustrated that AC016405.3, acting as an anti-oncogene, suppressed GBM cell proliferation and metastasis by regulating TET through miR-19a-5p sponging. Our present study might provide a new axis in the molecular treatment of GBM.		Yes	Functionally, we found that overexpression of AC016405.3 suppressed GBM cells' proliferation and metastasis using a gain of function experiment.	30888082
AC012668	LncRNA	Mus musculus	Non-alcoholic Fatty Liver Disease	free fatty acid-treated LO2 cells and high-fat diet-fed mice	Interaction(miR-380-5p/LRP2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Microarray//Oil Red O Staining//ELISA	AC012668 expression levels were significantly suppressed in NAFLD models, whereas AC012668 overexpression inhibited lipogenesis-related gene (SCD1, SREBP1, FAS) expression and TG/lipid accumulation in vitro.Subsequently, miR-380-5p was predicted and verified to target AC012668, and its expression was notably increased in the NAFLD cell model.  AC012668 inhibited NAFLD progression via the miR-380-5p/LRP2 axis. 		Yes	AC012668 expression levels were significantly suppressed in NAFLD models, whereas AC012668 overexpression inhibited lipogenesis-related gene (SCD1, SREBP1, FAS) expression and TG/lipid accumulation in vitro.	34511037
AC009948.5	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD samples and cells	Interaction(miR-186-5p/NCAPG2)	In Vivo Experiment//RNA Pull-Down//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	 LncRNA expression microarray data indicate that LncRNA-AC009948.5 is upregulated in LUAD samples. The present study confirmed the upregulation of LncRNA-AC009948.5 in LUAD tissues and cells. Conversely, LncRNA-AC009948.5 upregulated had opposite effects. Mechanistically, we elucidated that LncRNA-AC009948.5 could directly bind to miR-186-5p and subsequently suppress expression of the target gene of NCAPG2.	Encreased expression of LncRNA-AC009948.5 was correlated with tumor size, lymph nodes, distant metastasis and histological grade, and poor prognosis.	Yes	LncRNA-AC009948.5 knockdown significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. 	36059662
AC009022.1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Interaction[suppressing miR-497-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	AC009022.1 expression was abnormally elevated in CRC tissues and cells.  AC009022.1 enhanced CRC cell proliferation, migration, and invasion by promoting ACTR3B expression via suppressing miR-497-5p.	High AC009022.1 expression in CRC patients was significantly associated with poor prognosis.	Yes	 Much lower subcutaneous tumor volume and weight were found in the siAC009022.1 group compared with siNC group (P < .001).	31637768
91H	LncRNA	Homo sapiens	Osteosarcoma	Five pairs of osteosarcoma tissues and adjacent normal tissues	Interaction(CDK4)	CCK8//qRT-PCR//Western Blot	Knockdown of 91 H significantly inhibited the growth of osteosarcoma cells via inducing the cell apoptosis. Meanwhile, knockdown of 91 H inhibited the progression of osteosarcoma via inducing methylation of CDK4 promoter.		Yes	Knockdown of 91 H significantly inhibited the growth of osteosarcoma cells via inducing the cell apoptosis. In addition, 91 H siRNA notably suppressed the migration and invasion of osteosarcoma cells. 	33499776
34936303	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction(miR182/Foxo3a axis)	Western Blot//Transfection//qPCR//PCR//IF	 The expression of CRIM1 in adjacent tissues was significantly down-regulated and negatively correlated with distal migration.  After circRNA CRIM1 was overexpressed, the miR-182 was significantly down-regulated. The expression levels of Foxo3a mRNA and proteins were up-regulated after miR-182 silencing of bladder cancer cell line UMUC3.		Yes	. The overexpression of circRNA CRIM1 reduced migration and invasion processes in bladder cancer cells.	34994952
17A	LncRNA	Homo sapiens	Alzheimer Disease	cell lines	Expression[highly expressed]	Western Blot//Migration Assay//qRT-PCR//Cell Apoptosis Assay//Cell Cycle Assay//ELISA//Invasion Assay//IF	As shown in Figure 1., our data found that the expression level of 17A was significantly enhanced in negative control (NC) cells which had been treated with Aβ 1-42 peptide, compared with that of the normal cells (P < 0.05). 		Yes	These data demonstrated that 17A depletion inhibited cell apoptosis, whereas the up-regulation of 17A promoted apoptosis, as shown in Figure 2.	30652945
1700020I14Rik	LncRNA	Homo sapiens	Hepatitis, Alcoholic	AML12 cell 	Interaction(miR-137/AKR1B10 /Erk signaling)	In Vivo Experiment//Western Blot//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//ELISA//Bioinformatics Analysis//IF	We found elevated AKR1B10 and 1700020I14Rik but reduced miR-137 in AH.1700020I14Rik was able to elevated miR-137-mediated AKR1B10.  In vitro cell experiments and in vivo animal experiments validated that 1700020I14Rik reduced ethanol-induced hepatocyte damage and inflammation in AH mice through regulation of miR-137-mediated AKR1B10/Erk axis. 		Yes	 In vitro cell experiments and in vivo animal experiments validated that 1700020I14Rik reduced ethanol-induced hepatocyte damage and inflammation in AH mice through regulation of miR-137-mediated AKR1B10/Erk axis. 	36028503
hsa_circ_0009910	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Expression[highly expressed]	qRT-PCR//Western Blot	Circ_0009910 expression level was elevated in GC tissues and cell lines and associated with clinical stage (p = 0.032), distant metastasis (p = 0.028) and differentiation (p = 0.007).	Circ_0009910 expression level was elevated in GC tissues and cell lines and associated with clinical stage (p = 0.032), distant metastasis (p = 0.028) and differentiation (p = 0.007).Kaplan-Meier survival analysis indicated that circ_0009910 expression in positive group has a worse overall survival compared to the negative group (p = 0.0013). Multivariate analysis showed that circ_0009910 was an independent risk factor for GC (HR = 2.346, 95% CI: 1.673-3.775, p = 0.006). 	Yes	Knockdown of circ_0009910 expression can suppress BGC823 and AGS cells proliferation, migration and invasion in vitro experiments.	30556864
hsa_circ_0027599	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues 	interaction[miR-101-3p.1]	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	The circRNA expression profile in the gastric cancer tissues by circRNA microarray showed that hsa_circ_0027599 (circ_0027599) was significantly down-regulated in gastric cancer patients and cells when comparing with the controls.The study uncovered that PHLDA1 was regulated by circ_0027599/miR-101, which suppressed gastric cancer survival and metastasis in gastric cancer.		Yes	Circ_0027599 overexpression suppressed gastric cancer cell proliferation and metastasis.	30410722
circYAP1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[miR-367-5p/p27 Kip1 axis]	qRT-PCR//FISH//Luciferase Report Assay//Western Blot	CircYAP1 expression level was significantly lower in GC tissues than the adjacent normal tissues, and GC patients with circYAP1 low expression had shorter survival times as compared with those with circYAP1 high expression. Our findings demonstrate that circYAP1 functions as a tumor suppressor in GC cells by targeting the miR-367-5p/p27 Kip1 axis and may provide a prognostic indicator of survival in GC patients.	CircYAP1 expression level was significantly lower in GC tissues than the adjacent normal tissues, and GC patients with circYAP1 low expression had shorter survival times as compared with those with circYAP1 high expression. 	Yes	Functionally, circYAP1 overexpression inhibited cell growth and invasion in vitro and in vivo, but its knockdown reversed these effects.	30336780
hsa_circ_102958	CircRNA	Homo sapiens	Stomach Neoplasms	CRC tissues and adjacent normal tissues	Regulation[miR-585/CDC25B axis ]	Western Blot//ISH//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that hsa_circRNA_102958 level was increased in tumor tissues (n=58) compared to adjacent normal tissues.Taken together, our findings revealed the novel oncogenic roles of hsa_circRNA_102958 in CRC through miR-585/CDC25B axis.	 	Yes	We showed that hsa_circRNA_102958 silencing markedly suppressed CRC growth, migration and invasion.	31413634
circOSBPL10	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and adjacent tissues 	 Expression[highly expressed]	Western Blot//FISH//Luciferase Report Assay//RNA-seq//PCR	The expression levels of circOSBP10 were significantly higher in GC tissues than in noncancerous tissues (P = 0.0118, Fig. 2a).	 Furthermore, the level of circOSBPL10 was observed to be a prognostic marker of the overall survival and disease-free survival of patients with GC. 	Yes	 In vivo experiments showed that circOSBPL10 promotes tumor growth and metastasis in mice.	31409903
circGRAMD1B	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and noncancerous tissues	Interaction[miR-149]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining	 We screened differentially expressed circRNAs and found that circGRAMD1B expression was Expression[down-expression]regulated in GC tissues and cell lines. Functionally, circGRAMD1B acted as an anti-oncogene and inhibited the proliferation, migration, and invasion abilities of GC cells. Then, we verified that circGRAMD1B served as a sponge that targeted miR-130a-3p in GC cells; circGRAMD1B alleviated GC cell proliferation, migration, and invasion by targeting miR-130a-3p. A mechanistic analysis showed that PTEN and p21 were involved in circGRAMD1B/miR-130a-3p axis-inhibited GC tumorigenesis. Our findings suggest that circGRAMD1B plays an important role in GC progression by regulating miR-130a-3p-PTEN/p21, which may provide a potential biomarker and therapeutic target for GC.		Yes	 We screened differentially expressed circRNAs and found that circGRAMD1B expression was Expression[down-expression]regulated in GC tissues and cell lines. Functionally, circGRAMD1B acted as an anti-oncogene and inhibited the proliferation, migration, and invasion abilities of GC cells. Then, we verified that circGRAMD1B served as a sponge that targeted miR-130a-3p in GC cells; circGRAMD1B alleviated GC cell proliferation, migration, and invasion by targeting miR-130a-3p. A mechanistic analysis showed that PTEN and p21 were involved in circGRAMD1B/miR-130a-3p axis-inhibited GC tumorigenesis. Our findings suggest that circGRAMD1B plays an important role in GC progression by regulating miR-130a-3p-PTEN/p21, which may provide a potential biomarker and therapeutic target for GC.	31719211
hsa_circ_0001461	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Regulation[ miR-346/ FBXL2 axis]	qRT-PCR//FISH	We verified that circFAT1(e2) was significantly Expression[down-expression]regulated in GC tissues and cell lines and was correlated with overall survival of GC patients.Then, we investigated whether circFAT1(e2) acts as a sponge of microRNA-549g(miR-548g) and regulates the expression of tumor sExpression[Expression[up-expression]-expression]pressor RUNX1 in GC cells. Moreover, we found that nucleus-located circFAT1(e2) could directly interact with Y-box binding protein-1 (YBX1) and inhibit its function.		Yes	 Functional assays indicated that overexpression of circFAT1(e2) inhibited GC cell proliferation, migration and invasion.	30419346
circNF1	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[miR-16]	qRT-PCR//RNA-seq//Western Blot	We analyzed next-generation RNA sequencing data from GC tissues and cell lines, identifying 75,201 candidate circRNAs. Among these, we focused on one novel circRNA, circNF1 , which was Expression[Expression[up-expression]-expression]regulated in GC tissues and cell lines. Furthermore, luciferase reporter assays showed that circNF1 binds to miR-16, thereby derepressing its Expression[down-expression]stream target mRNAs, MAP7 and AKT3. Targeted silencing or overexpression of circNF1 had no effect on levels of its linear RNA counterpart, NF1. 		Yes	Loss- and gain-of-function studies demonstrated that circNF1 significantly promotes cell proliferation. 	30576282
circLMTK2	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Expression[Expression[lower expressed]-expression]	CCK8//qRT-PCR//Western Blot//Transwell Assay	CircLMTK2 expression was significantly Expression[down-expression]-regulated in gastric carcinoma tissue specimens (P<0.001) compared with its expression in paired normal tissues.	Furthermore, a Kaplan-Meier analysis revealed that lower levels of circLMTK2 expression were associated with decreased overall survival (OS) (P<0.001), and a multivariate Cox hazards analysis showed that high circLMTK2 expression was an independent factor for OS. 	Yes	Afterward, overexpression of circLMTK2 was performed in gastric cancer cell line MGC-803, and results indicated that malignant biological properties were inhibited by circLTMK2 overexpression. 	30988068
hsa_circ_0001368	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Regulation[miR-6506-5p/FOXO3 axis ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Microarray	In the current study, we found a broad Expression[down-expression]regulation of hsa_circ_0001368 in GC tissues and cells, which correlates with a worse prognosis in GC patients. Mechanically, we demonstrated that hsa_circ_0001368 served as a competing endogenous RNA (ceRNA) to sponge miR-6506-5p. Subsequently, FOXO3 may act as the functional target of miR-6506-5p, and the knockExpression[down-expression] of hsa_circ_0001368 decreased the expression of the tumor-sExpression[Expression[up-expression]-expression]pressive gene FOXO3. 		Yes	Functional experiments suggested that the knockExpression[down-expression] of hsa_circ_0001368 promoted cell viability and motility by cell proliferation and invasion assays.In addition, the knockExpression[down-expression] of hsa_circ_0001368 led to accelerated tumor growth in vivo.	30853185
circNRIP1	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction[AKT1/mTOR pathway]	RNA Pull-Down//Western Blot//CCK8//Luciferase Report Assay//RNA-seq	We detected higher circNRIP1 expression in gastric cancer by performing RNA-seq analysis.Western blot analysis and immunofluorescence assays were performed to demonstrate that the circNRIP1-miR-149-5p-AKT1/mTOR axis is responsible for the altered metabolism in GC cells and promotes GC development.		Yes	We discovered that knockdown of circNRIP1 successfully blocked proliferation, migration, invasion and the expression level of AKT1 in GC cells. 	30717751
hsa_circ_001569	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[absorbing miR-145]	RNA Pull-Down//Western Blot//CCK8//Luciferase Report Assay//PCR	Both circRNA_001569 and NR4A2 were overexpressed in tissues and cells of gastric cancer, while miR-145 was down-regulated.CircRNA_001569 regulated the expression of miR-145, the effect of pcDNA-circRNA_001569 was abolished by miR-145 mimic and the effect of si-circRNA_001569 was abolished by miR-145 inhibitor. MiR-145 targets NR4A2 to regulate its expression. Overexpressed miR-145 sExpression[up-expression]pressed cell viability and promoted cell apoptosis. 		Yes	Overexpressed circRNA_001569 significantly increased cell viability, and decreased cell apoptosis, while down-regulated circRNA_001569 dramatically decreased cell viability and promoted cell apoptosis.	30304349
hsa_circ_0000267	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[sponging MiR-503-5p and regulating HMGA2]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//BrdU//Transwell Assay	Circ_0000267 showed a significant upregulation in GC tissues and cell lines, and its high expression level was extremely linked to the increased tumor diameter and local lymph node metastasis. dual-luciferase reporter gene assay was adopted to verify the targeting relationship between circ_0000267 and miR-503-5p.From the perspective of mechanism, circ_0000267 promoted the progression of GC through adsorbing miR-503-5p and upregulating HMGA2 expression.	Circ_0000267 showed a significant upregulation in GC tissues and cell lines, and its high expression level was extremely linked to the increased tumor diameter and local lymph node metastasis. 	Yes	Circ_0000267 overexpression accelerated GC cell proliferation, metastasis, and EMT processes, while knocking down circ_0000267 led to the opposite effect. 	31845519
hsa_circ_0008035	CircRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissue	Regulation[miR-375/YBX1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	This study aims to uncover the mechanism by which circRNAs regulate gastric cancer tumorigenesis. Among the microarray data, we screened dysregulated circRNAs and identified an up-regulated circRNA, hsa_circ_0008035.  Functionally, the hsa_circ_0008035 silencing by the siRNA transfection inhibited the proliferation and invasion of gastric cancer cells. 		Yes	 Functionally, the hsa_circ_0008035 silencing by the siRNA transfection inhibited the proliferation and invasion of gastric cancer cells. 	31105852
circRanGAP1	CircRNA	Homo sapiens	Stomach Neoplasms	blood	Interaction[targeting miR-877-3p]	Western Blot//Wound Healing Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//IHC	Here, we identified that circ-RanGAP1 was significantly upregulated in both GC tissues and exosomes from the plasma of GC patients.Mechanistically, circ-RanGAP1 sponged miR-877-3p to upregulate VEGFA expression. Overexpression of miR-877-3p reversed the biological functions mediated by circ-RanGAP1 in GC cells. Interestingly, we demonstrated that circ-RanGAP1 was upregulated in plasma exosomes from preoperative GC patients. More importantly, the plasma exosomes derived from these patients enhanced the migration and invasion potential of GC cells.	High circ-RanGAP1 expression was closely associated with an advanced TNM stage, lymph node metastases, and worse survival. 	Yes	 Inhibition of circ-RanGAP1 decreased GC cell invasion and migration in vitro. Overexpression of circ-RanGAP1 had the opposite effect. Additionally, circ-RanGAP1 silencing remarkably suppressed tumor growth and metastasis of GC in vivo. 	31811909
A1BG-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[targeting miR-216a-5p]	qRT-PCR	Further analyses confirmed that A1BG-AS1 expression in HCC was markedly lower than that in noncancerous tissues based on our HCC cohort. A1BG-AS1 positively regulated the levels of phosphatase and tensin homolog and SMAD family member 7, which were reduced by miR-216a-5p in HCC cells. 	 Clinical association analysis revealed that low A1BG-AS1 expression correlated with poor prognostic features, such as microvascular invasion, high tumor grade, and advanced tumor stage. Follow-up data indicated that low A1BG-AS1 level evidently correlated with poor clinical outcomes of HCC patients.	Yes	Moreover, forced expression of A1BG-AS1 repressed proliferation, migration, and invasion of HCC cells in vitro. Conversely, A1BG-AS1 knockdown promoted these malignant behaviors in HepG2 cells. 	30556161
A1BG-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	Interaction(miR-485-5p/FLOT1 pathway)	Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Invasion Assay//Transwell Assay	We found A1BG-AS1 to be highly expressed in breast cancer tissues and cell lines. Mechanistic investigations confirmed that A1BG-AS1 directly interacted with miR-485-5p as a molecular sponge. We demonstrated that FLOT1 is a direct target of miR-485-5p, which could be positively regulated by A1BG-AS1 by competing for miR-485-5p. 		Yes	 In terms of function, depleted A1BG-AS1 markedly suppressed cell proliferation, accelerated cell apoptosis, and hindered cell migration and invasion in breast cancer. Furthermore, A1BG-AS1 interference reduced tumor growth in vivo. 	34115333
A2M-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues and cells	Interaction( miR-587/BMP3)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	In this study, A2M-AS1 was downregulated in LUAD tissues and cells and related to poor prognosis in LUAD patients. Mechanistically, A2M-AS1 directly bound with miR-587 to promote BMP3 expression in LUAD cells. 	In this study, A2M-AS1 was downregulated in LUAD tissues and cells and related to poor prognosis in LUAD patients.  Low expression of BMP3 was found in LUAD tissues and cells and was closely correlated with poor prognosis in LUAD patients. 	Yes	A2M-AS1 overexpression suppressed LUAD cell proliferation, migration and invasion in vitro and inhibited tumor growth in vivo. 	36461613
ABCB10	CircRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	cell lines	Interaction(miR‑1271‑mediated Capn4/Wnt/β‑catenin signaling pathway )	Western Blot//Transfection//qPCR//PCR//IF	circ‑ABCB10 expression was significantly increased in OVCAR3, SKOV3 and CAOV3 cells compared with IOSE80 cells, but was not significantly altered in UWB1.289 cells. miR‑1271 expression was significantly decreased in OVCAR3, UWB1.289, SKOV3 and CAOV3 cells compared with IOSE80 cells. In both SKOV3 and UWB1.289 cells, circ‑ABCB10 negatively regulated miR‑1271, whereas miR‑1271 did not affect circ‑ABCB10.  Moreover, miR‑1271 attenuated the proproliferative, proinvasive and antiapoptotic effects of circ‑ABCB10, and reversed the positive regulation of circ‑ABCB10 on the Capn4/Wnt/β‑catenin signaling pathway. Besides, the luciferase activity assay indicated that circ‑ABCB10 directly bound to miR‑1271.		Yes	Furthermore, circ‑ABCB10 enhanced cell proliferation, invasion and the Capn4/Wnt/β‑catenin signaling pathway, but inhibited cell apoptosis, whereas miR‑1271 suppressed cell proliferation, invasion and the Capn4/Wnt/β‑catenin signaling pathway, but facilitated cell apoptosis.	33760208
AC008972.1	LncRNA	Homo sapiens	Prostatic Neoplasms	 prostate cancer tissues and cell lines 	Interaction( miR-143-3p/TAOK2)	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	High expression of lncRNA AC008972.1 was associated with low overall survival in prostate cancer patients.LncRNA AC008972.1 bound with miR-143-3p and negatively regulated miR-143-3p expression. MiR-143-3p overexpression suppressed prostate cancer malignant behaviors in vitro. TAOK2 expression was decreased by miR-143-3p through the complementary targeting of TAOK2 mRNA. Downregulation of lncRNA AC008972.1 mitigated prostate cancer malignant behaviors in vitro based on miR-143-3p/TAOK2 node. 	High expression of lncRNA AC008972.1 was associated with low overall survival in prostate cancer patients.	Yes	 Downregulation of lncRNA AC008972.1 suppressed prostate cancer progression by inhibiting cell viability, proliferation, migration, and invasion, in addition to the EMT process, whereas cell apoptosis was significantly promoted. Furthermore, the data of xenograft model experiment showed that inhibition of lncRNA AC008972.1 suppressed tumor growth in vivo. 	36094409
AC007639.1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues	Expression(highly expressed)	qRT-PCR//Western Blot	We found that lncRNA AC007639.1 was overexpressed in hepatocellular carcinoma.		Yes	Knocking down of lncRNA AC007639.1 by specific siRNAs or shRNAs promoted cancer cell death. The growth of mouse xenograft tumor created using lncRNA AC007639.1 deficient HepG2 cells was significantly slowed down. 	34540685
AC007207.2	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cell lines	Interaction(miR-1306-5p/SIRT7 Axis)	qRT-PCR//Transwell Assay	We found lncRNA AC007207.2 was over-expressed in OS tissues and cell lines, and this phenomenon was associated with the worse prognosis of OS.Moreover, we found that AC007207.2 promotes proliferation and metastasis of OS cells via the miR-1306-5p/SIRT7 axis. Meanwhile, we found miR-1306-5p remarkably inhibits the malignant behavior of OS cells.	We found lncRNA AC007207.2 was over-expressed in OS tissues and cell lines, and this phenomenon was associated with the worse prognosis of OS.	Yes	Moreover, we found that AC007207.2 promotes proliferation and metastasis of OS cells via the miR-1306-5p/SIRT7 axis. Meanwhile, we found miR-1306-5p remarkably inhibits the malignant behavior of OS cells.	34584454
AC005592.2	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	Regulation(OLFM4)	CCK8//qRT-PCR//Western Blot//Transwell Assay	AC005592.2 was significantly increased in CRC tissues and cells. In addition, AC005592.2 positively regulated the expression of olfactomedin 4 (OLFM4), which was also upregulated in CRC tissues.	 High expression of AC005592.2 was significantly associated with TNM stage and tumor differentiation in CRC patients.	Yes	Knockdown of AC005592.2 suppressed CRC cell proliferation, invasion and migration but promoted apoptosis, while AC005592.2 overexpression exerted the opposite effects on CRC cells. 	33622275
AC002454.1	LncRNA	Homo sapiens	Endometriosis	endometrium tissues	Interaction[CDK6 ]	qRT-PCR	We confirmed AC002454.1 and CDK6 mRNA and protein were highly expressed in ectopic and eutopic endometrial tissue from patients with EMS and were clearly correlated. AC002454.1 and CDK6 may have synergistic effects, thereby affecting the biological behavior of endometrial cells, and thus promote the progression of EMS.		Yes	In vitro, both AC002454.1 and CDK6 positively regulated the proliferation, migration and invasion ability of eutopic endometrial cells and could promote the transformation of cells from G0/G1 phase to S phase.	30884467
ABCC6P2	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction[HNF4A ]	qRT-PCR	Quantitative real-time polymerase chain reaction (RT-PCR) implied that NR_023387 was significantly downregulated in RCC tissues and cell lines.Our combined analysis identifies a tumor-suppressive and prognosis-related lncRNA NR_023387, which is silenced in RCC via promoter hypermethylation and HNF4A deficiency, and may exert its tumor-suppressive roles by downregulating the oncogenic MGP.	Quantitative real-time polymerase chain reaction (RT-PCR) implied that NR_023387 was significantly downregulated in RCC tissues and cell lines, and lower expression of NR_023387 was correlated with shorter overall survival. 	Yes	Functional experiments demonstrated NR_023387 exerted tumor-suppressive roles in RCC via suppressing the proliferation, migration, invasion, tumor growth, and metastasis of RCC.	31432508
ABCC6P1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 PTC tissues and cells	Regulation(Wnt/β-catenin pathway)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay//Transwell Assay	The expression of ABCC6P1 was upregulated in PTC tissues and cells. In addition, knockdown of ABCC6P1 caused a significant decrease in levels of Wnt/β-catenin signaling pathway members (including β-catenin, c-myc, and cyclin D1) in PTC cells.		Yes	ABCC6P1 silencing could significantly suppress the proliferation, colony formation ability, migratory and invasive ability in PTC cells. Moreover, knockdown of ABCC6P1 induced cell cycle arrest at G0/G1 phase and inhibited epithelial-mesenchymal transition (EMT) process of PTC cells by increasing the E-cadherin expression, but downregulating N-cadherin and vimentin expression. 	33987362
ABCB10	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines 	Interaction(miR-1915-3p/Rac1 axis)	colony Formation Assay//Western Blot//Transfection//Colony Formation Assay//Flow Cytometry//qRT-PCR//IF//PCR//IHC//Transwell Assay	 Circ-ABCB10 expression was upregulated in GC tissues and cell lines and positively correlated with poor survival of GC patients. Circ-ABCB10 could upregulate Rac1 expression by directly sponging miR-1915-3p. Rescue experiments revealed that miR-1915-3p inhibitor obviously reversed the inhibitory effect of si-circ-ABCB10, and Rac1 overexpression obviously reversed the inhibitory effect of miR-1915-3p mimics on cell growth, invasion, migration, apoptosis, and cell cycle progression.		Yes	Circ-ABCB10 downregulation decreased cell viability, inhibited cell growth, invasion, and migration, while promoted cell apoptosis of GC cell lines SGC-7901 and MKN-48. Moreover, si-circ-ABCB10 effectively inhibited tumor growth in a xenograft model.	34987010
ABCB10	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC cells	Interaction(miR-588/CXCR4 axis)	colony Formation Assay//Western Blot//Wound Healing Assay//Colony Formation Assay//qRT-PCR//RIP//MTT//PCR//IP//Transwell Assay//IF	Here, we were interested in the role of circABCB10 in the modulation of LSCC progression. Mechanically, circABCB10 served as a sponge for microRNAs-588 (miR-588) and miR-588 could target and down-regulated chemokine receptor 4 (CXCR4) expression in LSCC cells. Thus, we concluded that circABCB10 was involved in the malignant progression of LSCC by regulating miR-588/CXCR4 axis. 		Yes	Our data demonstrated that the depletion of circABCB10 significantly inhibited the proliferation and induced the apoptosis of LSCC cells.Meanwhile, circABCB10 knockdown was able to remarkably reduce the invasion and migration of LSCC cells. 	34015764
A2M-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer cells	Interaction(PCBP3)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	The overexpression of A2M-AS1 promoted ferroptosis in the pancreatic cancer, which was inhibited by the silencing of A2M-AS1. Mechanically, A2M-AS1 could directly interact with the poly (rC) binding protein 3 (PCBP3), which plays an important role in the process of iron metabolism, thereby promoting the ferroptosis in pancreatic cancer. In addition, the A2M-AS1/PCBP3 axis could facilitate the p38 activation and inhibit the phosphorylation of the AKT-mTOR signaling pathway; all these participate in regulating ferroptosis. In conclusion, the regulation of ferroptosis by targeting the A2M-AS1/PCBP3 axis might provide a novel target for the treatment of pancreatic cancer in the future.		Yes	The overexpression of A2M-AS1 promoted ferroptosis in the pancreatic cancer, which was inhibited by the silencing of A2M-AS1. Mechanically, A2M-AS1 could directly interact with the poly (rC) binding protein 3 (PCBP3), which plays an important role in the process of iron metabolism, thereby promoting the ferroptosis in pancreatic cancer. 	35920801
ABCA15P	LncRNA	Homo sapiens	Stomach Neoplasms	 gastric cancer cells and tissues	Interaction(CRYM)	Western Blot//qRT-PCR//RIP//MTT//ChIP	 CRYM-AS1 was low expressed in gastric cancer cells and tissues compared with normal gastric cells and tissues respectively. Forced expression of CRYM rescued the decreased aerobic glycolysis and cell proliferation induced by CRYM-AS1 in gastric cancer cells.	 CRYM-AS1 was negatively correlated with TNM staging, tumor size, and overall survival (OS) rate in gastric cancer patients. 	Yes	CRYM-AS1 inhibited gastric cancer cell aerobic glycolysis and cell proliferation. CRYM-AS1 directly bound to EZH2 and mediated the CRYM promoter methylation and consequently negatively regulated the expression of CRYM. 	35414504
AB209371	LncRNA	Homo sapiens	ovarian carcinoma	OC tissues 	Regulation[down-regulating miR-203  ]	CCK8//qRT-PCR//Western Blot	We found that AB209371 gene and Survivin gene were up-regulated in OC and positively correlated with OC development.Therefore, AB209371 may down-regulate miR-203 to up-regulate Survivin, thereby promoting OC cell proliferation. Our study provided novel insights into the pathogenesis of OC.	AB209371 over-expression led to up-regulated Survivin in OC cells, while Survivin over-expression failed to affect AB209371. 	Yes	In addition, over-expressions of AB209371 and Survivin resulted in the increased proliferation rate of OC cells.	31601255
AATBC	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer patients	Interaction(YBX1 and activating the YAP1/Hippo signaling pathway)	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//Co-IP//RIP//IF//Luciferase Report Assay//IHC//Transwell Assay	 In this study, the lncRNA apoptosis-associated transcript in bladder cancer (AATBC) was found to be significantly highly expressed in breast cancer patients. Further studies revealed that AATBC activated the YAP1/Hippo signaling pathway through the AATBC-YBX1-MST1 axis. This is also an important supplement to the composition of the YAP1/Hippo signaling pathway. 		Yes	 In vitro and in vivo experiments indicated that AATBC promoted breast cancer metastasis. 	33951538
AATBC	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	Interaction(miR-1245b-5p)	Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Significant upregulation of AATBC and reduced miR-1245b-5p level in cervical cancer were observed, which showed a negative correlation between their expression levels. Close relationships of AATBC and miR-1245b-5p with the FIGO stage and lymph node metastasis were revealed. AATBC showed a significant prognostic value and miR-1245b-5p was found to mediate the tumor inhibitory effect of AATBC knockdown, which is speculated to be the underlying molecular mechanism of AATBC in cervical cancer development. 	Upregulation of AATBC indicted the malignant development and adverse prognosis of cervical cancer. 	Yes	 Close relationships of AATBC and miR-1245b-5p with the FIGO stage and lymph node metastasis were revealed. AATBC showed a significant prognostic value and miR-1245b-5p was found to mediate the tumor inhibitory effect of AATBC knockdown, which is speculated to be the underlying molecular mechanism of AATBC in cervical cancer development. 	36420764
AATBC	LncRNA	Homo sapiens	Nasopharyngeal carcinoma		regulation[miR-1237-3p-PNN-ZEB1 axis]	Western Blot//ISH//qRT-PCR//Luciferase Report Assay//Transwell Assay	 AATBC was found to be highly expressed in nasopharyngeal carcinoma (NPC), and increased AATBC expression was associated with poor survival in patients with NPC. Collectively, our results indicate that AATBC promotes NPC progression through the miR-1237-3p-PNN-ZEB1 axis.	 AATBC was found to be highly expressed in nasopharyngeal carcinoma (NPC), and increased AATBC expression was associated with poor survival in patients with NPC. 	Yes	 Furthermore, AATBC promoted migration and invasion of NPC cells in vitro, as well as metastasis in vivo.	32364663
AATBC	LncRNA	Homo sapiens	Prostatic Neoplasms	Pca tissues	Interaction(miR-1245b-5p/CASK Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	Firstly, we certified that the expression of AATBC was augmented in PCa, and knockdown of AATBC could significantly inhibit the growth of PCa in vitro and in vivo.  Mechanistically, our results manifested that AATBC could directly bind to miR-1245b-5p. In addition, miR-1245b-5p played cancer-suppressive role in PCa cells. Moreover, CASK was attested as the target of miR-1245b-5p, and CASK was demonstrated to exert as oncogene in the progression of PCa. 		Yes	Firstly, we certified that the expression of AATBC was augmented in PCa, and knockdown of AATBC could significantly inhibit the growth of PCa in vitro and in vivo. 	34234553
A2M-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	interaction[Sponging microRNA-146b to Upregulate MUC19]	RNA Pull-Down//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	A2M-AS1 and MUC19 were highly expressed in BC, while miR-146b was poorly expressed. Taken above together, an oncogenic role for A2M-AS1 in BC was elicited by acting as a miR-146b sponge to promote MUC19 expression. The findings will present some cues for a further approach to BC.		Yes	A2M-AS1 accelerated BC cell proliferation, invasion, and colony formation and suppressed apoptosis via the miR-146b/MUC19/Hippo axis, which was confirmed in vivo.	33273850
A2M-AS1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	Of these lncRNAs, A2M-AS1, a lncRNA that has not been previously reported, was significantly upregulated in human breast cancer tissues compared with adjacent nontumour tissues.		Yes	 The results revealed that A2M-AS1 significantly promotes human breast cancer cell proliferation, invasion, and migration.	32352014
ARHGAP10	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues, cells, and serum-derived exosomes	Interaction( miR-638/FAM83F Axis)	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	circARHGAP10 was upregulated in NSCLC tissues, cells, and serum-derived exosomes.Serum-derived exosomes boosted the expression of circARHGAP10 in NSCLC cells. Also, miR-638 acted as a target of circARHGAP10, miR-638 overexpression overturned circARHGAP10 upregulation-mediated acceleration of proliferation, migration, invasion, and glycolysis of NSCLC cells. Besides, miR-638 targeted FAM83F and FAM83F overexpression abolished miR-638 enhancement-mediated proliferation, migration, invasion, and glycolysis of NSCLC cells.		Yes	circARHGAP10 depletion repressed proliferation, migration, invasion, and glycolysis of NSCLC cells in vitro, and curbed tumor growth in vivo.	32783691
ARHGAP27P1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines,blood	Interaction[regulating p15 and p16]	IHC//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//RIP//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//ChIP	Herein, we confirmed that ARHGAP27P1 was significantly downregulated in GC tissues, plasma and cells. Mechanistic investigations showed that ARHGAP27P1 had a key role in G0/G1 arrest. We further demonstrated that ARHGAP27P1 was associated with Jumonji-domain containing 3 (JMJD3) and that this association was required for the demethylation of H3K27me3, thereby epigenetically activating expression of p15, p16 and p57. Moreover, knockdown of JMJD3, p15, or p16 consistently reversed the inhibitory effects of ARHGAP27P1 in cell proliferation and cell cycle progression. 	Low expression of ARHGAP27P1 was closely associated with advanced TNM stage, increased invasion depth and lymphatic metastasis. Low ARHGAP27P1 expression also predicted a poor prognosis in GC patients.	Yes	Functionally, overexpression of ARHGAP27P1 inhibited proliferation, invasion, and migration in GC cells, while silencing of ARHGAP27P1 showed the opposite effects.	31665700
ARHGAP42	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal carcinoma tissues and cell lines	Regulation[PI3K/Akt signaling pathway]	Transwell Assay//qRT-PCR//IHC//Western Blot	We confirmed the elevated expression of ARHGAP42 in metastatic NPC tissues of mRNA and protein for the first time.	Immunohistochemical analysis indicated that NPC patients with highly ARHGAP42 expression were significantly associated with shorter metastasis-free survival.	Yes	Knockdown of ARHGAP42 resulted in significant inhibition of nasopharyngeal cancer cell migration and invasion in vitro, and the overexpression of ARHGAP42 showed the opposite effects. 	29936709
CASC15	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues	Interaction[downregulate miR-124]	qRT-PCR	We found that CASC15 was upregulated, while miR-124 was downregulated in TSCC tissues than in non-cancer tissues of TSCC patients. CASC15 and miR-124 predict TSCC patients' survival and CASC15 may downregulate miR-124 to inhibit TSCC cell migration and invasion.		Yes	CASC15 overexpression resulted in the increased, while miR-124 overexpression resulted in the decreased migration and invasion rates of TSCC cells.	31665008
CASC15	LncRNA	Homo sapiens	Ischemic Stroke	AIS patients	Interaction(miR-338-3p/ETS1 Axis)	Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//ELISA	The expression of CASC15 was increased and the levels of miR-338-3p were decreased in AIS patients.. A positive association between CASC15 and NIHSS score and an inverse association between CASC15 and miR-338-3p were revealed by Pearson correlation. Silenced CASC15 exerted neuroprotective roles on cell viability, apoptosis, and inflammation via the miR-338-3p/ETS1 axis.	A positive association between CASC15 and NIHSS score and an inverse association between CASC15 and miR-338-3p were revealed by Pearson correlation. 	Yes	Silenced CASC15 exerted neuroprotective roles on cell viability, apoptosis, and inflammation via the miR-338-3p/ETS1 axis.	34629895
CASC15	LncRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues 	Regulation(PRDX2/PI3K/AKT Axis)	Western Blot//Transfection//qPCR//Flow Cytometry//FISH//IF//Transwell Assay	CASC15 is highly expressed in ICC tissues and is related to higher TNM stage. Downregulation of CASC15 inhibited phosphoinositide 3-kinase (PI3K)/AKT/c-Myc pathway through downregulating of PRDX2 and overexpressed PRDX2 rescued the block. 	CASC15 is highly expressed in ICC tissues and is related to higher TNM stage. 	Yes	Knockdown of CASC15 in ICC cells reduced cell proliferation, migration, invasiveness and increased apoptosis, and G1/S block. PRDX2 bound to CASC15. Knockdown of CASC15 decreased PRDX2 expression which was rescued by the inhibition of proteasome formation.  Downregulation of PRDX2 resulted in G1/S block, reduced ICC cell invasion. CASC15 knockout in ICC xenografts suppressed tumor development in vivo, decreased the expression of PRDX2 and Ki67 and inhibited PI3K/AKT pathway.	33017884
CASC15	LncRNA	Homo sapiens	Neonatal Sepsis	Serum	Interaction(miR-144-3p )	qRT-PCR//Transfection//ELISA//Luciferase Report Assay	 Serum CASC15 was upregulated in NS patients, and it had the ability to distinguish NS patients from NP patients.  Besides, serum miR-144-3p was reduced in NS patients, and luciferase reporter genes showed that miR-144-3p was a direct target of CASC15. 		Yes	 LPS stimulation increased the expression of CASC15 and simultaneously stimulated the secretion of inflammatory cytokines, while the knockdown of CASC15 alleviated the inflammatory response induced by LPS stimulation. 	34870560
CASC11	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Expression[highly expressed]	qRT-PCR//Transwell Assay	LINC01116 and lncRNA CASC11 were both upregulated in cancer tissues compared to cancer-adjacent tissues.	 Expression levels of LINC01116 and CASC11 were increased with the increase in clinical stages. 	Yes	Overexpression of LINC01116 and CASC11 led to promoted invasion and migration of gastric cancer cells.	31632064
CASC11	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues ,cell lines (A547, H157 and SPC-A-1) 	Regulation[microRNA-302/CDK1 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 CASC11 and CDK1 were highly expressed, whereas microRNA-302 was lowly expressed in lung cancer tissues. Identically, CASC11 was highly expressed in lung cancer cell lines (A547, H157 and SPC-A-1) than controls as well.Dual-luciferase reporter gene assay verified that CASC11 could bind to microRNA-302 and microRNA-302 could bind to CDK1. CDK1 expression in lung cancer cells was negatively regulated by CASC11. MicroRNA-302 knockdown reversed the inhibitory effect of CASC11 on CDK1 expression. The proliferation of lung cancer cells co-transfected with microRNA-302 inhibitor and si-CASC11 decreased compared with those transfected with microRNA-302 inhibitor.		Yes	CASC11 knockdown attenuated proliferative capacity of lung cancer cells.	31378894
CASC11	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells	Interaction(miR-646 and miR-381-3p/RAB11FIP2 axis)	CCK8//qRT-PCR//Western Blot	 We found that CASC11 binds to miR-646 and miR-381-3p in the cytoplasm of CRC cells.We further confirmed that RAB11FIP2 is a mutual target of miR-646 and miR-381-3p. The expression levels of CASC11 and RAB11FIP2 in CRC were positively correlated and reciprocally regulated. Further study showed that CASC11 played an important role in regulating PI3K/AKT pathway by miR-646 and miR-381-3p/RAB11FIP2 axis.		Yes	Moreover, miR-646 and miR-381-3p inhibitors reversed the suppressive effect of CASC11 silencing on CRC growth and metastasis in vitro and in vivo. 	33937069
CASC11	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[inhibiting miRNA-188-5p]	CCK8//qRT-PCR	In the present study, we found that CASC11 was up-regulated, while miR-188-5p was down-regulated in tumor tissues of HCC patients.Expression levels of CASC11 and miR-188-5p were inversely correlated in tumor tissues. CASC11 overexpression mediated the down-regulation of miR-188-5p, while miR-188-5p overexpression failed to affect CASC11 expression. In addition, miR-188-5p overexpression attenuated the enhancing effects of CASC11 overexpression on cancer cell proliferation. Therefore, LncRNA CASC11 promoted cancer cell proliferation in HCC possibly by inhibiting miR-188-5p.	 Follow-up study showed that high levels of CASC11 were significantly correlated with poor survival.	Yes	CASC11 overexpression led to promoted, while miR-188-5p overexpression led to inhibited proliferation of cells of HCC cell lines. CASC11 overexpression showed no significant effects on cancer cell migration and invasion.	30910841
CASC11	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[binding with EZH2]	Northern Blot//ChIP//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//IF	 CASC11 was found to be overexpressed in HCC tissues and cell lines and predicted a poor prognosis.Mechanically, the enhancer of zeste homolog 2 (EZH2) was found to be a binding partner of CASC11. Moreover, CASC11 epigenetically silenced PTEN by binding with EZH2. 	 CASC11 was found to be overexpressed in HCC tissues and cell lines and predicted a poor prognosis.	Yes	 Loss of CASC11 function efficiently suppressed cell migration, invasion and epithelial-mesenchymal transition (EMT). 	30503497
CASC11	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Interaction(UBE2T)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 In this context, here, it was found that CASC11 was upregulated in HCC tissues and associated with tumor grades, metastasis, and prognosis of HCC patients. Mechanistically, CASC11 associated with and stabilized Ubiquitin-conjugating enzyme E2T (UBE2T) mRNA. 	 In this context, here, it was found that CASC11 was upregulated in HCC tissues and associated with tumor grades, metastasis, and prognosis of HCC patients. 	Yes	 Functionally, CASC11 facilitated HCC cell proliferation, migration, and invasion in vitro, and enhanced tumor growth and metastasis in vivo.	34900723
CASC11	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	blood	Interaction[miRNA-150 ]	CCK8//qRT-PCR//Transwell Assay	 In this study we showed that plasma lncRNA CASC11 was upregulated.Altered expression of plasma lncRNA CASC11 and miRNA-150 separated patients with bladder cancer from healthy controls. lncRNA CASC11 expression was inversely correlated with miRNA-150 expression in patients with bladder cance but not in healthy controls. Overexpression of lncRNA CASC11 mediated the inhibition of miRNA-150 expression in cancer cells, while miRNA-150 overexpression did not significantly alter lncRNA CASC11 expression.		Yes	 lncRNA CASC11 overexpression promoted, while miRNA-150 overexpression inhibited cancer cell proliferation. 	30916832
CASC11	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	regulation[Wnt/β-catenin and JAK2/STAT3 signaling pathways]	Western Blot//Flow Cytometry//qRT-PCR//BrdU//Transwell Assay	 CARLo-7 was dramatically upregulated in BC tissues and cell lines.Collectively, CARLo-7 plays a critical role in regulating BC development by regulating cell proliferation, migration, invasion, and EMT through Wnt/β-catenin and JAK2/STAT3 signaling. Therefore, CARLo-7 might be a promising therapeutic target for BC.		Yes	Silencing CARLo-7 by sh-CARLo-7 significantly suppressed proliferation and induced apoptosis of BC cells, while enforced CARLo-7 expression promoted cell proliferation. 	33209690
CASC11	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues , cell lines	Regulation[activating Wnt/beta-catenin signaling pathway]	qRT-PCR//Luciferase Report Assay//Western Blot	 We discovered that CASC11, the expression of which was positively associated with the tumor size and the FIGO staging and negatively related to the patients' survival rate, was Expression[Expression[up-expression]-expression]-regulated in the cervical cancer tissues and cell lines. 		Yes	Silencing CASC11 inhibited the proliferation, migration as well as invasion and promoted the cell apoptosis. Conversely, overexpression of CASC11 facilitated the cancer cell's proliferation, migration and invasion ability and sExpression[Expression[up-expression]-expression]pressed the apoptosis. 	31255182
CASC11	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	Interaction[SP1/CASC11/miR-498/FOXK1]	ChIP//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this work, we found that lncRNA CASC11 was significantly up-regulated in the glioma specimens and cells, and the ectopic overexpression indicated the poor prognosis of glioma patients. Taken together, the data suggest the regulation of SP1/CASC11/miR-498/FOXK1 in the gliomagenesis, which might provide a potential therapeutic strategy for glioma.		Yes	 In vivo and vitro, the knockdown of CASC11 impaired the proliferation, migration and tumor growth of glioma cells. 	31121483
CASC11	LncRNA	Homo sapiens	Atherosclerosis	blood	Regulation[downregulating IL-9 ]	qRT-PCR	 In the present study we found that CASC11 was downregulated, while IL-9 was upregulated in plasma of atherosclerosis patients compared with healthy controls.  Therefore, CASC11 may improve atherosclerosis by downregulating IL-9 and regulating VSMC apoptosis and proliferation.		Yes	CASC11 overexpression also resulted in the downregulation of proliferation and promoted apoptosis of VSMC.	30915898
CASC11	LncRNA	Homo sapiens	esophageal carcinoma	ECa tissues	Interaction[regulating KLF6]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	In this work, the qPCR results showed that the expression level of lncRNA CASC11 in the ECa tissues was remarkably higher than that of the adjacent normal tissues, and the difference was statistically significant (p<0.05).The Western Blot results revealed that protein expression of KLF6 was remarkably up-regulated after lncRNA CASC11 knockdown. In addition, the recovery experiments found that lncRNA CASC11 and KLF6 had mutual regulation, thereby promoting the malignant progression of ECa.	Compared with patients with a low level of lncRNA CASC11, the pathological stage of patients with high expression was significantly higher, while the overall survival rate was lower (p<0.05).	Yes	Compared with negative control (NC) group, the proliferation ability of the cells in the lncRNA CASC11 knockdown group CASC11 significantly decreased, whereas cell apoptosis remarkably increased (p<0.05). 	31696474
CASC11	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cells	Interaction(YBX1/p53 signaling axis)	In Vivo Experiment//Wound Healing Assay//Flow Cytometry//qRT-PCR//RNA-seq	 The present results revealed that CASC11 was dominantly distributed in the nuclei of PCa cells, and was highly expressed in PCa tissues and cells. In conclusion, the present study suggested that CASC11 may regulate PCa progression and elucidated a novel CASC11/YBX1/p53 signaling axis, providing a potential lncRNA‑directed therapeutic strategy particularly for the treatment of patients with PCa.		Yes	Overexpression of CASC11 was markedly associated with increased tumor proliferation and migratory ability. Functionally, decreased proliferation and migration, as well as inhibited xenograft tumor growth, were observed in CASC11?silenced PCa cells, whereas the opposite effects were detected in CASC11?overexpressing cells. 	35904175
CASC11	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	blood	Interaction[TGF-β1]	qRT-PCR	Plasma CASC11 and TGF-β1 were upregulated and positively correlated in SCLC patients, but not in healthy controls. Overexpression of CASC11 and TGF-β1 also resulted in the increased percentage of CDD133+ cells of SCLC cell lines, while TGF-β inhibitor attenuated the effects of CASC11 overexpression. CASC11 overexpression mediated the upregulation of TGF-β1 in SCLC cells, while treatment with exogenous TGF-β1 showed no significant effect on CASC11.	Upregulation of plasma CASC11 and TGF-β1 predicted poor survival of SCLC patients.	Yes	Overexpression of CASC11 and TGF-β1 also resulted in the increased percentage of CDD133+ cells of SCLC cell lines, while TGF-β inhibitor attenuated the effects of CASC11 overexpression. 	30965130
CASC11	LncRNA	Homo sapiens	Pituitary Neoplasms	PA tissues and cell 	Interaction( lncRNA MYMLR/miR-197-3p/CBR1)	In Vivo Experiment//IHC//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Transwell Assay	 LncRNA MYMLR was highly expressed in PA tissues compared with that in normal tissues. Mechanistically, MYMLR functioned as a competing endogenous RNA (ceRNA) sponging microRNA miR-197-3p. Furthermore, miR-197-3p exerted its tumor inhibitory role via negatively regulating carbonyl reductase 1 (CBR1). Overexpression of CBR1 antagonized the inhibitory effect of lncRNA MYMLR knockdown or miR-197-3p overexpression. In addition, xenograft tumor model revealed that knockdown of lncRNA MYMLR suppressed PA tumor development in vivo via regulating CBR1.		Yes	 Knockdown of MYMLR suppressed cell proliferation, migration and invasion, while promoting PA cell apoptosis.	36206098
CASC11	LncRNA	Homo sapiens	Neuroblastoma	neonatal neuroblastoma tissues and cells	Interaction[sequestered miR-676-3p]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Highly expressed CASC11 was observed in neonatal neuroblastoma tissues and cells. CASC11 sequestered miR-676-3p from NOL4L to facilitate neonatal neuroblastoma progression, hinting a CASC11-mediated therapeutic target for neonatal neuroblastoma.	High level of CASC11 indicated unsatisfactory survival of neonatal neuroblastoma patients. 	Yes	 CASC11 depletion inhibited cell proliferation and invasiveness. 	31645055
CASC15	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC samples and cell lines	interaction[miR-33a-5p]	qRT-PCR//Western Blot	Here, we identified that CASC15 expression was upregulated in TSCC samples and cell lines.  These results suggested that lncRNA CASC15 and miR-33a-5p might be exploited as new markers of TSCC and were potential treatment targets for TSCC patients.		Yes	We showed that overexpression of CASC15 promoted cell proliferation, cycle, and migration in TSCC.	29804249
CASC15	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Regulation[Wnt/β-Catenin Signaling Pathway]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The expression of CASC15 and β-catenin was upregulated in melanoma tissues and cells. Our study demonstrated that CASC15 promoted the proliferation, migration, and invasion of melanoma cells via activating Wnt/β-catenin signaling pathway, implying that CASC15 might be a potential therapeutic target and prognostic biomarker for melanoma.		Yes	 Furthermore, inhibition of CASC15 decreased proliferation and increased apoptosis of melanoma cells by downregulating Survivin and Bcl-2 and upregulating Bax in A375 and SK-MEL-28 cells. Silencing of CASC15 inhibited migration and invasion of melanoma cells by repressing EMT process.	31838468
CARMN	miRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[Wnt signaling pathway]	Western Blot//qPCR//CCK8//PCR//IF	miR143HG expression was markedly downregulated in HCC tissues and cells.miR143HG inhibits miR-155 expression; miR-155 directly targets APC, which is a negative regulator of the Wnt/β-catenin pathway, so miR143HG can act on the Wnt pathway. miR143HG was further found to reduce the expression of β-catenin and block the nuclear accumulation of β-catenin, ultimately inhibiting the activation of the Wnt pathway. It inhibits the expression of Wnt downstream target gene ZEB1, and then E-cadherin expression is increased and cell motility is inhibited. Furthermore, miR143HG exerts its antiproliferative function by influencing the MAPK signaling pathway and then inducing G2 /M arrest in cells.	 Additionally, miR143HG expression predicted a good prognosis and acted as an independent prognostic factor in HCC for overall survival.	Yes	Overexpression of miR143HG suppressed HCC cell proliferation and metastasis, and induced cell cycle arrest and apoptosis. Consistently, the depletion of miR143HG resulted in the opposite phenomenon of the aforementioned results. 	30945380
CASC15	LncRNA	Homo sapiens	Melanoma	melanoma tissues 	interaction[PDCD4]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//cell invasion assay//Cell Cycle Assay	We found that CASC15 expression was up-regulated in melanoma tissues and associated with advanced pathological stages. CASC15 acts as an oncogene by negatively regulating PDCD4 expression via recruiting EZH2 and subsequently increasing H3K27me3 level.		Yes	 Function experiments displayed that CASC15 knockdown hindered proliferation, facilitated apoptosis and suppressed invasion, while CASC15 overexpression facilitated proliferation and invasion in melanoma cells.	30013768
CASC19	LncRNA	Homo sapiens	Osteoarthritis	OA tissues and cells	Interaction(miR-152-3p/DDX6 axis)	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA	CASC19 was verified to exhibit higher expression in OA tissues and cells. Moreover, inhibition of CASC19 weakened proinflammatory cytokine (IL-6, IL-8, and TNF-α) production and cell apoptosis but facilitated cell viability. Experiments of the ceRNA mechanism elucidated that miR-152-3p was a sponge for CASC19, and miR-152-3p targeted DDX6, suggesting that CASC19 sponged miR-152-3p to release DDX6. Finally, results from rescue assays proved that the impacts of CASC19 silencing on chondrocytes apoptosis and proinflammatory cytokine production could be reversed by DDX6 overexpression.		Yes	 CASC19 was verified to exhibit higher expression in OA tissues and cells.Finally, results from rescue assays proved that the impacts of CASC19 silencing on chondrocytes apoptosis and proinflammatory cytokine production could be reversed by DDX6 overexpression.	34158095
CASC19	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[miR-454-3p/RAB5A axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//BrdU//Transwell Assay	The results revealed that CASC19 expression was significantly upregulated in glioma tissues and cell lines. The results demonstrated that the CASC19/miR‑454‑3p/RAB5A axis is involved in the promotion of glioma progression.	 CASC19 expression was also positively associated with tumor diameter and pathological grade. Additionally, its high expression was closely associated with tumor MRI signal heterogeneity and peritumoral edema. 	Yes	 CASC19 upregulation promoted glioma cell proliferation and metastasis, while CASC19?knockdown demonstrated the opposite effect.	33416169
CASC19	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	regulation[miR-148b/E2F7 axis]	qRT-PCR//MTT//Tunel//Transwell Assay	 The results elucidated that CASC19 expression was markedly increased in PC tissues and cell lines. The CASC19/miR-148b/E2F7 axis might be a new study direction for PC treatment.	 Patients with high expression of CASC19 had a short survival time.	Yes	Silencing of CASC19 attenuated PC cell proliferation, migration, and invasion.	33155202
CASC19	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cell lines	regulation[CASC19/miR-532/ETS1 regulatory pathway]	qRT-PCR//MTT//Colony Formation Assay	CASC19 was overexpressed in ccRCC tissues and cell lines.The CASC19/miR-532/ETS1 regulatory pathway is crucial for the malignant manifestations of ccRCC, which makes it an attractive target for potential treatments of ccRCC.	 High expression of CASC19 was closely associated with unfavorable clinicopathological parameters and predicted negative clinical outcomes in patients with ccRCC. 	Yes	Knockdown of CASC19 decreased ccRCC cell proliferation, colony formation, migration, and invasiveness, as well as attenuated tumor growth in vivo. 	32273759
CASC19	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[regulating miRNA-130b-3p]	qRT-PCR//Luciferase Report Assay	LncRNA CASC19 was upregulated in NSCLC tissues and cell lines. NSCLC patients with high expression of CASC19 presented a worse survival.	NSCLC patients with high expression of CASC19 presented a worse survival.	Yes	 Knockdown of CASC19 attenuated proliferative, migratory, and invasive capacities of A549 and PC9 cells. CASC19 sponged miRNA-130b-3p and negatively regulated its level. 	31389608
CASC15	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue specimens and cells	Regulation[miR-153-3p/KLF5 positive feedback loop]	ChIP//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	This study uncovered that CASC15 expression level was aberrantly high-expressed in breast cancer tissue specimens and cells. In conclusion, we validated the positive feedback loop of KLF5/CASC15/miR-153-3p/KLF5 in the acceleration of breast cancer malignant behaviors and tumorigenesis, suggesting the important biologic roles of CASC15 on the breast cancer tumorigenesis.		Yes	Functionally, the loss-of-functional experiments showed that knockdown of CASC15 suppressed the malignant behaviors of breast cancer cells, such as proliferation, invasion and tumor growth in vitro and vivo. 	30389133
CASC15	LncRNA	Homo sapiens	Breast Neoplasms	MCF-7 cells	Interaction(miR-654-5p/MEF2D axis)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	 In this study, high expression of CASC15 in MCF-7 CSCs was reported, relative to MCF-7 cells, and this phenomenon was associated with metastatic lymph nodes, higher TNM stage, and shorter breast cancer survival rates. Overall, breast cancer stemness and tumor development are regulated via the CASC15/miR-654-5p/MEF2D axis. Accordingly, this pathway can be explored for breast cancer therapy.	miR-654-5p/MEF2D axis	Yes	Further experiments revealed that CASC15 promoted the acquisition of stemness properties of breast cancer cells (BSCCs) by competing with endogenous RNA for miR-654-5p, resulting in overexpression of MEF2D in BCSCs. 	35235236
CASC15	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	regulation[ SIM2 stability]	Flow Cytometry//qRT-PCR//MTT//Western Blot	The results revealed that CASC15 expression was elevated in ESCC tissues, and patients with ESCC exhibiting high CASC15 expression had a poor prognosis.  In conclusion, CASC15 promoted ESCC tumorigenesis by decreasing SIM2 stability via FTO‑mediated demethylation.	The results revealed that CASC15 expression was elevated in ESCC tissues, and patients with ESCC exhibiting high CASC15 expression had a poor prognosis. 	Yes	CASC15?knockdown inhibited ESCC cell proliferation and facilitated apoptosis. Additionally, CASC15?knockdown decreased the growth of ESCC xenograft tumors.	33650646
CASC15	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	Interaction(miR-33a-5p/PTGS2 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	CASC15 was upregulated in ESCC tissues and cell lines. Mechanistically, it was confirmed that CASC15 acts as competing endogenous RNA for miR-33a-5p to regulate PTGS2 expression. In addition, rescue assay showed that miR-33a-5p knockdown or PTGS2 overexpression abolished the cell proliferation, migration, and invasion inhibition role of CASC15 knockdown. 	 CASC15 overexpression was associated with poorer prognosis in ESCC patients.	Yes	Functionally, CASC15 knockdown inhibited cell proliferation, migration, and invasion of ESCC cells. 	36111503
CASC15	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissue and cells	Regulation[miR-766-5p/ KLK12 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In lung cancer tissue and cells, CASC15 was upregulated, while miR-766-5p was downregulated. CASC15 promotes lung cancer through the miR-766-5p/KLK12 axis, indicating that CASC15 is a potential therapeutic in lung cancer.		Yes	Overexpression of CASC15 promoted lung cancer cell proliferation and invasion. 	31378128
CASC15	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells	Interaction(miR-582-5p/HMGB2)	qRT-PCR//RNA Pull-Down//RIP//Transwell Assay	The CASC15 level is revealed to be significantly elevated in CRC cells compared to that in normal cells.  Furthermore, CASC15 can bind with microRNA-582-5p (miR-582-5p) to modulate high mobility group box 2 (HMGB2) expression. We also showed that silencing of CASC15 inhibits tumor growth.		Yes	 In vitro assays revealed that CASC15 overexpression stimulates cell growth and invasion, whereas its down-expression has opposite effects. 	33395735
CASC15	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction(miR-7151-5p/WNT7A axis)	qRT-PCR//Colony Formation Assay//Western Blot	 The present study results showed that CASC15 was overexpressed in PTC tissues compared with normal tissues and acted as a potent oncogene to promote the proliferation and tumorigenesis of PTC cells both in vitro and in vivo. Mechanistic studies demonstrated that CASC15 could serve as an endogenous miRNA sponge to absorb and downregulate miR-7151-5p, thereby preventing the inhibition of WNT7A during PTC progression. Furthermore, the study demonstrated that CASC15 activated the WNT/β‑catenin signaling pathway by upregulating WNT7A in PTC. 		Yes	 The present study results showed that CASC15 was overexpressed in PTC tissues compared with normal tissues and acted as a potent oncogene to promote the proliferation and tumorigenesis of PTC cells both in vitro and in vivo. 	34325316
CASC15	LncRNA	Homo sapiens	Ovarian Neoplasms	Ovarian Cancer tissues	Regulation[miR-221/ARID1A Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	In this study, we found that the expression of CASC15 was lower in ovarian cancer tissues and cells by qRT-PCR.In addition, bioinformatics analysis, luciferase reporter assay, and biotin pull-Expression[down-expression] assay confirmed that CASC15 straightly interacted with miR-221. 	In addition, low expression of CASC15 was closely correlated with advanced TNM stage, moderate/poor differentiation, and larger size. Moreover, Kaplan-Meier survival analysis showed that patients with low CASC15 expression level had poorer overall survival and progression-free survival than those with high CASC15 expression. 	Yes	 Overexpression of CASC15 prohibited the malignancy of ovarian cancer cells, including proliferation, colony formation, cell cycle, migration, and invasion, and promoted cell apoptosis. 	31695430
CASC15	LncRNA	Homo sapiens	Ovarian Neoplasms	OC cells	Interaction( miR-23b-3p/miR-24-3p/SMAD3)	qRT-PCR//Luciferase Report Assay//Western Blot	In vitro and in vivo experiments validated CASC15 as an oncogenic lncRNA in ovarian cancer, which could enhance metastasis through TGF-β-induced epithelial-mesenchymal transition progress. MiR-23b-3p and miR-24-3p, which are members of the miR-23b cluster, were identified to directly target CASC15 through luciferase assays. Further mechanistic investigations indicated that CASC15-mediated miR-23b-3p/miR-24-3p sequestration cooperatively upregulated SMAD3 expression, which, in turn, would permit increased CASC15 mRNA level as a transcription activation factor. 		Yes	In vitro and in vivo experiments validated CASC15 as an oncogenic lncRNA in ovarian cancer, which could enhance metastasis through TGF-β-induced epithelial-mesenchymal transition progress. MiR-23b-3p and miR-24-3p, which are members of the miR-23b cluster, were identified to directly target CASC15 through luciferase assays. Further mechanistic investigations indicated that CASC15-mediated miR-23b-3p/miR-24-3p sequestration cooperatively upregulated SMAD3 expression, which, in turn, would permit increased CASC15 mRNA level as a transcription activation factor. 	35342355
CASC15	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues and cell lines,blood	regulation[miR-338-3p/RAB14 axis ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Upregulated CASC15 was observed in OS plasma exosomes compared with control, and the same expression was observed in the OS tissues and cell lines. Overall, our findings indicate that CASC15 plays a key role in OS progression by targeting the miR-338-3p/RAB14 axis and can serve as a possible therapeutic target for OS patients.		Yes	Further assays indicated that CASC15 knockdown could restrain the proliferation, migration, and invasion of OS cells, and inhibit the growth of OS in xenograft models.	33262606
CASC15	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and adjacent tissues,cell lines(g HeLa, Caski and C33A)	Expression[Expression[Expression[highly expressed]-expression]-expression]	CCK8//qRT-PCR//Western Blot	We demonstrated that lncRNA CASC15 expression was higher in cervical cancer tissues compared to adjacent normal tissues.	"By Chi-square test, 
we found that higher lncRNA CASC15 expression 
associated with lymph node metastasis and FIGO 
stage (All of p<0.05, Table I). Moreover, survival 
plots results showed that higher lncRNA CASC15 
expression predicted a poor prognosis of cervi_x0002_cal cancer compared to lower lncRNA CASC15 
expression in cervical cancer patients (Figure 1C, 
log rank test, p<0.05). Thus, these results indicated 
that higher lncRNA CASC15 expression showed 
an important role in cervical cancer."	Yes	Functional assays showed that knockExpression[down-expression] of lncRNA CASC15 sExpression[Expression[up-expression]-expression]pressed cell proliferation and cell cycle progression in cervical cancer. Moreover, we also found that knockExpression[down-expression] of lncRNA CASC15 inhibited cell invasion ability and Epithelial-Mesenchymal Transition (EMT) signaling pathway by Expression[Expression[up-expression]-expression]regulating E-cadherin and Expression[down-expression]regulating N-cadherin expression in cervical cancer.	30720157
CASC15	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues and cells	Interaction(miR-365/cyclin D1)	Cell Proliferation Assay//qRT-PCR//Western Blot	CASC15 was upregulated in LSCC and high expression levels of CASC15 predicted poor survival. In LSCC tissues, CASC15 was negatively correlated with miR-365 but positively correlated with cyclin D1. In LSCC cells, overexpression of CASC15 resulted in downregulation of miR-365 and upregulation of cyclin D1. Overexpression of miR-365 did not affect the expression of CASC15 but downregulated cyclin D1. Overexpression of Cyclin D1 did not affect the expression of miR-365 and CASC15. 	CASC15 was upregulated in LSCC and high expression levels of CASC15 predicted poor survival. 	Yes	Overexpression of CASC15 and cyclin D1 led to promoted, while overexpression of miR-365 led to inhibited LSCC cell proliferation. In addition, overexpression of miR-365 reduced the effects of overexpression of CASC15.	35216636
CARMN-208	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues,cell lines	Expression[lower expressed]	qRT-PCR//RNA-seq	Subsequently, four lncRNAs (upregulated ENST00000433108; downregulated ENST00000598996, ENST00000524265 and ENST00000398461) and two mRNAs (upregulated CCNB1 and CDK1) in 64 pairs of BC and adjacent normal tissues and four BC cell lines were detected using reverse transcription?quantitative PCR and these results were consistent with the sequencing data. 	The low expression level of ENST00000598996 and ENST00000524265 was correlated with unfavorable clinicopathological parameters, and shorter progression?free and overall survival time, whereas, ENST00000433108 was not associated with either.	Yes	 The in vitro functional experiments also revealed that the overexpression of ENST00000598996 and ENST00000524265 decreased the proliferation, migration, and invasion abilities of BC cells. 	33000254
CARMN	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues 	Regulation[miR-1275/AXIN2 axis]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	In the present study, we found that miR143HG expression was significantly downregulated in bladder cancer tissues (BCa) compared with normal tissues. In summary, our findings demonstrated that miR143HG/miR-1275/AXIN2 axis regulates BCa development by modulating the Wnt/β-catenin pathway.	We showed that miR143HG high expression was associated with a high survival rate in BCa patients.	Yes	Gain-of-function assays demonstrated that miR143HG overexpression suppressed the proliferation, arrested cell cycle progression, and attenuated migration and invasion of BCa cells in vitro. In vivo assay illustrated that ectopic expression of miR143HG inhibited BCa growth in vivo.	30471109
ZSCAN16-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells	Interaction( miR-181 c-5p/SPAG9 axis/JNK pathway)	qRT-PCR	ZSCAN16-AS1 was significantly up-regulated in HCC cells. ZSCAN16-AS1 worked as a competing endogenous RNA (ceRNA) to regulate sperm associated antigen 9 (SPAG9) expression through sponging miR-181 c-5p. Moreover, SPAG9 could activate the c-Jun-N-terminal kinase (JNK) pathway.		Yes	 ZSCAN16-AS1 silence inhibited HCC cell proliferation, migration and invasion, while it accelerated HCC cell apoptosis. 	34097562
CA3-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cell lines and tissues	Interaction(miR-93-5p/BTG3)	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	Firstly, we found that the expression level of CA3-AS1 was decreased in gastric cancer cell lines and tissues. Then, the relationship between CA3-AS1 and miR-93-5p was explored. Luciferase reporter assays results showed that miR-93-5p was a direct target of CA3-AS1 in SGC-7901 and BCG-823. Furthermore, BTG3 was identified as a direct target gene of miR-93-5p. Restore experiments showed that CA3-AS1 upregulated the expression level of BTG3 and inhibited the gastric cancer cells invasion by sponging miR-93-5p. 		Yes	Then, CA3-AS1 overexpression inhibited the gastric cancer cells migration and invasion and knockdown of CA3-AS1 enhanced the gastric cancer cells migration and invasion. Finally, we found that CA3-AS1 inhibited the metastasis ability of gastric cancer cells in vivo. 	33051589
C3orf85	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and their adjacent tissues	Expression[lower expressed]	CCK8//qRT-PCR//Western Blot//Microarray	The lncRNA FLJ22763 was found to be significantly downregulated with the largest fold change	 	Yes	The ectopic expression of lncRNA FLJ22763 significantly suppressed the biological malignant behavior of GC cells and inhibited xenograft tumor growth (both P < 0.001).	30716442
C2dat2	LncRNA	Homo sapiens	Cerebral Ischaemia/Reperfusion Injury	cell lines	Interaction(miR-30d-5p/DDIT4/mTOR axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Tunel//qRT-PCR//FISH//Luciferase Report Assay//Bioinformatics Analysis	Mechanistically, C2dat2 acts as a competing endogenous RNA (ceRNA) to negatively regulate miR-30d-5p expression. More specifically, miR-30d-5p targeted the 3'-untranslated region of DNA damage-inducible transcript 4 (DDIT4) and silenced its target mRNA DDIT4. Additionally, C2dat2 binding with heat shock cognate 70/heat shock protein 90 blocked RNA-induced silencing complex assembly to abolish the miR-30d-5p targeting of DDIT4 and inhibited miR-30d-5p to silence its target mRNA DDIT4. Further analysis showed that C2dat2 knockdown conspicuously inhibited the up-regulation of DDIT4 and Beclin-1 levels and LC3B II/I ratio and the down-regulation of P62 and phosphorylated mammalian target of rapamycin (mTOR)/mTOR and phosphorylated-P70S6K/P70S6K ratio in Neuro-2a cells after oxygen-glucose deprivation/reoxygenation. 		Yes	C2dat2 up-regulation facilitated neuronal autophagy and apoptosis induced by CIRI. 	33833132
C2CD4D-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines.	Interaction(miR-3681-3p/NEK2 axis)	RNA Pull-Down//ChIP//Western Blot//Transfection//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	C2CD4D-AS1 was dramatically overexpressed in LUAD tissues and cell lines. To conclude, C2CD4D-AS1 up-regulation induced by ETV4 enhanced NEK2 expression by sequestering miR-3681-3p to contribute to the malignant behaviors of LUAD cells.		Yes	 As a result, depletion of C2CD4D-AS1 significantly repressed cell proliferation, migration, invasion and stimulated cell apoptosis in LUAD. 	34850664
C20orf204-203	LncRNA	Homo sapiens	Hematologic Neoplasms	leukemia cell lines and THP-1 cell line	Regulation	RNA-seq	Here, we used short hairpin RNA (shRNA) library combined with high-throughput sequencing to screen lncRNAs that may affect the proliferation of leukemia cell lines, and identified lncRNA C20orf204-203 among 74 candidate lncRNAs in this study.  We observed the increased mRNA level of BAD gene while decreased protein level of TP53 and BCL2. The expression of Caspase 3 decreased and Caspase 3-cleaved protein increased in THP-1 cell line. However, their changes were inconsistent in the two cell lines. 		Yes	 C20orf204-203 knockdown decreased the proliferation of K562 and THP-1 cell lines accompanied with the increased proportion of early apoptotic cells.  Our experimental results showed that knockdown of lncRNA C20orf204-203 in leukemia cell lines affected cell proliferation although the mechanism of action in different cell lines may differ. 	36151809
C20orf204	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	20 primary HCC	Expression(highly expressed)	qRT-PCR	We report here that a protein, C20orf204-189AA, was detected in the nucleus of 14 out of 20 primary HCC, but not in control livers. 	Furthermore, the expression of C20orf204-189AA upregulates the protein level of nucleolin. Nucleolin and C20orf204 mRNA levels in HCC are correlated with tumor differentiation grade and patient survival, suggesting that C20orf204-189AA is a cancer type-specific fine tuner in some HCC that presents itself for potential targeting therapy and cancer biomarker. 	Yes	Strikingly, overexpression of C20orf204-189AA enhanced cell proliferation and ribosomal RNA transcription. 	33731669
C20orf204	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues,cell lines	Regulation[LINC00176/BCL3/CP axis]	qRT-PCR	Bioinformatics prediction in combination with RT-qPCR analysis for the expression pattern of LINC00176 revealed that LINC00176 was highly expressed in ovarian cancer tissues as well as in ovarian cancer cell lines, respectively. Investigations with regard to the correlation between LINC00176 and promoter region of CP turned out to be positive via B-cell CLL/lymphoma 3 (BCL3) by means of dual-luciferase reporter gene assay, ChIP and RIP assays. Furthermore, oncogenic properties of the LINC00176/BCL3/CP axis were also demonstrated by tumour formation in vivo generated upon injecting cells in nude mice. Our results demonstrate that restored LINC00176 initiates tumorigenesis in ovarian cancer by increasing CP expression via recruiting BCL3, the mechanism of which represented a potential and promising therapeutic target for the disease.		Yes	 Promoted proliferation, migration and invasion along with reduced apoptosis were observed in cells treated with oe-LINC00176, while si-BCL3 and si-CP were able to block the promoting effects.	31668012
C1RL-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[AKT/β-Catenin/c-Myc Pathway]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	C1RL-AS1 was upregulated in GC tissues, and high expression levels of C1RL-AS1 were associated with poor prognosis.C1RL-AS1 probably exerts its biological function by mediating the AKT/β-catenin/c-Myc pathway, indicating a novel therapeutic target in GC.	C1RL-AS1 was upregulated in GC tissues, and high expression levels of C1RL-AS1 were associated with poor prognosis.	Yes	Further in vitro functional assays revealed that silencing C1RL-AS1 attenuated the proliferation rate and migration ability and enhanced the apoptotic rate and the senescence of GC cells. 	32983994
C10orf95-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	CRC tissues and multiple CRC cell lines	Interaction(miR125a-5p Axis)	CCK8//qRT-PCR	In the study, we found that the expression of RPARP-AS1 was significantly up-regulated in CRC tissues and multiple CRC cell lines, which was closely related to poor prognosis of CRC patients.Results of research on the mechanisms showed that RPARP-AS1 functioned as a competitive endogenous RNA (ceRNA) to sponge miR-125a-5p, therefore promoting CRC procession.	In the study, we found that the expression of RPARP-AS1 was significantly up-regulated in CRC tissues and multiple CRC cell lines, which was closely related to poor prognosis of CRC patients.	Yes	Loss-of-function studies indicated that knockdown of RPARP-AS1 inhibited CRC cell proliferation, migration and invasion in HCT116 and LoVo cell lines. 	34675548
BX357664	LncRNA	Homo sapiens	Stomach Neoplasms	cancer specimens 	Interaction( miR-183-3p/PTEN/PI3K/AKT pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Invasion Assay	It was found that BX357664 level was lowered in cancer specimens than adjacent non-cancer tissues and correlated with tumor size and TNM stage. In the dual-luciferase report analysis, BX357664 acted as a miR-183-3p ceRNA to target and regulate the expression of PTEN and affect the PI3K/AKT pathway. 	It was found that BX357664 level was lowered in cancer specimens than adjacent non-cancer tissues and correlated with tumor size and TNM stage. 	Yes	Also, we used cell counting kit 8 (CCK8), cell clone formation assay and transwell assay, which affirmed that up-regulation of BX357664 inhibited the proliferation, migration, and invasion of GC cells, but promoted apoptosis. 	33607219
BX357664	LncRNA	Homo sapiens	Lung Neoplasms	Tumor tissues and their adjacent non-cancerous tissues,cell lines(A549，H1975,H-125,95D,SPC-A-1,293T)	Expression[lower expressed]	Wound Healing Assay//CCK8//qRT-PCR//Microarray//Colony Formation Assay//Transwell Assay	In the present study, it was initially demonstrated that BX357664 was downregulated in clinical lung cancer tissues and in a series of lung cancer cell lines.	 	Yes	Transwell analysis and a wound-healing assay also demonstrated that overexpression of BX357664 in A549 and 95D cells significantly inhibited cell migration and invasion. 	30854036
BX357664	LncRNA	Homo sapiens	Colorectal Neoplasms	 colorectal cancer tissues and cell lines	Expression[lower expressed]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	The results demonstrated that BX357664 was significantly downregulated in clinical colorectal cancer tissues and cell lines.		Yes	Overexpression of BX357664 decreased cell proliferation rates and cell colony formation capacities in HCT116 and HT-29 cells. 	29844809
BTN3A2	LncRNA	Homo sapiens	Bacterial Infections	cecum tissue and DF-1 cells	Expression(highly expressed)	In Vivo Experiment//qRT-PCR//ELISA//RNA-seq	 Moreover, through cis regulation network analysis of the differentially expressed lncRNAs, we found that a novel lncRNA termed lncRNA BTN3A2 was significantly increased in both cecum tissue and DF-1 cells after coccidia infection or sporozoite stimulation. 		Yes	Functional test data showed that the overexpression of lncRNA BTN3A2 reduced the production of inflammatory cytokines, including IL-6, IL-1β, TNF-α and IL-8, while lncRNA BTN3A2 knockdown promoted the production of these inflammatory cytokines. 	36091044
BTG3-7:1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms		regulation[GRB2-RAS-RAF-MEK-ERK and GRB2-PI3K-AKT-GSK3β-β-catenin pathways]	Flow Cytometry//FISH//Western Blot	Abundant Lnc-BTG3-7:1, which targets gene C21ORF91, was specifically observed in TNBC biopsies and cell lines.Meanwhile, investigation of molecular mechanism indicated that Lnc-BTG3-7:1, cooperated with transcription factor JUND, cis-regulated the transcription of C21ORF91 gene, and down-regulation of Lnc-BTG3-7:1/C21ORF91 suppressed GRB2-RAS-RAF-MEK-ERK and GRB2-PI3K-AKT-GSK3β-β-catenin pathways.		Yes	Knockdown of Lnc-BTG3-7:1 or C21ORF91 strongly inhibited cell proliferation, promoted cell apoptosis and cell cycle G1-arrested.	33585557
BTG2	LncRNA	Homo sapiens	Glioma	 RBP-J OE Mφ-Exos	Interaction(miR-25-3p/PTEN)	In Vivo Experiment//cell invasion assay//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Microarray//Cell Proliferation Assay	We found that circRNA BTG (circBTG2) is upregulated in RBP-J OE Mφ-Exos compared to WT Mφ-Exos.  In conclusions, Exo-circBTG2 secreted from RBP-J OE Mφ inhibits tumor progression through the circBTG2/miR-25-3p/PTEN pathway, and circBTG2 is probably a diagnostic biomarker and potential target for glioma therapy.		Yes	RBP-J OE Mφ-Exos co-culture and circBTG2 overexpression inhibited proliferation and invasion of glioma cells, whereas circBTG2 knockdown promotes tumor growth in vivo. The effects of RBP-J OE Mφ-Exos on glioma cells can be reversed by the circBTG2 knockdown. 	35643814
BSN-DT	LncRNA	Homo sapiens	Osteosarcoma	 OS cells	regulation[miR-654-3p/SYTL2 axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	Our study identified that BSN-AS2 expression was boosted in spinal OS tissues and cell lines. In conclusion, the availability of miR-654-3p was antagonized by E2F1-induced BSN-AS2 for SYTL2-meidated spinal OS progression.		Yes	 Afterwards, loss-of-function assays indicated that BSN-AS2 depletion reduced cell proliferation, migration and invasion as well as promoted cell apoptosis in spinal OS.	32351327
BSG-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tissues with high hypoxia score.	Regulation(BSG )	qRT-PCR//RNA Pull-Down//Western Blot	We found that lncRNA BSG-AS1 was highly expressed in tissues with high hypoxia score. RNA-seq was used to find the downstream target genes of lncRNA BSG-AS1. Sequencing data and wet experiments showed that mRNA of BSG decreased after knockout of lncRNA BSG-AS1, and mediated the promotive effect of lncRNA BSG-AS1 on proliferation and migration in HCC cells. 		Yes	Then we verified the response of lncRNA BSG-AS1 to hypoxia in the cell hypoxia model in vitro. Through functional phenotypic analysis, we found that lncRNA BSG-AS1 can mediate the promoting effect of hypoxia on the proliferation and migration in HCC cells. 	34119821
BRE-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[NR4A3]	RNA Pull-Down//Western Blot//RIP//qRT-PCR//EdU Staining//ChIP	In this study, using public NSCLC microarray data we identified a novel lncRNA BRE antisense RNA 1 (BRE-AS1). BRE-AS1 is significantly down-regulated in NSCLC tissues and cell lines.  Collectively, our data demonstrate that BRE-AS1 represses NSCLC cell growth and survival via up-regulating NR4A3 and suggest that enhancing BRE-AS1 may be potential therapeutic strategy for NSCLC.		Yes	Gain-of-function and loss-of-function assays showed that BRE-AS1 reduces NSCLC cell viability, represses NSCLC cell proliferation, and induces NSCLC cell apoptosis in vitro, and represses NSCLC tumor growth in vivo.	30227111
BRE-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	regulation[ mediating STAT3]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	 LncRNA BRE-AS1 showed significantly decreased expression in BC tissues than the paired normal tissues.Over-expression of lncRNA BRE-AS1 inhibited BC cell proliferation in vitro and in vivo via repressing the phosphorylation of STAT3. 		Yes	 In vitro experiments demonstrated that over-expression of lncRNA BRE-AS1 inhibited cell proliferation but promoted cell apoptosis of EJ and T24 cells. STAT3 was determined as a target for lncRNA BRE-AS1. In vivo, up-regulation of lncRNA BRE-AS1 reduced cancer growth in nude mice bearing BC via repressing the phosphorylation of STAT3.	32495865
CA3-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues,cell lines(HCT-116，SW480，SW620，SW1116,HT29)	Regulation[miRNA-93/PTEN axis]	CCK8//qRT-PCR//Transwell Assay//Western Blot	We found that lncRNA CA3-AS1 mainly located in cytoplasm, and overexpression of lncRNA CA3-AS1 inhibits cell proliferation, invasion and promotes cell apoptosis. Our results revealed that miR-93 could directly bind to CA3-AS1, and verified the oncogenic role of miR-93. Furthermore, we found that miR-93 played its role through regulating PTEN, the tumor-sExpression[Expression[up-expression]-expression]pressor gene, which was inversely correlated with miR-93.		Yes	We found that lncRNA CA3-AS1 mainly located in cytoplasm, and overexpression of lncRNA CA3-AS1 inhibits cell proliferation, invasion and promotes cell apoptosis. Our results revealed that miR-93 could directly bind to CA3-AS1, and verified the oncogenic role of miR-93. Furthermore, we found that miR-93 played its role through regulating PTEN, the tumor-sExpression[Expression[up-expression]-expression]pressor gene, which was inversely correlated with miR-93.	30415006
CARMN	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Interaction[sponging miR-125a ]	qRT-PCR//Cell Apoptosis Assay//Western Blot	We found that the down-regulation of miR143HG in EC predicted poor survival.MiR143HG may up-regulate p53 in EC by sponging miR-125a to promote cancer cell apoptosis.	We found that the down-regulation of miR143HG in EC predicted poor survival.	Yes	 Cell apoptosis analysis showed that miR143HG and p53 over-expression led to an increased cell apoptotic rate.	31819644
CACNA1C-AS2	LncRNA	Homo sapiens	Glioma	glioma cells	Regulation(Fbxo45)	In Vivo Experiment//Western Blot//Wound Healing Assay//Tunel//Migration Assay//qRT-PCR//MTT//Invasion Assay//Transwell Assay	In the current study, we discovered that an antisense lncRNA, CACNA1C-AS2, suppressed growth, migration and invasion of glioma cells, suggesting that CACNA1C-AS2 functions as a tumor suppressor.Furthermore, we found that CACNA1C-AS2 negatively regulated Fbxo45 protein expression in glioma cells.		Yes	In the current study, we discovered that an antisense lncRNA, CACNA1C-AS2, suppressed growth, migration and invasion of glioma cells, suggesting that CACNA1C-AS2 functions as a tumor suppressor.	36038736
CARMN	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-92a-3p/BTG2/Wnt/β-catenin axis)	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 RT-qPCR and clinical analysis revealed that CARMN and B-cell translocation gene 2 (BTG2) were downregulated, whereas miR-92a-3p was upregulated in CC tissues and cells and their expressions were correlated with clinicopathological characteristics and prognosis. Mechanically, CARMN repressed miR-92a-3p to promote BTG2 transcription. Functional rescue assays revealed that miR-92a-3p overexpression or BTG2 downregulation reversed the inhibitory role of CARMN overexpression in CC cell growth. Western blot analysis elicited that Wnt3a and β-catenin were elevated in CC cells and CARMN blocked the Wnt/β-catenin signaling pathway via the miR-92a-3p/BTG2 axis. 	 RT-qPCR and clinical analysis revealed that CARMN and B-cell translocation gene 2 (BTG2) were downregulated, whereas miR-92a-3p was upregulated in CC tissues and cells and their expressions were correlated with clinicopathological characteristics and prognosis. 	Yes	MTT assay, flow cytometry, and Transwell assays revealed that CARMN overexpression reduced proliferation, migration, and invasion and increased apoptosis rate in CC cells.	36314369
CARMN	LncRNA	Homo sapiens	Glioblastoma	GBM tissues 	Interaction(miR-504/p53 )	Cell Proliferation Assay//qRT-PCR//Western Blot	 We found that miR143HG was downregulated in GBM and predicted poor survival. 	 We found that miR143HG was downregulated in GBM and predicted poor survival. The mRNA expression levels of miR143HG and p53 were positively correlated in GBM tissues.Bioinformatics analysis suggested that miR143HG could form base paring with miR-504, which has been reported to target p53. 	Yes	Moreover, overexpression of miR143HG and p53 decreased GBM cell proliferation, while overexpression of miR-504 increased GBM cell proliferation. In addition, overexpression of miR-504 attenuated the effect of miR143HG overexpression on GBM cell proliferation.	33461388
CARMN	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	 breast tissue	Interaction(miR143-3p/MCM5)	Cell Proliferation Assay//qRT-PCR//Western Blot	 CARMN is downregulated at different phase of malignant transformation of breast tissue. We confirmed CARMN can produce miR143-3p from its exon5 which is DROSHA and DICER dependent, resulting binding and decrease of MCM5. 	CARMN can predict both better prognosis and higher response rate of cisplatin-based neoadjuvant chemotherapy in breast cancer. 	Yes	Through in vitro and in vivo studies, we confirmed CARMN can also inhibit tumorigenesis and enhance sensitivity to cisplatin in TNBC cells. 	34162418
CARD8-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	tissues and cell lines 	Interaction(miR-650)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The expression of CARD8-AS1 was decreased in lung adenocarcinoma tissues and cell lines (p < 0.001). The Bcl-2 protein levels were decreased while Bax levels were increased by overexpression of CARD8-AS1 (p < 0.001). miR-650 may thus be a direct target of CARD8-AS1 and Bax may be a direct target of miR-650. 	 Low expression of CARD8-AS1 was related to tumor size (p = 0.042), TNM stage (p = 0.021), lymph node metastasis (p = 0.025), and poor overall survival (p < 0.05). 	Yes	Elevated expression of CARD8-AS1 could suppress cellular viability, migration potential, and invasion ability (p < 0.05). 	35996500
CARD11	LncRNA	Homo sapiens	Uveal melanoma	immune cells	Expression(highly expressed)	qRT-PCR	CARD11 expression had notable correlation with UVM clinicopathological features, which was also an independent predictor for overall survival (OS). Intriguingly, CARD11 had a positively correlation to autophagy, cellular senescence and apoptosis. Infiltration of monocytes was significantly higher in low CARD11 expression group, and infiltration of T cells regulatory was lower in the same group. Functional enrichment analyses revealed that CARD11 was positively related to T cell activation pathways and cell adhesion molecules. The expressions of hub-genes were all increased in the high CARD11 expression group and the ceRNA network showed the interaction among mRNA, miRNA and lncRNA. These findings show that high CARD11 expression in UVM is associated with poor OS	high CARD11 expression in UVM is associated with poor OS	Yes	Functional enrichment analyses revealed that CARD11 was positively related to T cell activation pathways and cell adhesion molecules. The expressions of hub-genes were all increased in the high CARD11 expression group and the ceRNA network showed the interaction among mRNA, miRNA and lncRNA.	34370778
CAR10	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Regulation(Non-Small Cell Lung Cancer)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	The present study demonstrated that CAR10 was upregulated in patients with NSCLC, which was also associated with a poor prognosis. Functionally, CAR10 was confirmed to be oncogenic and promoted NSCLC cell migration and invasion, using overexpression and knockdown Transwell assays. Furthermore, GJB2 expression was revealed to be upregulated and was positively correlated with CAR10 expression in NSCLC. A further mechanistic study revealed that GJB2 was a downstream target of CAR10, which induced the migration and invasive potential of the A549 and H1299 cell lines. More specifically, miR-892a was found to serve as a bridge between CAR10 and GJB2, via similar miRNA response elements. The RNA pull-down and luciferase assays indicated that miR-892a directly binds both CAR10 and GJB2.	The present study demonstrated that CAR10 was upregulated in patients with NSCLC, which was also associated with a poor prognosis.	Yes	Functionally, CAR10 was confirmed to be oncogenic and promoted NSCLC cell migration and invasion, using overexpression and knockdown Transwell assays.	33664589
CAR10	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cells	regulation[CAR10/miR-125b-5p/PDPK1 network ]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay	We found that CAR10 is significantly increased in4 cervical cancer tissues and cells, which can promote the proliferation of cervical cancer cells in vitro and in vivo, indicating that CAR10 is involved in the progression of cervical cancer as an oncogene.  In addition, our study also suggests that intervention of CAR10/miR-125b-5p/PDPK1 network may be a new strategy for targeted therapy of cervical cancer.		Yes	We found that CAR10 is significantly increased in4 cervical cancer tissues and cells, which can promote the proliferation of cervical cancer cells in vitro and in vivo, indicating that CAR10 is involved in the progression of cervical cancer as an oncogene. 	32025520
CAR10	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cell lines	regulation[miR-125b-5p/RAB3D axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 LncRNA CAR10 was upregulated in melanoma tissues and cell lines.Our work suggests that lncRNA CAR10 promotes melanoma growth and metastasis through modulating miR-125b-5p/RAB3D axis.	Upregulation of CAR10 predicted a poor prognosis in patients with melanoma. 	Yes	CAR10 knockdown suppressed proliferation, migration and invasion of melanoma cells in vitro.	32636644
CAMK2B	LncRNA	Homo sapiens	Carcinoma, Renal Cell	infiltrating stromal cells	Interaction(GUSBP11/miR-432-5p/CAMK2B)	qRT-PCR//Transfection//Immunoblotting//IHC	We further evaluated the relationship between immune scores (ISs) and stromal scores (SSs) and disease progression and found that high SSs were associated with a poor prognosis in KIRP. Differentially expressed genes (DEGs) were therefore screened based on SS scores, resulting in 2509 DEGs, including 1668 mRNAs, 783 long noncoding (lnc)RNAs, and 58 micro (mi)RNAs. DEGs were then filtered using the random variance and subjected to hierarchical clustering using EPCLUST. Weighted gene co-expression network analysis (WGCNA) was used to assess the prognostic capacity of these DEGs and identify target ceRNA networks, and lncRNA GUSBP11/miR-432-5p/CAMK2B in the turquoise module was selected as a promising ceRNA network. From this analysis CAMK2B was selected as the core gene predicted to be involved in stromal TMA regulation. We therefore explored the expression and function of CAMK2B in vitro and in vivo and provide evidence that this protein promotes stromal TME remodulation and inhibits proliferation in KIRP. Lastly, we show that vascular endothelial growth factor (VEGF), transforming growth factor (TGF)β, and close homolog of L1 (CHL1) act as downstream effectors of CAMK2B in KIRP. Thus, in this study, we show that the TME determines prognosis of KIRP patients via the core effector molecule CAMK2B, which mediates both microenvironmental remodeling and tumor progression. Based on these findings, we propose that remodeling of the stromal microenvironment could represent an improved therapeutic approach relative to immunotherapy for KIRP.	We further evaluated the relationship between immune scores (ISs) and stromal scores (SSs) and disease progression and found that high SSs were associated with a poor prognosis in KIRP.	Yes	We therefore explored the expression and function of CAMK2B in vitro and in vivo and provide evidence that this protein promotes stromal TME remodulation and inhibits proliferation in KIRP.	35127542
CALML3-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	Interaction[ Wnt/β-catenin pathway]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay	We found that CALML3-AS1 was upregulated in CC tissues and this upregulation was associated with FIGO stage, histological grade, and reduced overall survival.Mechanistic investigations revealed that inhibiting the expression of CALML3-AS1 decreased the levels of β-catenin, cyclin D1, and c-myc via Western blot.	We found that CALML3-AS1 was upregulated in CC tissues and this upregulation was associated with FIGO stage, histological grade, and reduced overall survival.	Yes	Functional assays suggested that knockdown of CALML3-AS1 suppressed the proliferation, migration, and invasion of CC cells, and induced apoptosis. 	31298313
CALML3-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Interaction(miR-20a-5p/RBM38 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The results indicated that the expression of both CALML3A-S1 and RBM38 were significantly downregulated in PTC tissues (p < 0.01), while the expression of miR-20a-5p was increased in PTC (p < 0.01). Mechanistically, CALML 3-AS1 sponged miR-20a-5p, which in turn leads to the suppression of RBM38 expression and PTC progression.		Yes	Functionally, CALML3-AS1 overexpression inhibited PTC cell proliferation in vitro and in vivo.	35351042
CAIF	LncRNA	Rattus norvegicus	Myocardial Infarction	cardiomyocytes	Interaction(miR‑488/AVEN )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//RIP//FISH//Luciferase Report Assay//H&E Staining//IHC//EdU Staining	CAIF was downregulated in the myocardium of I/R rats and cardiomyocytes treated with hydrogen peroxide (H2O2).  Mechanistically, CAIF sponged microRNA (miR)‑488‑5p; this interaction was confirmed by rescue experiments. Moreover, miR‑488‑5p targeted apoptosis and caspase activation inhibitor (AVEN) and inhibited its expression. In summary, the present data identified a novel CAIF/miR‑488‑5p/AVEN signaling axis as a key regulator of myocyte apoptosis, which may be a potential therapeutic target for the treatment of MI.		Yes	Further experiments demonstrated that CAIF overexpression inhibited I/R‑induced cardiac infarction and apoptosis in vivo. CAIF decreased H2O2‑induced apoptosis and oxidative stress of cardiomyocytes. 	35795990
CAHM	LncRNA	Homo sapiens	Intervertebral Disc Degeneration	BMSC-Exo, THP-1 and NPCs	Expression(highly expressed)	qRT-PCR//ELISA//Western Blot	Compared with BMSCs, the expression of CAHM in BMSC-Exo was significantly higher.  Using co-cultured experiments, we proved that BMSC-Exo reduced apoptosis and ECM degradation of NPCs by inhibiting M1-type macrophage polarization by delivering CAHM. In addition, BMSC-Exo could improve IDD in vivo, including increased proteoglycan content, reduced macrophage infiltration and ECM degradation, and decrease expression of inflammatory factors by delivering CAHM.		Yes	 Using co-cultured experiments, we proved that BMSC-Exo reduced apoptosis and ECM degradation of NPCs by inhibiting M1-type macrophage polarization by delivering CAHM. In addition, BMSC-Exo could improve IDD in vivo, including increased proteoglycan content, reduced macrophage infiltration and ECM degradation, and decrease expression of inflammatory factors by delivering CAHM.	36334792
CADM1-AS1	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissue, cell lines	Regulation[PTEN/AKT/GSK-3β  axis]	Western Blot//Wound Healing Assay//CCK8//Cell proliferation assay//PCR//Microarray//Colony Formation Assay//EdU Staining//Transwell Assay	CADM1-AS1 expression was reduced in HCC. Meanwhile, we revealed that CADM1-AS1 inhibited the phosphorylation of AKT and GSK-3β. Furthermore, our study showed that CADM1-AS1 decreased the cell cycle associated proteins expression of cyclinD, cyclinE, CDK2 CDK4, CDK6, and enhanced the levels of p15, p21 and p27. More importantly, SC79, a specific activator for AKT;, apparently attenuated the effects of CADM1-AS1 on above cell-cycle associated proteins, confirming that CADM1-AS1 inhibited cell cycles through the AKT signaling pathway. And we also found the CADM1-AS1 has antitumor effect in vivo by a xenograft HCC mouse model. In conclusion, the present findings show that the CADM1-AS1 inhibits proliferation of HCC by inhibiting AKT/GSK-3β signaling pathway, then upregulate p15, p21, p27 expression and downregulate cyclin, CDK expression to inhibit the G0/G1 to S phase transition both in vitro and in vivo. 	Clinical data showed that this downregulation was associated with advanced tumor stage, high TNM stage and reduced survival in HCC patients.	Yes	CADM1-AS1 overexpression inhibited HCC cells proliferation, migration and invasion, while inducing G0/G1 phase arrest.	31118799
CACS15	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cell lines 	Interaction[recruiting EZH2]	RNA Pull-Down//ChIP//CCK8//qRT-PCR//RIP//Transwell Assay	CACS15 was upregulated in OC tissues and cell lines relative to matched ones. LncRNA CACS15 inhibits the expression of APC by recruiting EZH2, thus accelerating the progression of ovarian cancer as an oncogene.		Yes	Knockdown of CACS15 attenuated proliferative, migratory and invasive abilities of OC cells. 	31737207
CACNA1G-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[downregulating p53]	qRT-PCR//Western Blot//RIP//ChIP	CACNA1G-AS1 was upregulated in CRC tissues compared to adjacent normal ones.  CACNA1G-AS1 downregulates p53 level by forming a carcinogenic complex with EZH2, thereby enhancing the proliferative and invasive abilities of CRC cells.		Yes	Knockdown of CACNA1G-AS1 reduced proliferative and invasive abilities of HTC116 and SW480 cells.	31957825
CACNA1G-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[miR-2392/C1orf61 pathway]	RNA Pull-Down//ISH//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Invasion Assay	 Through bioinformatics analysis, we found that CACNA1G-AS1 expression was significantly upregulated in HCC tissues compared with that in the adjacent normal tissues. Collectively, CACNA1G-AS1 promotes HCC progression through regulating the miR-2392/C1orf61 pathway.		Yes	 Knockdown of CACNA1G-AS1 attenuated the proliferation, migration, and invasion of HCC cells.  In vivo assay also showed that CACNA1G-AS1 silencing HCC cells have smaller tumor volumes and weights. 	30908634
CACNA1G-AS1	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cells 	Interaction( miR-3160-5p)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	 It was revealed that CACNA1G-AS1 was highly expressed in DLBCL tissues and cells and that expression of CACNA1G-AS1 was associated with the clinical stage of DLBCL. In addition, CACNA1G-AS1 could downregulate miR-3160-5p by targeting binding in DLBCL cells. Overexpression of miR-3160-5p had the same effects on the cytotoxicity and apoptosis of DLBCL cells as CACNA1G-AS1-knockdown. 	 It was revealed that CACNA1G-AS1 was highly expressed in DLBCL tissues and cells and that expression of CACNA1G-AS1 was associated with the clinical stage of DLBCL. 	Yes	 Functionally, CACNA1G-AS1-knockdown was demonstrated to increase cytotoxicity and expedite apoptosis in DLBCL cells in vitro and in vivo. 	36160896
CACNA1G-AS1	LncRNA	Homo sapiens	Keloid	keloid tissues	regulation[miR-205]	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	CACNA1G-AS1 level was up-regulated in keloid tissues and keloid fibroblasts.CACNA1G-AS1 suppressed miR-205 expression to promote proliferation and invasion and inhibit apoptosis in human keloid fibroblasts.		Yes	CACNA1G-AS1 overexpression promoted proliferation and invasion and suppressed apoptosis of keloid fibroblasts.	32495824
CASC19	LncRNA	Homo sapiens	Colorectal Neoplasms	colon tissues,cell lines	Regulation[CASC19/miR-140-5p/CEMIP axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Transwell Assay	 CASC19 expression was markedly upregulated in CRC tissues and CRC cell lines (P < 0.05).MiR-140-5p was found to be able to bind directly to CASC19 and CEMIP. Overexpression of miR-140-5p reversed the effect of CASC19 on cell proliferation and tumor migration, as well as suppressed CASC19-induced CEMIP expression.	qRT-PCR revealed that CASC19 expression was higher in 25 tissue samples from patients with aggressive CRC compared with the 27 tissue samples from patients with nonaggressive CRC (P < 0.05). Higher CASC19 expression was associated with poorer patient prognoses.	Yes	Furthermore, in vitro experiments demonstrated that CASC19 overexpression enhanced CRC cell invasion, migration, and proliferation. CASC19 overexpression enhanced the expression of cell migration inducing hyaluronidase 1 (CEMIP) and epithelial-mesenchymal transition markers. 	31011255
CASC19	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cells 	regulation[miR-301b-3p/LDLR axis]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	CASC19 is markedly overexpressed in NSCLC.CASC19 facilitates NSCLC cell proliferation and metastasis by targeting the miR-301b-3p/LDLR axis, offering a possible strategy for lncRNA-targeted treatment in NSCLC.		Yes	 Finally, rescue experiments showed that miR-301b-3p inhibition or LDLR overexpression counteracted the CASC19 knockdown-mediated function on cell proliferation and metastasis in NSCLC.	32677267
CASC19	LncRNA	Homo sapiens	Stomach Neoplasms	cell lines (AGS, BGC-823, MGC-803, and HGC-27) 	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay	Furthermore, quantitative real-time PCR assay confirmed that CASC19 expression in four human gastric cancer cells (AGS, BGC-823, MGC-803, and HGC-27) was significantly upregulated compared with human normal gastric mucosal epithelial cell line (GES-1). 	Cancer susceptibility 19 (CASC19) was the top hub lncRNA among the lncRNAs included in the gene module most significantly correlated with AGC's pathological variables. CASC19 was upregulated in AGC clinical samples and was significantly associated with higher pathologic TNM stage, pathologic T stage, lymph node metastasis, and poor overall survival.Multivariable Cox analysis confirmed that CASC19 overexpression is an independent prognostic factor for overall survival.	Yes	 Functionally, CASC19 knockdown inhibited GC cell proliferation and migration in vitro. 	31422382
CASC9	LncRNA	Homo sapiens	Colonic Neoplasms	CC cells and tissues	Interaction[sponging miR-145-5p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 LncRNA CASC9 was high-expressed in CC cells and tissues, especially in CC at advanced TNM stages.LncRNA CASC9 is an oncogene in CC cells through sponging miR-145-5p. The findings in the current study provide a new understanding on CASC9 in CC.		Yes	 In HCT116 and SW480 cells, knockdown of CASC9 suppressed cell proliferation, promoted cell apoptosis and arrested cell cycle at G0/G1 phase.	35117034
CASC9	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues/ cells	regulation[down-regulating miR-424-5p]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Higher expression of CASC9 was observed in HCC tissues/ cells than in adjacent normal tissues/ human hepatic epithelial cells, and was closely linked to poor prognosis of HCC, tumor size, TNM stage, differentiation degree, lymph node metastasis and alpha-fetoprotein (AFP).  CASC9 promoted proliferation, invasion and migration and inhibited apoptosis in HCC cells by inhibiting miR-424-5p.	Higher expression of CASC9 was observed in HCC tissues/ cells than in adjacent normal tissues/ human hepatic epithelial cells, and was closely linked to poor prognosis of HCC, tumor size, TNM stage, differentiation degree, lymph node metastasis and alpha-fetoprotein (AFP). 	Yes	Down-regulation of CASC9 decreased the proliferation, invasion and migration of HCC cells while enhancing apoptosis. 	33346094
CASC9	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues,cell lines	interaction[FZD6/Wnt/β-catenin signaling pathway]	CCK8//qRT-PCR//FISH	This study found that CASC9 expression was markedly upregulated in bladder cancer and related to histological grade, TNM stage and prognosis. In summary, lncRNA CASC9 plays a critical regulatory role in bladder cancer. The CASC9/miR-497-5p/ FZD6 axis provides insights for regulatory mechanism of bladder cancer, and new strategies for clinical practice.	This study found that CASC9 expression was markedly upregulated in bladder cancer and related to histological grade, TNM stage and prognosis. 	Yes	 Knockdown of CASC9 inhibited tumor growth and metastasis of bladder cancer in vitro and in vivo.	32677984
CASC9	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder tissues,cell lines	interaction[sponges miR-758-3p]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//FISH//EdU Staining//Transwell Assay	CASC9 expression was significantly upregulated in BC cell lines and specimens compared to that in adjacent normal bladder tissues.Collectively, these results indicated that CASC9 sponged miR‑758‑3p to regulate the expression of TGF‑β2, which activated the TGF‑β signaling pathway and promoted proliferation and EMT in BC.	Upregulated CASC9 was associated with increased invasion ability and poor prognosis of BC. 	Yes	CASC9 knockdown inhibited BC cell proliferation, migration and invasion.	33200222
CASC9	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 BC tissues and cell lines	interaction[EZH2 ]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	CASC9 was upregulated in BC tissues and cell lines, and correlated with the staging and metastasis in BC. Upregulation of CASC9 induced by STAT3 promoted the progression of BC by interacting with EZH2 and affecting the expression of PTEN, representing a novel regulatory mechanism for BC progression.	CASC9 was upregulated in BC tissues and cell lines, and correlated with the staging and metastasis in BC.	Yes	 Knockdown of CASC9 inhibited the proliferation, migration, and invasion of BC cells. Similarly, silencing of CASC9 inhibited tumor growth in vivo. 	32982303
CASC9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines 	Regulation[AKT/mTOR pathway]	Western Blot//ISH//Tunel//Flow Cytometry//qRT-PCR//MTT//IHC	In this study, we found for the first time that CASC9 was remarkably upregulated in OSCC tissues and cell lines compared with paired noncancerous tissues and normal oral epithelial cells. In conclusion, our findings demonstrate that lncRNA CASC9 promotes OSCC progression through enhancing cell proliferation and suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway. 	Highly expressed CASC9 is strongly associated with tumor size, clinical stage, regional lymph node metastasis and overall survival time in OSCC patients. 	Yes	 In vitro, CASC9 knockdown in OSCC cells SCC15 and CAL27 significantly promotes autophagy and apoptosis, while inhibiting proliferation. 	30674868
CASC9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction(microRNA-545-3p/LAMC2)	Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Bioinformatics Analysis	 Our study confirmed that lncRNA CASC9 and LAMC2 were upregulated in OSCC, whereas miR-545-3p expression was reduced.  In addition, we proved for the first time that lncRNA CASC9 can sponge miR-545-3p to upregulate LAMC2. 		Yes	After performing a series of cell functional experiments, it was found that knockdown of lncRNA CASC9 or LAMC2 resulted in the inhibition of proliferation, colony formation, and migration of OSCC cells, but their negative effects could be partly impaired by the miR-545-3p inhibitor.	34612783
CASC9	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction( miR-874-3p/SOX12 axis)	In Vivo Experiment//IHC//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	LncRNA CASC9 was found to be up-regulated in OS.Besides, miR-874-3p was identified as the target of CASC9, and SOX12 acted as a potential target of miR-874-3p. The down-regulation of miR-874-3p recovered the reduction in cell invasion and proliferation in vitro which were induced by CASC9 knockdown and delayed the tumor progression in vivo.		Yes	Knockdown of CASC9 inhibited the proliferation and invasion of OS cells. 	36266695
CASC9	LncRNA	Homo sapiens	Glioma	glioma specimens and cells	Regulation[CASC9/miR-519d/STAT3]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Results manifested that CASC9 was highly expressed in glioma specimens and cells, moreover, the ectopic overexpression was correlated with glioma patients' clinic.  In conclusion, our results concluded that CASC9 promotes STAT3 expression via sponging miR-519d, in return, STAT3 activate CASC9 transcription, forming a positive feedback loop of CASC9/miR-519d/STAT3.	Results manifested that CASC9 was highly expressed in glioma specimens and cells, moreover, the ectopic overexpression was correlated with glioma patients' clinic. 	Yes	Functional studies found that siRNA-mediated CASC9 silencing inhibited the proliferative ability, invasion in vitro, and impaired the tumour growth in vivo. 	30270508
CASC9	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Interaction[regulating miR-145]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The expression level of CASC9 was upregulated in NPC tissues and cells. CASC9 knockdown inhibited cell migration and invasion but increased cell apoptosis in NPC cells by regulating miR-145, providing a novel insight for the treatment of NPC.		Yes	knockdown of CASC9 evidently suppressed migration and invasion but promoted apoptosis in NPC cells.	31933798
CASC9	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal carcinoma cells	Interaction(miR-497-5p/Wnt3a/β-catenin Signaling Pathway)	In Vivo Experiment//Western Blot//Invasion Assay//Migration Assay//Flow Cytometry//qRT-PCR//FISH//MTT//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis	Mechanism research confirmed CASC9 regulated the malignant biological behavior of nasopharyngeal carcinoma cells by targeting miR-497-5p/Wnt3a/β-catenin signaling pathway. 	 In this study, we found that CASC9 was overexpressed and associated with worse prognosis in NPC. 	Yes	CASC9 knockdown significantly inhibited the cell proliferation, migration and invasion in vitro and enhanced the sensitivity of tumor cells to cisplatin and paclitaxel. 	35419295
CASC9	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	regulation[miR-488-3p/ADAM9 pathway]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We found that CASC9 expression was augmented in human PTC tissues and cells.In conclusion, lncRNA CASC9 promoted the malignant phenotypes of PTC via modulating miR-488-3p/ADAM9 pathway.	Higher CASC9 expression was associated with large tumor size, advanced stage, or lymph node metastasis. 	Yes	Downregulation of CASC9 significantly attenuated the proliferative, migrative, and invasive abilities of PTC cells, and suppressed tumorigenesis in vivo. 	31943867
CASC9	LncRNA	Homo sapiens	Retinoblastoma	 RB tissues and cells	interaction[interacting with miR-145-5p]	qRT-PCR//Luciferase Report Assay//RIP	We found that CASC9 expression was elevated in RB tissues and cells.These findings suggested that CASC9 contributed to RB development by regulating E2F3 via sponging miR-145-5p. 		Yes	Overexpression of CASC9 significantly facilitated the proliferation, invasion and EMT of RB cells. On the contrary, knockdown of CASC9 inhibited the proliferation, invasion and EMT, while enhanced the apoptosis of RB cells. 	32772636
CASC9	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues and cells	regulation[ miR-423-5p/SOX12 Axes]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	CASC9 was up-regulated in the TSCC tissues and cells, and predicted a poor prognosis. miR-423-5p was predicted as the targeting miRNA of CASC9; this was verified by a luciferase reporter assay. CASC9 expression showed a negative correlation with miR-423-5p expression and a positive correlation with SOX12 expression. 	CASC9 was up-regulated in the TSCC tissues and cells, and predicted a poor prognosis. 	Yes	CASC9 silencing significantly inhibited cell proliferation, migration, and invasion of the TSCC cells compared with the non-targeting control small interfering RNA (siCtrl) treatment.	32021442
CASC9	LncRNA	Homo sapiens	laryngeal carcinoma	laryngeal carcinoma tissues,cell lines	Interaction[GLUT-1]	qRT-PCR//MTT//Transwell Assay	 Using quantitative reverse transcriptase PCR, we found higher expression of CASC9 and GLUT-1 in laryngeal carcinoma tissues and cells, compared to adjacent tissues and cells. The results showed that transfection with an overexpressed GLUT-1vector reversed the effects of silencing CASC9 on proliferation, migration, and apoptosis in TU212 and Hep-2 cells. 		Yes	An MTT assay of TU212 and Hep-2 cells showed increased cell proliferation after transfection with overexpressed CASC9 and decreased cell proliferation after transfection with silenced CASC9.A Transwell assay showed that overexpressing CASC9 increased and silencing CASC9 decreased cell migration of TU212 and Hep-2 cells. A flow cytometry assay showed that overexpressing CASC9 reduced and silencing CASC9 increased cell apoptosis. In other words, we found that overexpressing CASC9 increased cell proliferation and cell migration and decreased apoptosis both in TU212 and Hep-2 cells, whereas silencing CASC9 had the opposite effects. 	31669650
CASC9	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck		Expression[highly expressed]	CCK8//qRT-PCR	Finally, the potential function of two lncRNAs (CASC9 and LINC00152) that were upregulated in OC tissues and associated with patients' survival time was verified by loss-of-function assays in OC cells. 	Moreover, lots of lncRNAs expression levels are associated with OC patients' overall survival and recurrence-free survival; for example, higher CASC9, LINC01232, and MIR4435-1HG expression levels are related to shorter overall survival and recurrence-free survival in OC patients.	Yes	Next, CCK8 assays showed that knockdown of CASC9 and LINC00152 inhibited SCC4 and SCC25 cells’ proliferation compared with control cells (Fig. 4c–f). 	30543527
CASC9	LncRNA	Homo sapiens	Ovarian Neoplasms	OC cells 	Interaction(miR-488-3p/cyclinG1/TP53/MMP7 signaling)	Bioinformatics Analysis	The results of our study revealed that CASC9 expression was upregulated while miR-488-3p and CCNG1 expression was downregulated in OC cells with significant higher TP53 and MMP7 protein levels compared with normal ovarian surface epithelial cells. Additionally, luciferase reporter assay confirmed CASC9 bond to miR-488-3p/CCNG1. 		Yes	CASC9 silencing inhibited cell proliferation, migration, and invasion whereas promoted cell inhibition rate and apoptosis in vitro and in vivo . However, CASC9 overexpression showed the opposite effects. 	34595994
CASC9	LncRNA	Homo sapiens	Pneumonia	 serum samples 	Expression(lower expressed)	Transfection//CCK8//qRT-PCR//Cell Apoptosis Assay//ELISA	The relative expression of CASC9 was downregulated in serum samples of severe pneumonia patients.	The low expression of CASC9 in severe pneumonia was negatively correlated with several clinical data. The CASC9 had the relatively high area under ROC curve (AUC) values for distinguishing severe pneumonia from pneumonia children and healthy control.	Yes	The elevated expression of CASC9 accelerated cell viability and diminished apoptosis in LPS-induced MRC-5 cells. The CASC9 expression was decreased in serum samples of severe pneumonia, and upregulation of CASC9 facilitated LPS-induced cell viability and inhibited apoptosis.	35587261
CASC9	LncRNA	Homo sapiens	Colonic Neoplasms	serum	Expression(highly expressed)	qRT-PCR	Patients with CC showed notably higher lncRNA CASC9 expression than controls	ncRNA CASC9 presented an association with the clinical stage of the patients. In addition, lncRNA CASC9 demonstrated a clinical value in predicting efficacy on patients and acted as one independent prognostic factor for PFS in patients with ACC.	Yes	lncRNA CASC9 demonstrated a clinical value in predicting efficacy on patients and acted as one independent prognostic factor for PFS in patients with ACC.	34589129
CASC9	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC specimens and cell lines 	Interaction(MiR-542-3p/ILK)	CCK8//qRT-PCR//Western Blot//Transwell Assay	We demonstrated long non-coding RNA cancer susceptibility candidate 9 in CRC specimens and cell lines overexpressed via real-time quantitative polymerase chain reaction. This study testified that silencing long non-coding RNA cancer susceptibility candidate 9 could inhibit proliferation and invasion of CRC cells by miR-542-3p/integrin-linked kinase.		Yes	Once long non-coding RNA cancer susceptibility candidate 9 was knocked down, it significantly inhibited proliferation, invasion, and migration of CRC cells in real-time quantitative polymerase chain reaction, cell counting kit-8, 5-ethynyl-2'-deoxyuridine, and transwell assays, which also was validated in vivo. 	35427373
CASC2	LncRNA	Mus musculus	Hypertension, Pulmonary	pulmonary artery smooth muscle cells	Expression[lower expressed]	qRT-PCR//Wound Healing Assay//EdU Staining//Western Blot	 The expression of lncRNA CASC2 was decreased in hypoxia-induced rat pulmonary arterial tissues and pulmonary artery smooth muscle cells (PASMCs). Western blot analysis and immunochemistry showed that up-regulation of lncRNA CASC2 greatly decreased the expression of phenotype switch-related marker α-SMA in hypoxia-induced PH. Furthermore, it was indicated by the pulmonary artery morphometric analysis that lncRNA CASC2 suppressed vascular remodeling of hypoxia-induced rat pulmonary arterial tissues.		Yes	Up-regulation of lncRNA CASC2 inhibited cell proliferation, migration yet enhanced apoptosis in vitro and in vivo in hypoxia-induced PH.	30857524
CASC9	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines 	regulation[CASC9/miR-576-5p/AKT3 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining	In this study, we found that CASC9 was significantly upregulated in CRC tissues and cell lines compared to normal controls and that aberrant expression was associated with the tumor-node-metastasis (TNM) stage of CRC.In summary, we identified CASC9 as an oncogenic lncRNA in CRC and defined the CASC9/miR-576-5p/AKT3 axis, which might be considered a potential therapeutic target for CRC patients, as a novel molecular mechanism implicated in the proliferation and apoptosis of CRC.	In this study, we found that CASC9 was significantly upregulated in CRC tissues and cell lines compared to normal controls and that aberrant expression was associated with the tumor-node-metastasis (TNM) stage of CRC.	Yes	Functionally, CASC9 depletion efficiently inhibited the proliferation of CRC cells and induced cell apoptosis in vitro.	33298846
CBR3-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cell lines	Interaction(miR-3163/LASP1 pathway)	Other	Besides, we identified that lncRNA CBR3-AS1 interacted with miR-3163, and miR-3163 targeted to LASP1. Moreover, the correlation between lncRNA CBR3-AS1 and miR-3163, as well as the correlation between miR-3163 and LASP1 was confirmed. 		Yes	 LncRNA CBR3-AS1 knockdown suppressed cervical cancer cell viability and inhibited cancer stem cell-like properties. Finally, lncRNA CBR3-AS1 knockdown inhibited tumor growth and suppressed cancer stem cell-like properties of cervical cancer in vivo.	36591804
CBR3-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LAD and cell lines	Regulation(Wnt/β-catenin signaling)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Colony Formation Assay	LncRNA CBR3-AS1 is highly-expressed in LAD and cell lines. LncRNA CBR3-AS1 shows physical association with β-catenin. CBR3-AS1 could facilitate Wnt/β-catenin signaling activation thought promoting nuclear localization of β-catenin.		Yes	 CBR3-AS1 promotes LAD cell proliferation, migration and invasion by targeting Wnt/β-catenin signaling.	33422081
CBR3-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues 	Regulation(PTEN/Akt axis)	In Vivo Experiment//Western Blot//qRT-PCR//FISH//Cell Cycle Assay//IHC	We found that PlncRNA-1 was up-regulated in 85.29% of PCa tissues and could predict the T stage of PCa patients to a certain extent. PlncRNA-1 can promote the occurrence and development of PCa via the PTEN/Akt pathway.		Yes	Results showed that inhibition of PlncRNA-1 expression potentially promoted cell apoptosis, suppressed the proliferation, migration, and invasion of cells, and triggered G2/M cycle arrest in vitro and in vivo. 	33848262
CBR3-AS1	CircRNA	Homo sapiens	gestational choriocarcinoma	GC cells	Interaction(PTBP1/SETD4 )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	CBR3-AS1 was markedly upregulated in GC cells, and its downregulation suppressed cell proliferation, induced cell cycle arrest, but promoted cell apoptosis in GC. . SETD4 was determined as the downstream mRNA of CBR3-AS1 and positively regulated by CBR3-AS1 in GC cells. Furthermore, CBR3-AS1 could interact with its RNA binding protein (RBP) PTBP1, thereby stabilizing SETD4 mRNA. Rescue assays verified that CBR3-AS1 facilitates GC cell malignant proliferation via SETD4.		Yes	CBR3-AS1 was markedly upregulated in GC cells, and its downregulation suppressed cell proliferation, induced cell cycle arrest, but promoted cell apoptosis in GC. 	35655916
CATIP-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	 THCA tissues and cells	Interaction(miR-515-5p/Smad4 )	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	The result shows that the CATIP-AS1 was significantly downregulated in THCA tissues and cells and was associated with a poor prognosis of patients diagnosed with THCA.Summarily, we demonstrated that the CATIP-AS1 promotes the progression and metastasis of THCA via EMT pathway partly through regulating the miR-515-5p and Smad4 expression in THCA cell. 	The result shows that the CATIP-AS1 was significantly downregulated in THCA tissues and cells and was associated with a poor prognosis of patients diagnosed with THCA.	Yes	The overexpression of CATIP-AS1 significantly inhibited THCA cell proliferation, migration, and epithelial-mesenchymal transition (EMT) but increased the THCA cell apoptosis. We found that CATIP-AS1 endogenously sponges miR-515-5p and its overexpression could inhibit miR-515-5p regulatory effect. 	35264071
CASP5	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cell lines	Expression [highly expressed]	CCK8//Transwell Assay//Flow Cytometry//Western Blot	We observed that lncRNA CASP5 was highly expressed in GBM tissues and cell lines.We demonstrate for the first time the potential oncogenic role of lncRNA CASP5 which may be helpful for identifying novel therapeutic targets in GBM.		Yes	Knockdown of CASP5 greatly inhibited GBM proliferation and resulted in G1 cell cycle arrest along with higher apoptosis ratios in vitro and in vivo, while overexpression led to the opposite phenomenon. Furthermore, the migration and invasion ability of GBM cells were significantly decreased after CASP5 down-regulation, while increased migration and invasion can be observed after CASP5 up-regulation.	29715460
CASC9-1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	 cervical SCC cells	Interaction( miR-383-5p/MAPKAP1)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Tunel//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	 CASC9-1 was up-regulated in cervical SCC cells.  In terms of mechanism, CASC9-1 directly targeted miR-383-5p, and MAPKAP1 was the target gene of miR-383-5p in cervical SCC cells. CASC9-1 could exacerbate malignant behaviors of cervical SCC cells via binding to miR-383-5p and regulating MAPKAP1.		Yes	 CASC9-1 knockdown repressed cervical SCC cell proliferation, migration and invasion while elevating apoptosis. Via in-vivo experiments, CASC9-1 down-regulation was proved to restrict cervical SCC tumor growth.	34857398
CASC9	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[Regulating BMI1]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP	LncRNA CASC9 was upregulated in GC tissue and GC cells.LncRNA CASC9 could interact with BMI1 and positively regulate BMI1 expression. Silencing CASC9 promoted the ubiquitination of BMI1. In addition, lncRNA CASC9 regulated the apoptosis of GC cells through BMI1. Furthermore, interfering CASC9 inhibited the tumor growth of GC. LncRNA CASC9 could interact with BMI1 to regulate the degradation of BMI1, thus to affect the apoptosis of GC cells and suppressed tumor growth.	LncRNA CASC9 was upregulated in GC tissue and GC cells, and high CASC9 expression was positively correlated with TNM stage and lymph node metastasis.	Yes	Silencing CASC9 promoted the apoptosis of GC cells. 	31642035
CASC9	CircRNA	Homo sapiens	Stomach Neoplasms	Eighty GC tissues and paired adjacent normal tissues	Interaction(miR-370/EGFR axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Bioinformatics Analysis//CCK8//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Cell Apoptosis Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	 Our results showed that CASC9 was up-regulated significantly in both GC tissues and cell lines. Further analysis indicated that CASC9 directly targeted miR-370 and negatively regulated miR-370 expression in GC. Besides, EGFR (epidermal growth factor receptor) was identified as a direct target gene of miR-370. 		Yes	Conversely, CASC9 knockdown inhibited GC growth in vitro. 	33478874
CASC9	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction[sponging miR‑195/497]	Western Blot//ISH//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	 In the present study, lncRNA CASC9 was found to be significantly upregulated in both BC tissues and cell lines. Moreover, mechanical experiments demonstrated that lncRNA CASC9 positively regulated checkpoint kinase 1 (CHK1) by competitively binding to the miR‑195/497 cluster in BC cells. Additionally, the knockdown of lncRNA CASC9 was observed to suppress breast tumor growth in vivo. Taken together, the results of this study indicate that lncRNA CASC9 plays an oncogenic role in BC through sponging the miR‑195/497 cluster, and that lncRNA CASC9 may be used as a novel therapeutic target and as a potential diagnostic marker for BC.		Yes	Furthermore, functional analyses revealed that lncRNA CASC9 accelerated BC cell proliferation, promoted cell cycle progression and suppressed cell apoptosis. 	30816435
CASC9	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(miR-590-3p)	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	CASC9 protein was overexpressed in BC cells and tissues, while CASC9 knockdown inhibited BC cell growth, invasion, and migration and promoted apoptosis. 		Yes	CASC9 protein was overexpressed in BC cells and tissues, while CASC9 knockdown inhibited BC cell growth, invasion, and migration and promoted apoptosis. 	34711117
CASC9	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cell lines	Interaction(STAT3-activated CASC9 )	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay//ChIP	 CASC9 was found to be highly expressed in BC tissues and cell lines, and ectopic overexpression was positively associated with tumor volume, TNM stage, and lymph node metastasis.Mechanical studies demonstrated that CASC9 could be transcriptionally activated by STAT3 and elevate SOX4 expression by enhancing the acetylation of its promoter region. Our results illustrated that STAT3-activated CASC9 served as a tumor-promoting gene involved in promoting BC invasion and BC-associated formation of lymphatic vessels by upregulating SOX4 through altering H3K27ac level. 	CASC9 was found to be highly expressed in BC tissues and cell lines, and ectopic overexpression was positively associated with tumor volume, TNM stage, and lymph node metastasis.	Yes	In addition, CASC9 silencing significantly inhibited the proliferation and invasion of BC cells, as well as BC-associated invasion and formation of lymphatic vessels of human dermal lymphatic endothelial cells. 	35860965
CASC9	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[Binding to HuR]	CCK8//qRT-PCR//RIP//Flow Cytometry//Transwell Assay	CASC9, CDC6 and HuR expression were found significantly upregulated in NSCLC tissues, which predicted poorer 5-year overall survival in NSCLC patients.	CASC9, CDC6 and HuR expression were found significantly upregulated in NSCLC tissues, which predicted poorer 5-year overall survival in NSCLC patients.	Yes	Inhibition of CASC9 significantly reduced the malignancy of NSCLC cells, such as proliferation, migration and cell cycle. In vivo experiments further demonstrated that CASC9 knockdown reduced the tumor growth and the Ki-67 expression. 	33061598
CASC9	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-335-3p/S100A14 axis]	qRT-PCR	In this study, we found CASC9 expression was upregulated in NSCLC tissues and cell lines. Taken together, our study suggested CASC9 could promote NSCLC progression via miR-335-3p/S100A14 axis. 	 High CASC9 expression was identified as a predictor for poorer overall survival of NSCLC patients.	Yes	 Furthermore, functional assays showed CASC9 knockdown suppressed NSCLC cell proliferation, migration, and invasion, while CASC9 overexpression caused opposite effects.	32606808
CASC9	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	regulation[APOBEC3G]	Western Blot//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay	The expression of lncRNA ESCCAL-1 is upregulated in esophageal squamous cell carcinoma (ESCC). This study demonstrates that the lncRNA ESCCAL-1 promotes malignant features of ESCC by relieving the inhibitory effect of miR-590-3p on APOBEC3G expression and identifies potential biomarkers or therapeutic targets to improve ESCC treatment outcomes.		Yes	Furthermore, depletion of ESCCAL-1 in ESCC models inhibited the cellular processes associated with malignancy, including proliferation, migration and invasion, resistance to apoptosis, and impaired tumor growth in mice.	32905814
CASC9	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(ESCCAL-1/miR-590/LRP6 signaling pathway )	CCK8//qRT-PCR//Western Blot	The present work discovered the ESCCAL-1 up-regulation within ESCC. . Furthermore, ESCCAL-1 was found to interact with miR-590 and consequently restrict its expression. Importantly, it was confirmed that LRP6 was miR-590's downstream target and LRP6 over-expression also partly abolished the role of miR-590 overexpression in ESCC cells.		Yes	Functionally, knocking down ESCCAL-1 or over-expressing miR-590 hindered ESCC cell growth, invasion, and migration in vitro.  Moreover, inhibition of miR-590 could reverse the effect of knockdown of ESCCAL-1 on cells.	35655441
CASC9	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(Gal-1/NF-κB signaling)	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//Cell Proliferation Assay//IP//Transwell Assay	Multiple LncRNA expression datasets as well as our own data together reveal that ESCCAL-1 is evidently up-regulated in ESCC tissues and exhibits promising diagnostic value.  Mechanistically, LncRNA ESCCAL-1 directly binds to Gal-1 and positively regulates its protein level without affecting its mRNA level. Up-regulation of Gal-1 facilitated ESCC cell proliferation and cell-cycle progress. Knockdown of Gal-1 mitigated the effects of ESCCAL-1-mediated high cellular proliferation, NF-κB signaling activation and tumorigenicity of ESCC cells. 		Yes	Over-expression of ESCCAL-1 augmented ESCC cell proliferation and cell-cycle progression, whereas down-regulation of ESCCAL-1 resulted in the opposite effects.	35233069
CASC9	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	Interaction[CASC9/HIF-1α axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	CASC9 was overexpressed in lung cancer specimens and cell lines. Our findings demonstrated a novel regulatory signaling pathway, namely the CASC9/HIF-1α axis, which was involved in lung cancer progression. 		Yes	Knockdown of CASC9 inhibited cell proliferation, migration, invasion and EMT in lung cancer cells. While overexpression of CASC9 in normal lung epithelial cells did the opposite.	31802910
CASC9	LncRNA	Homo sapiens	Colorectal Neoplasms		Regulation[CASC9-CPSF3-TGFβ2 axis]	qRT-PCR//RNA Pull-Down//RIP//Western Blot	 CASC9 was frequently upregulated in CRC, which was correlated with advanced TNM stage, and higher CASC9 levels were associated with poor patient outcomes.CASC9 is a promising prognostic predictor for patients with CRC and the CASC9-CPSF3-TGFβ2 axis is a potential therapeutic target for CRC treatment.	 CASC9 was frequently upregulated in CRC, which was correlated with advanced TNM stage, and higher CASC9 levels were associated with poor patient outcomes.	Yes	Knockdown of CASC9 inhibited growth and promoted apoptosis in CRC cells, whereas ectopic CASC9 expression promoted cell growth in vitro and in vivo.	31186036
CASC9	LncRNA	Rattus norvegicus	Spinal Cord Injuries	 SCI rats and LPS-induced PC12 cells.	Interaction(miR-383-5p/ Furthermore, miR-383-5p was a direct target of CASC9 and was negatively regulated by CASC9. LDHA was a direct target of miR-383-5p and was negatively regulated by CASC9. )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA	 The results showed that lncRNA CASC9 was downregulated and miR-383-5p was upregulated in SCI rats and LPS-induced PC12 cells.  Furthermore, miR-383-5p was a direct target of CASC9 and was negatively regulated by CASC9. LDHA was a direct target of miR-383-5p and was negatively regulated by CASC9. 		Yes	Severe histological injury and increased water content were also found in SCI rats. Increased levels of LDH, MDA, lactic acid, TNF-α, and IL-1β were found in SCI rats and LPS-induced PC12 cells. These changes could be reversed by MP treatment in vivo or overexpression of CASC9 in vitro.Besides, overexpression of CASC9 decreased cell apoptosis and protein expression of LDHA and increased protein expression of Nrf2 and HO-1 in LPS-induced PC12 cells. 	33438067
CASC8	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction(hnRNPL/Bcl2/caspase3 pathway)	ISH//qRT-PCR//RNA Pull-Down//RIP	CASC8 was highly overexpressed in ESCC tissues and upregulation of CASC8 predicted poor prognosis in ESCC patients. Mechanistically, CASC8 interacted with heterogeneous nuclear ribonucleoprotein L (hnRNPL) and inhibited its polyubiquitination and proteasomal degradation, thus stabilizing hnRNPL protein levels and activating the Bcl2/caspase3 pathway. Additionally, AlkB Homolog 5, RNA demethylase (ALKBH5)-mediated m6A demethylation stabilized the CASC8 transcript, resulting in CASC8 upregulation. 	CASC8 was highly overexpressed in ESCC tissues and upregulation of CASC8 predicted poor prognosis in ESCC patients. 	Yes	 Moreover, CASC8 decreased the cisplatin sensitivity of ESCC cells and promoted ESCC tumor growth in vivo. 	35982900
CASC2c	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and corresponding non-cancer tissues,cell lines(H292、H226、H1975、H460)	Regulation[ERK1/2 and β-catenin signaling pathways ]	qRT-PCR//MTT//Transwell Assay//Western Blot	The results showed that CASC2c expression was significantly down-regulated in NSCLC tissues compared to matched adjacent non-tumor tissues (2.765 ± 1.605 v.s. 1.137 ± 0.754, p < 0.05, Fig. 1a). Furthermore, the expression of CASC2c in NSCLC cell lines (including H292, H226, H1975 and H460) were significantly lower than that in BEAS-2B cells (p < 0.05).Western blot assay showed that the high-expressed CASC2c can decrease the expression of phosphorylated-ERK1/2 (p-ERK1/2) and β-catenin.	  In addition, the CASC2c expression was remarkably correlated with TNM staging, tumor cell differentiation, lymph node metastasis, smoking and other pathological indicators of patients with NSCLC (p < 0.05). 	Yes	What's more, it inhibited the proliferation and migration of NSCLC cells by inhibiting the expression of p-ERK1/2 and β-catenin and reversed NSCLC cells' resistance to the chemotherapy drug cisplatin. 	31300295
CASC2c	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Regulation[ERK1/2 and Wnt/β-catenin signaling pathway]	qRT-PCR	In the present work, we observed that CASC2c was significantly down-regulated in HCC tissues and cells.Furthermore, we demonstrated that CASC2c overexpression decreased p-ERK1/2 levels in HCC, GC, and CRC cells. Interestingly, while overexpression of CASC2c decreased β-catenin expression in HCC and GC cells, it increased that in CRC cells.		Yes	 Moreover, its overexpression remarkably inhibited the growth, migration, and invasion of HCC cells in vitro and promoted their apoptosis.	31625123
CASC2	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cell lines	Regulation[PTEN/Akt signaling]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//BrdU//ChIP	According to recent studies, long noncoding RNA-CASC2 is involved in the development and progression of many malignant tumors; in the present study, we demonstrated that lncRNA-CASC2 was specifically downregulated in PC tissues and cell lines, and a lower CASC2 expression in PC was related with a poorer prognosis.CASC2 suppressed PC cell proliferation.		Yes	CASC2 suppressed PC cell proliferation.	28865121
CASC2	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues,cell lines	regulation[miR‑24/MUC6 axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	CASC2 and MUC6 were downregulated, and miR?24 was upregulated in pancreatic cancer specimens and cell lines. CASC2 exerted tumor‑suppressive functions in pancreatic cancer through the miR‑24/MUC6 axis, which may be a promising target for pancreatic cancer therapy.		Yes	 Functionally, CASC2 overexpression or miR?24 knockdown suppressed pancreatic cancer cell proliferation, colony formation, migration and invasion, and promoted apoptosis. 	31894271
CASC2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	adenocarcinoma tissues,cell lines	Interaction[miR-4735-3p and mTOR]	qRT-PCR	We found that long noncoding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2), a putative tumor suppressor, was downregulated in both patient adenocarcinoma tissues and cultured lung cancer cells.  Furthermore, the lncRNA and miR-4735-3p interplay likely the suppressed tumor growth through the downstream mammalian target of rapamycin signaling pathway. The results have revealed molecular details that may be critical for the development of lung adenocarcinoma, opening opportunities for the development of novel, and therapeutic tools.		Yes	Changing the levels of CASC2 and miR-4735-3p in the cultured adenocarcinoma cells could affect the malignant phenotypes as well as growth of tumors derived from the cells injected into nude mice.	30450692
CASC2	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD patients and LUAD cell lines	Interaction(miR-21/p53 axis)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay	CASC2 was expressed at a low level in LUAD patients and LUAD cell lines. Mechanistically, CASC2 overexpression dramatically inhibited miR-21 expression and increased p53 expression by directly targeting miR-21. 		Yes	CASC2 overexpression markedly suppressed cell proliferation and enhanced apoptosis. 	34337857
CASC2	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and cells	regulation[miR-18a/SOCS5 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	 It was found that CASC2 was expressed at a significantly lower level in CCA tissues and cell lines. CASC2 was downregulated in CCA tissues and cells. It could inhibit cell proliferation, invasion, migration and EMT via sponging miR-18a/SOCS5 axis. 		Yes	 The overexpression of CASC2 inhibited QBC939 cell proliferation, invasion and migration when the knockdown of CASC2 accelerated HUCCT1 cell growth and metastasis. 	32894543
CASC2	LncRNA	Homo sapiens	Prostatic Neoplasms	PC tissues and cell lines	Expression[lower expressed]	qRT-PCR	 Herein, CASC2 and SPRY2 expression was down-regulated in PC tissues and cell lines		Yes	 the overexpression of CASC2 and SPRY2 could suppress PC cell proliferation, promote PC cell apoptosis	29373811
CASC2	LncRNA	Homo sapiens	Melanoma	MM tissues	Interaction[miR-18a-5p/RUNX1]	MTT//Luciferase Report Assay//Transwell Assay	The levels of CASC2 and RUNX1 were significantly reduced in MM tissues compared with normal skin tissues or cells, while the miR-18a-5p level was obviously increased (all p < 0.01). The luciferase reporter assay revealed that CASC2 acted as a molecular sponge for miR-18a-5p, and RUNX1 was a target gene of miR-18a-5p. Moreover, CASC2 overexpression promoted the expression of RUNX1, while upregulated miR-18a-5p significantly reversed the effect of CASC2 on the RUNX1 level (all p < 0.05). Upregulated CASC2 may inhibit cell proliferation, migration, and invasion through regulating miR-18a-5p and its target gene RUNX1 in MM.		Yes	Cell viability, colony number, migration, and invasion were significantly decreased in cells with pc-CASC2 compared with cells transfected with pcDNA3.1 (all p < 0.05).	29422114
CASC2	LncRNA	Homo sapiens	Diabetic Nephropathies	serum 	regulation[miR-133b/FOXP1 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay	The expression of CASC2 was reduced in serum from DN patients and HG-induced HMCs.CASC2 upregulation suppressed HG-induced proliferation, ECM accumulation and oxidative stress of HMCs through miR-133b /FOXP1 regulatory axis, suggesting that CASC2 was a novel biomarker for DN treatment.		Yes	CASC2 upregulation inhibited HG-induced HMCs proliferation, ECM accumulation and oxidative stress. 	32016985
CASC2	LncRNA	Homo sapiens	stomach carcinoma	GC tissues and cell lines	Regulation[E2F6/CASC2 axis]	Flow Cytometry//qRT-PCR//Transwell Assay//Western Blot	Our data revealed that CASC2 was downregulated while E2F6 was upregulated in GC tissues and cell lines. Furthermore, downregulation of E2F6 decreased the expression of MMP-2 and increased the activity of caspase-3. However, these changes triggered by E2F6 knockdown could be reversed by inhibition of CASC2. Moreover, we also proved that downregulation of CASC2 reverses the effect of E2F6 knockdown on tumor growth in vivo.	Remarkably, lower expression of CASC2 was associated with poor survival in GC patients.	Yes	Subsequently, reliable data showed that downregulation of E2F6 suppressed the proliferation and invasion, and promoted the apoptosis of GC cells.	31301415
CASC2	LncRNA	Homo sapiens	Sepsis	serum 	regulation[miR-155 and NF-κB pathway]	qRT-PCR	The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects.  In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis‑induced AKI by inhibiting the miR‑155 and NF‑κB pathway‑mediated inflammation.		Yes	 Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide?stimulated human renal tubular epithelial HK?2 cells.	32323747
CASC2	LncRNA	Homo sapiens	Asthma	ASMCs	Interaction(miR-31-5p)	CCK8//qRT-PCR//Luciferase Report Assay//ELISA//Transwell Assay	CASC2 was at a low level in asthma children in comparison with the healthy controls. Serum CASC2 can distinguish healthy individuals from asthma children. In PDGF-BB treated ASMCs, the reduced expression of contractile phenotype marker (α-SMA) was detected, but the trend was reversed by CASC2 upregulation. LncRNA CASC2 serves as a ceRNA of miR-31-5p, overexpression of miR-31-5p reversed the influence of CASC2 on asthma in vitro.		Yes	Overexpression of CASC2 inhibited PDGF-BB induced cell proliferation and migration. CASC2 upregulation inhibited the release of Th2 related cytokines (IL-4 and IL-10), but promoted the release of Th1-related cytokine (IFN-γ). 	35185342
CASC2	LncRNA	Homo sapiens	Arthritis, Rheumatoid	plasma 	regulation[downregulating IL-17]	Flow Cytometry//qRT-PCR//ELISA//Western Blot	Our preliminary microarray data showed that lncRNA CASC2 was downregulated in the plasma of patients with rheumatoid arthritis (RA), indicating the involvement of this lncRNA in RA.Therefore, downregulation of lncRNA CASC2 is involved in RA and lncRNA CASC2 overexpression may promote the apoptosis of HFLS by downregulating IL‑17.		Yes	Overexpression of lncRNA CASC2 promoted, while treatment with IL?17 inhibited the apoptosis of human fibroblast?like synoviocytes (HFLSs) isolated from RA patients.	32186765
CASC2	LncRNA	Homo sapiens	Arthritis, Rheumatoid	 patients with RA	Interaction(miR-18a-5p/BTG3 signaling axis )	Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//ELISA	Compared with the healthy subjects, lncRNA CASC2 was downregulated, whereas miR-18a-5p was upregulated in patients with RA. Overall, lncRNA CASC2 alleviated RA by adjusting the miR-18a-5p/BTG3 signaling axis and could serve as a novel therapeutic option for RA.		Yes	 Overexpression of lncRNA CASC2 decreased the viability of human fibroblast-like synoviocytes (HFLSs) and induced apoptosis, as revealed by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and flow cytometry analyses. F	35045800
CASC2	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive	Serum of fifty smokers with COPD and another 50 smokers without COPD 	Interaction(miR-18a-5p/IGF1 axis)	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA	Serum CASC2 was dramatically decreased in COPD patients compared with smokers without COPD, and was positively associated with FEV1 (forced expiratory volume in one second). CASC2 was overexpressed in severe COPD patients, and had the diagnostic accuracy to distinguish COPD patients from smokers.  CASC2 functions as a ceRNA of miR-18a-5p. Upregulation of miR-18a-5p reversed the influence of CASC2 on cell apoptosis and inflammation in 16HBE cells. IGF1 was the target gene of miR-18a-5p.		Yes	CASC2 overexpression alleviated CSE-induced apoptosis and inflammation in 16HBE cells. CASC2 functions as a ceRNA of miR-18a-5p. Upregulation of miR-18a-5p reversed the influence of CASC2 on cell apoptosis and inflammation in 16HBE cells. IGF1 was the target gene of miR-18a-5p.	34266334
CASC2	LncRNA	Homo sapiens	Diabetic Foot	 tissues of ulcers of DFU mice and patients	Interaction(miRNA-155/HIF-1 α)	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	According to our study, the lncRNA CASC2's expression was low in the tissues of ulcers of DFU mice and patients. In addition, lncRNA CASC2 directly targets miR-155 and HIF-1α functions as miR-155's target gene. Overexpression of miR-155 abrogated the function of lncRNA CASC2.		Yes	 lncRNA CASC2's overexpression promoted fibroblasts migration, proliferation, and inhibited apoptosis and was beneficial for the healing of wounds, preferably in the DFU mice.	35845734
CASC2	LncRNA	Homo sapiens	Lymphoma, Non-Hodgkin	cell lines	regulation[LncRNA-CASC2/miR-155-5p/APC Axis ]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 CASC2 was downregulated in NHL cell lines.Overexpression of CASC2 suppresses the proliferation and invasion of NK-92 cells, promote the apoptosis of NK-92 cells via targeting miR-155-5p and upregulating APC expression.		Yes	 Overexpression of CASC2 could inhibit the proliferation and invasion of NK-92 cells, and promote its apoptosis.	33283723
CASC2	LncRNA	Homo sapiens	Acute Lung Injury	Serum specimens	Interaction(miR-152-3p/PDK4 Axis)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//ELISA	CASC2 and PDK4 were down-regulated, while miR-152-3p was up-regulated in sepsis patients and LPS-stimulated HPAEpiC. In addition, miR-152-3p was a miRNA target of CASC2 and CASC2 alleviated cell injury in LPS-disposed HPAEpiC by sponging miR-152-3p. Moreover, miR-152-3p directly targeted PDK4 and CASC2 increased the PDK4 expression by depending on the sponge effect on miR-152-3p. 		Yes	Overexpression of CASC2 relieved the LPS-resulted cell viability inhibition, apoptosis promotion, inflammatory and oxidative damages in HPAEpiC.	34165388
CASC2	LncRNA	Homo sapiens	Acute Kidney Injury	sepsis patients' serums and LPS-treated HK2 and HEK293 cells	Interaction(MiR-545-3p/PPARA Axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	 CASC2 level was decreased in sepsis patients' serums and LPS-treated HK2 and HEK293 cells.CASC2 was identified as a sponge for miR-545-3p to regulate PPARA expression. MiR-545-3p overexpression restored the impact of CASC2 on LPS-induced injury in HK2 and HEK293 cells. Moreover, miR-545-3p overexpression aggravated LPS-induced cell injury in HK2 and HEK293 cells by targeting PPARA.		Yes	CASC2 overexpression facilitated cell viability and restrained cell apoptosis, migration, epithelial-mesenchymal transition (EMT) and oxidative stress in LPS-triggered HK2 and HEK293 cells.	33957574
CASC2	LncRNA	Mus musculus	Diabetic Nephropathies	urine 	regulation[miR-144/SOCS2 axis]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	The expression of CASC2 in diabetic mouse models and HG-induced HRMCs was lower than that in the control (p < 0.05). CASC2 could alleviate the degree and process of apoptosis, inflammation, and fibrosis in diabetic nephropathic models by regulating the miR-144/SOCS2 axis.		Yes	Overexpression of CASC2 resulted in a decrease in the apoptosis rate, inflammatory factor release (TNF-α, IL-6, and IL-1β), expression of cleaved caspase-3, and fibrotic proteins (fibronectin, Col-IV, and TGF-β1) and an increase in Bcl-2 expression. 	33227790
CASC2	LncRNA	Homo sapiens	Pancreatic Neoplasms	cell lines	Interaction[downregulating miR-21]	qRT-PCR//Transwell Assay	 CASC2 expression was downregulated in the pancreatic cancer cell lines CAPAN-1, BxPC-3, JF305, PANC-1 and SW1990 compared with levels in normal human pancreatic HPDE6-C7 cells. MiR-21 was a direct target of CACS2. The overexpression of miR-21 significantly abolished the antimetastatic effects of CASC2 on PANC-1 cells. Moreover, the downregulation of PTEN significantly abolished the antimetastatic effects of CASC2.		Yes	 CACS2 overexpression inhibited the migration and invasion of PANC-1 cells and significantly inhibited the expression of miR-21 and PTEN. 	30675129
CASC2	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	tumor tissues and plasma 	Regulation[EMT pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	We demonstrated that lncRNA CASC2 expression was significantly downregulated in tumor tissues and plasma samples in patients with PTC compared with those in nodular goiters (P< 0.05).  Moreover, we demonstrated that overexpression of lncRNA CASC2 suppressed cell epithelial-mesenchymal transition (EMT) process of PTC by increasing the E-cadherin expression, but downregulating ZEB1 and N-cadherin expression.	Decreased plasma lncRNA CASC2 expression associated with lymph node metastasis (LNM) of PTC patients and was identified as an independent risk for patients with LNM (P< 0.05). 	Yes	Furthermore, functional assays demonstrated that overexpression of lncRNA CASC2 inhibited cell proliferation, migration and invasion of PTC. 	30175973
CASC2	CircRNA	Homo sapiens	Thyroid Neoplasms	 thyroid cancer	Interaction( miR-18a-5p/FIH1 axis)	Western Blot//Transfection//Migration Assay//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	We demonstrated that CASC2 was downregulated in thyroid cancer. Bioinformatics analysis predicted that hypoxia inducible factor 1 subunit alpha inhibitor (FIH-1) was potentially targeted by miR-18a-5p, which was confirmed by luciferase reporter assay. Upregulation of FIH-1 abrogated the promotive effect of miR-18a-5p on the growth and invasion of thyroid cancer cells.		Yes	e noted that CASC2 overexpression restrained the growth, migration, and invasion of thyroid cancer cells, whereas CASC2 depletion caused opposite trends. 	33336500
CASC2	LncRNA	Homo sapiens	Colonic Neoplasms	 cancer cell lines	Interaction(miR-19a)	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	Expression of lncRNA CASC2 lower in cancer cell lines and the overexpression reduced the cell viability of HT29 and SW480. 		Yes	Furthermore, Bcl-2 was suppressed by overexpressed lncRNA CASC2, while Bax was upregulated. LC3-Ⅰ and p62 were both inhibited, but LC3-Ⅱ was promoted. MiR-19a was predicted to bind lncRNA CASC2 and expressed higher in cancer cell lines. 	33983643
CASC21	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Regulation[miR-7-5p/YAP1 axis]	Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	By bioinformatics analysis, CASC21 was found to be significantly up-regulated in colorectal cancer tissues.Mechanistically, CASC21 could competently bind to miR-7-5p, resulting in increased YAP1 expression. Furthermore, up-regulation of YAP1 could rescue the inhibitory effects of CASC21 knockdown on EMT and cell invasion.		Yes	 Moreover, CASC21 knockdown displayed significant depression in cell viability, proliferation, migration, and invasion in colorectal cancer cells, as well as EMT process, while cell apoptosis was promoted by regulating the Bcl-2/Bax axis and Caspase cascade.	31731190
CASC21	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues 	regulation[regulating CDK6]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//ChIP	CASC21 is overexpressed in CRC and high CASC21 expression is associated with poor survival.Mechanistically, we found that CASC21 expressed predominantly in the cytoplasm. CASC21 could interact with miR-539-5p and regulate its target CDK6.	CASC21 is overexpressed in CRC and high CASC21 expression is associated with poor survival.	Yes	Functional experiments revealed that CASC21 promotes CRC cell growth.	32584787
CASC21	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell	Interaction(miR-485-5p/POU5F1B)	RNA Pull-Down//qRT-PCR//RIP//IF//Luciferase Report Assay//IHC//ChIP	 In addition, CASC21 was co-expressed with and bound to transcription factor POU5F1B (POU class 5 homeobox 1B). CASC21 recruited POU5F1B to HGH1 promoter to activate the transcription of HGH1 homolog. Also, CASC21 served as a competitive endogenous RNA (ceRNA) to up-regulate HGH1 via endogenously sponging miR-485-5p. 		Yes	The results revealed that CASC21 facilitated CRC cell proliferation, migration, epithelial-mesenchymal transition (EMT) and stemness. 	34375566
CASC20	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tumor tissues and various GC cell lines	Interaction(miR-143-5p/MEMO1 molecular axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 The expression of CASC20 was increased in GC tumor tissues and various GC cell lines.Mechanistic studies revealed that CASC20 exhibits oncogenic functions by regulating MEMO1 expression through competitive endogenous binding to miR-143-5p, leading to induction of epithelial-mesenchymal transition.	 High CASC20 expression was correlated with a high risk of lymphatic metastasis and poor prognosis in GC patients.	Yes	 In vitro assays showed that silencing CASC20 reduced cell proliferation, migration, and invasion in GC cells	35581960
CASC2	LncRNA	Homo sapiens	Breast Neoplasms	Breast Cancer tissues,cell line( HCC1937 , LCC9, MDA-MB-231,MCF-7)	Interaction[TGF-β]	qRT-PCR//MTT//Western Blot	In the present study, lncRNA CASC2 was found to be significantly Expression[down-expression]regulated in breast cancer tissues and cell lines using real-time quantitative PCR.Additionally, based on the above research, we illustrated that inactivation of the TGF-β signaling pathway was involved in the function of lncRNA CASC2.		Yes	Furthermore, gain-of-function assays demonstrated that overexpression of lncRNA CASC2 significantly repressed breast cancer cell proliferation and metastasis. 	29523222
CASC2	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction[increasing SOCS1 ]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	In the present study, we found that CASC2 was significantly downregulated in ESCC tissues and positively correlated with overall survival time of patients with ESCC.Conclusively, these results demonstrated that CASC2 could exert as a tumor suppressive lncRNA in ESCC progression via regulating SOCS1.	In the present study, we found that CASC2 was significantly downregulated in ESCC tissues and positively correlated with overall survival time of patients with ESCC.	Yes	Functional assays demonstrated that CASC2 suppressed proliferation, migration and invasion, as well as enhanced drug sensitivity in ESCC cells.	31728180
CASC2	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues 	Interaction(miR-18a-5p/BTG3 Pathway)	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	CASC2 was decreased in CRC tissues and cell lines, and its low expression in CRC tissues was associated with larger tumor size and lymph node metastasis. CASC2 could function as a molecular sponge for miR-18a-5p and repress the expression of miR-18a-5p. Furthermore, the inhibitory effects of CASC2 on the malignant phenotypes of CRC cells was counteracted by miR-18a-5p mimics. Additionally, CASC2 could positively regulate BTG3 expression via suppressing miR-18a-5p.		Yes	CASC2 overexpression restrained proliferative, migrative and invasive capabilities of CRC cells.	36377216
CASC2	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cell lines	regulation[TRIM16 expression]	qRT-PCR//Luciferase Report Assay//Western Blot	The gene expression analysis showed that LncRNA CASC2 is significantly suppressed in colon cancer tissues and cell lines. Additionally, silencing of TRIM16 resulted in the inhibition of HT-29 cell growth similar to that of CASC2 overexpression. 		Yes	Overexpression of CASC2 inhibited the growth of HT-29 cells. 	32655801
CASC2	LncRNA	Homo sapiens	Osteoarthritis	blood	Interaction[IL-17]	qRT-PCR	Our new findings showed that both lncRNA CASC2 and IL-17 were up-regulated in plasma of osteoarthritis patients. Therefore, lncRNA CASC2 is up-regulated in osteoarthritis and participates in the regulation of IL-17 expression and chondrocyte proliferation and apoptosis. ®		Yes	In addition, overexpression of lncRNA CASC2 inhibited the proliferation, and promoted the apoptosis of chondrocyte. 	31015370
CASC2	LncRNA	Homo sapiens	Thyroid Neoplasms	 thyroid cancer tissues,cell lines	interaction[ sponging miR-24-3p]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 CASC2 was significantly downregulated in thyroid cancer. In addition, upregulation of CASC2 could inhibit the tumorigenesis of TC via sponging miR-24-3p. 		Yes	Overexpression of CASC2 inhibited the proliferation, migration, and invasion of thyroid cancer cells.	33194032
CASC2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Expression[lower expressed]	Western Blot//Wound Healing Assay//Flow Cytometry//Colony Formation Assay//Transwell Assay	In tissues and cells of HCC, decreased CASC2 expressions were confirmed.		Yes	Meanwhile, the overexpression of CASC2 played significant roles in inhibiting the proliferation, migration, and invasion of HCC cells. Furthermore, In vivo experiment indicated that CASC2 restrained the growth of tumors.	30362539
CASC2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cell lines	Regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CASC2 was down-regulated in HCC tissues and cell lines, while miR-183 was up-regulated.  Overexpression of CASC2 inhibited cell viability, colony formation, migration, and invasion in HCC cells, as well as Wnt/β-catenin signaling pathway activity. CASC2 inhibited cell viability and the colony formation, migration, and invasion abilities of HCC cells by directly downregulating miR-183 through inactivation of the Wnt/β-catenin signaling pathway.		Yes	Overexpression of CASC2 inhibited cell viability, colony formation, migration, and invasion in HCC cells, as well as Wnt/β-catenin signaling pathway activity. 	31538425
CASC2	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue	Interaction[PDCD4 ]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	The results demonstrated that CASC2 was significantly downregulated in clinical OSCC tissue samples and cultured OSCC cell lines.Furthermore, bioinformatics analysis and dual-luciferase reporter assay showed that CASC2 might act as a competing endogenous RNA of miR-21 to promote the expression of PDCD4. Rescue experiments also showed that miR-21 blocked the tumor-suppressive role that CASC2 exerted in OSCC cells. Finally, in vivo study indicated that overexpression of CASC2 restrained OSCC tumor growth in volume and weight.		Yes	 Functionally, overexpression of CASC2 remarkably inhibited cell proliferation partly through inducing cell cycle arrest and cell apoptosis.	31123403
CASC2	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	Interaction[MAPK pathway]	CCK8//qRT-PCR//Western Blot	 CASC2 levels in human cervical cancer tissues and cell lines were significantly downregulated compared to para-cancerous tissues and the immortalized human keratinocyte line HaCaT.  Moreover, the expression of p-JNK and p-ERK1 levels in the MAPK pathway was significantly decreased in pcDNA3.1-CASC2 group.		Yes	Compared to scramble group, CASC2 overexpression significantly inhibited the proliferation, migration, invasion, and angiogenesis of cervical cancer cells. However, the inhibition of CASC2 had the opposite effect. 	31081078
CASC2	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues, cell lines	Regulation[CASC2/miR‑18a‑5p axis]	CCK8//qRT-PCR//Luciferase Report Assay//RIP	 We showed that the CASC2 level is reduced in NPC tissues and cells.There were putative binding sites of microRNA (miR)‑18a‑5p in the promoter of CASC2. The level of miR‑18a‑5p was upregulated in NPC tissues and cells. We further confirmed that CASC2 could directly bind with miR‑18a‑5p and inhibit miR‑18a‑5p expression, using reporter gene and RNA immunoprecipitation assays. miR‑18a‑5p suppressed CASC2 upregulation‑mediated decrease in proliferation and increase in apoptotic cell death. Bioinformatics predicted the putative binding site of miR‑18a‑5p in the 3' untranslated region of C‑terminal binding protein interacting protein (CtIP)/RBBP8. It was further confirmed that miR‑18a‑5p could directly bind with RBBP8 and inhibit RBBP8 expression. Downregulation of RBBP8 inhibited the anti‑miR‑18a‑5p‑mediated increase in apoptosis and decrease in proliferation. Downregulation of CASC2 increased tumor growth, increased the level of miR‑18a‑5p and decreased RBBP8 expression in vivo. In summary, CASC2 regulates NPC malignancy through modulation of RBBP8 via sponging miR‑18a‑5p.		Yes	CASC2 downregulation promoted proliferation and inhibited apoptotic cell death in NPC cells. In contrast, CASC2 upregulation inhibited proliferation and increased apoptosis.	30569153
CASC2	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tumor tissues and cells (T98 and A172)	regulation[CASC2- miR-18a axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Colony Formation Assay//Transwell Assay	 As a result, CASC2 was downregulated and miR-18a was upregulated in glioblastoma tumor tissues and cells (T98 and A172). Collectively, this study demonstrated that CASC2 served as tumor suppressor in glioblastoma by inhibiting cell growth, metastasis and EMT both in vitro and in vivo partially via CASC2- miR-18a axis.		Yes	Overexpression of CASC2 promoted apoptosis rate and E-cadherin expression, but suppressed cell viability, colony-forming ability, migration, invasion, and expression of N-cadherin and Vimentin in T98 and A172 cells, accompanied with tumor growth inhibition in vivo; whereas, silencing of CASC2 exerted the opposite effect on cell growth, metastasis and EMT of T98 and A172 cells in vitro.	32975234
CASC2	LncRNA	Homo sapiens	Atherosclerosis	blood	regulation[miR-532-3p/PAPD5]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The expression levels of CASC2 were decreased, while the expression levels of miR-532-3p were elevated in AS patient samples and VSMCs.CASC2 suppressed cell reproduction and promoted cell apoptosis by regulating the miR-532-3p/PAPD5 axis in ox-LDL-mediated VSMCs. This might be important for AS therapeutics.		Yes	 Overexpression of CASC2 inhibited the proliferation and migration of VSMCs and enhanced cell apoptosis.	32698757
BRE-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Interaction(miR-21)	RNA Pull-Down//Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC.	Low expression levels of lncRNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes. BRE-AS1 and miRNA-21 were inversely correlated across TNBC samples, not control samples. BRE-AS1 decreased miR-21 expression and increased PTEN expression while miR-21showed no role in BRE-AS1 expression. RNA pull-down assay illustrated that BRE-AS1 may sponge premature miR-21 to suppress it maturation. 	Yes	Overexpression of BRE-AS1 decreased cell behaviors, while overexpression of miR-21 promoted cell behaviors. MiR-21	34182945
BRE-AS1	LncRNA	Homo sapiens	prostate carcinoma	prostate carcinoma tissues	Interaction[miR-145-5p]	CCK8//PCR	In the present study we found that plasma BRE-AS1 and miR-145-5p were both down-regulated in PC patients than in healthy controls.BRE-AS1 overexpression mediated miR-145-5p Expression[up-expression]-regulation in PC cells, while miR-145-5p overexpression did not significantly affect BRE-AS1. miR-145-5p inhibitor attenuated the effects of BRE-AS1 overexpression on cancer cell behaviors. 	Down-regulation of BRE-AS1 and miR-145-5p effectively distinguished early-stage PC patients from healthy controls. 	Yes	 Overexpression of BRE-AS1 and miR-145-5p led to inhibited proliferation and promoted apoptosis of PC cells. 	30833361
BORG	LncRNA	Homo sapiens	Breast Neoplasms	murine and human TNBC cells	Interaction(TRIM28 complexes )	Flow Cytometry//qRT-PCR//RNA-seq	Indeed, we found BORG expression to: (i) correlate with stem cell markers Nanog, Aldh1a3, and Itga6 (α6 integrin/CD49f); (ii) enhance stem cell phenotypes in murine and human TNBC cells, and (iii) promote TNBC tumor initiation in mice. Collectively, these findings implicate BORG:TRIM28 complexes as novel drivers of BCSC phenotypes in developing and progressing TNBCs. 		Yes	Indeed, we found BORG expression to: (i) correlate with stem cell markers Nanog, Aldh1a3, and Itga6 (α6 integrin/CD49f); (ii) enhance stem cell phenotypes in murine and human TNBC cells, and (iii) promote TNBC tumor initiation in mice. 	34497119
B3GALT5-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissues	Regulation[B3GALT5-AS1/miR-203/EMT axis]	qRT-PCR	 In this study, we identified a novel lncRNA B3GALT5-AS1, which is reduced in colon cancer tissues and further reduced in colon cancer liver metastasis tissues.Our data suggested that the activating B3GALT5-AS1/miR-203/EMT axis may be potential therapeutic strategy for colon cancer liver metastasis.	Reduced expression of B3GALT5-AS1 is associated with liver metastasis and poor outcome of colon cancer patients.	Yes	 Gain-of-function and loss-of-function assays revealed that B3GALT5-AS1 inhibited proliferation but promoted migration and invasion of colon cancer cells. 	30530918
AY343892	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	regulation[BRCA1-mediated transcription of PTEN]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//ChIP	 In this research, we found that lncRNA AY343892 was significantly down-regulated in breast cancer tissues and cells. In conclusion, this study illustrated that AY343892 inhibited breast cancer development by positively regulating BRCA1-mediated transcription of PTEN. 		Yes	Functional assays indicated that overexpression of AY343892 significantly inhibited proliferation and promoted apoptosis in breast cancer cells. 	32754899
AXL	CircRNA	Homo sapiens	Alzheimer Disease	 AD models, cell line	Interaction(miR-328/BACE1)	Western Blot//Transfection//qPCR//PCR//IF	Additionally, circ-AXL negatively regulated miR-328 but positively modulated BACE1; besides, miR-328 negatively regulated BACE1; further luciferase reporter gene assay presented that circ-AXL directly bound miR-328, and miR-328 directly bound BACE1. Furthermore, miR-328 overexpression decreased apoptosis rate, elevated neurite outgrowth, and declined inflammatory cytokines in cellular AD models; but miR-328 knockdown presented opposite effects. Notably, miR-328 knockdown attenuated the effect of circ-AXL knockdown on cellular AD models. 		Yes	Circ-AXL overexpression increased apoptosis rate and declined neurite outgrowth, as well as elevated inflammatory cytokines in cellular AD models; but circ-AXL knockdown exhibited opposite effects. 	35167942
AWPPH	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and adjacent normal tissues	Regulation[miR-203a/DKK2 axis]	qRT-PCR//Luciferase Report Assay//Western Blot	It turned out that lncRNA AWPPH was significantly decreased in GC tissues, comparing to adjacent noncancerous gastric tissues. Upregulation of miR-203a attenuated the repressive effects of AWPPH on GC cell proliferation and invasion. AWPPH inhibited GC cell proliferation and invasion via miR-203a/DKK2 axis.	 	Yes	CCK8 and transwell assays proved that AWPPH inhibited cell proliferation and invasion in GC cells. 	31489578
AWPPH	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[ TGF-β1]	qRT-PCR//ELISA//Western Blot	It was observed that AWPPH was significantly Expression[Expression[up-expression]-expression]regulated in patients with NSCLC, while AWPPH expression level did not increase with the increase of tumor size. AWPPH overexpression promoted TGF-β1 expression in NSCLC cells, while TGF-β1 treatment showed no significant effects on AWPPH expression. AWPPH overexpression promoted NSCLC cell migration and invasion, while TGF-β signaling inhibition reduced this enhancing effect.		Yes	 AWPPH overexpression promoted TGF-β1 expression in NSCLC cells, while TGF-β1 treatment showed no significant effects on AWPPH expression. AWPPH overexpression promoted NSCLC cell migration and invasion, while TGF-β signaling inhibition reduced this enhancing effect.	31516619
AWPPH	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	interaction[miRNA-204 ,CDK6]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Upregulated AWPPH and downregulated miRNA-204 were determined in NSCLC tissues.  LncRNA AWPPH serves as the miRNA-204 sponge to upregulate CDK6 level, thus aggravating the progression of NSCLC.	AWPPH level was negatively correlated to overall survival in NSCLC patients and miRNA-204 level in NSCLC tissues.	Yes	Silence of AWPPH attenuated proliferative, migratory, and invasive capacities in A549 cells.	32373964
AWPPH	LncRNA	Homo sapiens	Colonic Neoplasms	cc tissues	Interaction[GLUT-1]	CCK8//qRT-PCR//ELISA//Western Blot	It was observed that serum levels of lncRNA AWPPH and GLUT-1 were significantly higher in patients with colon cancer patients compared with healthy controls. AWPPH-silencing significantly inhibited GLUT-1 expression and inhibited cancer cell proliferation. GLUT-1 overexpression promoted cancer cell proliferation and attenuated the inhibitory effects of AWPPH-silencing on cancer cell proliferation. 		Yes	Furthermore, AWPPH-silencing significantly inhibited GLUT-1 expression and inhibited cancer cell proliferation. GLUT-1 overexpression promoted cancer cell proliferation and attenuated the inhibitory effects of AWPPH-silencing on cancer cell proliferation. 	31423271
AWPPH	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	bone marrow	interaction[ROCK2 ]	CCK8//qRT-PCR//Western Blot	The results of the present study revealed that the expression levels of lncRNA AWPPH and Rho-associated protein kinase 2 (ROCK2) were upregulated in the bone marrow of patients with pediatric T-cell acute lymphoblastic leukemia compared with healthy controls.		Yes	 lncRNA AWPPH and ROCK2 overexpression promoted the proliferation and inhibited the apoptosis of Loucy cells, an acute lymphoblastic leukemia cell line. 	32973953
AWPPH	LncRNA	Homo sapiens	colorectal adenocarcinoma	colorectal adenocarcinoma tissues	Interaction[TGF-β1]	qRT-PCR	AWPPH was significantly upregulated in tumor tissues compared with adjacent healthy tissues.AWPPH overexpression promoted and silencing inhibited TGF-β1 expression. Therefore, lncRNA-AWPPH promoted colorectal adenocarcinoma by promoting tumor growth, increasing tumor cell viability and activating the TGF-β1 signaling.		Yes	AWPPH overexpression in colorectal adenocarcinoma cell lines promoted cell proliferation and increased cell viability, while AWPPH silencing resulted in opposite effects.	31611981
AWPPH	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells	Interaction[PI3K/AKT pathway]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	The results demonstrated that AWPPH was highly expressed in OS tissues and cells.Furthermore, AWPPH downregulation significantly inhibited the PI3K/AKT pathway. The present study demonstrated that AWPPH was highly expressed in OS, and that AWPPH promoted OS cell proliferation and migration, and inhibited OS cell apoptosis, which may be mediated by PI3K/AKT pathway activation.		Yes	Functional analyses revealed that AWPPH depletion significantly inhibited OS cell proliferation and migration, and promoted OS cell apoptosis.	31612016
AWPPH	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Regulation[miR-93-3p/FZD7 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In this research, results indicated AWPPH levels were increased in OS tissues in contrast to paracancerous controls.Mechanistically, AWPPH was demonstrated to sponge miR-93-3p and promote FZD7 expression, causing activation of Wnt/β-catenin. Inhibition of miR-93-3p effectively reversed the effects of AWPPH knockdown on OS cells. Collectively, our findings suggested AWPPH may be a prognostic biomarker and potential therapeutic target. AWPPH enhances FZD7-mediated activation of Wnt/β-catenin by sponging miR-93-3p to promote OS progression.	Up-regulated AWPPH was associated with advanced stage, tumor size and metastasis. Besides, AWPPH up-regulation indicated a low survival rate in OS patients.	Yes	Silencing of AWPPH suppressed proliferation, migration and invasion of OS cells.	31092328
AWPPH	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	blood	Interaction[miRNA-21]	CCK8//qRT-PCR//MTT	The current study aimed to explore the involvement of AWPPH in triple-negative breast cancer (TNBC). In the current study, we found that plasma levels of lncRNA AWPPH and microRNA-21 (miRNA-21) were Expression[Expression[up-expression]-expression]regulated in patients with TNBC than in healthy controls, and the Expression[Expression[up-expression]-expression]regulation of plasma lncRNA AWPPH and miRNA-21 distinguished early-stage patients with TNBC from healthy controls		Yes	 LncRNA AWPPH and miRNA-21 overexpression led to promoted cancer cells proliferation and improved cancer cell viability under carboplatin treatment, while lncRNA AWPPH small interfering RNA (siRNA) silencing played an opposite role. In addition, miRNA-21 overexpression attenuated the effects of lncRNA AWPPH siRNA silencing on of cancer cell behaviors. LncRNA AWPPH overexpression led to Expression[Expression[up-expression]-expression]regulated miRNA-21 in TNBC cells, while miRNA-21 overexpression also led to significantly Expression[Expression[up-expression]-expression]regulated lncRNA AWPPH expression.	31033015
AWPPH	LncRNA	Homo sapiens	Glioma	blood	Interaction[TGF-β pathway]	qRT-PCR//ELISA//Western Blot//Transwell Assay	 It was identified that AWPPH expression levels in tumor tissues were higher in patients with metastatic glioma.The plasma levels of AWPPH were positively correlated with the plasma levels of TGF-β1 in patients with glioma but not in healthy controls. In addition, AWPPH overexpression enhanced cancer cell migration and invasion, and upregulated TGF-β1 expression. Treatment with TGF-β1 demonstrated no significant effect on AWPPH expression; however, a TGF-β inhibitor attenuated the effects of AWPPH overexpression on cell migration and invasion. Therefore, the present study proposed that AWPPH may promote the migration and invasion of glioma cells by activating the TGF-β pathway.		Yes	 In addition, AWPPH overexpression enhanced cancer cell migration and invasion, and upregulated TGF-β1 expression.	31788066
AWPPH	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC cells	interaction[interacting with LSD1 and EZH2]	ChIP//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//EdU Staining//Transwell Assay	In this study, AWPPH expression was markedly upregulated in NPC cells. Collectively, our study shows that AWPPH inhibits PTEN expression to drive NPC progression through interacting with LSD1 and EZH2, providing potential biomarkers for NPC treatment.		Yes	Further, loss- and gain-of-function assays indicated that AWPPH facilitates cell proliferation and migration and hinders apoptosis in NPC cells.	32663416
AWPPH	LncRNA	Homo sapiens	ovarian carcinoma	 ovarian carcinoma tissues,blood	Regulation[Wnt/β‑catenin signaling pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	It was revealed that the expression levels of AWPPH were significantly upregulated in OC tissues and serum compared with healthy controls. Therefore, it was revealed that AWPPH may promote OC via activation of the Wnt/β‑catenin signaling pathway.	The serum levels of AWPPH were able to effectively diagnose and predict the prognosis of patients with OC. 	Yes	AWPPH overexpression promoted the proliferation, migration and invasion of OC cells, and upregulated β‑catenin expression. Treatment with a Wnt agonist markedly altered AWPPH expression; however, inhibition of Wnt suppressed the effects of AWPPH overexpression on proliferation, migration and invasion of OC cells. 	30896797
AWPPH	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	lung tissues,blood	Regulation[Wnt/β‑catenin signaling pathway]	Cell Proliferation Assay//qRT-PCR//Cell Apoptosis Assay//Western Blot	The results demonstrated that AWPPH expression levels were significantly upregulated in the lung tissues and serum samples of patients with NSCLC compared with in healthy controls. Therefore, it was concluded that lcRNA AWPPH could promote the growth of NSCLCs by activating the Wnt/β‑catenin signaling pathway.	In addition, patients with high expression levels of AWPPH had significantly shorter survival time.	Yes	AWPPH overexpression in NSCLC cells promoted proliferation and inhibited apoptosis, and activated the Wnt/β‑catenin signaling pathway, which is a classic signaling pathway involved in the development and progression of different types of cancers. 	30942396
AWPPH	LncRNA	Homo sapiens	Osteoporosis	osteoporosis patients	Expression(lower expressed)	qRT-PCR//Transfection//Western Blot	We observed that the expression of lncRNA AWPPH was downregulated in osteoporosis patients than that in healthy controls.	Downregulated expression of lncRNA AWPPH distinguished osteoporosis patients from healthy controls. 	Yes	In vitro cell experiments showed that knockdown of lncRNA AWPPH led to upregulated α1 but downregulated expression of α2 in osteoblasts, which made the α1 to α2 ratio higher than 2:1. In contrast, overexpression of lncRNA AWPPH led to downregulated α1 but upregulated α2 in osteoblasts, which made the α1 to α2 ratio lower than 2:1.	32552067
AWPPH	LncRNA	Homo sapiens	Femur Head Necrosis	mesenchymal stem cells,blood	Regulation[upregulating Runx2]	qRT-PCR	It was demonstrated that AWPPH was significantly downregulated in non-traumatic ONFH patients compared with in healthy controls in both MSCs and serum.Therefore, it was concluded that lncRNA AWPPH may participate in the development of ONFH by upregulating Runx2.		Yes	AWPPH overexpression promoted, while AWPPH short hairpin RNA silencing inhibited the expression of Runx2 expression in hMSC-BM cells. 	31853285
AURKAP1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCCtissues	Interaction[regulating miR-142, miR-155 and miR-182]	qRT-PCR//Luciferase Report Assay//Western Blot	The mRNA expression of AURKAPS1 in HCC tumor tissues was significantly higher, which is associated with tumor size and TNM stage. AURKAPS1 can increases the protein expression of RAC1, promotes the activation of ERK, and enhance the formation of membrane ruffles by binding with miR-182, miR-155 and miR-142 competively. Thus, AURKAPS1 could be a useful marker, and the combination of AURKAPS1/miRNAs (miR-142, miR-155 and miR-182) may be a new theoretical basis for the treatment of HCC.	The mRNA expression of AURKAPS1 in HCC tumor tissues was significantly higher, which is associated with tumor size and TNM stage. 	Yes	The high expression of AURKAPS1 promotes cell movement, migration and invasion.	31873123
B3GALT5-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-934/UFM1 Axis)	CCK8//qRT-PCR//Western Blot	 We found that the B3GALT5-AS1 expression level was of significant reduction in both HCC tissues and cell lines; B3GALT5-AS1 overexpression (ov) may inhibit the malignant features of HCC. Our results demonstrated that B3GALT5-AS1 was an excellent HCC suppressant by regulating miR-934 and UFM1 to achieve negative regulation of HCC cell proliferation, invasion, and metastasis, indicating that B3GALT5-AS1 is a promising potential therapeutic target for HCC treatment.	 We found that the B3GALT5-AS1 expression level was of significant reduction in both HCC tissues and cell lines; B3GALT5-AS1 overexpression (ov) may inhibit the malignant features of HCC. 	Yes	Our results demonstrated that B3GALT5-AS1 was an excellent HCC suppressant by regulating miR-934 and UFM1 to achieve negative regulation of HCC cell proliferation, invasion, and metastasis, indicating that B3GALT5-AS1 is a promising potential therapeutic target for HCC treatment.	34721576
B3GALT5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	MKN-45 cells	Regulation(CSNK2A1)	RNA Pull-Down//Western Blot//Invasion Assay//Migration Assay//CCK8//RIP//qRT-PCR//Cell Apoptosis Assay//Bioinformatics Analysis	The results showed that B3GALT5-AS1 expression was upregulated in MKN-45 cells compared with the control group.  In addition, B3GALT5-AS1 could bind to CSNK2A1 to regulate its expression.B3GALT5-AS1 knockdown attenuated cell viability, invasion and migration, whilst promoting cell apoptosis. These effects were partly reversed by CSNK2A1 overexpression. 		Yes	B3GALT5-AS1 knockdown attenuated cell viability, invasion and migration, whilst promoting cell apoptosis. These effects were partly reversed by CSNK2A1 overexpression. 	34306196
BANCR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	regulation[IGF1R/Raf/MEK/ERK pathway]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 It was found that BANCR and IGF1R were upregulated, while miR?338?3p was downregulated in ESCC tissues and cells.On the whole, the findings of the present study demonstrate that BANCR inhibition blocks ESCC progression by inactivating the IGF1R/Raf/MEK/ERK pathway by sponging miR‑338‑3p.		Yes	Both BANCR and IGF1R knockdown suppressed the proliferation, migration, invasion and epithelial?mesenchymal transition (EMT) of ESCC cells. IGF1R enhancement reversed BANCR knockdown?mediated effects on the proliferation, migration, invasion and EMT of ESCC cells. 	32945416
B4GALT1-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cells spheres	Regulation[YAP]	RIP//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Transwell Assay	 LncRNA B4GALT1-AS1 expression was significantly increased in OS tissues and cells spheres. Mechanistically, B4GALT1-AS1 recruited HuR to enhance YAP mRNA stability and thus its transcriptional activity.		Yes	 Knockdown of B4GALT1-AS1 inhibited OS cells proliferation, migration, stemness and chemotherapeutic sensitivity.	30182452
BANCR	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(LINC00586/LSD1/ASXL1 axis )	qRT-PCR	LINC00586 was overexpressed in CRC tissues and associated with patient survival. Overall, discovery of the LINC00586/LSD1/ASXL1 axis partially explains epigenetic mechanism regulating EMT in CRC, providing a therapeutic target to limit CRC metastasis.	LINC00586 was overexpressed in CRC tissues and associated with patient survival. 	Yes	 LINC00586 knockdown repressed HCT116 and LoVo cell viability, migration, their phenotypic switch from epithelial to a mesenchymal, and tumorigenesis in vivo.	35586041
BANCR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	regulation[MAPK signaling pathway]	qRT-PCR	 In this study, we found that the expression of BANCR was upregulated in OSCC tissues and cell lines compared to the negative control.  The results also showed that the expression of MAPK signaling-related proteins (p-erk, p-akt, and p-p-38) was positively correlated with that of BANCR.		Yes	The decreased expression of BANCR in vitro markedly inhibited OSCC cell proliferation, migration, and invasion while the opposite was observed for the overexpression of BANCR. 	31654433
BANCR	LncRNA	Homo sapiens	Atherosclerosis	 plasma and HASMCs	Interaction(miR-34c methylation )	CCK8//qRT-PCR//Transfection//Luciferase Report Assay	In this study, we found that BANCR was upregulated, while miR-34c was downregulated in atherosclerosis.Bioinformatics analysis showed that BANCR and miR-34c could directly interact with each other. Moreover, overexpression of BANCR could decrease the expression of miR-34c in HASMCs, but overexpression of miR-34c could not affect the expression of BANCR. Furthermore, overexpression of BACNR increased miR-34c methylation, and knockdown of endogenous BANCR decreased miR-34c methylation.		Yes	In addition, overexpression of BANCR reduced the effects of miR-34c on HASMCs proliferation and reversed the effects of miR-34c on HMGB1, TNF-ɑ and Bcl-2 expression. BANCR overexpression could induce HASMCs proliferation by downregulating the miR-34c methylation. 	33151462
BANCR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	thyroid tumor tissues	Regulation[RAF/MEK/ERK signaling pathway]	Flow Cytometry//qRT-PCR//Western Blot	We observed that BANCR was expressed at a higher level in human thyroid tumor tissues than that noted in the adjacent normal tissues.Taken together, these results suggest that BANCR plays a role in PTC development by regulating the expression of cancer stem cell markers LGR5 and EpCAM via the c-Raf/MEK/ERK signaling pathway.		Yes	In the xenograft mouse model, BANCR overexpression in the thyroid cancer cells significantly increased tumor growth. 	29917164
BANCR	LncRNA	Homo sapiens	Pancreatic Neoplasms	 SW1990 and PANC-1 PC cell lines	Interaction(HIF-1α/VEGF-C/VEGFR-3 pathway )	qRT-PCR//Transfection//Western Blot	The results showed that the expression of BANCR in the SW1990 and PANC-1 PC cell lines was significantly higher than that in human pancreatic duct endothelial cells. Additionally, the expression of BANCR was significantly increased in PC cells under hypoxic conditions compared with normoxic conditions. These results indicate that BANCR positively regulated the expression of HIF-1α in PC cells at the transcriptional and translational levels. Finally, the expression levels of VEGF-C and VEGFR-3 in PC cells were significantly reduced when BANCR or HIF-1α expression was knocked down.		Yes	 These results indicate that BANCR positively regulated the expression of HIF-1α in PC cells at the transcriptional and translational levels. Finally, the expression levels of VEGF-C and VEGFR-3 in PC cells were significantly reduced when BANCR or HIF-1α expression was knocked down.	36284647
BANCR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//BrdU//IHC//Transwell Assay	Overexpression of BANCR in these six NSCLC cell lines attenuated the cell viability and invasion.		Yes	Furthermore, we identified the effect of BANCR overexpression on tumor growth in NSCLC mouse model.	31114383
BANCR	LncRNA	Homo sapiens	Polycystic Ovary Syndrome	granulosa cells	Interaction[upregulation of Bax and p53]	CCK8//qRT-PCR//MTT//Western Blot	The results revealed that the expression levels of lncRNA BANCR in GCs were significantly higher in patients with PCOS compared with in non‑PCOS patients.Transfection with the BANCR expression vector significantly inhibited proliferation and promoted apoptosis of KGN cells, and significantly promoted the expression levels of pro‑apoptotic Bax and p53.		Yes	Transfection with the BANCR expression vector significantly inhibited proliferation and promoted apoptosis of KGN cells, and significantly promoted the expression levels of pro‑apoptotic Bax and p53.	30592281
BAIAP2-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(miR-361-3p/SOX4 Axis)	CCK8//qRT-PCR//Colony Formation Assay//EdU Staining	In this study, the expressions of BAIAP2-AS1 and SOX4 were distinctly upregulated in HCC cells and tissues, and high BAIAP2-AS1 may be a novel biomarker for HCC. E2F1 activated BAIAP2-AS1 expression. Assays for relationship verification showed that BAIAP2-AS1 regulated the expression of SOX4 and miR-361-3p. Rescue experiments further confirmed the positive interaction between miR-361-3p and BAIAP2-AS1 as well as between miR-361-3p and SOX4. 	In this study, the expressions of BAIAP2-AS1 and SOX4 were distinctly upregulated in HCC cells and tissues, and high BAIAP2-AS1 may be a novel biomarker for HCC.	Yes	The silence of BAIAP2-AS1 inhibited the proliferation and metastasis of HepG2 and PLC5 cells. 	34616498
BACE1-AS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-377-3p/CELF1 axis)	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	This study found that BACE1-AS was overexpressed in HCC tissues and cell lines. MiR-377-3p was negatively modulated by BACE1-AS in HCC tumor tissues and cells.  Moreover, CELF1 was identified as a downstream regulator of miR-377-3p and served as an oncogene in HCC cells.		Yes	Knockdown of BACE1-AS could restrain HCC progression in vitro, and inhibit pulmonary metastasis in vivo. 	33667514
BACE1-AS	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines, HCC tissues, and serum samples of HCC patients 	Interaction(miR-214-3p/APLN axis)	qRT-PCR	In the present study, we found that the relative expression of BACE1-AS in HCC cell lines, HCC tissues, and serum samples of HCC patients was significantly increased, and its high expression was correlated with the poor prognosis of HCC patients.These findings suggest that the BACE1-AS/miR-214-3p/APLN axis is a novel signaling pathway that facilitates HCC.	In the present study, we found that the relative expression of BACE1-AS in HCC cell lines, HCC tissues, and serum samples of HCC patients was significantly increased, and its high expression was correlated with the poor prognosis of HCC patients.	Yes	 In addition, overexpression of BACE1 promoted HCC cell proliferation, cell cycle progression, migration, and invasion, but inhibited cell apoptosis, while knockdown of BACE1 exerted the opposite role. 	34636395
BACE1-AS	LncRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(miR-762/SOX7 axis)	qRT-PCR//Western Blot//Transwell Assay	 In addition, LncRNA BACE1-AS is validated as a sponge of miR-762 through the prediction of lncRNASNP. Further, luciferase reporter and RIP assays are conducted to confirm the binding sites between LncRNA BACE1-AS and miR-762. SRY-box transcription factor 7 (SOX7) target to miR-762 and regulated by LncRNA BACE1-AS. Moreover, inhibition of miR-762 attenuate the role of sh-LncRNA BACE1-AS in OS cells, at meanwhile reduce the expression of SOX7.		Yes	Furthermore, using Cell counting kit-8 (CCK-8), transwell, wound healing and westernblot assays, overexpression LncRNA BACE1-AS remarkably reduce cell proliferation, migration and invasion abilities in OS. 	35332412
BACE1-AS	LncRNA	Homo sapiens	Parkinson Disease	SH-SY5Y cells	Interaction(miR-214-3p/CDIP1 signaling axis)	qRT-PCR//Luciferase Report Assay	Results suggested that lncRNA BACE1-AS was over-expressed and miR-214-3p was under-expressed in MPP+-stimulated SH-SY5Y cells.In addition, we found that CDIP1 was directly targeted by miR-214-3p and up-regulated in MPP+-stimulated SH-SY5Y cells. Further functional assays suggested that CDIP1-plasmid reversed the effects of miR-214-3p mimic on MPP+-stimulated SH-SY5Y cells. 		Yes	Further analyses revealed that MPP+ inhibited cell viability; enhanced cell apoptosis, Cleaved Caspase-3 expression and Cleaved Caspase-3/GAPDH ratio; induced oxidative stress and inflammation in SH-SY5Y cells were inhibited by lncRNA BACE1-AS-siRNA transfection; and all these inhibitions were reversed by miR-214-3p inhibitor. 	35481549
BACE1-AS	LncRNA	Homo sapiens	Alzheimer Disease	blood samples from AD patients	Expression[highly expressed]	CCK8//qRT-PCR//ELISA//Western Blot	It was demonstrated that lncRNA BACE1-AS expression was highly expressed in blood samples from AD patients, and also upregulated in peripheral blood samples and hippocampi from an AD animal model.		Yes	Knockdown of BACE1-AS by short interfering RNA increased the primary hippocampal neurons proliferation in vitro. Knockdown of BACE1-AS mediated by lentivirus in vivo improved the memory and learning behaviors of SAMP8 mice, inhibited BACE1 and amyloid precursor protein production, and phosphorylation of tau protein in hippocampi.	30186443
BACE1-AS	LncRNA	Homo sapiens	Alzheimer Disease	blood	regulation[iR-214-3p/ATG5 Signalling Axis]	qRT-PCR	The BACE1-AS level was found to be upregulated in serum samples of AD patients, brain tissues of AD transgenic (Tg) mice and Aβ1-42-treated SH-SY5Y cells.Our findings demonstrate that silencing of BACE1-AS alleviated neuronal injury by regulating autophagy through the miR-214-3p/ATG5 signalling axis in AD.		Yes	BACE1-AS knockdown alleviated Aβ1-42-induced cell injury. 	33197504
BAALC-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Interaction(G3BP2/c-Myc feedback loop )	RNA Pull-Down//Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay	 The expression of BAALC-AS1 was highly up-regulated and associated with malignant phenotypes in ESCC tissues and cell lines.  BAALC-AS1 directly interacted with G3BP2, and thereby inhibited the degradation of c-Myc RNA 3'-UTR by G3BP2, thus leading to the accumulation of c-Myc expression. Additionally, c-Myc acted as a transcription factor that can induce the expression of BAALC-AS1 by directly binding to its promoter region.		Yes	 In vivo and in vitro assays showed that BAALC-AS1 promoted ESCC cell proliferation, migration, and invasion. 	33476486
B4GALT1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues and cell lines	regulation[B4GALT1-AS1/miR-30e/SOX9 axis ]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	An elevated B4GALT1-AS1 mRNA level was observed in NSCLC tissues compared with adjacent healthy tissues (Fig. 1A).The findings of the present study indicated that the B4GALT1-AS1/miR-30e/SOX9 axis maybe an effective target for NSCLC treatment and management.		Yes	The results of the present study demonstrated that knockdown of B4GALT1-AS1 significantly attenuated the proliferative ability and clonality of H1299 and A549 cells. 	33014162
B4GALT1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 cell lines and tissues 	Interaction(miR-144-3p/ZEB1 )	CCK8//qRT-PCR	We showed significant upregulation of B4GALT1-AS1 in cell lines and tissues of NSCLC. The demonstration of the binding capacity of B4GALT1-AS1 and miR-144-3p was predicted by bioinformatics and luciferase reporter activity assay. The B4GALT1-AS1 and miR-144-3p interaction was shown by using rescue experiments. NSCLC has a positive association with its target, zinc finger e-box binding homeobox 1 (ZEB1).		Yes	B4GALT1-AS1 knockdown impeded the in vitro proliferation-related characteristics of the NSCLC cells.	35402178
ATXN8OS	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues,cell lines	Interaction[sequestering miR‑204]	qRT-PCR//Luciferase Report Assay	 It was found that ATXN8OS was markedly up‑regulated in BC tissue and cell lines, and that its level of overexpression was inversely linked with the overall survival rate of patients with BC. In conclusion, the present study suggested that ATXN8OS acts as a tumour promoter by sequestering miR‑204 during the development of BC, therefore providing a mechanistic insight which may facilitate the diagnosis and treatment of BC.	 It was found that ATXN8OS was markedly up‑regulated in BC tissue and cell lines, and that its level of overexpression was inversely linked with the overall survival rate of patients with BC. 	Yes	Knockdown of ATXN8OS inhibited proliferation, viability and invasion in the human MCF7 and MDA‑MB‑231 BC cell lines.	31173245
ATXN7	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tissues	Expression[highly expressed]	qRT-PCR	The results revealed that circATXN7 was upregulated in 45 NSCLC tissues compared with its expression in non-tumor tissues. 	It was also observed that the survival time of patients with high circATXN7 levels was shorter compared with that of patients with low circATXN7 levels, although the difference was not statistically significant (P>0.05).	Yes	Furthermore, silencing of circATXN7 by small interfering RNA inhibited the proliferation and invasion of NSCLC cells in vitro. 	31186686
Atxn2l-203	CircRNA	Rattus norvegicus	Neuralgia	NP rat and cell models 	Interaction(miR-216a-5p/TXNIP axis)	Western Blot//ISH//Transfection//qPCR//Flow Cytometry//RIP//PCR//IP//ELISA//IF	 The results exposed that circSMEK1 and TXNIP were up-regulated in NP, while miR-216a-5p was down-regulated. The claw retraction threshold and claw retraction latency in rats were elevated and reduced separately via knockdown circSMEK1 and miR-216a-5p. Mechanism studies demonstrated that circSMEK1 mediated TXNIP expression through competitive adsorption of miR-216a-5p. Functional rescue experiments manifested that the suppressive effect of circSMEK1 knockdown on NP was reversed by declined miR-216a-5p simultaneously. 	    	Yes	 Meanwhile, knockout circSMEK1 or elevated miR-216a-5p declined inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL6 in spinal cord, and the activation of microglia, but promoted the polarization of microglia into anti-inflammatory type, while up-regulation of circSMEK1 or knockdown of miR-216a-5p was opposite. 	34517790
ATP1A1-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	 THCA cells and tissues	Interaction(miR-620/IRF2BP2 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//FISH//Luciferase Report Assay	ATP1A1-AS1 was decreased in THCA cells and tissues. MiR-620, which was upregulated in THCA, was identified as a direct target of ATP1A1-AS1. Furthermore, IRF2BP2 was discovered to be a target of miR-620, which displayed low expression in THCA cells and tissues. Importantly, IRF2BP2 knockdown reversed the influence of ATP1A1-AS1 overexpression on THCA cell proliferation and apoptosis.		Yes	 ATP1A1-AS1 overexpression attenuated cell growth and promoted apoptosis. 	36002076
ASB16-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC samples	Regulation(NF-kappa B (NF-κB) pathway )	In Vivo Experiment//RNA Pull-Down//Northern Blot//IHC//Western Blot//Co-IP//CCK8//qRT-PCR//FISH//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//IF	ASB16-AS1 was upregulated in GC samples according to GEO data and qRT-PCR analysis.Mechanistically, ASB16-AS1 strengthened TRIM37 expression by sequestering miR-3918 and miR-4676-3p. ASB16-AS1 activated NF-kappa B (NF-κB) pathway by cooperating with ATM serine/threonine kinase (ATM) to induce TRIM37 phosphorylation.		Yes	ASB16-AS1 strengthened the proliferative ability and stem cell-like characteristics in GC cells. More importantly, ASB16-AS1 encouraged GC cell growth in vivo. 	32572790
ASB16-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells	Interaction(miR-185-5p/TEAD1 axis)	RNA Pull-Down//Western Blot//Tunel//RIP//qRT-PCR	 In our research, we discovered that ASB16-AS1 was with high expression in CRC cells.  In addition, ASB16-AS1 silencing restrained the proliferation, migration, invasion, and stemness while accelerating cell apoptosis of CRC cells. Mechanism experiments were applied to explore the regulatory mechanism of ASB16-AS1. It turned out that miR-185-5p could interact with ASB16-AS1 and inhibited the progression of CRC cells. TEAD1 (TEA domain transcription factor1) - a major effector of the Hippo signaling was proved to serve as the target of miR-185-5p and promote CRC development. 		Yes	 In addition, ASB16-AS1 silencing restrained the proliferation, migration, invasion, and stemness while accelerating cell apoptosis of CRC cells. 	34870557
ASB16-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissues 	Interaction(miR-1258)	qRT-PCR//MTT	The expression levels of ASB16-AS1 and miR-1258 in esophageal cancer tissues were 2.95±0.27 and 0.62±0.06, respectively.  ASB16-AS1 targeted negative regulation of miR-1258 expression. 		Yes	The cell viability of the si-NC group at 48 h and 72 h were 0.81±0.07 and 1.15±0.11, while those of si-ASB16-AS1 group were 0.46±0.04 and 0.62±0.06 (P<0.05). The numbers of cell migration and invasion in the si-NC group were 86.32±8.24 and 71.29±7.15, respectively, while those of si-ASB16-AS1 group were 43.22±4.31 and 32.36±3.58, respectively, the differences were statistically significant (P<0.05). The cell viability of the miR-NC group at 48 h and 72 h were 0.84±0.08, 1.18±0.12, while those of miR-1258 group were 0.55±0.05, 0.71±0.07 (P<0.05). The migration and invasion numbers of the miR-NC group were (83.15±8.31) and (75.33±7.51), while those of miR-1258 group were (49.58±4.23) and (38.42±3.84), respectively, the differences were statistically significant (P<0.05). The cell viability of the si-ASB16-AS1+ anti-miR-NC group at 48 h and 72 h were 0.45±0.04, 0.61±0.06, while those of si-ASB16-AS1+ anti-miR-1258 group were 0.72±0.07, 0.98±0.08; The migration and invasion numbers of cells in the si-ASB16-AS1+ anti-miR-NC group were 44.36±4.41 and 31.69±3.85, respectively, while those of si-ASB16-AS1+ anti-miR-1258 group were 72.65±7.27 and 61.22±6.14, respectively, and the differences were statistically significant (P<0.05). 	34289570
ASB16-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and CC cells	regulation[miR-1305/Wnt/β-catenin axis ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In our study, we showed that the expression of ASB16-AS1 was increased while miR-1305 reduced was re in CC.This study reveals that ASB16-AS1 promotes cell proliferation, migration, invasion via binding miR-1305 with Wnt2, and enhancing the Wnt/β-catenin pathway. ASB16-AS1 may play a new therapeutic target for CC.	Clinically, ASB16-AS1 and miR-1305 were correlated with poor-associated clinicopathological features of CC patients.	Yes	Knockdown of ASB16-AS1 reduced CC cells proliferation, migration and invasion abilities by regulating miR-1305 in vitro and in vivo.	32058219
ASB16-AS1	LncRNA	Homo sapiens	Glioma	Glioma tissues	Expression[highly expressed]	Flow Cytometry//qRT-PCR//Western Blot	RT-qPCR was used to detect the expression of ASB16-AS1 in human glioma tissues. The results indicated that the expression of ASB16-AS1 was obviously increased in 77 glioma tissues in comparison with 15 normal tissues.		Yes	It was observed that the proliferation, invasion, and migration abilities of the cells were significantly suppressed upon knocking down ASB16-AS1 in U87GS and U251GS cells (Figure 4).	30949502
ASB16-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues	interaction[miR-185-5p/miR-214-3p]	RNA Pull-Down//Western Blot//qRT-PCR//FISH//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	 In this study, we found that the expression of the long noncoding RNA (lncRNA) ASB16-AS1 was downregulated in ccRCC tissues compared with non-diseased tissues and was also associated with advanced tumor stage and larger tumors.ASB16-AS1 promotes ccRCC progression via a miR-185-5p-miR-214-3p-LARP1 pathway. 		Yes	By constructing cell and mouse models, it was found that downregulated lncRNA ASB16-AS1 enhanced cell proliferation, migration, invasion, and promoted tumor growth and metastasis. 	33680937
ASB16-AS1	LncRNA	Homo sapiens	Adrenocortical Carcinoma	adrenocortical carcinoma tissues	regulation[HuR]	RNA Pull-Down//ISH//Immunoblotting//CCK8//qRT-PCR//RIP//RNA-seq//Cell Cycle Assay//IHC//EdU Staining	Here, we found that lncRNA ASB16-AS1 was down-regulated in adrenocortical carcinoma and ASB16-AS1 functions as tumor suppressor in vitro and in vivo. We then found that inhibition of ASB16-AS1 attenuates the binding of ubiquitin E3 ligase BTRC to HuR and subsequently inhibits HuR protein unbiquitination and degradation. BTRC knock-down could reverse the effect of AB16-AS1 on HuR, CDK6, and IGF1R levels.		Yes	Here, we found that lncRNA ASB16-AS1 was down-regulated in adrenocortical carcinoma and ASB16-AS1 functions as tumor suppressor in vitro and in vivo. 	33219221
ASB16-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissues	Regulation	cell invasion assay//Transfection//Migration Assay//qRT-PCR//Cell Apoptosis Assay//Cell Proliferation Assay	In terms of comprehensive analysis, compared with non-tumor tissues, ASB16-AS1 was highly expressed in tumor tissues, and indicated the value of poor prognosis in multiple cancer types. 		Yes	Functional assays, such as counting kit-8 assay, transwell assay and scratch-wound assay verified that high ASB16-AS1 expression promoted tumor progression in LIHC. 	34709970
ASAP1‑IT1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian tumor samples and ovarian cancer cells	Interaction(miR‑2278/LATS2)	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	The analysis indicated that lncRNA ASAP1‑IT1 expression was downregulated in ovarian tumor samples and ovarian cancer cells. Bioinformatics analysis predicted that miR‑2278, a previously reported upregulated miRNA in ovarian tumors, may bind to ASAP1‑IT1. Dual luciferase assay confirmed the direct regulatory association between ASAP1‑IT1 and miR‑2278. In addition, the data demonstrated that large tumor suppressor 2 (LATS2) was a target gene of miR‑2278, whose expression was upregulated by ASAP1‑IT1 in ovarian cancer cells. 		Yes	The overexpression of ASAP1‑IT1 inhibited ovarian cancer cell proliferation and induced cell apoptosis. 	33576454
ASAP1-IT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues, cancer cells and spheres of cancer stem cells	Interaction(miR-509-3p/YAP1 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	knockdown of ASAP1-IT1 or overexpression of miR-509-3p repressed tumor growth in nude mice via reducing expression of tumorigenic genes. 		Yes	knockdown of ASAP1-IT1 or overexpression of miR-509-3p repressed tumor growth in nude mice via reducing expression of tumorigenic genes. 	34715859
ASAP1-IT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells 	Interaction(miR-221-3p)	qRT-PCR	ASAP1-IT1 levels were significantly increased in HCC tissues and cells compared with controls. Mechanistically, ASAP1-IT1 might exert its role in HCC progression, at least in part, by directly interacting with miR-221-3p. 	 Notably, higher ASAP1-IT1 levels were significantly associated with poorer prognosis of HCC patients. 	Yes	 Furthermore, knockdown of ASAP1-IT1 significantly suppressed cell proliferation and migration, while its overexpression significantly promoted cell proliferation and migration of HCC cells. 	35712508
ASAP1-IT1	LncRNA	Homo sapiens	Cholangiocarcinoma	Cholangiocarcinoma tissues and cells 	Regulation( Smo and Gli1 )	Cell Proliferation Assay//qRT-PCR//migration assay//Western Blot	 The high expression level of ASAP1-IT1 was tested in Cholangiocarcinoma tissues and cells with qRT-PCR.As a results, the Cholangiocarcinoma progression was inhibited. Hedgehog signaling pathway has been discovered to be a treatment target in Cholangiocarcinoma. In this study, the interaction between ASAP1-IT1 and hedgehog pathway was specifically investigated. Smo and Gli1, two hedgehog-related proteins were examined in Cholangiocarcinoma cells. The results of qRT-PCR and western blot assay suggested that ASAP1-IT1 could positively modulate Smo and Gli1 in Cholangiocarcinoma. Finally, rescue assays were carried out to prove that ASAP1-IT1 could improve Cholangiocarcinoma progression and development via hedgehog signaling pathway.	Upregulation of ASAP1-IT predicted the unfavorable prognosis for Cholangiocarcinoma patients.	Yes	Next, ASAP1-IT1 was knocked down in cancerous cells for loss-of function assay. MTT, colony formation and transwell and western bot assays were performed to demonstrate the specific impacts of ASAP1-IT1 on proliferation, migration and EMT progression of Cholangiocarcinoma. Cells. 	29653361
AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cells and prostate cancer cells (PCCs)	Expression(highly expressed)	Cell Cycle Assay//qPCR//Transwell Assay//Western Blot	LncRNA NCK1-AS1 is highly expressed in PCa, so its down-regulation can inhibit PCCs from proliferating and reduce the number of invasive cells.	The prognosis of patients with high LncRNA NCK1-AS1 expression was remarkably poorer than that of those with low expression.	Yes	Compared with the Blank group, cell proliferation and the number of plate cloned cells remarkably reduced in the sh-NCK1-AS1 group.	34151833
ARRDC1-AS1	LncRNA	Homo sapiens	Glioma	glioma specimens and cell lines	regulation[miR-432-5p/PRMT5 axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	In this study, we firstly reported that ARRDC1-AS1 expression was distinctly increased in both glioma specimens and cell lines, and high ARRDC1-AS1 expression was associated with advanced clinical progression and poor prognosis of glioma patients.Overall, our findings highlighted the importance of STAT1/ARRDC1-AS1/miR-432-5p/PRMT5 axis in glioma progression and offered novel strategies for glioma treatments.	In this study, we firstly reported that ARRDC1-AS1 expression was distinctly increased in both glioma specimens and cell lines, and high ARRDC1-AS1 expression was associated with advanced clinical progression and poor prognosis of glioma patients.	Yes	 Functional studies revealed that knockdown of ARRDC1-AS1 suppressed the proliferation, migration and invasion of glioma cells. 	33220929
ARRDC1-AS1	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	 DLBCL tissues and cell lines	Interaction(miR-2355-5p to regulate ATG5)	Western Blot//Flow Cytometry//qRT-PCR//Colony Formation Assay//Transwell Assay	We found that ARRDC1-AS1 was upregulated in DLBCL tissues and cell lines. ARRDC1-AS1 was activated by transcription factor PAX5. 		Yes	Knockdown of ARRDC1-AS1 suppressed DLBCL autophagy to aggravate proliferation, repress apoptosis, and facilitate invasion and migration. Furthermore, ARRDC1-AS1 sponged miR-2355-5p to upregulate ATG5.	34499929
ARHGEF26-AS1	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC patients	Interaction(miR-372-3p)	qRT-PCR//Luciferase Report Assay	The findings revealed that low expression of ADAM23 and ARHGEF26-AS1 as well as high expression of miR-372-3p was associated with poor prognosis and a lower FPI score in EC patients. Mechanistically, ARHGEF26-AS1 upregulated the expression of ADAM23 by competitively binding to miR-372-3p.	The findings revealed that low expression of ADAM23 and ARHGEF26-AS1 as well as high expression of miR-372-3p was associated with poor prognosis and a lower FPI score in EC patients. 	Yes	 Functionally, overexpression of ADAM23 and ARHGEF26-AS1 and the miR-372-3p inhibitor not only promoted ferroptosis in ESCC cells in vitro but also inhibited the proliferation and migration of cells. 	35003396
ARHGAP5-AS1	LncRNA	Homo sapiens	Breast Neoplasms	cell lines	Interaction(SMAD7)	RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//FISH//IF//RIP//Luciferase Report Assay//Transwell Assay	We analyzed the RNA-seq data of MDA-MB-231 and its highly metastatic derivative MDA-MB-231-LM2 cell lines (referred to as LM2) and identified a novel lncRNA (NR_027263) named as ARHGAP5-AS1, which expression was significantly downregulated in LM2 cells. Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2. 		Yes	Further functional investigation showed ARHGAP5-AS1 could inhibit cell migration via suppression of stress fibers in breast cancer cell lines. 	34370213
ASMTL-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cells 	Regulation(U2AF2/SAT1 )	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//FISH//RIP//Luciferase Report Assay//IF//Colony Formation Assay//Transwell Assay	 Results showed that ASMTL-AS1 was down-regulated in LUAD cells and ASMTL-AS1 up-regulation resulted in retarded LUAD cell and xenograft tumor growth along with stimulated ferroptosis. ASMTL-AS1 recruited U2AF2 to stabilize SAT1 mRNA. Furthermore, SAT1 exerted a cancer suppressor role in LUAD cells.  In conclusion, we first demonstrated that ASMTL-AS1 positively regulated SAT1 to promote ferroptosis and could stabilize SAT1 mRNA via recruiting U2AF2, shedding a light on a novel molecular mechanism in LUAD progression.		Yes	 Results showed that ASMTL-AS1 was down-regulated in LUAD cells and ASMTL-AS1 up-regulation resulted in retarded LUAD cell and xenograft tumor growth along with stimulated ferroptosis. 	34658100
ASMTL-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Interaction(miR-1228-3p/SOX17/β-catenin axis )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 ASMTL-AS1 was significantly downregulated in TNBC tissues compared to normal tissues, which was closely associated with aggressive clinical features and unfavorable prognosis.  RNA pull-down and luciferase reporter assays revealed that miR-1228-3p directly bound to ASMTL-AS1, ASMTL-AS1 increased SOX17 expression via sponging and repressing miR-1228-3p. Subsequently, the upregulated SOX17 trans-suppressed β-catenin expression, resulting in the inactivation of carcinogenic Wnt/β-catenin signaling, thereby restraining TNBC cell growth and dissemination. 		Yes	Lentivirus-mediated ASMTL-AS1 overexpression evidently reduced the ability of TNBC cell colony formation, activity and invasion by more than 2.5 times. 	34006305
ASMTL-AS1	LncRNA	Homo sapiens	Osteosarcoma	 OS tissues	Interaction(miR-342-3p/ADAM9 axis.)	CCK8//qRT-PCR	ASMTL-AS1 expression in OS was elevated in both TCGA database and our own cohort. Mechanistically, ASMTL-AS1 could act as a competing endogenous RNA for microRNA-342-3p (miR-342-3p) and inhibit its activity in OS cells, consequently causing an increase in ADAM metallopeptidase domain 9 (ADAM9) levels. Furthermore, inhibiting miR-342-3p or upregulating ADAM9 abated silenced ASMTL-AS1-induced antitumour activity in OS cells.		Yes	Interfering with ASMTL-AS1 restricted cell proliferation, migration and invasion while increasing cell apoptosis in vitro. Additionally, silencing ASMTL-AS1 blocked tumour growth in vivo. 	34597997
ATB	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	Interaction(EZH2)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//IHC//ChIP	n our research, lnc-ATB expression in OC tissues was elevated compared with adjacent normal tissues and high expression of lnc-ATB was associated with poor outcomes of OC patients. RNA immunoprecipitation and RNA pull-down results showed that lnc-ATB positively regulated the expression of EZH2 via directly interacting with EZH2. 	n our research, lnc-ATB expression in OC tissues was elevated compared with adjacent normal tissues and high expression of lnc-ATB was associated with poor outcomes of OC patients. 	Yes	The silencing of lnc-ATB blocked cell proliferation, invasion and migration in SKOV3 and A2780 cells. 	33336896
ATB	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction[increasing miR-141-3p]	qRT-PCR//Western Blot	Here, we found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells.  Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression. Down-regulation of lnc-ATB resulted in a morphological change of breast cancer cells from spindle-like to a round shape, and in a remarkable inhibition of cell migration and invasion, which were reversed by miR-141-3p inhibitor. Furthermore, we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects. Moreover, we proved that miR-141-3p directly bound to the 3' untranslated region (UTR) of ZEB1 and ZEB2 and negatively regulated ZEB1 and ZEB2 expression. Taken together, our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-3p, indicating that lnc-ATB might serve as a novel therapeutic target for breast cancer.		Yes	Down-regulation of lnc-ATB resulted in a morphological change of breast cancer cells from spindle-like to a round shape, and in a remarkable inhibition of cell migration and invasion, which were reversed by miR-141-3p inhibitor. 	30352165
ATB	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[suppressing miR-141-3p]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay	In this study, lncRNA-ATB was significantly up-regulated in NSCLC tissues and cell lines, and high lncRNA-ATB expression indicated poor prognosis.Further mechanism studies demonstrated that lncRNA-ATB was a target of miR-141-3p. MiR-141-3p expression was negatively related to lncRNA-ATB expression in NSCLC tissues.	In this study, lncRNA-ATB was significantly up-regulated in NSCLC tissues and cell lines, and high lncRNA-ATB expression indicated poor prognosis.	Yes	 Knockdown of lncRNA-ATB suppressed NSCLC cell growth, colony formation, migration, invasion and reversed epithelial-mesenchymal transition. In vivo study showed that silencing lncRNA-ATB inhibited tumor growth.	32092085
ATB	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues ,cell lines	interaction[ sponging miR-141-3p]	IHC//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 lncRNA-ATB was upregulated in CRC tissues and cell lines compared with healthy tissues and cells, respectively. 	 Moreover, high expression of lncRNA-ATB was significantly associated with advanced TNM stage and metastasis in CRC.  In addition, the results indicated that lncRNA-ATB expression predicted the prognosis and overall survival of patients with CRC. 	Yes	Compared with small interfering RNA-negative control, lncRNA-ATB knockdown inhibited CRC cell proliferation, migration and invasion, whereas, compared with vector, lncRNA-ATB overexpression promoted CRC cell proliferation, migration and invasion. Furthermore, the in vivo experiment suggested that lncRNA-ATB knockdown inhibited tumor growth. 	33199986
ATB	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 tumor tissues	interaction[TGF-β1]	qRT-PCR//Western Blot//Transwell Assay	 lncRNA-ATB expression level was higher in tumor tissues than in adjacent healthy tissues in most PTC patients.Upregulation of lncRNA-ATB by TGF-b1 promotes migration and invasion of PTC cells.		Yes	lncRNA-ATB overexpression promoted tumor cell migration and invasion, lncRNA-ATB overexpression showed no significant effects on TGF-β1 expression, and TGF-β1 treatment increased the expression level of lncRNA-ATB.	30042377
ATB	LncRNA	Homo sapiens	Carcinoma, Renal Cell		Interaction[downregulating p53 via binding to DNMT1]	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Our previous study found that lncRNA ATB was highly expressed in renal cell carcinoma (RCC). To sum up, our study revealed that high expression of lncRNA ATB could accelerate the proliferative and migratory rates of RCC cells and inhibit cell apoptosis through downregulating p53 via binding to DNMT1.		Yes	The results showed that lncRNA ATB knockdown in RCC cell line ACHN inhibited proliferative and migratory capacities and promoted apoptosis. 	30536843
ATB	LncRNA	Homo sapiens	Osteoarthritis	cell line( ATDC5)	Interaction[microRNA-5]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ELISA	Additionally, we observed that lncRNA-ATB expression was Expression[down-expression]-regulated in LPS-injured cells, and lncRNA-ATB overexpression significantly alleviated LPS-induced inflammatory injury in ATDC5 cells.		Yes	Additionally, we observed that lncRNA-ATB expression was Expression[down-expression]-regulated in LPS-injured cells, and lncRNA-ATB overexpression significantly alleviated LPS-induced inflammatory injury in ATDC5 cells.	30771739
ATB	LncRNA	Homo sapiens	Ovarian Neoplasms	cell line(SKOV3)	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	The results indicated that lncRNA-ATB was expressed at significantly higher levels in SKOV3 cells compared with the healthy cell line. 		Yes	LncRNA-ATB downregulation significantly reduced SKOV3 cell proliferation, invasion and migration, promoted apoptosis, decreased the expression of p-STAT3 and vimentin, and increased E-cadherin expression. 	32010258
ATB	LncRNA	Homo sapiens	Ovarian Neoplasms	 tissues or cells	interaction[Targeting miR-204-3p]	RNA Pull-Down//Flow Cytometry//qRT-PCR//CCK8//Luciferase Report Assay//Transwell Assay	In addition, luciferase activity suggested that lncRNA-ATB negatively regulated miR-204-3p in ovarian cancer. Besides, Nidogen 1 (NID1) was the direct target of miR-204-3p.		Yes	 LncRNA-ATB silencing significantly inhibited the proliferation and induced apoptosis of ovarian cancer cells.	32021299
ATB	LncRNA	Homo sapiens	Ovarian Neoplasms	HUVECs	Interaction(miR-204-3p/TGFβR2 Axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Ovarian cancer cells-derived exosomes promoted the viability, angiogenesis and migration of HUVECs; however, knockdown of lncRNA ATB in HUVECs reversed these phenomena.  In addition, exosomal lncRNA ATB promoted the tumorigenesis of ovarian cancer via regulating miR-204-3p/TGFβR2 axis. Furthermore, ovarian cancer cells-secreted exosomal lncRNA ATB increased tumor growth in vivo.		Yes	Ovarian cancer cells-derived exosomes promoted the viability, angiogenesis and migration of HUVECs; however, knockdown of lncRNA ATB in HUVECs reversed these phenomena.  Furthermore, ovarian cancer cells-secreted exosomal lncRNA ATB increased tumor growth in vivo.	35115831
ASMTL-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	 tumorous tissues and cell lines	Interaction(miR-1228-3p)	qRT-PCR	 In tumorous tissues and cell lines, ASMTL-AS1 was lowly expressed compared with normal ones. ASMTL-AS1 overexpression strongly decreased cell proliferation, migration, and invasion in vitro partly by moderating miR-1228-3p. 	 This downregulation was associated with the advanced FIGO stage, positive ascites cytology, and lymph node.  In particular, low levels of ASMTL-AS1 were revealed to have a high prognostic impact on EOC.	Yes	ASMTL-AS1 overexpression strongly decreased cell proliferation, migration, and invasion in vitro partly by moderating miR-1228-3p. 	35835145
ATB	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues	Interaction[miR-200c signals]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	CCA tissues have increased Lnc-ATB and reduced miR-200a/b/c levels, but the down-regulated miR-200c was most prominent. Overexpressed Lnc-ATB functioned as an oncogene for CCA growth and metastasis via miR-200 signals.		Yes	Inhibition of Lnc-ATB significantly impaired cell vitality and induced apoptosis and G0/G1 arrest, which, however, was rescued by miR-200c inhibitor.	31571907
ATB	LncRNA	Homo sapiens	Melanoma	MM tissues and cells	interaction[miR-590-5p]	qRT-PCR	In the present study, it was identified that lncRNA activated by transforming growth factor?β (lncRNA?ATB) was upregulated in MM tissues and cells compared with benign nevus cells and human melanocytes, via comparative lncRNA screening from Gene Expression Omnibus datasets and reverse transcription?quantitative polymerase chain reaction analysis.		Yes	Furthermore, lncRNA?ATB promoted the cell proliferation, cell migration, and cell invasion of MM cells in vitro, and tumor growth in vivo. 	29956757
ATB	LncRNA	Homo sapiens	lung squamous cell carcinoma	LSC tissues and cell lines	regulation[microRNA-590-5p/NF90 Axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//IF//Colony Formation Assay//Transwell Assay	 In our study, lncRNA-ATB expression also markedly increases in LSC tissues and cell lines in comparison to the adjacent normal tissues and normal lung epithelial cells, respectively.Taken together, our initial data suggest that lncRNA-ATB overexpression may promote the progression of LSC by modulating the microRNA-590-5p/NF-90 axis.		Yes	Functional experiments indicate that lncRNA-ATB overexpression improves the proliferative, migratory, and invasive capabilities of normal lung epithelial cells compared with control group. 	31934791
ATAD1	CircRNA	Homo sapiens	Leukemia, Myeloid, Acute	 patients with AML	Interaction(miR-34b)	BrdU//qRT-PCR	 circ-ATAD1 expression was found to be elevated, and inversely correlated with that of miR-34b, in patients with AML.  In addition, circ-ATAD1 overexpression in AML cells decreased miR-34b expression and increased miR-34b gene methylation. 		Yes	Moreover, AML cell proliferation was increased by circ-ATAD1 overexpression, but decreased by miR-34b overexpression, and the effect of circ-ATAD1 overexpression on AML cell proliferation was reduced by miR-34b overexpression. 	34630706
ASNR	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	Interaction(miR-519e-5p/FGFR2)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//IHC//Invasion Assay	High expressed Lnc_ASNR was detected in both GC cells and tissues using qRT-PCR. The bioinformatics analysis, luciferase assay, and Western blot demonstrated that Lnc_ASNR inhibited miR-519e-5p expression but increased FGFR2 expression.  Lnc_ASNR and FGFR2 were both targeted to miR-519e-5p, and they were negatively correlated with the expression of miR-519e-5p. 		Yes	Downregulated Lnc_ASNR could reduce proliferation, migration, and invasion in GC cells, while upregulated Lnc_ASNR could promote the cell proliferation, migration, and invasion. Moreover, the effect of Lnc_ASNR on migration and invasion ability is closely related to epithelial-mesenchymal transition (EMT). 	34307360
ASMTL-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 gastric cancer tissues  and cell lines	Interaction(ASMTL-AS1/microRNA-1270 )	RNA Pull-Down//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	ASMTL-AS1 was significantly downregulated while miR-1270 was upregulated in gastric cancer tissues as compared with normal tissue and cell lines.In summary, ASMTL-AS1 and miR-1270 are associated with poor prognosis of patients with gastric cancer. ASMTL-AS1 inhibited gastric cancer progression by regulating miR-1270. 	According to the studies, ASMTL-AS1 and miR-1270 were related to unfavorable clinical parameters, such as the advanced TNM stage. Downregulated ASMTL-AS1 and upregulated miR-1270 were associated with reduced 5-year overall survival. 	Yes	 Functional studies suggested that ASMTL-AS1 inhibits proliferation, migration, and invasion of HGC-27 and NCI-N87 cells by regulation of miR-1270.	34986743
ASMTL-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissue 	regulation[miR-93-3p/miR-660/FOXO1 axis ]	qRT-PCR	In the current study, we found that a novel lncRNA, ASMTL antisense RNA 1 (ASMTL-AS1), was significantly downregulated in PTC.Collectively, our data clearly indicate that ASMTL-AS1 functions as a novel tumor suppressor in PTC through regulation of miR-93-3p/miR-660/FOXO1 pathway.	And its downregulation was positively linked to larger tumor size, advanced clinical stage and unfavorable outcome. 	Yes	Overexpression of ASMTL-AS1 evidently inhibited PTC cell proliferation and glycolysis, while knockdown of ASMTL-AS1 resulted in the opposite effect. 	31953163
ASMTL-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cells,	Interaction(miR-1343-3p/LAMC1 axis)	qRT-PCR	 ASMTL-AS1 and LAMC1 were highly expressed in HCC tissues and cells, whereas miR-1343-3p showed low expression. Clinically, miR-1343-3p expression in HCC tissues showed a negative correlation with ASMTL-AS1 or LAMC1 expression. More interestingly, ASMTL-AS1 sponged miR-1343-3p and miR-1343-3p to target the 3'-UTR of LAMC1, thereby interfering with the malignant behavior of HCC cells. In conclusion, ASMTL-AS1 acts as a carcinogen in HCC through competing endogenous RNA (ceRNA) activity in the miR-1343-3p/LAMC1 axis. 		Yes	 Functional assays demonstrated that ASMTL-AS1 silencing suppressed HCC cell proliferation and migration and increased cell apoptosis.	34859735
BANCR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cell lines	Expression [highly expressed]	qRT-PCR//MTT//Western Blot	The results revealed that lncRNA BANCR was highly expressed in ESCC cells compared with in normal esophageal cells.		Yes	 BANCR overexpression enhanced proliferation, migration and invasion of ESCC cells, and BANCR silencing exerted opposite effects. Moreover, BANCR overexpression induced activation of the Raf/MEK/ERK signaling pathway in ESCC cells. 	33880577
BANCR	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Expression(highly expressed)	Western Blot//Migration Assay//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	The expression level of lncRNA BANCR in breast cancer tissues was significantly higher than that in para-carcinoma normal tissues. Results of Western blotting revealed that the expressions of B-cell lymphoma 2 associated X protein (BAX), cleaved-Caspase-3 and cleaved-poly adenosine diphosphate-ribose polymerase (PARP) in knockdown group were significantly up-regulated compared with those in control group. Both wound-healing assay and transwell migration assay showed that the down-regulation of lncRNA BANCR could inhibit the invasion and metastasis capacities of MCF-7 cells, whose mechanism was related to the inhibition of EMT process and down-regulation of MMP expressions in cells.	The prognosis of patients in low-expression BANCR group was significantly superior to that of patients in high-expression BANCR group. 	Yes	After BANCR knockdown in breast cancer MCF-7 cells, the cell proliferation and colony formation capacities were significantly inhibited. Further mechanism research showed that inhibiting BANCR could promote the apoptosis of MCF-7 cells.	29565494
BMPR1B-DT	LncRNA	Homo sapiens	Endometrial Neoplasms	 EC cells	Interaction(miR-7-2-3p/DCLK1 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//IHC//Transwell Assay	In this study, we analyzed the RNA transcripts of EC cells from The Cancer Genome Atlas (TCGA) and first reported a novel lncRNA, BMPR1B-AS1, that was more highly expressed in endometrial cancer tissues than in adjacent tissues, and BMPR1B-AS1 could promote endometrial cancer cell proliferation and metastasis.  Bioinformatics prediction and experimental results both suggested that BMPR1B-AS1 could modulate the malignant behaviors of endometrial cancer cell lines by sponging miR-7-2-3p to modulate DCLK1, and a DCLK1 inhibitor blocked the activation of the PI3K/Akt/NF-κB signaling pathway. 		Yes	 Bioinformatics prediction and experimental results both suggested that BMPR1B-AS1 could modulate the malignant behaviors of endometrial cancer cell lines by sponging miR-7-2-3p to modulate DCLK1, and a DCLK1 inhibitor blocked the activation of the PI3K/Akt/NF-κB signaling pathway. 	35404759
BISPR	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	 TPC tissues	Regulation[miR-21-5p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	BISPR in TPC tissues was over-expressed.  BISPR stimulated propagation and invasiveness of TPC cells by depressing miR-21-5p.		Yes	BISPR knockdown restrained the propagation and invasiveness and enhanced the iodine uptake of TPC cells. The tumor-forming rate reduced after BISPR knockdown.	29856242
BICDL3P	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction[miR-1254-WNT11 pathway]	qRT-PCR	In the study, we found that ABHD11-AS1 was highly expressed in CRC tissues and cell lines. Investigation of the underlying mechanism showed that ABHD11-AS1 could act as a molecular sponge of miR-1254, and WNT11 was a downstream target of miR-1254 in CRC. Moreover, there was a negative association between ABHD11-AS1 expression (or WNT11) and miR-1254 in CRC tissues. The rescue assays showed that WNT11 overexpression partially rescued the effects of ABHD11-AS1 inhibition on CRC progression.	 High ABHD11-AS1 expression was correlated with poor overall survival of patients with CRC. 	Yes	 High ABHD11-AS1 expression was correlated with poor overall survival of patients with CRC. 	30537177
BICDL3P	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC and normal tissues	Interaction( ITGA5/Fak/PI3K/Akt signaling pathway)	CCK8//qRT-PCR//Western Blot	In the present study, public database analysis and quantitative reverse transcription PCR of CRC and normal tissues showed that ABHD11-AS1 was overexpressed in CRC and associated with poor prognosis in CRC patients. Taken together, our studies suggest that lncRNA ABHD11-AS1 promotes proliferation, migration, and invasion in CRC by activating the ITGA5/Fak/PI3K/Akt signaling pathway, and that the ITGA5/Fak/PI3K/Akt axis is a promising target for CRC therapy.		Yes	Additionally, we noted that ABHD11-AS1 deficiency reduced integrin subunit alpha (ITGA)5 expression, and impaired the phosphorylation of P85, focal adhesion kinase (FAK), and Akt1 in CRC cell lines and tumor tissues of nude mice. Furthermore, we observed that ITGA5 overexpression abrogated the effect of ABHD11-AS1 knockdown on the proliferation and invasion abilities of CRC cells. 	34375304
BICDL3P	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cell lines	Regulation[ PI3K/AKT signalling pathway and miR-1301-3p/STAT3 axis]	Other	High expression of ABHD11-AS1 predicted poor prognosis for patients with PTC and promoted cell proliferation and metastasis in vitro and in vivo. STAT3-induced lncRNA ABHD11-AS1 promoted PTC progression by regulating PI3K/AKT signalling pathway and miR-1301-3p/STAT3 axis.	High expression of ABHD11-AS1 predicted poor prognosis for patients with PTC and promoted cell proliferation and metastasis in vitro and in vivo. 	Yes	High expression of ABHD11-AS1 predicted poor prognosis for patients with PTC and promoted cell proliferation and metastasis in vitro and in vivo. 	30657221
BICDL3P	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues and cells	Regulation(EPS15L1/EGFR signaling pathway)	qRT-PCR//MTT//Western Blot	High expression of ABHD11-AS1 was found in PTC tissues (P < 0.01), which was significantly correlated with lymph node metastasis (P < 0.05). ABHD11-AS1 positively regulated EGFR/EPS15L1 pathway, as EGFR, EPS15L1, STAT3, and p-STAT3 were activated.		Yes	 ABHD11-AS1 overexpression noticeably promoted cell proliferation, migration, and invasion capabilities, which were obviously decreased upon ABHD11-AS1 knockdown. 	35098448
BICDL3P	LncRNA	Homo sapiens	Ovarian Neoplasms	EOC tissues and cell lines	Interaction[suppressing TIMP2]	qRT-PCR//Wound Healing Assay//Colony Formation Assay//Transwell Assay	EGFR and ABHD11-AS1 were highly expressed in EOC tissues and cell lines.We defined the regulatory relationship between the EGFR signaling pathway, ABHD11-AS1, EZH2, and TIMP2 suggesting that ABHD11-AS1 may act as an oncogene and a potential target for antitumor therapies in ovarian cancer.		Yes	Knockdown of EGFR or ABHD11-AS1 inhibited cell growth, migration, and invasion of EOC cells. 	31568657
BICDL3P	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer samples	Interaction(EZH2/ABHD11-AS1/miR-133a-3p axis )	qRT-PCR//Transwell Assay	The expression of ABHD11-AS1 was significantly upregulated in ovarian cancer samples, and its levels were closely associated with lymph node metastasis, tumor stage and 3-year survival rate. In summary, EZH2-mediated enrichment of H3K27me3 on ABHD11-AS1 promoter could regulate the progression of ovarian cancer via miR-133a-3p. 	The expression of ABHD11-AS1 was significantly upregulated in ovarian cancer samples, and its levels were closely associated with lymph node metastasis, tumor stage and 3-year survival rate.	Yes	Furthermore, interference of ABHD11-AS1 suppressed the proliferation, migration and invasion of ovarian cancer cells, while cell apoptosis was promoted	33491971
BICDL3P	LncRNA	Homo sapiens	Endometrial Neoplasms	endometrial tissue	interaction[cyclin D1]	qRT-PCR//RNA Pull-Down	 lncRNA ABHD11-AS1 was significantly overexpressed in endometrial carcinoma. LncRNA ABHD11-AS1 functions as an oncogene to promote cell proliferation and invasion in endometrial carcinoma by positively targeting cyclin D1.		Yes	Overexpression of lncRNA ABHD11-AS1 promoted the proliferation, G1-S progression, invasion and migration of endometrial cancer cells; inhibited apoptosis; up-regulated cyclin D1, CDK1, CDK2, CDK4, Bcl-xl and VEGFA; and down-regulated p16, while ABHD11-AS1 down-regulation has the opposite effect. 	29799152
BICDL3P	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC cells	Interaction(miR-330-5p/MARK2 axis)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//ISH//Transfection//Tunel//qRT-PCR//FISH//RIP//Luciferase Report Assay//H&E Staining//Colony Formation Assay//EdU Staining//Transwell Assay	ABHD11-AS1 expression was abnormally high in CC cells. Moreover, miR-330-5p was corroborated to bind with ABHD11-AS1 in CC cells and microtubule affinity regulating kinase 2 (MARK2) was confirmed to be targeted by miR-330-5p. 		Yes	In vitro experiments showed ABHD11-AS1 downregulation restrained CC cell malignant phenotypes. In vivo experiments proved ABHD11-AS1 knockdown impeded tumor growth. 	34793775
BICDL3P	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues,cell lines	Regulation[miR-199a-5p/SLC1A5 axis]	qRT-PCR	We found that ABHD11-AS1 was remarkably overexpressed in PTC, and high expression was related to tumor size, lymph node metastasis, extrathyroidal extension and advanced TNM stage.  Taken together, the data show that ABHD11-AS1 acts as a competing endogenous RNA (ceRNA) to exert malignant properties in PTC through the miR-199a-5p/SLC1A5 axis. 	We found that ABHD11-AS1 was remarkably overexpressed in PTC, and high expression was related to tumor size, lymph node metastasis, extrathyroidal extension and advanced TNM stage. 	Yes	Moreover, ABHD11-AS1 enhanced the abilities of cell proliferation, migration, and invasion, inhibited apoptosis in vitro, promoted tumorigenesis in vivo via sponging miR-199a-5p and then induced SLC1A5 activation.	31409775
BICDL3P	LncRNA	Homo sapiens	Pancreatic Neoplasms		interaction[Sponging miR-1231]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	To explore the gene expression data of pancreatic cancer and adjacent normal tissue, TCGA data were used. As indicated in Figure 1A, the expression of ABHD11-AS1 in pancreatic cancer tissues was significantly upregulated, compared with adjacent normal tissues. In addition, high expression of ABHD11-AS1 was negatively correlated with the survival rate of patients with pancreatic cancer (Figure 1B). Meanwhile, ABHD11-AS1 bound to miR-1231 and cyclin E1 was found to be the target of miR-1231. Moreover, ABHD11-AS1 knockdown-induced G1 arrest in pancreatic cancer cells was reversed by miR-1231 antagomir.	ABHD11-AS1 was found to be negatively correlated with the survival rate of patients with pancreatic cancer. 	Yes	ABHD11-AS1 silencing significantly inhibited the proliferation and induced the apoptosis of pancreatic cancer cells. Additionally, knockdown of ABHD11-AS1 greatly inhibited the migration and invasion of pancreatic cancer cells. Finally, knockdown of ABHD11-AS1 obviously inhibited the tumor growth of pancreatic cancer in vivo.	33177842
BICDL3P	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue specimens and cells	Expression[highly expressed]	qRT-PCR//MeRIP	 Here, lncRNA ABHD11-AS1 was upregulated in NSCLC tissue specimens and cells and the ectopic overexpression was closely correlated with unfavorable prognosis of NSCLC patients. 	 Here, lncRNA ABHD11-AS1 was upregulated in NSCLC tissue specimens and cells and the ectopic overexpression was closely correlated with unfavorable prognosis of NSCLC patients. 	Yes	Functionally, ABHD11-AS1 promoted the proliferation and Warburg effect of NSCLC.	32892348
BICDL3P	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	serum and carcinoma tissues of cervical carcinoma patients, cells	Interaction(miR-1254)	Transfection//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 ABHD11-AS1 was upregulated, and miR-1254 was reduced in serum and carcinoma tissues of cervical carcinoma patients (P < 0.05). The expression levels of the two were negatively correlated (P < 0.001). ENCORI online website found that LncRNA ABHD11-AS1 and miR-1254 had binding sites. Bifluorescein reporter enzyme experiment found that ABHD11-AS1-WT fluorescence activity was inhibited by transfected miR-1254-mimics (P < 0.05). LncRNA ABHD11-AS1 accelerates proliferation, invasion, and migration of cervical carcinoma cells through targeted regulation of miR-1254, which may become the key to the treatment of cervical carcinoma.	High ABHD11-AS1 and low miR-1254 had a close correlation with the poor prognosis of cervical carcinoma patients (P < 0.05). 	Yes	Silencing LncRNA ABHD11-AS1 could inhibit the activity of cervical carcinoma cells (P < 0.05), while inhibiting miR-1254 could promote the activity of cervical carcinoma cells (P < 0.05).	35186240
BGLT3	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Regulation(PTEN stability)	qRT-PCR//Wound Healing Assay//Co-IP//Western Blot	BGL3 was significantly decreased in PTC tissues compared to adjacent normal thyroid tissues, and it was transcriptionally repressed by oncogene Myc. BGL3 was mainly located in the cytoplasm, in which interacted with PTEN and recruited OTUD3, enhancing the de-ubiquitination effect of OTUD3 on PTEN, resulting in increasing PTEN protein stability and inactivating carcinogenic PI3K/AKT signaling.	Low BGL3 is positively related to larger tumor size, lymph node metastasis, later TNM stage and poor prognosis. 	Yes	Overexpression of BGL3 inhibited PTC cell proliferation and migration in vitro, and reduced tumor size and lung metastasis nodules in vivo. 	33543443
BG981369	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell line	Interaction(SOX4 )	Migration Assay//qRT-PCR//MTT//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	The results indicated that lncRNA BG981369 was significantly higher in GC tissues than in normal tissues. Furthermore, we found that SOX4 may act as a downstream mediator of BG981369, suggesting that BG981369 inhibits proliferation, migration, and invasion, and promotes apoptosis by targeting SOX4 in the GC cell lines.		Yes	Overexpression of BG981369 inhibited the proliferation, migration, and invasion and promoted apoptosis of gastric adenocarcinoma (AGS) cells, and silencing of BG981369 promoted proliferation, migration, and invasion, and inhibited cell apoptosis of SNU-5 cells. 	29398692
BE503655	LncRNA	Homo sapiens	Osteosarcoma	cell lines	Regulation[Wnt/β-catenin pathway]	qRT-PCR//Western Blot//Transwell Assay	LncRNA BE503655 is overexpressed in human osteosarcoma and osteosarcoma cell lines.Moreover, we also provided evidences that lncRNA BE503655 played its functions dependent on regulation of Wnt/β-catenin signaling in osteosarcoma.		Yes	Knockdown lncRNA BE503655 suppresses cell proliferation, invasion and migration.	31316000
BDNF-AS	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction[repressing GSK-3β]	qRT-PCR//ChIP//RIP//Transwell Assay	 LncRNA BDNF-AS expression was significantly decreased, while GSK-3β was highly expressed in human CRC tissues and cell lines. Mechanistically, BDNF-AS led to GSK-3β promoter silencing in CRC cells through recruitment of EZH2. In conclusion, lncRNA BDNF-AS functioned as an oncogene in CRC and shed new light on lncRNA-directed therapeutics in CRC.		Yes	Moreover, lncRNA BDNF-AS induced inhibition of proliferation, migration, and invasion of CRC cells via inhibiting GSK-3β expression. 	31062382
BDNF-AS	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tissues and cells	regulation[PABPC1-BDNF-AS-RAX2-DLG5]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Cell Apoptosis Assay//ChIP	In this study, we confirmed that lncRNA brain-derived neurotrophic factor antisense (BDNF-AS) was downregulated in glioblastoma tissues and cells, interacted and stabilized by polyadenylate-binding protein cytoplasmic 1 (PABPC1). In general, this study elucidated that the PABPC1-BDNF-AS-RAX2-DLG5 mechanism may contribute to the anticancer potential of glioma cells and may provide potential therapeutic targets for human glioma.		Yes	 Overexpression of BDNF-AS inhibited the proliferation, migration, and invasion, as well as induced the apoptosis of glioblastoma cells.	32015336
BDNF-AS	LncRNA	Homo sapiens	Multiple Myeloma	MM serum and corresponding cancer cell lines	Interaction(miR-125a/b-5p-BCL2 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining	BDNF-AS was significantly upregulated, while miR-125a-5p and miR-125b-5p were downregulated in MM serum and corresponding cancer cell lines. Knockdown of BDNF-AS effectively inhibited the proliferation and migration of MM.1S and U266 cells, and co-transfection of miR-125a-5p or miR-125b-5p inhibitor and sh-BDNF-AS enhanced cell proliferation and migration compared with that in sh-BDNF-AS group. Knockdown of miR-125a-5p or miR-125b-5p significantly enhanced the proliferation and migration of MM.1S and U266 cells, and co-transfection of sh-Bcl-2 and miR-125a/b-5p inhibitor inhibited cell proliferation compared with that in miR-125a/b-5p inhibitor group. Moreover, knockdown of BDNF-AS increased the expression levels of apoptosis-related proteins (cleaved caspase 3 and cleaved PARP), while knockdown of miR-125a-5p or miR-125b-5p reduced the expression levels of these apoptosis-related proteins compared with knockdown of BDNF-AS. Furthermore, knockdown of BDNF-AS effectively suppressed MM tumor growth in vivo.		Yes	Knockdown of BDNF-AS effectively inhibited the proliferation and migration of MM.1S and U266 cells, and co-transfection of miR-125a-5p or miR-125b-5p inhibitor and sh-BDNF-AS enhanced cell proliferation and migration compared with that in sh-BDNF-AS group. 	34980181
BICDL3P	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[miR-361-3p/PDPK1 signalling]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In summary, ABHD11-AS1 boosts GC development by regulating miR-361-3p/PDPK1 signalling.		Yes	 ABHD11-AS1 knockdown repressed cell proliferation but enhanced cell apoptosis in function.	32678870
BLACAT1	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[BLACAT1/miR-605-3p/VASP axis]	qRT-PCR	BLACAT1 levels were increased in glioma tissues.Summarily, this study highlights the important roles of BLACAT1/miR-605-3p/VASP axis in glioma progression.		Yes	Silencing of BLACAT1 markedly repressed glioma proliferation, migration, and invasion, and suppressed glioma growth in vivo. 	31093978
BASP1-AS1	LncRNA	Homo sapiens	Melanoma	melanoma tissues 	Interaction(YBX1/NOTCH3)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//RIP//CHIP//Colony Formation Assay//Invasion Assay	 The expression of BASP1-AS1 was upregulated in melanoma tissues and various melanoma cell lines. Mechanically, BASP1-AS1 interacted with YBX1 and recruited it to the promoter of NOTCH3, initiating its transcription process. The activation of the Notch signaling then resulted in the transcription of multiple oncogenes, including c-MYC, PCNA, and CDK4, which contributed to melanoma progression. 		Yes	Functionally, the ectopic expression of BASP1-AS1 promoted cell proliferation, migration, and invasion in both A375 and SK-MEL-2 cells. 	34533860
BLACAT1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC tissue 	Expression[highly expressed]	qRT-PCR//Transwell Assay	We showed that BLACAT1 was upregulated in CSCC tissue comparing to adjacent non-cancer tissue of CSCC patients.	Patients with higher BLACAT1 level in CSCC tissues showed a significantly lower overall 5-year survival rate. 	Yes	 Overexpression of miR-424 and miR-143 led to inhibited migration and invasion, while BLACAT1 overexpression led to promoted migration and invasion of CSCC cells.	32046460
BMI1	CircRNA	Homo sapiens	Esophageal Neoplasms	serum and tissues of esophageal cancer patients	Expression [lower expressed]	Transfection//qPCR//Proliferation Assay//RIP//Cell Apoptosis Assay//PCR//Cell Proliferation Assay//IP//IF	Expression of circ-BMI1 in serum and tissues of esophageal cancer patients was significantly decreased compared to controls (P < 0.001 and P = 0.003, respectively). Area under the receiver operating characteristic curve (ROC) was 0.726. 		Yes	 Cell proliferation, migration and colony forming ability of circBMI1-Eca109 cells were obviously decreased than that of NC-Eca109 cells (P < 0.05). circBMI1-Eca109 cells were more sensitive to 5-fluorouracil and cisplatin, and tumor volume of nude mice in circBMI1-Eca109 group was smaller (P < 0.05).	34278876
BM466146	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Expression[lower expressed]	CCK8//qRT-PCR//EdU Staining	It was found that the expression of lncRNA BM466146 in breast cancer tissues was significantly lower than that in normal breast tissues (P < 0.001). 	Kaplan-Meier survival analysis showed that breast cancer patients with overexpression of BM466146 had longer overall survival. 	Yes	EDU and CCK8 experiments showed that overexpression of BM466146 inhibited the proliferation of breast cancer cells. 	33585256
Blnc1	LncRNA	Mus musculus	Cerebral Hemorrhage	brain tissue	regulation[PPAR-γ/SIRT6/FoxO3 pathway]	Western Blot//CCK8//qRT-PCR//Cell Apoptosis Assay//ELISA//Transwell Assay	Blnc1 was upregulated in perihematomal edema, hematoma and microvessel in the brain of ICH mice. Silencing Blnc1 alleviated nerve injury and inflammatory response caused by ICH through activating PPAR-γ/SIRT6/FoxO3 pathway.		Yes	Silencing Blnc1 restrained OGD plus hemin-caused reduction of BMVEC viability and migration and the induction of apoptosis, permeability and inflammation response, and suppressed PPAR-γ/SIRT6-mediated FoxO3 activation, which could be reversed by T0070907 (PPAR-γ inhibitor). 	33359247
BLACAT2	LncRNA	Homo sapiens	Stomach Neoplasms	Primary gastric cancer tissues and the normal samples 	Interaction(miR-193b-5p/METTL3 pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Our study discovered that lncRNA-BLACAT2 was significantly upregulated in gastric cancer. Furthermore, BLACAT2 was verified to perform its function through interaction with miR-193b-5p using a luciferase reporter assay.  Additional studies also discovered that Methyltransferase Like 3 (METTL3) was the downstream target of miR-193b-5p.		Yes	 Different studies have illustrated that BLACAT2 promoted gastric cancer progression through regulating proliferation, migration, invasion, and apoptosis in terms of biological function.	33976730
BLACAT1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[miR-150-5p/CCR2]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay	We found BLACAT1 took part in breast cancer cell aggressive phenotype. The real-time PCR result showed that BLACAT1 was up-regulated in tumor tissues compared to adjacent normal tissues. The molecular mechanism experiments demonstrated that BLACAT1 down-regulation suppressed the proliferation and metastasis of human breast cancer cells by regulating miR-150-5p targeting CCR2. 	The clinical studies indicated that lack of BLACAT1 was related to tumor size, metastasis.	Yes	The molecular mechanism experiments demonstrated that BLACAT1 down-regulation suppressed the proliferation and metastasis of human breast cancer cells by regulating miR-150-5p targeting CCR2. 	30733855
BLACAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Expression[highly expressed]	qRT-PCR	In our results, BLACAT1 expression was increased in SCLC tissues and cell lines compared with paired adjacent normal tissues and bronchial epithelial cell lines, respectively. 	 In addition, BLACAT1 high-expression was obviously associated with advanced clinical stage, large tumor size, more lymph node metastasis, present distant metastasis, and poor prognosis.	Yes	The loss-of-function studies suggested that of BLACAT1 suppressed SCLC cell proliferation, migration, and invasion, and induced G0/G1 phase arrest. 	30203450
BLACAT1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissues	Regulation(Sonic Hedgehog Pathway)	qRT-PCR//Western Blot//Colony Formation Assay//Transwell Assay	Here, we reported BLACAT1 was significantly up-regulated in lung cancer tissues in comparison to the adjacent normal tissues, which suggested BLACAT1 might act as an oncogene in lung cancer. Sonic hedgehog (shh) signaling is able to exert a significant role in carcinogenesis, including lung cancer. Currently, we proved that up-regulation of BLACAT1 activated shh signaling pathway, via inducing shh, Gli-1 and Smo expression. shh pathway inhibitor GANT-61 reversed the effect of overexpression of BLACAT1 on non-small cell lung cancer. 		Yes	 As shown, we proved up-regulation of BLACAT1 greatly induced the growth of non-small cell lung cancer cells. Reversely, knockdown of BLACAT1 reduced A549 and PC9 cell proliferation, migration and invasion. 	33937028
BLACAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	colon tissues,cell lines	Expression[highly expressed]	CCK8//qRT-PCR	BLACAT1 level was higher in CRC tissues and cell lines than in normal colon mucosal tissues and cell lines. 	Correlation of data from the GEO and GEPIA databases with several clinical parameters revealed that CRC patients with high BLACAT1 expression showed poor OS. Multivariate analysis indicated that high BLACAT1 expression is an independent risk factor in patients with CRC.	Yes	Furthermore, siRNA-mediated knockdown of BLACAT1 suppressed proliferation and invasion of CRC cells in vitro. 	35116731
BLACAT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[BLACAT1/miR-519d-3p/CREB1 Axis ]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	The expression of BLACAT1 was promoted in CRC tissues and cells, and correlated to the TNM (tumor, node, metastasis) stage, distant metastasis, and overall survival rate. Moreover, our data showed that miR-519d-3p directly targeted CREB1 and BLACAT1 sponged miR-519d-3p to regulate CREB1 expression. Besides, CREB1 disrupted the bio-functional results above from BLACAT1 suppression.	The expression of BLACAT1 was promoted in CRC tissues and cells, and correlated to the TNM (tumor, node, metastasis) stage, distant metastasis, and overall survival rate. 	Yes	Silencing of BLACAT1 limited the proliferation, migration, and invasion, facilitated the apoptosis, and re-sensitized OXA-resistance in CRC cells.	33376405
BLACAT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[BLACAT1/ has-miR-485-5p regulatory axis ]	qRT-PCR//Luciferase Report Assay	BLACAT1was found to be overexpressed in both HCC cells and human HCC tumors.The BLACAT1/ has-miR-485-5p regulatory axis may be a molecular target for future HCC therapy.		Yes	In HeG2 and MHCC97 L cells, lentivirus-induced BLACAT1 downregulation inhibited cancer cellin vitro proliferation and invasion, and in vivo xenograft growth.	31174090
BLACAT1	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues 	regulation[Wnt/β-catenin signaling pathway,miR-519d-3p]	Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	Quantitative RT-PCR showed that BLACAT1 was aberrantly up-regulated in ovarian cancer tissues compared with normal tissues.Taken together, BLACAT1 knockdown inhibited the progression of ovarian cancer by suppressing the Wnt/β-catenin signaling pathway via regulating miR-519d-3p. 		Yes	 In vitro, BLACAT1 knockdown induced cell cycle arrest and inhibited the proliferation, migration and invasion of ovarian cancer cells using flow cytometry, MTT and EdU assays, wound healing assay and transwell assay, respectively.	32095930
BLACAT1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	cell lines	Interaction[targeting miR-142-5p]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The expression of BLACAT1 was increased and the expression of miR-142-5p was decreased in OSCC cells.LncRNA BLACAT1 knockdown suppressed the viability, migration and invasion of OSCC cells by sponging miR-142-5p, indicating that BLACAT1 might be a novel target for the treatment of OSCC.		Yes	The knockdown of BLACAT1 suppressed the viability, migration and invasion of OSCC cells. 	31841186
BLACAT1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction[regulating STAT3]	qRT-PCR//RNA Pull-Down//Western Blot	BLACAT1 was upregulated in OS tissues and cells. Upregulation of BLACAT1 predicted unfavorable prognosis for patients with OS.  More importantly, BLACAT1 could interact with STAT3 and regulat the phosphorylation of STAT3.		Yes	Downregulation of BLACAT1 inhibited cell proliferation and invasion, whereas upregulation of BLACAT1 accelerated cell proliferation and invasion.	30665678
BLACAT1	LncRNA	Homo sapiens	Glioma	lioma tissues and adjacent non-tumor tissues,cell lines (NHA,U251, T98G, H4, A172, LN229) 	Regulation[Wnt/β-catenin signaling pathway ]	Western Blot//Wound Healing Assay//qPCR//Cell Proliferation Assay//Transwell Assay	Results demonstrated that BLACAT1 mRNA expression was significantly increased in glioma tissues compared to adjacent non-tumor (ANT) tissues.Results determined that BLACAT1 was highly expressed in glioma cell lines (U251, T98G, H4, A172 and LN229) compared with the NHA cell line.In conclusion, BLACAT1 may serve as an oncogenic lncRNA in glioma progression via activation of the Wnt/β-catenin signaling pathway. 	 	Yes	Functional assays determined that BLACAT1 promoted glioma cell proliferation, migration, invasion and epithelial-mesenchymal transition in vitro. 	31086604
BLACAT1	LncRNA	Homo sapiens	Pancreatic Neoplasms		regulation[Repressing CDKN1C via EZH2-Induced H3K27me3]	qRT-PCR//Western Blot	Based on bioinformatic prediction, EZH2 and BLACAT1 were highly expressed in PC, while CDKN1C was lowly expressed (all P < 0.05). Interference with BLACAT1 inhibits H3K27 trimethylation of CDKN1C gene by blocking EZH2 recruitment to promote CDKN1C expression and inhibit CCNE expression, thus suppressing PC cell proliferation, migration and aerobic glycolysis, and promoting mitochondrial oxidative phosphorylation.		Yes	Interference with EZH2 and BLACAT1 inhibited cell proliferation, migration and aerobic glycolysis, and promoted mitochondrial oxidative phosphorylation (all P < 0.05).In vivo results showed that BLACAT1 interference inhibited tumor formation (all P < 0.05).	33072570
BLACAT1	LncRNA	Homo sapiens	Prostatic Neoplasms	 prostate cancer samples 	Interaction(miR-29a-3p/DVL3 Axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	BLACAT1 expression was significantly up-regulated in cancerous tissues of prostate cancer samples and positively correlated with the expression of DVL3, while negatively associated with miR-29a-3p. the luciferase activity of BLACAT1 reporter was inhibited by miR-29a-3p, and DVL3 was validated as a target gene of miR-29a-3p.		Yes	After the transfection of BLACAT1 shRNAs into prostate cancer cells, the proliferative ability and metastatic ability of cancer cells were significantly inhibited; BLACAT1 shRNAs could reduce the expression of DVL3 on both mRNA and protein expressions levels, 	33641528
BLACAT1	LncRNA	Homo sapiens	Melanoma	Melanoma tissue and noncancerous tissue 	Interaction(miR-374b-5p/U2-associated factor homology motif kinase 1 axis)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	the collected data showed that BLACAT1 was highly expressed in melanoma.BLACAT1 upregulated UHMK1 expression by acting as a competing endogenous RNA for miR-374-5b. BLACAT1 deficiency resulted in the upregulation of miR-374b-5p expression and the downregulation of UHMK1 expression in melanoma cells. Moreover, BLACAT1 activated PI3K and AKT signaling by upregulating UHMK1 expression, as shown by western blotting analyses.		Yes	Functionally, UHMK1 overexpression or miR-374b-5p knockdown reversed the suppressive effect of BLACAT1 depletion on melanoma cell proliferation and invasion.	34708547
BDNF-AS	LncRNA	Homo sapiens	Prostatic Neoplasms	 CaP tumors, CaP cell lines	Expression(lower expressed)	qRT-PCR	BDNF-AS was downregulated in human CaP tumors. BDNF-AS was also found to be lowly expressed in CaP cell lines. In LNCaP and PC-3 cells, lentivirus-driven BDNF-AS overexpression exerted significantly tumor-suppressing effects on hindering cancer cell proliferation and invasion in vitro, and explant growth in vivo.	Low BDNF-AS expression was correlated with CaP patients' poor prognosis and shorter overall survival.	Yes	In LNCaP and PC-3 cells, lentivirus-driven BDNF-AS overexpression exerted significantly tumor-suppressing effects on hindering cancer cell proliferation and invasion in vitro, and explant growth in vivo.	29710528
BCYRN1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells and tissue	Expression[highly expressed]	qRT-PCR//RNA-seq	Our results show that BC200 is upregulated in nulliparous women, and breast cancer cells and tissue. 		Yes	When overexpressed in luminal and triple negative breast cancer cell lines, BC200 shows increased proliferation, migration, and invasion in vitro.In vivo, overexpression of BC200 increased tumor size.	31646972
BCYRN1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines(A549, SPC-A1, H460 and H1650)	Interaction [Wnt/β-catenin pathway]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We found that BCYRN1 was increased in NSCLC, and its Expression[down-expression]regulated expression could sExpression[Expression[up-expression]-expression]press NSCLC cell proliferation and cell cycle progression by inhibiting the Wnt/β-catenin pathway. Our results showed that the expression of BCYRN1 was higher in lung cancer cells compared with a normal bronchial epithelial cell line. Moreover, Expression[down-expression]regulation of BCYRN1 expression could inhibit cell proliferation and migration and induce apoptosis.		Yes	 KnockExpression[down-expression] of BCYRN1 in NSCLC cells reduced a cohort of molecules (β-catenin, c-Myc and cyclin D1) which are critical for cell proliferation and apoptosis. 	30486938
BCYRN1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction[PI3K/AKT pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	Higher expression of BC200 was found in NSCLC tissues than that of adjacent normal tissues. Western blot results showed that protein expressions of PI3K, AKT and STAT3 were downregulated after BC200 knockdown in LC cells. Additionally, the IC50 in H1299/DDP cells transfected with si-BC200 was lower than in those transfected with si-NC. The apoptotic rate in H1299 cells transfected with si-BC200 was remarkably lower than those transfected with si-NC.	BC200 expression was positively correlated with tumor stage, lymph node metastasis and distant metastasis of NSCLC patients, whereas not correlated to age and sex. 	Yes	 Knockdown of BC200 inhibited proliferation, invasion and migration of LC cells. 	30779077
BCAR4	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-139-3p)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Here, we unraveled that lncRNA BCAR4 was upregulated in ESCC and predicted poor prognosis. Mechanistically, lncRNA BCAR4 sponged miR-139-3p to upregulate ELAVL1, thereby inhibiting p53/p21 pathway in ESCC cells.	Here, we unraveled that lncRNA BCAR4 was upregulated in ESCC and predicted poor prognosis.	Yes	Functionally, lncRNA BCAR4 knockdown induced cell apoptosis and G1/S arrest, while inhibited cell proliferation and migration in vitro; conversely, overexpressing lncRNA BCAR4 promoted proliferation and metastasis. 	33602031
BCAN-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical carcinoma tissues and cell lines	regulation[RP11-284F21.9/miR-769-3p/PPWD1 axis ]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay	We found that RP11-284F21.9 was down-regulated in cervical carcinoma tissues and cell lines. Taken together, our results demonstrate that RP11-284F21.9 functions as tumor suppressor and regulates PPWD1 expression through competitively binding to miR-769-3p in cervical carcinoma, suggesting that RP11-284F21.9/miR-769-3p/PPWD1 axis could serve as a promising prognostic biomarker and therapeutic target for cervical carcinoma.		Yes	Overexpression of RP11-284F21.9 inhibits proliferation, invasion and migration of cervical carcinoma cells in vitro. 	32936290
BCAN-AS1	LncRNA	Homo sapiens	lung carcinoma	lung cell lines and tissues 	regulation[miR-627-3p/CCAR1]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	An increased expression of RP11?284F21.9 was identified in both lung carcinoma tissues and cells.Mechanistically, it was demonstrated that RP11‑284F21.9 promoted the proliferation and invasiveness of lung carcinoma cells, in part, via the regulation of miR‑627‑3p. Furthermore, cell division cycle and apoptosis regulator 1 (CCAR1) was identified as a target gene of miR‑627‑3p. 		Yes	 Knockdown of RP11?284F21.9 in lung carcinoma cells inhibited cell proliferation and invasion, but promoted cell apoptosis. 	32945522
BC050642	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction[down-regulating the expression of c-myc]	CCK8//qRT-PCR//Colony Formation Assay//Cell Apoptosis Assay	BC050642 levels showed distinctive increases in osteosarcoma tissues and cell lines compared with controls. BC050642 is up-regulated in osteosarcma and its over-expression promotes tumor development via down-regulating the expression of c-myc.		Yes	Up-regulated BC050642 could promote cell proliferation, induce colony formation and meanwhile inhibit cell apoptosis.	31397185
BC037916	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	regulation[miR-3145-3p]	qRT-PCR	Quantitative RT-PCR analysis showed that 86.0% (74/86) pancreatic cancer tissues had increased BC037916 expression as compared with normal counterparts.Further experiments suggested that BC037916 positively regulated the expression of Twist through miR-3145-3p.		Yes	 Functionally, knockdown of BC037916 repressed cell proliferation, inhibited cell invasion, halted cell cycle progression, and promoted apoptosis in both PANC-1 and SW1990 cells. 	33447050
BBOX1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cells	Interaction(miR-361-3p/Mucin 13 signaling axis)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis	 The results showed that BBOX1-AS1 was significantly upregulated in GC tissues.  MiR-361-3p was significantly downregulated in GC and counteracted the inhibitory effects of BBOX1-AS1 on GC progression. MUC13, which is targeted by miR-361-3p, is significantly upregulated in GC. MUC13 silencing inhibited GC progression was aborgated by miR-361-3p inhibitor. 		Yes	 Silencing of BBOX1-AS1 inhibited GC cell proliferation and invasion and inhibited tumor growth in vivo, whereas it promoted apoptosis. 	36700475
BBOX1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	Interaction(HOXB7/β-catenin axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	 Herein, we validated that BBOX1-AS1 was notably overexpressed in ESCC tissues compared to the adjacent non-tumor tissues and significantly correlated with tumor sizes. Mechanistically, BBOX1-AS1 regulated HOXB7 expression, and rescue experiments indicated that silencing of HOXB7 could abolish the malignant phenotypes mediated by BBOX1-AS1 to a certain extent. Moreover, HOXB7 participated in the activation of the Wnt/β-catenin signaling pathway. 		Yes	BBOX1-AS1 enhanced the malignant behavior of ESCC cells in vitro, such as cell proliferation, migration, and invasion. In addition, knockdown of BBOX1-AS1 augmented the proportion of apoptotic cells in ESCC cells. 	35351402
BBOX1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cell lines	Interaction(hsa-miR-361-3p/SH2B1)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	 We observed that BBOX1-AS1 is overexpressed in CRC cell lines, and BBOX1-AS1 knockdown enhances cell proliferation, migration and invasion while reducing cell apoptosis. miR-361-3p is present at a low level in CRC and is negatively modified by BBOX1-AS1. Moreover, miR-361-3p was validated to be targeted by BBOX1-AS1. Src homology 2 B adaptor protein 1 (SH2B1) was notably upregulated in CRC cell lines and was identified as a downstream gene of miR-361-3p. In addition, we found that miR-361-3p amplification can suppress the expression of SH2B1. 		Yes	 We observed that BBOX1-AS1 is overexpressed in CRC cell lines, and BBOX1-AS1 knockdown enhances cell proliferation, migration and invasion while reducing cell apoptosis. 	31984680
BBOX1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-361-3p/PHF8 axis.)	In Vivo Experiment	Previously, we showed that lncRNA BBOX1-AS1 was highly expressed and played an oncogenic role in HCC.  This study revealed that BBOX1-AS1 could promote tumor progression, autophagy, and drug resistance by upregulating PHF8 in HCC cells.Mechanistically, BBOX1-AS1 enhanced the stability of PHF8 mRNA by targeting the PHF8 inhibitor miR-361-3p to regulate tumor progression and autophagy in HCC. The functional rescue experiments showed that PHF8 acted as a key factor in regulating the biological effects induced by BBOX1-AS1 and miR-361-3p in HCC, indicating that BBOX1-AS1 promotes tumor progression and sorafenib resistance by regulating miR-361-3p/PHF8. 		Yes	 This study revealed that BBOX1-AS1 could promote tumor progression, autophagy, and drug resistance by upregulating PHF8 in HCC cells.	36699616
BBOX1-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	regulation[miR-361-3p/PODXL pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	As a result, we demonstrated the extremely high BBOX1-AS1 expression in OC tissues and cells. All the results above explained that BBOX1-AS1 was overexpressed in OC and that BBOX1-AS1 caused carcinogenic influences on OC cell growth via miR-361-3p/PODXL pathway, highlighting BBOX1-AS1 as a novel potential target for OC treatment.		Yes	BBOX1-AS1 silence inhibited OC progression by suppressing cell proliferation and promoting cell apoptosis. 	33159291
BBOX1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues	regulation[HOXC6,miR-361-3p]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Microarray//Colony Formation Assay//Transwell Assay	BBOX1 antisense RNA 1 antisense RNA 1 was revealed to be highly expressed in CC. Decreased expression of BBOX1-AS1 had suppressive effects on CC cell growth and migration.BBOX1 antisense RNA 1 facilitates CC progression by upregulating HOXC6 expression via miR-361-3p and HuR.		Yes	BBOX1 antisense RNA 1 antisense RNA 1 was revealed to be highly expressed in CC. Decreased expression of BBOX1-AS1 had suppressive effects on CC cell growth and migration.	32515533
BBOX1-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	carcinoma tissues&NPC cells	Interaction(BBOX1-AS1/miR-3940-3/KPNA2 axis)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//EdU Staining//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	High BBOX1-AS1 levels were detected in the nasopharyngeal carcinoma tissues. BBOX1-AS1 silencing considerably suppressed the proliferative, migratory, and invasive abilities of NPC cells in vitro. Interestingly, BBOX1-AS1 could specifically bind to miR-3940-3 and abrogate the inhibition of KPNA2 induced by miR-3940-3. Additionally, analysis of tissue samples showed that miR-3940-3 was inversely correlated with BBOX1-AS1 and KPNA2.		Yes	BBOX1-AS1 silencing considerably suppressed the proliferative, migratory, and invasive abilities of NPC cells in vitro.	34938119
BBOX1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells	Interaction(miR-513a-3p/SLC7A11 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//IHC//EdU Staining//Transwell Assay	BBOX1-AS1 expression was significantly higher in ESCC tissues, indicating poor prognosis.miR-513a-3p was verified as a specific target of BBOX1-AS1 in ESCC, whereas knockdown of miR-513a-3p reversed the suppressive function of BBOX1-AS1 silencing in TE-1 cells. Moreover, solute carrier family 7 member 11 (SLC7A11) is regulated by miR-513a-3p, which is mediated by BBOX1-AS1 in ESCC cells. 	BBOX1-AS1 expression was significantly higher in ESCC tissues, indicating poor prognosis.	Yes	 Inhibition of BBOX1-AS1 reduced cell proliferation, slowed cell invasion and migration, and promoted apoptosis and ferroptosis in vitro. 	36216119
BBOX1-AS1	LncRNA	Homo sapiens	lung squamous cell carcinoma	LUSC tissues	Expression(highly expressed)	CCK8//qRT-PCR//Wound Healing Assay//Flow Cytometry	The results of the RT-qPCR analysis and data obtained from the TCGA database, GEO datasets, in-house gene microarray and standard mean deviation analysis all supported the upregulated expression level of BBOX1-AS1 in LUSC. 		Yes	 Furthermore, silencing of BBOX1-AS1 inhibited the proliferation and migration of LUSC cells according to in vitro assays. In addition, the cells were arrested in S-phase after knockdown of BBOX1-AS1.	34820016
BBOX1-AS1	LncRNA	Homo sapiens	Pituitary Neoplasms	pituitary adenoma tissues and cells	Interaction(miR-361-3p/E2F1 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 The expression of BBOX1-AS1 in pituitary adenoma tissues and cells has been increased, according to our findings.  We identify BBOX1-AS1 bind to miR-361-3p and to suppress its expression in a negative way. Moreover, miR-361-3p has been shown to bind with E2F1 and inhibit its expression. E2F1 also corrected miR-361-3p-mediated cell invasion, proliferation and apoptosis in BBOX1-AS1-dysregulated pituitary adenoma cells in rescue tests. 		Yes	Furthermore, it is also noted that downregulation of BBOX1-AS1causes the inhibition of pituitary adenoma cells which result in invasion, apoptosis and proliferation, as well as boosting tumor development in vivo . In addition, BBOX1-AS1 knockdown inhibited tumor development in vivo .	35324526
BBOX1-AS1	LncRNA	Homo sapiens	Primary Ovarian Insufficiency	 POF patients and granulosa cells	Interaction(miR-146b)	RNA Pull-Down//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay	 We found that the expression levels of BBOX1-AS1 were increased, while the expression levels of miR-146b were decreased in POF patients. BBOX1-AS1-WT, but not BBOX1-AS1-mut, directly interacted with miR-146b. 		Yes	BBOX1-AS1 suppressed the role of miR-146b in cell apoptosis. Therefore, BBOX1-AS1 may increase the apoptosis of granulosa cells in POF by sponging miR-146b.	35188872
BBOX1-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 EC tissues and cells	Interaction(miR-361-3p/COL1A1 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 BBOX1-AS1 was remarkably elevated in EC tissues and cells.Moreover, BBOX1-AS1 was found to be a sponge of miR-361-3p, which downregulated miR-361-3p expression. MiR-361-3p inhibitor rescued the anti-tumour effect of BBOX1-AS1 knockdown on the progression of EC. Furthermore, we discovered that miR-361-3p specially bound to COL1A1 3'UTR and downregulated COL1A1 and COL1A1 reduction declined the promoting effect of silencing miR-361-3p on EC cell malignant phenotypes.		Yes	 In addition, the silencing of BBOX1-AS1 attenuated the cell viability, cell migration and enhanced cell apoptosis of EC, as well as suppressed EC tumour formation in vivo. 	36453878
BCAR4	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues	interaction[sponging miR-1261]	CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the present study, the expression of lncRNA BCAR4 was notably elevated in liver cancer compared with adjacent non?tumor tissues. Collectively, the results of the present study demonstrated that lncRNA BCAR4 may promote liver cancer development by directly binding to miR‑1261 and targeting ANAPC11.		Yes	 Functional in vitro assays demonstrated that knockdown of lncRNA BCAR4 inhibited the proliferation, migration and invasion of Huh?7 cells. 	32319544
BCAR4	LncRNA	Homo sapiens	Liver Neoplasms	LC tissues 	Expression[highly expressed]	qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	The present study measured the expression levels of BCAR4 in LC cells and tissues, and discovered that BCAR4 was upregulated in LC tissues compared with adjacent normal tissues. 	Furthermore, high BCAR4 expression was associated with the presence of multiple tumors and advanced Tumor-Node-Metastasis stages (III/IV). Survival analysis found that high BCAR4 expression indicated poor overall survival (OS) and progression-free survival (PFS). By analyzing the risk factors of poor OS and PFS using univariate analysis and multivariate analysis, high BCAR4 expression was revealed to be an independent risk factor of poor prognosis. 	Yes	In addition, the role of BCAR4 was further investigated in vitro, which revealed overexpression of BCAR4 to markedly promote the proliferation, migration and invasion of LC cells. Conversely, the loss of BCAR4 expression repressed the proliferation, migration and invasion of LC cells. 	32782595
BCAR4	LncRNA	Homo sapiens	Glioma	glioma tissues,cell lines	Regulation[BCAR4/miR-2276/MMP7 axis]	RNA Pull-Down//Western Blot//qPCR//CCK8//Transwell Assay	BCAR4 expression was increased in glioma tissues and GBM cell lines, and its high expression positively correlated with advanced grades and worse prognosis.Our findings identified the essential roles of the BCAR4/miR-2276/MMP7 axis in gliomagenesis and provided novel insights on glioma therapy.	BCAR4 expression was increased in glioma tissues and GBM cell lines, and its high expression positively correlated with advanced grades and worse prognosis.	Yes	Functional assays verified that knockdown of BCAR4-inhibited cell growth and invasion in vitro, and impaired tumor formation in vivo. 	31849498
BCYRN1	LncRNA	Homo sapiens	Glioma		regulation[miR-125a-5p]	qRT-PCR//Wound Healing Assay//Transwell Assay	 Mechanistically, upregulated expression of BCYRN1 in glioma acts as a sponge to sequester the endogenous tumor suppressor miR-125a-5p and to further increase the expression TAZ.		Yes	The upregulation of BCYRN1 promoted the proliferation, migration and invasion of glioma cells. 	32104095
BCYRN1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-30b-3p/ROCK1 axis)	qRT-PCR//Luciferase Report Assay//Transwell Assay//Western Blot	The expression levels of BCYRN1 and ROCK1 were upregulated in NSCLC tissues and cells, while miR-30b-3p was downregulated.LncRNA BCYRN1 was involved in the metastasis of NSCLC through modulating the miR-30b-3p/ROCK1 axis.	Higher BCYRN1 expression indicated lymph node metastasis and advanced tumor-node-metastasis (TNM) stage of NSCLC patients.	Yes	 Loss of BCYRN1 suppressed cell migration and invasion.  In vivo, BCYRN1 silencing reduced the growth of A549 cells.	35225646
BCYRN1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tumor tissues	Regulation[NPR3 ]	qRT-PCR	 The results showed that BCYRN1 expression was significantly upregulated in 96 CRC tumor tissues compared with para-carcinoma control tissues.  Furthermore, NPR3 was identified to be a target of BCYRN1 and was downregulated by BCYRN1 knockdown.	Additionally, BCYRN1 overexpression was associated with larger tumor size and advanced pathological stages in CRC patients.	Yes	In vitro BCYRN1 knockdown significantly inhibited the proliferation and apoptosis of CRC cells.	30114690
BCYRN1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines(HIEC,SW620)	Expression[Expression[lower expressed]-expression]	qRT-PCR//Western Blot	" The results showed that the expres_x0002_sion level of lncRNA BCYRN1 in CRC tissues 
was significantly higher than that in para-cancer 
tissues (Figure 1). "	"We performed a 60-month prognostic follow-Expression[Expression[up-expression]-expression] 
of these patients and analyzed their prognosis using 
the Kaplan-Meier method. Fortunately, no patient 
was lost to follow-Expression[Expression[up-expression]-expression]. The results were shown in 
Figure 2. Patients with high expression of lncRNA 
BCYRN1 had a poor prognosis, and their survival 
curve was significantly weaker than patients with 
low expression of lncRNA BCYRN1"	Yes	In vitro study, Expression[down-expression]-regulation of lncRNA BCYRN1 expression by si-BCYRN1 could significantly inhibit invasion and migration of CRC cells.	31773686
BCYRN1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tumour tissues and cell lines 	regulation[miR-204-3p/KRAS axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	" We found that compared with normal tissues and human intestinal epithelial cells (HIECs), CRC tumour tissues and cell lines had significantly increased BCYRN1 levels.Our findings suggest that BCYRN1 plays a carcinogenic role in CRC by regulating the miR-204-3p/KRAS axis.
"		Yes	We further determined that knockdown of BCYRN1 inhibited the proliferation, migration, and invasion and promoted the apoptosis of CRC cells.	32944001
BCYRN1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples	regulation[BCYRN1/miR-490-3p/POU3F2]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our results exhibited that BCYRN1 was over expressed in HCC samples, which was connected with unfavorable prognosis in HCC patients.BCYRN1, served as a competing endogenous RNA, up-regulated the expression of POU3F2 to promote the development of HCC through sponging miR-490-3p, supplying novel molecular targets and underlying prognostic biomarkers for HCC therapy.		Yes	 In addition, a series of experiments exhibited that overexpression of BCYRN1 significantly expedited HCC cells growth, clone formation, and movement abilities, and vice versa.	31920461
BCYRN1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell and tissues	Interaction(TM4SF1/BATF )	qRT-PCR	BCYRN1 upregulation was associated with poorer clinical outcomes in HCC patients, and knocking down this lncRNA impaired HCC cell migration and invasion.  From a mechanistic perspective, BATF was recruited to the TM4SF1 promoter by BCYRN1, and reducing the expression of this lncRNA was sufficient to constrain xenograft tumor growth in mice. 	BCYRN1 upregulation was associated with poorer clinical outcomes in HCC patients, and knocking down this lncRNA impaired HCC cell migration and invasion. 	Yes	BCYRN1 upregulation was associated with poorer clinical outcomes in HCC patients, and knocking down this lncRNA impaired HCC cell migration and invasion. 	35730016
BCYRN1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	urinary-EXO from patients with BCa	Regulation（WNT5A/VEGF-C/VEGFR3 ）	qRT-PCR//ChIP	LncRNA BCYRN1 was substantially upregulated in urinary-EXO from patients with BCa, and associated with the LN metastasis of BCa. Mechanistically, BCYRN1 epigenetically upregulated WNT5A expression by inducing hnRNPA1-associated H3K4 trimethylation in WNT5A promoter, which activated Wnt/β-catenin signaling to facilitate the secretion of VEGF-C in BCa.		Yes	We demonstrated that exosomal BCYRN1 markedly promoted tube formation and migration of human lymphatic endothelial cells (HLECs) in vitro and lymphangiogenesis and LN metastasis of BCa in vivo. 	34323412
BCYRN1	LncRNA	Homo sapiens	Glioma	glioma tissues	regulation[PTEN/AKT/p21 pathway]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//migration assay//Colony Formation Assay	Among them, BCYRN1 was the most downregulated lncRNA, and its low expression positively correlated with glioma progression. BCYRN1 functioned as a ceRNA to inhibit glioma progression by sponging miR-619-5p to regulate CUEDC2 expression and PTEN/AKT/p21 pathway. 		Yes	 Functionally, BCYRN1 overexpression inhibited cell proliferation, migration in glioma cell lines, whereas BCYRN1 depletion resulted in the opposite way. 	32978519
BCYRN1	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 In the present study, it was found that BC200 expression level was higher in hepatocellular carcinoma (HCC) tissues than that in adjacent tissues.  Interestingly, it was found that BC200 affected the expression of c‑Myc protein but did not affect the mRNA expression level of c‑MYC. BC200 KO cells exhibited a reduced protein expression level of Bax protein and an increased protein expression level of Bcl‑xL. Conversely, BC200 overexpression reduced the expression of Bcl‑xL protein and increased the expression of Bax protein. Importantly, it was found that BC200 affected the formation of subcutaneous tumors in nude mice. In conclusion, the present results suggested that lncRNA BC200 may play an important role in liver cancer.		Yes	 Cell function was examined by constructing BC200 knockout (KO) and BC200‑overexpression in vitro models. It was found that BC200 affected the proliferation and migration of HepG2 cells.	31894342
BCAR4	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer cell lines	interaction[miR-644a,TLX1 ]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	The expression of BCAR4 was higher in bladder cancer cell lines than normal urothelial cell line. We showed that BCAR4 sponged miR-644a to modulate the expression of TLX1 and promote bladder cancer development.	Moreover, the expression of BCAR4 was associated with the advanced stage and metastasis of bladder cancer. 	Yes	Through knockdown of BCAR4, we discovered that knockdown of BCAR4 significantly decreased the proliferation, migration and invasive abilities of bladder cancer cells. 	32273720
BCYRN1	LncRNA	Homo sapiens	stomach carcinoma	 GC samples and cell lines	Regulation(EpCAM)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//migration assay//Cell Proliferation Assay//Colony Formation Assay	We found BCYRN1 was significantly upregulated in GC samples, and its expression was positively correlated with advanced TNM stage (p = 0.0012) and tumor size (p = 0.027).Moreover, the results of RT-qPCR and western blotting indicated that knockdown of BCYRN1 notably decreased the expression of epithelial cell adhesion molecules (EpCAM). Otherwise, overexpression of BCYRN1 in GC cells (BGC-823 and SGC-7901) could reverse the effects of BCYRN1 knockdown.	We found BCYRN1 was significantly upregulated in GC samples, and its expression was positively correlated with advanced TNM stage (p = 0.0012) and tumor size (p = 0.027).	Yes	Functionally, BCYRN1 knockdown by siRNA could inhibit cell proliferation, induce G1/G0 cell cycle arrest, increase apoptosis and impair migratory ability of AGS cells. 	29435146
BCYRN1	LncRNA	Homo sapiens	Myelodysplastic Syndromes	MDS patients,  MDS cells 	Interaction(LncRNA BC200/miR-150-5p/MYB )	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay//EdU Staining//ChIP	we found that BC200 was highly expressed in MDS patients compared with normal individuals. Mechanistic investigations revealed that BC200 functioned as a miRNA sponge to positively regulate the expression of MYB through sponging miR-150-5p and subsequently promoted malignant proliferation of MDS cells. Conversely, we found that BC200 was a direct transcriptional target of MYB, and knockdown of MYB abolished the oncogenic effect of BC200/miR-150-5p. 		Yes	Knockdown of BC200 inhibited MDS cell proliferation, colony formation, and cell cycle progression in vitro and suppressed the growth and invasiveness of MDS cells in vivo.	35136029
BCRC-3	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	Regulation[miR-182-5p/p27 axis]	Flow Cytometry//Western Blot//PCR//IF	BCRC-3 was lowly expressed in bladder cancer tissues and cell lines.BCRC-3 functions as a tumor inhibitor to suppress BC cell proliferation through miR-182-5p/p27 axis, which would be a novel target for BC therapy.		Yes	Proliferation of BC cells was suppressed by ectopic expression of BCRC-3 in vitro and in vivo. 	30285878
BCLIN25	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer  tissues	Interaction[upregulating ERBB2]	Western Blot//Tunel//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	Mechanistically, BCLIN25 was shown to increase the expression of ERBB2 by enhancing promoter CpG methylation of miR-125b, leading to miR-125b downregulation. In turn, ERBB2 mRNA degradation was found to be abolished due to decreased binding of miR-125b to the 3'-untranslated region (UTR) of ERBB2. These findings reveal the role of novel lincRNAs in breast cancer and provide a comprehensive landscape of breast cancer MS-lincRNAs, which may complement the current molecular classification system in breast cancer.		Yes	 BCLIN25 was found to contribute to tumorigenesis in vitro and in vivo. 	31801944
BCAR4	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[MAPK/ERK signaling]	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	LncRNA BCAR4 was highly expressed in both GC tissues and cell lines.Besides, Western blotting revealed that lncRNA BCAR4 played an oncogenic role in GC via regulating MAPK/ERK signaling.		Yes	CCK-8 assay, colony formation assay, and flow cytometry results indicated that up-regulated lncRNA BCAR4 significantly promoted cell proliferation and suppressed cell apoptosis in GC. 	32329841
BCAR4	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[GLI2]	qRT-PCR//IHC//Transwell Assay	qRT-PCR was used to determine the expression of BCAR4 and GLI2 downstream genes in NSCLC tissues and cell lines. The expression of BCAR4 in NSCLC tissues and cells was significantly higher than the normal level.  In summary, the cooperative mechanism of lncRNA BCAR4 and GLI2 might provide a new opportunity for treating NSCLC.		Yes	The overexpression of BCAR4 promoted NSCLC cell viability, migration, and invasion. The suppression of BCAR4 and GLI2 showed the opposite effects.	29615150
BCAR4	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 LO2 cells 	Regulation(LATS2)	Luciferase Report Assay//Invasion Assay//Migration Assay	 The relative expression of LncRNA BCAR4 in HepG2 cells was critically higher than that in LO2 cells (P<0.05), while LATS2 mRNA in HepG2 cells was significantly less than that in LO2 cells (P<0.05).LncRNA BCAR4 can regulate the LATS2 expression, and inhibiting the expression of LncRNA BCAR4 can inhibit proliferation, invasion of HepG2 cells and induce its apoptosis, which finding provides a certain reference for the targeted therapy of liver cancer.		Yes	LncRNA BCAR4 can regulate the LATS2 expression, and inhibiting the expression of LncRNA BCAR4 can inhibit proliferation, invasion of HepG2 cells and induce its apoptosis, which finding provides a certain reference for the targeted therapy of liver cancer.	34150042
BCAR4	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Regulation[Wnt signaling]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	In the present study, elevated levels of lncRNA breast cancer anti‑estrogen receptor 4 (BCAR4) were identified in BC tissues compared with matched healthy tissues.Downregulation of BCAR4 led to the inactivation of Wnt signaling. Mechanistically, BCAR4 directly sponged microRNA (miR)‑370‑3p and elevated Wnt7a expression. Endogenous expression of Wnt7a reversed BCAR4 silencing‑mediated cell growth arrest and induction of apoptosis in BC cells accompanied with a re‑activation of Wnt signaling. Reverse transcription‑quantitative PCR indicated that there was a strong association between BCAR4, miR‑370‑3p and Wnt7a expression in tumors from patients with BC compared with healthy control tissues. 		Yes	Silencing of BCAR4 inhibited cell proliferation and induced apoptosis in BC cell lines 5637 and T24.	31894304
MANCR	LncRNA	Homo sapiens	Thyroid Carcinoma, Anaplastic	ATC tissues,cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay	One of the lncRNAs, mitotically associated long non-coding RNA (MANCR; LINC00704), was significantly overexpressed in ATC cell lines and patient samples compared with NT and papillary thyroid cancer (PTC).		Yes	 MANCR depletion in ATC cells significantly inhibited cancer cell proliferation and invasion, and induced apoptosis.	33178758
MANCR	LncRNA	Homo sapiens	esophageal carcinoma	esophageal carcinomas tissues 	Interaction(PDE4D)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay	MANCR was highly expressed in esophageal carcinomas tissues than non-tumoral ones. PDE4D was the target gene binding MANCR, which was downregulated in esophageal carcinoma tissues. Its level was negatively regulated by MANCR. Importantly, PDE4D could abolish the role of MANCR in stimulating the malignant progression of esophageal carcinoma.		Yes	MANCR promoted proliferative ability and inhibited apoptosis in TE-1 and EC-109 cells. In nude mice with xenografted esophageal carcinoma, knockdown of MANCR markedly slowed down tumor growth. 	34565013
SLC16A1-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM tissues	Interaction(miR-149)	CCK8//qRT-PCR//Colony Formation Assay	We found that SLC16A1-AS1 expression was upregulated in GBM tissues, and the upregulated expression of SLC16A1-AS1 predicted poor survival of GBM patients. MiR-149 was downregulated in GBM tissues and inversely correlated with the expression of SLC16A1-AS1. In GBM cells, overexpression of SLC16A1-AS1 downregulated the expression of miR-149 and increased the methylation of miR-149 gene. 	We found that SLC16A1-AS1 expression was upregulated in GBM tissues, and the upregulated expression of SLC16A1-AS1 predicted poor survival of GBM patients. 	Yes	. In cell proliferation and colony formation assay, overexpression of SLC16A1-AS1 reduced the inhibitory effects of miR-149 on GBM cell proliferation.	33603467
SLC16A1-AS1	LncRNA	Homo sapiens	Breast Neoplasms	BC patients and cells	Interaction(miR-552-5p/WIF1 Signaling Pathway)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	Lower SLC16A1-AS1 expression in BC tissues was related to poor prognosis of BC patients. Lower SLC16A1-AS1 expression in BC tissues was related to poor prognosis of BC patients.	Lower SLC16A1-AS1 expression in BC tissues was related to poor prognosis of BC patients.	Yes	Lower SLC16A1-AS1 expression in BC tissues was related to poor prognosis of BC patients.	35372039
SLC16A1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Expression[lower expressed]	Western Blot//ISH//CCK8//qRT-PCR//Flow Cytometry//MTT//IHC	 It was showed that SLC16A1-AS1 was remarkably downregulated in NSCLC tissues and cell lines.	Clinical sample analysis showed that SLC16A1-AS1 had a favorable impact on the overall survival and progression-free survival of patients with NSCLC. 	Yes	Functionally, SLC16A1-AS1 overexpression could inhibit the viability and proliferation of lung cancer cell, block the cell cycle and promote cell apoptosis in vitro which may result from reduced phosphorylation of rat sarcoma (RAS)/ proto-oncogene serine/threonine-protein kinase (RAF)/ mitogen-activated protein kinase kinase (MEK)/ extracellular regulated protein kinases (ERK) pathway caused by elevated expression of SLC16A1-AS1.	31371390
SLC16A1-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC cells and tissues 	Interaction(miR-143-3p/SLC7A11 Signaling)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//FISH//Flow Cytometry//Luciferase Report Assay//IHC//Transwell Assay	Our study revealed that SLC16A1-AS1 has high expression and was associated with overall survival in renal cancer. The present results suggest that silencing lncRNA SLC16A1-AS1 can induce ferroptosis through miR-143-3p/SLC7A11 signaling in renal cancer. 	Our study revealed that SLC16A1-AS1 has high expression and was associated with overall survival in renal cancer.	Yes	Knockdown SLC16A1-AS1 inhibited cell viability, proliferation, and migration of renal cancer cells. 	35167383
SLC16A1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients and cells	Interaction(miR-141)	qRT-PCR	SLC16A1-AS1 was upregulated in HCC and its high expression levels predicted poor survival of HCC patients.  Expression levels of miR-141 were lower in HCC patients and were inversely correlated with the expression levels of SLC16A1-AS1. In HCC cells, overexpression of SLC16A1-AS1 led to downregulation of miR-141, while overexpression of miR-141 did not regulate the expression of SLC16A1-AS1. In addition, overexpression of SLC16A1-AS1 led to increased methylation of miR-141. 	SLC16A1-AS1 was upregulated in HCC and its high expression levels predicted poor survival of HCC patients. 	Yes	And overexpression of SLC16A1-AS1 attenuated the inhibitory effects of miR-141 on HCC cell proliferation.	33744723
SLC16A1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-411/MITD1 axis)	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Invasion Assay	 The expression of SLC16A1-AS1 markedly increased in HCC tissues and cell lines.  Subsequent studies identified SLC16A1-AS1 as a downstream target of miR-411. In addition, SLC16A1-AS1 knockdown and miR-411 overexpression significantly stagnated the progression of HCC cells. SLC16A1-AS1 knockdown also downregulated MITD1 levels.		Yes	In addition, SLC16A1-AS1 knockdown and miR-411 overexpression significantly stagnated the progression of HCC cells. 	35293026
SLC16A1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC samples	Expression[highly expressed]	Flow Cytometry//qRT-PCR//Western Blot	To identify the differentially expressed lncRNAs between OSCC tissue and normal tissue, RNA-Seq data were used. lncRNA SLC16A1-AS1 was significantly highly expressed in OSCC samples than that in normal samples. 	Systematic bioinformatics analysis revealed that SLC16A1-AS1 was associated with histological tumor grades and overall survival status, as well as copy number variation, somatic mutation, tumor mutation burden, tumor stemness, tumor microenvironment and infiltrating immune cells. 	Yes	 Loss-of-function experiments were performed to determine the biological functions of SLC16A1-AS in OSCC cells. Silencing SLC16A1-AS1 significantly reduced the cell proliferation rate and colony-forming ability in both CAL27 and SCC25 cell lines. 	32450050
SLC16A1-AS1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue samples, OSCC cells	Interaction(miR-5088-5p)	BrdU//qRT-PCR//RNA Pull-Down	OSCC tissue samples exhibited decreased expression levels of SLC16A1-AS1 and premature miR-5088-5p, but increased the expression levels of mature miR-5088-5p. SLC16A1-AS1 was detected in both nucleus and cytoplasm samples of OSCC cells and its direct interaction with premature miR-5088-5p was confirmed. Overexpression of SLC16A1-AS1 in OSCC cells resulted in inhibited maturation of miR-5088-5p. SLC16A1-AS1 suppressed the enhancing effects of miR-5088-5p on cell proliferation. SLC16A1-AS1 was downregulated in OSCC and it may inhibit cell proliferation by suppressing maturation of miR-5088-5p.		Yes	SLC16A1-AS1 was detected in both nucleus and cytoplasm samples of OSCC cells and its direct interaction with premature miR-5088-5p was confirmed. Overexpression of SLC16A1-AS1 in OSCC cells resulted in inhibited maturation of miR-5088-5p. SLC16A1-AS1 suppressed the enhancing effects of miR-5088-5p on cell proliferation. SLC16A1-AS1 was downregulated in OSCC and it may inhibit cell proliferation by suppressing maturation of miR-5088-5p.	35829849
SLC16A1-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	 TNBC tissues and cells	Interaction(miR-182/PDCD4 axis)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay	 SLC16A1-AS1 expression was downregulated in TNBC tissues. SLC16A1-AS1 interacted with miR-182, whereas SLC16A1-AS1 and miR-182 overexpression failed to affect their expression. SLC16A1-AS1 overexpression upregulated the expression of PDCD4, a downstream target of miR-182. SLC16A1-AS1 and PDCD4 overexpression suppressed cell cycle progression from the G1 phase to the G2 phase. MiR-182 and silencing of PDCD4 played the opposite role. 		Yes	Additionally, miR-182 overexpression inhibited the role of SLC16A1-AS1 overexpression on cell cycle progression in both BT-549 and BT20 cells. The cell proliferation assay showed that SLC16A1-AS1 and PDCD4 overexpression decreased the cell proliferation rate.	35316129
SLC16A1-AS1	LncRNA	Homo sapiens	Glioblastoma	 LN-229 , LN-18 cells and tissues	Interaction( miR-1269 )	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//BrdU//Transwell Assay	 SLC16A1-AS1 was also overexpressed in GBM.  The direct interaction of SLC16A1-AS1 with premature miR-1269 was observed. SLC16A1-AS1 partly reversed the effects of miR-1269 on GBM cell proliferation, movement and apoptosis. 		Yes	SLC16A1-AS1 suppressed miR-1269 maturation and promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while miR-1269 displayed the opposite trend.  Moreover, SLC16A1-AS1 overexpression increased the level of ki-67, CDK4 and Bcl-2 in LN-229 and LN-18 cells. 	35609320
SLC25A21-AS1	LncRNA	Homo sapiens	Glioma	 glioma specimens and cell lines	Interaction(miR-221-3p/miR-222-3p)	Transfection//Invasion Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	SLC25A21-AS1 was significantly downregulated in glioma specimens and cell lines compared to non-cancerous ones. miR-221-3p/miR-222-3p were the target miRNAs for SLC25A21-AS1. Overexpression of SLC25A21-AS1 inhibited glioma cell growth, invasion, and migration while miR-221-3p/miR-222-3p-overexpressed groups could offset this effect.Downregulation of SLC25A21-AS1 in gliomas carries a universally poor prognosis. Overexpression of SLC25A21-AS1 inhibited glioma progression via miR-221-3p/miR-222-3p.	Significant associations were found between SLC25A21-AS1 downregulation and WHO stage, IDH status, poor disease-free survival/overall survival.	Yes	miR-221-3p/miR-222-3p were the target miRNAs for SLC25A21-AS1. Overexpression of SLC25A21-AS1 inhibited glioma cell growth, invasion, and migration while miR-221-3p/miR-222-3p-overexpressed groups could offset this effect.	35266110
SLC16A1-AS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC and non-tumor tissue samples	Interaction(miR-194/SOCS2 Axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	SLC16A1-AS1 was down-regulated in CSCC and correlated with poor survival. In addition, SLC16A1-AS1 could sponge miR-194 and increase the expression levels of SOCS2, ultimately inhibiting the proliferation of cervical cancer cells.	SLC16A1-AS1 was down-regulated in CSCC and correlated with poor survival.	Yes	Overexpression of SLC16A1-AS1 could inhibit the proliferation of cervical cancer cells. 	33603475
hsa_circ_0119872	CircRNA	Homo sapiens	Uveal melanoma	UM cell lines and tissues	Interaction(circ_0119872/miR-622/G3BP1 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	We found that circ_0119872 is upregulated in UM cell lines and tissues. Moreover, overexpression of circ_0119872 promotes the malignancy of UM cells, while silencing of circ_0119872 inhibits it. In addition, circ_0119872 can directly interact with miR-622 as a miRNA sponge that regulates the expression of the miR-622 target gene G3BP1 as well as downstream Wnt/β-catenin and mTOR signalling pathways.		Yes	overexpression of circ_0119872 promotes the malignancy of UM cells, while silencing of circ_0119872 inhibits it. 	33579337
SH3PXD2A-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation(p53)	ISH//Wound Healing Assay//qRT-PCR//RIP//FISH//ChIP	 RNA ISH revealed that SH3PXD2A-AS1 was overexpressed in CRC compared with adjacent normal colon tissues and indicated poor prognosis in CRC. Mechanistically, SH3PXD2A-AS1 can directly interact with p53 protein and regulate p53-mediated gene transcription in CRC. 	 RNA ISH revealed that SH3PXD2A-AS1 was overexpressed in CRC compared with adjacent normal colon tissues and indicated poor prognosis in CRC. 	Yes	Functional analyses showed that SH3PXD2A-AS1 enhanced cell proliferation, angiogenesis, and metastasis. 	34131400
circFNDC3B	CircRNA	Homo sapiens	microinvasive gastric cancer	gastric cancer (GC) cells and patients	Interaction(miR-942/CD44 and miR-510/CDH1)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//IHC	 In summary, our study demonstrated that a higher level of circFNDC3B could lead to the increased expression of CD44 and CDH1 via modulating the signaling pathways of miR-942/CD44 and miR-510/CDH1 in EGC patients. 		Yes	And circFNDC3B was proved to increase the migration and invasion of gastric cancer (GC) cells. 	35418175
SGO1-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients and cell	Regulation	qRT-PCR	We demonstrated that SGOL1-AS1 interacts with chromatin-modifying proteins involved in gene repression and that SGOL1-AS1 knockdown is associated with increased heterochromatin formation. In AML patients, high expression of SGOL1-AS1 correlates with both pro-inflammatory gene expression and poor survival. Altogether, our data reveal that SGOL1-AS1 is an essential regulator of cell survival in AML cell lines and a possible regulator of pro-inflammatory signaling in AML patients.	 In AML patients, high expression of SGOL1-AS1 correlates with both pro-inflammatory gene expression and poor survival. 	Yes	 We also observed that loss of SGOLl-AS1 results in increased apoptosis and the downregulation of pro-inflammatory genes. 	36387443
SGO1-AS1	LncRNA	Homo sapiens	stomach carcinoma	 gastric carcinoma tissues	Interaction(TGFB1/2/PTBP1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//ISH//Transfection//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Microarray//Cell Proliferation Assay//ChIP	SGO1-AS1 was downregulated in gastric carcinoma tissues compared to adjacent normal tissues, and its downregulation was positively correlated with advanced clinical stage, metastasis status and poor patient prognosis. Mechanistically, SGO1-AS1 facilitated TGFB1/2 mRNA decay by competitively binding the PTBP1 protein, resulting in reduced TGFβ production and, thus, preventing the epithelial-to-mesenchymal transition (EMT) and metastasis. In addition, in turn, TGFβ inhibited SGO1-AS1 transcription by inducing ZEB1. 		Yes	The functional experiments revealed that SGO1-AS1 inhibited GC cell invasion and metastasis in vitro and in vivo. 	34706749
SGMS1-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cells and tissues	Interaction(miR-106a-5p/MYLI9 axis)	qRT-PCR//Luciferase Report Assay//Migration Assay//Colony Formation Assay	 SGMS1-AS1 was downregulated in LUAD tissue as well as cells, which was related to good prognosis of patients with lung adenocarcinoma.  Furthermore, miR-106a-5p was the direct target of SGMS1-AS1 and transfecting miR-106a-5p inhibitor could reversed the impact induced by knockdown of SGMS1-AS1. Subsequently, we found that MYLIP was the target of miR-106a-5p, which was negatively correlated with miR-106a-5p, but had high positive correlation with SGMS1-AS1.	 SGMS1-AS1 was downregulated in LUAD tissue as well as cells, which was related to good prognosis of patients with lung adenocarcinoma. 	Yes	Additionally, knockdown of SGMS1-AS1 promoted proliferation, migration, invasion, and epithelial mesenchymal transition (EMT) progression of LUAD cells, which meant that SGMS1-AS1 inhibited the progression of LUAD cells. 	34061466
circCTNNB1	CircRNA	Homo sapiens	Cerebral Ischemia/Reperfusion Injury	OGD/R-treated mAS cells	Interaction(miR-96-5p/SRB1 )	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//ELISA//IF	CircCTNNB1 and SRB1 interacted with miR-96-5p, and the overexpression of miR-96-5p efficiently reversed the function of circCTNNB1 in OGD/R-treated mAS cells. CircCTNNB1 protected against cerebral ischemia-reperfusion injury by up-regulating SRB1 in vivo.		Yes	 Overexpression of circCTNNB1 alleviated cell apoptosis, oxidative stress and the inflammatory response induced by OGD/R in vitro. Up-regulation of circCTNNB1 increased SRB1 expression levels to protect mAS cells from OGD/R-induced damage.	35435123
circLPAR1	CircRNA	Homo sapiens	Urinary Bladder Neoplasms	MIBC tissues	Interaction[miR-762]	qRT-PCR//Wound Healing Assay//Luciferase Report Assay//RNA-seq	 circLPAR1 was identified to be lowly expressed in MIBC tissues in a cohort of 125 cases, and predicted a poor disease-specific survival time, compared with patients with high circLPAR1 expression (52.4 vs. 56.0 months; P=0.001) by univariate and multivariate Cox regression analyses. 	 circLPAR1 was identified to be lowly expressed in MIBC tissues in a cohort of 125 cases, and predicted a poor disease-specific survival time, compared with patients with high circLPAR1 expression (52.4 vs. 56.0 months; P=0.001) by univariate and multivariate Cox regression analyses. 	Yes	 Matrigel and wound healing assays also demonstrated that the invasion of 5637 and T24 bladder cancer cells were significantly enhanced following the knockdown of circLPAR1 by small interfering RNA (si-circLPAR1-1 in T24 cell line, P=0.01; si-circLPAR1-2 in 5637 cell line, P=0.003; si-circLPAR1-2 in T24 cell line, P=0.002; si-circLPAR1-2 in 5637 cell line, P=0.006).	30867795
SLC25A21-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	PA tisssues	Interaction(NPM1/c-Myc axis and SLC25A21)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ChIP	LncRNA SLC25A21-AS1 expression was downregulated by PA and associated with the proliferation and migration of ESCC cells in vitro and in vivo. SLC25A21-AS1 promotes the proliferation and migration of ESCC cells by regulating the NPM1/c-Myc axis and SLC25A21 expression. 		Yes	LncRNA SLC25A21-AS1 expression was downregulated by PA and associated with the proliferation and migration of ESCC cells in vitro and in vivo.	35735113
SFTA3	LncRNA	Homo sapiens	Pulmonary Arterial Hypertension	PAs of PAH patients and hypoxic human pulmonary artery smooth muscle cells (PASMCs)	Interaction(miR-23a-3p)	Western Blot//Transfection//CCK8//RIP//Flow Cytometry//qRT-PCR//Luciferase Report Assay//H&E Staining//Cell Proliferation Assay//Cell Cycle Assay//EdU Staining	LncRNA PAHRF was down-regulated in both the PAs of PAH patients and hypoxic human pulmonary artery smooth muscle cells (PASMCs). Luciferase activity assay proved molecular binding between PAHRF and hsa-miR-23a-3p. Moreover, MST1 was confirmed to be the putative target gene and regulated by PAHRF/miR-23a-3p. In addition, we explored the molecular mechanism regulating the expression of miR-23a-3p, and found that lncRNA PAHRF acted as an endogenous sponge for miR-23a-3p, and silencing lncRNA PAHRF could up-regulate the expression of miR-23a-3p.		Yes	The overexpression of PAHRF inhibited the proliferation and promoted the apoptosis of PASMCs. Similarly, we also found PAHRF overexpression decreased the proliferation under hypoxia condition. Knockdown of PAHRF exerted the opposite effects. 	34126237
SLC44A3-AS1	LncRNA	Homo sapiens	Glioblastoma	GBMs	Regulation( NF-κB signaling )	In Vivo Experiment//cell invasion assay//Western Blot//ISH//Transfection//Flow Cytometry//qRT-PCR//RIP//Cell Proliferation Assay//IHC//IF	Here, we report that LINC01057 as a lncRNA is overexpressed in GBMs, especially in MES subtype. LINC01057 interacts with IKKα and maintains IKKα nucleus localization, leading to effective chromatin accessibility at NF-κB responsive promoters via histone modification and final NF-κB activation. IKKα knockdown disrupts the effect of LINC01057 overexpression on PN to MES transition (PMT). LINC01057 level is negatively correlated with patient prognosis in MES-subtype GBM.		Yes	LINC01057 knockdown suppresses proliferation, invasion and radioresistance of GBM cells in vitro, and tumor growth in vivo. LINC01057 knockdown leads to loss of MES signature in MES subpopulation of GBM cells, but LINC01057 overexpression promotes MES differentiation in proneural (PN) subpopulation.	33130316
SLCO4A1	LncRNA	Homo sapiens	Mucocutaneous Lymph Node Syndrome	 serum of KD patients, HUVECs	Interaction(miR-335-5p/POU5F1 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Tunel//qRT-PCR//Luciferase Report Assay//H&E Staining//ELISA//Bioinformatics Analysis	LncRNA Slco4a1 was significantly upregulated in the serum of KD patients compared with healthy controls. LncRNA Slco4a1 was upregulated in human umbilical vein endothelial cells (HUVECs) stimulated with KD serum.lncRNA Slco4a1 is a sponge of miR-335-5p and negatively regulated the expression of miR-335-5p. POU5F1 was the downstream target of miR-335-5p, and miR-335-5p overexpression could upregulate the expression of POU5F1. 		Yes	 LncRNA Slco4a1 overexpression could promote the expression of inflammatory factors and apoptosis in HUVECs. The number of inflammatory cells and the infiltration area of the coronary artery in KD rats were decreased after lncRNA Slco4a1 silencing. 	35282018
Slco3a1-206	LncRNA	Rattus norvegicus	Arthritis, Gouty	THP-1 cell line	Regulation(AP3D1)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//ELISA	SNHG8 expression was identified to be upregulated after MSU treatment. Ablation of SNHG8 decreased the MSU-induced enhancement of paw swelling and foot thickness. In addition, SNHG8 depletion decreased the protein levels of proinflammatory factors in GA mice. Mechanically, SNHG8 was verified to be a sponge of miR-542-3p, and miR-542-3p targeted AP3D1 3' untranslated region. SNHG8 competitively bound with miR-542-3p to upregulate AP3D1 expression. Finally, results of rescue assays illustrated that AP3D1 upregulation offset the SNHG8-mediated inhibition on paw swelling and protein levels of proinflammatory factors in GA mice. In conclusion, SNHG8 accelerates acute GA development by upregulating AP3D1 in an miR-542-3p-dependent way in mice, providing an effective therapeutic approach to treat acute GA.		Yes	Ablation of SNHG8 decreased the MSU-induced enhancement of paw swelling and foot thickness. In addition, SNHG8 depletion decreased the protein levels of proinflammatory factors in GA mice. Mechanically, SNHG8 was verified to be a sponge of miR-542-3p, and miR-542-3p targeted AP3D1 3' untranslated region.	34874227
SLCC1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC patients	Regulation(HK2)	qRT-PCR//RNA Pull-Down	Further validation in two independent CRC cohorts confirmed the upregulation of lncSLCC1 in CRC tissues, and revealed that increased lncSLCC1 expression was associated with poor survival in CRC patients. Mechanistically, lncRNA-SLCC1 interacted with AHR and transcriptionally activated HK2 expression, the crucial enzyme in glucose metabolism, thereby driving the glycolysis pathway and accelerating CRC tumor growth.  The functional assays revealed that lncSLCC1 induced glycolysis activation and tumor growth in CRC mediated by HK2. 	Further validation in two independent CRC cohorts confirmed the upregulation of lncSLCC1 in CRC tissues, and revealed that increased lncSLCC1 expression was associated with poor survival in CRC patients. 	Yes	Mechanistically, lncRNA-SLCC1 interacted with AHR and transcriptionally activated HK2 expression, the crucial enzyme in glucose metabolism, thereby driving the glycolysis pathway and accelerating CRC tumor growth. 	33602893
SLC9A3-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(microRNA-760 )	CCK8//qRT-PCR	 SLC9A3-AS1 was upregulated in NSCLC tissues and cell lines. Mechanistically, SLC9A3-AS1 acted as competing endogenous RNA for miR-760 to regulate NSCLC progression. In addition, rescue assay showed that downregulation of miR-760 could reverse the modulatory activity of SLC9A3-AS1 knockdown on NSCLC cells.	SLC9A3-AS1 possessed a favorable ability in diagnosing NSCLC. A high level of SLC9A3-AS1 was associated with poor prognosis in NSCLC patients. 	Yes	Functionally, SLC9A3-AS1 knockdown inhibited cell proliferation, migration, and invasion of NSCLC cells.	35300063
SLC8A1-AS1	LncRNA	Homo sapiens	Glioma	 glioma tissues	Expression [highly expressed]	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	 A validation experiment was conducted to confirm a high expression level of lncRNA SLC8A1-AS1 in glioma tissues.		Yes	 Down-regulation of lncRNA SLC8A1-AS1 suppressed the proliferation, colony formation, migration, and invasion of glioma cells in vitro and in vivo. Moreover, lncRNA SLC8A1-AS1 silencing decreased the activity of the Wnt/β-catenin pathway and suppressed the epithelial to mesenchymal transition (EMT) in glioma cells. 	34474120
SLC8A1-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	clinical PTC samples and PTC cell lines	Interaction(FUS/Numbl axis)	Western Blot//Wound Healing Assay//qPCR//CCK8//RIP//Cell Apoptosis Assay//Bioinformatics Analysis//Transwell Assay	We observed that the expression of SLC8A1-AS1 was downregulated in clinical PTC samples and PTC cell lines compared to that in normal controls. Mechanistically, SLC8A1-AS1 maintained NUMB like endocytic adaptor protein (Numbl) mRNA stability by interacting with FUS RNA Binding Protein (FUS) in PTC cells. Depletion of Numbl reversed the inhibitory effect of SLC8A1-AS1 overexpression on PTC. Thus, we concluded that SLC8A1-AS1 suppresses PTC progression via the FUS/Numbl axis. 		Yes	 Cell counting kit (CCK)-8 assays demonstrated that the overexpression of SLC8A1-AS1 significantly reduced the proliferation of PTC cells.  Consistently, apoptosis of PTC cells was enhanced by SLC8A1-AS1 overexpression. SLC8A1-AS1 overexpression attenuated the invasion and migration of PTC cells.	35599603
SLC7A11-AS1	LncRNA	Homo sapiens	Lung Neoplasms	Lung cancer tissues 	regulation[Inhibiting miR-4775, Facilitating TRAIP ]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The up-regulated SLC7A11-AS1 in lung cancer patients was associated with metastasis and advanced tumor stage (P < 0.05). SLC7A11-AS1 promoted lung cancer development by enhancing TRAIP expression via suppressing miR-4775.	The up-regulated SLC7A11-AS1 in lung cancer patients was associated with metastasis and advanced tumor stage (P < 0.05).	Yes	Silencing of SLC7A11-AS1 prominently inhibited H1299 and A549 cells proliferation, migration and invasion in vitro (P < 0.05).	32636648
SLC30A10	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues and cell lines	regulation[miR-21c/APC axis]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	SLC30A10 was down-regulated in colorectal cancer tissues and cell lines, and its low expression was positively correlated with colorectal cancer progression and metastasis.Bioinformatics prediction and luciferase assay indicated that miR-21c is a direct target of SLC30A10, which plays the role of ceRNA in regulating colorectal cancer metastasis. In addition, miR-21c specifically targets APC gene.	SLC30A10 was down-regulated in colorectal cancer tissues and cell lines, and its low expression was positively correlated with colorectal cancer progression and metastasis.	Yes	Functionally, SLC30A10 depletion promotes cell proliferation and migration in colorectal cancer cells, while SLC30A10 overexpression has the opposite effect.	32633358
SLC25A21-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cell line	regulation[miR-324-3p/IL-6 Axis]	CCK8//qRT-PCR	 In this study, we found that SLC25A21-AS1 expression was increased in NPC tissues and cell line, and knockdown of SLC25A21-AS1 inhibited cell growth and MDR in NPC cell.Our findings demonstrated the role of SLC25A21-AS1/miR-324-3p/IL-6 axis in cell growth and MDR in NPC, which might be a potential prognostic and diagnostic marker in NPC patients and provide new insight into the molecular mechanism of MDR in NPC chemotherapy.		Yes	 In this study, we found that SLC25A21-AS1 expression was increased in NPC tissues and cell line, and knockdown of SLC25A21-AS1 inhibited cell growth and MDR in NPC cell.	32547230
SLC2A1-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples	regulation[ STAT3/FOXM1/GLUT1 pathway]	ChIP//ISH//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In the current study, we report that lncRNA SLC2A1-AS1 is frequently downregulated in HCC samples, as shown by quantitative real-time polymerase chain reaction analysis. Results from fluorescence in situ hybridization, ChIP and luciferase reporter assays demonstrated that SLC2A1-AS1 exerts its regulatory role on GLUT1 by competitively binding to transketolase and signal transducer and activator of transcription 3 (STAT3) and inhibits the transactivation of Forkhead box M1 (FOXM1) via STAT3, thus resulting in inactivation of the FOXM1/GLUT1 axis in HCC cells.	 SLC2A1-AS1 deletion is significantly associated with recurrence-free survival in HCC.	Yes	 In vitro Cell Counting Kit-8, colony formation, transwell assays as well as in vivo tumorigenesis and metastasis assays showed that SLC2A1-AS1 overexpression significantly suppressed proliferation and metastasis in HCC through the transcriptional inhibition of GLUT1.	32174012
SLC26A4-AS1	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	regulation[NPTX1,NFKB1 ]	qRT-PCR	We determined that SLC26A4-AS1 was downregulated in human glioma tissues and cells. Taken together, we demonstrate that SLC26A4-AS1 promotes NPTX1 transcriptional activity by recruiting NFKB1 and thus exerting antiangiogenic effects on glioma cells.		Yes	Furthermore, overexpression of SLC26A4-AS1 or NPTX1 restrained the aggressiveness of glioma cells and their pro-angiogenic ability.	32255252
SLC26A4-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid cancer tissues 	interaction[DDX5]	RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//RIP//Transwell Assay//IF	We found that lncRNA SLC26A4-AS1 was continuously, significantly down-regulated in normal tissues, thyroid cancer, and lymph node metastasis specimens.  Intriguingly, SLC26A4-AS1 could simultaneously interact with DDX5 and the E3 ligase TRIM25, which promoting DDX5 degradation through the ubiquitin-proteasome pathway. 	We found that lncRNA SLC26A4-AS1 was continuously, significantly down-regulated in normal tissues, thyroid cancer, and lymph node metastasis specimens. Low SLC26A4-AS1 levels in tissues were significantly associated with poor prognosis of thyroid cancer patients.	Yes	LncRNA SLC26A4-AS1 markedly inhibited migration, invasion, and metastasis capability of cancer cells in vitro and in vivo.	32939012
SLC26A4	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(microRNA-15a)	Transfection//qPCR//RIP//PCR//IP	circSLC26A4 expression was upregulated in NSCLC tissues, and its high expression was significantly associated with poor survival of patients with NSCLC. The expression levels of circSLC26A4 were correlated with the expression levels of mature miR-15a, but not the expression levels of miR-15a precursor in NSCLC tissues. 		Yes	A cell proliferation assay revealed that overexpression of circSLC26A4 reduced the inhibitory effects of overexpression of miR-15a on cell proliferation.	34429762
SLC25A5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[miR-19a-3p/PTEN/PI3K/AKT signalling pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Microarray	The results showed that the expressions of SLC25A5-AS1 in GC were significantly lower than that of adjacent normal tissues. Dual-luciferase reporter assay confirmed the direct interaction between SLC25A5-AS1 and miR-19a-3p, rescue experiment showed that co-transfection miR-19a-3p mimics and pcDNA-SLC25A5-AS1 could partially restore the ability of GC cell proliferation and the inhibition of cell apoptosis. The mechanism analyses further found that SLC25A5-AS1 might act as a competing endogenous RNAs (ceRNA), which was involved in the derepression of PTEN expression, a target gene of miR-19a-3p, and regulate malignant phenotype via PI3K/AKT signalling pathway in GC. Taken together, this study indicated that SLC25A5-AS1 was down-regulated in GC and functioned as a suppressor in the progression of GC. Moreover, it could act as a ceRNA to regulate cellular behaviours via miR-19a-3p/PTEN/PI3K/AKT signalling pathway. Thus, SLC25A5-AS1 might be served as a potential target for cancer therapeutics in GC.	The results showed that the expressions of SLC25A5-AS1 in GC were significantly lower than that of adjacent normal tissues, which were significantly associated with tumour size, TNM stage and lymph node metastasis. 	Yes	Moreover, SLC25A5-AS1 could inhibit GC cell proliferation, induce G1/G1 cell cycle arrest and cell apoptosis in vitro, as well as GC growth in vivo.	30793479
SLC25A25-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	regulation[EMT pathway]	qRT-PCR	 Here, we identified one lncRNA HRCEG, whose expression was decreased in the gastric cancer tissues compared with adjacent normal tissues.These findings suggest that HRCEG might be regulated by HDAC1 to inhibit gastric cancer progress and metastatic capability via EMT pathway.		Yes	Overexpression of HRCEG significantly promoted cell apoptosis and inhibited cell proliferation.	31964588
SLC25A25-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines.	Interaction(microRNA-195-5p/ITGA2 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	As compared with normal lung tissues, increased expression of SLC25A25-AS1 was demonstrated in NSCLC tissues using The Cancer Genome Atlas database.. In addition, SLC25A25-AS1 was overexpressed in both NSCLC tissues and cell lines.Mechanistically, SLC25A25-AS1 was demonstrated to be an miR-195-5p sponge in NSCLC cells. miR-195-5p mimics decreased ITGA2 expression in NSCLC cells by directly targeting ITGA2, and SLC25A25-AS1 interference decreased ITGA2 expression by sequestering miR-195-5p. 	High SLC25A25-AS1 expression was markedly associated with shorter overall survival time of patients with NSCLC.	Yes	SLC25A25-AS1 silencing impeded NSCLC cell proliferation and triggered apoptosis, while restricting cell migration and invasion. Tumour growth in vivo was also impaired by SLC25A25-AS1 silencing. 	34055094
SFTA1P	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	regulation[PI3K-AKT signaling pathway ]	qRT-PCR	We found that the expression of SFTA1P was significantly downregulated in NSCLC tissues with high diagnostic value (AUC = 0.87), which was consistent with the results of TCGA and microarray data.Taken together, this work supported that SFTA1P may play a suppressing role in the tumorigenesis of NSCLC by modulating PI3K-AKT signaling pathway to influence cell cycle, which provides a potential and prospective biomarker for NSCLC.		Yes	Furthermore, the cell function results suggested that the overexpression of SFTA1P triggered cell cycle arrest in the S-phase (P < 0.05).	32825934
SLCO4A1-AS1	LncRNA	Homo sapiens	Melanoma	melanoma cell 	Interaction(miR-1306-5p/PCGF2)	qRT-PCR//Transfection	Our study suggested that SLCO4A1-AS1 promoted the melanoma cell malignant behaviours via targeting miR-1306-5p/PCGF2, which might facilitate the discovery of novel biomarkers for melanoma treatment.		Yes	Additionally, proliferation, migration and invasion of melanoma cells were weakened but apoptosis was facilitated due to SLCO4A1-AS1 down-regulation. 	35427425
hsa_circ_0132817	CircRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	Regulation(miR-432-5p/NOL4L axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	In this paper, the levels of circ_0132817 and NOL4L were induced in NB tissues and cells, and miR-432-5p expression was on the contrary. MiR-432-5p was verified as a target of circ_0132817 and miR-432-5p could bind to NOL4L. The inhibitory effects of miR-432-5p overexpression on cell proliferation, migration, invasion and glycolysis could be reversed by circ_0132817 facilitation. The suppression of NOL4L knockdown on NB cells progression could be rescued by miR-432-5p inhibition. Besides, knockdown of circ_0132817 repressed tumor growth in vivo. Thus, we came to a conclusion that circ_0132817 promoted the tumorigenesis of NB cells by up-regulating NOL4L and acting as a sponge for miR-432-5p.		Yes	The inhibitory effects of miR-432-5p overexpression on cell proliferation, migration, invasion and glycolysis could be reversed by circ_0132817 facilitation. The suppression of NOL4L knockdown on NB cells progression could be rescued by miR-432-5p inhibition. Besides, knockdown of circ_0132817 repressed tumor growth in vivo. 	33837793
circHIPK3	CircRNA	Homo sapiens	Diabetic Cardiomyopathies	AC16 cells	Regulation(PTEN )	Western Blot//Transfection//qRT-PCR//Cell Apoptosis Assay//ELISA	The result showed that CircHIPK3 was downregulated in diabetes and further downregulated in DC. Across DC samples, the expression of circHIPK3 was inversely correlated with PTEN. In AC16 cells, overexpression of circHIPK3 decreased the expression levels of PTEN. 		Yes	 CircHIPK3 may suppress AC16 cell apoptosis induced by high glucose and inhibited the role of PTEN in cell apoptosis. Therefore, circHIPK3 may downregulate PTEN to protect cardiomyocytes from high glucose-induced cell apoptosis.	35200097
circTRPS1	CircRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues or cell lines	regulation[miR-124-3p/EZH2 axis-mediated stemness]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//IHC//Transwell Assay	The result showed that circ-TRPS1 was upregulated significantly in high-grade PCa tissues or cell lines. In summary, data demonstrated that circ-TRPS1 suppressed PCa progression through functioning similar to a miR-124-3p sponge to enhance EZH2 expression and cancer stem-like cell differentiation.		Yes	Knockdown of circ-TRPS1 suppressed PCa proliferation and metastasis through targeting miR-124-3p/EZH2 axis-mediated stemness in PCa, which was validated by luciferase reporter assays.	33415005
SDPR-AS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[p38 MAPK/ERK signals]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	SDPR-AS was lowly expressed in NSCLC tissues and cells, but had no changes in SCLC tissues and cells.  Our findings indicate that SDPR-AS was lowly expressed in NSCLC cells and down-regulation of SDPR-AS may promote the malignant behaviors of NSCLC cells possible through regulating SDPR expression and involving in p38 MAPK/ERK signaling pathway. SDPR-AS may serve as a prospective target for NSCLC diagnosis and therapy.		Yes	Down-regulation of SDPR-AS enhanced the proliferation, migration and invasion and inhibited apoptosis of NSCLC cells (H522, H661 and H520). Overexpression of SDPR-AS exhibited opposite effects. 	31352804
hsa_circ_0135889	CircRNA	Homo sapiens	Neuroblastoma	NB cells	Interaction(miR-127-5p/NEUROD1)	In Vivo Experiment//RNA Pull-Down//Western Blot//qPCR//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//IHC//Transwell Assay	" Circ_0135889 and neuronal differentiation 1 (NEUROD1) were upregulated whilst microRNA (miR)-127-5p, was downregulated in NB tumors and immortalized NB cells. Circ_0135889 was a sponge for miR-127-5p, and inhibition of miR-127-5p counteracted the inhibitory impact of circ_0135889 knockdown on the malignant behaviors of NB cells. Moreover, NEUROD1 was a direct target of miR-127-5p, and miR-127-5p exerted the anti-tumor role in NB cells by targeting NEUROD1. Furthermore, circ_0135889 regulated NEUROD1expression by sponging miR-127-5p.
"		Yes	 Silencing of circ_0135889 could suppress cell proliferation, migration and invasion, but enhance apoptosis rate of NB cells in vitro. More importantly, circ_0135889 depletion inhibited xenograft tumor growth of NB cells.	35772185
hsa_circ_0125803	CircRNA	Homo sapiens	Neuroblastoma	neuroblastoma samples	Interaction(miR-197-5p-E2F1 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	We identified hsa_circ_0125803 (circ0125803) as an extremely upregulated circRNA in neuroblastoma samples.  Our data demonstrated upregulation of circ0125803 promotes the neuroblastoma progression by blocking miR-197-5p and upregulating E2F1 expression.		Yes	 Knockdown of circ0125803 significantly decreased the growth rate and invasion rate in neuroblastoma.	35358781
SDCBP-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	Interaction(hnRNP K to destabilize β-catenin)	RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//RIP//RNA-seq//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//IF	SDCBP2-AS1 was significantly downregulated in GC tissues and predictive of poor patient prognosis.  Mechanically, SDCBP2-AS1 physically bound to hnRNP K to repress SUMOylation of hnRNP K and facilitated ubiquitination of hnRNP K and β-catenin, thereby promoting the degradation of β-catenin in the cytoplasm. 	SDCBP2-AS1 was significantly downregulated in GC tissues and predictive of poor patient prognosis. 	Yes	 Silencing of SDCBP2-AS1 promoted the proliferation and migration of GC cells both in vitro and in vivo. 	36209503
SDCBP2-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues and OC cell lines (COC1, A2780, and SKOV3) 	Interaction(miR-100-5p)	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	 LncRNA SDCBP2-AS1 and EPDR1 levels were suppressed whilst miR-100-5p level was elevated in OC. 		Yes	After upregulating lncRNA SDCBP2-AS1 or EPDR1, viability, migration, and invasion of OC cells were impaired, and apoptosis rate was increased. Downregulating EPDR1 or upregulating miR-100-5p partially mitigated upregulated lncRNA SDCBP2-AS1-induced impacts on the biological functions of OC cells. 	34218800
circKIF2A	CircRNA	Homo sapiens	Neuroblastoma	 21 neuroblastoma tissues and cells	Interaction( miR-377-3p/PRPS1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Invasion Assay//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//EdU Staining	The expression levels of CircKIF2A and PRPS1 were increased and that of miR-377-3p were decreased in 21 neuroblastoma tissues and cells.Mechanically, circKIF2A could work as a sponge of miR-377-3p to enhance PRPS1 expression. CircKIF2A knockdown impedes cell proliferation, metastasis, and glycolysis partly by regulating the miR-377-3p/PRPS1 axis, suggesting that targeting circKIF2A can be a feasible therapeutic strategy for neuroblastoma.		Yes	Functionally, the silencing of circKIF2A inhibited cell proliferation, migration, invasion, and glycolysis, boosted apoptosis in neuroblastoma cells in vitro, and blocked the growth of subcutaneously transplanted tumors in nude mice. 	35039981
circACAP2	CircRNA	Homo sapiens	Neuroblastoma	neuroblastoma tissues and cell lines	Interaction(neuroblastoma cells)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	The abundances of ACAP2 and HK2 were remarkedly increased in neuroblastoma tissues and cell lines.		Yes	silencing ACAP2 significantly constrained neuroblastoma cell migration, invasion, and glycolysis, and promoted apoptosis. Bioinformatics prediction, luciferase assay, and RNA pull-down assay consistently demonstrated that ACAP2 sponged miR-143-3p to downregulate its expression in neuroblastoma cells.	35070838
SEMA3B	LncRNA	Homo sapiens	Glioblastoma	glioblastoma cells	Interaction(miR-195/cyclin D1)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//BrdU	 We observed downregulation of SEMA3B-AS1 in GBM. The expression of SEMA3B-AS1 was inversely correlated with the expression of cyclin D1 but positively correlated with the expression of miR-195.  In GBM cells, overexpression of SEMA3B-AS1 and miR-195 caused reduced expression levels of cyclin D1. MiR-195 inhibitor reduced the effects of overexpression of SEMA3B-AS1 on the expression of cyclin D1. Moreover, overexpression of SEMA3B-AS1 increased the expression levels of miR-195. 		Yes	 Cell proliferation data showed that, SEMA3B-AS1 and miR-195 decreased cell proliferation, while overexpression of cyclin D1 increased GBM cell proliferation. In addition, miR-195 inhibitor inhibited the role of overexpression of SEMA3B-AS1 in cancer cell proliferation. 	35287551
hsa_circ_0013401	CircRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	Interaction( miR-195/PAK2)	In Vivo Experiment//Transfection//Colony Formation Assay//CCK8//FISH//qRT-PCR//Flow Cytometry//IHC//Transwell Assay	hsa_circ_0013401 was highly expressed, miR-195 was lowly expressed, and there was a negative correlation between hsa_circ_0013401 and miR-195 in NB. Luciferase reporter assays showed that miR-195 was a direct target of hsa_circ_0013401, and PAK2 was the downstream target gene of miR-195.		Yes	The inhibitory effects of hsa_circ_0013401 knockdown suppressed the proliferation, migration, and invasion and induced the apoptosis and autophagy of NB cells by targeting miR-195 to downregulate PAK2 expression. In vivo studies showed that hsa_circ_0013401 promotes tumor formation.	34853631
circPDE5A	CircRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	Interaction(miR-362-5p/NOL4L axis)	In Vivo Experiment//Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Invasion Assay//Transwell Assay	Our results revealed that circPDE5A was up-regulated in NB tissues and cells. Moreover, circPDE5A directly targeted miR-362-5p by binding to miR-362-5p. CircPDE5A silencing impeded NB malignant progression in vitro through up-regulating miR-362-5p. Furthermore, NOL4L was a direct target of miR-362-5p, and NOL4L mediated the regulation of miR-362-5p on NB malignant progression in vitro. Additionally, circPDE5A functioned as a regulator of NOL4L expression via targeting miR-362-5p.		Yes	The silencing of circPDE5A suppressed NB cell proliferation, migration, invasion, and glycolysis in vitro and diminished tumour growth in vivo. 	33635749
SCIRT	LncRNA	Homo sapiens	Lung Neoplasms	cancer cell exosomes	Interaction(miR-665)	qRT-PCR	We further demonstrated that lncRNA SCIRT was also increased in cancer cell exosomes and may facilitate the exosomal loading of miR-665 with the help of hnRNPA1.		Yes	 In addition, we found that miR-665 and SCIRT were significantly upregulated in tumor tissue and plasma of patients with lung cancer, and both of them showed increased expression in metastatic disease samples. 	34349799
SCIRT	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues	Interaction(miR-221/lncRNA GAS5)	qRT-PCR//RNA Pull-Down	SCIRT and GAS5 were downregulated, while miR-221 was overexpressed in OSCC. CIRT was detected in both nucleus and cytoplasm and directly interacted with miR-221, while SCIRT overexpression failed to affect miR-221 expression. In addition, GAS5 expression was increased by SCIRT and decreased by miR-221. 		Yes	 Moreover, SCIRT suppressed the role of miR-221 in suppressing GAS5 expression and OSCC cell apoptosis.	34547134
SCIRT	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Expression(highly expressed)	Western Blot//Transfection//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay//Transwell Assay	 LncRNA SCIRT was highly expressed in CC tissues and cells, and significantly linked with clinical/pathology-based characteristics of patients, including Federation Internationale of Gynecologie and Obstetrigue (FIGO) stage, tumor dimensions, and lymph-node metastasis. Western blotting analysis demonstrated that SCIRT knockdown upregulated e-cadherin and downregulated n-cadherin, vimentin, MMP-9, and MMP-2. Meanwhile, overexpressing SCIRT of lncRNA SCIRT had the opposite effect. 	 LncRNA SCIRT was highly expressed in CC tissues and cells, and significantly linked with clinical/pathology-based characteristics of patients, including Federation Internationale of Gynecologie and Obstetrigue (FIGO) stage, tumor dimensions, and lymph-node metastasis. 	Yes	 SCIRT knockdown markedly reduced CC proliferative, colony forming, and invasive properties, while overexpressing SCIRT promoted the proliferative and invasive properties of CC.Western blotting analysis demonstrated that SCIRT knockdown upregulated e-cadherin and downregulated n-cadherin, vimentin, MMP-9, and MMP-2. Meanwhile, overexpressing SCIRT of lncRNA SCIRT had the opposite effect.  Tumorigenic experiment showed that SCIRT knockdown could markedly reduce CC proliferative property the nude mouse.	35979035
SCIRT	LncRNA	Homo sapiens	Atherosclerosis	HAOSMCs	Regulation(miR-146a)	BrdU//qRT-PCR//Transfection//RNA Pull-Down	SCIRT was downregulated by atherosclerosis, while miR-146a was upregulated by atherosclerosis. SCIRT was detected in both cytoplasm and nuclear samples, and it directly interacted with miR-146a. In HAOSMCs, overexpression of SCIRT and miR-146a did not affect the expression of each other. Interestingly, SCIRT suppressed the proliferation of HAOSMCs and reduced the enhancing effects of miR-146a on cell proliferation.		Yes	In HAOSMCs, overexpression of SCIRT and miR-146a did not affect the expression of each other. 	34742341
SCHLAP1	LncRNA	Homo sapiens	Glioblastoma	glioma tissue	Regulation[NF-κB signaling]	RNA Pull-Down//ISH//Co-IP//Colony Formation Assay//qRT-PCR//RIP//Luciferase Report Assay//IHC	SChLAP1 was increased in primary GBM samples and cell lines. SChLAP1 was found to bind heterogeneous nuclear ribonucleoprotein L (HNRNPL), which stabilized the lncRNA and led to an enhanced interaction with the protein actinin alpha 4 (ACTN4). ACTN4 was also highly expressed in primary GBM samples and was associated with poorer overall survival in glioma patients. The SChLAP1-HNRNPL complex led to stabilization of ACTN4 through suppression of proteasomal degradation, which resulted in increased nuclear localization of the p65 subunit of NF-κB and activation of NF-κB signaling, a pathway associated with cancer development.		Yes	SChLAP1 was increased in primary GBM samples and cell lines, and knockdown of the lncRNA suppressed growth.	31492748
SCHLAP1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	 50 paired TNBC tissues and matched adjacent normal tissues	Interaction(miR‑524‑5p/HMGA2 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay//Bioinformatics Analysis	The present study determined that SChLAP1 was upregulated in TNBC tissues and was associated with the long‑distant lymph node metastasis of patients with TNBC.  Bioinformatics analysis suggested that SChLAP1 acted as a sponge of microRNA (miR)‑524‑5p and negatively modulated the expression of miR‑524‑5p.  An inverse correlation was also identified between the expression levels of SChLAP1 and miR‑524‑5p in TNBC tissues. 	The present study determined that SChLAP1 was upregulated in TNBC tissues and was associated with the long‑distant lymph node metastasis of patients with TNBC.	Yes	Knockdown of SChLAP1 significantly inhibited cell viability and colony formation, and triggered apoptosis of TNBC cells. 	33846810
SEMA3B	LncRNA	Homo sapiens	gastric cardia adenocarcinoma	GCA tissues,cell lines	Interaction[ZNF143 ]	qRT-PCR//RNA Pull-Down//IHC//Western Blot	Frequent downregulation of SEMA3B, SEMA3B-AS1, and miR-6872 was detected in GCA tissues and gastric cancer cells. ZNF143 might be the target gene of miR-6872-5p and miR-6872-5p functioning synergistically with SEMA3B to suppress cell invasion. 		Yes	Overexpression of SEMA3B and SEMA3B-AS1 inhibited gastric cancer cell proliferation, migration, and invasion in vitro. 	30656427
SEMA3B-AS1	LncRNA	Homo sapiens	gastric cardia adenocarcinoma	GCA tissues,cell lines	Interaction[MLL4]	qRT-PCR	Frequent downregulation of SEMA3B, SEMA3B-AS1, and miR-6872 was detected in GCA tissues and gastric cancer cells. SEMA3B-AS1 induced the expression of SEMA3B by interacting with MLL4. 		Yes	Overexpression of SEMA3B and SEMA3B-AS1 inhibited gastric cancer cell proliferation, migration, and invasion in vitro. 	30656427
SFTA1P	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 cell lines	Interaction( Hippo-YAP/TAZ signaling)	qRT-PCR//RNA Pull-Down//Western Blot	Using non-small cell lung cancer (NSCLC) cell lines, we show that SFTA1P is transcriptionally activated by YAP/TAZ in a TEAD-dependent manner. Mechanistically, SFTA1P knockdown decreased TAZ protein abundance and consequently, the expression of YAP/TAZ transcriptional targets. 		Yes	Functionally, knockdown of SFTA1P in NSCLC cell lines inhibited proliferation, induced programmed cell death, and compromised their tumorigenic potential.	34845189
circRANBP9	CircRNA	Homo sapiens	Polycystic Ovary Syndrome	plasma of patients with PCOS 	Interaction(microRNA-136-5p/ XIAP axis)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	First, the circ_RANBP9 level was found to be increased in the plasma of patients with PCOS and ovarian granulosa cells (GCs) using Reverse Transcription-Quantitative Polymerase Chain Reaction (RT-qPCR). Furthermore, bioinformatics analysis showed that circ_RANBP9 and XIAP can be targeted by the microRNA, miR-136-5p. 		Yes	 In GCs, loss of circ_RANBP9 decelerated proliferation and accelerated apoptosis of KGN and COV434 cells, as determined by MTT assay, colony formation assay, and flow cytometry. 	34546853
SFTA1P	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[miR-4766-5p via PI3K/AKT/mTOR Signaling Pathway]	qRT-PCR//Luciferase Report Assay//Western Blot	SFTA1P was up-regulated in HCC tissues and cell lines. lncRNA SFTA1P could promote tumor development in HCC by down-regulating miR-4766-5p expression via PI3K/AKT/mTOR signaling pathway. It may be a potential therapeutic target for HCC.	SFTA1P expression was closely related to tumor size, vascular invasion and TNM stage.	Yes	Knockdown of SFTA1P inhibited HCC cell viability, migration and invasion and promoted cell apoptosis. 	33061455
SFTA1P	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	tumor tissues and cells	Interaction( SFTA1P-PTBP1-TPM4 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Migration Assay//qRT-PCR//Survival Analysis//RIP//RNA-seq//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	SFTA1P is upregulated in cervical tumor tissues and its high expression is associated with poor prognosis. Mechanistically, SFTA1P was shown to interact with polypyrimidine tract binding protein 1 (PTBP1) to regulate the stability of tropomyosin 4 (TPM4) mRNA, thereby resulting in malignant cell phenotypes. TPM4 knockdown could attenuate the suppression of cell progression induced by either SFTA1P or PTBP1 knockdown. 	SFTA1P is upregulated in cervical tumor tissues and its high expression is associated with poor prognosis.	Yes	Biologically, knockdown of SFTA1P inhibited the proliferation, migration, and invasion of cervical cancer cells in vitro, as well as tumorigenesis and metastasis in vivo. 	36344495
SFTA1P	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cell and tissues	Interaction(miR-4766-5p/LATS1/YAP pathway)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR	"SFTA1P was lowly expressed in LUAD, which was associated with the poor prognosis of patients with LUAD. MiR-4766-5p acted as an intermediate ""bridge"" for SFTA1P to regulate LATS1. "	SFTA1P was lowly expressed in LUAD, which was associated with the poor prognosis of patients with LUAD. 	Yes	Up-regulated SFTA1P prevented the metastasis of LUAD cells and the nuclear translocation of YAP. Hypoxia-induced exosomes stimulated LUAD cell metastasis, but inhibited the SFTA1P and LATS1/YAP axes. SFTA1P repressed xenograft growth and LUAD cell metastasis. 	36283586
hsa_circ_0043532	CircRNA	Homo sapiens	Polycystic Ovary Syndrome	GCs and KGN cells	Interaction(miR-182/SGK3 axis )	Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//EdU Staining	irc_0043532 was markedly elevated in PCOS granulosa cells (GCs) and KGN cells. Silencing of circ_0043532 suppressed cell proliferation and cell cycle process and promoted cell apoptosis in PCOS GCs and KGN cells. For mechanistic analysis, circ_0043532 was identified as a sponge of miR-182 and SGK3 was confirmed to be a target gene of miR-182. Inhibition of miR-182 rescued the impacts of circ_0043532 interference on PCOS GCs and KGN cell progression. Moreover, miR-182 overexpression suppressed cell proliferation and cell cycle process and promoted cell apoptosis in PCOS GCs and KGN cells by targeting SGK3.		Yes	For mechanistic analysis, circ_0043532 was identified as a sponge of miR-182 and SGK3 was confirmed to be a target gene of miR-182. Inhibition of miR-182 rescued the impacts of circ_0043532 interference on PCOS GCs and KGN cell progression.	34740363
SERPINE2	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[sponging miR-375 and modulating YWHAZ]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//EdU Staining	Circ-SERPINE2 and YWHAZ were upregulated, and miR-375 was downregulated in GC tissues and cells. Circ-SERPINE2 and YWHAZ targetedly bound to miR-375. Circ-SERPINE2 promoted cell proliferation and cell cycle progress and inhibited cell apoptosis by sponging miR-375 and regulating YWHAZ expression in vitro. 		Yes	Circ-SERPINE2 repressed solid tumour growth through enhancing miR-375 expression and reducing YWHAZ expression in vivo.	31199037
SERPINE2	CircRNA	Homo sapiens	Glioblastoma	glioblastoma cell lines and tissues	Interaction(miR-361-3p/miR-324-5p/ BCL2)	colony Formation Assay//RNA Pull-Down//Western Blot//Transfection//qPCR//RIP//Cell Apoptosis Assay//PCR//IP//Colony Formation Assay//IF	In our study, we identified a novel upregulated circRNA, circSERPINE2, through analyzing circRNAs microarray data of glioblastoma from GEO datasets (GSE146463).Mechanistically, circSERPINE2 could directly sponge miR-324-5p and miR-361-3p. BCL2, known as a novel anti-apoptosis gene, is a target gene both of miR-324-5p and miR-361-3p. 		Yes	Silencing circSERPINE2 inhibits glioblastoma proliferation in vivo and in vitro through cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry analysis, and western blot analysis and xenograft tumor model. 	34553034
SERPINB9P1	LncRNA	Homo sapiens	Ischemic Stroke	 patients with IS 	Mutation(rs375556 )	qRT-PCR//Genotyping	We found that the SERPINB9P1 expression was significantly downregulated in patients with IS compared with that in healthy controls. After stratification by gender, the rs375556 polymorphism was significantly associated with susceptibility to female IS in the recessive model, and the significant association remained after adjusting for age. 		Yes	After adjusting for gender and age, rs318429 was significantly associated with FPG and D-D levels, and rs375556 was significantly associated with INR and PTA levels in IS cases. Besides, the lncRNA SERPINB9P1 expressed downregulated in OGD/reoxygenation-treated human A172 cells. In conclusion, the lncRNA SERPINB9P1 may protect against cerebral ischemia-reperfusion injury and neurological impairment after IS. 	34273050
circFURIN	CircRNA	Homo sapiens	Polycystic Ovary Syndrome	GCs	Interaction(miR-195-5p/BCL2 axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Colony Formation Assay	Circ-FURIN was upregulated in PCOS patients and granular cells (GCs). Knockdown of circ-FURIN inhibited cell proliferation and promoted apoptosis of KGN cells, along with the increased expression of caspase-3 and Bax and the decreased levels of p-PI3K. Gene ontology (GO) analysis indicated circ-FURIN is associated with apoptotic signaling pathway and cell death. Subsequently, BCL2 expression was elevated in patients with PCOS and positively regulated by circ-FURIN. Furthermore, circ-FURIN was served as a sponge of miR-195-5p to directly target to BCL2. The levels of miR-195-5p were reduced in PCOS and KGN cells. Knockdown of circ-FURIN decreased the expression of BCL2, which was abolished by miR-195-5p inhibitor. At last, rescue experiments revealed that overexpression of BCL2 reversed the effects of circ-FURIN knockdown on cell proliferation and apoptosis of KGN cells.		Yes	Knockdown of circ-FURIN inhibited cell proliferation and promoted apoptosis of KGN cells, along with the increased expression of caspase-3 and Bax and the decreased levels of p-PI3K.	34784951
circRHBG	CircRNA	Homo sapiens	Polycystic Ovary Syndrome	granular cells of PCOS patients	Interaction(miR-515/SLC7A11 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//EdU Staining	CircRNA high-throughput chips and qRT-PCR verified that circRHBG was significantly upregulated in granular cells of PCOS patients. Luciferase reporter assays and Ago2-RIP detection showed that circRHBG competes with SLC7A11 to bind to miR-515-5p. 		Yes	 Knockdown of circRHBG inhibits KGN and SVOG cell proliferation.	34532485
SEMA3B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[PTEN ]	qRT-PCR//Western Blot	 We found that SEMA3B-AS1 was downregulated in HCC tissues compared with noncancer tissues and was not affected by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections.Therefore, miR-718 may mediate the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.		Yes	 SEMA3B-AS1 and PTEN overexpression resulted in a reduced proliferation rate of HCC cells	31251699
circPSMC3	CircRNA	Homo sapiens	Polycystic Ovary Syndrome	PCOS tissues	regulation[ circPSMC3/miR-296-3p/PTEN axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//H&E Staining//EdU Staining	 In this study, we determined the abnormal reduction in circPSMC3 expression by comparing the ovarian tissue samples of PCOS patients and normal individuals. Collectively, we preliminarily characterized the role and possible insights of circPSMC3/miR-296-3p/PTEN axis in the proliferation and apoptosis of KGN cells.		Yes	 In vitro functional experiments confirmed that circPSMC3 can inhibit cell proliferation and promote apoptosis by blocking the cell cycle in human-like granular tumour cell lines.	32808450
SENCR	LncRNA	Homo sapiens	Aortic Aneurysm, Abdominal	VSMCs & aortic tissues	Expression(lower expressed)	In Vivo Experiment//qRT-PCR//Transfection//Western Blot	SENCR was decreased in AAA. Overexpression of SENCR inhibited AAA formation via inhibition of VSMC apoptosis and extracellular matrix degradation.		Yes	Overexpression of SENCR inhibited AAA formation via inhibition of VSMC apoptosis and extracellular matrix degradation. 	32903173
SENCR	LncRNA	Homo sapiens	Coronary Disease	blood 	Expression[lower expressed]	qRT-PCR	The results showed that SENCR was downregulated in the peripheral blood of CHD, and negatively related to the Gensini score. 		Yes	Overexpression of SENCR significantly inhibited HA-VSMCs proliferation, migration, and block cell cycle, while the knockdown of SENCR had the opposite effects.	32401347
circCTNNA1	CircRNA	Homo sapiens	Lymphoma, Mantle-Cell	MCL patientsand cells	Interaction(miR-34a)	RNA Pull-Down//Transfection//qPCR//Cell Proliferation Assay//BrdU	The results showed that circCTNNA1 was upregulated in MCL and high expression levels of circCTNNA1 predicted the poor survival of MCL patients. MiR-34a was downregulated in MCL and inversely correlated with circCTNNA1. CircCTNNA1 was predicted to interact with miR-34a, and the interaction between them was confirmed by RNA pull-down assay. Interestingly, overexpression of circCTNNA1 and miR-34a did not affect the expression of each other. 	The results showed that circCTNNA1 was upregulated in MCL and high expression levels of circCTNNA1 predicted the poor survival of MCL patients	Yes	 Cell proliferation analysis showed that overexpression of circCTNNA1 reversed the inhibitory effects of overexpression of miR-34a on cell proliferation.	35865405
circCDYL	CircRNA	Homo sapiens	Lymphoma, Mantle-Cell	blood	Expression[highly expressed]	qRT-PCR	CircCDYL was high expressed in the plasma of MCL patients.		Yes	Functionally, circCDYL knockdown inhibited MCL cell proliferation. 	31819653
SEMA3B-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 PM tissues and cell line	Interaction(SEMA3B-AS1/HMGB1/FBXW7 Axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	The mRNA expression level of SEMA3B-AS1 was downregulated in GC and PM tissues compared to normal stomach tissues; however, BGN was highly expressed at the mRNA level.Mechanistically, SEMA3B-AS1 could combine with HMGB1 to regulate the transcription of FBXW7, thus facilitating the ubiquitination of BGN. In conclusion, our study demonstrated that the SEMA3B-AS1/HMGB1/FBXW7 axis plays an inhibitory role in the PM of GC by regulating BGN protein ubiquitination. It also provides a new biological marker for the diagnosis and treatment of the PM of GC.	SEMA3B-AS1 was closely related to PM and the overall survival (OS) of GC patients.	Yes	Functionally, the overexpression of SEMA3B-AS1 was related to GC progression, PM, and prognosis. 	35273678
SEMA3B-AS1	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues and cells	Interaction(SMAD3/lncRNA SEAS1/miR-3940-3p/KLLN axis)	ChIP//Western Blot//CCK8//qRT-PCR//FISH//Flow Cytometry//RIP//RNA-seq//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 SEAS1 was downregulated in the triple-negative breast cancer (TNBC) tissues compared with the para-carcinoma tissues, which was associated with poor prognosis of TNBC patients. Bioinformatics analysis demonstrated that microRNA (miR)-3940-3p was a potential target of SEAS1. Mechanistically, RNA immunoprecipitation (RIP) and luciferase reporter assays confirmed that lncRNA SEMA3B-AS1 acted as sponge for miR-3940-3p, preventing the degradation of its target gene KLLN, which acts as a tumor-inhibiter in TNBC. Moreover, RNA pulldown, mass spectrometry, ChIP, and luciferase reporter assays confirmed that SMAD3 directly interacted with the promoter of SEAS1 and suppressed its transcription, thereby promoting TNBC progression. 	 SEAS1 was downregulated in the triple-negative breast cancer (TNBC) tissues compared with the para-carcinoma tissues, which was associated with poor prognosis of TNBC patients. The clinical samples of TNBC confirmed SEAS1 was correlated inversely with lymphatic and distant metastasis.	Yes	 We demonstrated that SEAS1 knockdown significantly increased the proliferation, migration, and invasion of TNBC cell lines, whereas SEAS1 overexpression reversed these effects. 	36123344
SEMA3B-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues ,cell lines	Expression[lower expressed]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	Frequent downregulation of SEMA3B and SEMA3B-AS1 was detected in esophageal cancer cells and ESCC tissues, SEMA3B and SEMA3B-AS1 shared the same CpG island in the promoter region and the expression of both genes might be regulated by the promoter methylation status. Furthermore, transcription factor Sp1 activated SEMA3B or SEMA3B-AS1 transcription and the promoter hypermethylation of SEMA3B and SEMA3B-AS1 influenced Sp1 binding ability. Moreover, over-expression of SEMA3B and SEMA3B-AS1 suppressed the viability and invasion of esophageal cancer cells in vitro. SEMA3B-AS1 influenced the protein expression of SEMA3B. SEMA3B or SEMA3B-AS1 expression and promoter methylation status were correlated with ESCC patients' survival. 	the expression level of SEMA3B and SEMA3B-AS1 in ESCC tissues was correlated with TNM stage and lymph node metastasis. 	Yes	Moreover, over-expression of SEMA3B and SEMA3B-AS1 suppressed the viability and invasion of esophageal cancer cells in vitro.	30915595
SLCO4A1-AS1	LncRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	 ALL tissues and cell lines	Interaction(miR-876-3p/RBBP6 axis)	RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining	SLCO4A1-AS1 was upregulated in ALL tissues and cell lines. Our result confirmed that SLCO4A1-AS1 acted as a ceRNA by sponging microRNA 876-3p (miR-876-3p) to upregulate retinoblastoma binding protein 6 (RBBP6) expression in ALL cells. Moreover, SLCO4A1-AS1 activated the JNK signaling pathway by upregulating RBBP6. 		Yes	We found that suppression of SLCO4A1-AS1 suppressed ALL cell proliferation and facilitated cell apoptosis. 	33683013
SLCO4A1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-223-3p/IKKα/NF-κB signaling]	qRT-PCR	qRT-PCR revealed that SLCO4A1-AS1 level was upregulated in NSCLC. In conclusion, SLCO4A1-AS1 drove NSCLC progression by activating NF-κB signaling pathway via sponging miR-223-3p to enhance IKKα expression. 		Yes	Function assays manifested that silence of SLCO4A1-AS1 attenuated NSCLC cell proliferation, migration and invasion but promoted NSCLC cell apoptosis. 	32687454
circTBC1D4	CircRNA	Homo sapiens	Neuroblastoma	Five paired neuroblastoma tumor and adjacent normal fetal adrenal medulla samples	Expression(lower expressed)	qRT-PCR//circRNA-seq//migration assay//Cell Proliferation Assay//Colony Formation Assay//Bioinformatics Analysis	A total of 4704 differentially expressed circRNAs were found, including 2462 up-regulated and 2242 down-regulated circRNAs. According to our previous studies, the predicted target circRNAs of miR-21 involved in tumorigenic signaling pathways were selected, including circRNA-TBC1D4, circRNA-NAALAD2 and circRNA-TGFBR3. These circRNAs were associated with clinical features, and the circRNA expression was significantly lower (P < 0.05) in the NB tissues than in normal adrenal tissues. 		Yes	Overexpression of circRNA-TBC1D4 promotes NB cell migration, but not proliferation and colony-formation in vitro.Besides that, xenograft analysis showed that circLDLR knockdown suppressed tumor growth in vivo via regulating LMO4 and miR-637.	34093041
Snhg1	LncRNA	Mus musculus	Epilepsy	 EP tissues,cell line	regulation[miR-181a/BCL-2 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	 SNHG1 expression was down-regulated in EP tissues and kainic acid (KA)-induced CTX-TNA2 cells. SNHG1 alleviated the progression of EP by modulating the miR-181a/BCL-2 axis in vitro, thus SNHG1 could act as a possible therapeutic target for treating EP.		Yes	Both the up-regulation of miR-181a and down-regulation of BCL-2 reversed the inhibiting effects of SNHG1 on apoptosis and inflammatory response of KA-induced CTX-TNA2 cells, and the promoting effect upon cell viability.	33359246
SNHG1	LncRNA	Homo sapiens	oral cavity cancer		regulation[miR-421/HMGB2 axis]	qRT-PCR	In this research, we found that lncRNA SNHG1 was up-regulated in oral cancer. Then we revealed a new mechanism that lncRNA SNHG1 regulated the growth of oral cancer via controlling the miR-421/HMGB2 axis, which provided new therapy for patients with oral cancer.		Yes	 Knockdown of lncRNA SNHG1 would inhibit the proliferation of oral cancer cells. 	34174971
SNHG1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue and cells	Expression[highly expressed]	CCK8//qRT-PCR	We found that SNHG1 was overexpressed in OSCC tissue and cells and was associated with OSCC progression.		Yes	 In addition, knockdown of SNHG1 suppressed cell proliferation in vitro and in vivo.	33376352
SNHG1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tumor tissues	Interaction(SOCS2/JAK2/STAT pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//qRT-PCR//RIP//FISH//RNA-seq//Cell Proliferation Assay//Invasion Assay//Transwell Assay	In this study, we investigated the clinical significance and function of lncRNA SNHG1 in GC. SNHG1 was significantly downregulated in GC tumor tissues compared with adjacent noncancerous tissues. Mechanically, SNHG1 was found interacted with ILF3, NONO and SFPQ. RNA-seq combined with bioinformatic analysis identified a serial of downstream genes of SNHG1, including SOCS2, LOXL2, LTBP3, LTBP4. 		Yes	Overexpression of SNHG1 in BGC-823 cells remarkably inhibited not only cell proliferation, migration, invasion in vitro, but also tumorigenesis and lung metastasis in the chick embryo chorioallantoic membrane (CAM) assay in vivo.  Conversely, inhibition of SNHG1 by transfection of siRNA in AGS cells resulted in opposite phenotype changes. 	34179518
SNHG1	LncRNA	Homo sapiens	Arthritis, Rheumatoid	RA-FLSs	Interaction(PTBP1 )	RNA Pull-Down//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//RIP//Cell Cycle Assay//Invasion Assay//IF	Here, we found that lncRNA small nucleolar RNA host gene 1 (SNHG1) is up-regulated in RA-FLSs compared with FLSs from trauma arthritis and osteoarthritis patients. Furthermore, the regulation mechanism depends on the interaction between SNHG1 and polypyridine tract-binding protein 1 (PTBP1). This interaction influences PTBP1 expression that participates in the regulation of RA-FLSs biological behaviors. 		Yes	The results suggest that SNHG1 in RA-FLSs helps to sustain the cellular functions of proliferation, migration and invasion. 	33218941
circZNF91	CircRNA	Homo sapiens	Leukemia, Lymphocytic, Chronic, B-Cell	CLL samples and cells	Interaction(miR-1283/WEE1 Axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//EdU Staining	 circZNF91 was upregulated in CLL samples.  circZNF91 could sponge miR-1283 to suppress its activity, which in turn upregulated WEE1 expression. Silencing circ-TTBK2 reduced WEE1 expression, while the inhibitor of miR-1283 enhanced WEE1 expression. The miR-1283/WEE1 axis mediated the effects of circZNF91 on cell proliferation and apoptosis, as well as induced cell cycle regulation.		Yes	Silencing circZNF91 attenuated CLL cell proliferation and induced apoptosis and cell cycle arrest. 	35572733
SNHG1	LncRNA	Homo sapiens	oral squamous cell carcinoma	 OSCC samples and cells	Interaction(SNHG1/miR-145-5p/KLF5 Axis)	Migration Assay//Transection//qRT-PCR//CCK8//Luciferase Report Assay//EdU Staining//Transwell Assay	SNHG1 was abnormally upregulated in OSCC samples and linked to a poor prognosis of OSCC patients. miR-145-5p was a key downstream target inducing the oncogenic role of SNHG1 in the OSCC process with KLF5 as its downstream gene. SNHG1/miR-145-5p/KLF1 axis is responsible for driving the malignant process of OSCC.	SNHG1 was abnormally upregulated in OSCC samples and linked to a poor prognosis of OSCC patients. 	Yes	 Serving as an oncogene, SNHG1 strengthened proliferative and migratory functions of Tca8113 and CAL-27 cells.	35281530
Snhg1	LncRNA	Mus musculus	Parkinson Disease	brain tissue,cell line	Regulation[miR-221/222 /p27/mTOR pathway ]	Western Blot//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//IHC	We observed that SNHG1 expression was gradually upregulated in PD cellular and animal models.  In conclusion, these results demonstrated that downregulation of SNHG1 attenuated MPP-induced decreases in LC3-II (an autophagic marker) levels and cytotoxicity through the miR-221/222/p27/mTOR pathway, suggesting that SNHG1 may be a therapeutic target for neuroprotection and disease treatment in PD. ++		Yes	 Furthermore, silencing SNHG1 promoted autophagy and prevented MPP-induced cell death, similar to the overexpression of the miR-221/222 cluster. 	31499060
Snhg1	LncRNA	Mus musculus	Neuralgia	spinal 	regulation[regulating CDK4 level]	qRT-PCR//ELISA//Luciferase Report Assay//RIP	SNHG1 was upregulated in rats undergoing SNL.SNHG1 induced NP by directly regulating CDK4 level.		Yes	 Knockdown of SNHG1 alleviated the development of NP and overexpression of SNHG1 was capable of inducing NP symptoms in uninjured rats.	33336721
Snhg1	LncRNA	Mus musculus	Epilepsy	hippocampus tissue	regulation[miR-154-5p/TLR5 axis]	Tunel//qRT-PCR//Luciferase Report Assay//H&E Staining//ChIP	Elevated SNHG1 and decreased miR-154-5p were observed in both in vivo mouse model and in vitro cell model of epilepsy.  In summary, SP1 transcriptionally activated-SNHG1 contributes to the development of epilepsy via directly regulating miR-154-5p/TLR5 axis, which provides novel targets in treatment of epilepsy.		Yes	Knockdown of SNHG1 or transfection with miR-154-5p mimics significantly ameliorated Mg2+ free-induced neuronal injury in SH-SY5Y cells. 	33096314
SNHG1	LncRNA	Homo sapiens	gallbladder carcinoma	GBC tissues and cells	Interaction(miR-194-5p/ LIF and PDGFA)	Other	 High expression of SNHG1 was observed in both GBC tissues and cells, and it was associated with tumor sizes. MiR-194-5p could competitively bind with SNHG1 and was low-expressed in GBC, revealing the negative correlation between SNHG1 and miR-194-5p. Downregulated miR-194-5p reversed the effects of SNHG1 silencing on viability, proliferation, invasion and EMT-related marker expressions in GBC cells. Additionally, LIF and PDGFA were the target genes of miR-194-5p.	 High expression of SNHG1 was observed in both GBC tissues and cells, and it was associated with tumor sizes. 	Yes	 ShSNHG1 inhibited SNHG1 expression and retarded the viability, proliferation and invasion of GBC cells, accompanied with downregulated N-Cadherin and Vimentin yet upregulated E-Cadherin. 	36261179
Snhg1	LncRNA	Mus musculus	Abortion, Spontaneous	trophoblast cells, RSA mice	Interaction(microRNA-183-5p/ZEB2 axis)	Western Blot//Transfection//Wound Healing Assay//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Microarray//EdU Staining//Transwell Assay	Microarray analysis was applied in RSA mice, and SNHG1 was identified as a significantly downregulated lncRNA. Mechanistically, SNHG1 bound to miR-183-5p in trophoblast cells. Moreover, miR-183-5p directly targeted ZEB2. Rescue experiment showed that ZEB2 silencing reversed the ameliorative effect of SNHG1 on pregnancy outcome and the promotion of trophoblast activity in RSA mice by impaired the Wnt/β-catenin pathway. 		Yes	SNHG1 improved pregnancy outcome and reduced embryo resorption in RSA mice. Trophoblast cell proliferation, apoptosis, migration, and invasion were investigated by CCK8, EdU, TUNEL, wound healing, and Transwell assays. SNHG1 promoted proliferation, migration, and invasion of trophoblast cells, and reduced apoptosis.	35121558
SNGH3	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	Expression [highly expressed]	qRT-PCR//ELISA	LncRNA SNGH3 (small nucleolar RNA host gene 3) is highly expressed in numerous forms of cancer, serving as an oncogene in cancer progression. Herein, the findings exhibited upregulation of SNGH3 in bladder cancer tissues, along with the cell lines. 	Furthermore, overexpressed SNGH3 was positively linked to the TNM stage, as well as the histological grade of bladder cancer. 	Yes	Moreover, the silencing of SNGH3, using CRISPR-dCas9, suppressed cell growth along with migration, but elevated bladder cancer cell apoptosis. 	33859998
SNG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[miR-302a-3p/FGF19 axis]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//Western Blot	 Here, we showed that SNG16 was up-regulated and associated with poor prognosis in HCC.Moreover, our result indicated that SNHG16/miR-302a-3p axis regulated the expression of FGF19 in liver cancer cells. Finally, we investigated the biological function of SNHG16 in HCC and showed that SNHG16 promoted liver cancer cells proliferation via the SNHG16/miR-302a-3p/FGF19 axis. 		Yes	Finally, we investigated the biological function of SNHG16 in HCC and showed that SNHG16 promoted liver cancer cells proliferation via the SNHG16/miR-302a-3p/FGF19 axis.	30784284
SND1-IT1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC cells and tissues	Interaction(miR-1245b-5p/DDX54/USP3/SNAIL1)	RNA Pull-Down//Western Blot//Wound Healing Assay//Co-IP//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 Long non-coding RNA (lncRNA) SND1 intronic transcript 1 (SND1-IT1) is highly expressed in exosomes secreted by GC cells.   SND1-IT1 was verified to bind to microRNA-1245b-5p (miR-1245b-5p) through competitive adsorption to promote ubiquitin specific protease 3 (USP3) messenger RNA (mRNA) expression. SND1-IT1 was validated to recruit DEAD-box helicase 54 (DDX54) to promote USP3 mRNA stability. SND1-IT1 induces malignant transformation of GES-1 cells through USP3. USP3 mediates the deubiquitination of snail family transcriptional repressor 1 (SNAIL1).		Yes	Exosome-mediated lncRNA SND1-IT1 from GC cells enhances malignant transformation of GES-1 cells via up-regulating SNAIL1.	35739527
SND1-IT1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells.	Interaction(SND1-IT1/miR-124/COL4A1 axis )	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	LncRNA SND1-IT1 was upregulated in GC tissues and cells. LncRNA SND1-IT1 participated in TGF-β1-stimulated EMT in GC by sponging miR-124. MiR-124 attenuated TGF-β1-stimulated EMT in GC by targeting COL4A1.		Yes	 TGF-β1-stimulated EMT and regulated lncRNA SND1-IT1, miR-124, and COL4A1 expressions in HGC-27 cells. LncRNA SND1-IT1 knockdown tempered HGC-27 cell viability, migration and invasion.	35184134
circSOS2	CircRNA	Homo sapiens	cervical squamous cell carcinoma	SCC tissues and cells	Interaction(miR-543/FNDC3B axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircSOS2 was highly expressed in SCC tissues and cells; besides, its expression level was closely associated with poor prognosis. Loss-of-functional experiments revealed that suppression of circSOS2 repressed proliferation, cell cycle process, migration, invasion, and glycolysis while induced apoptosis in SCC cells, which was overturned by inhibition of miR-543. 	 CircSOS2 was highly expressed in SCC tissues and cells; besides, its expression level was closely associated with poor prognosis.	Yes	Loss-of-functional experiments revealed that suppression of circSOS2 repressed proliferation, cell cycle process, migration, invasion, and glycolysis while induced apoptosis in SCC cells, which was overturned by inhibition of miR-543.	34023283
SND1-IT1	LncRNA	Homo sapiens	Retinoblastoma	RB specimens and cells	Interaction(miR-132-3p/SMAD2 axis)	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We observed that SND1-IT1 was highly expressed in both RB specimens and cells, and associated with poorer prognosis of RB patients.MiR-132-3p was predicted to interact with SND1-IT1. RT-qPCR and dual-luciferase reporter assays verified the regulation of miR-132-3p by SND1-IT1 in RB cells. In addition, SND1-IT1 enhanced the expression of SMAD2 by sponging miR-132-3p. 		Yes	Functional investigation revealed that downregulation of SND1-IT1 suppressed RB cell proliferation, migration and invasion in vitro and restrained RB tumorigenesis in vivo. 	34969359
hsa_circ_0065898	CircRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC cell lines	Expression(highly expressed)	CCK8//qRT-PCR//Transwell Assay	Hsa_circ_0065898 was significantly overexpressed in the CSCC cell lines. Hsa_circ_0065898 facilitated cell proliferation, migration, and invasion in CSCC.		Yes	Hsa_circ_0065898 was significantly overexpressed in the CSCC cell lines. Hsa_circ_0065898 facilitated cell proliferation, migration, and invasion in CSCC.	35116238
SNHG1	LncRNA	Homo sapiens	Epilepsy	EP tissues	Interaction(miR-181a/BCL-2 axis )	In Vivo Experiment//Western Blot//qRT-PCR//MTT//Luciferase Report Assay//ELISA	SNHG1 expression was down-regulated in EP tissues and kainic acid (KA)-induced CTX-TNA2 cells. In addition, we confirmed that SNHG1 targeted miR-181a, whereas BCL-2 was a target gene of miR-181a. Negative correlations between SNHG1 and miR-181a, as well as miR-181a and BCL-2 were exhibited. 		Yes	The apoptosis and release of inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) in KA-induced CTX-TNA2 cells were suppressed by SNHG1 overexpression and promoted by miR-181a up-regulation.	33359246
SNHG1	LncRNA	Homo sapiens	Meningioma	cell lines	Regulation[Wnt signaling pathway]	qRT-PCR	In this work, it was discovered that SNHG1 was overexpressed in meningioma cell lines.Then mechanism experiments demonstrated that SNHG1 functioned as the role of sponging miR-556-5p and negatively regulated miR-556-5p expression. Moreover, it was verified that TCF12 is the direct downstream target of miR-556-5p. Furthermore, SNHG1/miR-556-5p/TCF12 axis promoted cell proliferation and suppressed cell apoptosis in meningioma via activating the Wnt signaling pathway. In the end, it was confirmed that TCF12 expression was positively regulated by SNHG1, and TCF12 could promote transcription of SNHG1 through binding with the promoter region of SNHG1. In conclusion, the SNHG1/miR-556-5p/TCF12 feedback loop promotes the tumorigenesis of meningioma through the Wnt signaling pathway.		Yes	SNHG1 deficiency restrained cell growth as well as accelerated apoptosis. 	31692066
snaR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	blood	Interaction[TGF-β1]	qRT-PCR	 In the present study, we found that plasma levels of snaR were upregulated in patients with laryngeal squamous cell carcinoma (LSCC) than in healthy controls.Therefore, overexpression of lncRNA snaR is correlated with progression and predicts poor survival of LSCC and the mechanism of its actions is likely related to TGF-β1.	Follow-up study showed that high plasma levels of snaR were correlated with poor overall survival. 	Yes	snaR overexpression and exogenous TGF-β1 treatment promoted LSCC cell proliferation, migration, and invasion. 	30506952
SNHG1	LncRNA	Homo sapiens	Prostatic Neoplasms	cancer tissues	regulation[miR-195-5p ]	qRT-PCR	SNHG1 was enhanced in PC, while miR-195-5p was decreased (p<0.05). SNHG1 can mediate the proliferation, invasion and EMT of PC by regulating miR-195-5p expression.		Yes	After transfection of DU-145 and PC-3, it was found that silence of SNHG1 or overexpression of miR-195-5p could evidently inhibit the proliferation and invasion, increase the apoptosis (p<0.05).	33090391
SNHG1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PCa tissues,cell lines	Interaction[miR-195]	qRT-PCR//Western Blot	 The results demonstrated that the expression levels of SNHG1 were increased in PCa cell lines and human tissue samples.We further confirmed that, in PCa cells, SNHG1 can negatively regulate miR-195 expression by acting as a ceRNA, and Cyclin D1 is a direct target of miR-195. Overexpression of miR-195 abrogated the oncogenic role of SNHG1 in PCa cells.	High SNHG1 expression was notably correlated with adverse characteristics and poor survival of PCa patients.	Yes	 Knockdown of SNHG1 sExpression[up-expression]pressed PCa cell proliferation in vitro and PCa tumor growth in vivo, and these effects might be associated with the induction of cell cycle arrest.	31933880
SNHG1	LncRNA	Homo sapiens	Pancreatic Neoplasms	cell lines	Regulation[Notch-1 signaling pathway ]	Western Blot//Wound Healing Assay//qPCR//MTT//Transwell Assay	SNHG1 was significantly upregulated in PC cells.Furthermore, SNHG1 knockdown inhibited the activation of the Notch-1 signaling pathway and inhibited the expression of N-cadherin, Hes1, Vimentin, Notch-1. The inhabitation was reversed when Notch-1 was overexpressed in si-SNHG1 cells.		Yes	 Knockdown of SNHG1 could obviously suppress cell proliferation, invasion, and migration. 	30520072
SNHG1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC cells	Interaction(miR-497/FGFR1)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Downregulation of SNHG1 blocked cell proliferation, migration and invasion, and induced apoptosis in vitro, while also inhibiting the EMT, shown by changes in the biomarkers E-cadherin, N-cadherin, and Vimentin. The opposite results were observed on upregulation of SNHG1. In vivo experiments showed that downregulation of SNHG1 inhibited tumor development in nude mice.Furthermore, experiments investigating the regulatory mechanism of SNHG1 indicated that SNHG1 acted as a competitive endogenous RNA, positively regulating the expression of fibroblast growth factor receptor 1 (FGFR1) through sponging miR-497. Rescue experiments demonstrated that the effects of SNHG1 downregulation on PC cells were attenuated when simultaneously inhibiting the levels of miR-497.		Yes	Downregulation of SNHG1 blocked cell proliferation, migration and invasion, and induced apoptosis in vitro, while also inhibiting the EMT, shown by changes in the biomarkers E-cadherin, N-cadherin, and Vimentin. The opposite results were observed on upregulation of SNHG1. In vivo experiments showed that downregulation of SNHG1 inhibited tumor development in nude mice.	35141164
hsa_circ_0007331	CircRNA	Homo sapiens	Endometriosis	 ectopic endometrial cells 	regulation[miR-200c-3p/HiF-1α axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	 In this study, we identified aberrant high expression of circ_0007331 in ectopic endometrial cells by comparing the endometrial samples from patients with and without endometriosis. Collectively, we preliminarily characterized the role and possible insights of circ_0007331/miR-200c-3p/HIF-1α axis in the proliferation and invasion of ectopic endometrial cells.		Yes	Further functional experiments revealed that circ_0007331 knock-down effectively suppressed the viability, proliferation and invasive capacity of ectopic endometrial cells. 	32960511
SNHG1	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues	interaction[CDKN1A ]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//ChIP	Herein, we have figured out that lncRNA SNHG1, with substantially enhanced expression in CCA, is capable of acting as the oncogenic molecule of CCA. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology. 		Yes	As revealed by our data, SNHG1 knockdown extensively inhibited CCA cell migration as well as proliferation in vitro and in vivo. 	29970899
SNHG1	LncRNA	Homo sapiens	Cholangiocarcinoma	cell lines	Interaction[TLR4/NF-κB Pathway]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 In this study, the SNHG1 levels were boosted in CCA cell lines.The data also demonstrated that miR-140 could act as a target of SNHG1 in CCA and inhibited CCA cell proliferation and invasion, whereas the inhibition effects were relieved by overexpression of SNHG1. In addition, Toll-like receptor 4 (TLR4), an NF-κB-activating signal, was identified to be a target of miR-140. SNHG1, as a competing endogenous RNA (ceRNA) for miR-140, enhanced TLR4 expression and activated NF-κB signaling, thereby regulating growth and tumorigenesis in CCA. Animal experiments further confirmed this conclusion. Collectively, these findings not only uncovered a key role of SNHG1/miR-140/TLR4/NF-κB signaling axis in CCA tumorigenesis and progression but also denoted the probable utilization of SNHG1 as a therapeutic target for CCA.		Yes	In this study, the SNHG1 levels were boosted in CCA cell lines, and knockdown of SNHG1 repressed CCA cell proliferation and invasion in vitro.	30764893
SNHG1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissue and cells	regulation[Wnt/β-catenin and PI3K/AKT/mTOR signaling pathways ]	RNA Pull-Down//Transwell Assay//qRT-PCR//MTT//Colony Formation Assay//IF	We found that SNHG1 and EZH2 were up-regulated in PCa tissue and cells.This study reveals that lncRNA-SNHG1 regulates Wnt/β-catenin and PI3K/AKT/mTOR signaling pathways via EZH2 gene to affect proliferation, apoptosis and autophagy of PCa cells.		Yes	The proliferation, colony formation, migration and invasion of LNCaP and PC3 cells were significantly reduced with the interference with SNHG1or EZH2 compared with the control group.	33194612
SNHG1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tumor tissues	Expression[highly expressed]	qRT-PCR//MTT//Tunel	The SNHG1 expression was significantly upregulated in PCa tumor tissues compared with paired adjacent non-cancerous tissues.	The SNHG1 expression was obviously associated with the TNM stage, Gleason Score, lymph node invasion, and long-term metastasis mortality rate. 	Yes	Silencing of SNHG1 inhibited cell proliferation and promoted apoptosis in PC3 and DU145 PCa cell lines in vitro, while overexpression of SNHG1 led to opposite results.	33154308
SNHG1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues and cells	Interaction(miR-383-5p)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	In this study, we found the level of SNHG1 was significantly upregulated in prostate cancer tissues and cells. MiR-383-5p was identified to be a target of SNHG1 by bioinformatics analysis, dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. MiR-383-5p was significantly downregulated in prostate cancer tissues and cells. 		Yes	Knockdown of SNHG1 significantly suppressed proliferation, migration and invasion and promoted cell apoptosis in prostate cancer cells. In addition, knockdown of SNHG1 significantly downregulated proliferating cell nuclear antigen and upregulated cleaved caspase-3. 	33470616
SNHG1	LncRNA	Homo sapiens	Myocardial Reperfusion Injury	 H/R-induced AC16 cells	Interaction(miR‑450b‑5p/IGF1 axis )	Western Blot//Transfection//Tunel//qRT-PCR//MTT//Luciferase Report Assay	 lncRNA SNHG1 expression was significantly downregulated in H/R-induced AC16 cells.  lncRNA SNHG1 overexpression significantly inhibited apoptosis and decreased oxidative stress levels in H/R‑induced AC16 cells, which was mediated via regulation of the miR‑450b‑5p/IGF1 axis and activation of the PI3K/Akt signaling pathway. 		Yes	 lncRNA SNHG1 overexpression significantly inhibited apoptosis and decreased oxidative stress levels in H/R?induced AC16 cells, which was mediated via regulation of the miR?450b?5p/IGF1 axis and activation of the PI3K/Akt signaling pathway. 	35315499
SNHG1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC cells	Interaction(SNHG1/miR-194-5p/MTFR1 Axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Importantly, SNHG1 promoted EMT, invasion and migration of TSCC cells by upregulating MTFR1. SNHG1/miR-194-5p/MTFR1 axis promotes TGFβ1-induced EMT, migration and invasion of cells in TSCC, which could be potential targets for treating TSCC patients.		Yes	 Importantly, SNHG1 promoted EMT, invasion and migration of TSCC cells by upregulating MTFR1. SNHG1/miR-194-5p/MTFR1 axis promotes TGFβ1-induced EMT, migration and invasion of cells in TSCC, which could be potential targets for treating TSCC patients.	35107755
SNHG1	LncRNA	Homo sapiens	Liver Neoplasms	LC tissues, cell lines	Interaction[inhibiting p53 expression via binding to DNMT1]	ChIP//Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	NHG1 expression was higher in LC tissues than that of paracancerous tissues. LC patients with stage III-IV presented higher expression level of SNHG1 than those with stage I-II.Similarly, SNHG1 was highly expressed in LC cells than that of normal liver cells. RIP and ChIP results demonstrated that SNHG1 could bind to DNMT1 and inhibit p53 expression. Overexpression of p53 partially reversed the inhibitory effects of SNHG1 on proliferative and invasive abilities of LC cells.	LC patients with stage III-IV presented higher expression level of SNHG1 than those with stage I-II. 	Yes	 SNHG1 knockdown inhibited the proliferative and invasive abilities, and arrested the cell cycle in the G0/G1 phase of SMMC-7721 and SK-HEP-1 cells.	31002127
SNHG1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	esophageal squamous cell cancer tissues	regulation[miR-204/HOXC8 Axis]	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	High expression of SNHG1 was exhibited in esophageal squamous cell cancer and indicated poor outcomes of patients. SNHG1 knockdown suppresses migration and invasion but induces apoptosis of esophageal squamous cell cancer cells by increasing miR-204 and decreasing HOXC8.		Yes	SNHG1 silence led to cell cycle arrest at G0-G1 phase, inhibition of migration and invasion and increase of apoptosis.	32158227
SNHG1	LncRNA	Homo sapiens	Esophageal Neoplasms	EC tissues and cell lines	regulation[SNHG1/miR-195/Cdc42 axis ]	qRT-PCR	It was found SNHG1 and Cdc42 were significantly upregulated, and miR-195 was significantly downregulated in both EC tissues and cell lines. This study might provide deeper insights into the SNHG1/miR-195/Cdc42 axis in EC.		Yes	In addition, the inhibition of either SNHG1 or Cdc42 resulted in suppression of cell proliferation, migration, and invasion, while inhibition of miR-195 led to opposite results and reversed the effects of si-SNHG1.	33171523
SNHG1	LncRNA	Homo sapiens	Laryngeal Neoplasms	LC tissues	Regulation[Notch1 signaling pathway]	CCK8//qRT-PCR//Western Blot	SNHG1 was upregulated in LC tissues than that of controls. Besides, its level was higher in LC with T3-T4 relative to those of T1-T2.Notch1 overexpression could reverse the regulatory effects of SNHG1 on viability and proliferation of LC cells.	SNHG1 was upregulated in LC tissues than that of controls. Besides, its level was higher in LC with T3-T4 relative to those of T1-T2. Higher abundance of SNHG1 was identified in LC patients with lymph node metastasis compared with those non-metastatic patients. Survival analysis indicated that LC patients with high-level SNHG1 had worse overall survival.	Yes	Knockdown of SNHG1 in Tu212 and Hep2 cells downregulated relative levels of Notch1 and Hes1. Moreover, SNHG1 knockdown resulted in decreased viability and proliferative ability of LC cells.	31378897
SNHG1	LncRNA	Homo sapiens	Liver Neoplasms	HCC tissues	Interaction(miR-326/PKM2 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Microarray//ChIP	SNHG1 expression was dramatically increased in HCC and positively correlated with poor prognosis.  E2F1 bound to the SNHG1 promoter region to activate SNHG1 transcription. Furthermore, SNHG1 served as a molecular sponge for miR-326 to sequester the interaction of miR-326 and pyruvate kinase M2 (PKM2), facilitating the expression of PKM2. 	SNHG1 expression was dramatically increased in HCC and positively correlated with poor prognosis. 	Yes	E2F1-activated SNHG1 modulates the miR-326/PKM2 axis to facilitate glycolysis and the proliferation of HCC cells.	35816558
SNHG1	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	Interaction[targeting miR-338-3p to regulate PLK4 ]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	The expression levels of SNHG1 and PLK4 were increased in NB tissues and cells, and miR-338-3p expression was on the contrary. PLK4 was verified as a direct target of miR-338-3p and miR-338-3p could specially bind to SNHG1. The negative effect of SNHG1 down-regulation on cell proliferation, migration, and invasion could be rescued by miR-338-3p inhibition. The suppression of miR-338-3p mimics on cell proliferation, migration, and invasion could be reversed by PLK4 overexpression.		Yes	The negative effect of SNHG1 down-regulation on cell proliferation, migration, and invasion could be rescued by miR-338-3p inhibition. In addition, SNHG1 knockdown weakened the volume and weight of tumor in vivo.	31696485
snaR	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues	Interaction[LncRNA NRON ]	CCK8//qRT-PCR	In contrast, lncRNA snaR was up-regulated in TNBC tissues and was inversely correlated with NRON.The snaR overexpression resulted in promoted cancer cell proliferation but did not significantly affect NRON expression. NRON overexpression inhibited cancer cell proliferation and down-regulated snaR. The snaR overexpression reduced the effects of NRON overexpression. We therefore conclude that NRON may down-regulate lncRNA snaR to inhibit cancer cell proliferation in TNBC.		Yes	The snaR overexpression resulted in promoted cancer cell proliferation but did not significantly affect NRON expression. 	30996114
snaR	LncRNA	Homo sapiens	ovarian carcinoma	plasma 	Regulation[GAB2 expression]	CCK8//qRT-PCR//Western Blot	It was observed that plasma levels of lncRNA snaR and GAB2 were significantly higher in OC patients than those in healthy controls.  LncRNA snaR may promote proliferation of ovarian carcinoma cells by upregulating GAB2 expression.	 In effect, high levels of plasma lncRNA snaR and GAB2 distinguished OC patients from healthy controls. Plasma lncRNA snaR and GAB2 were positively correlated in OC patients but not in healthy controls.	Yes	LncRNA snaR overexpression promoted cancer cell proliferation and upregulated GAB2 expression.	30093110
SLCO4A1-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues	Regulation[miR-335-5p/OCT4 axis]	CCK8//qRT-PCR//Transwell Assay	SLCO4A1-AS1 expression was more upregulated in BC tissues than in adjacent normal tissues. High SLCO4A1-AS1 expression level was associated with the progression of BC, and SLCO4A1-AS1 promoted the malignant phenotypes of BC cells through the miR-335-5p/OCT4 axis.	Moreover, SLCO4A1-AS1 level was positively correlated with the advanced stage and metastasis in BC. The upregulation of SLCO4A1-AS1 indicates poor prognosis in BC patients.	Yes	The knockdown of SLCO4A1-AS1 downregulated the proliferation, migration, and invasion of EJ and T24 cells in vitro. 	30863101
SMARCA5	CircRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues 	Expression[lower expressed]	qRT-PCR	 Circ-SMARCA5 expression was reduced in ICC tumor tissues compared to adjacent tissues. 	Tumor circ-SMARCA5 high expression was negatively associated with Eastern Cooperative Oncology Group performance score, T stage, N stage, TNM stage, and abnormal CA199 status. Furthermore, OS was increased in patients with tumor circ-SMARCA5 high expression compared with those with low expression, and further multivariate Cox's regression demonstrated that tumor circ-SMARCA5 high expression was an independent predictive factor for longer OS. 	Yes	In TFK-1 and HuH-28 ICC cells, circ-SMARCA5 upregulation decreased cell proliferation, reduced relative cell viability in cisplatin-treated as well as gemcitabine-treated cells, and also decreased inhibitory concentration by 50% value (IC50 ) of cisplatin and gemcitabine.	31880360
circRTN4IP1	CircRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues and cells	Interaction(miR-541-5p)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay	In contrast, ICC tissues and cells showed high expression of circRTN4IP1 and HIF1A, but low expression of miR-541-5p.		Yes	 Knockdown of circRTN4IP1 led to repression of cell proliferation and glucose metabolism, but promotion of cell apoptosis; however, circRTN4IP1 overexpression had opposite effects. 	34974242
circACTN4	CircRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues 	Interaction(miR-424-5p/YBX1 /FZD7)	qRT-PCR//RIP//Luciferase Report Assay//Microarray//ChIP	 In addition, circACTN4 upregulated Yes-associated protein 1 (YAP1) expression by sponging miR-424-5p. More importantly, circACTN4 also recruited Y-box binding protein 1 (YBX1) to stimulate Frizzled-7 (FZD7) transcription. Furthermore, circACTN4 overexpression in ICC cells enhanced the interaction between YAP1 and β-catenin, which are the core components of the Hippo and Wnt signaling pathways, respectively.	High circACTN4 expression in ICC was associated with a worse 3-year overall survival and higher recurrence than low circACTN4 expression.	Yes	High circACTN4 expression was associated with enhanced tumor proliferation and metastasis in vitro and in vivo, as well as a worse prognosis following ICC resection. 	34509526
SMASR	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer cells	Regulation( TGF-β/Smad signaling pathway)	RNA Pull-Down//Northern Blot//Western Blot//qRT-PCR//FISH//Luciferase Report Assay//IF	Here, we report a novel lncRNA adjacent to Smad3, named Smad3-associated long non-coding RNA (SMASR). SMASR is downregulated by TGF-β via Smad2/3 in lung cancer cells. Mechanistically, SMASR interacts with Smad2/3 and inhibits the expression of TGFBR1, the TGF-β type I receptor responsible for phosphorylation of Smad2/3, thus leading to inactivation of TGF-β/Smad signaling pathway. 		Yes	Knockdown of SMASR induces EMT and increases the migration and invasion of lung cancer cells. Moreover, knockdown of SMASR promotes the phosphorylation of Smad2/3. 	33931741
SMARCC2	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer cells	Interaction(SMARCC2/miR-551b-3p/TMPRSS4 axis )	Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Invasion Assay	LncRNA SMARCC2 inhibits the expression of miR-551b-3p through binding to its mRNA response elements in gastric cancer cells. TMPRSS4 is a direct target gene of miR-551b-3p. We conclude that miR-551b-3p functions as a tumour suppressor gene in gastric cancer, and its function is regulated by LncRNA SMARCC2/miR-551b-3p/TMPRSS4 axis.		Yes	Overexpression of LncRNA SMARCC2 enhances the proliferation and migration of gastric cancer cells, while inhibition of LncRNA SMARCC2 does the opposite. 	29337109
SMARCA5	CircRNA	Homo sapiens	Stomach Neoplasms	GC tissues,cell lines(MGC803, SGC7901, N87 and AGS)	Interaction[miR-150-5p]	qRT-PCR//Western Blot//PCR//IF	Our results showed that circSMARCA5 expression was significantly decreased in human gastric cancer tissues and cell lines.Luciferase reporter assays proved that circSMARCA5 acted as a sponge for miroRNA-346 (miR-346) and regulated the expression of F-Box and leucine rich repeat protein 2 (FBXL2). 		Yes	Transfection efficiency assay showed that circSMARCA5 expression was markedly increased after transfection with pLCDH-circSMARCA5 when compared with pLCDH-transfected SGC7901 cells (Fig. 2A). Next, we detected the effect of circSMARCA5 overexpression on proliferation, migration and invasion. CCK-8 assay demonstrated that circSMARCA5 overexpression dramatically sExpression[Expression[up-expression]-expression]pressed the cell proliferation of SGC7901 cells (Fig. 2B). In addition, cell migration and invasion were also reduced by circSMARCA5 overexpression (Fig. 2C and D).	35515212
SMARCA5	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	regulation[miR-670-5p/RBM24 axis]	qRT-PCR//Luciferase Report Assay	 The results showed that circsSMARCA5 was expressed at low level in NSCLC tissues and cells, while miR-670-5p had high level in NSCLC tissues. Thus, circsSMARCA5 may serve as an NSCLC suppressor by regulating the miR-670-5p/RBM24 axis, and it may have the potential to be a biomarker or therapeutic target for NSCLC.		Yes	Moreover, circsSMARCA5 obviously inhibited tumor growth in vivo, reduced cell proliferation and increased cell apoptosis in vitro, while miR-670-5p mimic or RBM24 knockdown could reverse these effects. 	33085761
SMARCA5	CircRNA	Homo sapiens	Colorectal Neoplasms	CRC cell lines and tissues	regulation[downregulating miR-39-3p and upregulating ARID4B]	qPCR//PCR//IF	Circ-SMARCA5 expression was dramatically decreased in CRC cell lines and tissues.Circ-SMARCA5 functions as a tumor suppressor by upregulating ARID4B expression via sponging miR-39-3p, and thereby inhibited CRC progression.		Yes	 Circ-SMARCA5 overexpression inhibited CRC cell proliferation, migration and invasion. 	32807692
SMARCA5	CircRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and cell lines	Interaction(SND1 /YWHAB)	RNA Pull-Down//cell invasion assay//Western Blot//Transfection//qPCR//Proliferation Assay//Cell Apoptosis Assay//PCR//Cell Proliferation Assay//IP//Invasion Assay//IF	Quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) results showed that the expression of SMARCA5 was downregulated in cervical cancer tissues and cell lines. Our results showed that overexpression of circ SMARCA5 inhibits the binding of SND1 to YWHAB, and inhibits the proliferation and invasion, but promotes apoptosis in cervical cancer cells, thus inhibiting the metastasis of cervical cancer.		Yes	 Then we found that overexpression of SMARCA5 inhibited proliferation and invasion, but promoted apoptosis in cervical cancer cells. Overexpression of SMARCA5 inhibited cervical cancer metastasis in vivo. 	33588586
SMAD7	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and HCC cell lines	regulation[miR-125b/SIRT6 axis]	qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	This study uncovered that Linc-smad7 was increased in HCC samples and HCC cell lines using RT-qPCR assays.In conclusion, the current study first identified Linc-smad7 is increased in HCC, facilitating HCC cells proliferation, migration, invasion and EMT via regulating the miR-125b/SIRT6 axis.		Yes	Functionally, it was demonstrated that Linc-smad7 could bind with microRNA-125b (miR-125b), and the restoration of miR-125b rescued the promoting effects of Linc-smad7 on HCC cells.	33037850
circNFIB	CircRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues 	Interaction(MEK1)	Bioinformatics Analysis	cNFIB was significantly down-regulated in human ICC tissues with postoperative metastases. Mechanistically, cNFIB competitively interacted with MEK1, which induced the dissociation between MEK1 and ERK2, thereby resulting in the suppression of ERK signaling and tumor metastasis.	cNFIB was significantly down-regulated in human ICC tissues with postoperative metastases.The loss of cNFIB was highly associated with aggressive characteristics and predicted unfavorable prognosis in ICC patients. 	Yes	 Functional studies revealed that cNFIB inhibited the proliferation and metastasis of ICC cells in vitro and in vivo. 	35039066
SMAD5-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and NPC cell lines	Interaction[SMAD5]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay//EdU Staining//Transwell Assay	High expression of SMAD5-AS1 and SMAD5 but low miR-195 expression was determined in NPC tissues and NPC cell lines by RT-qPCR and western blot analysis. SMAD5-AS1 could upregulate SMAD5 expression by competitively binding to miR-195 in NPC cells. 		Yes	 Downregulation of SMAD5-AS1 or SMAD5 or overexpression of miR-195 led to inhibited NPC cell proliferation, invasion and migration and reversed EMT, enhanced apoptosis in vitro as well as restrained tumor growth in vivo.	31921616
SMAD5-AS1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cell lines	Interaction[microRNA-106a-5p ]	RNA Pull-Down//Western Blot//ISH//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	SMAD5-AS1 was highly expressed and miR-106a-5p was poorly expressed in NPC tissues and cell lines.Long noncoding RNA SMAD5-AS1 acts as a microRNA-106a-5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma.		Yes	Taken together, SMAD5-AS1 silencing suppressed EMT, cell proliferation, migration, and invasion in NPC by elevating miR-106a-5p to down-regulate SMAD5, which provided a novel therapeutic target for NPC treatment.	31557058
SLNCR1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Tumor tissues and paired healthy tissues 	Interaction[sPLA2]	Western Blot//qRT-PCR//ELISA//Invasion Assay//Transwell Assay	Compared with adjacent healthy tissues, the expression levels of lncRNA SLNCR1 were significantly increased in tumor tissues.In conclusion, lncRNA SLNCR1 may regulate cancer cell migration, invasion and stemness in NSCLC through interactions with sPLA2.	 	Yes	 lncRNA SLNCR1 siRNA silencing inhibited, whereas sPLA2 overexpression promoted cell migratory and invasive abilities and stemness.	31524254
SLCO4A1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC samples and cell lines	Interaction(miR-149/XIAP Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//Invasion Assay	SLCO4A1-AS1 was significantly upregulated in the GC samples and cell lines, and a high level of SLCO4A1-AS1 was associated with an advanced tumor stage and shortened patient survival. Mechanistically, SLCO4A1-AS1 post-transcriptionally regulated XIAP by functioning as competing endogenous RNA in GC to sponge miR-149. Further functional assays revealed that the overexpression of miR-149 and knockdown of XIAP considerably inhibited GC cell viability and its migratory and invasive characteristics in vitro. 	SLCO4A1-AS1 was significantly upregulated in the GC samples and cell lines, and a high level of SLCO4A1-AS1 was associated with an advanced tumor stage and shortened patient survival.	Yes	SLCO4A1-AS1 knockdown also determined the function of GC cells but was diminished by the miR-149 inhibitor in vitro. Finally, we demonstrated that the deletion of SLCO4A1-AS1 suppressed tumor growth and metastasis in vivo.	34650909
SLCO4A1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	Interaction( miR-149-5p/STAT3 Axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 The expressions of SLCO4A1-AS1 and STAT3 were increased, while the expression of miR-149-5p was suppressed in gastric cancer tissues and cell lines.  In addition, STAT3 expression was negatively correlated with miR-149-5p expression but was positively correlated with SLCO4A1-AS1 expression. SLCO4A1-AS1 bound to miR-149-5p and targeted STAT3. Moreover, miR-149-5p mimic inhibited the malignant development of gastric cancer cells and obviously reversed the function of SLCO4A1-AS1 overexpression. 		Yes	Overexpression of SLCO4A1-AS1 promoted cell viability, migration, invasion, and STAT3 expression but suppressed apoptosis, while knockdown of SLCO4A1-AS1 had the opposite effect.	34712324
SLCO4A1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 control tissues	Regulation[miR-508-3p/PARD3 axis ]	ISH//qRT-PCR	 In addition, the expression of SLCO4A1-AS1 was significantly up-regulated in 23 CRC tissues compared with the control tissues (Figure 1C).  The current study demonstrates that the SLCO4A1-AS1/miR-508-3p/PARD3/autophagy pathway play a critical role in CRC cell proliferation, and might provide novel targets for developing therapeutic strategies for CRC.		Yes	In vitro and in vivo studies revealed that SLCO4A1-AS1 knockdown repressed cytoprotective autophagy as assayed by transmission electron microscopy (TEM), and inhibited cell proliferation by directly targeting partition-defective 3 (PARD3).	31308265
SLCO4A1-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation(Cdk2/c-Myc signalling)	qRT-PCR//IHC//RIP//FISH	SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter.  Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth.		Yes	 Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. 	35039060
SLCO4A1-AS1	LncRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissues	Interaction(miR-150-3p to elevate SLCO4A1 )	qRT-PCR//FISH	 SLCO4A1-AS1 and SLCO4A1 were screened as the differentially expressed lncRNA and mRNA in colon cancer tissues.  SLCO4A1-AS1 was confirmed to competitively bind to miR-150-3p to elevate SLCO4A1 expression. 		Yes	Moreover, knockdown of SLCO4A1-AS1 decreased SLCO4A1 expression, thus inhibiting cell migration, invasion, sphere formation, and tumorigenesis abilities and enhancing the apoptosis of CD133+CD44+ cells. 	33958701
circHMGCS1	CircRNA	Homo sapiens	Cholangiocarcinoma	ICC tissues 	Interaction(miR-1236-3p/CD73 and GAL-8 axis)	In Vivo Experiment//Western Blot//ISH//Transfection//qRT-PCR//Luciferase Report Assay//Microarray//ELISA//IHC	We identified that compared with peritumor tissues, ICC tissues expressed hsa_circ_0008621 (circHMGCS1-016) high by RNA-seq, which was further identified by qRT-PCR and in situ hybridization.  By SILAC and circRNA-pull down, we demonstrated that circHMGCS1-016 induced ICC cell invasion and reshaped the tumor immune microenvironment via the miR-1236-3p/CD73 and GAL-8 axis. 	Moreover, the expression of circHMGCS1-016 was revealed to be associated with survival and recurrence of ICC patients.	Yes	By regulating circHMGCS1-016 expression, we found that elevated circHMGCS1-016 promoted ICC development both in vitro and in vivo. 	34526098
circSETDB1	CircRNA	Homo sapiens	Ovarian Neoplasms	SOC tissues and cells	Interaction(miR-129-3p)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//Invasion Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	 CircSETDB1 and MAP3K3 expression were apparently upregulated, whereas miR-129-3p expression was downregulated in SOC tissues and cells in comparison with normal fallopian tube tissues or normal ovarian epithelial cells. Additionally, miR-129-3p inhibitor impaired circSETDB1 silencing-mediated SOC malignant progression. 		Yes	CircSETDB1 knockdown inhibited cell proliferation, invasion and migration, but induced cell apoptosis in SOC cells. 	34789310
snaR	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues	Interaction[TGF-β1]	qRT-PCR//ELISA//Western Blot	 The expression of snaR and TGF-β1 was significantly increased in the patients with HCC compared with the healthy controls.snaR overexpression significantly promoted cancer cell migration and invasion, and additionally increased TGF-β1 expression. Treatment with TGF-β1 did not significantly affect snaR expression. A TGF-β1 inhibitor attenuated the effects of snaR overexpression in cancer cell migration and invasion. snaR may promote the metastasis of liver cancer through TGF-β1.		Yes	snaR overexpression significantly promoted cancer cell migration and invasion, and additionally increased TGF-β1 expression.	31186778
SMIM31	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells and tissues	Interaction(microRNA-1301-3p/lactate dehydrogenase isoform A axis)	CCK8//qRT-PCR//Luciferase Report Assay//RIP	We found that LINC01207 was overexpressed in OSCC cells and tissues. LINC01207 interacted with microRNA-1301-3p (miR-1301-3p) while lactate dehydrogenase isoform A (LHDA) was targeted by miR1301-3p. Effects caused by LINC01207 downregulation on OSCC cells were reversed by overexpression of LDHA. Overall, LINC01207 promotes OSCC progression via the miR-1301-3p/LDHA axis.		Yes	LINC01207 silencing inhibited OSCC cell proliferation and migration but promoted apoptosis and autophagy, and LINC01207 overexpression had an opposite result. 	34463208
snaR	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	SPC-A1 and A549 wild-type EGFR cell lines	Expression(highly expressed)	cell invasion assay//qRT-PCR//Transfection//MTT	The expression of snaR was remarkably up-regulated in SPC-A1 and A549 wild-type EGFR cell lines. 		Yes	Down regulation of snaR with small interfering RNA significantly inhibited cell invasion as well as proliferation of SPC-A1 and A549 cells. 	35875332
circATAD1	CircRNA	Homo sapiens	cervical squamous cell carcinoma	CSCC tissues	Interaction(miR-218)	Transfection//qRT-PCR//Cell Apoptosis Assay//BrdU//Transwell Assay	CSCC tissues exhibited upregulated expression of circ-ATAD1, which was localized to both nucleus and cytoplasm. Mature miR-218 was downregulated in CSCC tissues and was inversely correlated with circ-ATAD1, while premature miR-218 was not differentially expressed in CSCC.  Circ-ATAD1 is upregulated in CSCC and may regulate cell proliferation and apoptosis by suppressing the maturation of miR-218.		Yes	 In addition, overexpression of circ-ATAD1 increased cell proliferation and decreased cell apoptosis, while overexpression of miR-218 decreased cell proliferation and increased cell apoptosis, and it also attenuated the effects of overexpression of circ-ATAD1 on cell proliferation. However, CSCC cell invasion, migration, and stemness were not affected by circ-ATAD1 and miR-218.	34254279
SNAI3-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	interaction[miR-27-3p and miR-34a-5p]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	In this study, qRT-PCR analysis revealed that the expression of SNAI3-AS1 was elevated and was correlated with the levels of PEG10 in HCC tissues. Further bioinformatics analysis and mechanistic experiments showed that SNAI3-AS1 functions as a competing endogenous RNA (ceRNA) to activate PEG10 by acting as a sponge for miR-27-3p and miR-34a-5p. 		Yes	Through functional experiments, we determined that knockdown of SNAI3-AS1 and PEG10 inhibited the proliferation and metastasis, whereas overexpression of SNAI3-AS1 and PEG10 promoted the proliferation and metastasis of HCC cells.	32826862
circPOLA2	CircRNA	Homo sapiens	cervical squamous cell carcinoma	CESC tissues	regulation[ miR-326/ GNB1]	qRT-PCR	Circ_POLA2 was highly expressed in CESC tissues and positively correlated with poor prognosis in CESC patients.  In conclusion, circ_POLA2 promotes cervical squamous cell carcinoma development and progression via regulating the miR-326/GNB1 axis, which might serve as a novel therapeutic target for CESC patients.	Circ_POLA2 was highly expressed in CESC tissues and positively correlated with poor prognosis in CESC patients. 	Yes	 Knockdown of circ_POLA2 using shRNA inhibited cervical cancer cell proliferation, migration, and invasion both in vitro and in vivo.	32766125
SMO-193a	CircRNA	Homo sapiens	Glioblastoma	glioblastoma tissues	Regulation(FUS/Gli1)	Northern Blot//ChIP//TUNEL//ISH//Transfection//Immunoblotting//Tunel//Proliferation Assay//qRT-PCR//FISH//RNA-seq//PCR//IP//IHC//IF	Moreover, circ-SMO/SMO-193a.a. is positively regulated by FUS, a direct transcriptional target of Gli1. Shh/Gli1/FUS/SMO-193a.a. form a positive feedback loop to sustain Hedgehog signaling activation in glioblastoma.	Clinically, SMO-193a.a. is more specifically expressed in glioblastoma than SMO and is relevant to Gli1 expression. Higher expression of SMO-193a.a. predicts worse overall survival of glioblastoma patients, indicating its prognostic value.	Yes	Deprivation of SMO-193a.a. in brain cancer stem cells attenuates Hedgehog signaling intensity and suppresses self-renewal, proliferation in vitro, and tumorigenicity in vivo. 	33446260
SMO	CircRNA	Homo sapiens	Glioma	glioma tissues	Interaction[sponging miR-338-3p]	Western Blot//qRT-PCR//MTT//PCR//IF	CircSMO742 and SMO were highly expressed in glioma tissues, while miR-338-3p expression was reduced. CircSMO742 promoted glioma growth by sponging miR-338-3p to regulate SMO expression. Our research revealed a new molecular mechanism of glioma growth and provide a fresh perspective on circRNAs in glioma progression.		Yes	Knocking down of circSMO742 suppressed glioma growing in vivo. 	31895689
SMIM45	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 esophageal cancer tissues	regulation[miR-342-3p/Bcl2L1 Axis]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	The results showed that the expression of LINC00634 in these tissues was higher than that in nontumor tissues and associated with tumor-node-metastasis (TNM) stage of patients. We also show that the knockdown of LINC00634 decreased cell viability and increased cell apoptosis levels in EC9706 and EC1 cells through the miR-342-3p/Bcl2L1 axis.		Yes	Knockdown of LINC00634 decreased cell viability and increased cell apoptosis levels in EC9706 and EC1 cells.	32583748
SMIM31	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue and cells	Interaction( miR-525-5p/ARHGAP11A axis )	qRT-PCR//Western Blot	 LINC01207 was up-regulated in NSCLC tissue and cells, which was mainly localized in the cytoplasm. LINC01207 could sponge and inhibit the expression of miR-525-5p in NSCLC cells, and inhibiting LINC01207 and miR-525-5p simultaneously could reverse the effect of miR-525-5p on the progression of NSCLC cells. Further study on downstream target genes showed that miR-525-5p could restrain the expression of ARHGAP11A, and then affect the progression of NSCLC. LINC01207 acting as a competing endogenous RNA (ceRNA) could regulate the expression of ARHGAP11A by competitively binding with miR-525-5p.		Yes	LINC01207 knockdown could inhibit the proliferation, migration and invasion of cancer cells and induce cell apoptosis. In addition, silencing LINC01207 could suppress tumor growth in vivo.	34487020
SMIM31	LncRNA	Homo sapiens	Pancreatic Neoplasms	pancreatic cancer tissues	Interaction[sponging miR-143-5p]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	LINC01207 and AGR2 were highly expressed while miR-143-5p was poorly expressed in pancreatic cancer. Functionally, LINC01207 can bind to miR-143-5p, and AGR2 was a target gene of miR-143-5p.		Yes	Moreover, silencing of LINC01207 and up-regulation of miR-143-5p promoted cell apoptosis and autophagy, corresponding to increased expression of autophagy- and apoptosis-related proteins, in addition to inhibited cell growth.	30991076
circPVT1	CircRNA	Homo sapiens	Small Cell Lung Carcinoma	 lung cells	Interaction( PVT1/AKT3)	Northern Blot//Western Blot//Transfection//Flow Cytometry//qRT-PCR	 In detail, circPVT1 activated a pro-proliferative and anti-apoptotic program when over-expressed in lung cells, and knockdown of chimPVT1 induced a decrease in cell growth and an increase of apoptosis in SCLC in vitro. Moreover, the investigated PVT1 transcripts underlined a functional connection between MYC and YAP1/POU2F3, suggesting that they contribute to the transcriptional landscape associated with MYC amplification. 		Yes	 In detail, circPVT1 activated a pro-proliferative and anti-apoptotic program when over-expressed in lung cells, and knockdown of chimPVT1 induced a decrease in cell growth and an increase of apoptosis in SCLC in vitro. Moreover, the investigated PVT1 transcripts underlined a functional connection between MYC and YAP1/POU2F3, suggesting that they contribute to the transcriptional landscape associated with MYC amplification. 	36562080
SMIM31	LncRNA	Homo sapiens	Prostatic Neoplasms		regulation[microRNA-1972 ,LIM ,SH3 protein 1]	qRT-PCR//Luciferase Report Assay//RIP//FISH	Quantitative real-time polymerase chain reaction revealed that LINC01207 and LASP1 were highly expressed in prostate cancer, while miR-1972 expression was lower.  The interaction among LINC01207, miR-1972, and LASP1 was confirmed by RNA-fluorescence in situ hybridization, RNA immunoprecipitation, and dual luciferase reporter assay, which verified that LINC01207 could bind to miR-1972 and downregulate miR-1972, and miR-1972 targeted LASP1 and negatively regulated its expression.		Yes	 Both in vitro and in vivo experiments found that silencing LINC01207 inhibited cell proliferation, migration, invasion and tumor formation and enhanced apoptosis in prostate cancer cells, suggesting that LINC01207 functioned as a tumor promoter in prostate cancer and that it may represent a novel therapeutic target.	32726517
SMIM31	LncRNA	Homo sapiens	Prostatic Neoplasms	 PC cells and tumor tissues 	Interaction(miR-1182)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	LINC01207 expression was significantly increased in PC cells and tumor tissues compared with in normal prostate cells (RWPE1) and normal prostate tissues, respectively. Mechanistic experiments showed that LINC01207 promoted carcinogenesis by sponging miR-1182 to regulate the protein levels of AKT3 in PC cell lines. 		Yes	Furthermore, LINC01207 silencing inhibited PC cell proliferation and colony formation and induced apoptosis. 	34992689
SMIM30	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	human AML	Interaction(ZFP36/mTORC2 axis)	CCK8//qRT-PCR	LINC00998 was significantly decreased in human AML, which was linked to relapse and poor prognosis.  LINC00998 was mainly located in the cytoplasm, in which interacted with ZFP36 ring finger protein (ZFP36), a mRNA destabilizing factor, resulting in increased decay of mammalian target of rapamycin complex 2 (mTORC2), a well-known proto-oncogene in AML. 		Yes	 Stable overexpression of LINC00998 inhibited AML cell viability, colony ability, DNA synthesis rate and increased apoptosis. Importantly, LINC00998 shortened in vivo AML cell survival in xenograft tumor model.	34699314
SMIM30	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tissues	regulation[ CBX3-mediated c-Met/Akt/mTOR axis]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay//IF	Through screening using TCGA database, we found that LINC00998 was downregulated in glioblastoma tissues and that low expression of LINC00998 was associated with poor prognosis. Mechanistically, RNA pull-down and mass spectrometry results showed an interaction between LINC00998 and CBX3. IP assays demonstrated that LINC00998 could stabilize CBX3 and prevent its ubiquitination degradation. GSEA indicated that LINC00998 could regulate the c-Met/Akt/mTOR signaling pathway, which was further confirmed by a rescue assay using siRNA-mediated knockdown of CBX3 and the Akt inhibitor MK2206. In addition, dual-luciferase assays showed that miR-34c-5p could directly bind to LINC00998 and downregulate its expression. 		Yes	 Overexpression of LINC00998 inhibited glioma cell proliferation in vitro and in vivo and blocked the G1/S cell cycle transition, which exerted a tumor-suppressive effect on glioma progression.	33268783
hsa_circ_0000615	CircRNA	Homo sapiens	Nasopharyngeal Neoplasms	NPC tissues and cells	regulation[miR-338-3p/FGF2 axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 We detected increased levels of circ_0000615 and FGF2, along with a decreased level of miR-338-3p in NPC tissues and cells.  In conclusion, our findings demonstrated that circ_0000615 knockdown suppressed the growth of NPC cells via modulating miR-338-3p/FGF2 axis, providing a theoretical basis for the treatment of NPC.		Yes	Circ_0000615 knockdown suppressed the proliferation, migration, invasion, and EMT of NPC cells. 	32453598
SMIM27	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer cell 	Interaction(VDR/Wnt/β-catenin signaling )	qRT-PCR//RIP//IP//Colony Formation Assay//ChIP	 Analysis of tumor cell transcriptomes indicated TOPORS-AS1's influence on the Wnt/β-catenin signaling. Additional experiments revealed that TOPORS-AS1 increased the phosphorylation of β-catenin and suppressed the expression of CTNNB1, disrupting the Wnt/β-catenin pathway. Our experiments further discovered that vitamin D receptor (VDR) upregulated TOPORS-AS1 expression and that inhibition of β-catenin by TOPORS-AS1 required a RNA binding protein, hnRNPA2B1 (heterogeneous nuclear ribonucleoprotein A2B1). 	 Patients with high TOPORS-AS1 expression had favorable overall survival compared to low expression. 	Yes	In vitro experiments demonstrated that overexpressing TOPORS-AS1 in ovarian cancer cells suppressed cell proliferation and inhibited aggressive cell behaviors, including migration, invasion, and colony formation. 	33820921
circVAPA	CircRNA	Homo sapiens	Small Cell Lung Carcinoma	 SCLC cell lines, clinical tissues, and serum from SCLC patients 	Interaction(miR-377-3p and miR-494-3p/IGF1R/AKT axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//FISH//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay	We revealed that circVAPA, derived from exons 2-4 of the vesicle-associated membrane protein-associated protein A (VAPA) gene, exhibited higher expression levels in SCLC cell lines, clinical tissues, and serum from SCLC patients than the controls, and facilitated SCLC progression in vitro and in vivo. Mechanistically, circVAPA activated the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway by modulating the miR-377-3p and miR-494-3p/insulin-like growth factor 1 receptor (IGF1R) axis to accelerate SCLC progression. 		Yes	We revealed that circVAPA, derived from exons 2-4 of the vesicle-associated membrane protein-associated protein A (VAPA) gene, exhibited higher expression levels in SCLC cell lines, clinical tissues, and serum from SCLC patients than the controls, and facilitated SCLC progression in vitro and in vivo. Furthermore, circVAPA depletion markedly enhanced the inhibitory effects of BMS-536924, an IGF1R kinase inhibitor in cellular and xenograft mouse models.	35668527
SMILR	LncRNA	Homo sapiens	Pulmonary Arterial Hypertension	blood 	regulation[RhoA/ROCK signaling ]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//MTT//Luciferase Report Assay	SMILR and RhoA expression were upregulated, while miR-141 expression was downregulated in PAH patients.Knockdown of SMILR effectively elevated miR-141 expression and in turn inhibited the RhoA/ROCK pathway to regulate vascular remodeling and reduce blood pressure in PAH.		Yes	Knockdown of SMILR suppressed PASMC proliferation and migration induced by hypoxia.	32559140
SCHLAP1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell	Interaction( AUF1/PD-L1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//EdU Staining//Transwell Assay	In conclusion, our data for the first time uncover that SChLAP1 functions an oncogene in NSCLC by promoting cancer cell immune evasion via regulating the AUF1/PDL1 axis, targeting of SChLAP1 may be a potential approach to improve the efficacy of immunotherapy in NSCLC patients.		Yes	 In this study, we found that depletion of SChLAP1 significantly inhibited NSCLC cell proliferation, migration and invasion in vitro, and retarded tumour growth and lung metastasis in vivo. SChLAP1 facilitated NSCLC cell immune evasion against CD8+ T cells through PD-1/PD-L1 immune checkpoint.	33904361
SCARNA2	LncRNA	Homo sapiens	Skin Neoplasms	cSCC tissues,cell lines 	regulation[miR-342-3p expression]	CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	We found that SCARNA2 expression is up-regulated in cSCC cell lines and SCARNA2 expression is higher in cSCC tissues than in adjacent non-tumor specimens. We found that elevated expression of SCARNA2 promotes cell growth, cell cycle and invasion via regulating miR-342-3p expression in SCC13 cells.		Yes	Ectopic expression of SCARNA2 promoted cell growth, cell cycle and invasion in SCC13 cells. 	32558970
circMCTP2	CircRNA	Homo sapiens	bladder carcinoma	 BC tissues and cell lines	Interaction(miR-498/MDM2)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In our study, circMCTP2 expression was strongly increased in BC tissues and cell lines. In BC cells, circMCTP2 deficiency enhanced the translation of E-cadherin, while diminishing the translation of N-cadherin, Vimentin, and Snail. Moreover, circMCTP2 acted as a sponge of miR-498 to regulate murine double minute-2 (MDM2) expression. In BC tissues, a negative correlation was observed between the expression levels of circMCTP2 and miR-498. Additionally, either miR-498 silencing or MDM2 over-expression augmented the carcinogenic action of circMCTP2 on BC.	 High expression of circMCTP2 predicted a poor prognosis of BC patients. 	Yes	CircMCTP2 deficiency impaired the cell growth, migration as well as invasive ability of BC cell lines (J82 and T24). In vivo, circMCTP2 deficiency cut the tumor growth rates and the tumor weight.	35475453
hsa_circ_0000592	CircRNA	Homo sapiens	stomach carcinoma	cell line 	Expression[highly expressed]	qRT-PCR//circRNA-seq//FISH	 When compared with GES-1-N cells, hsa_circ_0000592 was obviously Expression[up-expression]-regulated in GES-1-T cells, as well as in other gastric cancer cell lines.		Yes	The silencing of hsa_circ_0000592 mRNA led to a decrease in cell proliferation, cell cycle arrest at the G0/G1 phase, an increased rate of apoptosis, and a reduction in cell migration. 	31189743
RP9P	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-133a-3p/FOXQ1 Axis)	CCK8//Luciferase Report Assay//IHC//Western Blot	 RP9P was overexpressed in CRC compared to normal control tissues and cells. RP9P directly interacted with miR-133a-3p, and miR-133a-3p downregulation abrogated the tumor-suppressing effect of RP9P knockdown. miR-133a-3p directly targeted FOXQ, which was positively regulated by RP9P. RP9P knockdown decreased FOXQ1 expression levels in CRC cells by directly targeting miR-133a-3p via a sponge mechanism. 		Yes	Knockdown of RP9P inhibited CRC cell viability.  In addition, in vivo experiments in a xenograft model revealed that downregulated RP9P expression inhibited CRC cell tumorigenesis.	35600345
circPRRX1	CircRNA	Homo sapiens	stomach carcinoma	tissues and cells	Interaction(MicroRNA-665/YWHAZ Axis)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Compared with normal tissues and cells, circ-PRRX1 and YWHAZ levels were upregulated, and miR-665 was downregulated in GC tissues and cells. Mechanistically, circ-PRRX1 was confirmed as a sponge of miR-665 to regulate YWHAZ expression. 		Yes	 Functionally, circ-PRRX1 knockdown inhibited the viability, migration, and invasion and promoted apoptosis in GC cells, whereas anti-miR-665 abolished these effects.  Xenograft mouse model suggested that circ-PRRX1 knockdown reduced GC cells growth in vivo.	33201331
circMTO1	CircRNA	Homo sapiens	stomach carcinoma	GC tissues and cells	regulation[miR-3200-5p/PEBP1 axis]	Western Blot//CCK8//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In this study, our experimental results delineated that circMTO1 exhibited much lower expression level in GC tissues and cells. In a word, this study was the first to indagate the underlying mechanism of circMTO1 in GC and confirmed circMTO1 exerted its anti-cancer effects by miR-3200-5p/PEBP1 axis, implying that circMTO1 may become a new promising therapeutic target for GC patients.		Yes	 CircMTO1 overexpression slowed down GC progression via inhibiting cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process. 	32194149
circFOXO3	CircRNA	Homo sapiens	stomach carcinoma		interaction[USP44, miR-143-3p]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	All the data indicate that circFOXO3 promotes GC cell proliferation and migration by upregulating USP44 expression via targeting of miR-143-3p.		Yes	CircFOXO3 enhanced GC cell proliferation and migration in vitro and promoted tumor growth of GC cells in vivo.	32445925
RP5-916L7.2	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues	Interaction[targeting miR-328-5p and miR-939-5p]	qPCR//CCK8//FISH//Luciferase Report Assay//Colony Formation Assay	lncRNA RP5-916L7.2 was increased in tumor tissue compared with paired adjacent tissue. lncRNA RP5-916L7.2 was up regulated in tumor tissue and positively correlated with tumor stage, and promoted cells proliferation while inhibited cells apoptosis by targeting miR-328-5p and miR-939-5p in TSCC.	 lncRNA RP5-916L7.2 was increased in tumor tissue compared with paired adjacent tissue, and correlated with higher T stage, N stage as well as TNM stage in TSCC patients. 	Yes	 In vitro experiments revealed that lncRNA RP5-916L7.2 promoted cells proliferation and repressed cells apoptosis in Tca-8113 cells. 	30825424
circPTK2	CircRNA	Homo sapiens	stomach carcinoma	GC tissues and cells	regulation[miR-139-3p]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	High expression of circPTK2 was presented in GC tissues and cells. CircPTK2 promotes GC development by sponging miR-139-3p, which may function as an effective gene target for managing GC.		Yes	 The circPTK2 knockdown notably suppressed cell proliferation and promoted cell apoptosis in GC.	32504353
hsa-circ-0007766	CircRNA	Homo sapiens	stomach carcinoma	GC tissues and GC cell lines	regulation[miR-1233-3p/ GDF15 axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//FISH	 Interestingly, we found that hsa-circ-0007766 was highly expressed in human GC tissues and GC cell lines.This study unveils a mechanism by which hsa-circ-0007766 regulates GDF15 via hsa-circ-0007766/miR-1233-3p/GDF15 axis, which may provide new insight for GC therapeutic strategies.		Yes	Knock-down of hsa-circ-0007766 inhibited cell proliferation, migration, invasion, and down-regulated the expression of GDF15.	32669960
RP5-881L22.5	LncRNA	Homo sapiens	Colorectal Neoplasms	 4 pairs of colorectal cancer patients	Expression(highly expressed)	qRT-PCR//Transwell Assay	 When quantitative reverse transcription PCR was performed on tumor tissues from 4 pairs of colorectal cancer patients, the results showed that RP5-881L22.5 was highly expressed. 		Yes	Subsequently, knocking down the expression of RP5-881L22.5, the invasiveness of colorectal cancer cell lines was reduced, and the apoptosis rate was increased.	36438707
RP5-1120P11.3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[miR-196b-5p-WIPF2 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	To evaluate the role of lncRNAs in HCC, we examined six lncRNAs and found that only RP5-1120P11.3 was significantly increased in the HCC cell line HepG-2 compared with the human immortalized liver cell line HL-7702 (Fig. 1A). Next, we assessed the expression level of RP5-1120P11.3 in 12 paired HCC tissues and adjacent noncarcinoma control tissues from HCC patients, and our results showed that RP5-1120P11.3 was dramatically increased in tumor tissues in comparison with adjacent normal tissues (Fig. 1B). These findings suggested that the RP5-1120P11.3-miR-196b-5p-WIPF2 axis is a potential target for treatment of HCC.		Yes	Further characterization of RP5-1120P11.3 revealed that it promoted proliferation and invasion of HCC cells while inhibiting apoptosis. 	31299165
hsa_circ_0000979	CircRNA	Homo sapiens	stomach carcinoma	 GC samples	Interaction(miR-136/SP1 )	qRT-PCR	We found that circ-0000979 is significantly upregulated in GC samples.  CircRNA interactome predicted miR-136 as circ-0000979 targeting miRNA, while starbase prediction result showed that miR-136 targeted the 3'UTR region of SP1 mRNA. Taken together, our results demonstrated that circ-0000979, as a carcinogenic circRNA, promotes the progression of GC by regulating the miR-136/SP1 pathway.		Yes	 Functionally, silencing circ-0000979 leads to a significant reduction in GC cell proliferation and migration. In vivo assays showed that circ-0000979 knockdown markedly reduced GC tumor growth.	36629013
RP4-773N10.4	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP4-758J18.10	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP4-694A7.2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines	Regulation(PSAT1)	qRT-PCR//FISH//Colony Formation Assay//Transwell Assay	RP4-694A7.2 levels were higher in HCC tissues than in normal liver tissues in published GSE datasets and were elevated in HCC cell lines.  Finally, phosphoserine aminotransferase 1 (PSAT1) was found to be regulated by RP4-694A7.2 to modulate growth and metastasis in HCC cells using a rescue assay.		Yes	Cell function assays revealed that RP4-694A7.2 promotes cell proliferation, invasion, and migration. 	34405023
RP1-86C11.7	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction(hsa-miR-144-3p/TFRC signaling)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay	We also found that the lncRNA RP1-86C11.7 sponges hsa-miR-144-3p to suppress its protective role in glioma. By contrast, silencing RP1-86C11.7 upregulated the hsa-miR-144-3p level, resulting in decreased TFRC expression and repressed glioma progression. echanistically, our data indicated that RP1-86C11.7 exacerbates the malignant behavior of glioma through the hsa-miR-144-3p/TFRC axis.		Yes	RP1-86C11.7 overexpression in glioma cells elevated TFRC expression, increased the intracellular free iron level, and deteriorated oncogenicity, with a significant reduction in hsa-miR-144-3p. 	34571345
RP1-85F18.6	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Expression[highly expressed]	qRT-PCR	lncRNA, RP1?85F18.6, was upregulated in colorectal cancer (CRC) tissues and cell lines.		Yes	Knockdown of lncRNA RP1?85F18.6 served a key role in tumor inhibition, reduced cell proliferation and invasion, disrupted the cell cycle, and increased apoptosis and pyroptosis of CRC cells.	30226619
RP11-89K21.1	LncRNA	Homo sapiens	Peste-des-Petits-Ruminants	 LUAD tissues and cell lines	Interaction(miR-146a/b-5p/RhoA/ROCK Pathway)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis	The authors identified that RP11-89K21.1 was highly expressed in LUAD tissues and cell lines.Mechanistically, RP11-89K21.1 could directly bind miR-146a-5p and miR-146b-5p and decrease their expression to upregulate RHPN2, and subsequently activated RhoA/ROCK pathway.	Moreover, upregulated RP11-89K21.1 was strongly associated with unfavorable overall survival of patients with LUAD.	Yes	Knockdown of RP11-89K21.1 significantly suppressed proliferation and sensitized cell to gefitinib. 	33877886
RP11-867G2.8	LncRNA	Homo sapiens	Chordoma	chordoma tissues and cells	Interaction(EIF4B and PABPC1/FUT4)	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//MTT//Microarray//Colony Formation Assay	We found that RP11-867G2.8 is highly expressed in chordoma tissues and cells, and RP11-867G2.8 overexpression promotes the malignant biological behavior of chordoma cells. RP11-867G2.8 overexpression alters the expression pattern of genes modulating signaling pathway. FUT4 is accumulated in chordoma tissues, and RP11-867G2.8 is antisense RNA of FUT4. RP11-867G2.8 can bind to FUT4 mRNA, increasing FUT4 mRNA stability and facilitating translation of FUT4. RP11-867G2.8 binds to EIF4B and PABPC1, which increases the translation of FUT4. Further studies found that FUT4 silence counteracts the effect of RP11-867G2.8 in vivo and in vitro. 		Yes	We found that RP11-867G2.8 is highly expressed in chordoma tissues and cells, and RP11-867G2.8 overexpression promotes the malignant biological behavior of chordoma cells. RP11-867G2.8 overexpression alters the expression pattern of genes modulating signaling pathway.	35411246
RP11-805J14.5	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cell and tissues	Interaction(miR‑34b‑3p and miR‑139‑5p/CCND2 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	 RP11‑805J14.5 was highly expressed in LUAD and associated with poor survival of LUAD patients.  Our study demonstrated that the regulation of RP11‑805J14.5 on LUAD was mediated by CCND2 whose expression was regulated by sponging miR‑34b‑3p and miR‑139‑5p. 	 RP11‑805J14.5 was highly expressed in LUAD and associated with poor survival of LUAD patients. 	Yes	 Knockdown of RP11‑805J14.5 suppressed LUAD cell growth, invasion, migration and tumor growth, indicating that RP11‑805J14.5 is an important regulator of LUAD. 	35866595
circGSPT1	CircRNA	Homo sapiens	stomach carcinoma	GC tissues and cells	Interaction(GSPT1-238aa)	qRT-PCR	In our study, circRNA sequencing was carried out using five pathologically diagnosed gastric carcinoma (GC) samples and their paired adjacent normal tissues, we characterized the circRNA GSPT1 (circGSPT1), which is expressed at low levels in GC. Our study reveals that GSPT1-238aa, a novel protein encoded by circGSPT1, halts GC tumorigenesis. 		Yes	 CircGSPT1 and GSPT1-238aa halted the proliferation, migration, and invasion in GC cells in vitro. 	35839920
circAPC	CircRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues	Regulation[Wnt/β-catenin signaling]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Microarray//ChIP	We identified a novel and highly stable circRNA originating from the back-splicing of APC exon 7 to exon 14, circ-APC (hsa_circ_0127621), which was Expression[down-expression]regulated in DLBCL tissues, cell lines and plasma.Cytoplasmic circ-APC functioned as a sponge for miR-888, thus post-transcriptionally Expression[Expression[up-expression]-expression]regulating APC by alleviating the repressive effects of miR-888 on this gene. Further, nuclear circ-APC bound to the APC promoter and recruited the DNA demethylase TET1, thereby transcriptionally Expression[Expression[up-expression]-expression]regulating APC. Expression[Expression[up-expression]-expression]on its Expression[Expression[up-expression]-expression]regulation, APC dampened the canonical Wnt/β-catenin signaling pathway by reducing the accumulation of β-catenin in the nucleus, thereby retarding DLBCL growth.		Yes	 In gain-of-function experiments, ectopic expression of circ-APC inhibited DLBCL cell proliferation in vitro and tumor growth in vivo. 	31631067
RP11-757G1.5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	regulation[RP11-757G1.5/miR-139-5p/YAP1 regulatory axis]	RNA Pull-Down//ISH//Wound Healing Assay//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We discovered a novel oncogenic lncRNA RP11-757G1.5, that was overexpressed in CRC tissues, especially in aggressive cases.Altogether, these results reveal a novel RP11-757G1.5/miR-139-5p/YAP1 regulatory axis that participates in CRC carcinogenesis and progression.	Moreover, up-regulation of RP11-757G1.5 strongly correlated with poor clinical outcomes of patients with CRC.	Yes	Functional analyses revealed that RP11-757G1.5 promoted cell proliferation in vitro and in vivo. Furthermore, RP11-757G1.5 stimulated cell migration and invasion in vitro and in vivo.	33023613
circABCB10	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	Regulation[miR-1252/FOXR2 axis]	CCK8//qRT-PCR//Transwell Assay	 The results showed that the expression of circABCB10 in NSCLC cell lines was increased. Fluorescein reporting experiments confirmed that circABCB10 expression increased FOXR2 levels by sponging miR-1252, and in vivo experiments found that knockExpression[down-expression] of circABCB10 decreased tumor growth. 		Yes	Expression[down-expression]regulation of circABCB10 sExpression[Expression[up-expression]-expression]pressed NSCLC cell proliferation and migration by promoting microRNA miR-1252 expression and sExpression[Expression[up-expression]-expression]pressing Forkhead box 2 (FOXR2).	30417418
RPL34-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tumor tissues and the CRC cell lines	Regulation( HSP70 and PI3K/AKT signaling pathway)	In Vivo Experiment//cell invasion assay//Western Blot//qRT-PCR//RNA-seq//Cell Apoptosis Assay//Cell Proliferation Assay	 From the results, we found that RP11-462C24.1 was significantly decreased in CRC tumor tissues and the CRC cell lines, which were most significant in SW480 and HT-29 cell lines;  additionally, 70 kD heat shock proteins (HSP70) has been identified as one of the most significantly deferentially expressed genes by RNA-seq, and we further confirmed that RP11-462C24.1 may affect the growth and metathesis of CRC cells via regulating HSP70 and PI3K/AKT signaling pathway. 		Yes	moreover, transient overexpression of RP11-462C24.1 suppressed the growth and migration while promoted apoptosis of SW480 and HT-29 cells, while knockdown of RP11-462C24.1 has shown the opposite effects; RP11-462C24.1 may also inhibit the growth of CRC tumors in xenograft mice models; 	32946066
RPL34-DT	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	" PTC
tissues,cell lines"	Interaction[miR-3663-3p/RGS4 ]	Western Blot//CCK8//RIP//Luciferase Report Assay//Transwell Assay	"We used qRT‐PCR analysis to examine
the RPL34‐AS1 expression in 77 PTC and adjacent normal tissues, and
RPL34‐AS1 expression was significantly downregulated in the PTC
tissues compared with that in normal tissues (Figure 2b). The RPL34‐AS1
expression was also verified in both normal thyroid cells (Nthy‐ori 3‐1)
and PTC cell lines (BCPAP, KTC‐1, and K1 cells), and the RPL34‐AS1
expression in PTC cells was significantly lower than that in normal
thyroid cells; among these cell lines, the decrease of K1 in these PTC cells
is most obvious (Figure 2c). "		Yes	We found that overexpression of RPL34-AS1 could inhibit proliferation and invasion while promoting apoptosis in PTC cell lines. 	31587286
circABCC2	CircRNA	Homo sapiens	Liver Neoplasms		Interaction[MiR-665]	Western Blot//CCK8//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	qRT-PCR verified that circABCC2 was overexpressed in HCC. Luciferase assays and RIP showed that circABCC2 and ABCC2 could directly bind to miR-665 and that circABCC2 could regulate ABCC2 expression by sponging miR-665. 		Yes	 Inhibition of circABCC2 suppressed HCC cell proliferation and invasion, but promoted apoptosis. 	31417632
hsa_circ_0091570	CircRNA	Homo sapiens	Liver Neoplasms	HCC tissues,cell lines	Interaction[sponging hsa-miR-1307]	CCK8//qRT-PCR//Wound Healing Assay//EdU Staining	 RNA immunoprecipitation assay verified the interaction of hsa_circ_0091570 and miR-1307. The miR-1307 inhibitor inhibited the function induced by hsa_circ_0091570 siRNA. 	 The decreased expression of hsa_circ_0091570 was associated with the pathological staging of HCC patients.	Yes	Furthermore, inhibition of hsa_circ_0091570 promoted cell proliferation and migration, blocked cell apoptosis in HCC cell lines, and promoted tumor growth in the mouse xenograft model. 	31207319
hsa_circ_0007841	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell line	Interaction(miR-199a-5p/SphK2 axis)	In Vivo Experiment//IHC//Western Blot//Transfection//Migration Assay//qRT-PCR//RIP//IF//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	Experimental studies have shown that the higher expression of circ_0007841 in NSCLC tissues, and circ_0007841 strengthen cell viability, cell proliferation and cell adhesion. In addition, miR-199a-5p exerts an inhibitory effect in NSCLC cells by inhibiting SphK2. And Sphk2 regulates cell proliferation and adhesion. 		Yes	Experimental studies have shown that the higher expression of circ_0007841 in NSCLC tissues, and circ_0007841 strengthen cell viability, cell proliferation and cell adhesion.  In addition, in-vivo silencing of circ_0007841 was found to inhibit the growth of NSCLC tumors. 	36066393
circHMGA2	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-331-3p/HMGA2 axes)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	CircHMGA2 was overexpressed in NSCLC, and high circHMGA2 level might be related to NSCLC metastasis and poor prognosis. Through interacting with miR-331-3p, circHMGA2 could regulate the expression of HMGA2. In addition, circHMGA2/miR-331-3p and miR-331-3p/HMGA2 axes were affirmed in NSCLC regulation. 	CircHMGA2 was overexpressed in NSCLC, and high circHMGA2 level might be related to NSCLC metastasis and poor prognosis. 	Yes	 In-vitro assays suggested that NSCLC cell growth, metastasis and glycolysis were retarded by downregulation of circHMGA2. Upregulation of HMGA2 was shown to return the anticancer response of circHMGA2 knockdown in NSCLC cells.  In-vivo analysis indicated that circHMGA2 inhibition also reduced tumorigenesis and glycolysis of NSCLC via the miR-331-3p/HMGA2 axis. 	36066399
circABCB10	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue 	regulation[miR-584-5p/E2F5 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	We analyzed the human circRNA expression profile in NSCLC tissues. CircABCB10 was identified as a circRNA that increased in NSCLC tissues.  CircABCB10 promoted the progression of NSCLC by modulating the miR-584-5p/E2F5 axis.	 CircABCB10 was noticeably raised in NSCLC, and high circABCB10 expression was related to low survival in NSCLC patients.	Yes	Silencing of circABCB10 suppressed non-small cell lung cancer cell migration, cell proliferation, and invasion.	32420810
circCDYL	CircRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expressionhighly expressed]	Microarray	Circ-CDYL (chromodomain Y like) is specifically Expression[Expression[up-expression]-expression]-regulated in the early stages of HCC and therefore contributes to the properties of epithelial cell adhesion molecule (EPCAM)-positive liver tumor-initiating cells. irc-CDYL interacts with mRNAs encoding hepatoma-derived growth factor (HDGF) and hypoxia-inducible factor asparagine hydroxylase (HIF1AN) by acting as the sponge of miR-892a and miR-328-3p, respectively. Subsequently, activation of the phosphoinositide 3-kinase (PI3K)-AKT serine/threonine kinase-mechanistic target of rapamycin kinase complex 1/β-catenin and NOTCH2 pathways, which promote the expression of the effect proteins, baculoviral IAP repeat containing 5 (BIRC5 or SURVIVIN) and MYC proto-oncogene, is influenced by circ-CDYL.		Yes	 A treatment incorporating circ-CDYL interference and traditional enzyme inhibitors targeting PI3K and HIF1AN demonstrated highly effective inhibition of stem-like characteristics and tumor growth in HCC.	31148183
RPL13AP20	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[ miRNA-335]	qRT-PCR//Luciferase Report Assay	 HANR was significantly upregulated in glioma tissues and cell lines. In addition, HANR aggravates the progression of glioma by negatively regulating miRNA-335.	Glioma patients with a high expression level of HANR presented remarkably higher rates of lymphatic metastasis and distant metastasis, as well as worse prognosis. 	Yes	The silence of HANR remarkably attenuated the proliferative, migratory, and invasive capacities of U251 and SHG44 cells.	32016979
hsa_circ_0001578	CircRNA	Homo sapiens	Diabetes, Gestational	 placental villous tissues	Expression(lower expressed)	Western Blot//Transfection//Wound Healing Assay//CCK8//ELISA//Colony Formation Assay//Transwell Assay	In particular, using qRT-PCR, we verified previous RNA-seq results showing that circ_0001578 is significantly downregulated in the placental villous tissues of pregnant women with GMD. 		Yes	 Furthermore, in HTR-8/SVneo trophoblasts, the downregulation of circ_0001578 inhibited proliferation and migration and induced apoptosis. These changes may induce chronic inflammation in the placenta. 	36263320
hsa_circ_0005243	CircRNA	Homo sapiens	Diabetes, Gestational	placenta and plasma 	regulation[ β-catenin and NF-κB pathways]	qRT-PCR//RNA-seq	 Expression of hsa_circ_0005243 was significantly reduced in both the placenta and plasma of GDM patients.Downregulation of hsa_circ_0005243 may be associated with the pathogenesis of GDM via the regulation of β-catenin and NF-κB signal pathways, suggesting a new potential therapeutic target for GDM.		Yes	Knockdown of hsa_circ_0005243 in trophoblast cells significantly suppressed cell proliferation and migration ability. 	32434530
circPCBP2	CircRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	human DLBCL specimens and cultured DLBCL cells	Interaction(miR-33a/b/PD-L1)	In Vivo Experiment//Western Blot//Transfection//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Apoptosis Assay	circPCBP2 was upregulated in human DLBCL specimens and cultured DLBCL cells while miR-33a/b was reduced. circPCBP2 directly bound with miR-33a/b while miR-33a/b targeted PD-L1 3'-UTR. circPCBP2 disinhibited PD-L1 signaling via sponging miR-33a/b. miR-33a/b inhibitor and activating PD-L1 reversed the effects of circPCBP2 knockdown and miR-33a/b mimics, respectively. 		Yes	Knockdown of circPCBP2 or miR-33a/b overexpression inhibited the stemness of DLBCL cells and promoted cancer cell apoptosis upon CHOP treatment.  circPBCP2 knockdown restrained DLBCL growth in vivo and potentiated the anti-tumor effects of CHOP. 	35579082
circZNF609	CircRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	OCI-LY19 cells	Interaction(miR-153)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay	Down-regulation of circZNF609 inhibits the proliferation of diffuse large B-cell lymphoma OCI-LY19 cells and induces apoptosis by targeting miR-153.		Yes	Down-regulation of circZNF609 inhibits the proliferation of diffuse large B-cell lymphoma OCI-LY19 cells and induces apoptosis by targeting miR-153.	35316873
hsa_circ_0000877	CircRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cell lines	Interaction(miR-370-3p/MAP4K4/Hippo pathway)	In Vivo Experiment//Transfection//Invasion Assay//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//IHC//EdU Staining	The expression of circ_0000877 was markedly elevated in DLBCL tissues and cell lines. Then, miR-370-3p directly interacted with circ_0000877 and MAP4K4. Circ_0000877 promoted MAP4K4 level by sponging miR-370-3p. MAP4K4 depletion inhibited the activation of Hippo pathway. Finally, circ_0000877 silencing significantly prevented the growth of DLBCL cells in vivo . Our findings revealed that circ_0000877 could regulate the malignant evolution of DLBCL by miR-370-3p/MAP4K4/Hippo pathway.		Yes	The decreased expression of circ_0000877 significantly inhibited proliferation, migration, and invasion of DLBCL cell lines. In addition, silencing circ_0000877 promoted cell apoptosis and induced cell cycle arrest in G0/G1 phase. 	36066383
RPL13AP20	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miRNA-140-5p]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	HANR expression was significantly up-regulated in NSCLC tissues and cell lines.LncRNA HANR accelerates the proliferative, migratory and invasive abilities of NSCLC via negatively mediating miRNA-140-5p.	HANR expression was positively correlated with lymphatic metastasis and distant metastasis of NSCLC patients, whereas it was negatively correlated with the overall survival of NSCLC patients. 	Yes	Knockdown of HANR markedly suppressed the proliferative, migratory and invasive abilities of NSCLC cells. 	32016972
circOTUD7A	CircRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	50 pairs of DLBCL tissues (DLBCL) and adjacent normal  tissues (Normal) 	Interaction(miR-431-5p/FOXP1 axis)	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_OTUD7A was highly expressed in DLBCL, and its knockdown could inhibit DLBCL cell proliferation and metastasis, while promote cell cycle arrest and apoptosis. Similarly, FOXP1 also was upregulated in DLBCL, and its silencing could restrain the progression of DLBCL cells. Further experiments revealed that circ_OTUD7A could sponge miR-431-5p and miR-431-5p could target FOXP1. 		Yes	Circ_OTUD7A was highly expressed in DLBCL, and its knockdown could inhibit DLBCL cell proliferation and metastasis, while promote cell cycle arrest and apoptosis. Similarly, FOXP1 also was upregulated in DLBCL, and its silencing could restrain the progression of DLBCL cells. 	33830472
circCFL1	CircRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse		regulation[CircCFL1/MiR-107 Axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Results showed that the circRNA CircCFL1 could regulate the expression of HMGB1 through miR-107 to promote the proliferation and migration of DLBCL.		Yes	 After CircCFL1 was overexpressed, cell migration and proliferation were enhanced. The tumor volume and weight in the lentivirus CircCFL1 group were higher than those in the lentivirus NC group.	33061624
RP11-77H9.2	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP11-732M18.3	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[14-3-3β/α]	Flow Cytometry//qRT-PCR//FISH	Among these aberrantly expressed lncRNAs, lncRNA RP11-732M18.3 was over-expressed in glioma (2.53-fold change, p < .05) and consistently over-expressed in small group glioma tissues (data not show).Here, we describe the newly discovered noncoding RNA RP11-732M18.3, which is highly overexpressed in glioma cells and interacts with 14-3-3β/α to promote glioma growth, acting as an oncogene.Mechanistically, the interaction of lncRNA RP11-732M18.3 with 14-3-3β/α increases the degradation of the p21 protein. lncRNA RP11-732M18.3 promoted the recruitment of ubiquitin-conjugating enzyme E2 E1 to 14-3-3β/α and the binding of 14-3-3β/α with ubiquitin-conjugating enzyme E2 E1 (UBE2E1) promoted the degradation of p21.		Yes	 Overexpression of lncRNA RP11-732 M18.3 was associated with the proliferation of glioma cells and tumor growth in vitro and in vivo.	31202814
RPL34-DT	LncRNA	Homo sapiens	Glioma	 glioma tissues 	Regulation(ERK/AKT signaling)	Western Blot//Transfection//Tube Formation Assay//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay	RPL34-AS1 was upregulated in glioma tissues and was correlated with tumor grade.RPL34-AS1 expression was also higher in glioma cells than in normal astrocytes. RPL34-AS1 expression was also higher in glioma cells than in normal astrocytes. Knockdown of RPL34-AS1 blocked glioma cell proliferation by inhibiting angiogenesis. This effect occurred through decreased ERK/AKT signaling. 	RPL34-AS1 was upregulated in glioma tissues and was correlated with tumor grade.	Yes	Knockdown of RPL34-AS1 blocked glioma cell proliferation by inhibiting angiogenesis. 	34539892
RP11-2B6.2	LncRNA	Homo sapiens	Lupus Nephritis	kidney tissues	Interaction[IFN-I pathway]	qRT-PCR//ELISA//Western Blot	Elevated lncRNA RP11-2B6.2 was observed in kidney biopsies from LN patients and positively correlated with disease activity and IFN scores. Knockdown of LncRNA RP11-2B6.2 inhibited the phosphorylation of JAK1, TYK2, and STAT1 in IFN-I pathway, while promoted the chromatin accessibility and the transcription of SOCS1. 		Yes	Knockdown of lncRNA RP11-2B6.2 in renal cells inhibited the expression of IFN stimulated genes (ISGs), while overexpression of lncRNA RP11-2B6.2 enhanced ISG expression. 	31130957
RP11-390F4.3	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tissues	Interaction(miR-148a/ROCK1 )	Western Blot//qPCR//Luciferase Report Assay//Migration Assay	RP11-390F4.3 and ROCK1 were both upregulated in glioblastoma, while miR-148a was downregulated in glioblastoma.In glioblastoma, RP11-390F4.3 was positively correlated with ROCK1 but negatively correlated with miR-148a. 		Yes	Cell invasion and migration analysis showed that overexpression of RP11-390F4.3 and ROCK1 resulted in increased, and overexpression of miR-148a resulted in deceased invasion and migration rates of glioblastoma cells.	34050115
RP11-386G11.10	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction(ZBTB7A-RP11-386G11.10-HNRNPU positive feedback loop )	qRT-PCR	 RP11-386G11.10 was overexpressed in HCC and positively correlated with tumour size, TNM stage, and poor prognosis in HCC patients.  Mechanistically, RP11-386G11.10 acted as a competing endogenous RNA (ceRNA) for miR-345-3p to regulate the expression of HNRNPU and its downstream lipogenic enzymes, leading to lipid accumulation in HCC cells and promoting their growth and metastasis. In addition, we identified ZBTB7A as a transcription factor of RP11-386G11.10. Moreover, HNRNPU promoted the expression of ZBTB7A in HCC cells, thereby increasing the transcriptional activity of RP11-386G11.10, and forming a positive feedback loop, ultimately leading continuous lipid accumulation, growth and metastasis in HCC cells.	 RP11-386G11.10 was overexpressed in HCC and positively correlated with tumour size, TNM stage, and poor prognosis in HCC patients. 	Yes	 RP11-386G11.10 promoted the proliferation and metastasis of HCC cells in vitro and in vivo. 	35798238
RP11-363E7.4	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	interaction[p53, Bax/Bcl-2, β-catenin pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	The results showed that lncRNA RP11-363E7.4 was significantly downregulated in GC cell lines and 82 paired tissues. Western blot assay revealed that lncRNA RP11-363E7.4 functioned via the p53, Bax/Bcl-2, β-catenin pathway.	 The correlation between expression and clinicopathological features indicated that low expression of lncRNA RP11-363E7.4 was associated with T stage (P = .010). 	Yes	Functional experiments showed that overexpression of lncRNA RP11-363E7.4 prevented proliferation, migration, and invasion and induced apoptosis of GC cells.	32141108
RP11-361F15.2	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[RP11-361F15.2/miR-30c-5p/CPEB4 loop]	qRT-PCR	The results indicate that RP11-361F15.2 is significantly increased in OS tissues, and its expression is positively correlated with cytoplasmic polyadenylation element binding protein 4 (CPEB4) expression and negatively associated with miR-30c-5p expression.This RP11-361F15.2/miR-30c-5p/CPEB4 loop could be used as a potential therapeutic strategy for the treatment of OS.		Yes	 Further, overexpression of RP11-361F15.2 increased OS cell migration/invasion and M2-Like polarization of TAMs in vitro, as well as promoted xenograft tumor growth in vivo.	31904478
RP11-357H14.17	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer patients	Regulation(ATF2 signaling )	qRT-PCR//IHC	We found that the high expression of RP11-357H14.17 was closely associated with shortened overall survival (OS) and poor prognosis in gastric cancer patients. Functional enrichment analysis revealed that RP11-357H14.17 is closely related to enhanced DNA replication and metabolism; ssGSEA analysis implied the oncogenic roles of RP11-357H14.17 was related to ATF2 signaling and Treg cell differentiation. 	We found that the high expression of RP11-357H14.17 was closely associated with shortened overall survival (OS) and poor prognosis in gastric cancer patients.  We also found that its expression was related to clinical features including tumor volume, metastasis, and differentiation. 	Yes	Functional enrichment analysis revealed that RP11-357H14.17 is closely related to enhanced DNA replication and metabolism; ssGSEA analysis implied the oncogenic roles of RP11-357H14.17 was related to ATF2 signaling and Treg cell differentiation. 	34195276
RP11-323N12.5	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(c-MYC/ YAP)	In Vivo Experiment//ChIP//Western Blot//ISH//Colony Formation Assay//CCK8//qRT-PCR//Migration Assay//Flow Cytometry//Luciferase Report Assay//ELISA//IHC//Invasion Assay//IF	RP11-323N12.5 was the most up-regulated lncRNA in human GC, based on data from the TCGA database. Its transcription was significantly positively correlated with YAP1 transcription, YAP1 downstream gene expression which contribute to tumor growth and immunosuppression.  RP11-323N12.5 promoted YAP1 transcription by binding to c-MYC in the YAP1 promoter region. 		Yes	 RP11-323N12.5 had tumor- and immnosuppression-promoting effects by enhancing YAP1 downstream genes in GC cells. Excessive RP11-323N12.5 was also observed in tumor-infiltrating leukocytes (TILs), which may be exosome-derived and also be related to enhanced Treg differentiation as a result YAP1 up-regulation. Moreover, RP11-323N12.5 promoted tumor growth and immunosuppression via YAP1 up-regulation in vivo.	32623586
RP11-315I20.1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP11-301G19.1	LncRNA	Homo sapiens	Multiple Myeloma	 MM cell lines	Interaction(miR-582-5p/HMGB2/PI3K/AKT signalling pathway)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay	Our results demonstrated that RP11-301G19.1 was upregulated in MM cell lines and that its downregulation inhibited the proliferation and cell cycle progression and promoted the apoptosis of MM cells.Bioinformatic analysis and luciferase reporter assay results revealed that RP11-301G19.1 can upregulate the miR-582-5p-targeted gene HMGB2 as a competing endogenous RNA (ceRNA). Furthermore, Western blot results indicated that RP11-301G19.1 knockdown decreased the levels of PI3K and AKT phosphorylation without affecting their total protein levels. 		Yes	Our results demonstrated that RP11-301G19.1 was upregulated in MM cell lines and that its downregulation inhibited the proliferation and cell cycle progression and promoted the apoptosis of MM cells. Additionally, in a xenograft model of human MM, RP11-301G19.1 knockdown significantly inhibited tumour growth by downregulating HMGB2. 	33707625
RP11-286H15.1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC samples and cell lines	regulation[ promoting PABPC4 ubiquitination]	qRT-PCR//RNA Pull-Down//RIP//FISH	The transcript abundance of RP11-286H15.1 in 80 pairs of HCC samples and cell lines was evaluated by qRT-PCR analysis.Our study demonstrates that a novel lncRNA, RP11-286H15.1, represses HCC progression by promoting PABPC4 ubiquitination. These findings highlight potential therapeutic targets for HCC.	The qRT-PCR and FISH assays revealed that RP11-286H15.1 was significantly decreased in HCC, and implied a shorter survival time.	Yes	RP11-286H15.1 overexpression inhibited HCC cell proliferation and metastasis in vitro and in vivo, whereas RP11-286H15.1 knockdown produced the opposite results. 	33259899
RP11-40C6.2	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients and cell line	Regulation(Hippo signaling pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transwell Assay//Co-IP//CCK8//qRT-PCR//migration assay//Luciferase Report Assay//IHC//Bioinformatics Analysis//ChIP	 RP11-40C6.2 was overexpressed in HCC patients with HBV infection compared to those without HBV infection.  Luciferase gene reporter and ChIP assays revealed that YAP1/TAZ/TEADs complex enhanced RP11-40C6.2 transcription by binding to its promoter area. RP11-40C6.2 showed oncogenic characteristics in HCC cell lines and in animal models that were mediated via activation of YAP1. In vitro ubiquitylation assay revealed that RP11-40C6.2 can promote the stabilization of YAP1 by stopping phosphorylation at its s127 residue and further stopping its degradation through binding to 14-3-3.		Yes	 Luciferase gene reporter and ChIP assays revealed that YAP1/TAZ/TEADs complex enhanced RP11-40C6.2 transcription by binding to its promoter area. RP11-40C6.2 showed oncogenic characteristics in HCC cell lines and in animal models that were mediated via activation of YAP1. In vitro ubiquitylation assay revealed that RP11-40C6.2 can promote the stabilization of YAP1 by stopping phosphorylation at its s127 residue and further stopping its degradation through binding to 14-3-3.	36643034
RP11-283G6.5	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues	Interaction(miR-188-3p/TMED3/Wnt/β-catenin signalling)	In Vivo Experiment//Western Blot//Migration Assay//qRT-PCR//IF//Luciferase Report Assay//IHC//Invasion Assay//Transwell Assay	In this study, we identified a novel lncRNA RP11-283G6.5 which was lowly expressed in breast cancer and whose low expression was correlated with poor overall survival and disease-free survival of breast cancer patients.  Collectively, these findings demonstrated that RP11-283G6.5 is a tumour suppressive lncRNA in breast cancer via modulating miR-188-3p/TMED3/Wnt/β-catenin signalling. This study indicated that RP11-283G6.5 might be a promising prognostic biomarker and therapeutic target for breast cancer.	In this study, we identified a novel lncRNA RP11-283G6.5 which was lowly expressed in breast cancer and whose low expression was correlated with poor overall survival and disease-free survival of breast cancer patients. 	Yes	Functional experiments revealed that ectopic expression of RP11-283G6.5 confined breast cancer cellular growth, migration, and invasion, and promoted cellular apoptosis. Conversely, RP11-283G6.5 silencing facilitated breast cancer cellular growth, migration, and invasion, and repressed cellular apoptosis.  Moreover, RP11-283G6.5 was found to confine breast cancer tumour growth and metastasis in vivo.	34130584
RP11-279C4.1	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Interaction(miR-1273g-3p/CBX3 Axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	In the present study, we identified and verified the expression of the novel lncRNA RP11-279C4.1 by analyzing the TANRIC database and performing qRT-PCR assays, the results of which revealed its upregulation in glioma tissues and cell lines. Mechanistically, RP11-279C4.1 induced CBX3 activation via competitively sponging miR-1273g-3p, and rescue assay results confirmed the importance of the RP11-279C4.1/miR-1273g-3p/CBX3 axis.		Yes	 The results of multiple functional experiments demonstrated that RP11-279C4.1 knockdown inhibited glioma malignant phenotypes, including cell proliferation, migration, invasion and cell self-renew ability in vitro. In addition, RP11-279C4.1 downregulation suppressed tumour growth in vivo.	33694060
RP11-264B17.2	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP11-259O2.3	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
circMTUS1	CircRNA	Homo sapiens	malignant conjunctival melanoma	conjunctival melanoma tissues	Interaction[binding to hsa-miR-622 and hsa-miR-1208 ]	RIP//RNA-seq	We identified 9300 different circRNAs in conjunctival melanoma tissues compared with adjacent normal tissues.CircMTUS1 was Expression[Expression[up-expression]-expression]regulated in conjunctival melanoma.CircMTUS1 may serve as an oncogene by binding to hsa-miR-622 and hsa-miR-1208 to regulate several tumor-related pathways.		Yes	Silencing of circMTUS1 inhibited conjunctival melanoma proliferation in vitro and in vivo.	30892069
RP11-214F16.8	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer patients	Expression(highly expressed)	RNA Pull-Down//ChIP//Western Blot//Wound Healing Assay//Co-IP//qRT-PCR//RIP//FISH//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	We identified that up-regulation of the lncRNA RP11-214F16.8 is subtype-independently associated with a higher overall death rate in breast cancer patients. Mechanistically, the oncogenic property of RP11-214F16.8 lies to its post-translational repression on the tumor suppressor NISCH via recruiting SENP3-mediated de-SUMOylation and ubiquitin-proteasome-mediated protein degradation. NISCH in turn inhibits the transcription of RP11-214F16.8 through restraining the expression of the transcription factors located downstream of RAC1, PAK1 and ERK1/2 signaling transduction pathways. 		Yes	 Increased RP11-214F16.8 expression endows breast cancer cells enhanced capabilities in the aspects of proliferation, invasion, migration and tumor-initiation, while loss of the lncRNA exerts the opposite effects.	35108640
hsa_circ_0070934	CircRNA	Homo sapiens	Cutaneous Squamous	CSCC and matched normal tissues	Interaction[miR-1238 and miR-1247-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The quantification data revealed that circ_0070934 was significantly overexpressed in a large subset of CSCC specimens when compared with their paired normal specimens (Fig. 1A).  Circ_0070934 expression was negatively correlated with miR-1238 and miR-1247-5p expression in CSCC and luciferase reporter experiment verified the binding ability between circ_0070934 and miR-1238/miR-1247-5p. Rescue experiments further identified that the oncogenic role of circ_0070934 is attributed to its sExpression[Expression[up-expression]-expression]pression of miR-1238 and miR-1247-5p.		Yes	Loss-of-function and gain-of-function assays were performed to detect cell proliferation, apoptosis, migration and invasion in vitro.	30967263
RP11-395G23.3	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	regulation[microRNA-205-5p/PTEN axis]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Transwell Assay	We discovered that low RP11-395G23.3 expression was significantly related to advanced histological grade and lymphovascular space invasion in EC patients.  We demonstrated for the first time that RP11-395G23.3 may inhibit the development and pathogenesis of EC by acting as a sponge for miRNA-205-5p and increasing PTEN expression. RP11-395G23.3 may be a target for the diagnosis and treatment of EC.	We discovered that low RP11-395G23.3 expression was significantly related to advanced histological grade and lymphovascular space invasion in EC patients. 	Yes	 In addition, overexpression of RP11-395G23.3 significantly inhibited the proliferation, invasion, migration, and induced apoptosis of Ishikawa and HEC-1A cells in vitro. 	32913516
RP11-422N16.3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma cancer tissues and cells	Interaction[Sponging miR-23b-3p]	RNA Pull-Down//Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Expressions of RP11-422N16.3 and DMGDH were down-regulated while that of miR-23b-3p were up-regulated in hepatocellular carcinoma cancer tissues and cells.Our data suggested that LncRNA RP11-422N16.3, by competitively binding to miR-23b-3p, promoted DMGDH expression, contributing to inhibit cell proliferation and EMT, and induce cell apoptosis in hepatocellular carcinoma cells.		Yes	Up-regulation of RP11-422N16.3 and down-regulation of miR-23b-3p contributed to increased expressions of DMGDH and E-cadherin, and decreased expressions of miR-23b-3p, ZEB1, Snail and Vimentin, resulting in inhibiting cell proliferation and promoting cell apoptosis. 	31849497
RP11-732M18.3	LncRNA	Homo sapiens	Glioma	 endothelial cell 	Regulation(EP300/VEGFA)	Western Blot//Transfection//Co-IP//qRT-PCR//migration assay//H&E Staining//IHC//IF	 lncRNA RP11-732M18.3 increased CD31+ microvessel density, and overexpression of lncRNA RP11-732M18.3 resulted in poor mouse survival. lncRNA RP11-732M18.3 promoted endothelial cell migration and tube formation. Mechanistically, lncRNA RP11-732M18.3 promotes angiogenesis by increasing the nuclear level of EP300 and facilitating the transcription and secretion of VEGFA. Our study contributes to the latest understanding of glioma angiogenesis and prognosis. lncRNA RP11-732M18.3 may be a potential treatment target in glioma.		Yes	 lncRNA RP11-732M18.3 increased CD31+ microvessel density, and overexpression of lncRNA RP11-732M18.3 resulted in poor mouse survival. lncRNA RP11-732M18.3 promoted endothelial cell migration and tube formation. 	35785190
RP11-59J16.2	LncRNA	Homo sapiens	Alzheimer Disease	SH-SY5Y cells, AD patients	Interaction(MCM2 )	qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Western Blot	 The result showed that RP11-59J16.2 was up-regulated and MCM2 was down-regulated in serum of AD patients.  Dual luciferase reporter gene analysis verified that RP11-59J16.2 could directly interact with 3'UTR of MCM2 and further regulate the expression of MCM2. 		Yes	Inhibition of RP11-59J16.2 or overexpression of MCM2, CCK-8 assay and Annexin V FITC/PI apoptosis assay kit results showed that RP11-59J16.2 could reduce cell viability, aggravate apoptosis and increase Tau phosphorylation in AD cell model by inhibiting MCM2. 	36092938
RP11-705C15.3	LncRNA	Homo sapiens	Melanoma	melanoma tissues	regulation[RP11-705C15.3/miR-145-5p/NRAS/MAPK signaling axis]	Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay	Furthermore, we investigated the expression of RP11-705C15.3 in clinical melanoma tissues and found that RP11-705C15.3 was increased in melanoma tissues. Taken together, our findings suggest RP11-705C15.3 as a novel oncogene in melanoma, and highlight that the RP11-705C15.3/miR-145-5p/NRAS/MAPK signaling axis may be potential therapeutic targets for melanoma.	High expression of RP11-705C15.3 was positively correlated with thickness, ulceration, metastasis, and inferior overall survival.	Yes	 Silencing of RP11-705C15.3 repressed melanoma cell proliferation, induced apoptosis, and repressed migration and invasion.	33311650
RP1-163G9.1	LncRNA	Homo sapiens	gastric adenocarcinoma	GA tissues and cell lines	Expression[lower expressed]	Western Blot//CCK8//qRT-PCR//FISH//Colony Formation Assay//Transwell Assay	 lncRNA RP1‑163G9.1 expression in GA tissues and cells was significantly decreased when compared with that in control gastric tissues (P<0.001) or gastric epithelial cells GES‑1 (P<0.05). 	 lncRNA RP1‑163G9.1 expression in GA tissues and cells was significantly decreased when compared with that in control gastric tissues (P<0.001) or gastric epithelial cells GES‑1 (P<0.05). This finding was associated with the depth of invasion (P=0.001), lymph node metastasis (P=0.009), tumor size (P=0.037) and immunocytochemistry marker Ki‑67 (P=0.010). 	Yes	Notably, overexpression of lncRNA RP1‑163G9.1 significantly decreased cell proliferation (P<0.01), colony formation (P<0.01), invasion (P<0.01) and the number of cells at the S‑phase of the cell cycle (P<0.05); However, it did not exert a significant effect on apoptosis (P>0.05). Furthermore, tumor formation experiments revealed that overexpression of lncRNA RP1‑163G9.1 inhibited cancer cell proliferation in nude mice. 	31002370
RP11-63A11.1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	pRCC cells and tissues	Expression(lower expressed)	Cell Proliferation Assay//qRT-PCR//Cell Apoptosis Assay//Western Blot	RP11-63A11.1 was mainly expressed in renal tissues and it correlated with the tumor stage, T, M, N classifications, OS, PFS, and DSS of pRCC patients. Consistent with the expression in pRCC tissue samples, RP11-63A11.1 was also down-regulated in pRCC cells. 	RP11-63A11.1 was mainly expressed in renal tissues and it correlated with the tumor stage, T, M, N classifications, OS, PFS, and DSS of pRCC patients. Consistent with the expression in pRCC tissue samples, RP11-63A11.1 was also down-regulated in pRCC cells. 	Yes	 More importantly, up-regulation of RP11-63A11.1 attenuated cell survival and induced apoptosis.	34663322
RP11-626G11.3	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	regulation[miR-375-SP1 axis]	qRT-PCR	Results indicated that lncRNA RP11-626G11.3 was up-regulated in glioma tissues and cell lines, moreover, its overexpression positively correlated with the poor prognosis and advanced pathological stages.Overall, our study shows that lncRNA RP11-626G11.3 promotes glioma progression by sponging miR-375 to regulate SP1 expression, which may provide a novel therapeutic strategy for glioma.	Results indicated that lncRNA RP11-626G11.3 was up-regulated in glioma tissues and cell lines, moreover, its overexpression positively correlated with the poor prognosis and advanced pathological stages.	Yes	Gain and loss of functional experiments demonstrated that lncRNA RP11-626G11.3 promoted the proliferation and invasion of glioma cells in vitro. The knockdown of lncRNA RP11-626G11.3 repressed the tumor growth in vivo.	32128886
RP11-624L4.1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues	regulation[CDK4/6-Cyclin D1-Rb-E2F1 Pathway]	ISH//qRT-PCR//RIP	As a result, we found that RP11-624L4.1 is hyper-expressed in NPC tissues, which was associated with unfavorable prognosis and clinicopathological features in NPC.Taken together, RP11-624L4.1 is required for NPC unfavorable prognosis and proliferation through the CDK4/6-Cyclin D1-Rb-E2F1 pathway, which may be a novel therapeutic target and prognostic in patients with NPC.	As a result, we found that RP11-624L4.1 is hyper-expressed in NPC tissues, which was associated with unfavorable prognosis and clinicopathological features in NPC.	Yes	By knocking down and overexpressing RP11-624L4.1, we also found that it promotes the proliferation ability of NPC in vitro and in vivo through the CDK4/6-Cyclin D1-Rb-E2F1 pathway.	33078086
RP11-619L19.2	LncRNA	Homo sapiens	Colonic Neoplasms	CC tissues and cell lines	regulation[miR-1271-5p/CD164 axis]	Western Blot//Migration Assay//CCK8//qRT-PCR//Invasion Assay	RP11?619L19.2 was found to be highly expressed in CC tissues and cell lines, and it was associated with advanced TNM stage and lymph node metastasis.In conclusion, the findings of the present study indicated that RP11‑619L19.2 regulates CD164 expression and EMT by sponging miR‑1271‑5p, which may provide novel targets for lncRNA‑directed diagnosis and therapy for patients with CC.	RP11?619L19.2 was found to be highly expressed in CC tissues and cell lines, and it was associated with advanced TNM stage and lymph node metastasis.	Yes	Furthermore, knockdown of RP11?619L19.2 inhibited CC cell proliferation, migration, invasion and epithelial?to?mesenchymal transition (EMT).	33125110
RP11-603J24.7	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[lower expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP11-59H7.3	LncRNA	Homo sapiens	Colorectal Neoplasms		regulation[miR-139-5p/NOTCH1 axis]	qRT-PCR//Luciferase Report Assay	 Taken together, these results demonstrated that the RP11-59H7.3/miR-139-5p/NOTCH1 axis functions as a key regulator in CRC metastasis. RP11-59H7.3 represents a potential biomarker for CRC diagnosis and could be an important target for development of novel therapies to manage the disease.		Yes	Functional analyses of this lncRNA revealed its role in promoting proliferation and progression of the cell cycle, as well as enhancement of cell migration and invasion.	32507766
RP11-443B7.1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
RP11-569A11.1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Expression(lower expressed)	qRT-PCR//Colony Formation Assay//Western Blot	Of which, RP11-569A11.1 was found to be significantly downregulated in CRC tissues and cells. 		Yes	 Functionally, overexpression of RP11-569A11.1 inhibited CRC cell proliferation, migration and invasion, and induced cell apoptosis, while knockdown of RP11-569A11.1 generated an opposite effect.	33942366
RP11-552M11.4	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues and corresponding non-tumor tissues	Regulation[miR-3941/ATF1 signaling ]	Migration Assay//RIP//qRT-PCR//FISH//Luciferase Report Assay//Invasion Assay	Our results demonstrated that the expression of lncRNA RP11-552M11.4 was markedly increased in cervical cancer tissues compared with the adjacent non-tumor tissues.Our observations elucidated the carcinogenic role of lncRNA RP11-552M11.4 in CC was mediated through miR-3941/ATF1 axis, giving a new insight into the effective target for the treatment and prognosis of cervical cancer.	 Additionally, CC patients with high lncRNA RP11-552M11.4 level suffered from poor clinical outcomes.	Yes	Moreover, silenced lncRNA RP11-552M11.4 restrained cell proliferation, migration and invasion in CC cells. 	30790638
RP11-552D4.1	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tissues and cell	Regulation	CCK8	 The RP11-552D4.1 is found to facilitate neuronal proliferation. 		Yes	 The RP11-552D4.1 is found to facilitate neuronal proliferation. 	35852867
RP11-551L14.4	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cells	Interaction(miR-4472)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	The results of qRT-PCR showed that RP11-551L14.4 expression in breast cancer tissues was significantly lower than in adjacent tissues. Bioinformatics technology showed that RP11-551L14.4 could complementarily bind to miR-4472. qRT-PCR results indicated that the expression levels of miR-4472 and RP11-551L14.4 in breast cancer were negatively correlated. 	 RP11-551L14.4 expression was negatively associated with the advanced tumor stage. Breast cancer patients with low RP11-551L14.4 expression manifested a poorer prognosis.	Yes	 Meanwhile, overexpression of RP11-551L14.4 significantly decreased the cell proliferation and cell cycle.	36523479
RP11-51O6.1	LncRNA	Homo sapiens	Colorectal Neoplasms	six CRC tissues and three adjacent non-tumor tissues 	Interaction(miR-206/YAP1)	RNA Pull-Down//Western Blot//ISH//qRT-PCR//Luciferase Report Assay//IHC	In this context, we explored the differentially expressed profiles of lncRNAs in six CRC tissues and three adjacent non-tumor tissues from RNA-sequencing (RNA-seq) study and noted a lncRNA, RP11-51O6.1, which is markedly overexpressed in CRC tissues, particularly in aggressive cases. Mechanistic studies (Bioinformatics binding site analyses, the Luciferase reporter, Ago2 immunoprecipitation, the RNA pull-down, immunofluorescence colocalization, rescued assays and western blotting) implicated that RP11-51O6.1 could regulate YAP1 expression by competitively sponging miR-206 and blocking its activity in promoting CRC progression. 	Impressively, an elevated RP11-51O6.1 level was highly correlated with poor prognosis in clinical patients. 	Yes	Functional analyses revealed that RP11-51O6.1 could promote cell proliferation in vitro and in vivo. Furthermore, we reported that RP11-51O6.1 enhances cell migration and invasion in vitro. 	34038520
RP11-499E18.1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(PAK2-SOX2 Interaction)	qRT-PCR//RNA Pull-Down//Western Blot	 RP11-499E18.1 was downregulated, while PAK2 and SOX2 was upregulated in OC tissues and cells.  There is an interaction between RP11-499E18.1 and PAK2, as well as PAK2 and SOX2 in OC cells. Alteration of RP11-499E18.1 and PAK2 expression both had no influence on PAK2 and SOX2 levels, but PAK2 upregulation notably augmented p-SOX2 level. Additionally, RP11-499E18.1 overexpression reduced PAK2-SOX2 interaction and SOX phosphorylation, and increased the binding of RP11-499E18.1 by PAK2.		Yes	RP11-499E18.1 overexpression suppressed OC cell proliferation, migration, and colony formation, as well as SOX2 nuclear translocation. Besides, it inhibited tumor growth in nude mice. However, these effects were notably reversed by PAK2 upregulation and eventually offset by SOX2 knockdown. 	34621737
RP11-468E2.5	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Regulation[JAK/STAT signaling pathway]	qRT-PCR	CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. 		Yes	Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results.	31718693
RP11-465B22.8	LncRNA	Homo sapiens	Esophageal Neoplasms	 EC tissues	Interaction(miR-765/KLK4 axis)	qRT-PCR//Western Blot	LncRNA RP11-465B22.8 was upregulated in EC tissues and high lncRNA RP11-465B22.8 expression was associated with poor survival of EC patients. Mechanistically, lncRNA RP11-465B22.8 sponged miR-765 to increase the expression of KLK4.	LncRNA RP11-465B22.8 was upregulated in EC tissues and high lncRNA RP11-465B22.8 expression was associated with poor survival of EC patients. 	Yes	Ectopic expression of lncRNA RP11-465B22.8 enhanced the proliferation, migration, and invasion of EC cells, whereas knockdown of lncRNA RP11-465B22.8 led to the opposite effects.	34561425
RPL34-DT	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal cancer tissue, cell line(TE-1, TE-13, KYSE150 and KYSE450 , Het-1A)	Interaction[RPL34 ]	CCK8//qRT-PCR//Transwell Assay	In our study, we found RPL34-AS1 expression levels in esophageal cancer tissue and specimens and cell lines were lower than in adjacent normal tissue specimens and normal esophageal cell line, respectively.In survival analysis suggested esophageal cancer patients with low RPL34-AS1 expression had short overall survival than those with high RPL34-AS1 expression. Our in vitro experiments suggested RPL34-AS1 inhibits esophageal cancer cell proliferation, migration and invasion through Expression[down-expression]-regulating RPL34 expression. In conclusion, RPL34-AS1 functions as tumor sExpression[Expression[up-expression]-expression]pressor in esophageal cancer.	"For investigating the clinical significance of RPL34-AS1 in esophageal cancer patients, total 56 esophageal cancer cases in our study were divided into two groExpression[Expression[up-expression]-expression]s based on clinicopathological features including clinical stage (Ⅰ-Ⅱ vs. Ⅲ-Ⅳ), T classification (T1-T2 vs. T3-T4) and lymph node metastasis (Negative vs. Positive). As shown in the Fig. 2A–C, esophageal cancer patients with Ⅲ-Ⅳ, T3-T4 or positive lymph node metastasis had lower RPL34-AS1expression levels than esophageal cancer patients with Ⅰ-Ⅱ, T1-T2 or negative lymph node metastasis, respectively.
"	Yes	CCK-8 assay was used to investigate the effect of RPL34-AS1 on esophageal cancer cell proliferation. As shown in Fig. 5A, RPL34-AS1 overexpression profoundly inhibited esophageal cancer cell proliferation at 72 h and 120 h. 	31574377
SCARNA10	LncRNA	Homo sapiens	Liver Cirrhosis	liver tissues,blood	Interaction[ ECM and TGFβ pathway]	RIP//ChIP	It was found lncRNA ENSMUST00000158992, named as Scarna10, was remarkably up-regulated in mouse fibrotic livers according to the microarray data. We observed that the transcript of SCARNA10 was increased in the serum and liver from patients with advanced hepatic fibrosis.Mechanistically, RNA immunoprecipitation (RIP) assays demonstrated that SCARNA10 physically associated with polycomb repressive complex 2 (PRC2). Additionally, our results demonstrated that SCARNA10 functioned as a novel positive regulator of TGFβ signaling in hepatic fibrogenesis by inhibiting the binding of PRC2 to the promoters of the genes associated with ECM and TGFβ pathway, thus promoting the transcription of these genes.		Yes	 Furthermore, we found that SCARNA10 promoted liver fibrosis both in vitro and in vivo through inducing hepatocytes (HCs) apoptosis and HSCs activation.	31281502
SAP30-2:1	LncRNA	Homo sapiens	Heart Defects, Congenital	CHD	Interaction(HAND2)	Western Blot//Transfection//qPCR//CCK8//RIP//Cell Apoptosis Assay//EdU Staining	We used Gene Expression Omnibus data mining, bioinformatics analysis, and analysis of clinical tissue samples and observed that the novel lncRNA SAP30-2:1 with unknown function was significantly downregulated in damaged cardiac tissues from patients with CHD.  Moreover, lncRNA SAP30-2:1 was associated with HAND2 by RNA immunoprecipitation. 		Yes	 Knockdown of lncRNA SAP30-2:1 inhibited the proliferation of human embryonic kidney and AC16 cells and decreased the expression of heart and neural crest derivatives expressed 2 (HAND2).	32820380
SBF2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR-520a-3p)	Transfection//CCK8//RIP//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In NSCLC tissues, SBF2-AS1 was highly expressed, while miR-520a-3p expression has decreased.  More importantly, the suppression of SBF2-AS1 silencing on the proliferation, migration, and invasion in NSCLC cells was counteracted by miR-520a-3p inhibition.	The overall survival of NSCLC patients with high SBF2-AS1 expression was lower. 	Yes	 SBF2-AS1 silencing repressed the proliferation, migration, and invasion of NSCLC cells. SBF2-AS1 directly interacted with miR-520a-3p, and a negative relationship was observed between their expression levels in NSCLC tissues. 	35444785
SBF2-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma		Interaction(miR-362-3P/E2F1 axis )	In Vivo Experiment//RNA Pull-Down//IHC//Western Blot//Transfection//qPCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay	 It was further found that the higher the expression of SBF2-AS1, the lower the survival rate.In mechanism, SBF2-AS1/miR-338-3P, miR-362-3P/E2F1 axis are involved in the regulation of ESCC growth.	 It was further found that the higher the expression of SBF2-AS1, the lower the survival rate.COX multivariate analysis showed that the expression of SBF2-AS1 was an independent prognostic factor.	Yes	Functional experiments show that inhibition of SBF2-AS1 can inhibit the proliferation of ESCC through in vivo and in vitro, and overexpression of SBF2-AS1 can promote the proliferation of ESCC and inhibit its apoptosis. 	33436941
SBF2-AS1	LncRNA	Homo sapiens	Aortic Aneurysm, Abdominal	VSMCs	Interaction(miRNA-520f-3p/SMARCD1 Axis)	qRT-PCR//Transfection//RNA Pull-Down//Western Blot	 SBF2-AS1 enhances SMARCD1 expression by forming miR-520f-3p in VSMC and HASMC. Overexpression of SMARCD1 or miR-520f-3p inhibitor reversed cell viability and caspase-3 activity mediated by SBF2-AS1 depletion in VSMC and HASMC. 		Yes	Depletion of SBF2-AS1 enhanced the cell viability and proliferation of VSMCs. Conversely, SBF2-AS1 knockdown inhibited VSMC apoptosis. Caspase-3 activity was inhibited by depletion of SBF2-AS1, whereas overexpression of SBF2-AS1 in VSMC promoted Caspase-3 activity. 	35968497
SBF2-AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	SOC tissues	Interaction(microRNA-338-3p)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	 In this study, the aberrant upregulation of SBF2-AS1 is detected in SOC after analysis of differentially expressed genes between SOC tissues and normal fallopian tubes from the public Gene Expression Omnibus (GEO) database. MiR-338-3p acts as a tumor suppressor in SOC, and E26 transformation specific-1 (ETS1) is identified as a potential target of miR-338-3p regulation. Furthermore, SBF2-AS1 could modulate ETS1 by operating as a competing endogenous RNA for miR-338-3p. 		Yes	We determine that knockdown of SBF2-AS1 inhibits SOC cell proliferation and invasion by sponging miR-338-3p.	34850542
SATB2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal tissues	Interaction[regulating SATB2]	ISH//qRT-PCR//RIP//ChIP	SATB2-AS1 is specifically expressed in colorectal tissues and downregulated in CRC. Mechanistically, SATB2-AS1 directly binds to WDR5 and GADD45A, cis-activating SATB2 (Special AT-rich binding protein 2) transcription via mediating histone H3 lysine 4 tri-methylation (H3K4me3) deposition and DNA demethylation of the promoter region of SATB2.	 Survival analysis indicates that decreased SATB2-AS1 expression is associated with poor survival.	Yes	 Functional experiments and bioinformatics analysis revealed that SATB2-AS1 inhibits CRC cell metastasis and regulates TH1-type chemokines expression and immune cell density in CRC.	31492160
SATB2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal carcinoma cells and tissues	Regulation[SATB2-Snail axis]	RNA Pull-Down//ISH//qRT-PCR//RIP//Microarray//ChIP	SATB2-AS1 was frequently downregulated in colorectal carcinoma cells and tissues. SATB2-AS1 suppressed colorectal carcinoma progression by serving as a scaffold to recruit p300, whose acetylation of H3K27 and H3K9 at the SATB2 promoter upregulated expression of SATB2, a suppressor of colorectal carcinoma growth and metastasis. SATB2 subsequently recruited HDAC1 to the Snail promoter, repressing Snail transcription and inhibiting epithelial-to-mesenchymal transition. Taken together, these data reveal SATB2-AS1 as a novel regulator of the SATB2-Snail axis whose loss facilitates progression of colorectal carcinoma. SIGNIFICANCE: These data show that the lncRNA SATB2-AS1 mediates epigenetic regulation of SATB2 and Snail expression to suppress colorectal cancer progression.	 SATB2-AS1 was frequently downregulated in colorectal carcinoma cells and tissues, and patients whose tumors expressed SATB2-AS1 at low levels had a shorter overall survival and poorer prognosis.	Yes	Downregulation of SATB2-AS1 significantly promoted cell proliferation, migration, and invasion in vitro and in vivo, demonstrating that it acts as a tumor suppressor in colorectal carcinoma. 	30858153
SAP30L-AS1	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues and cell lines	Interaction[repressing SAP30L]	CCK8//qRT-PCR//Western Blot	 The expression of SAP30L-AS1 is found to be increased in prostate cancer tissues and cell lines compared with adjacent noncancerous tissues and normal prostate epithelial cell line, respectively. Mechanistic investigation revealed that SAP30L-AS1 physically binds to the promoter of SAP30L and represses SAP30L expression. The expression of SAP30L is negatively associated with that of SAP30L-AS1 in prostate cancer tissues. Rescue assays demonstrated that overexpression of SAP30L attenuated the roles of SAP30L-AS1 in promoting prostate cancer proliferation and inhibiting prostate cancer apoptosis. In conclusion, SAP30L-AS1 is upregulated and has oncogenic roles in prostate cancer via repressing SAP30L. Our data suggest that SAP30L-AS1 may be a promising prognostic biomarker and therapeutic target for prostate cancer.	Increased expression of SAP30L-AS1 is associated with greater Gleason score, advanced pathological T stage, and poor over survival of prostate cancer patients. 	Yes	 Functional assays demonstrated that ectopic expression of SAP30L-AS1 promotes prostate cancer proliferation and inhibits prostate cancer apoptosis. SAP30L-AS1 knockdown represses prostate cancer proliferation and induces prostate cancer apoptosis. Furthermore, SAP30L-AS1 knockdown represses prostate cancer xenograft growth in vivo. 	30599235
SAMMSON	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells 	Expression[highly expressed]	qRT-PCR//Wound Healing Assay//Transwell Assay	 QRT-PCR results showed that lncRNA-SAMMSON was abnormally overexpressed in GC tissues and cells (p<0.05). 	Kaplan-Meier survival analysis represented that GC patients with high lncRNA-SAMMSON expression had significantly shorter progression-free survival time and overall survival time (p<0.05). 	Yes	Transwell assay and wound healing assay proved that inhibition of lncRNA-SAMMSON in GC cells dramatically reduced the invasion and migration abilities of GC cells, respectively (p<0.05).	32572923
SBF2-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung		Regulation[SBF2-AS1-miR-338-3p/362-3p-E2F1 regulatory axis ]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//RNA-seq	Five early LUAD-specific lncRNAs were filtered out, and only SBF2-AS1 was upregulated in LUAD. The SBF2-AS1-miR-338-3p/362-3p-E2F1 regulatory axis may serve as a prognostic marker and potential therapeutic target for LUAD.	High expression of SBF2-AS1 indicates poor survival of LUAD, especially the early-stage LUAD, but not lung squamous cell carcinoma. 	Yes	SBF2-AS1 promotes LUAD cells proliferation in vitro, and RNA-sequencing data shows that many cell-cycle-related genes were downregulated after SBF2-AS1 knockdown.	31071530
SAMMSON	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC cells, tissues, and plasma	Regulation[p300/Sp1 axis]	qRT-PCR	SAMMSON was identified to be notably upregulated in PTC cells, tissues, and plasma, and could be used as an effective diagnostic and prognostic biomarker for PTC patients. Mechanistically, SAMMSON was transcriptionally elevated by oncogenic Sp1, in turn, upregulated SAMMSON was capable of acting as a scaffold to recruit p300 to increase H3K9ac and H3K27ac levels on Sp1 promoter region, leading to transcriptional activation of Sp1, thereby facilitating PTC progression. Taken together, our data demonstrate that SAMMSON is an oncogenic lncRNA and unveil the crucial role of SAMMSON/Sp1 positive feedback loop in tumorigenesis and aggressiveness of PTC.		Yes	 Knockdown of SAMMSON significantly inhibited PTC cell proliferation and invasion in vitro as well as tumorigenicity and metastasis in vivo.	31478331
SAMMSON	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Regulation[regulates miR-9-3p ]	qRT-PCR	We found that SAMMSON was up-regulated in HCC tissues, and patients with high levels of SAMMSON in HCC tissues had significantly lower overall rate within 5 years after admission. 	We found that SAMMSON was up-regulated in HCC tissues, and patients with high levels of SAMMSON in HCC tissues had significantly lower overall rate within 5 years after admission. 	Yes	 SAMMSON overexpression led to increased, while miR-9-3p overexpression resulted in decreased migration and invasion rates of HCC cells. 	31164410
SAMMSON	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cells	regulation[PI3K/Akt Pathway]	CCK8//qRT-PCR//Western Blot	We found that SAMMSON was highly expressed in GBM tissues and cells.  Taken together, lncRNA SAMMSON knockdown inhibited the malignancy of GBM cells by inactivation of the PI3K/Akt pathway.		Yes	Moreover, SAMMSON silencing impeded the invasive ability of GBM cells by regulating epithelial-to-mesenchymal transition (EMT).	32236901
SAMMSON	LncRNA	Homo sapiens	Uveal melanoma	uveal melanoma cell lines	Regulation	Bioinformatics Analysis	Antisense oligonucleotide (ASO)-mediated SAMMSON inhibition impaired the growth and viability of a genetically diverse panel of uveal melanoma cell lines. These effects were accompanied by an induction of apoptosis and were recapitulated in two uveal melanoma patient derived xenograft (PDX) models through subcutaneous ASO delivery. 		Yes	Antisense oligonucleotide (ASO)-mediated SAMMSON inhibition impaired the growth and viability of a genetically diverse panel of uveal melanoma cell lines. These effects were accompanied by an induction of apoptosis and were recapitulated in two uveal melanoma patient derived xenograft (PDX) models through subcutaneous ASO delivery. 	34508176
SAMD12-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	Interaction( DNMT1/p53 Axis)	Western Blot//CCK8//qRT-PCR//FISH//RIP//Transwell Assay//IF	 SAMD12-AS1 was highly up-regulated in human gastric cancer tissues and cell lines compared to their normal counterparts. Mechanistically, SAMD12-AS1 might performed its biological roles in GC via directly interacting with DNMT1 and facilitating DNMT1 repress the P53 signaling pathway.	 High SAMD12-AS1 expression was closely related to TNM stage, and shorter survival span of patients with GC. 	Yes	 Moreover, SAMD12-AS1 was also found to promote the oncogenic role of GC cells via inhibiting the P53 signaling pathway. 	33962804
SAMD12-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissues	Regulation(p53 Signaling Pathway)	CCK8//qRT-PCR	The level of lncRNA SAMD12-AS1 expression in tumor tissues was remarkably higher than that in paracancerous liver tissues (p < 0.01). It was found that the lncRNA SAMD12-AS1 expression was largely correlated with TNM stage of tumor, vascular invasion, and hepatitis B surface (HBs) antigen in liver cancer patients (p < 0.05). Cell function experiments showed that lncRNA SAMD12-AS1 overexpression promoted liver cancer development, migration, and invasion (p < 0.05), while lncRNA SAMD12-AS1 knockdown inhibited the activity of liver cancer cells to invade and migrate (p < 0.05). Western blot analysis showed that overexpression of lncRNA SAMD12-AS1 markedly inhibited p21, p53, and E-cadherin expression and promoted vimentin expression. Conversely, knockdown of lncRNA SAMD12-AS1 significantly promoted p21, p53, and E-cadherin expression and inhibited vimentin expression (p < 0.05).	It was found that the lncRNA SAMD12-AS1 expression was largely correlated with TNM stage of tumor, vascular invasion, and hepatitis B surface (HBs) antigen in liver cancer patients (p < 0.05).	Yes	Cell function experiments showed that lncRNA SAMD12-AS1 overexpression promoted liver cancer development, migration, and invasion (p < 0.05), while lncRNA SAMD12-AS1 knockdown inhibited the activity of liver cancer cells to invade and migrate (p < 0.05). Western blot analysis showed that overexpression of lncRNA SAMD12-AS1 markedly inhibited p21, p53, and E-cadherin expression and promoted vimentin expression.	36052283
SAMD12-AS1	LncRNA	Homo sapiens	Glioma	Glioma tissues	Interaction[P53]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	qPCR results in the study revealed that SAMD12-AS1 expression in tumor tissue specimens of glioma patients was remarkably higher than that in the adjacent ones, and the difference was statistically significant.In addition, compared to the NC group, knocking down SAMD12-AS1 markedly attenuated the proliferation rate, as well as the invasiveness and migration ability of glioma cells. Subsequently, in glioma tissues, it was verified that P53 expression was remarkably decreased and negatively correlated with SAMD12-AS1. Finally, cell recovery experiment also demonstrated that there may exist a mutual regulation between SAMD12-AS1 and P53, which then together affected the malignant progression of glioma.	Compared with patients with low expression of SAMD12-AS1, patients with high expression of SAMD1-AS1 had a higher incidence of lymph node or distant metastasis.	Yes	 In addition, compared to the NC group, knocking down SAMD12-AS1 markedly attenuated the proliferation rate, as well as the invasiveness and migration ability of glioma cells. 	31646576
SBF2-AS1	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cell lines	Interaction(miR-494-3p/FGFR2 axis )	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Long non-coding RNA (lncRNA) SBF2-AS1 was highly expressed in DLBCL tissues and cell lines. Furthermore, SBF2-AS1 acted as a sponge of miR-494-3p and inhibited its expression. And miR-494-3p directly targeted FGFR2. 		Yes	Silencing of SBF2-AS1 inhibited the viability and growth of OCI-LY-3 cells. 	33519236
SBF2-AS1	LncRNA	Homo sapiens	Laryngeal Neoplasms	LSCC tissues and cell lines	Interaction(miR-302b-3p/TGFBR2 axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//qRT-PCR//RNA-seq//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	We verified that SBF2-AS1 was significantly downregulated in LSCC tissues and cell lines using qRT-PCR analysis. Subsequent mechanistic studies revealed that SBF2-AS1 acted as a competing endogenous RNA that upregulated the expression of TGFBR2 by endogenous sponging for miR-302b-3p in LSCC cell lines. 	 Its low expression was correlated to lymph node metastasis and an advanced clinical stage. More importantly, LSCC patients with low expression of SBF2-AS1 tended to have a poor prognosis. 	Yes	Based on this, we performed gain-of-function and loss-of-function experiments in LSCC cell lines. The results confirmed that knocking down SBF2-AS1 can promote the metastasis of LSCC cells and enhance epithelial-mesenchymal transition phenotype, while the upregulation of SBF2-AS1 expression resulted in the opposite. Our in vivo model verified that SBF2-AS1 overexpression could inhibit LSCC cell metastasis. 	34644425
RUSC1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[hsa-miR-7-5p/NOTCH3 axis]	qRT-PCR//Luciferase Report Assay//RIP	 In this study, we found that RUSC1-AS1 was upregulated in HCC tissues and cells, and predicted unfavorable prognosis of HCC patients.In conclusion, lncRNA RUSC1-AS1 promoted the proliferation and reduced the apoptosis of HCC cells through activation of NOTCH signaling via hsa-miR-7-5p/NOTCH3 axis.		Yes	The function assays including colony formation, EdU, TUNEL assay revealed that RUSC1-AS1 facilitated HCC cell proliferation and inhibited HCC cell apoptosis.	32701359
SBF2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	regulation[miR-338-3p/ADAM17 axis]	Northern Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//ELISA//Colony Formation Assay//Transwell Assay	In this study, we revealed that SBF2-AS1 was overexpressed in NSCLC tissues compared with that in normal tissues. Finally, we revealed that SBF2-AS1 contributed to the proliferation and metastatic phenotypes of NSCLC cell via regulating miR-338-3p/ADAM17 axis.		Yes	SBF2-AS1 silencing restrained the growth and aggressive phenotypes of NSCLC cell in vitro. Consistently, SBF2-AS1 knockdown hindered the growth of NSCLC cell in nude mice. 	32976115
SCARB1	CircRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and RCC cell	regulation[Mir- 510-5p/SDC3 Axis]	qRT-PCR//Microarray	Circ-SCARB1 was elevated in 30 pairs of RCC tissues and multiple RCC cell lines. Circ-SCARB1 promotes RCC progression via sequestering miR-510-5p and indirectly up-regulating SDC3 expression. 		Yes	Knockdown of Circ-SCARB1 inhibited cell proliferation, migration, and invasion while inducing cell apoptosis. 	32271695
SCAMP1-TV2	LncRNA	Homo sapiens	Breast Neoplasms		regulation[SCAMP1-TV2/PUM2/INSM1 pathway]	RNA Pull-Down//CCK8//RIP//Luciferase Report Assay//ChIP	SCAMP1-TV2/PUM2/INSM1 pathway plays an important role in regulating the biological behavior of breast cancer cells.		Yes	Silenced SCAMP1-TV2 inhibited the proliferation, migration, and invasion of breast cancer cells, and promoted cell apoptosis.	32670859
SCAMP1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction[miR-429]	RNA Pull-Down//Western Blot//qRT-PCR//MTT//Luciferase Report Assay	SCAMP1 was elevated in RCC cells and tumors.Then, miR-429 was identified as downstream effector for SCAMP1-mediated tumorigenesis under H2O2 treatment. Besides, miR-429 was downregulated in human clinical tumors. ZEB1 and JUN were both found to be involved in the role of miR-429 in RCC. More interestingly, autophagy obviously affected miR-429-modulated RCC tumorigenesis. Eventually, we also showed that SCAMP1 played an oncogenic role in vivo.		Yes	SCAMP1 depletion attenuated cell viability and promoted apoptosis under H2O2 treatment.	31550675
SCAMP1	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC tissues	regulation[miR-137/CXCL12 Axis]	qRT-PCR//Western Blot//Luciferase Report Assay//Transwell Assay	 Finally, through TCGA database, we found that SCAMP1 (or CXCL12) was upregulated as well as miR-137 was downregulated in OC tissues, and high (or low) level of them was associated with poor prognosis. In summary, our study clarified the role of SCAMP1/miR-137/CXCL12 axis in OC, and this finding may provide a potential therapeutic target of OC.	 Finally, through TCGA database, we found that SCAMP1 (or CXCL12) was upregulated as well as miR-137 was downregulated in OC tissues, and high (or low) level of them was associated with poor prognosis. 	Yes	In this study, we found that SCAMP1 was highly expressed in OC cells, which promoted OC cell invasion and angiogenesis.	32401536
SCAMP1	LncRNA	Homo sapiens	Glioma	cell lines	Regulation[miR-499a-5p/LMX1A/NLRC5 pathway]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	 The present study demonstrated that LncRNA secretory carrier membrane protein 1 (SCAMP1) was up-regulated and functioned as an oncogene in glioma cells. In conclusion, our study clarifies that SCAMP1/miR-499a-5p/LMX1A/NLRC5 axis plays a critical role in modulating malignant progression of glioma cells, which provide a novel therapeutic strategy for glioma treatment.		Yes	Subsequently, inhibition of SCAMP1 significantly restrained the cell proliferation, migration and invasion, as well as promoted apoptosis by acting as a molecular sponge of miR-499a-5p. 	31207033
SBF2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[miR-545/EMS1 Axis]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	LncRNA SBF2-AS1 expression was upregulated in GC tissues, especially in advanced clinical stage cases.These findings elucidated a crucial role of SBF2-AS1 as a miR-545 sponge in GC cells, suggesting that SBF2-AS1 might be a potential target for GC.	Moreover, increased SBF2-AS1 indicated a poor survival rate.	Yes	Functionally, the downregulation of SBF2-AS1 by siRNA in GC cells suppressed the proliferation, migration, and invasion.	32626753
SBF2-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	 GC cell lines, GC tissues	Regulation(Wnt/LRP5 Signaling Pathway)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//cell invasion assay	 SBF2-AS1 was aberrantly expressed in GC cell lines (p<0.05) and GC tissues (p<0.05).  Additionally, online database analysis uncovered a positive correlation between SBF2-AS1 and the Wnt/LRP5 signaling pathway (p<0.05). SBF2-AS1 knockdown blocked the Wnt/LRP5 signaling pathway, whereas the effects of SBF2-AS1 knockdown on the malignant genotype of MKN74 as well as NCI-N87 cells were partially restored by triggering the Wnt/ LRP5 signaling pathway. 		Yes	 Cell invasive and proliferative capabilities were inhibited via SBF2-AS1 knockdown, resulting in apoptosis of NCI-N87 and MKN74 cells. 	36549764
SBF2-AS1	LncRNA	Homo sapiens	Breast Neoplasms	 BC tissues and cells	interaction[miR-143,RRS1]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//FISH//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	SBF2-AS1 and RRS1 were amplified, while miR-143 was reduced in BC tissues and cells.We have discovered in this study that down-regulated SBF2-AS1 could inhibit tumorigenesis and progression of BC by up-regulation miR-143 and repressing RRS1, which provides basic therapeutic considerations for a novel target against BC.		Yes	Reduced SBF2-AS1 and elevated miR-143 could repress the proliferation, invasion and migration via restraining RRS1 expression.	31952549
SBF2-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tumors and cells	regulation[miR-494 ,PFN2 ]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	 In the present research, we found that the expression of SBF2-AS1 and PFN2 was up-regulated, while miR-494 was down-regulated in ESCC tumors and cells using quantitative real-time polymerase chain reaction (qRT-PCR).In conclusion, SBF2-AS1 contributed to cell proliferation, migration, invasion and EMT in ESCC by enhancing PFN2 expression via sponging miR-494, providing promising biomarkers for ESCC diagnosis and treatment.		Yes	3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and transwell assay demonstrated that silencing of SBF2-AS1 suppressed proliferation, migration and invasion.	32229486
SBF2-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction(miR-338-3p/ ETS1)	In Vivo Experiment//Western Blot//ISH//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//IHC//Bioinformatics Analysis//Transwell Assay	 SBF2-AS1 was found to be highly expressed in ccRCC tissues and cells. SBF2-AS1 specifically bound to miR-338-3p and inhibited its expression. Moreover, ETS1 was targeted by miR-338-3p. The knockdown of SBF2-AS1 or ETS1 or overexpression of miR-338-3p resulted in reduced cell proliferation, migration and invasion but elevated cell apoptosis and autophagy. In vivo experiments verified the tumor-suppressive role of silencing SBF2-AS1 in tumor growth of nude mice xenografted with ccRCC cells. 		Yes	Ectopic expression and knockdown of SBF2-AS1 and miR-338-3p were performed in ccRCC 768-O cells to explore their effects on cell proliferation, migration, invasion, apoptosis and autophagy by EdU assay, scratch test, Transwell assay, calcein-AM/PI, and GFP-LC3 immunofluorescence assays, respectively. 	32719443
SBF2-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	Cell lines	Interaction[inhibiting miR-619-5p]	qRT-PCR//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	Accordingly, SBF2-AS1 possesses higher expression in CRC cell lines than in normal cell line.  In terms of mechanism, SBF2-AS1 upregulation restrained the activity of miR-619-5p and led to overexpression of HDAC3. Importantly, downregulation of miR-619-5p or HDAC3 overexpression reversed SBF2-AS1-silencing-caused suppression on proliferation and metastasis. 		Yes	Functionally, SBF2-AS1 knockdown suppressed the proliferation, migration, and invasion of CRC cells. 	30912164
SBF2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Regulation[EMT pathway]	qRT-PCR//MTT//Western Blot//Transwell Assay	We found that SBF2-AS1 expression levels were significantly up-regulated in HCC tissues and cell lines compared with the corresponding noncancerous liver tissues and normal hepatic cell line.  Mechanistically, we found that SBF2-AS1 could promote the activation of EMT pathway, which was demonstrated by measuring the expression levels of EMT-related markers.	 In addition, high SBF2-AS1 expression levels were correlated with vein invasion (p = 0.008) and TNM stage (p = 0.013). Furthermore, Kaplan-Meier survival analysis indicated that high expressions of SBF2-AS1 were correlated with shorter overall survival of HCC patients.	Yes	Further functional analysis demonstrated that knockdown of SBF2-AS1 significantly inhibited HCC cells proliferation, migration and invasion. 	30338801
SBF2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells 	Interaction(miR-361-5p/TGF-β1 signaling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay	lncRNA SBF2-AS1 concentration in HCC cells exceeded that in a normal hepatocyte cell line. The downregulation of lncRNA SBF2-AS1 upregulated miR-361-5p levels in HCC cells. And, miR-361-5p negatively regulate TGF-β1 expression in HCC cells.		Yes	 The suppression of miR-361-5p attenuated the influence of lncRNA SBF2-AS1 downregulation on the viability, proliferation, and migration capability of HCC cells. Further, the downregulation of lncRNA SBF2-AS1 inhibited neoplasm growth in an XMM of HCC. 	34341185
SBF2-AS1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	cell lines	Interaction[binding with miR-188-5p]	CCK8//qRT-PCR//Flow Cytometry	QRT-PCR results showed that SBF2-AS1 expression was upregulated in AML cells. Mechanistically, miR-188-5p was identified as a direct target of SBF2-AS1. SBF2-AS1 upregulated the expression level of ZFP91 by sponging miR-188-5p. And the effects of SBF2-AS1 suppression on AML cells progression could be abolished by miR-188-5p inhibitors. Moreover, we found that SBF2-AS1 inhibition reduced tumor growth in vivo. Taken together, our findings elucidated that SBF2-AS1 could act as a miRNA sponge in AML progression, and provided a potential therapeutic strategy for AML treatment.		Yes	CCK-8 assay revealed that SBF2-AS1 inhibition decreased AML cells proliferation ability in vitro.Moreover, we found that SBF2-AS1 inhibition reduced tumor growth in vivo.	31062614
SBF2-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Regulation[miR-361-5p/FOXM1 axis]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	In the present study, our data showed that SBF2-AS1 expression was significantly increased in CC. Mechanistically, we showed that SBF2-AS1 Expression[Expression[up-expression]-expression]regulation restrained the activity of miR-361-5p and led to overexpression of FOXM1 in CC cells. Furthermore, we found that miR-361-5p inhibitors could rescue the effects of SBF2-AS1 inhibition on CC cells proliferation.	High SBF2-AS1 expression was associated with advanced FIGO stage and lymph node metastasis of CC patients.	Yes	Function assays showed that SBF2-AS1 inhibition significantly reduced CC cells proliferation both in vitro and in vivo.	30856345
SBF2-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	regulation[miR-431-5p/CDK14 axis]	qRT-PCR	First, differentially expressed SBF2-AS1 between PTC and normal adjacent thyroid tissues was determined, and result indicated a higher SBF2-AS1 expression in PTC tissues than adjacent normal tissues. Moreover, SBF2-AS1 could bind with miR-431-5p and showed negative correlation with miR-431-5p in PTC patients. Furthermore, miR-431-5p bind with cyclin-dependent kinase (CDK) 14 and showed negative correlation with CDK14 in PTC patients. 	Moreover, highly SBF2-AS1 expression predicted a poor prognosis in PTC patients.	Yes	Second, SBF2-AS1 overexpression promoted cell viability and cycle of PTC, while inhibited cell apoptosis.	32602632
SBF2-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-362-3p/GRB2 Axis]	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay//ChIP	We found that SBF2-AS1 was upregulated in both NSCLC tissues and cell lines.These results demonstrate that E2F1-induced overexpression of SBF2-AS1 promotes the expression of GRB2 by targeting miR-362-3p to facilitate the metastasis of NSCLC.	Patients with high levels of SBF2-AS1 have larger tumors, higher malignancy, and poor prognosis.	Yes	Knockdown of SBF2-AS1 significantly inhibited tumor growth in vivo and cell proliferation, migration, and invasion in vitro. 	32364763
RUSC1-AS-N	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Regulation[Wnt/β‑catenin signaling]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	A total of 100 patients with breast cancer were recruited for this study and it was revealed that RUSC1‑AS‑N was upregulated in tumor tissues compared with in adjacent non‑cancerous counterparts. In addition, using several breast cancer cell lines, it was demonstrated that the mRNA levels of RUSC1‑AS‑N were highest in the notably metastatic cell lines MDA‑MB‑231 and MDA‑MB‑468. The present study demonstrated that lncRNA RUSC1‑AS‑N promoted cell viability and metastasis via Wnt/β‑catenin signaling in human breast cancer, which may indicate novel targets for the treatment of breast cancer in clinic.		Yes	Knockdown of RUSC1‑AS‑N in breast cancer cells inhibited cell proliferation in the colony formation and cell proliferation assays. Furthermore, depletion of RUSC1‑AS‑N suppressed cell metastasis, as revealed by wound‑healing and western blot assays. 	30569097
RUSC1-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and HCC cell lines	Interaction(miR-340-5p/CREB1 axis)	CCK8//qRT-PCR//Wound Healing Assay	When compared with normal groups, RUSC1-AS1 expression in HCC tissues and HCC cell lines was higher. Further studies demonstrated that the expression of RUSC1-AS1 negatively correlated with miR-340-5p expression in HCC cells. In addition, miR-340-5p was identified as a direct target of RUSC1-AS1 and tightly associated with the prevention of tumor progression. Moreover, miR-340-5p bound directly to CREB1. CREB1 overexpression reversed the impact of miR-340-5p on HCC cells. Together, lncRNA RUSC1-AS1 plays a regulatory role in the PI3K/AKT signaling pathway in HCC cells.		Yes	We also found that knockdown of RUSC1-AS1 inhibited HCC cell progression, including proliferation, migration, and invasion, and suppressed tumorigenesis in vivo. 	33841637
RPL34-DT	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-3656 )	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//BrdU	In this study, increased expression levels of miR-3656 and decreased expression levels of RPL34-AS1 were observed in CRC tissues.  MiR-3656 directly interacted with RPL34-AS1, but not the RPL34-AS1 mutant with disrupted binding sites. RPL34-AS1 and miR-3565 did not affect the expression of each other. RPL34-AS1 positively regulated the expression of ACAP2 at both mRNA and protein levels. 		Yes	 RPL34-AS1 suppressed the role of miR-3565 in enhancing cell proliferation, while RPL34-AS1 mutant did not affect cell behaviors and the role of miR-3565 in cell proliferation.	35773374
RPPH1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines	regulation[miR-326/WNT2B axis]	CCK8//qRT-PCR//Colony Formation Assay	RPPH1 was significantly upregulated in NSCLC cell lines, compared with a normal lung epithelial cell line. In conclusion, RPPH1 promoted NSCLC progression and lung cancer cell resistance to CDDP through miR-326 and WNT2B.	 Moreover, high RPPH1 expression was associated with poor overall survival and disease progression. 	Yes	Compared with the negative control, RPPH1 silencing significantly reduced the number of invading cells, increased E-cadherin expression and reduced vimentin protein expression. 	32831924
circFOXM1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[ circFOXM1/miR-614/FAM83D ]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	We found that circFOXM1 was significantly upregulated in NSCLC tissues, and its upregulation was positively correlated with advanced clinical stage and poor prognosis of NSCLC patients. circFOXM1/miR-614/FAM83D regulatory network may serve as a potential therapeutic target for NSCLC patients.	We found that circFOXM1 was significantly upregulated in NSCLC tissues, and its upregulation was positively correlated with advanced clinical stage and poor prognosis of NSCLC patients.	Yes	Gain or loss-of-function assay showed that circFOXM1 promoted cell proliferation and cell cycle progression. 	32228656
hsa_circ_0008003	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	regulation[miR-488/ZNF281 axis]	qRT-PCR//Microarray	 Then, it was unveiled that the expression of circ-0008003 examined via qRT-PCR was elevated in tumour tissues relative to the non-tumour tissues, which was associated with TNM stage and lymphatic metastasis in NSCLC. It was validated in this research that circ-0008003 triggered tumour formation in NSCLC, which was adjusted via miR-488/ZNF281 axis, casting a novel light on the resultful target for treating NSCLC and predicting the prognosis.	 Then, it was unveiled that the expression of circ-0008003 examined via qRT-PCR was elevated in tumour tissues relative to the non-tumour tissues, which was associated with TNM stage and lymphatic metastasis in NSCLC. Additionally, the prognosis of NSCLC patients with high circ-0008003 level was poor. 	Yes	Besides, circ-0008003 silencing dampened the invasion and proliferation of NSCLC cells. 	33320427
hsa_circ_0058357	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and NSCLC cells	Interaction(hsa‑miR‑24‑3p/AVL9 axis)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//CCK8//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results demonstrated that hsa_circ_0058357 was highly expressed in human NSCLC tissues and NSCLC cells compared with para?cancerous tissues and human bronchial epithelial (HBE) cells, respectively.  As a competing endogenous RNA, hsa_circ_0058357 knockdown contributed to the increase of miR‑24‑3p expression in NSCLC cells. Mechanistically, as a signaling molecule in late secretory pathway, AVL9 was also expressed at a high level in NSCLC tissues and cells, which could be directly suppressed by miR‑24‑3p. In the tumor tissues, along with growth inhibition, hsa_circ_0058357 knockdown also mediated the elevation of miR‑24‑3p and the reduction of AVL9.		Yes	 Knockdown of hsa_circ_0058357 significantly suppressed cell viability, migration and tumor growth, while it promoted apoptosis in NSCLC cells. Of note, overexpression of miR‑24‑3p markedly abolished the exogenous hsa_circ_0058357‑induced excessive proliferation, migration and apoptosis resistance of NSCLC cells. 	33880595
hsa_circ_0000735	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[miR-1179/1182]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Circ_0000735 was elevated in both NSCLC tissues and cells. Moreover, we proved circ_0000735 could bound to miR-1179/1182 to exert its biological functions in NSCLC cells. 	This upregulation of circ_0000735 is associated with more advanced TNM stages and lymph node invasion. 	Yes	Gain and loss of function experiments documented that circ_0000735 significantly facilitated cell proliferation, migratory and invasive abilities and inhibit cell apoptosis. 	30737027
hsa_circ_0043278	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction[regulating miR-520f]	RNA Pull-Down//Wound Healing Assay//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	In the present study, we screened the dysregulated circRNAs in paired NSCLC and normal samples from GEO database and identified circ_0043278 was to be significantly up-regulated in NSCLC and demonstrated it promotes NSCLC progression in vitro and in vivo. In addition, we revealed that circ_0043278 sponged miR-520f, which was demonstrated to target ROCK1, CDKN1B, and AKT3 in NSCLC cells. In conclusion, circ_0043278 promoted NSCLC cell proliferation, invasion, and migration by increasing ROCK1, CDKN1B, and AKT3 expressions through direct inhibition of miR-520f.		Yes	In the present study, we screened the dysregulated circRNAs in paired NSCLC and normal samples from GEO database and identified circ_0043278 was to be significantly up-regulated in NSCLC and demonstrated it promotes NSCLC progression in vitro and in vivo. Then, we revealed the expression of miR-520f, a downstream factor of circ_0043278, was significantly down-regulated in NSCLC and acted as a tumor inhibitor. 	30873868
RPS10P7	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells and tissues	Expression[highly expressed]	IHC//Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay	Bioinformatics analysis demonstrated that lnc-MCEI was involved in the tumorigenesis of ESCC and lnc-MCEI levels were significantly increased in ESCC cells and tissues.		Yes	Additionally, lnc-MCEI knockdown retarded cell proliferation, colony formation of ESCC cells, but induced cell apoptosis. 	33061807
RPPH1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	regulation[repressing P21]	Western Blot//Wound Healing Assay//qRT-PCR//EdU Staining//Transwell Assay	 It was shown in qRT-PCR assay results that the expression of RPPH1 was upregulated in 60 cases of GC tissues.Highly expressed RPPH1 promotes the proliferation and metastasis of GC cells by regulating p21 expression.	Statistical analysis revealed that RPPH1 expression was positively correlated with the TNM stage, lymph node metastasis, and infiltration depth in GC patients. Besides, highly expressed lncRNA RPPH1 suggested poor prognosis of GC patients.	Yes	After interfering in RPPH1 expression, both colony formation assay and EdU staining indicated that the proliferative capacity of GC cells was repressed.	33215423
RPPH1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[TUBB3]	ISH//RNA Pull-Down//IHC//RNA-seq	In this study, we report that lncRNA RPPH1 was significantly upregulated in CRC tissues.Mechanistically, RPPH1 induced epithelial-mesenchymal transition (EMT) of CRC cells via interacting with β-III tubulin (TUBB3) to prevent its ubiquitination. 	In this study, we report that lncRNA RPPH1 was significantly upregulated in CRC tissues, and the RPPH1 overexpression was associated with advanced TNM stages and poor prognosis.	Yes	RPPH1 was found to promote CRC metastasis in vitro and in vivo.	31685807
circFBXW8	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues, cells and the exosomes 	Interaction(miR-370-3p/TRIM44)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 CircFBXW8 and TRIM44 expression were upregulated, while miR-370-3p was downregulated in NSCLC tissues, cells and the exosomes from NSCLC cells compared with respective controls.  CircFBXW8 acted as a sponge of miR-370-3p and regulated NSCLC cell malignancy by binding to miR-370-3p. Additionally, miR-370-3p repressed NSCLC cell processes by regulating TRIM44. 		Yes	CircFBXW8 depletion repressed NSCLC cell proliferation, migration and invasion, but promoted cell apoptosis. CircFBXW8 knockdown inhibited tumor formation in vivo. Further, circFBXW8 secretion was mediated by exosomes. 	34988777
RPPH1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML tissues and cell lines	Regulation[RPPH1/miR-330-5p axis]	Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//cell invasion assay	 RPPH1 was expressed in the AML tissues and cell lines and its high expression predicted worse overall survival in AML patients. Our work highlights the contributions of RPPH1 in promoting AML progression through targeting miR-330-5p, and suggests that the RPPH1/miR-330-5p axis is a potential target for AML treatments.	 RPPH1 was expressed in the AML tissues and cell lines and its high expression predicted worse overall survival in AML patients. 	Yes	Knockdown of RPPH1 suppressed the proliferation, invasion and migration ability of human AML cells, which was partially reversed by additional administration with miR-330-5p inhibitor. RPPH1 knockdown significantly inhibited the growth of xenografted THP-1 tumor in nude mice. 	31645843
Rpph1	LncRNA	Mus musculus	Alzheimer Disease	cortical tissues	Regulation[miR-122/Wnt1 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay	Both lncRNA Rpph1 and miR-122 were up-regulated in AD mouse. Both lncRNA Rpph1 and miR-122 were up-regulated in AD mouse and Rpph1 activated Wnt/β-catenin signaling to ameliorate amyloid-β induced neuronal apoptosis in SK-N-SH cells via direct targeting miR-122.		Yes	Either over-expression of Rpph1 or inhibition of miR-122 restored the cell viability or decreased cell apoptosis rate in Aβ induced SK-N-SH cells.	31718352
Rpph1	LncRNA	Mus musculus	Diabetic Nephropathies	renal tissues	Regulation[Gal-3/Mek/Erk signaling pathway]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//FISH//RNA-seq//ELISA//EdU Staining	In this study, we identified differentially expressed lncRNAs in DN using RNA-sequencing. Among these lncRNAs, we identified seven DN-related lncRNAs in vivo and in vitro using quantitative real-time PCR. One lncRNA in particular, Rpph1 (ribonuclease P RNA component H1), exhibited significantly increased expression. The results revealed that Rpph1 directly interacts with the DN-related factor galectin-3 (Gal-3). Further, over-expression of Rpph1 promoted inflammation and cell proliferation through the Gal-3/Mek/Erk signaling pathway in MCs under low glucose conditions, while knockdown of Rpph1 inhibited inflammation and cell proliferation through the Gal-3/Mek/Erk pathway in MCs under high glucose conditions. These results provide new insight into the association between Rpph1 and the Gal-3/Mek/Erk signaling pathway during DN progression.		Yes	Further, over-expression or knockdown of Rpph1 was found to regulate cell proliferation and the expression of inflammatory cytokines in mesangial cells (MCs). 	31285427
RPLP0P2	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissue	Expression(highly expressed)	CCK8//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	 The results demonstrated that the expression levels of RPLP0P2 were higher in CRC tissue compared with those in normal tissue, and RPLP0P2 was associated with prognosis. 	. The results demonstrated that the expression levels of RPLP0P2 were higher in CRC tissue compared with those in normal tissue, and RPLP0P2 was associated with prognosis. 	Yes	 RPLP0P2 knockdown significantly decreased cell colony formation, migration and invasion, and arrested CRC cells in the S phase to G2/M phase transition. Furthermore, apoptosis was significantly increased in CRC cells infected with the RPLP0P2 shRNA lentivirus compared with in the control group. 	33649783
F-circEA-2a	CircRNA	Homo sapiens	gastric adenocarcinoma	GA tissues	Interaction(miR-3940-5p)	BrdU//qRT-PCR//Transfection//RNA Pull-Down	We found that F-circEA-2a and premature miR-3940-5p were overexpressed in GA, while mature miR-3940-5p was under-expressed in GA.F-circEA-2a suppressed miR-3940-5p maturation in GA cells. MiR-3940-5p directly bound to F-circEA-2a wild type (-wt), but not mutant (-mut).		Yes	 F-circEA-2a promoted GA cell proliferation and inhibited the role of miR-3940-5p in reducing cell proliferation. Therefore, F-circEA-2a might suppress mature miR-3940-5p formation by sponging premature miR-3940-5p to promote cell proliferation in GA. 	35235752
circABCB10	CircRNA	Homo sapiens	laryngeal carcinoma	HaCat cells	Expression(lower expressed)	Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry	 The results of RT-qPCR detection indicated that the expression of circ-ABCB10 in all three laryngeal carcinoma cells was downregulated by 3.2 times compared with that of HaCat cells. There is low expression of circ-ABCB10 in most laryngeal carcinoma tissues, the diagnostic cutoff value of circ-ABCB10 is 0.0008, the area under the curve is 0.718, the sensitivity is 0.981, and the specificity is 0.556. The expression of circ-ABCB10 in laryngeal carcinoma was significantly higher compared to that in paracancerous tissues. Silencing circ-ABCB10 could significantly inhibit the growth and proliferation of laryngeal adenocarcinoma cells, while overexpression of circ-ABCB10 could significantly promote the growth of laryngeal adenocarcinoma cells, probably by inhibiting KLF6 to enhance the proliferation of laryngeal carcinoma and inhibit apoptosis.		Yes	The expression level of KLF6 in laryngeal carcinoma is on the rise, which is significantly higher compared to healthy tissues (P < 0.05); 48 hours after transfection, RT-qPCR analysis confirmed the transfection efficiency, and upregulation of circ-ABCB10 could significantly promote cell proliferation. Compared with the control group, silencing circ-MTCL1 could inhibit cell proliferation, overexpression of circ-ABCB10 promoted cell migration, and downregulation of circ-ABCB10 significantly inhibited cell movement (P < 0.001). Upregulation of circ-ABCB10 significantly enhanced the invasiveness and motility of laryngeal cancer cells, while downregulation of circ-ABCB10 was the opposite. 	35756421
hsa_circ_0008450	CircRNA	Homo sapiens	Liver Neoplasms	HCC tissues ,cells	regulation[miR-431/AKAP1 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	Circ_0008450 was upregulated in HCC tissues and hypoxia-disposed HCC cells. In conclusion, circ_0008450 repression mitigated the progression of HCC under hypoxia by downregulating AKAP1 via miR-431, providing a potential target for HCC treatment.		Yes	 Depletion of circ_0008450 suppressed tumor growth in vivo and reversed the repression of apoptosis and the acceleration of viability and glycolysis of HCC cells induced by hypoxia treatment in vitro. 	33193848
RPL34-DT	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-575/ACAA2 axis)	Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	RPL34-AS1 was significantly down-regulated in ESCC tissues and cells, which was negatively correlated with overall survival in ESCC patients. Functionally, upregulation of RPL34-AS1 dramatically suppressed ESCC cell proliferation, colony formation, invasion and migration in vitro, whereas knockdown of RPL34-AS1 elicited the opposite function. Consistently, overexpression of RPL34-AS1 inhibited tumor growth in vivo. Mechanistically, RPL34-AS1 acted as a competing endogenous RNA (ceRNA) of miR-575 to relieve the repressive effect of miR-575 on its target ACAA2, then suppressed the tumorigenesis of ESCC.	RPL34-AS1 was significantly down-regulated in ESCC tissues and cells, which was negatively correlated with overall survival in ESCC patients. 	Yes	Functionally, upregulation of RPL34-AS1 dramatically suppressed ESCC cell proliferation, colony formation, invasion and migration in vitro, whereas knockdown of RPL34-AS1 elicited the opposite function. Consistently, overexpression of RPL34-AS1 inhibited tumor growth in vivo.	36162992
hsa_circ_0072309	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC  samples	Interaction(miR-607/FTO axis )	In Vivo Experiment//RNA Pull-Down//cell invasion assay//qRT-PCR//Luciferase Report Assay//migration assay//Cell Proliferation Assay//IHC	 Based on a microarray assay, we found that hsa_circ_0072309 was significantly upregulated in NSCLC compared with matched normal samples. Through the above work, we found that hsa_circ_0072309 interacted with miR-607 via its miRNA response element to upregulate the expression of FTO, an m6A demethylase and downstream target of miR-607, thus promoting tumorigenesis of NSCLC.		Yes	 Moreover, functional experiments demonstrated that hsa_circ_0072309 promotes the proliferation, migration, and invasion of NSCLC cells. 	33879631
RUSC1-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma cell line U2OS and HOS, human samples	Interaction(miR-340-5p and PI3K/AKT pathway)	qRT-PCR//RIP	 The results showed that the expression of RUSC1-AS1 was significantly upregulated in osteosarcoma cell line U2OS and HOS compared to that in human osteoblast cell line hFOB1.19. Similar results were found in human samples.  Mechanically, we showed that RUSC1-AS1 directly binds to and inhibits miR-340-5p and activates the PI3K/AKT signaling pathway. 		Yes	Silencing RUSC1-AS1 by siRNA significantly inhibited U2OS and HOS cell proliferation and invasion, measured by CCK-8 and transwell assay. Besides, knockdown of RUSC1-AS1 increased cell apoptosis in osteosarcoma cell lines.In addition, RUSC1-AS1 promoted the epithelial-mesenchymal transition (EMT) process of osteosarcoma cells. In vivo experiments confirmed that RUSC1-AS1 knockdown had an inhibitory effect on osteosarcoma tumor growth.	34048366
RUBCNL	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[NF-κB pathway ]	Western Blot//Wound Healing Assay//qRT-PCR//FISH//MTT//Luciferase Report Assay//ELISA//Colony Formation Assay//Transwell Assay	 RT-qPCR analysis revealed that PACER was highly expressed in CRC tissues and cells, and a high PACER-expression level was associated with poor prognosis.PACER modulates COX-2 expression through the nuclear factor kappa B (NF-κB) pathway in CRC. 	 RT-qPCR analysis revealed that PACER was highly expressed in CRC tissues and cells, and a high PACER-expression level was associated with poor prognosis.	Yes	MTT assay, wound-healing assay, colony-formation assay, and transwell assay revealed that PACER enhanced CRC-cell proliferation, invasion, and metastasis in vitro. Mouse xenograft models of CRC revealed that PACER promoted colorectal tumorigenesis in vivo.	34316376
RUNX1-IT1	LncRNA	Homo sapiens	Lung Neoplasms	cancerous lung cells and tissues	Expression(lower expressed)	CCK8//qRT-PCR//Western Blot//Transwell Assay	Low expression levels of lncRNA RUNX1-IT1 were detected in the cancerous lung cells and tissues. The findings of the Western blot assessment showed that the overexpression or knockdown of lncRNA RUNX1-IT1 significantly affected the expression of cluster of differentiation 44, cluster of differentiation 133, sex-determining region Y-box 2, octamer-binding transcription factor 4, and Nanog, and regulated the sphere-forming ability of cells.		Yes	The overexpression of lncRNA RUNX1-IT1 significantly restricted the ability of cells to proliferate, produce clones, form spheres, and invade lung cancer cells, while the knockdown of lncRNA RUNX1-IT1 had the opposite effect. Additionally, the overexpression or knockdown of lncRNA RUNX1-IT1 regulated the invasion ability of cells by affecting expressions of E-cadherin, N-cadherin, and Vimentin.	35116340
RUNX1-IT1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,CRC cell lines (HCT116, HT29, and RKO) 	Expression[lower expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Significant down regulation of lncRNA RUNX1-IT1 was measured in CRC tissues and three CRC cell lines (HCT116, HT29, and RKO) compared with paired nontumorous adjacent tissues (P < 0.01) or the normal colonic epithelial cell line FHC (P < 0.05), respectively. The protein levels of PCNA, Ki67, and MMP9 were upregulated by overexpressing lncRNA RUNX1-IT1 and down regulated in si-RUNX1-IT1 cells. Besides, lncRNA RUNX1-IT1 could also promote the apoptosis of CRC cells. In conclusion, lncRNA RUNX1-IT1 is downregulated in CRC and plays a tumour-suppressive role due to the regulatory of cell proliferation, migration, and apoptosis. SIGNIFICANCE OF THE STUDY: We demonstrated that lncRNA RUNX1-IT1 was down regulated both in CRC tissues and cell lines. Besides, lncRNA RUNX1-IT1 could serve as a potential diagnostic biomarker and play a tumour-suppressive role owing to its good diagnostic efficacy and inhibition of CRC cell proliferation and migration		Yes	 Moreover, the proliferative and migration potential of CRC cells were inhibited by overexpressing lncRNA RUNX1-IT1, which could be obviously improved by knocking down lncRNA RUNX1-IT1. 	30499136
RUNX1-IT1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC Tissues,cell lines (Huh7, Hep3B, and HCCLM3) 	Interaction[MAPK pathways]	CCK8//qRT-PCR//Western Blot	"he expression level of lncRNA RUNX1-IT1 significantly decreased in HCC tissues. The 
protein changes of P-P38, P-ERK, and P-JNK in 
cells overexpressing lncRNA RUNX1-IT1 were 
significantly lower than those of the vector groExpression[Expression[up-expression]-expression] 
(p<0.05). However, no significant changes were 
found in the protein expressions of P38, ERK, 
and JNK (Figures 4A, 4B). In addition, the pro_x0002_tein changes of P-P38, P-ERK, and P-JNK in the 
cells with Expression[down-expression]-expression of lncRNA RUNX1-
IT1 were remarkably higher than those of the 
vector groExpression[Expression[up-expression]-expression] (p<0.05). Similarly, no significant 
changes were found in the protein expressions of 
P38, ERK, and JNK (Figures 4C, 4D). "		Yes	The overexpression of lncRNA RUNX1-IT1 remarkably inhibited the proliferation and induced the apoptosis of HCC cells. On the contrary, the knockExpression[down-expression] of lncRNA RUNX1-IT1 remarkably enhanced the ability of proliferation and repressed the apoptosis of the HCC cells. 	31646558
RUNX1-IT1	LncRNA	Homo sapiens	Glioblastoma	GBM tissues 	Interaction(miR-195/cyclin D1)	Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay	 RUNX1-IT1 was upregulated in GBM. RUNX1-IT1 and miR-195 interacted with each other, but failed to regulate the expression of each other. Overexpression of RUNX1-IT1 resulted in the upregulation of cyclin D1, and also reduced the effects of miR-195 overexpression on cyclin D1 expression. RUNX1-IT1 and cyclin overexpression increased cell proliferation, while miR-195 overexpression decreased cell proliferation. In addition, RUNX1-IT1 overexpression reduced the effects of miR-195 overexpression on cell proliferation.		Yes	RUNX1-IT1 and cyclin overexpression increased cell proliferation, while miR-195 overexpression decreased cell proliferation. In addition, RUNX1-IT1 overexpression reduced the effects of miR-195 overexpression on cell proliferation.	33507136
RUNX1-IT1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues	regulation[RUNX1 ]	qRT-PCR//RNA-seq	 In this study, we identified a novel PC-associated lncRNA, RUNX1-IT1, that was significantly upregulated in PC patient samples from multiple centers and associated with poor prognosis. Overall, RUNX1-IT1 is a crucial oncogenic lncRNA that activates C-FOS expression by regulating and recruiting RUNX1 and is a potential prognostic biomarker and therapeutic target for PC.	 In this study, we identified a novel PC-associated lncRNA, RUNX1-IT1, that was significantly upregulated in PC patient samples from multiple centers and associated with poor prognosis. 	Yes	 In vitro and in vivo, alterations in RUNX1-IT1 expression markedly affected PC proliferation, migration and invasion. 	32487998
RUNX1-IT1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues 	regulation[miR-21]	CCK8//qRT-PCR//RNA Pull-Down//Luciferase Report Assay	We found that RUNX1-IT1 was downregulated in EC and inversely correlated with mature miR-21 but not miR-21 precursor. RUNX1-IT1 is downregulated in EC and inhibits cancer cell proliferation by suppressing the maturation of miR-21.		Yes	 Overexpression of RUNX1-IT1 suppressed the role of miR-21 in increasing cell proliferation.	33408517
RUNDC3A-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	THCA cells	Interaction(miR-151b/SNRPB Axis)	Western Blot//Bioinformatics Analysis//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining	 RUNDC3A-AS1 exhibited high expression in THCA cells.  Importantly, RUNDC3A-AS1 targeted miR-151b to regulate the SNRPB expression. In rescue assays, SNRPB overexpression partially reversed the suppressive effect of RUNDC3A-AS1 knockdown on cell proliferation and the promotive effect of RUNDC3A-AS1 knockdown on cell apoptosis. The RUNDC3A-AS1/miR-151b/SNRPB axis regulated THCA cell proliferation and apoptosis, which provides novel insight into THCA investigation at the molecular level.		Yes	RUNDC3A-AS1 knockdown suppressed cell proliferation but induced cell apoptosis. 	35242185
RUNDC3A-AS1	LncRNA	Homo sapiens	Thyroid Cancer Lung Metastasis	thyroid cancer tissues and cell lines	Interaction(miR-182-5p/ADAM9)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The results indicated that RUNDC3A-AS1 was highly expressed in the thyroid cancer tissues and cell lines.Mechanistically, RUNDC3A-AS1 served as an inhibitor of miR-182-5p in tumor tissues and cell lines. RUNDC3A-AS1 inhibited the expression of miR-182-5p to increase the expression level of ADAM9, thus further aggravating the malignancy of thyroid cancer. 		Yes	 Functionally, knockdown of RUNDC3A-AS1 could repress the migration and invasion of thyroid cancer cells in vitro, and inhibit thyroid cancer metastasis to lung in vivo. 	34046406
RUBCNL	LncRNA	Homo sapiens	Pulmonary Disease, Chronic Obstructive	blood	Expression[highly expressed]	CCK8//qRT-PCR//Transwell Assay	PACER was upregulated in serum of COPD patients, which was a potential biomarker for diagnosing COPD.		Yes	Overexpression of PACER in primary rat alveolar epithelial cells enhanced proliferative and migratory abilities.	33378047
circHMGCS1	CircRNA	Homo sapiens	Hepatoblastoma	HB tissues	Regulation[IGF Signaling Pathway ]	ISH//qRT-PCR//circRNA-seq	 In this report, we analyzed the expression prolife of circRNAs in HB tissues and identified circHMGCS1 (3-hydroxy-3-methylglutaryl-CoA synthase 1; hsa_circ_0072391) as a remarkably upregulated circRNA.CircHMGCS1 regulates IGF2 and IGF1R expression via sponging miR-503-5p, and affects the downstream PI3K-Akt signaling pathway to regulate HB cell proliferation and glutaminolysis.	 HB patients with high circHMGCS1 expression have shorted overall survival.	Yes	Knockdown of circHMGCS1 inhibits HB cells proliferation and induces apoptosis.	30809316
RUBCNL	LncRNA	Homo sapiens	Mycoplasma Pneumoniae-Induced Inflammatory	A549 cells	Interaction(NF-κB)	Other	 First, we observed that PACER was upregulated in MP infected A549 cells. By performing luciferase reporter assay, we found PACER knockdown inhibited NF-κB activation induced by MP. Furthermore, RNA immunoprecipitation showed that PACER could physically bind to NF-κB p50 in MP-treated A549 cells.		Yes	 Knockdown of PACER suppressed the production of inflammatory cytokines as well as the expression of COX-2 in A549 cells after MP infection. 	35181614
RSU1P2	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues and cells	Interaction(microRNA let-7a/Tex10)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//cell invasion assay//Colony Formation Assay//Transwell Assay	In this study, the expression of LncRNA RSU1P2 was significantly elevated in liver cancer tissues and cells. In addition, LncRNA RSU1P2 can interact with microRNA let-7a (let-7a), and repress let-7a expression. Testis-Expressed Protein 10 (Tex10) was identified to be a target of let-7a, and let-7a repressed Tex10 expression. 		Yes	 Besides, knockdown of RSU1P2 repressed cell viability, invasion, epithelial-mesenchymal transition (EMT) of liver cancer cells and the expressions of cancer stem cell-related genes, whereas facilitated the apoptosis of liver cancer cells.  Finally, RSU1P2 knockdown suppressed tumor volume, tumor weight, and EMT in a xenograft model. 	35156514
RPSAP52	LncRNA	Homo sapiens	Stomach Neoplasms	 GC cells	Interaction( miR-665/STAT3)	RNA Pull-Down//Northern Blot//Western Blot//Flow Cytometry//qRT-PCR//CCK8	 LncRNA RPSAP52 is significantly elevated in GC cells. MiR-665 was verified as the target of lncRNA RPSAP52. A ceRNA-sponge mechanism of lncRNA RPSAP52 on miR-665 was identified. Meanwhile, miR-665 functions as STAT3 sponge. MiR-665 overexpression and STAT3 depletion served the same functions as lncRNA RPSAP52 depletion in GC cells. LncRNA RPSAP52 exerted anti-cancer effects via modulating miR-665/STAT3 in GC.		Yes	Deletion of lncRNA RPSAP52 restrained cell proliferation and induced G0-G1 phase arrest, while expediting apoptosis in GC cells. Tumor growth in vivo was suppressed following lncRNA RPSAP52 depletion. 	35322746
RPSAP52	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	TSCC samples	Interaction( miR-423-5p/MYBL2)	Transfection//qPCR//Luciferase Report Assay//Cell Proliferation Assay//ELISA	We indicated that RPSAP52 was higher in TSCC samples compared with that in control samples.  We found that the overexpression of RPSAP52 suppressed miR-423-5p expression in SCC-4 cell.Pearson's correlation indicated that miR-423-5p was negatively associated with that of RPSAP52 in TSCC tissues. Furthermore, MYBL2 was one direct gene of miR-423-5p and elevated expression of miR-423-5p suppressed MYBL2 expression and ectopic expression of RPSAP52 increased MYBL2 expression in SCC-4 cell. 	The higher expression of RPSAP52 was positively correlated with higher T stage and TNM stage.	Yes	Ectopic expression of RPSAP52 induced TSCC cell growth and cycle and induced cytokine secretion including IFN-γ, IL-1β and IL-6, IL-8, IL-10 and TGF-β. 	33787061
RPSAP52	LncRNA	Homo sapiens	Pituitary Neoplasms	pituitary tissues	Interaction[HMGA proteins]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Microarray	We report that RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues.		Yes	 Moreover, functional studies indicate that RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle.	31076808
hsa_circ_0001187	CircRNA	Homo sapiens	Colitis, Ulcerative	UC patients	Interaction(miR-1236-3p/MYD88 axis)	Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA//EdU Staining	 Circ_0001187 was overexpressed in UC patients.  Our data confirmed that circ_0001187 facilitated UC progression through miR-1236-3p/MYD88 axis, which might be a potential treatment and diagnosis biomarker for UC.		Yes	Circ_0001187 knockdown enhanced the proliferation, while suppressed apoptosis, inflammation and oxidative stress of TNF-α-induced FHC cells. Circ_0001187 acted as miR-1236-3p sponge, and the effects of circ_0001187 downregulation on TNF-α-induced FHC cell injury were overturned by miR-1236-3p inhibitor. 	35609334
circSETD3	CircRNA	Homo sapiens	Hepatoblastoma	HB clinical tissues and cell lines	Interaction(miR-423-3p/Bcl-2)	In Vivo Experiment//RNA Pull-Down//Immunoblotting//qPCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	Here, we identified that circSETD3 downregulated in both HB clinical tissues and cell lines, compared to that of normal tissues and cells. Next, we validated that miR-423-3p targeted both circSETD3 and 3' untranslated region (3'UTR) of Bim, and circSETD3 positively regulated Bim in HB cells through sponging miR-423-3p in a competing endogenous RNA (ceRNA)-dependent manner.		Yes	 Further gain-of-function experiments validated that circSETD3 overexpression inhibited cell proliferation, viability, migration, epithelial-mesenchymal transition (EMT) and tumorigenesis, and induced cell apoptosis in HB cells. 	34659347
hsa_circ_0000594	CircRNA	Homo sapiens	Hepatoblastoma	 HB tissues	Expression[ Mechanically, hsa_circ_0000594 was identified to have a critical role in HB development through the hsa_circ_0000594/mir-217/SIRT1 regulatory axis, which might become a novel diagnostic marker and potential therapeutic target in HB.]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Expression levels of hsa_circ_0000594 were significantly upregulated in HB tissues compared with those in paired normal liver tissues and showed a clear association with the subtype of HB. Mechanically, hsa_circ_0000594 was identified to have a critical role in HB development through the hsa_circ_0000594/mir-217/SIRT1 regulatory axis, which might become a novel diagnostic marker and potential therapeutic target in HB.		Yes	The knockdown of hsa_circ_0000594 inhibited the malignant phenotype of HB. 	31646606
SNHG1	LncRNA	Homo sapiens	Thyroid Neoplasms	PTC tissue,cell lines	Interaction[SP1/SNHG1/miR-199a-5p]	ChIP//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Among these candidate lncRNAs, SNHG1 was identified to be Expression[Expression[up-expression]-expression]-regulated in both PTC tissue and cells. Mechanistically, SNHG1 sponged miR-199a-5p by complementary binding with specificity protein 1 (SP1) 3'-UTR. Interestingly, transcription factor SP1 targeted the promoter region of SNHG1 to promote its transcriptional level. The interaction within lncRNA, miRNA and target mRNA constructed the feedback loop of SP1/SNHG1/miR-199a-5p/SP1 in PTC.		Yes	Functionally, knockExpression[down-expression] of SNHG1 repressed the proliferation, invasion and tumor growth in vitro and in vivo.	31791587
SNHG1	LncRNA	Homo sapiens	Atherosclerosis	blood	Regulation[miR-17-5p/NF-κB signaling pathway  ]	CCK8//qRT-PCR//ELISA//Luciferase Report Assay	We found that SNHG16 was increased in AS patients and THP-1 macrophage-derived foam cells. Most importantly, we uncovered a previously unappreciated SNHG16/miR-17-5p/ NF-κB signaling axis in promoting proliferation and inflammatory response in AS patients and THP-1 macrophages, which might provide a potential target for treating AS.		Yes	Furthermore, SNHG16 overexpression promoted proliferation, inflammatory response and increased levels of IKKβ, p-IkBα, p-p65 in THP-1 macrophages, while SNHG16 downregulation led to the opposite results.	31646601
SNHG1	LncRNA	Homo sapiens	Glioblastoma	U138MG cells	Expression(Among them, 27 lncRNAs were identified as therapy-resistant lncRNAs that remained dysregulated after both radiotherapy and chemoradiotherapy; while 21 lncRNAs were identified as therapy-sensitive lncRNAs whose expressions were reversed by both radiotherapy and chemoradiotherapy.)	Western Blot//Transfection//qRT-PCR//Microarray//Cell Proliferation Assay	We identified 51 lncRNAs aberrantly expressed in GBM specimens compared with either normal brain samples or epilepsy non-tumor brain samples. Among them, 27 lncRNAs were identified as therapy-resistant lncRNAs that remained dysregulated after both radiotherapy and chemoradiotherapy; while 21 lncRNAs were identified as therapy-sensitive lncRNAs whose expressions were reversed by both radiotherapy and chemoradiotherapy. We further investigated the potential functions of the therapy-resistant and therapy-sensitive lncRNAs and demonstrated their relevance to cell proliferation. We also found that the expressions of several lncRNAs, including SNHG1 and UBL7-AS1, were positively correlated with cell-cycle genes' expressions. Finally, we experimentally confirmed the function of a therapy-resistant lncRNA, SNHG1, and a therapy-sensitive lncRNA, UBL7-AS1, in promoting cell proliferation in GBM U138MG cells. Our in vitro results demonstrated that knockdown of SNHG1 and UBL7-AS1 showed an additive effect in reducing cell proliferation in U138MG cells.		Yes	Among them, 27 lncRNAs were identified as therapy-resistant lncRNAs that remained dysregulated after both radiotherapy and chemoradiotherapy; while 21 lncRNAs were identified as therapy-sensitive lncRNAs whose expressions were reversed by both radiotherapy and chemoradiotherapy. 	35313638
SNHG16	LncRNA	Homo sapiens	Colonic Neoplasms		Regulation[miR-302a-3p/AKT Axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	Furthermore, the starBase database predicted that miR-302a-3p was the target gene of SNHG16, which was supported by dual luciferase assay. The effect of promoting cell proliferation ability induced by SNHG16 overexpression could be partly reversed by co-transfection of miR-302a-3p mimic. Application of the miRanda database indicated that AKT may be modulated by SNHG16, further evidenced by western blot and quantitative PCR assays. AKT overexpression could partly reverse the attenuated colon cancer cell growth caused by miR-302a-3p mimic transfection. Meanwhile, the combination of miR-302a-3p inhibitor and shAKT achieved the parallel result. In conclusion, our study revealed the SNHG16/miR-302a-3p/AKT axis might play a crucial role in colon cancer cell proliferation, thus participating in the process of colon cancer development.		Yes	 In our study, with the aim to identify the role of SNHG16 on colon cell proliferation, SNHG16 was overexpressed or knocked down in vitro, respectively. SNHG16 overexpression accelerated colon cancer cell growth, while cell growth ability was impaired in SNHG16 silencing cells.	31502038
SNHG16	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer cells	regulation[miR-520/VEGF axis]	qRT-PCR//MTT//Transwell Assay	Compared with normal cells, SNHG16 is highly expressed in lung cancer cells.LncRNA SNHG16 as ceRNA promotes the migration of lung cancer cells by regulating the miR-520/VEGF axis.		Yes	Silent SNHG16 has a negative effect on the migration of lung cancer cells.	33015794
SNHG16	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	Interaction(ALDH2)	Western Blot//Wound Healing Assay//Luciferase Report Assay//Cell Viability Assay//Colony Formation Assay//Transwell Assay	The results showed a significant (P < 0.05) transcriptional upregulation of SNHG16 in lung cancer tissues and cell lines. Bioinformatic analysis revealed that SNHG16 interacted with ALDH2 to exert its effects in human lung cancer cells. The expression of ALDH2 was found to be significantly (P < 0.05) suppressed in human lung cancer tissues and cell lines. 		Yes	 However, downregulation of SNHG16 resulted in significant (P < 0.05) inhibition of lung cancer A549 and SK-LU-1 cell proliferation. DAPI and annexin V/PI assays revealed apoptosis to be responsible for inhibition of cell proliferation and colony formation observed upon SNHG16 knockdown.  This was accompanied by enhancement of Bax and suppression of Bcl-2 expression in A549 and SK-LU-1 cells. Transwell assays revealed that silencing of SNHG16 also significantly (P < 0.05) inhibited migration and invasion of A549 and SK-LU-1 cells.	35646120
SNHG16	LncRNA	Homo sapiens	Colorectal Neoplasms	CC tissues and adjacent normal tissues	Interaction[ sponging miR-200a-3p]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	A revealed that SNHG16 level was significantly higher in CRC tissues compared with normal tissues.MiR-200a-3p was inversely correlated with SNHG16 expression in CRC tissues.	 	Yes	 Further, in vivo study also revealed that overexpression of SNHG16 could promote tumor growth.	30962265
SNHG16	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal tumors or cells	regulation[miR-124-3p/MCP-1]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//MTT//Luciferase Report Assay//H&E Staining//Transwell Assay	 SNHG16 and miR-124-3p were dysregulated in human colorectal tumors or cells. In summary, our data suggest that SNHG16 plays a contributory role in proliferation, migration, and EMT of CRC cells via miR-124-3p/MCP-1 axis, which offers a rationale for targeting SNHG16 and developing therapeutic drugs to treat CRC.		Yes	Knockdown of SNHG16 led to attenuate cell proliferation, migration, invasion, and EMT of CRC cells. And xenograft tumor experiment showed that SNHG16 might influence tumor growth. 	32859986
SNHG16	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cells	regulation[SNHG16/miR-132-3p/USP22 pathway ]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 SNHG16 was highly expressed in CRC tissues and cells.The discovery of the SNHG16/miR-132-3p/USP22 pathway provided new thinking for the treatment of CRC.		Yes	 Knockdown of SNHG16 reduced the proliferation, migration, invasion, and promoted the apoptosis of CRC cells.	32547062
SNHG16	LncRNA	Homo sapiens	Colorectal Neoplasms	CTC tissues and cells	Interaction(miR-195-5p/Ago2)	qRT-PCR//RIP//ChIP	Mechanistically, SNHG16 acted as a miRNA sponge to sequester miR-195-5p on Ago2, thereby protecting YAP1 from repression. Moreover, YAP1 bound TEA domain transcription factor 1 (TEAD1) to form a YAP1/TEAD1 complex, which in turn bound two sites in the promoter of SNHG16 and regulate SNHG16 transcription. 		Yes	Finally, in vivo experiments showed that the inhibition of SNHG16 suppressed tumor progression, and that YAP1 rescued the effect of SNHG16 on tumor progression.  Furthermore, loss- and gain-of-function assays revealed that SNHG16 promoted CRC colony formation, proliferation, migration, invasion, EMT, mesenchymal-like CTC generation, and liver metastasis through YAP1. 	36147462
SNHG16	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-214-3p/ABCB1 )	qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	 SNHG16 was found to be significantly elevated in human CRC tissues and cell lines.Mechanistically, we identified that SNHG16 is expressed predominantly in the cytoplasm. SNHG16 could interact with miR-214-3p and up-regulated its target ABCB1. 		Yes	Functional studies suggested that SNHG16 promoted CRC cell growth both in vitro and in vivo.	35965433
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	Hepatocellular Carcinoma tissues	Interaction[Regulating miR-186]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our findings showed for the first time that SNHG16 was up-regulated in HCC tissues and cell lines. Further molecular mechanism studies reported that the expression of SNHG16 was negatively correlated with the level of miR-186 and SNHG16 directly bound to miR-186. SNHG16 and miR-186 repressed each other. Notably, rescue experiments were conducted and showed that miR-186 reversed the effect of SNHG16 on cell. 	The expression of SNHG16 in cancer tissues was highly correlated with tumor size, TNM stage, ALT expression level and HBV DNA level. 	Yes	As revealed by our data, SNHG16 accelerated the proliferation, migration and invasion of HCC cell. SNHG16 facilitated tumor formation in vivo	31293662
SNHG16	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	Lung cancer tissues and adjacent normal tissues,cell lines(A292，NCI-H460，NCI-H1703,NCI-H16)	Expression[highly expressed]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//ELISA	In this study, we report that lncRNA SNHG16 is upregulated in non-small cell lung cancer (NSCLC) tissues, and correlates with tumor size, TNM stage and lymph node metastasis.	 Kaplan-Meier analysis shows that the patients with high SNHG16 expression have poorer disease-free survival (DFS) and overall survival (OS) than the patients with low SNHG16 expression. Multivariate Cox regression analysis reveals that SNHG16 expression could be regarded as an independent predictor for DFS and OS in NSCLC patients. 	Yes	Cell experiments show that SNHG16 promotes NSCLC cell proliferation, migration and invasion. miR-146a is further identified and confirmed to be the target of SNHG16, and SNHG16 functions by targeting miR-146a. 	30287374
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues,cell lines	Interaction[ miR-195]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 In our study, our observations showed that the expression level of SNHG16 in HCC tissues and cell lines was upregulated compared with adjacent noncancerous tissues and normal cells. miR-195 expression was significantly decreased in HCC tissues and negatively correlated with SNHG16 expression. Furthermore, RIP and dual luciferase reporter assays showed that SNHG16 acted as an endogenous sponge by directly binding to miR-195 and downregulated its expression. SNHG16 overexpression inverted the inhibitory effect of miR-195 on proliferation and invasion of SMMC7721 and HepG2 cells. Additionally, SNHG16 depletion resulted in lower tumor growth and weight loss, in vivo.		Yes	n vitro, loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation and weakened invasion of SMMC7721 and HepG2 cells. 	31306653
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Interaction[regulating p62]	Western Blot//Wound Healing Assay//Flow Cytometry//FISH//qRT-PCR//MTT//Luciferase Report Assay//Microarray//Transwell Assay	LncRNA SNHG16 is upregulated in HCC and correlates with poorer prognosis.Altering SNHG16 expression altered levels of miR-17-5p, which in turn modified expression of p62, which has been shown to regulate the mTOR and NF-κB pathways. Indeed, altering SNHG16 expression in HCC cells activated mTOR and NF-κB signaling. These results reveal a potential mechanism for the oncogenic role of SNHG16 in HCC. SNHG16 may therefore be a promising diagnostic marker as well as therapeutic target in HCC.	LncRNA SNHG16 is upregulated in HCC and correlates with poorer prognosisPatients with high SNHG16 expression showed lower rates of overall and disease-free survival than patients with low SNHG16 expression. Multivariate Cox regression revealed that SNHG16 expression was an independent predictor of poor overall and disease-free survival.	Yes	 In vitro, SNHG16 promoted HCC cell proliferation, migration, and invasion while inhibiting apoptosis; in vivo, it accelerated tumor development.	31256427
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Expression[highly expressed]	qRT-PCR	We found that SNHG16 was upregulated in HCC tissues and cell lines and that it was negatively correlated with survival time in HCC patients. 	We found that SNHG16 was upregulated in HCC tissues and cell lines and that it was negatively correlated with survival time in HCC patients. 	Yes	Furthermore, downregulation of SNHG16 inhibited proliferation, migration, invasion.	30893293
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[miR-4500/STAT3 axis]	qRT-PCR	In this study, our results delineated that SNHG16 presented much higher expression levels in HCC tissues and cells, particularly in advanced stages of HCC. In other words, this study was the first to investigate the potential mechanism of SNHG16 in HCC and verified SNHG16 exerted its carcinogenesis by miR-4500/STAT3 axis, suggesting SNHG16 may be a new underlying therapeutic target for HCC treatment.	Enhanced SNHG16 expression was strongly related to poor prognosis. 	Yes	 SNHG16 facilitated HCC progression by promoting cell proliferation, migration, invasion, and epithelial-mesenchymal transition process as well as inhibiting cell apoptosis. 	30779219
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[let-7b-5p/CDC25B/CDK1 axis ]	qRT-PCR	 The results revealed that SNHG16 was highly expressed in HCC tissues and cell lines, which predicted poor prognosis of HCC patients. SNHG16 facilitated the G2/M cell cycle transition by directly acting on the let-7b-5p/CDC25B/CDK1 axis, and promoted cell metastasis and EMT progression by regulating the let-7b-5p/HMGA2 axis in HCC.		Yes	On one hand, the downregulation of SNHG16 induced G2/M cell cycle arrest, inducing cell apoptosis and suppression of cell proliferation. On the other hand, it inhibited cell metastasis and EMT progression demonstrated by in vitro loss-of-function cell experiments. Besides, knockdown of SNHG16 increased the sensitivity of HCC cells to cisplatin.	31696971
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	tumor tissues and HCC cell line	Expression(highly expressed)	qRT-PCR//Cell Viability Assay	SNHG16 expression was upregulated in tumor tissues and HCC cell lines.Mechanistic analyses indicated that the ECM-receptor interaction pathway was remarkably activated by SNHG16.	 High expression of SNHG16 was associated with tumor recurrence and poor prognosis after surgery. 	Yes	Moreover, inhibition of SNHG16 in HepG2, Hep3B, and BEL-7402 cells significantly reduced cell invasiveness and proliferation. 	34600815
SNHG16	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC cells	Interaction(miR-942-3p/MMP9 )	qRT-PCR	 Exosomal LncSNHG16 was phagocytized by TCs and downregulated miR-942-3p, which induced targeted MMP9 upregulation, and it had specific binding sites with miR-942-3p in TCs to facilitate the migration of HCC cells in vitro and in vivo. Exosomal LncSNHG16 was found to act as a competing endogenous RNA of the miR-942-3p/MMP9 axis in TCs.		Yes	 Exosomal LncSNHG16 was phagocytized by TCs and downregulated miR-942-3p, which induced targeted MMP9 upregulation, and it had specific binding sites with miR-942-3p in TCs to facilitate the migration of HCC cells in vitro and in vivo.	36434360
MANCR	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cells	Expression(highly expressed)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	MANCR was significantly upregulated in LUAD cells. 	It also resulted in a poor prognosis.	Yes	When MANCR expression was down-regulated, the expression of proteins related to invasion and migration, cell cycle and proliferation was decreased, while the expression of proteins associated with apoptosis was elevated. Furthermore, in vitro experiments revealed that silencing MANCR inhibited cancer cell functions, blocked cell cycle progression while promoting cell apoptosis.	34418982
SNHG16	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[miR-520a-3p/EphA2 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	We found that SNHG16 was upregulated in NSCLC tissues and cell lines, knockdown of SNHG16 inhibited cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. SNHG16 promoted NSCLC development by regulating the miR-520a-3p/EphA2 axis, suggesting novel insights for the pathogenesis of NSCLC and new potential therapeutic targets for the treatment of NSCLC.		Yes	We found that SNHG16 was upregulated in NSCLC tissues and cell lines, knockdown of SNHG16 inhibited cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo.	31953899
SNHG16	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-892b/PPAPDC1A Axis)	Western Blot//RIP//qRT-PCR//Luciferase Report Assay//H&E Staining//IHC	This study demonstrated that SNHG16 expression was significantly increased in BC tissues and cells. Bioinformatics analysis predicted that SNHG16 regulated PPAPDC1A expression by sponging miR-892b, which was confirmed by RNA-fluorescence in situ hybridization (FISH), RT-qPCR, dual-luciferase gene reporter assay, and RNA immunoprecipitation (RIP).In conclusion, EVs derived from BC cells transferred SNHG16 via the miR-892b/PPAPDC1A axis, thus promoting EMT, migration, and invasion of BC.		Yes	Overexpression of SNHG16 promoted the migration, invasion, and epithelial-mesenchymal transition (EMT) of BC cells.  The results confirmed that enhanced miR-892b expression partially eliminated the increase of migration, invasion, and EMT of BC cells mediated by SNHG16 or EVs. The lung metastasis model in nude mice was established by injecting HS578T cells via tail vein. The results showed that si-SNHG16 reduced the metastatic nodules and decreased the vimentin expression. 	34249903
SNHG16	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction[c-Myc ]	qRT-PCR	 In this paper, we found that c-Myc and SNHG16 were overexpressed in OSCC tissues and cell lines compared with normal tissues and normal human oral keratinocytes cells. Moreover, depletion of SNHG16 induced cell apoptosis and inhibited epithelial-to-mesenchymal transition as indicated by induction of cleaved caspase-3 and epithelial cadherin (E-cadherin) along with reduction of N-cadherin and Snail. Intriguingly, c-Myc knockdown led to the similar functional effects as that of SNHG16 knockdown in TSCCA cells. However, these changes caused by c-Myc knockdown were abrogated by SNHG16 overexpression.  Similarly, silencing of c-Myc markedly inhibited tumor growth and reduced SNHG16 expression in nude mice. Moreover, overexpression of SNHG16 blocked the inhibitory effect of c-Myc silencing on tumor growth in vivo. Thus, we conclude that c-Myc-induced upregulation of SNHG16 enhances progression and carcinogenesis in OSCC.		Yes	Depletion of SNHG16 in CAL-27 cells strikingly inhibited cell proliferation, migration and invasion, as indicated by downregulation of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2 and MMP-9.  Knockdown of SNHG16 conspicuously repressed tumor growth in nude mice.	30607006
SNHG17	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD tissues and cells	Interaction(microRNA-193a-5p/NETO2 axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	 The results demonstrated that SNHG17 expression was significantly upregulated in LUAD tissues and cells, and high SNHG17 expression was associated with tumor-node-metastasis stage and poor prognosis of patients with LUAD.  In addition, the results revealed that SNHG17 functions as a competing endogenous RNA of miR-193a-5p. The results of the dual-luciferase reporter assay confirmed that miR-193a-5p can directly target SNHG17. NETO2 was also predicted as a target protein of miR-193a-5p, which was confirmed via the dual-luciferase reporter assay. 	 The results demonstrated that SNHG17 expression was significantly upregulated in LUAD tissues and cells, and high SNHG17 expression was associated with tumor-node-metastasis stage and poor prognosis of patients with LUAD. 	Yes	SNHG17 knockdown inhibited cell migration, invasion, proliferation and the EMT process. 	34671432
SNHG17	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissue 	regulation[FOXA1]	CCK8//qRT-PCR//Western Blot//Transwell Assay	qRT-PCR results indicated that SNHG17 expression was remarkably enhanced in ovarian cancer tissue samples compared with that in adjacent ones. LncRNA SNHG17 can promote ovarian tumor cell proliferative ability and invasiveness by upregulating FOXA1, and serve as a potential therapeutic target for ovarian cancer.		Yes	However, down-regulating SNHG17 attenuated the cell proliferation and invasive ability. 	33015769
SNHG17	LncRNA	Homo sapiens	Ovarian Neoplasms	 EOC cells	Interaction(miR-485-5p/AKT1 axis)	Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 SNHG17 knockdown reduced the proliferation and promoted the apoptosis of EOC cells.MiR-485-5p was proved to be the target miRNA of SNHG17, and SNHG17 negatively regulated the level of miR-485-5p. MiR-485-5p inhibitor significantly abolished the anti-tumor impact of si-SNHG17 on EOC. AKT1 was identified to be targeted by miR-485-5p, and miR-485-5p negatively modulated AKT1 and p-mTOR levels. Moreover, miR-485-5p mimics reduced the proliferation, migration and promoted the apoptosis of EOC cells via targeting AKT1. 		Yes	Consistently, si-SNHG17 obviously reduced the invasion and epithelial-to-mesenchymal transition (EMT) process of EOC cells.  Furthermore, si-SNHG17 markedly suppressed EOC growth in vivo.	36399797
SNHG17	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cell lines	Interaction(miR-384/ELF1 axis )	Tunel//CCK8//qRT-PCR//Colony Formation Assay//EdU Staining	Herein, SNHG17 was disclosed to be remarkably upregulated in OSCC cell lines and promoted OSCC cell growth. Collectively, it can be concluded that SNHG17/miR-384/ELF1 axis contributed to OSCC cell growth via promoting CTNNB1 expression, thus activating Wnt/β-catenin signaling pathway.		Yes	Herein, SNHG17 was disclosed to be remarkably upregulated in OSCC cell lines and promoted OSCC cell growth. 	33531646
SNHG17	LncRNA	Homo sapiens	Osteosarcoma	Five pairs of primary OS adjacent tumor-free tissues and tumor tissues	Interaction(miR-2861)	qRT-PCR//RIP//Migration Assay	We found that SNHG17 was upregulated in the tumor tissues and presented a pro-tumorigenic effect on OS both in vitro and in vivo. CAFs-released exosomal SNHG17 acted as an essential molecular sponge for miR-2861 in OS cells. 		Yes	 It also was an essential exosomal cargo of CAFs and could affect OS cell proliferation and migration in vitro.	34650683
SNHG17	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	serum of CC patients	Interaction(microRNA-375-3p)	Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay	SNHG17 showed an ascending expression while miR-375-3p descended in the serum of CC patients. Serum SNHG17 expression was negatively correlated with miR-375-3p expression, and miR-375-3p was the target miRNA of SNHG17.		Yes	Knockdown of SNHG17 inhibited proliferation, migration, and invasion of CC cells. 	34188550
SNHG17	LncRNA	Homo sapiens	Glioma	glioma tissues	regulation[miR-23b-3p/ZHX1 axis]	CCK8//qRT-PCR//Western Blot//Transwell Assay	"SNHG17 expression was markedly raised in glioma tissues, which was positively correlated with ZHX1 expression and negatively associated with the expression of miR-23b-3p. SNHG17 is a ""competing endogenous RNA"" with respect to modulating ZHX1 expression by adsorbing miR-23b-3p and thereby promoting glioma progression."		Yes	After transfection of SNHG17 shRNAs into glioma cells, the proliferation, migration and invasion of cancer cells was markedly restrained. 	32602607
SNHG17	LncRNA	Homo sapiens	Glioma	 glioma tissues and cells	regulation[miR-506-3p/CTNNB1 axis,Wnt/β-catenin signaling pathway]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining	SNHG17 expression was up-regulated in glioma tissues and cells.The findings that YY1-induced SNHG17 facilitated the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway offered a brand-new prospects to molecular-targeted treatment for glioma.		Yes	 SNHG17 silence attenuated cell proliferation and promoted apoptosis and repressed tumor growth. 	32009853
SNHG17	LncRNA	Homo sapiens	Adenocarcinoma of Lung	cell lines	interaction[sponging miR-485-5p]	RNA Pull-Down//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	SNHG17 and WLS were up-regulated in LUAD cell lines. 		Yes	SNHG17 curbed LUAD cell proliferation, migration and invasion but facilitated apoptosis. SNHG17 acted as miR-485-5p sponge to upregulate WLS expression.	33109341
SNHG17	LncRNA	Homo sapiens	Adenocarcinoma of Lung	NSCLC tissues	Interaction( lncRNA MIR503HG/SNHG17/miR-330-3p/regulatory axis)	CCK8//qRT-PCR//Transfection//migration assay	Finally, we identified the upstream regulatory axis of IRRGs in NSCLC, namely, lncRNA MIR503HG/SNHG17/miR-330-3p/regulatory axis. 		Yes	Finally, knockdown of SNHG17 expression inhibited lung adenocarcinoma (LUAD) cell proliferation and migration.	35719962
SNHG16	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue	regulation[SNHG16/miR-30a axis ]	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Recent studies have reported that the lncRNA small nucleolar RNA host gene 16 (SNHG16) is highly expressed in breast cancer tissue.  Our results indicated that the SNHG16/miR-30a axis regulated the expression of ribonucleotide reductase M2 (RRM2) in breast cancer cells. 		Yes	We found that SNHG16 inhibition reduced the proliferation and invasion of breast cancer cells in vitro. 	32122142
SNHG17	LncRNA	Homo sapiens	Rectal Neoplasms	rectal cancer tissues and cells	Interaction(miR-361-3p/STC2 Axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Bioinformatics Analysis	The upregulation status of SNHG17 was identified in rectal cancer tissues and cells. Furthermore, we showed that microRNA-361-3p (miR-361-3p) has decreased expression in tumor tissues and cells, and SNHG17 functions as a sponge for miR-361-3p. 		Yes	Functionally, knockdown the expression of SNHG17 inhibits rectal cancer cell proliferation via stimulating cell apoptosis. In vivo assay showed that the knockdown of SNHG17 inhibits tumor growth. 	34249085
SNHG17	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	interaction[SNORA71B]	RNA Pull-Down//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//ChIP	Results depicted that transcript 6 of SNHG17 and SNORA71B were upregulated in PC. In conclusion, current study first revealed that lncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop, which might do help to the pursuit of better PC treatment.		Yes	Knockdown of SNHG17 or SNORA71B weakened proliferation, invasion, migration, and epithelial-to-mesenchymal transition (EMT) and strengthened apoptosis.	32447342
SNHG17	LncRNA	Homo sapiens	Prostatic Neoplasms	CRPC tissues and cells	regulation[miR-144/CD51 Axis]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//FISH//Transwell Assay	Our results further confirmed that both SNHG17 and CD51 were up-regulated in CRPC tissues and cells. Taken together, our study reveals the role of the SNHG17/miR-144/CD51 axis in accelerating CRPC cell proliferation and invasion, and suggests that SNHG17 may serve as a novel therapeutic target for CRPC.		Yes	Functionally, down-regulation of SNHG17 or up-regulation of miR-144 inhibited the proliferation, migration, and invasion of CRPC cells, whereas up-regulation of SNHG17 and down-regulation of miR-144 promoted the proliferation, migration and invasion of CRPC cells in vitro and in vivo.	32351538
SNHG17	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tumor and cell lines 	Expression [highly expressed]	qRT-PCR//Invasion Assay//Western Blot	The clinicopathological analysis revealed that SNHG17 mRNA expression level was increased in the PCa tumor samples, and its high expression levels were associated with poor patient outcomes, indicating that SNHG17 may act as a biomarker for the prognosis of PCa. SNHG17 mRNA expression level was also increased in different PCa tumor cell lines. 	 its high expression levels were associated with poor patient outcomes	Yes	Functionally, SNHG17 increased C4-2 tumor cell growth and aggressiveness by stimulating tumor cell proliferation, survival, invasion and resistance to chemotherapy. Furthermore, SNHG17 promoted in vivo tumor growth in a xenograft mouse model. 	33907582
SNHG17	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells 	Expression[highly expressed]	qRT-PCR	High expressions of SNHG17 were observed in both melanoma tissues and cells. 	Up-regulation of SNHG17 in melanoma patients was associated with lymph node metastasis and tumor stage. Survival assays revealed that those patients with high SNHG17 expression had significantly shorter survival time. SNHG17 was also confirmed to be independently associated with overall survival of melanoma patients.	Yes	. Functional studies confirmed that the proliferation, migration, and invasion of melanoma cells were noticeably reduced by the down-regulation of SNHG17.	31599425
SNHG17	LncRNA	Homo sapiens	Pancreatic Carcinoma	 human PC specimens and cell lines	Interaction(miR-942)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//MTT//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	SNHG17 expression was markedly higher in human PC specimens and cell lines than in normal healthy tissues and pancreatic epithelial cells. MiR-942 expression displayed the opposite trend. Bioinformatics prediction and a dual luciferase reporter assay confirmed that SNHG17 serves as a sponge for miR-942. 		Yes	Loss-of-function assay revealed that SNHG17 silencing reduced the proliferation and viability of PC cells, impaired their migratory and invasive capacities, and led to their apoptosis. All these changes could be reversed by miR-942 inhibition. Further mechanical studies showed that SNHG17 silencing decreased the expression of several tumor modulators, including XXX, and this decrease was countered by miR-942 inhibition. 	33841638
SNHG17	LncRNA	Homo sapiens	Colonic Neoplasms	 COAD tissues and cells	regulation[SNHG17/miR-375/CBX3]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay	We showed SNHG17 was upregulated expression in COAD tissues and cells.In conclusion, we demonstrated a novel SNHG17/miR-375/CBX3 triplets that participates in COAD progression, which may provide promising therapeutic targets for COAD.		Yes	Functionally, SNHG17 could promote COAD cell proliferation, colony formation, migration, and invasion in vitro.	33042419
SNHG16	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction[JAK2/STAT3 pathway]	Western Blot//qRT-PCR//RIP//FISH//Luciferase Report Assay	The expression level of SNHG16 in GC cell lines (BGC823, MGC803, MKN45, SGC7901) were all up regulated in different degrees.In addition, the expression level of SNHG16 in GC tissues was measured by qRT-PCR (Fig. ​Fig.11C) and results showed that SNHG16 was up-regulated in GC tissues compared with normal tissues. Collectively, it was suggested that SNHG16 can serve as a miR-135a sponge and block the function of miR-135a in JAK2/STAT3 pathway.		Yes	SNHG16 gene knockdown experiment indicated that the expression level of SNHG16 can influence GC cells proliferation, colony formation, invasion ability and apoptosis in a miR-135a dependent manner. 	30854107
SNHG16	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	tissues and cell lines of bladder cancer	Regulation(p21)	qRT-PCR	 It was discovered that the level of SNHG16 was evidently enhanced both in tissues and cell lines of bladder cancer.  Finally, mechanism experiments revealed that SNHG16 could epigenetically silence the expression of p21. 	Patients with highly expressed SNHG16 suffered from poor overall survival. Multivariable Cox proportional hazards regression analysis implied that highly expressed SNHG16 could be used as an independent prognostic marker.	Yes	It could be known from functional assays that silenced SNHG16 impaired cell proliferation, owing to the effects of SNHG16 on cell cycle and apoptosis.	29234154
SNHG16	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Interaction(miR-17-5p/CCND1 axis )	CCK8//qRT-PCR	LncRNA SNHG16 and CCND1 were upregulated, while miR-17-5p was downregulated in OSCC tissues and cell lines, compared to their normal counterparts. Also, miR-17-5p negatively correlated with both LncRNA SNHG16 and CCND1 mRNA, but LncRNA SNHG16 was positively relevant to CCND1 mRNA in OSCC tissues.  Furthermore, our dual-luciferase reporter gene system evidenced that LncRNA SNHG16 sponged miR-17-5p to upregulate CCND1 in OSCC cells, and the inhibiting effects of LncRNA SNHG16 ablation on OSCC progression were abrogated by both downregulating miR-17-5p and overexpressing CCND1. 		Yes	 By performing the gain- and loss-of-function experiments, we noticed that LncRNA SNHG16 overexpression aggravated the malignant phenotypes, such as cell proliferation, viability, migration and epithelial-mesenchymal transition (EMT) in OSCC cells, while LncRNA SNHG16 knock-down had opposite effects. 	33654431
SNHG17	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Expression(highly expressed)	Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Invasion Assay	Our data showed that SNHG17 expression was significantly upregulated in cancer regions of HCC compared with adjacent regions. 	Increased SNHG17 expression level was correlated with tumor size, TNM stage and poor survival prognosis in HCC patients.	Yes	 Further functional experiments indicated that inhibition of SNHG17 significantly inhibited HCC cell proliferation, migration and invasion, caused cell cycle G0/G1 phase arrest and apoptosis.	34227089
SNHG16	LncRNA	Homo sapiens	Diabetic Retinopathy	hRMECs	Interaction(microRNA (miR)-146a-5p and miR-7-5p/IRAK1/IRS1)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Tube Formation Assay//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Proliferation Assay//ELISA//Transwell Assay	We found that SNHG16 expression was significantly upregulated in hRMECs treated with HG. Moreover, SNHG16 was associated with nuclear factor κB (NF-κB) and phosphatidylinositol 3-kinase (PI3K)/AKT pathways. Mechanistically, SNHG16 could promote hRMEC dysfunction by sequestering microRNA (miR)-146a-5p and miR-7-5p to act as a competing endogenous RNA (ceRNA) with interleukin-1 receptor-associated kinase 1 (IRAK1) and insulin receptor substrate 1 (IRS1). 		Yes	Functionally, SNHG16 could facilitate hRMEC proliferation, migration, and angiogenesis. 	33898104
SNHG16	LncRNA	Homo sapiens	prostate carcinoma	 prostate carcinoma tissues	regulation[GLUT1 ]	Cell Proliferation Assay//qRT-PCR	Overexpression of lncRNA-SNHG16 effectively distinguished prostate carcinoma patients from normal ones.		Yes	 lncRNA-SNHG16 siRNA silencing also significantly inhibited prostate carcinoma cell proliferation.	32210616
SNHG16	LncRNA	Homo sapiens	Neuroblastoma	NB tissues	Expression[highly expressed]	Wound Healing Assay//qRT-PCR//Cell Cycle Assay//Colony Formation Assay//Transwell Assay	Analysis of NB tissue samples (Table I) revealed that SNHG16 expression was increased alongside clinical staging of NB tumor progression (Fig. 1F) and in MYCN-amplified NB (Fig. 1G). 	The expression of SNHG16 was revealed to be in line with the clinical staging of NB, and high SNHG16 expression was positively associated with poor clinical outcome.	Yes	Furthermore, SNHG16 silencing inhibited cell proliferation, repressed migration, and induced cell cycle arrest at the G0/G1 phase in SH‑SY5Y cells. Additionally, apoptosis was undetectable in SH‑SY5Y cells following SNHG16 silencing. 	31180520
SNHG16	LncRNA	Homo sapiens	Neuroblastoma	neuroblastoma tissues and cells	regulation[miR-15b-5p/PRPS1 axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found SNHG16 and PRPS1 levels were increased in neuroblastoma tissues and cells. In conclusion, SNHG16 downregulation suppressed neuroblastoma tumorigenicity by regulating cell cycle, proliferation, and metastasis via miR-15b-5p/PRPS1 axis.		Yes	 SNHG16 knockdown inhibited cell proliferation, increased the cell cycle distribution at G0/G1 phase, and decreased the cells at S phase. SNHG16 overexpression caused an opposite effect. SNHG16 silence suppressed neuroblastoma cell metastasis. PRPS1 knockdown constrained cell proliferation and metastasis and regulated cell cycle distribution. 	33105440
SNHG16	LncRNA	Homo sapiens	Neuroblastoma	NB tissues 	regulation[SNHG16/miR-542-3p/HNF4α axis]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our data revealed that SNHG16 and hepatocyte nuclear factor 4 α (HNF4α) were up-regulated, but miR-542-3p was down-regulated in NB. Therefore, SNHG16/miR-542-3p/HNF4α axis modified NB progression via RAS/RAF/MEK/ERK signaling pathway, might highlight a novel therapeutic approach for NB.		Yes	Knockdown of SNHG16 or HNF4α could impede cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro.	32412051
SNHG16	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	interaction[miR-542-3p,ATG5 ]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	SNHG16 was upregulated in NB tissues and cells and associated with clinical stage and poor prognosis of NB. SNHG16 facilitated proliferation, migration, invasion and autophagy of NB cells via sponging miR-542-3p and upregulating ATG5 expression in NB.		Yes	Knockdown of SNHG16 impeded proliferation, migration, invasion and autophagy of NB cells in vitro, and suppressed tumor growth in vivo. 	32021273
SNHG16	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	regulation[SNHG16/miR-128-3p/HOXA7 axis]	Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	 The levels of SNHG16 and HOXA7 were conspicuously increased in NB tissues and cells, while the expression of miR-128-3p was obviously declined, compared with corresponding normal tissues and cells. Knockdown of SNHG16 impeded proliferation, migration, invasion and induced apoptosis through the SNHG16/miR-128-3p/HOXA7 axis in NB cells.		Yes	 SNHG16 silencing inhibited proliferation, migration and invasion and induced apoptosis of NB cells. 	31919621
SNHG16	LncRNA	Homo sapiens	Leukemia	cell lines	regulation[miR-193a-5p/CDK8]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	 SNHG16 was found to be abnormally highly expressed in acute myeloblastic leukemia cell lines, the knockdown of which weakened the viability of the leukemia cells, suppressed cell proliferation and promoted cell apoptosis.The knockdown of SNHG16 suppressed the viability of the leukemia cells, suppressed cell proliferation, and induced cell apoptosis by regulating miR‑193a‑5p/CDK8. 		Yes	 SNHG16 was found to be abnormally highly expressed in acute myeloblastic leukemia cell lines, the knockdown of which weakened the viability of the leukemia cells, suppressed cell proliferation and promoted cell apoptosis.	32705162
SNHG16	LncRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	blood	Interaction[hsa-miR-124-3p]	qPCR//Luciferase Report Assay	SNHG16 gene expression was evaluated by quantitative real-time PCR (qPCR) in both in vitro ALL cell lines and in vivo human samples of T lymphocytes. Hsa-miR-124-3p was inhibited in SNHG16-downregulated MOLT3 and SUP-B15 cells to further evaluate the functional correlation between SNHG16 and hsa-miR-124-3p in ALL. SNHG16 is upregulated in both in vitro ALL cell lines and in vivo human leukemic T-cells. SNHG16 downregulation suppressed ALL proliferation and migration in vitro, and ALL explant in vivo. Hsa-miR-124-3p was demonstrated to interact with SNHG16, and upregulated in SNHG16-downregulated ALL cells. 		Yes	Lentivirus-mediated SNHG16 downregulation was performed in MOLT3 and SUP-B15 cells, to evaluate its functional effects on ALL cell proliferation, migration in vitro, and ALL transplant in vivo. 	30380185
SNHG16	LncRNA	Homo sapiens	pneumonia	blood	Regulation[miR-370-3p/IGF2 axis]	CCK8//qRT-PCR//ELISA//RIP	SNHG16 and IGF2 were upregulated while miR-370-3p was downregulated in serum of acute pneumonia patients and LPS-induced A549 cells. SNHG16 impeded cell viability and promoted apoptosis, inflammatory injury by targeting IGF2 mediated by miR-370-3p in LPS-induced A549 cells.		Yes	SNHG16 regulated proliferation, apoptosis and inflammatory cytokines by inhibiting miR-370-3p in LPS-induced A549 cells.	31841752
SNHG16	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction(miR-205-5p/PAK2 Axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	Here, we found that SNHG16 was up-regulated in melanoma. NHG16 can promote the expression of P21-activated kinases 2 (PAK2) by sponging miR-205-5p. PAK2 is the target gene of miR-205-5p. We demonstrated that SNHG16 promotes the metastasis and growth of melanoma through miR-205-5p/PAK2 axis.		Yes	SNHG16 enhances the growth and metastasis of melanoma. 	35983126
hsa_circ_0066715	CircRNA	Homo sapiens	Arthritis, Rheumatoid	macrophage 	Interaction(miR-486-5p)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//RIP//FISH//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	Here, we show that RA was closely associated with low expression of circ_0066715.  Interestingly, the overexpression of miR-486-5p significantly suppressed the attenuation of the cell function and the effect on M1 macrophage polarization caused by circ_0066715 positive expression. WTAP may be involved in the methylation process of ETS1 in RA. ETS1 m6A methylation levels were altered upon WTAP intervention. The overexpression or interference of circ_0066715 decreased or increased WTAP expression. 		Yes	The overexpression of circ_0066715 significantly increased the ETS1 levels in RA-FLS cells, decreased cytokine secretion by M1-type macrophages, elevated M2-type cytokines, and inhibited FLS proliferation. 	36541909
SNHG16	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(EIF4A3/RhoU)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//Colony Formation Assay//qRT-PCR//FISH//RIP//RNA-seq//IHC	 SNHG16 was highly expressed in ESCC and intraepithelial neoplasia (IEN) samples, and its expression level was correlated with tumour differentiation and T stage.  Mechanistically, we noticed that SNHG16 could bind RNA binding protein (RBP)-eukaryotic translation initiation factor (EIF4A3) and interact with it to form a complex. Importantly, the coalition of SNHG16 and EIF4A3 ultimately regulated Ras homologue family member U (RhoU). SNHG16 modulated RhoU expression by recruiting EIF4A3 to regulate the stability of RhoU mRNA. Knockdown of RhoU further alleviated the effect of the SNHG16 oncogene in ESCC cells.	 SNHG16 was highly expressed in ESCC and intraepithelial neoplasia (IEN) samples, and its expression level was correlated with tumour differentiation and T stage. 	Yes	Overexpression of SNHG16 can facilitate ESCC cell proliferation and metastasis. 	36221055
Snhg16	LncRNA	Mus musculus	Osteoarthritis	 OA tissue	Interaction(miR‑373‑3p)	Western blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	lncRNA SNHG16 was upregulated in OA tissue compared with normal joint tissue. Furthermore, the luciferase activity assay suggested that SNHG16 negatively regulated miR‑373‑3p in OA. Finally, the results suggested that the proinflammatory effect of IL‑1β on CHON‑001 cells was significantly reduced by SNHG16 knockdown. 		Yes	SNHG16 knockdown significantly increased the expression levels of aggrecan, and decreased the expression levels of MMP13, cleaved caspase?3 and p21 in IL?1β?treated CHON?001 cells. In addition, IL?1β induced CHON?001 cell apoptosis, while SNHG16 knockdown decreased IL?1β?induced apoptosis.	33300061
hsa_circ_0044235	CircRNA	Homo sapiens	Arthritis, Rheumatoid	plasma	Expression(highly expressed)	qRT-PCR	 Hsa-circ0044235 was found to be significantly decreased in plasma from patients with new-onset RA compared with HC and OA + UA patients, but was significantly increased compared with SLE patients. The expression of plasma hsa-circ0000175 in new-onset RA patients was associated with platelet count (PLT), plateletcrit (PCT), and platelet large cell ratio (PLR), the expression of plasma hsa-circ0044235 new-onset RA patients was associated with swollen joint count (SJC), painful joint count (PJC), and disease activity score 28 (DAS28). ROC curve analysis suggested that the combination of hsa-circ0000175 and hsa-circ0044235 has some value in the diagnosis of new-onset RA from HC, patients with SLE and patients with OA + UA. The logistic regression analysis revealed that the expression of hsa-circ0000175 and hsa-circ0044235 in plasma were risk factors for RA. This study suggests that the combination of plasma hsa-circ0000175 and hsa-circ0044235 improves the diagnostic accuracy for new-onset RA. Moreover, the expression levels of plasma hsa-circ0000175 and hsa-circ0044235 were associated with disease activity and severity of RA.	the expression of plasma hsa-circ0044235 new-onset RA patients was associated with swollen joint count (SJC), painful joint count (PJC), and disease activity score 28 (DAS28). ROC curve analysis suggested that the combination of hsa-circ0000175 and hsa-circ0044235 has some value in the diagnosis of new-onset RA from HC, patients with SLE and patients with OA + UA. The logistic regression analysis revealed that the expression of hsa-circ0000175 and hsa-circ0044235 in plasma were risk factors for RA. 	Yes	We confirmed that hsa-circ0000175 was significantly elevated in plasma from patients with new-onset RA compared with HC and patients with new-onset SLE, but significantly was reduced when compared with OA + UA patients.	34008433
hsa_circ_0000175	CircRNA	Homo sapiens	Arthritis, Rheumatoid	plasma	Expression(highly expressed)	qRT-PCR	 Hsa-circ0044235 was found to be significantly decreased in plasma from patients with new-onset RA compared with HC and OA + UA patients, but was significantly increased compared with SLE patients. The expression of plasma hsa-circ0000175 in new-onset RA patients was associated with platelet count (PLT), plateletcrit (PCT), and platelet large cell ratio (PLR), the expression of plasma hsa-circ0044235 new-onset RA patients was associated with swollen joint count (SJC), painful joint count (PJC), and disease activity score 28 (DAS28). ROC curve analysis suggested that the combination of hsa-circ0000175 and hsa-circ0044235 has some value in the diagnosis of new-onset RA from HC, patients with SLE and patients with OA + UA. The logistic regression analysis revealed that the expression of hsa-circ0000175 and hsa-circ0044235 in plasma were risk factors for RA. This study suggests that the combination of plasma hsa-circ0000175 and hsa-circ0044235 improves the diagnostic accuracy for new-onset RA. Moreover, the expression levels of plasma hsa-circ0000175 and hsa-circ0044235 were associated with disease activity and severity of RA.	the expression of plasma hsa-circ0044235 new-onset RA patients was associated with swollen joint count (SJC), painful joint count (PJC), and disease activity score 28 (DAS28). ROC curve analysis suggested that the combination of hsa-circ0000175 and hsa-circ0044235 has some value in the diagnosis of new-onset RA from HC, patients with SLE and patients with OA + UA. The logistic regression analysis revealed that the expression of hsa-circ0000175 and hsa-circ0044235 in plasma were risk factors for RA. 	Yes	We confirmed that hsa-circ0000175 was significantly elevated in plasma from patients with new-onset RA compared with HC and patients with new-onset SLE, but significantly was reduced when compared with OA + UA patients.	34008433
SNHG15	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Interaction(miR-506-5p)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	 In the present study, we found that SNHG15 was up-regulated in GC tissues and cell lines.  More importantly, microRNA-506-5p (miR-506-5p) was predicted as a direct target of SNHG15 by binding its 3'-UTR and further verified using luciferase reporter assay. Meanwhile, the results of rescue experiments revealed that knockdown of miR-506-5p expression reversed the functional effects of SNHG15 silenced cell proliferation, migration, invasion and apoptosis. 		Yes	Silencing SNHG15 suppressed proliferation migration, invasion and promoted apoptosis of AGS cells. 	33899079
SNHG15	LncRNA	Homo sapiens	Breast Neoplasms	BC cells and clinical tissues	Interaction(miR-451/c-Myc signaling )	IHC//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Our data indicated LncRNA SNHG15 upregulated c-Myc to facilitate BC progression by sponging miR-451 in a competing endogenous RNA (ceRNA)-dependent manner in vitro and in vivo. Specifically, LncRNA SNHG15 and c-Myc were upregulated, while miR-451 was downregulated in BC cells and clinical tissues, compared to their normal counterparts. 		Yes	 Our data indicated LncRNA SNHG15 upregulated c-Myc to facilitate BC progression by sponging miR-451 in a competing endogenous RNA (ceRNA)-dependent manner in vitro and in vivo.	33952250
SNHG15	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissues 	Expression[highly expressed]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	Results of qRT-PCR showed that the expression of SNHG15 in cancer tissues was increased compared with that in para-carcinoma tissues.		Yes	Results of cell counting kit-8 (CCK-8) assay showed that knocking down SNHG15 could significantly inhibit the proliferation of lung cancer A549 cells. 	29771418
SNHG16	LncRNA	Homo sapiens	Rhinitis, Allergic	AR tissues	Interaction(miR-106b-5p/LIF JAK1/STAT3 pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//ELISA//IF	RT-qPCR results showed that the expression of SNHG16 in AR was up-regulated. In conclusion, SNHG16 up-regulates LIF expression by binding with miR-106b-5p, thus promoting the activity of JAK1/STAT3 pathway, and promoting the development of AR. These results provide new targets for the treatment of AR and may help reduce the damage caused by AR.		Yes	The results showed that SNHG16 promoted cell apoptosis and inflammation. 	34407675
SNHG16	LncRNA	Homo sapiens	Melanoma	melanoma tissues and cell lines	interaction[sponging miR-132]	CCK8//qRT-PCR//Transwell Assay	 SNHG16 was overexpressed, and miR-132 was low expressed in melanoma tissues and cell lines.SNHG16 promotes the expression of LAPTM4B by sponging miR-132, thereby acting as an oncogene in melanoma. 	 Moreover, overexpression of SNHG16 was associated with poor prognosis of melanoma patients. 	Yes	 Knockdown of SNHG16 or overexpression of miR-132 inhibited SK-MEL-2 cell proliferation and migration. 	32864914
SNHG16	LncRNA	Homo sapiens	pancreatic adenocarcinoma	 PC tissues and cell lines	Interaction(miR-302b-3p/SLC2A4 axis)	qRT-PCR//Luciferase Report Assay//Western Blot	SNHG16 expression was significantly elevated in PC tissues and cell lines and was associated with poor prognosis of PC patients.Knockdown of SNHG16 reduced PC cell proliferation, migration and invasion. SNHG16 acted as a sponge to regulate miR-302b-3p expression in PC cells. In addition, miR-302b-3p targeted SLC2A4 directly.	SNHG16 expression was significantly elevated in PC tissues and cell lines and was associated with poor prognosis of PC patients.	Yes	Knockdown of SNHG16 reduced PC cell proliferation, migration and invasion. SNHG16 acted as a sponge to regulate miR-302b-3p expression in PC cells. In addition, miR-302b-3p targeted SLC2A4 directly.	33435953
SNHG16	LncRNA	Homo sapiens	Esophageal Neoplasms	CSCs	Interaction(microRNA-802/PTCH1 Axis)	qRT-PCR//MeRIP//RIP	Upregulated SNHG16 expression was found in CSCs, whose expression was decreased during the differentiation of CSCs. SNHG16 or PTCH1 overexpression or miR-802 inhibition promoted the proliferation, colony formation, and tumorsphere formation of EC9706 and KYSE150 cells as well as SOX2, OCT4, Bmi-1, and PTCH1 expression. Moreover, SNHG16 and PTCH1 were competitively bound to miR-802, and SNHG16 orchestrated the miR-802/PTCH1 axis to activate the Hedgehog pathway.		Yes	SNHG16 or PTCH1 overexpression or miR-802 inhibition promoted the proliferation, colony formation, and tumorsphere formation of EC9706 and KYSE150 cells as well as SOX2, OCT4, Bmi-1, and PTCH1 expression. Consistently, SNHG16 knockdown or miR-802 overexpression inhibited EC progression. SNHG16 silencing repressed the tumorigenicity of EC9706 in nude mice.	35579168
SNHG16	LncRNA	Homo sapiens	Endometrial Neoplasms	ECa tissue and cells	Regulation[TFAP2A/SNHG16/miR-490-3p/HK2 axis]	Western Blot//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//ChIP	Results presented that SNHG16 expression was increased in the ECa tissue and cells, In conclusion, this finding illustrates the vital role of SNHG16 via the TFAP2A/SNHG16/miR-490-3p/HK2 axis in the ECa proliferation and glycolysis, providing an interesting insight for the ECa tumorigenesis.	Results presented that SNHG16 expression was increased in the ECa tissue and cells, and the ectopic SNHG16 overexpression was closely correlated with the poor survival rate and recurrence free survival of ECa.	Yes	 In functional experiments, SNHG16 knockdown suppressed the proliferation, glycolysis and tumor growth of ECa cells. 	31814916
SNHG16	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Interaction[sponges miR-98-5p]	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	The ectopic expression of SNHG16 was found in osteosarcoma tissues and cell lines.LncRNA SNHG16 regulated cellular processes in osteosarcoma by sponging miR-98-5p, and SNHG16 may be a new and effective molecular therapeutic target for osteosarcoma.	The ectopic expression of SNHG16 was found in osteosarcoma tissues and cell lines, which indicated poor prognosis and lower overall survival rate of osteosarcoma patients. 	Yes	 Knockdown of SNHG16 inhibited cell proliferation, migration, invasion, cell cycle and promoted apoptosis in osteosarcoma.	30923843
SNHG16	LncRNA	Homo sapiens	Osteosarcoma	OS tissues and cell lines	Interaction[Sponging miRNA-340 ]	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Viability Assay	We found that SNHG16 is overexpressed in OS tissues and cell lines.The results showed that SNHG16 involves in the migration and invasion of OS cells through sponging miRNA-340. 		Yes	Inhibition of SNHG16 reduced OS cells proliferation, stimulated apoptosis, and decreased migration and invasion. 	30726150
SNHG16	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Regulation[miR-1301/BCL9 axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In the current study, we confirmed that SNHG16 expression was markedly up-regulated in OS tissues compared to paracancerous tissues.SNHG16 promotes BCL9 expression by sponging miR-1301 to facilitate the proliferation, migration and invasion of OS cells.	 The elevated level of SNHG16 closely associated with advanced tumor stages, larger tumor size and more distance metastasis. Furthermore, OS patients with high SNHG16 level had a significant poorer overall survival compared to patients with low SNHG16 level.	Yes	Knockdown of SNHG16 suppressed the proliferation, migration and invasion of U2OS and MG63 cells.	30909141
SNHG16	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Expression[highly expressed]	qRT-PCR	 Small nucleolar RNA host gene 16 (SNHG16) and autophagy-related 4B (ATG4B) were significantly upregulated in osteosarcoma tissues than the normal ones, and the higher expression level of SNHG16 predicted a poor prognosis in osteosarcoma patients.	 Small nucleolar RNA host gene 16 (SNHG16) and autophagy-related 4B (ATG4B) were significantly upregulated in osteosarcoma tissues than the normal ones, and the higher expression level of SNHG16 predicted a poor prognosis in osteosarcoma patients.	Yes	SNHG16 was shown to promote cell growth, migration, and invasion, while miR-16 reversed this impact.	31427084
SNHG16	LncRNA	Homo sapiens	Osteosarcoma	tissues of patients with OS and OS cell lines	Interaction(miR-1285-3p)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	The present study demonstrated that SNHG16 is highly expressed in both the tissues of patients with OS, as well as OS cell lines, and its expression level was positively correlated with clinical stage and poor overall survival.In addition, the present study revealed that microRNA-1285-3p expression levels can be decreased by SNHG16 acting as a 'sponge', and that this pathway takes part in OS tumor growth in vivo, and OS cell proliferation, invasion, migration and apoptosis in vitro.	its expression level was positively correlated with clinical stage and poor overall survival	Yes	 Functional assays revealed that the depletion of SNHG16 inhibits OS growth, OS cell progression and promotes apoptosis both in vivo and in vitro. 	33823834
SNHG16	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	Interaction( miR-488/ ITGA6)	CCK8//qRT-PCR	 SNHG16 and ITGA6 were significantly increased while miR-488 was decreased in osteosarcoma. ITGA6 was screened as a target gene of miR-488, and SNHG16 was sponged by miR-488 in osteosarcoma cells. 		Yes	MiR-488 overexpression and SNHG16 knockdown suppressed migration, invasion and EMT of osteosarcoma cells. Moreover, rescue assays proved that the influences of SNHG16 on osteosarcoma cells migration, invasion and EMT were dependent on miR-488 and ITGA6. In addition, the promotive effects of SNHG16 on osteosarcoma tumor growth and metastasis were further supported by xenograft tumor growth assay.	33598394
SNHG16	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML patients and cells	Interaction(PTEN/PI3K/AKT axis)	qRT-PCR//Bioinformatics Analysis	This study showed that SNHG16 was upregulated in AML patients and cells. Taken together, the present study indicated that SNHG16 promoted proliferation and migration of AML cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein.		Yes	And SNHG16 overexpression remarkably enhanced the proliferation and migration capacities of HL60 and AML-193 cells, while SNHG16 knockdown acted the opposite way. 	33576342
SNHG16	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cell lines	Interaction[recruiting transcriptional factor SPI1 to upregulate PARP9]	RIP//Luciferase Report Assay//ChIP	Here, quantitative analysis of SNHG16 and PARP9 expression levels in cervical cancer tissues and cell lines indicated that both SNHG16 and PARP9 were highly expressed compared with controls. These data indicate that SNHG16 recruits SPI1 to upregulate PARP9, which promotes the tumorigenicity of cervical cancer cells. The regulation of their expression might provide a new direction for treating cervical cancer.		Yes	After ectopic expression and knockdown experiments were conducted, it was observed that silencing SNHG16 inhibited PARP9 expression, proliferation, and invasion of cervical cancer cells, which was rescued by co-transfection of SNHG16 silencing and PARP9 overexpression. Moreover, in vivo experimental results showed that silencing SNHG16 reduced the expression of PARP9 and suppressed tumor growth. 	31774223
SNHG16	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissue	Interaction(miR‑373‑3p/ TGF‑β‑R2/SMAD pathway )	Luciferase Report Assay	The results demonstrated that the expression levels of SNHG16 and TGF‑β‑R2 were significantly upregulated in PCa tissues, whereas miR‑373‑3p expression was significantly downregulated (P<0.001).  In addition, negative correlations were observed between SNHG16 and miR‑373‑3p (rho, ‑0.631) and miR‑373‑3p and TGF‑β‑R2 (rho, ‑0.516). 		Yes	Overexpression of SNHG16 significantly promoted the proliferation, migration and invasion of PCa cells (P<0.05), and significantly increased the protein expression levels of TGF‑β‑R2, phosphorylated (p)‑SMAD2, p‑SMAD3, c‑Myc and E2F4 (P<0.001).	34643247
SNHG16	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[Suppressing p21]	CCK8//qRT-PCR//Flow Cytometry	 The expression of SNHG16 were up-regulated in both glioma tissues and cell lines.Moreover, p21 could mediate cell proliferation and monoclonal formation, promote cell apoptosis in glioma, which was negatively correlated with lncRNA SNHG16. The molecule mechanism experiments revealed that SNHG16 could not only inhibit the expression of p21 but also suppressed the level of caspase 3 and 9, while promoted cyclinD1 and cyclinB1 expression. lncRNA SNHG16 could promote the cell proliferation and inhibit the apoptosis of glioma through suppressing p21, indicating that lncRNA SNHG16 might be quite vital for the diagnosis and progression of glioma and could even be a novel therapeutic target for glioma.		Yes	 Knockdown of SNHG16 was associated with poor proliferation, decreased monoclonal formation rates, but increased apoptosis rates, which also caused the high expression of p21.	30972632
SNHG16	LncRNA	Homo sapiens	Glioma	 glioma tissues and cell lines	Interaction( SNHG16-miR-4518-PRMT5 )	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//ELISA//Bioinformatics Analysis	 SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. Further investigation revealed that SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518. Moreover, SNHG16 also affects the expression of Bcl-2 family proteins and the activation of PI3K/Akt signaling pathway.	 SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. 	Yes	Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells.	29529599
SNHG16	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	Interaction(miR-520a-3p/MAPK1 axis)	In Vivo Experiment//IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	SNHG16 was overexpressed in NPC tissues and cells. Additionally, SNHG16 could directly bind to miR-520a-3p, thus positively regulating MAPK1 expression. Moreover, functional analysis indicated that miR-520a-3p exerted a tumor-suppressing role in NPC progression. 	 High SNHG16 expression indicated a poor prognosis. 	Yes	SNHG16 knockdown could cause significant inhibition on cell proliferation and metastasis, induce cell apoptosis in NPC cells, and repressed tumor growth and metastasis in vivo.	34045897
SNHG16	LncRNA	Homo sapiens	Multiple Myeloma	MM tissues	interaction[sponging miR-342-3p]	Flow Cytometry//qRT-PCR//Luciferase Report Assay	SNHG16 expression was up-regulated in MM tissues. Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG16 as a novel therapeutic target for MM.		Yes	SNHG16 knockdown suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted the apoptosis of MM cells. 	32025219
SNHG16	LncRNA	Homo sapiens	Pancreatic Neoplasms	cell lines	Regulation[miR-195/SREBP2 axis]	Wound Healing Assay//Transwell Assay	 LncRNA SNHG16 directly sponged miR-195 to modulate the lipogenesis via regulating the expression of SREBP2. 		Yes	Both the knock down of lncRNA SNHG16 and SREBP2 and overexpression of miR-195 suppressed the proliferation, migration, invasion and lipogenesis in pancreatic cancer cells.	31664866
SNHG16	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues	Interaction[targeting miR-218-5p]	RNA Pull-Down//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//cell invasion assay	An increase in expression of SNHG16 in PC samples against adjacent normal tissues was shown here.Mechanistically, SNHG16 might serve as a sponge competitive endogenous RNA (ceRNA) for miR-218-5p, thereby playing a role in regulating the expression of high mobility group box 1 (HMGB1) expression, a known direct miR-218-5p target in PC cells. These results provide novel insight into PC tumorigenesis and suggest that SNHG16 could serve as a likely therapeutic intervention in PC.	Increased SNHG16 was linked intimately to the tumor-node-metastasis (TNM) stage, distant metastasis, tumor differentiation, and poor overall survival.	Yes	 Loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation, formation of colonies, ability to migrate and invade in vitro, along with a lowered growth of the tumor in a mouse model.	30981105
SNHG16	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA tissues and CCA cell lines.	Interaction( miR-146a-5p/GATA6 Axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	 SNHG16 was significantly elevated in CCA tissues from TCGA database and CCA cell lines. miR-146a-5p, a downstream target of SNHG16, was shown to be an intermediate mediator of GATA6 expression regulated by SNHG16. In addition, either the miR-146a-5p inhibitor or overexpression of GATA6 obviously impaired the regulatory effects of SNHG16 downregulation in RBE and HuCCT1 cells. 		Yes	Moreover, downregulation of SNHG16 restricted cell proliferation and increased apoptotic rate of RBE and HuCCT1 cells.	33797690
SNHG16	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues and cells	regulation[miR-877-5p/FOXP4 Axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 SNHG16 expression was increased in LSCC tissues and cells.LncRNA SNHG16 promotes the progression of LSCC by sponging miR-877-5p and upregulating FOXP4.	The abnormal expression of SNHG16 was associated with clinical stage and lymph node metastasis in LSCC patients. 	Yes	 In addition, knockdown of SNHG16 restrained cell proliferation, migration and invasion in LSCC.	32547087
SNHG17	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues and cell lines	Expression(highly expressed)	qRT-PCR	Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. . Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC.	tilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. 	Yes	 Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. 	34557456
SNHG17	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC human samples	Interaction(miR-3180-3p/RFX1)	CCK8//qRT-PCR//Western Blot	 Our study demonstrated that SNHG17 was upregulated in HCC human samples and involved cell proliferation, migration, invasion progress. Furthermore, we investigated the downstream factor of SNHG17, SNHG17 acted as a molecular sponge for miR-3180-3p, and SNHG17 regulated RFX1 expression via miR-3180-3p. SNHG17 promotes tumor-like behavior in HCC cells via miR-3180-3p/RFX1.		Yes	 Our study demonstrated that SNHG17 was upregulated in HCC human samples and involved cell proliferation, migration, invasion progress. SNHG17 promoted HCC cell growth and metastasis in vivo.	33519911
SNHG1	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	nasopharyngeal carcinoma tissues,cell lines	Interaction[miR-145a-5p]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	SNHG1 is highly expressed in nasopharyngeal carcinoma tissues and in cell lines.  Down-regulation of SNHG1 facilitated the expression of miR-145-5p and further suppressed the level of NAUK1 in CNE and HNE-1 cells. Silencing of SNHG1, up-regulation of miR-145-5p and inhibition of NAUK1 by relative transfection all attenuated the aggressiveness of CNE and HNE-1 cells both in vivo and in vitro. Moreover, the impaired cell migration and invasion by SNHG1 siRNA could be rescued by cotransfection of miR-145-5p in CNE and HNE-1 cells. LncRNA SNHG1 promoted the expression of NUAK1 by down-regulating miR-145-5p and thus promoted the aggressiveness of nasopharyngeal carcinoma cells through AKT signalling pathway and induced epithelial-mesenchymal transition (EMT).		Yes	 Down-regulation of SNHG1 facilitated the expression of miR-145-5p and further suppressed the level of NAUK1 in CNE and HNE-1 cells. Silencing of SNHG1, up-regulation of miR-145-5p and inhibition of NAUK1 by relative transfection all attenuated the aggressiveness of CNE and HNE-1 cells both in vivo and in vitro. 	29575772
SNHG22	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cells	regulation[miR-429/SESN3 axis]	CCK8//qRT-PCR//Colony Formation Assay//Flow Cytometry	Then, we found that SNHG22 was highly expressed in ESCC cells (Kyse-150, TE-10, and Eca109), especially in TE-10 and Eca109.  SNHG22 promotes the progression of ESCC by the miR-429/SESN3 axis.		Yes	 Inhibition of SNHG22 was found that can inhibit the progression and promotes autophagy and apoptosis of ESCC cells.	32953807
circFNDC3B	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cell line	Interaction(miR-214-3p/CDC25A axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	CircFNDC3B was highly expressed in ESCC, and high circFNDC3B expression was tightly associated with poor prognosis in ESCC patients. Mechanistically, circFNDC3B acted as a sponge for miR-214-3p to up-regulate the expression of its target CDC25A. Rescue experiments showed that miR-214-3p inhibitor reversed the anticancer effects of circFNDC3B knockdown. Moreover, forced expression of miR-214-3p suppressed the malignant phenotypes mentioned above, while this condition was abolished by CDC25A overexpression. 	CircFNDC3B was highly expressed in ESCC, and high circFNDC3B expression was tightly associated with poor prognosis in ESCC patients. 	Yes	Functionally, circFNDC3B knockdown not only suppressed ESCC cell growth, migration and invasion in vitro, but hindered ESCC tumour growth in vivo. 	36184488
SNHG29	LncRNA	Homo sapiens	Spontaneous Preterm Birth	HTR8/SVneo cells	Regulation(p53/p21 signaling )	Cell Proliferation Assay//qPCR//Western Blot	SNHG29 was overexpressed in the placentas of women who delivered preterm with labor and in HTR8/SVneo cells treated with H2O2 (p < 0.05). We observed an increase in the expression of IL-8 and TNF-α in senescent HTR8/SVneo cells (p < 0.05).		Yes	 The levels of mRNA of p53 and p21, protein levels of p53, phospho-p53, p21and phospho-p21, and β-galactosidase activity was decreased in HTR8/SVneo cells depleted of SNHG29, while the opposite trend was observed in HTR8/SVneo cells overexpressing SNHG29 (p < 0.05). 	33080448
SNHG26	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cells	Interaction( PGK1/Akt/mTOR signal pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Co-IP//qRT-PCR//FISH//RIP//RNA-seq//Cell Proliferation Assay//Cell Cycle Assay//IHC//Invasion Assay//Transwell Assay	The results of next-generation transcriptomic sequencing revealed that lncRNA-SNHG26 was differentially expressed and was associated with TSCC cisplatin resistance. Furthermore, in TSCC cells, SNHG26 was found to bind directly to the PGK1 protein, inhibiting its ubiquitination and activating the Akt/mTOR signaling pathway. 	 The Cancer Genome Atlas dataset and tumor tissue analysis revealed that high SHNG26 expression was associated with the occurrence, progression, and poor prognosis of TSCC. 	Yes	 Evidence from cell and animal experiments showed that SNHG26 expression was positively correlated with TSCC proliferation, epithelial-mesenchymal transformation, migration, invasion, and cisplatin resistance. 	35118193
SNHG25	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	30 ovarian cancer tissue samples and 30 normal ovarian tissue samples	Expression [highly expressed]	qRT-PCR//RNA-seq	n the present study, we showed that SNHG25 expression was up-regulated in EOC tissues relative to normal ovarian tissues. High-throughput sequencing and western blot analysis showed a significant decrease in the expression of COMP mRNA and protein in SNHG25 knockdown compared to control ovarian cancer cells. 		Yes	In vitro, functional experiments demonstrated that high expression of SNHG25 promoted proliferation, migration and invasion, and decreased apoptosis, in ovarian cancer cell lines. In vivo, downregulation of SNHG25 inhibited the growth (tumor volume) of subcutaneous xenografts in nude mice. 	33613753
SNHG25	LncRNA	Homo sapiens	Glioma	glioma cells and tissues	Interaction(miR-579-5p/MAP2K2 )	In Vivo Experiment//IHC//Western Blot//Transfection//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	In this study, we found that SNHG25 was upregulated in glioma cells and tissues. Further studies indicated that SNHG25 positively regulated MAP2K2 through sponging miR-579-5p. High expression of SNHG25 activated MAPK signaling through MAP2K2. These data suggest that SNHG25 is a potential target and biomarker for glioma.		Yes	 CCK-8, EDU, and colony formation assays demonstrated that SNHG25 knockdown markedly inhibited glioma cell proliferation. In vivo studies showed that SNHG25 knockdown significantly inhibited tumor growth. 	36071306
SNHG22	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cells	regulation[microRNA-361-3p/HMGA1/Wnt/β-Catenin Axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down	SNHG22 and HMGA1 were highly expressed but miR-361-3p was poorly expressed in GC tissues.Collectively, SNHG22 silencing possessed tumor-suppressing potentials in GC development via Wnt/β-catenin pathway by binding to miR-361-3p and downregulating HMGA1, highlighting a new promising road for GC treatment development.		Yes	Following SNHG22 or HMGA1 silencing or miR-361-3p upregulation, we observed a decline of proliferation, migration, and invasion of GC cells and HUVEC angiogenesis but acceleration of GC cell apoptosis and cell cycle arrest.	33364835
SNHG22	LncRNA	Homo sapiens	Stomach Neoplasms	 GC (Gastric Cancer) tissues and cells	Interaction(miR-200c-3p/Notch1 axis)	In Vivo Experiment//RNA Pull-Down//IHC//ChIP//Western Blot//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Here, we report that the expression of lncRNA SNHG22 (small nucleolar RNA host gene 22) was significantly increased in GC (Gastric Cancer) tissues and cells, which confers poor prognosis of patients. In addition, using RNA pull-down followed MS assay, we found that SNHG22 directly bound to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) to suppress the expression of tumor suppressor genes. At the same time, SNHG22 sponged miR-200c-3p to increase Notch1 (notch receptor 1) expression. 	 Here, we report that the expression of lncRNA SNHG22 (small nucleolar RNA host gene 22) was significantly increased in GC (Gastric Cancer) tissues and cells, which confers poor prognosis of patients. 	Yes	Knockdown of SNHG22 inhibited the proliferation and invasion ability of GC cells. Moreover, we identified that the transcriptional factor, ELK4 (ETS transcription factor ELK4), could promote SNHG22 expression in GC cells. 	34663788
SNHG22	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissue, TCGA database, GC cell lines, and clinical tissue samples	Interaction(miR-101-3p/e2f2 axis)	CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our result showed that SNHG22 was upregulated significantly in GC tissue samples from TCGA database, GC cell lines, and clinical tissue samples, and its expression was related to low survival rate of gastric cancer patients. Bioinformatics prediction predicted miR-101-3p as the potential target of SNHG22 and E2F2 genes as miR-101-3p target mRNA. We found that E2F2 expression was negatively associated with overall survival of GC patients. Functional study showed that silencing SNHG22 markedly inhibited the proliferation, migration, and invasion of GC cells as well as in vivo tumor growth. This was reversed after inhibiting miR-101-3p or overexpressing E2F2. The lncRNA SNHG22 promotes the proliferation, migration, and invasion of GC cells via the miR-101-3p/E2F2 axis. SNHG22 might be a potential prognostic indicator in gastric cancer.	Our result showed that SNHG22 was upregulated significantly in GC tissue samples from TCGA database, GC cell lines, and clinical tissue samples, and its expression was related to low survival rate of gastric cancer patients. Bioinformatics prediction predicted miR-101-3p as the potential target of SNHG22 and E2F2 genes as miR-101-3p target mRNA. We found that E2F2 expression was negatively associated with overall survival of GC patients.	Yes	Functional study showed that silencing SNHG22 markedly inhibited the proliferation, migration, and invasion of GC cells as well as in vivo tumor growth. 	36281526
SNHG22	LncRNA	Homo sapiens	Colorectal Neoplasms	 adenoma tissues and ANTs	Interaction(miR‑128‑3p/E2F3 )	CCK8//qRT-PCR//Western Blot	The present study revealed that SNHG22 expression was most highly expressed in TTs followed by adenoma tissues and ANTs. The mechanistic study revealed that SNHG22 bound to miR‑128‑3p and attenuated its inhibitory effects on E2F transcription factor 3 (E2F3) expression levels and activity.	 In addition, high SNHG22 expression levels were significantly associated with advanced clinicopathological factors and worse survival in patients with CRC. 	Yes	SNHG22 knockdown markedly inhibited CRC cell proliferation, apoptosis resistance, migration and invasion in vitro, and hindered tumor growth in vivo. 	34368861
Snhg3	LncRNA	Mus musculus	Cerebral Ischaemia/Reperfusion Injury	cell models (treated with OGD/R or LPS) and mouse models (tMCAO)	Interaction(HDAC3)	RNA Pull-Down//Western Blot//Transfection//Co-IP//qRT-PCR//RIP//H&E Staining//ELISA//IHC//IF	Levels of SNHG3, microglial activation marker Iba-1, proinflammatory factors (TNF-α and IL-6) were highly expressed in cell models (treated with OGD/R or LPS) and mouse models (tMCAO). Besides, SNHG3 could bind to HDAC3 and promote its expression. Through further study, we found that SNHG3 could stabilize the protein levels of HDAC3 and inhibit the ubiquitination of HDAC3. Furthermore, interference with SNHG3 down-regulated the levels of HDAC3, Iba-1, TNF-α, and IL-6, whereas the overexpression of HDAC3 reversed the results. 		Yes	The H&E staining assay demonstrated that the condition of vacuoles of different sizes, uneven cytoplasmic staining, and inflammatory infiltration in the brain tissue was improved by interference with SNHG3. The immunohistochemistry result showed that microglial activation marker Iba-1 was increased in the shRNA-SNHG3 group, indicating that interference with SNHG3 inhibited the activation of microglia in the brain. 	34411323
SNHG22	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(EZH2/DNMT1/miR-16-5p axis)	Western Blot//CCK8//qRT-PCR//RIP//ChIP	 In our report, we discovered the high level of SNHG22 in HCC tissues and cells, and the high expression of SNHG22 was correlated with unfavorable clinical outcome in HCC patients.  Mechanistic exploration revealed that SNHG22 recruited DNMT1 to miR-16-5p DNA promoter through EZH2 and inhibited miR-16-5p transcription via DNA methylation. Finally, we verified that the suppression of miR-16-5p countervailed the suppressive effect of SNHG22 deficiency on HCC cell proliferation, migration, invasion, and angiogenesis.		Yes	 Functional assays implied that SNHG22 deficiency suppressed cell proliferation, migration, invasion, and angiogenesis in vitro. Additionally, it was also confirmed that silenced SNHG22 suppressed tumor growth and angiogenesis in vivo. 	34652260
SNHG22	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	regulation[miR-324-3p,SUDS3]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	SNHG22 represented a high expression level in TNBC tissues and cells. LncRNA SNHG22 facilitated cell growth and motility in TNBC via sponging miR-324-3p and upregulating SUDS3, highlighting a new promising road for TNBC treatment development.		Yes	Besides, SNHG22 silencing restrained the proliferation, migration and invasion of TNBC cells. 	32565736
hsa_circ_0000745	CircRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	ALL patients and cell lines	Interaction(miR-494-3p/NET1 axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay	Circ_0000745 expression was elevated in ALL patients and cell lines.  Circ_0000745 acted as a molecular sponge for miR-494-3p in ALL cells. miR-494-3p silencing partly diminished circ_0000745 knockdown-induced anti-tumor effects in ALL cells. NET1 was a target of miR-494-3p, and miR-494-3p overexpression-induced anti-tumor influences were partly counteracted by the accumulation of NET1 in ALL cells. Circ_0000745 can positively regulate NET1 expression by sponging miR-494-3p in ALL cells.		Yes	 Circ_0000745 knockdown restrained cell cycle progression and glycolysis and triggered cell apoptosis and ferroptosis. 	34957935
SNHG214	LncRNA	Homo sapiens	Osteoarthritis	knee cartilage	regulation[miR-214-5p/PPARGC1B axis]	qRT-PCR//ELISA//Luciferase Report Assay//Western Blot	 The results showed that SNHG7 was distinctly downregulated, while miR-214-5p was significantly upregulated in OA patients and primary chondrocytes treated with IL-1β. Collectively, The above results confirmed that SNHG7 prevents IL-1β induced OA by inhibiting NLRP3 inflammasome and apoptosis through miR-214-5p/PPARGC1B axis.		Yes	 In addition, SNHG7 enhanced cell viability, inhibited apoptosis and inflammation of IL-1β-mediated chondrocytes.	33296783
SNHG20	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Regulation[SNHG20/miR-495-3p/ZFX axis ]	qRT-PCR	Here, our results showed that the lncRNA SNHG20 expression was significantly higher in GC tissues compared with adjacent normal tissues by quantitative real-time PCR (qRT-PCR) analysis.Furthermore, lncRNA SNHG20 expression negatively associated with miR-495-3p expression and regulated miR-495-3p expression	Higher lncRNA SNHG20 expression was highly associated with tumor size and lymphatic metastasis of patients. Patients with higher lncRNA SNHG20 expression predicted a short disease-free survival (DFS) and overall survival (OS). 	Yes	Function assays confirmed that lncRNA SNHG20 knockExpression[down-expression] using RNA interference sExpression[Expression[up-expression]-expression]pressed cell proliferation and invasion of GC by negatively regulating miR-495-3p expression. 	30520073
SNHG20	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines 	Interaction[sponging miR-154]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our results showed that SNHG20 was significantly up-regulated in NSCLC tissues and cells.  Furthermore, SNHG20 could function as a competing endogenous RNA (ceRNA) to elevate ZEB2 and RUNX2 expression by sponging miR-154. Rescue assays revealed that miR-154 inhibition could reverse the inhibitory effect of SNHG20 silence on proliferation, migration and invasion in NSCLC cells. More importantly, SNHG20 knockdown suppressed tumor growth in NSCLC in vivo through suppressing miR-154 and elevating ZEB2 and RUNX2 expression. In summary, knockdown of lncRNA SNHG20 suppressed proliferation, migration and invasion, and promotes apoptosis through up-regulating ZEB2 and RUNX2 expression by sponging miR-154 in NSCLC, providing a promising therapeutic target for NSCLC patients.		Yes	 Moreover, SNHG20 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NSCLC cells. 	30780105
SNHG20	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cancer tissues and serum	regulation[Wnt/β-catenin signaling pathway]	qRT-PCR//Luciferase Report Assay//Western Blot	LncRNA SNHG20 was highly expressed in the cancer tissues and serum of patients with NSCLC. LncRNA SNHG20 promotes the proliferation and inhibits the apoptosis of NSCLC cells by targeting miR-197 through the Wnt/β-catenin signaling pathway.		Yes	 LncRNA SNHG20 could promote the proliferation and inhibit the apoptosis of NSCLC cells.	31957836
SNHG20	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-495/STAT3 axis]	Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Viability Assay//Transwell Assay	 In the present study, SNHG20 expression was found to be significantly upregulated in CRC tissues and cell lines.Taken together, the results revealed that SNHG20 facilitated CRC progression by regulating STAT3 expression and by sponging miR‑495.	Association analysis indicated that high SNHG20 expression was significantly association with greater tumor size (P=0.014), tumor invasion depth (P=0.019), positive lymph node status (P=0.022), distant metastasis (P=0.017) and advanced tumor node metastasis stage (P=0.038).	Yes	 Loss?of?function experiments indicated that SNHG20 knockdown could significantly suppress proliferation, migration and invasion in vitro. Notably, SNHG20 knockdown significantly inhibited tumor growth and lung metastasis in vivo.	33179110
hsa_circ_30032	CircRNA	Homo sapiens	renal fibrosis	BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice	Interaction(miRNA-96-5p/HBEGF/KRAS axis)	Western Blot//Transfection//qRT-PCR//FISH//Luciferase Report Assay//IHC	These results demonstrate that circRNA_30032 promotes renal fibrosis via the miR-96-5p/HBEGF/KRAS axis and suggest that circRNA_30032 is a potential therapeutic target for treatment of renal fibrosis.		Yes	CircRNA_30032 silencing significantly reduced renal fibrosis in UUO model mice by increasing miR-96-5p levels and decreasing levels of HBEGF and KRAS. 	33973871
Snhg3	LncRNA	Mus musculus	Brain Injuries	brain tissue,cell line	Expression[lower expressed]	CCK8//qRT-PCR//MTT//Western Blot	In this study, we determined the role of Snhg3 in the pathogenesis of HIBD. Snhg3 expression was significantly down-regulated in the neonatal brain and primary hippocampal cells response to hypoxic/ischemic stress. 		Yes	 Snhg3 overexpression protected against hypoxic/ischemic-induced brain injury in vivo and hippocampal cell injury in vitro. 	31751562
SNHG20	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues	Expression[highly expressed]	CCK8//qRT-PCR//Western Blot	SNHG20 expression was markedly higher in serous EOC tissues than that in adjacent tissues and closely correlated with histological grade and lymph node (LN) status. 	Patients with high SNHG20 showed a shorter overall survival (OS) and SNHG20 was an independent risk factor for the prognosis of serous EOC.	Yes	. Knockdown of SNHG20 remarkably inhibited EOC cell proliferation, migration, and invasion, which was associated with dysregulation of P21, Cyclin D1, E-cadherin, and Vimentin. 	30846486
SNHG3	LncRNA	Homo sapiens	Prostatic Neoplasms	Pca tissues and cells	Interaction(microRNA-1827)	In Vivo Experiment//Western Blot//Wound Healing Assay//RIP//qRT-PCR//Luciferase Report Assay//Invasion Assay	The results demonstrated that SNHG3 expression was upregulated in PCa tissues downloaded from The Cancer Genome Atlas database, which was associated with poor prognosis. Bioinformatic analysis revealed that microRNA (miRNA/miR)-1827 was a downstream target of SNHG3. The direct interaction between SNHG3 and miR-1827 was validated via the dual-luciferase reporter and RNA immunoprecipitation assays. Pearson's correlation analysis demonstrated that SNHG3 expression was negatively correlated with miR-1827 expression at different stages of PCa. 	The results demonstrated that SNHG3 expression was upregulated in PCa tissues downloaded from The Cancer Genome Atlas database, which was associated with poor prognosis. 	Yes	 Furthermore, cell proliferation, migration and invasion were significantly inhibited following SNHG3 knockdown in vitro, the effects of which were reversed following overexpression of SNHG3 in PCa cells. 	35814830
SNHG3	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tumors and cell lines 	regulation[miR-326/ITGA5 axis,Vav2/Rac1 signaling pathway]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that the expression of SNHG3 and ITGA5 was upregulated and miR-326 was downregulated in TNBC tumors and cell lines (MDA-MB-231, BT-549, MDA-MB-468 and SUM159).  Silencing of SNHG3 suppressed the malignant development of TNBC cells, at least partially, through miR-326/ITGA5 axis and inhibiting Vav2/Rac1 signaling pathway.		Yes	Functionally, both SNHG3 silencing and miR-326 overexpression enhanced cell apoptosis, but depressed cell viability, migration and invasion in MDA-MB-231 and BT-549 cells, as well as inhibited Vav2 and Rac1 expression. 	32495883
SNHG3	LncRNA	Homo sapiens	Glioma	glioma tissues	regulation[miR-384/HDGF axis]	CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay	The expression of SNHG3 and HDGF was upregulated, whereas miR-384 was downregulated in glioma tissues, compared with the normal tissues. LncRNA SNHG3 promotes cell proliferation, migration, and invasion in glioma by enhancing HDGF expression via miR-384 sponging, representing the promising targets for the development of novel therapeutic strategies.		Yes	Moreover, SNHG3 or HDGF knockdown significantly suppressed proliferation, migration, and invasion and induced apoptosis in glioma.	33817254
SNHG3	LncRNA	Homo sapiens	Glioma	glioma tissues	Interaction(miR-485-5p/LMX1B axis)	In Vivo Experiment//qRT-PCR//Transfection//Luciferase Report Assay	 In addition, the expression of SNHG3 and LMX1B in advanced glioma tissues was significantly upregulated, while the expression of miR-485-5p was significantly downregulated. These results indicate that lncRNA SNHG3 can regulate the expression of LMX1B by sponging miR-485-5p, thereby promoting the proliferation, migration, and invasion of glioma cells. 		Yes	SNHG3 overexpression reduced the expression of miR-485-5p; increased the expression of LMX1B; and promoted the proliferation, migration, and invasion of glioma cells. In addition, subcutaneous and orthotropic xenograft models confirmed that lncRNA SNHG3 silencing or miR-485-5p overexpression significantly reduced the growth of glioma xenografts and prolonged survival time.	34153159
SNHG3	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues and cell lines	Interaction(miR-890)	Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//cell invasion assay//Colony Formation Assay	The results revealed that SNHG3 expression levels were downregulated in LUAD tissues and cell lines. Mechanistically, microRNA- (miR-) 890 was identified as a potential target of SNHG3, and its expression was negatively regulated by SNHG3. Notably, SNHG3 was found to promote LUAD progression by targeting miR-890.		Yes	Functionally, SNHG3 overexpression suppressed the proliferation, migration, and invasion of LUAD cells, while promoting apoptosis. 	34306585
SNHG3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 lung cancer tissues and cells	Interaction(miR-515-5p/SUMO2 Axis)	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	In the present study, SNHG3 was found to be highly expressed in lung cancer tissues and cells.  In addition, SNHG3 was found to have the ability to bind to miR-515-5p. Furthermore, Small Ubiquitin Like Modifier 2 (SUMO2) was identified to be the downstream target of miR-515-5p, which was negatively correlated with miR-515-5p expression. SNHG3 could positively regulate SUMO2 expression by sponging miR-515-5p. 		Yes	 Downregulation of SNHG3 could inhibit cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process.	34032148
SNHG3	LncRNA	Homo sapiens	Cholangiocarcinoma	CCA cells	Interaction(miR-3173-5p/ERG Axis)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Invasion Assay	SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells. Mechanistically, SNHG3-sponged miR-3173-5p, thus releasing the repression of ERG by miR-3173-5p. Rescue experiments showed that the miR-3173-5p/ERG axis mediated the oncogenic effect of SNHG3.		Yes	Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells.	34647226
SNHG3	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	 LSCC tissues and cells	regulation[Wnt/β-catenin pathway,miR-340-5p/YAP1 axis]	Flow Cytometry//qRT-PCR//Luciferase Report Assay//Western Blot	 We found that the levels of SNHG3 and YAP1 were increased but the miR-340-5p expression was decreased in LSCC tissues and cells.In conclusion, knockdown of SNHG3 inhibited LSCC progression via inactivating Wnt/β-catenin pathway by regulating the miR-340-5p/YAP1 axis.		Yes	The knockdown of SNHG3 or YAP1 inhibited cell viability and glycolysis but induced apoptosis in LSCC cells.	32538668
SNHG3	LncRNA	Homo sapiens	Prostatic Neoplasms	cell lines	interaction[miR-577 ]	RNA Pull-Down//Western Blot//Tunel//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this work, SNHG3 exerted high expression in prostate cancer cell lines.All the results above explained that SNHG3 accelerated prostate cancer progression by sponging miR-577 to up-regulate SMURF1 expression, suggesting that SNHG3 may act as a biomarker for prostate cancer patients.		Yes	Suppression of SNHG3 inhibited cell proliferation, migration, EMT (epithelial-mesenchymal transition) process and promoted cell apoptosis. 	32248648
SNHG3	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissue and cells	Interaction(SNHG3/miR-152-3p/SLC7A11)	In Vivo Experiment//IHC//Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Cycle Assay//Colony Formation Assay//Invasion Assay	 In this study, our analysis in the TCGA database revealed high SNHG3 expression in PCa tissue.  It was noted that SNHG3 as a molecular sponge of miR-152-3p stimulated proliferation, migration, and invasion, restrained methionine dependence and apoptosis, and affected the cell cycle of PCa cells via targeting SLC7A11. Additionally, we constructed xenograft tumor models in nude mice and confirmed that knockdown of SNHG3 could restrain PCa tumor growth and elevate methionine dependence in vivo.		Yes	 It was noted that SNHG3 as a molecular sponge of miR-152-3p stimulated proliferation, migration, and invasion, restrained methionine dependence and apoptosis, and affected the cell cycle of PCa cells via targeting SLC7A11. Additionally, we constructed xenograft tumor models in nude mice and confirmed that knockdown of SNHG3 could restrain PCa tumor growth and elevate methionine dependence in vivo.	35123415
SNHG3	LncRNA	Homo sapiens	Aortic Valve, Calcification of	human and mouse calcified aortic valves	Regulation(BMP2)	In Vivo Experiment	SNHG3 upregulation was verified in human and mouse calcified aortic valves.  In-depth functional assays showed SNHG3 physically interacted with polycomb repressive complex 2 to suppress the H3K27 trimethylation BMP2 locus, which in turn activated BMP2 expression and signaling pathways. Taken together, SNHG3 promoted aortic valve calcification by upregulating BMP2, which might be a novel therapeutic target in human calcific aortic valve disease.		Yes	Moreover, in vivo and in vitro studies showed SNHG3 silencing markedly ameliorated aortic valve calcification. 	36317131
SNHG3	LncRNA	Homo sapiens	Prostatic Neoplasms	bone metastasis-positive PC tissues	Interaction(SNHG3/miR-214-3p/TGF-β axis)	Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	 Our results indicated that SNHG3 was upregulated in bone metastasis-positive PC tissues compared to bone metastasis-negative PC tissues and adjacent normal tissues. Mechanistically, SNHG3 enhanced the expression of transforming growth factor beta receptor 1 (TGFBR1) and activated transforming growth factor-Beta (TGF-β) signaling by targeting miR-214-3p. 	High expression of SNHG3 indicates advanced clinicopathological features and predicts poor prognosis in patients with PC.	Yes	Meanwhile, SNHG3 knockdown suppressed the proliferation, migration, and invasion abilities of PC cells and inhibited PC cell metastasis to the bone. 	35030969
SNHG3	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cell lines	Interaction(miR-370-5p/EZH1 axis)	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	SNHG3 was upregulated in CRC tissues and cell lines. The SNHG3/miR-370-5p/EZH1 axis was ascertained. 	 Its high level was correlated to advanced tumor staging, positive lymph node metastasis and poor prognosis of CRC. 	Yes	Knockdown of SNHG3 reduced proliferative and invasive rates of SW480 and HT29 cells. 	34661273
SNHG3	LncRNA	Homo sapiens	Carcinoma, Renal Cell		Regulation[ SNHG3/miR-139-5p/TOP2A axis ]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	In this study, we analyzed the available public TCGA and GEO databases, and found that the expression of SNHG3 was increased in clear cell renal cell carcinoma (ccRCC), which was positively correlated with many clinicopathological parameters, and the higher expression of SNHG3 predicted worse clinical prognosis. Our work suggested that the SNHG3/miR-139-5p/TOP2A axis plays an important role in the proliferation and metastasis of ccRCC, and was expected to be a new biomarker for diagnosis, prognosis and a target for treatment of ccRCC.	In this study, we analyzed the available public TCGA and GEO databases, and found that the expression of SNHG3 was increased in clear cell renal cell carcinoma (ccRCC), which was positively correlated with many clinicopathological parameters, and the higher expression of SNHG3 predicted worse clinical prognosis. 	Yes	 Functional experiments indicated that knockdown of SNHG3 could significantly inhibit the proliferation and metastasis of ccRCC in vitro and in vivo.	31505165
SNHG3	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tissues	Interaction(microRNA-10b-5p/BIRC5)	Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//Luciferase Report Assay//Invasion Assay//Transwell Assay	The two novel lncRNAs (LINC00997, SNHG3) were up-regulated in ccRCC tissues and positively with the BICR5 protein expression. However, Suppressing SNHG3 expression reduced BIRC5 protein expression compared with the LINC00997, most importantly, Suppressing SNHG3 expression suppressed tumor progression in vitro. In addition, SNHG3 promotes the expression of BIRC5 protein by sponging microRNA-10b-5p.		Yes	However, Suppressing SNHG3 expression reduced BIRC5 protein expression compared with the LINC00997, most importantly, Suppressing SNHG3 expression suppressed tumor progression in vitro. In addition, SNHG3 promotes the expression of BIRC5 protein by sponging microRNA-10b-5p.	35116306
SNHG3	LncRNA	Homo sapiens	laryngeal carcinoma	LC tissues and cell lines	Regulation[miR-384/WEE1 axis]	qRT-PCR//Luciferase Report Assay	Our results showed increased SNHG3 in LC tissues and cell lines.Collectively, our results indicate that SNHG3 regulated LC cell migration and invasion via the miR-384/WEE1 axis.		Yes	 Loss of function of SNHG3 reduced cell viability, migration, and invasion of TU212 and TU686 cells.	31238052
SNHG3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues	Interaction(miR‑1343‑3p)	Western Blot//Bioinformatics Analysis//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	The findings indicated that lncRNA SNHG3 was highly expressed in NSCLC tissues and cell lines.		Yes	 Knockdown of lncRNA SNHG3 inhibited cell proliferation, migration and invasion, and accelerated cell apoptosis in NSCLC cell lines. The results of the bioinformatics analysis and the luciferase reporter assay indicated that lncRNA SNHG3 directly bound to miR‑1343‑3p and that it could downregulate the expression levels of miR‑1343‑3p to promote the progression of NSCLC.	34132359
circPTPN14	CircRNA	Homo sapiens	renal fibrosis	renal tubule epithelial cells, mouse kidneys	Interaction(FUBP1/FUSE/MYC )	Western Blot//qRT-PCR//Luciferase Report Assay//IHC//IF	We found that a circular RNA, circPTPN14, is highly expressed in human kidneys with biopsy-proved chronic interstitial fibrosis, mouse kidneys subjected to ischemia/reperfusion (IR) or unilateral ureteral obstruction (UUO), and TGFβ1-stimulated renal tubule epithelial cells (TECs). The binding of circPTPN14 to the KH3 and KH4 domains of far upstream element (FUSE) binding protein 1 (FUBP1) enhanced the interaction between FUBP1 and FUSE domain, which was required for the initiation of MYC transcription. In human kidneys (n = 30) with biopsy-proved chronic interstitial fibrosis, the expression of circPTPN14 positively correlated with MYC expression. 		Yes	The intrarenal injection of circPTPN14 shRNA alleviated the progression of fibrosis in kidneys subjected to IR or UUO. Knockdown of circPTPN14 in TECs inhibited TGFβ1-induced expression of profibrotic genes, whereas overexpressing circPTPN14 increased the profibrotic effect of TGFβ1.	36394649
circPlekha7	CircRNA	Homo sapiens	renal fibrosis	renal tissues	Interaction(miR-493-3p/KLF4)	qRT-PCR	 circPlekha7 was diminished in renal tissues from chronic kidney disease patients and TGF-β1-treated human kidney 2 cells and tubular epithelial cells, while miR-493-3p was upregulated. Overexpression of circPlekha7 or knockdown of miR-493-3p suppressed TGF-β1 induced enhancements on epithelial to mesenchymal transition and fibrogenesis, as well as attenuated renal fibrosis and injury in mice subjected to unilateral ureteral obstruction. 		Yes	Overexpression of circPlekha7 or knockdown of miR-493-3p suppressed TGF-β1 induced enhancements on epithelial to mesenchymal transition and fibrogenesis, as well as attenuated renal fibrosis and injury in mice subjected to unilateral ureteral obstruction. 	35172608
hsa_circ_0000745	CircRNA	Homo sapiens	Precursor Cell Lymphoblastic Leukemia-Lymphoma	leukemia cells	regulation[ERK pathway]	qRT-PCR	In this study, we observed circ-0000745 upregulated in leukemia cells (Kasumi-1 and KG-1). Altogether, these results revealed that upregulated circ-0000745 in leukemia cells could promoter cell viability by increasing the activation of ERK pathway.		Yes	Upregulated the expression of circ-0000745 significantly enhanced the proliferation of Kasumi-1 and KG-1 cells, and reduced the ratio of apoptosis cells. Knock down the endogenous expression of circ-0000745 suppressed the cell proliferation and increased the ratio of apoptosis cells. 	32360844
SNHG17	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines (PLC, Hep3B, Huh7 and 7721)	Expression [highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Cell Viability Assay//Cell Cycle Assay	We firstly found that expression levels of lncRNA SNHG17 in HCC tissues and cell lines was higher than that in para-carcinoma tissues and QSG-7701 cells (P<0.05). 	In addition, we observed that patients with tumor size ≥ 5cm, HCC stages III-IV or poor pathological histological types, lncRNA SNHG17 expression were significantly higher than those with tumor size <5 cm, HCC stages I-II or good histopathological types (P<0.05). 	Yes	 In vitro studies showcased that low expression of lncRNA SNHG17 restrained HCC cell proliferation and evoked cell cycle arrest. Further, silence of lncRNA SNHG17 up-regulated p57 expression in HCC cells.	34921029
rno_circ_0004002	CircRNA	Homo sapiens	Anorectal Malformations	anorectal tissues	Interaction[targeting miR-342-5p and Wnt3a]	qRT-PCR//RNA-seq	 Among the downregulated circRNAs, rno_circ_0004002 was selected as the candidate circRNA.		Yes	Functionally, silencing of rno_circ_0004002 was correlated with suppression of proliferation, and promotion of apoptosis and epithelial-mesenchymal transition (EMT) in anorectal development.	31074015
Snhg20	LncRNA	Mus musculus	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-2467-3p/E2F3)	Western Blot//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	SNHG20 and E2F3 was upregulation in NSCLC tissues and cell lines. Besides, SNHG20 activated protein kinase B (AKT) signaling pathway and increased E2F3 level in NSCLC cells through targeting miR-2467-3p.		Yes	 Mechanical experiment displayed that knockdown of SNHG20 or E2F3 silencing could inhibit proliferation, motility, and improve apoptosis in NSCLC cell lines. Restored expression of E2F3 could effectively reverse reduction of proliferation, motility, and promotion of apoptosis caused by SNHG20 silencing in NSCLC cells.	32456448
Snhg20	LncRNA	Mus musculus	Silicosis	lung tissues and TGF-β1 treated fibroblasts	Interaction(miR-490-3p/TGFBR1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//IF	MiR-490-3p was significantly downregulated in silica-induced fibrotic mouse lung tissues and TGF-β1 treated fibroblasts. Moreover, overexpressed miR-490-3p could relieve silica-induced lung fibrosis in vivo, and prevent the process of fibroblast-to-myofibroblast transition(FMT)in vitro. Mechanistically, TGFBR1 was one of the major target genes of miR-490-3p, and tightly associated with the process of fibroblasts activation. SNHG20, as opposed to miR-490-3p expression, was elevated in TGF-β1-treated fibroblast cell lines and contributed to decreased levels of miR-490-3p. Taken together, these data indicated that miR-490-3p plays a key role in silica-induced pulmonary fibrosis.		Yes	overexpressed miR-490-3p could relieve silica-induced lung fibrosis in vivo, and prevent the process of fibroblast-to-myofibroblast transition(FMT)in vitro. Mechanistically, TGFBR1 was one of the major target genes of miR-490-3p, and tightly associated with the process of fibroblasts activation.	33482250
SNHG18	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC specimens	Interaction(miR-211-5p/BRD4 axis)	ChIP//Western Blot//Wound Healing Assay//CCK8//RIP//Luciferase Report Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	SNHG18 upregulation in NSCLC specimens correlated with lymph node metastasis and reduced overall survival of NSCLC patients. SNHG18 expression served as an independent prognostic factor for NSCLC.  Mechanically, SNHG18 exerted its prometastatic effects on NSCLC cells through repression of miR-211-5p and induction of BRD4. Clinical evidence indicated that SNHG18 expression was negatively correlated with miR-211-5p expression in NSCLC tissues.	SNHG18 upregulation in NSCLC specimens correlated with lymph node metastasis and reduced overall survival of NSCLC patients. 	Yes	Knockdown of SNHG18 blocked MKL1-induced growth and invasion of NSCLC cells in vitro. Animal studies validated the requirement for SNHG18 in NSCLC growth and metastasis. Moreover, overexpression of SNHG18 promoted NSCLC cell proliferation and invasion.	33500406
hsa_circ_0056558	LncRNA	Homo sapiens	Spondylitis, Ankylosing	AS tissue	Regulation(microRNA-1290)	Western Blot//Transfection//Proliferation Assay//qRT-PCR//Cell Apoptosis Assay//PCR//Cell Proliferation Assay//Bioinformatics Analysis//IF	Our findings revealed that the expression levels of both circ_0056558 and CDK6 in AS tissue were significantly higher than that in normal samples. Besides, hsa_circ_0056558 could suppress cell proliferation and differentiation by facilitating CDK6 expression and suppressing miR-1290 expression in AS. Over-expression of miR-1290 negatively regulated CDK6 expression to enhance cell proliferation. The protein levels of p-AKT, p-NF-κB p65, and p-IκBα were promoted by hsa_circ_0056558 or CDK6 over-expression while suppressed by miR-1290 up-regulation. In conclusion, our study demonstrated that hsa_circ_0056558 and CDK6 suppressed cell proliferation and differentiation while enhanced cell apoptosis by competitive binding to miR-1290 in AS, which might be possibly achieved by PI3K/AKT/NF-κB pathway, providing us novel therapeutic strategy for AS.		Yes	Over-expression of miR-1290 negatively regulated CDK6 expression to enhance cell proliferation. The protein levels of p-AKT, p-NF-κB p65, and p-IκBα were promoted by hsa_circ_0056558 or CDK6 over-expression while suppressed by miR-1290 up-regulation.	33685301
hsa_circ_0121582	CircRNA	Homo sapiens	Leukemia	leukemia cells	regulation[Wnt/β-catenin signaling]	qRT-PCR//RNA Pull-Down//RIP//Western Blot	 A new and highly stable circRNA was found, which was derived from the reverse splicing of GSK3β exon 1 to exon 7, and hsa_circ_0121582 was down-regulated in leukemia cells.  The upregulated GSK3β inhibited the Wnt/β-catenin signaling pathway, and reduced the aggregation of β-catenin in the nucleus, thus inhibited the proliferation of leukemia cells.		Yes	 In gain-of-function experiments, the up-regulated hsa_circ_0121582 inhibited the proliferation of leukemia cells in vitro and in vivo.	32472455
SNHG18	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction(miR-338-5p/FOXD1 axis)	ChIP//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	 It was revealed that, SNHG18 expression in glioma was up-regulated and associated with unfavorable prognosis of the patients; MiR-338-5p was a target of SNHG18, and SNHG18 promoted the expression of FOXD1 by decoying miR-338-5p. Additionally, E2F1 could bind to the promoter of SNHG18 to elevate its expression. In conclusion, SNHG18 accelerates glioma progression via regulating the miR-338-5p/FOXD1 axis.	 It was revealed that, SNHG18 expression in glioma was up-regulated and associated with unfavorable prognosis of the patients;	Yes	 knockdown of SNHG18 repressed the malignant biological behaviors of glioma cells, enhanced E-cadherin expression and repressed N-cadherin and Vimentin expressions. 	34937497
SNHG18	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HBV-associated HCC cells	Expression(lower expressed)	Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Invasion Assay	Downregulated SNHG18 in HBV-associated HCC was demonstrated to be involved in disease development and predict patients' prognosis. 	Downregulated SNHG18 in HBV-associated HCC was demonstrated to be involved in disease development and predict patients' prognosis. 	Yes	 The downregulation of SNHG18 dramatically promoted cellular processes of HBV-associated HCC could reverse the inhibitory effect of OA.	35221722
SNHG17	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues and cell lines	Interaction[inhibiting P15 and P16]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	Analysis of The Cancer Genome Atlas (TCGA) database revealed that SNHG17 expression was remarkably higher in gastric carcinoma tissues than normal stomach mucosae (P=4.85×10-10). We confirmed that SNHG17 was overexpressed in gastric cancer tissues (P<0.0001) and cell lines (P<0.01) compared with corresponding noncancerous tissues and gastric epithelial cell line, respectively. Mechanistically, we found that SNHG17 inhibited P15 and P16, and enhanced CDK4 expression, resulting in a G0/G1 cell cycle arrest, and that SNHG17 inhibited cell apoptosis.	Furthermore, SNHG17 levels in tumor tissues were associated with lymph node metastasis (P=0.0006), pTNM stage (P=0.0061), and lymphovascular invasion (P=0.0005), but were not associated with overall survival (OS) (P=0.888). 	Yes	 Loss-of-function studies indicated that SNHG17 promoted gastric carcinoma cell proliferation in vitro and in vivo (P<0.01), and that SNHG17 enhanced gastric cancer cell migration (P<0.01). 	35116784
SNHG17	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines,blood	Interaction[silencing of p15 and p57]	qRT-PCR	Our results showed that SNHG17 expression was upregulated in GC tissues and cells, and its high expression was significantly correlated with increased invasion depth, lymphatic metastasis, and advanced TNM stage.  The expression of plasma SNHG17 was also found upregulated in patients with GC compared with healthy controls, with a moderate accuracy for diagnosis of GC (area under the receiver operating characteristic curve = 0.748; 95% CI, 0.666-0.830). Mechanistic investigations showed that SNHG17 was associated with polycomb repressive complex 2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15 and p57, thus contributing to the regulation of GC cell cycle and proliferation. Furthermore, rescue experiments indicated that SNHG17 functioned as an oncogene via activating enhancer of zeste homolog 2 in GC cells.	Our results showed that SNHG17 expression was upregulated in GC tissues and cells, and its high expression was significantly correlated with increased invasion depth, lymphatic metastasis, and advanced TNM stage. 	Yes	Gain- and loss-of-function of SNHG17 revealed that SNHG17 promoted GC cell proliferation, cell cycle progression, invasion, and migration and inhibited apoptosis.	30256413
SNHG20	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	interaction[miR-2467-3p/E2F3]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	SNHG20 and E2F3 was upregulation in NSCLC tissues and cell lines.SNHG20 contributed to NSCLC development through mediating AKT signaling pathway and sponging miR-2467-3p to elevate E2F3 expression in NSCLC cells.		Yes	Mechanical experiment displayed that knockdown of SNHG20 or E2F3 silencing could inhibit proliferation, motility, and improve apoptosis in NSCLC cell lines. 	32456448
SNHG17	LncRNA	Homo sapiens	Breast Neoplasms	BC samples and cell lines	interaction[sponging miR-124-3p]	Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	 An increased SNHG17 was observed in BC samples and cell lines compared with corresponding control.The present study demonstrated that the lncRNASNHG17 could regulate the progression of BC by sponging miR-124-3p.		Yes	 Increased SNHG17 was closely associated with poor prognosis.SNHG17 depletion suppressed cell proliferation, migration and invasion in vitro, as well as inhibited tumor growth in xenograft tumor models. 	32042267
SNHG17	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung		Expression[lower expressed]	Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//MTT//EdU Staining	In the present study, we analyzed The Cancer Genome Atlas (TCGA) data, and we found that lncRNA Small Nucleolar RNA Host Gene 17 (SNHG17) was upregulated in NSCLC driven by the amplification of copy number, indicating the special role of SNHG17 in NSCLC.		Yes	Results showed that the knockdown of SNHG17 inhibited the proliferation and migration and promoted the apoptosis of NSCLC cells.	31310946
SNHG17	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	 ESCC tissues and cell lines	Interaction(c-Jun/c-Myc axis )	CCK8//qRT-PCR//Western Blot	The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF-β1, and associated with poor survival. SNHG17 was found to directly regulate c-Myc transcription by binding to c-Jun protein and recruiting the complex to specific sequences of the c-Myc promoter region, thereby increasing its expression. Moreover, SNHG17 hyperactivation induced by TGF-β1 results in PI3K/AKT pathway activation, promoting cells EMT, forming a positive feedback loop. 	The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF-β1, and associated with poor survival. 	Yes	 It is also involved in the epithelial-to-mesenchymal transition (EMT) process.Furthermore, SNHG17 facilitated ESCC tumor growth in vivo. 	34714590
SNHG17	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues 	Interaction(miR-338-3p/SOX4 axis)	CCK8//qRT-PCR	" Results demonstrated SNHG17 to be markedly upregulated in ESCC.Mechanistic analysis suggested that SNHG17 acts as an endogenous ""sponge"" competing with miR-338-3p to regulate SOX4, thereby promoting tumor progression. "		Yes	Knockdown of SNHG17 significantly suppressed ESCC cell proliferation, invasion, and epithelial-mesenchymal transition in vitro and tumor growth in vivo. 	34429400
circZXDC	CircRNA	Homo sapiens	Moyamoya Disease	MMD plasma, VSMC	Interaction(circZXDC-miR-125a-3p-ABCC6 axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	The results from a series of in vitro experiments, such as dual luciferase reporter assays, cell transfection, CCK-8 assays, Transwell assays, and Western blotting, indicate a higher level of circZXDC in the MMD plasma, especially in those MMD patients with the RNF213 mutation. CircZXDC sponges miR-125a-3p to increase ABCC6 expression, which induces ERS (endoplasmic reticulum stress), and subsequently regulates VSMC transdifferentiation from the contractive phenotype to the synthetic phenotype, contributing to the intima thickness of MMD vessels. 		Yes	 Moreover, circZXDC overexpression results in a VSMC phenotype switching toward a synthetic status, with increased proliferation and migration activity. 	36497052
SNHG17	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-339-5p-FOSL2-SNHG17 positive feedback loop)	qRT-PCR	Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. SNHG17 impedes PES1 degradation by inhibiting Trim23-mediated ubiquitination of PES1. SNHG17 upregulates FOSL2 by sponging miR-339-5p, and FOSL2 transcription activates SNHG17 expression, uncovering a SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop.	Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. 	Yes	In vitro and in vivo functional assays indicated that SNHG17 facilitates CRC proliferation and metastasis. 	34782005
SNHG17	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissue samples and cell lines	Interaction(miR-328-3p)	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Invasion Assay	Highly expressed SNHG17 was evident in RCC tissue samples and cell lines, and SNHG17 overexpression was related to advanced TNM stage and reduced relapse-free and overall survival of patients with RCC.More importantly, SNHG17 could upregulate the expression of H2AX by acting as a miR-328-3p sponge. In vivo experiments confirmed that SNHG17 promoted the growth of RCC tumors. SNHG17/miR-328-3p/H2AXaxis might be involved in RCC progression, which provided a potential therapeutic target for RCC.	Highly expressed SNHG17 was evident in RCC tissue samples and cell lines, and SNHG17 overexpression was related to advanced TNM stage and reduced relapse-free and overall survival of patients with RCC.	Yes	Knockdown of SNHG17 prohibited malignant phenotypes, whereas ectopic SNHG17 expression showed the opposite effects. 	34497156
hsa_circ_0003307	CircRNA	Homo sapiens	Spondylitis, Ankylosing	 AS patients 	Regulation(PI3K/AKT pathway)	qRT-PCR//IF//ELISA//Western Blot	The expression level of hsa_circ_0003307 was significantly high in AS patients and was positively associated with erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and Bath Ankylosing Spondylitis Functional Index (BASFI). We found that hsa_circ_0003307 overexpression could promote the activation of the PI3K/AKT pathway and expression of inflammatory cytokines - tumor necrosis factor alpha (TNF-α) and TNF-α-induced protein 2 (TNFAIP2). However, hsa_circ_0003307 knockdown reduced the expression of TNF-α and TNFAIP2.		Yes	We found that hsa_circ_0003307 overexpression could promote the activation of the PI3K/AKT pathway and expression of inflammatory cytokines - tumor necrosis factor alpha (TNF-α) and TNF-α-induced protein 2 (TNFAIP2). However, hsa_circ_0003307 knockdown reduced the expression of TNF-α and TNFAIP2.	35275449
SNHG20	LncRNA	Homo sapiens	Retinoblastoma	RB tissues and cell lines	Interaction( miR‑335‑5p/E2F3 axis)	qRT-PCR//RNA Pull-Down	SNHG20 expression was significantly increased in RB tissues and cell lines. Moreover, mechanistic investigations demonstrated that SNHG20 could enhance the expression of E2F3 by sponging of miR‑335‑5p. 		Yes	 Silencing of SNHG20 in RB cells was shown to inhibit cell proliferation, clonogenic survival, migration and invasion.	34080033
SNHG20	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	regulation[miR-338-3p/MCL1 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 The levels of SNHG20 and MCL1 were upregulated, while miR-338-3p level was downregulated in OC tissues and cells.In conclusion, the present study demonstrated that SNHG20 regulates OC development via modulation of the miR-338-3p/MCL1 axis, providing the theoretical basis for the treatment of OC.		Yes	 Besides, mouse xenograft assay was carried out to explore the effect of SNHG20 on tumor growth in vivo.	33552251
SNHG20	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer cells and tissues	Interaction [miR-140-5p-ADAM10 axis]	In Vivo Experiment//RNA Pull-Down//cell invasion assay//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay	QRT-PCR showed that SNHG20 expression was significantly increased in cervical cancer. MiR-140-5p acted as a downstream target of SNHG20. SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. Furthermore, we identified that ADAM10 could act as a potential target of miR-140-5p. MEK/ERK signaling could be inhibited by miR-140-5p mimics in cervical cancer cells. In addition, ADAM10 overexpression abrogated the effect of miR-140-5p mimics on cervical cancer cells proliferation and invasion.		Yes	SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. 	29604594
SNHG20	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues and cell lines	Interaction(miR-217)	CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	SNHG20 was upregulated in ovarian cancer tissues and cell lines.  MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. 		Yes	Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion.	34302635
SNHG20	LncRNA	Homo sapiens	Ovarian Neoplasms	 OC cell lines	Interaction(miR-148a )	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Significant higher expression of SNHG20 was observed in OC cell lines. SNHG20 enhanced ROCK1 expression by sponging miR-148a, and the direct binding between SNHG20/ROCK1 and miR-148a was identified.		Yes	SNHG20 markedly promoted the invasion, migration, proliferation and inhibited the apoptosis of OC cells. 	34836544
SNHG20	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues and cell lines	Regulation[Wnt/β-catenin signalling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	The resulting data indicated that SNHG20 was significantly upregulated in bladder cancer tissues and cell lines, compared with its expression in adjacent non?tumour tissues and the SV?HUC?1 normal urinary tract epithelial cell line, respectively. Investigations into the mechanism revealed that the inhibition of SNHG20 suppressed the activation of Wnt/β‑catenin signalling and the expression of certain key genes in bladder cancer cells.	In addition, the high expression of SNHG20 was associated with advanced clinical stage, lymph node metastasis, and reduced patient survival rate. 	Yes	 The knockdown of SNHG20 caused a significant reduction in cancer cell survival, proliferation, colony formation, migration and invasion, and induced cell apoptosis. Additionally, the inhibition of SNHG20 reduced tumour growth in vivo. 	30106094
SNHG20	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues 	Regulation[targeting miR-197/LIN28 axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	LncRNA SNHG20 was Expression[up-expression]-regulated in OSCC tissue compared with adjacent non-tumour tissue. Meanwhile, SNHG20 was overexpressed in cancer stem-like cells. Bioinformatics and luciferase reporter assay revealed that miR-197 targeted the 3'-untranslated regions of SNHG20 and LIN28 by complementary binding. Validation experiments confirmed the associated functions of SNHG20/miR-197/LIN28 axis on OSCC proliferation and stemness.		Yes	vitro and in vivo, loss-of-function experiments showed that lncRNA SNHG20 knockdown inhibited proliferative ability, mammosphere-forming ability, ALDH1 expression, stem factors (LIN28, Nanog, Oct4, SOX2) and tumour growth. 	30394668
SNHG20	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissue 	Expression[highly expressed]	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	It was demonstrated that SNHG20 expression was significantly increased in OSCC tissue specimens, compared with in adjacent non-tumor tissue specimens.	The increased SNHG20 expression in OSCC tissue specimens was associated with tumor differentiation and Tumor-Node-Metastasis stage. Kaplan-Meier analysis and log-rank tests indicated that Higher SNHG20 expression predicted a poor overall survival (OS) rate in patients with OSCC. Multivariate Cox proportional hazards regression analysis demonstrated that increased SNHG20 expression was an independent predictor for the OS of patients with OSCC.	Yes	Knockdown of SNHG20 expression in OSCC cells suppressed proliferation.	30655853
SNHG20	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	tissues	Interaction(microRNA-19b-3p/RAB14 axis )	qRT-PCR//MTT	The results indicated that lncRNA SNHG20 was upregulated in the tissues. Furthermore, bioinformatic analysis showed that both SNHG20 and RAB14 could bind to miR-19b-3p. RAB14 was upregulated, and miR-19b-3p was downregulated in the tissues. 		Yes	The knockdown of SNHG20 inhibited cell proliferation, migration, and invasion. Contrarily, the knockdown of miR-19b-3p reversed the effects of si-SNHG20 on cell proliferation, migration, and invasion, and the overexpression of RAB14 reversed the effects of miR-19b-3p mimic on the cell biological functions. 	34282711
SNHG20	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues and cell lines	Expression[highly expressed]	qRT-PCR	Our results indicated SNHG20 was overexpressed in osteosarcoma tissues and cell lines compared with paired non-tumor tissues and normal human osteoblast cell line, respectively. 	 Moreover, we observed high-expression of SNHG20 was obviously associated with Enneking stage, distant metastasis, and histological grade. SNHG20 expression was negatively associated with overall survival, and high-expression of SNHG20 was an independent unfavorable prognostic factor in osteosarcoma patients. 	Yes	 Furthermore, SNHG20 promoted osteosarcoma cell migration and invasion through modulating epithelial-mesenchymal transition -associated genes. 	30120876
SNHG20	LncRNA	Homo sapiens	Glioma	Glioma tissues	Interaction[silencing P21]	CCK8//qRT-PCR//Colony Formation Assay//Western Blot	Our results suggested the high expression of lncRNA SNHG20 in human glioma tissues compared with normal brain tissues.Consequently, the expression of CCNA1 was inhibited, and the expression of P21 was up-regulated in U87 cells.	Our results suggested the high expression of lncRNA SNHG20 in human glioma tissues compared with normal brain tissues, which was related to recurrence-free survival and poor overall survival in glioma patients. According to the existing retrospective cohort study, high lncRNA SNHG20 expression was associated with tumor size, extent of resection, WHO grade, follow-up time, survival status and recurrence.	Yes	Besides, knocking down the expression of lncRNA SNHG20 could inhibit the proliferation and colony formation abilities of glioma U87 cells through cell cycle arrest.	30774368
SNHG20	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines	Regulation(DDX17)	Western Blot//Migration Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	SNHG20 is highly expressed in PCa tissues and cell lines. Mechanistically, SNHG20 was verified to act as a competing endogenous RNA (ceRNA) to upregulate DDX17. DDX17 is also highly expressed and has oncogenic roles in PCa. Furthermore, the expression of DDX17 is significantly positively correlated with that of SNHG20 in PCa tissues. Depletion of DDX17 reverses the oncogenic roles of SNHG20 in PCa.	High expression of SNHG20 is positively correlated with high Gleason score and advanced tumor stage. 	Yes	Functional experiments revealed that overexpression of SNHG20 promotes PCa cell proliferation and migration. SNHG20 knockdown represses PCa cell proliferation and migration. 	34900057
SNHG20	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Interaction[MDM2-p53 pathway ]	CCK8//qRT-PCR//Western Blot	SNHG20 was overexpressed in glioma tissues and cell lines.Molecular studies uncovered that SNHG20 acted as a competing endogenous RNA (ceRNA) to sponge the expression of miR-4486. MiR-4486 was down-regulated in glioma tissues and significantly inversely correlated with the expression of SNHG20. Restoration of miR-4486 remarkably attenuated the promotion effect of SNHG20 on the growth of glioma cells. Further study revealed that miR-4486 targeted the E3 ubiquitin ligase mouse double minute 2 (MDM2) and negatively regulated the expression of MDM2. Down-regulation of MDM2 by miR-4486 increased the abundance of p53 in glioma cells.		Yes	Down-regulation of SNHG20 suppressed the proliferation, migration and induced apoptosis of glioma cells.	31298384
SNHG20	LncRNA	Homo sapiens	Glioma	glioma tissues	Regulation[PTEN/PI3K/AKT signaling pathway]	CCK8//qRT-PCR//Tunel//Western Blot	The expression level of SNHG20 messenger RNA (mRNA) in glioma tissues was significantly higher than that in para-carcinoma tissues (p<0.05). After the inhibition of siRNA on SNHG20, the proliferation of U118 and U251 cells was significantly inhibited, and the expression of Bax was significantly up-regulated, while that of Bcl-2 was down-regulated. The TUNEL results showed that the number of apoptotic cells in SNHG20 siRNA group was about 12 times that in control group (p<0.05). After SNHG20 knockout, the protein expressions in the PTEN/PI3K/AKT signaling pathway were inhibited (p<0.05).		Yes	After the inhibition of siRNA on SNHG20, the proliferation of U118 and U251 cells was significantly inhibited	30657567
SNHG20	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tissues and cell lines	Regulation[PI3K/Akt/mTOR signaling pathway]	qRT-PCR	In this study, we found that SNHG20 was significantly upregulated in glioblastoma tissues and cell lines.Furthermore, western blotting demonstrated that the PI3K/Akt/mTOR signaling pathway was activated by SNHG20 in glioblastoma cells. At last, rescue assays validated that PI3K/Akt/mTOR signaling pathway involved in the glioblastoma progression mediated by SNHG20. Taken together, this study revealed that SNHG20 regulated PI3K/Akt/mTOR signaling pathway to promote tumorigenesis and stemness of glioblastoma.	Survival analysis suggested that high expression of SNHG20 indicated the low overall survival rate of glioblastoma patients.	Yes	expression of SNHG20 indicated the low overall survival rate of glioblastoma patients. Subsequently, gain or loss-of-function assays were carried out to examine the effect of SNHG20 on glioblastoma cell proliferation and apoptosis. We found that SNHG20 knockdown obviously suppressed cell proliferation, increased cell apoptosis and impaired stem properties, while SNHG20 overexpression led to the opposite results. In vivo experiment demonstrated that knockdown of SNHG20 efficiently suppressed cell growth in vivo.	30943748
SNHG20	LncRNA	Homo sapiens	Adenocarcinoma of Lung	lung adenocarcinoma tissues and cell lines	regulation[miR-342/DDX49 axis]	qRT-PCR//Luciferase Report Assay	SNHG20 and DDX49 were overexpressed, while miR-342 was lowly expressed in lung adenocarcinoma tissues and cell lines. Our findings demonstrate that SNHG20/miR-342/DDX49 axis plays an important role in lung adenocarcinoma, providing a novel insight into the treatment of lung adenocarcinoma.		Yes	Knockdown of SNHG20 suppressed cell proliferation, invasion and enhanced cell apoptosis.	33089952
hsa_circ_0000045	CircRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	HNSCC tissues and HNSCC cell lines	Regulation(HSP70)	RNA Pull-Down//Western Blot//Transfection//Migration Assay//qRT-PCR//RNA-seq//Invasion Assay	Great alterations in circRNA profiles were detected in HNSCC tissues, including the elevated expression of circ_0000045.  Results also showed that circ_0000045 was associated with multiple RNA-binding proteins in HNSCC cells, such as HSP70. Moreover, circ_0000045 knockdown enhanced HSP70 expression and inhibited JNK2 and P38's expression in HNSCC cells, which were oppositely regulated by circ_0000045's overexpression.		Yes	As observed, silencing of circ_0000045 effectively repressed the proliferation, migration, and invasion of HNSCC cell lines (FaDu and SCC-9). Contrarily, circ_0000045's overexpression promoted the proliferation, migration, and invasion in FaDu and SCC-9 cells. 	35854245
SNHG20	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues,cell lines	Interaction[regulating miR-140]	CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining	The SNHG20 expression in LSCC tissues or cells remarkably increased than controls, and the difference was statistically significant. MiR-140 was negatively correlated with SNHG20 in LSCC tissues and cells. Dual-luciferase reporter gene assay showed that SNHG20 could be targeted by miR-140 through a certain binding site. The cell rescue experiment also indicated that there was a mutual regulation between SNHG20 and miR-140, which could together affect the malignant progression of LSCC.	The LSCC patients with the high expression level of SNHG20 were more likely to develop advanced tumor compared with patients with low expression of SNHG20. Moreover, the LSCC patients with the high expression level of SNHG20 had a shorter overall survival than those with low level.	Yes	The cell proliferation ability significantly decreased in the SNHG20 knockdown group, while notably increased in SNHG20 overexpression group.	31081112
SNHG20	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines 	Regulation[miR-6516-5p/SCGB2A1 axis]	qRT-PCR//Luciferase Report Assay	SHNG20 expression was found markedly elevated in PCa tissues and cell lines. In conclusion, this finding suggests the SNHG20/miR-6516-5p/SCGB2A1 axis in PCa tumorigenesis, providing the novel insight for the molecular mechanism of PCa.		Yes	Overexpression of SNHG20 increased PCa cell proliferation and invasion but decreased cell apoptosis. However, the knockdown of SNHG20 will cause the opposite effects on PCa cell behaviors. 	31497231
circMAPK9	CircRNA	Homo sapiens	Arthritis, Rheumatoid	FLS	Interaction(miR-140-3p/PPM1A axis)	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//ELISA//Transwell Assay	CircMAPK9 and PPM1A were upregulated and miR-140-3p was downregulated in RA patients and FLSs from RA patients (RA-FLSs). CircMAPK9 silence suppressed cell proliferation, migration, invasion, inflammatory response, and promoted apoptosis in RA-FLSs. MiR-140-3p was a target of circMAPK9, and miR-140-3p downregulation attenuated the effects of circMAPK9 knockdown on cell progression and inflammatory response in RA-FLSs. PPM1A was targeted by miR-140-3p, and circMAPK9 could regulate PPM1A expression by sponging miR-140-3p. Furthermore, miR-140-3p could impede cell biological behaviors in RA-FLSs via targeting PPM1A.		Yes	CircMAPK9 silence suppressed cell proliferation, migration, invasion, inflammatory response, and promoted apoptosis in RA-FLSs.	34154607
SNHG15	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[inhibiting miR-338-3p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	Our results showed that SNHG15 was up-regulated in CRC tissues compared with paired NCTs (P < 0.0001). The results of mechanism experiments showed that SNHG15 could bind to miR-338-3p and block its inhibition on the expression and activity of FOS or RAB14. In conclusion SNHG15 promotes cell proliferation through SNHG15/miR-338-3p/FOS-RAB14 axis in CRC.		Yes	SNHG15 overexpression could promote cell proliferation and inhibit cell apoptosis. Animal experiments showed that up-regulation of SNHG15 promoted tumor growth in vivo.	30945457
SNHG15	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues,cell lines	Interaction[AIF]	RNA Pull-Down//Western Blot//qRT-PCR//RIP//RNA-seq//Colony Formation Assay//Transwell Assay	To confirm this observation, we obtained 36 fresh colorectal cancer tumors and their adjacent normal tissues immediately after surgery from Iranian CRC patients (Table ​(Table1).1). SNHG15 expression was examined by qRT-PCR and its upregulation was observed in tumoral samples (Fig. ​(Fig.1d,1d, p < 0.001). Moreover, we profiled SNHG15 expression in ten CRC cell lines (Caco-2, DLD-1, HCT 116, HT-29, LoVo, LS513, RKO, SW480, SW620 and T84) and found this lncRNA ubiquitously expressed in all tested CRC cell lines and with higher levels compared to the non-cancerous HDFa cell line (Fig. ​(Fig.11e).		Yes	The depletion of SNHG15 by siRNA or CRISPR-Cas9 inhibits cell proliferation and invasion, decreases colony formation as well as the tumorigenic capacity of CRC cells, whereas its overexpression leads to opposite effects.	31014355
SNHG10	LncRNA	Homo sapiens	Prostatic Neoplasms	PC cells and tissues	Expression [highly expressed]	ChIP//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay//Transwell Assay	In this study, we investigated the role of SNHG10 in PC and found that SNHG10 expression was significantly increased in datasets extracted from The Cancer Genome Atlas. Increased expression of SNHG10 was related to advanced clinical parameters. 	 Increased expression of SNHG10 was related to advanced clinical parameters. Receiver operating curve analysis revealed the significant diagnostic ability of SNHG10 (AUC = 0.805).	Yes	 In addition, immune infiltration analysis, and GSEA showed that SNHG10 expression was correlated with oxidative phosphorylation and immune infiltrated cells. Finally, we determined that SNHG10 regulated cell proliferation, migration, and invasion of PC in vitro. 	34676212
SNHG10	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues 	regulation[miR-21]	CCK8//qRT-PCR	We observed the expression of SNHG10 was down-regulated in non-small cell lung cancer (NSCLC) compared with that in non-tumor tissues.  SNHG10 may involve in NSCLC cell proliferation by regulating the miR-21 gene methylation.	Moreover, we found that high expression levels of SNHG10 predicted favorable survival of NSCLC patients, and the expression of miR-21 were increased in NSCLC and inversely correlated with SNHG10 expression.	Yes	 In NSCLC cells, overexpression of SNHG10 resulted in increased miR-21 gene methylation and decreased miR-21 expression. Moreover, overexpression of SNHG10 attenuated the enhancing effect of miR-21 overexpression on cell proliferation.	33081752
SNHG10	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	interaction[miR-543,SIRT1 ]	CCK8//qRT-PCR//Western Blot	We confirmed the downregulation of SNHG10 in NSCLC. In conclusion, SNHG10 sponges miR-543 to upregulate tumor suppressive SIRT1 in NSCLC to suppress cell proliferation.	 In addition, low expression level of SNHG10 predicted the poor survival of NSCLC patients.	Yes	Cell proliferation assay showed that SNHG10 and SIRT1 overexpression led to the decreased proliferation rate of NSCLC cells.	32319822
SNHG10	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue samples and cells	Expression(highly expressed)	CCK8//qRT-PCR//ELISA//Western Blot	RNA sequencing revealed that SNHG10 expression was upregulated in EMT-exo compared with that in non-EMT-exo.  Moreover, SNHG10 expression was upregulated in tumor tissues in CRC, which was associated with poor prognosis. 	 Moreover, SNHG10 expression was upregulated in tumor tissues in CRC, which was associated with poor prognosis. 	Yes	Overexpression of SNHG10 in exosomes (oe-lnc-SNHG10 exo) significantly suppressed the viability and cytotoxicity of NK cells.	34641864
SNHG10	LncRNA	Homo sapiens	Carcinoma, Ovarian Epithelial	EOC tissues and cells	Interaction(SNHG10/miR-200a-3p/BIN1 axis)	Western Blot//qRT-PCR//RIP//FISH//IHC	Altogether, SNHG10 sponges miR-200a-3p to upregulate BIN1 and thereby exerting its tumor-suppressive effects in EOC. Therefore, the SNHG10/miR-200a-3p/BIN1 axis may act as a potential predictive biomarker and therapeutic target for treating EOC.	 Kaplan-Meier analysis and COX proportional hazard progression model showed that low expression of SNHG10 was correlated with a poor prognosis of EOC patients. 	Yes	Overexpressing SNHG10 suppressed the proliferation, colony formation, migration, and invasion of EOC cells. 	35149697
circVPS13C	CircRNA	Homo sapiens	Pituitary Neoplasms	NFPA samples	Regulation(IFITM1/MAPK)	In Vivo Experiment//Western Blot//qPCR//FISH//migration assay//Cell Apoptosis Assay//Microarray//Colony Formation Assay	CircVPS13C is significantly upregulated in NFPA samples and cell lines. Mechanistically, circVPS13C silencing increases the expression of IFITM1 and subsequently activates its downstream genes involved in MAPK- and apoptosis-associated signaling pathways. Rescue experiments show that IFITM1 overexpression partly reverses the biological effects of circVPS13C. Further studies reveal that circVPS13C inhibits IFITM1 expression through a novel mechanism mainly by competitively interacting with RRBP1, a ribosome-binding protein of the endoplasmic reticulum membrane, and thereby alleviating the stability of IFITM1 mRNA.	Clinically, circVPS13C expression is markedly higher in high-risk NFPA samples and is downregulated in patient serum 7 days post-transsphenoidal adenoma resection.	Yes	 Gain- and loss-of-function experiments demonstrate that silencing circVPS13C inhibits the proliferation of pituitary tumor cells in vitro and in vivo. 	35091683
SNHG10	LncRNA	Homo sapiens	Osteosarcoma	 OS cells and tissues	Interaction(miR-141-3p/WTAP axis)	CCK8//qRT-PCR	The present work found that SNHG10 expression increased within OS cells and tissues, while suppressing its expression decreased OS cell proliferation, migration, invasion, but increased their apoptosis. . As for the mechanism, we confirmed that SNHG10 could bind to miR-141-3p, while the latter could bind to WTAP. SNHG10 upregulated WTAP through decreasing miR-141-3p expression.		Yes	The present work found that SNHG10 expression increased within OS cells and tissues, while suppressing its expression decreased OS cell proliferation, migration, invasion, but increased their apoptosis. More importantly, SNHG10 deletion remarkably reduced proliferation, migration, and invasion of cells, but accelerated their apoptosis. However, when cells were subjected to miR-141-3p inhibitor cotransfection or overexpressed WTAP, these effects were partially recovered. 	35274397
SNHG10	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	AML samples	Interaction(miR-621 methylation)	qRT-PCR	In this study, we found that the expression of SNHG10 was upregulated and the expression of miR-621 was downregulated in AML samples. Bioinformatics analysis showed that SNHG10 could be targeted by miR-621. In AML cells, miR-621 overexpression downregulated the expression of SNHG10, while SNHG10 overexpression could not affect the expression of miR-621. However, it was found that the reduction of miR-621 caused by SNHG10 overexpression might be due to the increase of miR-621 methylation. 	 Moreover, SNHG10 and miR-621 were inversely correlated across AML samples, and a high level of SNHG10 predicted poor survival of AML patients.	Yes	n addition, SNHG10 overexpression significantly promoted BMMNC proliferation, whereas miR-621 overexpression inhibited BMMNC proliferation and abolished the effect of SNHG10 overexpression on BMMNC proliferation.	33688254
SNHG10	LncRNA	Homo sapiens	Glioma	cell lines	regulation[miR-532-3p/FBXL19 axis]	RNA Pull-Down//ChIP//Wound Healing Assay//Tunel//qRT-PCR//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	High level of SNHG10 was detected in glioma cells.  SNHG10 was transcriptionally activated by ETS1 and played an oncogenic role in glioma by sponging miR-532-3p and up-regulating FBXL19.		Yes	 Functional assay confirmed that SNHG10 promoted the proliferation, migration, invasion and stemness of glioma cells.	33298070
SNHG1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines and tissues	Regulation[miR-140/ADAM10 axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay	Here, we reported that SNHG1 expression was significantly increased in GC cell lines and tissues.Mechanismly, it was found that SNHG1 functioned as a competing endogenous RNA to repress miR-140 expression and thereby elevated its down-stream target ADAM10. 		Yes	 Knockdown of SNHG1 impeded cell growth via disturbing cell cycle distribution and protecting cells from apoptosis.Nevertheless, SNHG1 down-regulation decreased cell invasive ability and reversed epithelial-mesenchymal transition (EMT) phenotype.	30391432
SNHG10	LncRNA	Homo sapiens	Stomach Neoplasms	cells	regulation[SNHG10/DDX54/PBX3 Feedback Loop ]	RNA Pull-Down//qRT-PCR//RIP//Luciferase Report Assay//ChIP	 SNHG10 was expressed at a high level in GC cells. SNHG10 facilitates cell growth by affecting DDX54-mediated PBX3 mRNA stability in GC.		Yes	SNHG10 knockdown resulted in the inhibition on GC cell proliferation, migration but induced cell apoptosis.	32712782
circNFIX	LncRNA	Homo sapiens	Pituitary Neoplasms	pituitary adenoma tissues	Interaction( miR-34a-5p/CCNB1)	In Vivo Experiment//Western Blot//Transfection//Migration Assay//qRT-PCR//Luciferase Report Assay//cell invasion assay//IHC	 In pituitary adenoma tissues, the expression of circNFIX and CCNB1 was upregulated, while miR-34a-5p expression was downregulated. In conclusion, CircNFIX affects cell invasion, migration, and proliferation in pituitary adenomas by sponging miR-34a-5p through CCNB1. 		Yes	 The silencing of circNFIX or overexpression of miR-34a-5p inhibited cell invasion, migration and proliferation. Inhibition of miR-34a-5p expression reversed the inhibitory effect of circNFIX silencing on the progression of pituitary adenoma.	33359304
SNHG1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction( miR-195-5p/YAP1 axis)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	SNHG1 and YAP1 levels were elevated and miR-195-5p level was reduced in GC.Downregulated SNHG1 suppressed tumor growth in vivo. SNHG1 bound to miR-195-5p, and miR-195-5p directly targeted YAP1.		Yes	 Reduction of SNHG1 or elevation of miR-195-5p retarded GC cell biological activity in vitro.	35819551
SNHG1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissue,cell lines (BT474、MCF7、MDA-MB-453、MDA-MB-231、HCC1937、MCF10A)	Expression[Expression[Expression[highly expressed]-expression]-expression]	CCK8//qRT-PCR//Western Blot	 LncRNA SNHG1 expression in tumor tissue was increased compared with paired adjacent tissue, and it correlated with higher T stage and worse overall survival (OS) in breast cancer patients. LncRNA SNHG1 expression was also elevated in breast cancer cell lines compared with normal breast epithelial cell line. 	 LncRNA SNHG1 expression in tumor tissue was increased compared with paired adjacent tissue, and it correlated with higher T stage and worse overall survival (OS) in breast cancer patients. LncRNA SNHG1 expression was also elevated in breast cancer cell lines compared with normal breast epithelial cell line. 	Yes	 Cell Counting Kit-8 (CCK8) assay revealed that lncRNA SNHG1 overexpression promoted while lncRNA SNHG1 shRNA reduced cell proliferation, and Annexin V-fluorescein isothiocyanate/propidium iodide staining (AV/PI) assay illustrated that lncRNA SNHG1 overexpression decreased while lncRNA SNHG1 shRNA increased cell apoptosis rate. In addition, Western Blot assay disclosed that lncRNA SNHG1 overexpression Expression[down-expression]regulated while lncRNA SNHG1 shRNA Expression[Expression[up-expression]-expression]regulated pro-apoptotic marker (C-Caspase3) expression, and lncRNA SNHG1 overexpression increased while lncRNA SNHG1 shRNA decreased anti-apoptotic marker (p-P38) expression.	35116793
SNHG1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction[regulating miR-382]	CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	SNHG1 upregulation was observed in breast cancer tissues and cells.SNHG1 promotes breast cancer through the regulation of miR-382-5p and EMT markers.		Yes	Knockdown of SNHG1 attenuated breast cancer proliferation, colony formation, migration and invasion. 	31354360
SNHG1	LncRNA	Homo sapiens	Breast Neoplasms	Breast cancer tissue	regulation[SNHG/miR-573/LMO4 axis]	Western Blot//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay	In the present study, increased expression levels of SNHG1 were noted in breast cancer tumors following analysis of differentially expressed lncRNAs between 1,063 tumor and 102 normal tissues derived from The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA‑BRCA) dataset. The present study demonstrated that SNHG1 acts as a novel oncogene in breast cancer via the SNHG/miR-573/LMO4 axis and that it could be a promising therapeutic target for patients with breast cancer.		Yes	In vitro experiments indicated that LMO4 overexpression could reverse siSNHG1‑induced cell growth arrest, cell cycle redistribution and inhibition of cell migration in breast cancer cells. Moreover, the tumor xenograft model indicated that SNHG1 knockdown inhibited MDA‑MB‑231 growth in vivo and LMO4 overexpression reversed the tumor growth inhibition induced by SNHG1 knockdown. 	32323846
SNHG1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cell lines	regulation[ SNHG1/miR-193a-5p/HOXA1]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Here, we found that SNHG1 expression was significantly upregulated in human breast cancer tissues and cell lines.  In summary, our study reveals a novel SNHG1/miR-193a-5p/HOXA1 competing endogenous RNA regulatory pathway in breast cancer progression and may provide new strategies for breast cancer therapy.		Yes	 We explored the function of SNHG1 in breast cancer cells using in vitro and in vivo experiments and found that SNHG1 promotes breast cancer metastasis and proliferation. 	32497022
SNHG1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues and cells	Interaction(EZH2)	qRT-PCR//RIP//MTT//Luciferase Report Assay//ChIP	Our findings demonstrated that SNHG1 is significantly upregulated in breast cancer tissues and cells.  	High SNHG1 levels were closely linked to reduced survival rates in breast cancer patients.	Yes	SNHG1 silencing has been shown to inhibit the proliferative, migratory, and invasive activity of breast cancer cells. Moreover, SNHG1 silencing enhanced cisplatin (DDP) sensitivity of these cells through improving DDP-induced cell apoptosis. Mechanistically, SNHG1 was found to interact with enhancer of zeste homolog 2 (EZH2), recruiting EZH2 to trigger trimethylation of histone H3 lysine 27 (H3K27me3), thus epigenetically inhibiting miR-381 transcription in these cells.	34806925
SNHG1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines,tissue	interaction[miR-497]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	The transcript level of lnc-SNHG1 was higher in lung adenocarcinoma specimens and NSCLC cell lines than in noncancer tissue and cells. Furthermore, our study demonstrated that the lnc-SNHG1 regulated the expression of the insulin-like growth factor 1 receptor (IGF1-R) by acting as a sponge of miR-497 in NSCLC.		Yes	 The inhibitory effect of si-lnc-SNHG1 on NSCLC cell proliferation, migration and invasion could be rescued by miR-497 inhibition, while the overexpression of miR-497 could reverse the effect of lnc-SNHG1 overexpression.	30454699
SNHG11	LncRNA	Homo sapiens	Pancreatitis	AP pancreatic tissue and AP cell models	Interaction(SNHG11/miR-7-5p/PLCB1/p38MAPK  Axis)	Western Blot//CCK8//qRT-PCR//RIP//RNA-seq//H&E Staining//ELISA//Bioinformatics Analysis	 Low expression of SNHG11 and PLCB1 and high expression of miR-7-5p were observed in AP pancreatic tissue and AP cell models. SNHG11 overexpression inhibited apoptosis and inflammatory responses induced by caerulein. 		Yes	SNHG11 overexpression inhibited apoptosis and inflammatory responses induced by caerulein. 	36611865
hsa_circ_0002594	CircRNA	Homo sapiens	Asthma	 asthma patients and HASMC	Interaction(miR-139-5p/TRIM8 axis)	Western Blot//Wound Healing Assay//Transfection//qRT-PCR//RIP//Luciferase Report Assay//ELISA//EdU Staining//Transwell Assay	Circ_0002594 and TRIM8 were elevated in asthma patients and PDGF-BB-treated HASMC, and the miR-139-5p level was decreased . Mechanism analysis exhibited that circ_0002594 could regulate TRIM8 expression through sponging miR-139-5p.		Yes	Furthermore, circ_0002594 knockdown could suppress PDGF-BB- stimulated HASMC damage. 	35470728
SNHG11	LncRNA	Homo sapiens	Stomach Neoplasms	Gastric Cancer tissues,cell lines	regulation[Wnt/β-Catenin Pathway]	RNA Pull-Down//ChIP//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Transwell Assay	We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes.Intriguingly, SNHG11 regulated autophagy in a manner dependent on ATG12 rather than the Wnt/β-catenin pathway, whereas SNHG11 contributed to the malignant behaviors of GC cells via both pathways. 	We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes.	Yes	 Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. 	33068778
SNHG12	LncRNA	Homo sapiens	stomach carcinoma	gastric carcinoma tissues and cell line	Interaction(microRNA-199a/b-5p)	Cell Proliferation Assay//RIP//ChIP	Higher lncRNA SNHG12 expression was observed in 6 gastric carcinoma tissues than the paracancerous tissues.  RIP experiment confirmed the binding abilities of lncRNA SNHG12, microRNA-199a/b-5p and Argo2. The distinct interaction between lncRNA SNHG12 and microRNA-199a/b-5p was verified by CHIP experiment.	 Clinical data analysis demonstrated that highly expressed lncRNA SNHG12 was related to tumor size and TNM staging. Survival analysis showed that highly expressed lncRNA SNHG12 in patients with gastric carcinoma was negatively correlated to the overall survival time.	Yes	Additionally, the expression of lncRNA SNHG12 was positively linked with the proliferative ability of BGC-823. 	29565487
SNHG12	LncRNA	Homo sapiens	Cerebral Ischemia/Reperfusion Injury	brain tissue of mice 	Interaction(miR-136-5p/Bcl-2/ PI3K/AKT pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//FISH//Flow Cytometry//RIP//qRT-PCR//Luciferase Report Assay	Here, we show that the expression of SNHG12 was upregulated in the brain tissue of mice exposed to middle cerebral artery occlusion/reperfusion (MCAO/R) and primary mouse cerebral cortex neurons treated with oxygen-glucose deprivation/reoxygenation (OGD/R).In addition, we found that SNHG12 acts as a competing endogenous RNA (ceRNA) with microRNA (miR)-136-5p, thereby regulating the inhibition of its endogenous target Bcl-2. Moreover, SNHG12 was proven to target miR-136-5p, increasing Bcl-2 expression, which finally led to the activation of PI3K/AKT signaling. 		Yes	Mechanistically, SNHG12 knockdown resulted in larger infarct sizes and worse neurological scores in MCAO/R mice.Consistent with the in vivo results, SNHG12 upregulation significantly increased the viability and prevented apoptosis of neurons cultured under OGD/R conditions. 	34839459
SNHG12	LncRNA	Homo sapiens	Cholangiocarcinoma	 ICC cells	Interaction(miR-199a-5p/Klotho)	Cell Proliferation Assay//qRT-PCR//Transfection//cell invasion assay	The expression of SNHG12 and Klotho was distinctly increased in ICC cells, while miR-199a-5p expressions were decreased. Mechanistically, Knockdown of SNHG12 significantly suppressed the expressions of miR-199a-5p by sponging it, and then increased Klotho expression. 		Yes	Functionally, the silence of SNHG12 inhibited the proliferation and metastasis of ICC cells, while miR-199a-5p overexpression exhibited an opposite result. The final in vivo experiments suggested that the silence of SNHG12 distinctly inhibited tumor growth.	34239888
SNHG12	LncRNA	Homo sapiens	cervical squamous cell carcinoma	 CSCC tissues	regulation[ERK/Slug pathway]	qRT-PCR	We found that SNHG12 was significantly overexpressed in CSCC tissues. In addition, SNHG12 could facilitate epithelial-mesenchymal transition through ERK/Slug/E-cadherin pathway at least in part. 		Yes	Functional experiments suggested that SNHG12 knockdown dramatically repressed CSCC cells proliferation, migration, and invasion while induced apoptosis in vitro as well as suppressed tumor growth in vivo. 	31943193
SNHG12	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cells	Interaction( miR-30a-3p)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay	 In the present study, we discovered that SNHG12 is up-regulated in ccRCC and that overexpression of SNHG12 predicted poor clinical outcome of ccRCC patients.  Furthermore, we discovered that miR-30a-3p, a putative ccRCC inhibitor, was competitively sponged by SNHG12. Via the crosstalk network, SNHG12 was capable of up-regulating multiple target genes of miR-30a-3p, namely, RUNX2, WNT2 and IGF-1R, which have been identified to facilitate tumorigenesis of ccRCC. 	 In the present study, we discovered that SNHG12 is up-regulated in ccRCC and that overexpression of SNHG12 predicted poor clinical outcome of ccRCC patients. 	Yes	SNHG12 knockdown notably inhibited proliferation and migration of RCC cells. 	33787057
Snhg12	LncRNA	Mus musculus	Cerebral Ischemia/Reperfusion Injury	brain tissue	Expression[highly expressed]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//EdU Staining//IF	We found the expression of SNHG12 was up-regulated by cerebral I/R in mice andSH-SY5Y cell model after OGD/R. 		Yes	On the contrary, down-regulation of SNHG12 exacerbated SH-SY5Y cell injury after OGD/R and inhibited autophagy. 	31056262
SNHG11	LncRNA	Homo sapiens	Pancreatic Carcinoma	serum of PC patients	Interaction(miR-324-3p/VEGFA axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR	LncRNA SNHG11 (SNHG11) has been found to display high expression in serum of PC patients, which implies that dysregulated SNHG11 may be related to the development of PC. Exosome-mediated SNHG11 regulated the expression of VEGFA through sponging miR-324-3p. Rescue assays validated that the inhibitory effect of SNHG11 depletion on cell proliferation, migration, and angiogenesis could be reversed by miR-324-3p downregulation or VEGFA upregulation, and the promoting effect of SNHG11 silence on cell apoptosis could be rescued by transfection of miR-324-3p inhibitor or pcDNA3.1-VEGFA. 		Yes	After conducting experiments with constructed models in vitro or in vivo, we found that exosomal SNHG11 promoted cell proliferation, migration, and angiogenesis but impeded cell apoptosis in PC in vitro, and additionally, it facilitated tumor growth in vivo. 	34519129
SNHG11	LncRNA	Homo sapiens	Stomach Neoplasms	GC samples and cell lines	Interaction(miR-194)	In Vivo Experiment//Western Blot//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	Compared with normal healthy gastric tissue and mucosal epithelial cell GES-1, SNHG11 and CDC25A expressions were dramatically increased in GC samples and cell lines, whereas microRNA-184 (miR-184) levels were reduced. SNHG11 silencing led to increased miR-184 and reduced CDC25A, whereas miR-184 downregulation recovered the expression of CDC25A. Additionally, miR-184 upregulation also played a role in regulating CDC25A ablation. 		Yes	Downregulated miR-184 expression in SNHG11 silenced GC cells showed that miR-184 inhibition reversed the effect of SNHG11 silencing on the growth, proliferation, apoptosis, and migration of GC cells. Moreover, in vivo xenograft experiments demonstrated that SNHG11 knockdown can inhibit tumor growth. 	33816469
SNHG11	LncRNA	Homo sapiens	Lung Neoplasms		regulation[Wnt/β-catenin signaling pathway]	qRT-PCR	Long noncoding RNA small nucleolar RNA host gene 11 (SNHG11) was found to be upregulated in lung cancer and facilitated lung cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition progression while suppressed cell apoptosis. Hence, SNHG11 was found to promote lung cancer progression by activating Wnt/β-catenin pathway in two different patterns, implying that SNHG11 might contribute to lung cancer treatment by acting as a therapeutic target.	Moreover, the high expression of SNHG11 was correlated with poor prognosis of lung cancer patients, TNM stage, and tumor size.	Yes	Long noncoding RNA small nucleolar RNA host gene 11 (SNHG11) was found to be upregulated in lung cancer and facilitated lung cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition progression while suppressed cell apoptosis. 	32239719
SNHG11	LncRNA	Homo sapiens	Colorectal Neoplasms		interaction[c-Myc]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay	Here, we found SNHG11, a highly conserved lncRNA, was commonly overexpressed in various cancer including CRC.Taken together, our findings suggested that reciprocal regulation of SNHG11 and c-Myc promotes cell proliferation in CRC.	 High expression of SNHG11 correlated with poor prognosis in patients with CRC.	Yes	Gain of function and loss-of function experiments showed that SNHG11 visibly promoted proliferation in CRC cells. 	32439170
SNHG11	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues,HCC cells	regulation[hsa-miR-184/AGO2]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Transwell Assay	LncRNA microarray assay and RT-PCR results revealed that the expression of SNHG11 was increased in HCC tumor tissues and also upregulated in HCC cells. Our study demonstrated that the expression of SNHG11 is higher in HCC; moreover, SNHG11 promotes proliferation, migration, apoptosis, and autophagy by regulating AGO2 via miR-184 in HCC.	 SNHG11 had a connection with poor survival rate in HCC. 	Yes	Our study demonstrated that the expression of SNHG11 is higher in HCC; moreover, SNHG11 promotes proliferation, migration, apoptosis, and autophagy by regulating AGO2 via miR-184 in HCC.	32021286
SNHG11	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cell lines	Interaction(miR-2355-5p/CBX5 axis)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	In the present study, the results indicated SNHG11 was highly expressed in TNBC tissues and cell lines.Furthermore, SNHG11 sponged microRNA 2355-5p (miR-2355-5p) in TNBC. Silencing SNHG11 increased miR-2355-5p expression.  In addition, chromobox 5 (CBX5) was identified to be targeted by miR-2355-5p in TNBC. It was also suggested that CBX5 silencing suppressed cell proliferation and migration. Furthermore, overexpressed CBX5 recovered the inhibitive influence of SNHG11 silencing on proliferative and migrative abilities of TNBC cells. 		Yes	Moreover, SNHG11 aggravated cell proliferation and migration, and whereas it attenuated cell apoptosis in TNBC. 	34257707
SNHG11	LncRNA	Homo sapiens	Glioma	glioblastoma tissues ,cell lines	interaction[miR-154-5p]	qRT-PCR//Luciferase Report Assay//Western Blot//Transwell Assay	SNHG11 was upregulated in glioblastoma tissues and five malignant glioma cell lines.SNHG11 functioned as an oncogene in glioma and promoted proliferation, invasion, and migration via EMT by sponging miR-154-5p. 	SNHG11 expression was negatively correlated with overall survival of glioma patients.	Yes	 Moreover, silencing of SNHG11 could decrease glioma cell viability both in vitro and in vivo. Furthermore, the inhibition of SNHG11 suppressed proliferation, invasion and migration via regulating epithelial-mesenchymal transition (EMT).	32432753
SNHG11	LncRNA	Homo sapiens	Adenocarcinoma of Lung	 LUAD cells 	Interaction(miR-193a-5p)	RNA Pull-Down//Wound Healing Assay//Migration Assay//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	SNHG11 was evidently high expressed in LUAD cells in comparison to normal lung epithelial cells. As for the mechanisms, SNHG11 activated Notch pathway via regulating Notch3. In addition, SNHG11 competitively bound with miR-193a-5p to up-regulate Notch3. The last rescue assays displayed that SNHG11 affecting LUAD cell malignant behaviors via regulating miR-193a-5p/SNHG11.		Yes	Moreover, down-regulation of SNHG11 hindered viability, proliferation and migration of LUAD cells as well as tumor growth.	35487027
SNHG11	LncRNA	Homo sapiens	Prostatic Neoplasms	30 PCa and adjacent normal tissue samples	Interaction(miR‑184)	In Vivo Experiment//IHC//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 It was revealed that the SNHG11 expression levels were significantly upregulated in PCa tissues, in comparison with those in adjacent normal tissues. Furthermore, SNHG11 was found to positively regulate insulin‑like growth factor 1 receptor (IGF‑1R) expression by sponging microRNA (miRNA/miR)‑184 in PCa cells. 		Yes	Functionally, SNHG11 knockdown significantly suppressed PCa cell proliferation, migration, invasion and metastasis in vitro and in vivo. 	34328198
SNHG1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Regulation[ miR-361-3p/FRAT1 axis]	Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our results indicated that SNHG1 and FRAT1 were highly expressed in NSCLC tissues and cells.SNHG1 sponged miR-361-3p and negatively regulated miR-361-3p expression. Meanwhile, miR-361-3p targeted FRAT1 and inversely modulated FRAT1 expression. In addition, miR-361-3p inhibition abated the effect of SNHG1 knockdown on FRAT1 expression.		Yes	SNHG1 silencing inhibited proliferation, induced apoptosis and blocked migration and invasion of NSCLC cells.	31788970
SNHG1	LncRNA	Homo sapiens	Lung Neoplasms	A549 and H1299 cell line	Regulation	qRT-PCR	The conclusion was that the A549 and H1299 groups of shLncRNA16 could significantly reduce the incidence by 64% and 40% percentage points compared with the experimental group, which indicates that LncRNA16 can be used as a potential treatment target for patients.		Yes	The conclusion was that the A549 and H1299 groups of shLncRNA16 could significantly reduce the incidence by 64% and 40% percentage points compared with the experimental group, which indicates that LncRNA16 can be used as a potential treatment target for patients.	36495499
circASH2L	CircRNA	Homo sapiens	Arthritis, Rheumatoid	normal synovial tissues and synovial tissues with RA	Interaction(miR-129-5p/HIPK2 axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//ELISA//EdU Staining//Transwell Assay	CircASH2L knockdown in RA-FLSs suppressed cell proliferative, migratory, and invasive capacities, triggered cell cycle arrest, promoted apoptosis, and inhibited inflammation. Mechanistically, circASH2L targeted miR-129-5p, and repression of miR-129-5p abolished the functions of circASH2L silencing on the growth, motility, and inflammation of RA-FLSs.		Yes	CircASH2L knockdown in RA-FLSs suppressed cell proliferative, migratory, and invasive capacities, triggered cell cycle arrest, promoted apoptosis, and inhibited inflammation. 	33964939
SNHG1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	blood	regulation[ miR-489-3p/SOX12/Wnt/β-catenin signaling]	qRT-PCR	The present study demonstrated that SNHG1 expression was upregulated in AML. Taken together, these data indicate that suppression of SNHG1 downregulates AML cell growth by inactivating SOX12/Wnt/β-catenin signaling via upregulating miR-489-3p.		Yes	SNHG1 silencing markedly repressed AML cell growth, whereas SNHG1 overexpression had the opposite effect. 	32592199
circATRNL1	CircRNA	Homo sapiens	Endometriosis	 endometrial cancer cells	Interaction(miR-103a-3p /ASIC1 )	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircATRNL1 and ASIC1 were upregulated but miR-103a-3p was downregulated in endometrial cancer cells. Mechanistically, circATRNL1 bound to miR-103a-3p to upregulate a target gene of miR-103a-3p, ASIC1. 		Yes	CircATRNL1 silencing contributed to the decline of proliferation, invasion, migration, and EMT in Ishikawa cells, while miR-103a-3p inhibitor reversed those changes. In addition, the EMT process was aggravated when miR-103a-3p was inhibited and this process was suppressed by silencing ASIC1 in the presence of downregulated miR-101a-3p.	35504053
SNHG1	LncRNA	Homo sapiens	Osteosarcoma	OS tissues,cell lines	Interaction[regulates miRNA‑101‑3p]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	In the present study, through reverse transcription‑quantitative polymerase chain reaction analysis, it was first found that the lncRNA SNHG1 was upregulated and miRNA‑101‑3p was downregulated in OS tissues and cell lines. Furthermore, according to a dual‑luciferase assay and western blot analysis, miRNA‑101‑3p was found to be a target of the lncRNA SNHG1 in OS, which further regulated the expression of Rho‑associated coiled‑coil‑containing protein kinase 1 (ROCK1). It was found that the phosphoinositide 3‑kinase/ATK pathway was inactivated and that epithelial‑mesenchymal transition was activated in OS cell lines with overexpression of the lncRNA SNHG1. 		Yes	Second, the knockdown of lncRNA SNHG1 induced cell apoptosis and maintained the cell cycle at the G0/G1 phase, which decreased the overall cell viability.	30592267
hsa_circ_0075503	CircRNA	Homo sapiens	Endometriosis	ESCs	Interaction(miR-15a-5p and KLF12)	Western Blot//Transfection//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Circ_0075503 expression was elevated in ectopic endometrium and ectopic ESCs. Down-regulation of circ_0075503 suppressed E2-induced promotion of cell viability, migration and invasion in eutopic ESCs. Circ_0075503 could act as a sponge for miR-15a-5p, and KLF12 was targeted by miR-15a-5p. Inhibition of miR-15a-5p reversed the effects of circ_0075503 knockdown on E2-treated ESCs migration and invasion. Besides, miR-15a-5p repressed E2-induced promotion effects on cell migration and invasion via targeting KLF12. Circ_0075503 could regulate KLF12 expression by sponging miR-15a-5p. Knockdown of circ_0075503 inhibited E2-induced enhancement of cell migration and invasion in eutopic ESCs by regulating miR-15a-5p/KLF12 axis, indicating a novel target for the treatment of endometriosis.		Yes	Inhibition of miR-15a-5p reversed the effects of circ_0075503 knockdown on E2-treated ESCs migration and invasion.	34117589
circPIP5K1A	CircRNA	Homo sapiens	Endometriosis	 EM tissues and cells	Interaction( miR-153-3p/TMSB4X axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	Herein, we found remarkable high circPIP5K1A expression in EM tissues and cells. Also, we found that circPIP5K1A regulated TMSB4X level via interaction with miR-153-3p in EM cells. Besides, circPIP5K1A promoted EM progression via TMSB4X. Moreover, TMSB4X could activate the TGF-β signaling in hEM15A cells. 		Yes	Silencing of circPIP5K1A suppressed proliferation, restrained cell cycle, increased cell apoptosis, and decreased migration and invasion in EM cells.In addition, miR-153-3p inhibition could abrogate the impacts of circPIP5K1A knockdown on EM progression in vitro. 	34546850
SNHG1	LncRNA	Homo sapiens	Parkinson Disease	neuroblastoma cells	Interaction( miR-181a-5p/CXCL12 axis)	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Viability Assay	 We discovered that SNHG1 was significantly elevated, while miR-181a-5p was decreased in N-methyl-4-phenylpyridinium (MPP+)-treated neuroblastoma cells in dose-dependent manners. SNHG1 directly bound to miR-181a-5p, and miR-181a-5p inhibition could block the action of SNHG1 knockdown on MPP+-induced neurotoxicity in neuroblastoma cells. CXCL12 was identified as a downstream target of miR-181a-5p, and the impact of miR-181a-5p on MPP+-induced neuronal damage could be attenuated by CXCL12 overexpression. 		Yes	MPP+ induced cell viability inhibition and apoptosis promotion, while these effects were reversed by SNHG1 knockdown or miR-181a-5p re-expression. 	33389428
SNHG1	LncRNA	Homo sapiens	Parkinson Disease	Human neuroblastoma cell lines	Regulation(miR-216a-3p/Bcl-2-associated X protein)	qRT-PCR//Luciferase Report Assay//Western Blot	The expression of miR-216a-3p was decreased in the PD model cells, and re-expression reversed the high apoptotic rate and cell vitality inhibition in PD model cells. SNHG1 interacted with miR-216a-3p and negatively regulated its upstream molecules, while miR-216a-3p attenuated the effect of SNHG1 knock-down on neurons. The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. At the same time, SNHG1 acted as a coordinator, mediating the regulation of BAX via miR-216a-3p, thereby affecting the activity and apoptotic rate of neurons in the PD model.		Yes	The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. 	34164485
SNHG1	LncRNA	Homo sapiens	Leukemia, Myeloid, Acute	bone marrow 	Expression[highly expressed]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	Here, we show that SNHG1 is highly expressed in AML specimens from non-M3 patients, as well as AML cell lines.Mechanistically, we found that an anti-tumor microRNA-101 (miR-101) is upregulated and its target genes are downregulated in AML cells after SNHG1 knockdown. Further investigations display that SNHG1 can serve as a competing endogenous RNA to inhibit miR-101. 		Yes	 Notably, SNHG1 facilitates the proliferation and inhibits the apoptosis of AML cells in vitro Consistent with these findings, knockdown of SNHG1 significantly inhibits AML progression in an immunodeficient mouse model. 	31615767
hsa_circ_0000673	CircRNA	Homo sapiens	Endometriosis	eutopic and normal endometrial cells	Interaction(Mir-616-3p/PTEN Axis)	Western Blot//Transfection//Wound Healing Assay//CCK8//FISH//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	We demonstrated that knockdown of circ_0000673 significantly increased the proliferation and migration of eutopic and normal endometrial cells. Bioinformatics analysis predicted that circ_0000673 might act as a sponge for miR-616-3p. We found that the effect of circ_0000673 knockdown could be recovered by miR-616-3p inhibitor and enhanced by miR-616-3p mimics. qPCR and western blot assays showed that circ_0000673 knockdown could decrease the expression of PTEN and increase the expression of PI3K and p-AKT. PTEN was confirmed to be a target of miR-616-3p. 		Yes	We demonstrated that knockdown of circ_0000673 significantly increased the proliferation and migration of eutopic and normal endometrial cells. 	34522177
circRTN4	CircRNA	Homo sapiens	Lupus Nephritis	human renal mesangial cells	Interaction(miR-513a-5p/FN axis)	In Vivo Experiment//Transfection//Flow Cytometry//qRT-PCR//FISH//IF	In the present study, we clarified that hsa_circ_0054595 (circRTN4) was upregulated in human renal mesangial cells (HRMCs). In cultured HRMCs, circRTN4 could enhance FN expression by directly interacting with miR-513a-5p. Our findings indicated that circRTN4 exacerbates mesangial cell dysfunction by activating the miR-513a-5p/FN axis in lupus nephritis.	Clinically, high levels of circRTN4 were found in peripheral blood mononuclear cells and kidney tissues of LN patients, hence serving as an effective biomarker for LN detection and a novel therapeutic target. 	Yes	High circRTN4 expression in monocytes disseminated into HRMCs in an exosomal manner, thereby accelerating cell proliferation and extracellular matrix deposition. In addition, knockdown of circRTN4 in the kidney or peripheral blood alleviated renal damage in MRL/lpr and BALB/c mice.	35523949
circZFPM2	CircRNA	Homo sapiens	Endometriosis	ectopic endometrial tissues	Interaction(miR-205-5p/ZEB1 )	Transfection//Wound Healing Assay//CCK8//qRT-PCR//FISH//Luciferase Report Assay//IHC//Bioinformatics Analysis	 The up-regulated circZFPM2 in ectopic endometrial tissues was previously screened by circRNA high-throughput sequencing and was furtherly validated by quantitative real time reverse transcriptase polymerase chain reaction (RT-qPCR) . Luciferase reporter assays validated that circZFPM2 could directly target miR-205-5p and miR-205-5p target ZEB1. 		Yes	Overexpression of circZFPM2 promoted the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in Ishikawa and End1/E6E7 cells, whereas silencing circZFPM2 produced the opposite effect. 	34517087
SNHG1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	Regulation[PI3K/AKT signaling pathway]	CCK8//qRT-PCR//Flow Cytometry//Western Blot	Herein, we found that SNHG1 was highly expressed in PDAC tissues in comparison with adjacent noncancerous tissues, being closely related to tumor size and TNM stage.Finally, an activator (740Y-P) and inhibitor (LY294002) of the PI3K/AKT signaling pathway were used in the western blot assays and the following rescue experiments, demonstrating that SNHG1 facilitates cell proliferation and tumorigenicity partly via the PI3K/AKT signaling pathway in PDAC.	Herein, we found that SNHG1 was highly expressed in PDAC tissues in comparison with adjacent noncancerous tissues, being closely related to tumor size and TNM stage.	Yes	Functionally, silencing of SNHG1 could significantly inhibit cell proliferation, promote cell apoptosis, as well as alter cell cycle progression, whereas the contrary results could be presented in the overexpression of SNHG1. In addition, in vivo xenograft experiment also further confirmed the above results. 	30087712
SNHG1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	regulation[miR-195/NEK2 Axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 The expression of lncRNA SNHG1 up-regulated while that of miR-195 down-regulated in CCCs. lncRNA SNHG1 promotes the progression of cervical cancer through the miR-195/NEK2 axis, so lncRNA SNHG1, miR-195 and NEK2 may have potential values for diagnosing and treating cervical cancer.		Yes	The down-regulation of lncRNA SNHG1 or the up-regulation of miR-195 led to the decrease of NEK2 and the reduction of cells' activity, migration and invasion, also resulting in the increase of cell apoptosis. 	33204155
SNHG1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and CC cell lines	regulation[miR-194/HCCR axis]	CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay	SNHG1 was highly expressed in CC tissues and CC cell lines.In vivo experiment, silencing of SNHG1 suppressed CC tumor growth by modulating miR-194/HCCR axis.		Yes	Knockdown of SNHG1 inhibited CC cell proliferation and enhanced the ability of cell apoptosis.	32456490
SNHG1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cervical cancer cell lines	Expression [highly expressed]	Transfection//Wound Healing Assay//qRT-PCR//Cell Proliferation Assay//Transwell Assay//Invasion Assay//ChIP	 SNHG1 was highly expressed in cervical cancer tissues and cervical cancer cell lines. After knock-down of SNHG1, cell proliferation and migration as well as invasiveness in HeLa and C-33A cells decreased.		Yes	After knock-down of SNHG1, cell proliferation and migration as well as invasiveness in HeLa and C-33A cells decreased.	28930646
hsa_circ_0061140	CircRNA	Homo sapiens	Endometriosis	endometriosis tissues 	regulation[ modulating miR-140-3p and Notch2]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Tissues from endometriosis women displayed an increased expression of circ_0061140.Decrease of circ_0061140 could depress endometriosis progression through modulating miR-140-3p and Notch2.		Yes	Then, we found loss of circ_0061140 significantly repressed ectopic endometrial cell proliferation, migration and invasion.	32621951
SNHG1	LncRNA	Homo sapiens	Glioma	glioma tissue and cell lines	Interaction[binding to miR-194 to regulate PHLDA1 expression]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	In this study, we show that SNHG1 is overexpressed in glioma tissues and cell lines. Next, through online databases, a luciferase reporter assay and an RNA pull-down assay, we confirmed that SNHG1 functions as a sponge for miR-194, which acts as a suppressor in glioma. We also verified that pleckstrin homology like domain family A, member 1 (PHLDA1) is the functional target of miR-194. Moreover, rescue experiments demonstrated that SNHG1 regulates PHLDA1 expression in a miR-194-dependent manner. Taken together, our study shows that SNHG1 promotes glioma progression by competitively binding to miR-194 to regulate PHLDA1 expression, which may provide a novel therapeutic strategy for glioma.		Yes	A series of functional assays suggested that SNHG1 promotes glioma progression in vitro and in vivo. 	31189920
circATRNL1	CircRNA	Homo sapiens	Endometriosis	ectopic tissues	regulation[miR-141-3p/miR-200a-3p-YAP1 axis ]	qRT-PCR//Western Blot	Based on the results of reverse transcription-quantitative polymerase chain reaction analysis, we found significant upregulation of circATRNL1 and Yes-associated protein 1 (YAP1), while downregulation of miR-141-3p and miR-200a-3p in ectopic tissues compared to eutopic tissues. Our findings demonstrate that abnormal upregulation of circATRNL1 regulates cell proliferation and motility and promotes EMT process via the miR-141-3p/miR-200a-3p-YAP1 axis in vitro, which could contribute to the progression of endometriosis.		Yes	The in vitro assays indicated that overexpression of circATRNL1 could promote the proliferation, migration, and invasion of Ishikawa cells, and induce EMT process, while circATRNL1 silencing showed the opposite effect.	32728069
SNHG1	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cell	Interaction(miR-186/FUT8)	qRT-PCR//RIP	SNHG1 was overexpressed in OSCC cells. Mechanistically, we demonstrated that SNHG1 could directly bind to miR-186 and positively regulated α1, 6-fucosyltransferase (FUT8) level. 		Yes	SNHG1 silencing prevented cell proliferation and increased the incidence of apoptosis, DNA fragments, cleaved-caspase 3, and Bax protein levels. Cell migration and invasion were reduced after SNHG1 deletion, and MMP2 and MMP9 protein levels were decreased. SNHG1 overexpression promoted cell survival, migration, and invasion, reduced DNA fragments formation. 	33872442
SNHG1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	Interaction(miR-137-3p/EZH2)	qRT-PCR//RIP	 SNHG1 was significantly overexpressed in BC tissues and cells. Regarding mechanism, the results of AGO2-RIP, ChIP or DLRA showed that SNHG1 played different roles at diverse subcellular sites. In the cytoplasm, SNHG1 acted as a competing endogenous RNA for miR-137-3p to promote EZH2 expression. In the nucleus, SNHG1 could interact with EZH2 to inhibit KLF2 transcription.	 Importantly, SNHG1 was associated with poor survival, and ROC curves revealed high diagnostic values. 	Yes	Moreover, by CCK8, wound healing, transwell, and Western blot analysis, SNHG1 knockdown significantly inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition of BC cells.  Additionally, in vivo experiments showed that silencing SNHG1 hindered tumorigenesis and tumor growth. 	36087568
SNHG1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	interaction[EZH2 and miR-154-5p]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Our analysis revealed that SNHG1 was upregulated in human colorectal cancer tissues, and high SNHG1 expression was associated with reduced patient survival. Mechanistic investigations demonstrated that SNHG1 could directly interact with Polycomb Repressive Complex 2 (PRC2) and modulate the histone methylation of promoter of Kruppel like factor 2 (KLF2) and Cyclin dependent kinase inhibitor 2B (CDKN2B) in the nucleus.	Our analysis revealed that SNHG1 was upregulated in human colorectal cancer tissues, and high SNHG1 expression was associated with reduced patient survival. 	Yes	Moreover, SNHG1 knockdown significantly repressed colorectal cancer cells growth both in vitro and in vivo.	30266084
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma and corresponding adjacent non-tumor tissues,cell lines (Huh7,HepG2,L02)	 Interaction[sponging miR-195]	qRT-PCR//MTT//Luciferase Report Assay//Western Blot	Generally, a significant increase in SNHG1 expression was observed in cancer cell lines compared to normal liver cell lines (Figure 1 A, p < 0.001). Consistent with this observation, SNHG1 was significantly up-regulated in hepatocellular carcinoma tissues in comparison to the levels in adjacent non-tumor tissues (Figure 1 B, p < 0.001). SNHG1 may promote cell invasion and migration in HCC cells by sponging miR-195.	 	Yes	When transfected with si-SNHG1, migration and invasion of HCC cells, as well as expression of astrocyte elevated gene 1 (AEG-1) protein, were significantly inhibited compared with the control cells.	32190150
SNHG1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues,cell lines	Interaction[miR-497/miR-195-5p]	qRT-PCR//Western Blot	 It seemed that there was a high potential for highly expressed SNHG1 and lowly expressed miR-497/miR-195 to symbolize CRC patients' unfavorable prognosis (p < .05). Concurrently, CRC cells were detected with higher SNHG1 expression and lower miR-497/miR-195 expression than CCC-HIE-2 cells (p < .05).Intriguingly, the strength of miR-195-5p collaborating with miR-497-5p in affecting the activity of CRC cells seemed to overweigh that of miR-497/miR-195-5p alone. Besides, both miR-195-5p and miR-497-5p were subjected to in vivo and in vitro modification of SNHG1 (p < .05). Conclusively, application of lncRNA SNHG1 for treating CRC might be promising, given its dual modulation of miR-497 and miR-195 underlying CRC pathogenesis.		Yes	In addition, the EMT process of CRC cells was facilitated markedly against the contexts of overexpressed SNHG1 and underexpressed miR-497-5p/miR-195-5p.	31276207
SNHG1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer tissues	Interaction[PI3K/AKT/mTOR pathway ]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//MTT//Transwell Assay	In the present study, it was demonstrated that SNHG6 expression was downregulated in colorectal cancer tissues by reverse transcription quantitative polymerase chain reaction assays.The overexpression of SNHG6 inhibited colon cell viability and proliferation by targeting ETS1 through the phosphoinositide 3‑kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. These results suggested that SNHG6 may directly suppress ETS1, which may be one of potential mechanisms through which it inhibits the viability and proliferation of colorectal cancer cells, and it provides novel insight into the carcinogenesis of colorectal cancer. 		Yes	Overexpression of SNHG6 not only inhibited the proliferation of colon cancer cells in vitro by inducing apoptosis, but also inhibited cell proliferation, invasion and migration.	31322251
SNHG1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Interaction[sponging miR-137]	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Transwell Assay	SNHG1 upregulation was observed in CRC tissues and cell lines, which was associated with the lymph node metastasis, advanced TNM stage and poorer prognosis.  SNHG1 regulated RICTOR expression by sponging miR-137 and promoted tumorgenesis in CRC.	SNHG1 upregulation was observed in CRC tissues and cell lines, which was associated with the lymph node metastasis, advanced TNM stage and poorer prognosis. 	Yes	 In addition, SNHG1 silencing inhibited CRC cell proliferation and migration in vitro and in vivo. 	31469189
SNHG1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancers tissues and cells	Interaction(miR-145)	qRT-PCR//Colony Formation Assay//Western Blot	In this study, SNHG1 was upregulated in colorectal cancers, and SNHG1 expression was correlated with advanced colorectal cancer stage and tumor recurrence.We found that SNHG1 promoted cell proliferation by acting as a sponge of miR-145, a well known tumor suppressor of colorectal cancer. 	In this study, SNHG1 was upregulated in colorectal cancers, and SNHG1 expression was correlated with advanced colorectal cancer stage and tumor recurrence.Furthermore, the survival analysis indicated that colorectal cancer patients with higher expression of SNHG1 had a worse prognosis. 	Yes	We found that SNHG1 promoted cell proliferation by acting as a sponge of miR-145, a well known tumor suppressor of colorectal cancer. 	29416759
SNHG1	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer tissues and cancerous cell lines	Expression[highly expressed]	CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay//Transwell Assay	In the present study, we referred to the Oncomine database and used RT-qPCR to determine that SNHG1 expression was significantly higher both in colon cancer tissues and cancerous cell lines than in normal samples.		Yes	Cell functional experiments were performed after knockdown of SNHG1, including Cell Counting Kit-8 assay, colony formation assay, Transwell? assay, and flow cytometric analyses of cell apoptosis, which suggested that SNHG1 stimulated colon cancer cell proliferation, promoted cell invasion and migration, and inhibited apoptosis.	29749530
SNHG1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and RCC cell lines	Regulation[miR-137]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	SNHG1 was identified to be overexpressed in RCC tissues and RCC cell lines.Overexpression of SNHG1 participates in RCC tumorigenesis by regulating miR-137.	 High levels of SNHG1 were correlated with poor prognosis of RCC patients.	Yes	Knockdown of SNHG1 suppressed the proliferation, invasion, and EMT capacity in RCC. 	29874202
SNHG1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC tissues and cells	Interaction(mmiR-129-3p/ STAT3 and PD-L1)	Wound Healing Assay//Transwell Assay//Western Blot	 Quantitative real-time PCR and western blotting results revealed that the expression of lncRNA SNHG1 and STAT3 were upregulated in RCC tissues and cells and that the expression of miR-129-3p was downregulated. 		Yes	 SNHG1 knockdown or miR-129-3p overexpression inhibited the proliferation and invasion of A498 and 786-O cells, while the proliferation and cytotoxicity of CD8+ T cells increased, which promoted the secretion of immune-related factors. 	33739543
SNHG1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tissues and cell lines	Interaction(miR-103a)	CCK8//qRT-PCR	 The expression of SNHG1 markedly increased in RCC tissues and cell lines. Subsequent studies identified SNHG1 as a miRNA sponge for miR-103a. In addition, SNHG1 knockdown and miR-103a overexpression significantly inhibited progression of RCC. miR-103a also regulated HMGA2 levels.		Yes	Subsequent studies identified SNHG1 as a miRNA sponge for miR-103a. In addition, SNHG1 knockdown and miR-103a overexpression significantly inhibited progression of RCC. miR-103a also regulated HMGA2 levels.	35466471
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	cell lines	Interaction[sponging miR-195-5p]	CCK8//qRT-PCR//Transwell Assay	Our results indicated a high expression of SNHG1 in hepatocellular carcinoma cells. Moreover, the expression of programmed cell death 4 (PDCD4) was positively regulated by SNHG1 through competing with miR-195-5p. These results indicated that SNHG1 participated in the development of hepatocellular carcinoma as a ceRNA to competitively bind to miR-195-5p and thus mediate PDCD4 expression. 		Yes	Downregulation of SNHG1 inhibited proliferative and migratory potentials of hepatocellular carcinoma cells in vitro and in vivo. 	31330233
SNHG1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer cells and tumor tissues	Interaction(miR-493-5p/ATG14/autophagy pathway)	qRT-PCR//MTT	The findings showed high expression of SNHG1 in the bladder cancer cells and tumor tissues. Further analysis of the mechanism of action of SNHG1 showed that it functions as a sponge of miRNA-493 in bladder cancer. miRNA-493 binds on the 3' -UTR of ATG14 mRNA thus affecting ATG14 protein expression, which is implicated in autophagy. 		Yes	 This finding implies that SNHG1 promotes bladder cancer cell invasion and proliferation via autophagy. 	34055628
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[CDKN1A and CDKN2B]	RNA Pull-Down//Flow Cytometry//qRT-PCR//RIP//FISH//Luciferase Report Assay	 SNHG1 was upregulated in HCC tissues and cells, and its knockdown significantly inhibited HCC cell cycle, growth, metastasis, and epithelial-mesenchymal transition (EMT) both in vitro and in vivo. Chromatin immunoprecipitation and RNA immunoprecipitation assays demonstrate that SNHG1 inhibit the transcription of CDKN1A and CDKN2B through enhancing EZH2 mediated-H3K27me3 in the promoter of CDKN1A and CDKN2B, thus resulting in the de-repression of the cell cycle.		Yes	 SNHG1 was upregulated in HCC tissues and cells, and its knockdown significantly inhibited HCC cell cycle, growth, metastasis, and epithelial-mesenchymal transition (EMT) both in vitro and in vivo. 	33009370
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	interaction[sponging miR-377-3p]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT	We found that SNHG1 was markedly upregulated in HCC tissues and cells.  In conclusion, SNHG1 inhibited apoptosis and induced proliferation, migration, invasion, and EMT by sponging miR-377-3p in HCC, which indicated that SNHG1 may be a potential biomarker and therapeutic target for HCC treatment.		Yes	Knockdown of SNHG1 induced apoptosis and inhibited proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) of HCC cells. SNHG1 knockdown suppressed the tumor growth of HCC in vivo. 	32122143
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	clinical HCC tissues of 75 patients with HCC	Interaction( miR-376a/FOXK1/Snail axis )	qRT-PCR//Luciferase Report Assay//FISH	SNHG1 and FOXK1 were upregulated, and miR-376a was downregulated in HCC. SNHG1 could competitively bind to miR-376a to upregulate its target gene FOXK1, which upregulated Snail. SNHG1 knockdown delayed cancer progression both in vitro and in vivo by upregulating miR-376a and downregulating FOXK1 and Snail. 		Yes	SNHG1 knockdown contributed to suppression of HCC cell viability, invasion, and migration properties and promotion of apoptosis. SNHG1 knockdown exerts anti-tumor activity in HCC, suggesting a therapeutic target.	34095464
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	Interaction(miR-326/LMNB2 )	qRT-PCR//Wound Healing Assay//Western Blot	Our results showed that SNHG1 expression was upregulated significantly in HCC tissues and cell lines. Furthermore, SNHG1 could regulate LMNB2 expression through binding to miR-326 in HCC cell lines.		Yes	Downregulation of both LMNB2, the target of miR-326 in HCC, and SNHG1 inhibited tumor proliferation and growth in vitro and in vivo. 	34917510
SNHG1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC patients	Expression(highly expressed)	qRT-PCR	 We found that SNHG1 was overexpressed and often amplified in HCC patients. 	In the SNHG1-associated network, high expression levels of SNHG1 (log-rank P value = 0.0643), E2F8 (log-rank P value = 0.000048), FANCE (log-rank P value = 0.00125) and LMNB2 (log-rank P value = 0.0392) were significantly associated with poor survival. 	Yes	 In addition, SNHG1 upregulation was associated with the promotion of several primary biological functions, including cell proliferation, transcription and protein binding. 	33499863
SNHG1	LncRNA	Homo sapiens	Ovarian Neoplasms	30 OC Tumor tissues and neighboring healthy tissues	Interaction(miR-454 and ZEB1)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Viability Assay//H&E Staining//Invasion Assay	We found that SNHG1 is overexpressed in OC. Downregulation of SNHG1 promoted miR-454 expression and reduced ZEB1 levels. Moreover, SNHG1 increased ZEB1 expression by downregulating miR-454 and activated Akt signaling, thereby promoting epithelial-mesenchymal transition and enhancing the invasiveness of OC cells. 		Yes	In addition, knockdown of SNHG1, also reduced the aggressiveness of A2780 and SK-OV3 cells. Furthermore, SNHG1 downregulation by siRNA hindered cell migration and invasion; however, this effect was reversed by co-transfection of miR-454 into A2780 and SK-OV3 cells. Tumor xenograft analyses confirmed that SNHG1 affects OC proliferation and metastasis in vivo.	33641229
SNHG1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer  tissues 	regulation[PI3K/AKT signaling pathway]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay	It was demonstrated that SNHG1 expression was significantly upregulated in bladder cancer tissues and cells.Therefore, it was speculated that SNHG1 functioned as a carcinogenic lncRNA in bladder cancer via activation of PI3K/AKT.		Yes	 Moreover, the loss-of-function experimental results suggested that knockdown of SNHG1 inhibited bladder cancer cell proliferation, migration and invasion, but increased apoptosis; however, SNHG1 overexpression promoted these processes. 	32989389
SNHG1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	interaction[ miR-143-3p and EZH2]	RNA Pull-Down//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//EdU Staining//ChIP	In the present study, SNHG1 was found to be substantially up-regulated in BC tissues and cells and was intimately correlated with the TNM stage, lymphatic invasion, metastasis and recurrence-free survival in BC patients.In the nucleus, SNHG1 could interact with EZH2 and regulate the histone methylation of the CDH1 promoter, altering the biological behaviours of BC cells.	In the present study, SNHG1 was found to be substantially up-regulated in BC tissues and cells and was intimately correlated with the TNM stage, lymphatic invasion, metastasis and recurrence-free survival in BC patients.	Yes	 Down-regulation of SNHG1 dramatically attenuated the proliferation, migration and invasion of BC cells, whereas the ectopic overexpression of SNHG1 had the opposite effects in vitro. The in vivo experimental results also indicated that SNHG1 down-regulation hampered the tumour growth and metastasis of BC cells.	32885590
SNHG12	LncRNA	Homo sapiens	Endometrial Neoplasms	EC cell lines	interaction[SNHG12/miR-4429 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	SNHG12 was overexpressed in EC cell lines with decreased expression of miR?4429.Therefore, targeting the SNHG12/miR‑4429 axis could serve as a potential future therapeutic target for treatment of EC.		Yes	Further experiments demonstrated that SNHG12 silencing and overexpression of miR?4429 markedly suppressed proliferation, migration and invasion of RL95?2 cells, arrested cells in the G1 phase, and markedly downregulated the expression of MMP2 and MMP9. 	32945395
SNHG12	LncRNA	Homo sapiens	Melanoma	melanoma cell lines	Interaction(miR-199b)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//EdU Staining//Transwell Assay	Overexpression of SNHG12 was found in melanoma cell lines, and SNHG12 promoted the proliferation, migration, and invasion of melanoma cells. MiR-199b is a target gene of SNHG12, which was expressed at low levels in melanoma cell lines, and SNHG12 regulated melanoma cell proliferation, migration, and invasion through miR-199b. We also revealed that SNHG12 promoted the expression of the target genes of miR-199b, namely ETS1, PXN, JAG1, and DDR1.		Yes	Overexpression of SNHG12 was found in melanoma cell lines, and SNHG12 promoted the proliferation, migration, and invasion of melanoma cells.	35280401
SNHG12	LncRNA	Homo sapiens	Carcinoma, Renal Cell	ccRCC tissues and cell lines	Interaction[Sponging miR-129-5p]	qRT-PCR//Luciferase Report Assay//RIP	MRNA microarray and quantitative real-time PCR revealed that SNHG12 was overexpressed in the ccRCC tissues and cell lines. Mechanistically, dual luciferase assay and RNA immunoprecipitation (RIP) assay showed that miR-129-5p could bind to SNHG12 directly. There was a negative relationship between SNHG12 and miR-129-5p. What's more, we used bioinformatics-based prediction software to predict the target genes of miR-129-5p. Through data analysis and experimental verification, we found MDM4, a regulatory factor in p53 pathway, was involved in this ceRNA network. Our findings demonstrated that SNHG12 served as a sponge for miR-129-5p to regulate the expression of MDM4 and p53 pathway in the development of ccRCC.		Yes	Functional inhibition of SNHG12 suppressed the viability and mobility of ccRCC cells. 	31824846
SNHG14	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[PABPC1]	CCK8//qRT-PCR//ChIP	SNHG14 was highly expressed in HCC tissues and cells, which promoted cell proliferation, migration, and angiogenesis in Hep3B and HepG2 cells. SNHG14 promoted cell proliferation and angiogenesis via upregulating PABPC1 through H3K27 acetylation and modulating PTEN signaling in the tumorigenesis of HCC.		Yes	SNHG14 was highly expressed in HCC tissues and cells, which promoted cell proliferation, migration, and angiogenesis in Hep3B and HepG2 cells. 	32811821
Snhg15	LncRNA	Mus musculus	Hypoxia-Ischemia, Brain	 brain tissues of mice 	Interaction(miR-153-3p/SETD7 axis)	Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//H&E Staining	Results showed that SNHG15 was elevated in brain tissues of mice with HI brain injury, and knockdown of SNHG15 attenuated HI-induced impairment of neurobehavioral function, brain edema, brain injury, and cell apoptosis.  Besides, SNHG15 acted as a miR-153-3p sponge. SETD7 was identified to be a target of miR-153-3p. Furthermore, down-regulation of SNHG15 inhibited the OGD-induced increase in SETD7 expression in PC12 cells. Moreover, SNHG15 modulated OGD-induced cell apoptosis and decrease of cell viability through the miR-153-3p/SETD7 axis. 		Yes	Results showed that SNHG15 was elevated in brain tissues of mice with HI brain injury, and knockdown of SNHG15 attenuated HI-induced impairment of neurobehavioral function, brain edema, brain injury, and cell apoptosis. 	35791576
SNHG14	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	Interaction(miR-543)	Western Blot//Bioinformatics Analysis//Migration Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Invasion Assay//Transwell Assay	Our data indicated that SNHG14 expression was increased in BC tissues and cells, and SNHG14 knockdown mitigated the proliferation, migration, and invasion and facilitated apoptosis of BC cells. SNHG14 directly interacted with miR-543. MiR-543 mediated the regulatory effects of SNHG14 silencing on BC cell behaviors. Moreover, KLF7 was a direct target of miR-543. Overexpressed miR-543-mediated anti-proliferation, anti-migration, anti-invasion, and pro-apoptosis effects were mediated by KLF7. Furthermore, SNHG14 modulated KFL7 expression through acting as a competing endogenous RNA (ceRNA) of miR-543 in BC cells.		Yes	SNHG14 knockdown mitigated the proliferation, migration, and invasion and facilitated apoptosis of BC cells. 	34783894
SNHG14	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and corresponding noncancerous tissues,cell lines(A549, NCI-H1975, NCI-H1299, SK-MES-1)	Interaction[miR-340]	CCK8//qRT-PCR//Luciferase Report Assay	"The results showed that SNHG14 expression was significantly higher in cancer tissues compared with that in matched noncancerous tissues (Figure 1A).We next examined the expression of SNHG14 in a number of NSCLC cell lines, and observed that increased SNHG14 expression could be observed in all four NSCLC cell lines, compared with normal 16HBE cells (Figure 1C).
"	As exhibited in Table 1, the high expression of SNHG14 in NSCLC was closely associated with larger tumor size (P=0.047) and advanced TNM stage (P=0.046). Kaplan–Meier analysis indicated that the prognosis was more unfavorable in NSCLC patients with high SNHG14 expression than those with low expression (P=0.04; Figure 1B).	Yes	KnockExpression[down-expression] of SNHG14 inhibited NSCLC cell proliferation through inducing cell cycle arrest and apoptosis, whereas SNHG14 overexpression exerted the opposite effects. Animal experiment further revealed that Expression[down-expression]-regulated SNHG14 greatly inhibited NSCLC tumor growth in vivo Further studies demonstrated that SNHG14 might serve as a competing endogenous RNA (ceRNA) by sponging miR-340 in NSCLC cells.	30254102
SNHG14	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	interaction[Sponging miR-382-5p]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	The levels of SNHG14 and SPIN1 were significantly increased, while the level of miR-382-5p was apparently reduced in NSCLC tissues and cells.SNHG14 facilitated NSCLC progression by regulating SPIN1 expression via targeting miR-382-5p.		Yes	SNHG14 depletion repressed cell viability, migration and invasion, but induced the apoptotic rate by targeting miR-382-5p. 	33061605
SNHG14	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissue	regulation[miR-206/G6PD pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found a higher expression of SNHG14 in NSCLC and upregulation of SNHG14 contributed to NSCLC cell proliferation, invasion and migration.LncRNA SNHG14 contributed to NSCLC progression through miR-206/G6PD axis, providing novel clues for understanding the mechanism of NSCLC.	We found a higher expression of SNHG14 in NSCLC and upregulation of SNHG14 contributed to NSCLC cell proliferation, invasion and migration.	Yes	knockdown of SNHG14 showed the opposite effect on the progression of NSCLC.	32153123
SNHG14	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction[targeting miR-92b-3p]	qRT-PCR	From the quantitative reverse transcription-polymerase chain reaction results, SNHG14 was found to be downregulated in CRC tissues compared with the normal mucous samples, and its low expression was significantly correlated with poor clinical outcomes.Consequently, SNHG14 exhibited low expression in CRC tissues and involved in CRC progression and metastasis by competing for miR-92b-3p, and SNHG14 could be used as a valuable biomarker and therapeutic target for CRC.	From the quantitative reverse transcription-polymerase chain reaction results, SNHG14 was found to be downregulated in CRC tissues compared with the normal mucous samples, and its low expression was significantly correlated with poor clinical outcomes.	Yes	Overexpression of SNHG14 inhibited cell growth, induced cell apoptosis, suppressed migration and invasion by inhibiting epithelial-mesenchymal transition process.	31692034
SNHG14	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC tissues and cells	Interaction(miR-519b-3p/DDX5 axis)	CCK8//qRT-PCR//Tunel//Western Blot	In our study, we found that SNHG14 is highly expressed in CRC tissues and cells, especially in SW480 and HT-29 cells.Furthermore, we found that SNHG14 functions as a sponge for miR-519b-3p, while the DEAD box protein 5 (DDX5) is a downstream target gene of miR-519b-3p, and the functions of miR-519b-3p inhibitors on the CRC progression could be rescued by downregulation of DDX5.		Yes	 In addition, sh-SNHG14 inhibits cell proliferation, cell migration and invasion, promotes cell apoptosis in CRC cell lines. 	34234865
SNHG14	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissues	Interaction[miR-4673/SOCS1]	CCK8//Luciferase Report Assay//Colony Formation Assay//Flow Cytometry	SNHG14 was found highly expressed in HCC cells and tissues. Dual-Luciferase reporter assays confirmed miR-4673 could bind with SNHG14 and SOCS1. In addition, we showed overexpression of miR-4673 or knockdown of SOCS1 could partially reverse the effects of SNHG14 overexpression on HCC cells. SNHG14 was revealed could promote HCC cell proliferation, colony formation but inhibit cell apoptosis by sponging miR-4673 to regulate SOCS1 expression.		Yes	In addition, we found SNHG14 overexpression could accelerate HCC cell proliferation and colony formation bur inhibit cell apoptosis. On the contrary, knockdown of SNHG14 could cause the exactly opposite effects on HCC cells.	31632558
SNHG14	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tissues	interaction[Sponging miR-217]	qRT-PCR//Luciferase Report Assay//Western Blot	The upregulation of lncRNA-SNHG14 was observed in HCC tissues compared with normal tissues via RT-qPCR and bioinformatic analysis of TCGA data.In summary, SNHG14 is involved in the development of HCC via sponging miR-217 and it may be a biomarker for patients with HCC.		Yes	Silencing of SNHG14 inhibited cell proliferation and induced cell apoptosis in HCC cells. 	32581548
SNHG15	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer cells	Interaction(miR-345-5p)	In Vivo Experiment//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	This present study revealed that the expression of lncRNA SNHG15 (lnc-SNHG15) was significantly upregulated in breast cancer cells, and its overexpression was associated with the tumor. The relative expression of lnc-SNHG15 could be downregulated using siRNAs, and silencing lnc-SNHG15 inhibited the proliferation and the migration of MDA-MB-231 cells. In vivo experiments using the zebrafish xenograft model showed similar results. Mechanistically, the knockdown effect of lnc-SNHG15 could be restored by inhibiting the expression of the miR-345-5p, confirming the negative regulation between lnc-SNHG15 and miR-345-5p. Interestingly, cisplatin treatment combined with SNHG15 knockdown effectively inhibited MDA-MB-231 cell proliferation and migration in the zebrafish xenograft compared to negative controls.		Yes	In vivo experiments using the zebrafish xenograft model showed similar results. Mechanistically, the knockdown effect of lnc-SNHG15 could be restored by inhibiting the expression of the miR-345-5p, confirming the negative regulation between lnc-SNHG15 and miR-345-5p.	36467335
SNHG14	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tumor tissues	Interaction(miR-206/SOX9)	qRT-PCR	SNHG14 and SOX9 were up-regulated in HCC tumor tissues compared with adjacent normal tissues, with decreased miR-206 expression. Besides, inverse correlations between SNHG14 and miR-206, as well as between miR-206 and SOX9, were noted. The dual luciferase reporter gene assay, RIP, and RNA pull-down experiments also revealed the targeting relationship between SNHG14 and miR-206 or between miR-206 and SOX9.	Moreover, SNHG14 expression was significantly associated with the TNM stage, lymphatic metastasis, and histological differentiation of HCC patients.	Yes	Silencing SNHG14 and SOX9 inhibited the proliferation, invasion, and migration of HCC cells, with increased apoptosis, which was all abolished by silencing miR-206.	33782806
SNHG14	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	Interaction(miR-876-5p/SSR2 axis)	qRT-PCR	we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC	we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. 	Yes	By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC	33485374
SNHG14	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian tissues 	Interaction[upregulating DGCR8]	qRT-PCR//Wound Healing Assay//Western Blot//Transwell Assay	SNHG14 level was dramatically higher in ovarian cancer specimens. In summary, SNHG14 could enhance cell migration and invasion via upregulating DGCR8 in ovarian cancer.		Yes	Moreover, cell migration and invasion were significantly attenuated via the inhibition of SNHG14, while enhanced via the SNHG14 overexpression.	31841176
SNHG14	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissues and cell lines	Interaction[targeting miRNA-150-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Flow Cytometry	SNHG14 was highly expressed in BCa tissues and cell lines.  LncSNHG14 overexpression accelerates proliferative potential and cell cycle progression of BCa cells through absorbing miRNA-150-5p to degrade VAMP2 expression.		Yes	overexpression of SNHG14 accelerated the proliferative potential and cell cycle progression of BCa cells. 	30779068
SNHG14	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 BCa tissues and cells	Interaction(microRNA-211-3p/ESM1 axis)	qRT-PCR//MTT	Enhanced SNHG14, ESM1 and suppressed miR-211-3p were found in BCa tissues and cells.SNHG14 up-regulated ESM1 via competitive binding with miR-211-3p. miR-211-3p inhibition or ESM1 overexpression reversed the effects of down-regulation of SNHG14 on BCa, and miR-211-3p up-regulation or ESM1 downregulation reversed the effect of SNHG14 overexpression on BCa. SNHG14 targeted miR-211-3p to regulate ESM1 expression.		Yes	Decreased SNHG14 or up-regulated miR-211-3p depressed cell cycle entry, colony formation, invasion, migration and proliferation abilities, and facilitated apoptosis of BCa cells. Decreased SNHG14 or up-regulated miR-211-3p reduced the tumor volume and weight of nude mice with BCa, as well as promoted apoptosis and restrained proliferation of tumor cells. 	33482820
SNHG14	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	regulation[miR-93-5p/ ZBTB7A Axis]	RNA Pull-Down//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	SNHG14 was underexpressed in EC.LncRNA SNHG14 hampered the viability, migration and invasion of EC cells via modulating miR-93-5p/ZBTB7A axis.	NHG14 expression was significantly relevant to menstruation, FIGO stage, histological grade and lymphatic metastasis of EC patients. 	Yes	 SNHG14 overexpression hampered viability, migration and invasion of EC cells.	33061638
SNHG14	LncRNA	Homo sapiens	Parkinson Disease	SK-N-SH cells	Interaction(miR-135b-5p/KPNA4 axis)	qRT-PCR//RIP//Western Blot	MPP+ treatment elevated the expression of SNHG14 in SK-N-SH cells in a dose and time-dependent manner.  SNHG14 interacted with miR-135b-5p, and SNHG14 silencing-mediated effects were partly overturned by miR-135b-5p knockdown in PD cell model. Besides, miR-135b-5p interacted with the 3' untranslated region (3'UTR) of KPNA4, and KPNA4 overexpression partly reversed miR-135b-5p overexpression-induced effects in PD cell model. SNHG14 knockdown reduced the protein level of KPNA4 partly by up-regulating miR-135b-5p in SK-N-SH cells.		Yes	 SNHG14 knockdown alleviated MPP+-induced apoptosis, inflammation, and cytotoxicity in SK-N-SH cells.	35781593
SNHG14	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissue	interaction[EZH2]	CCK8//qRT-PCR//Western Blot//Transwell Assay	 In the study, we found that SNHG14 expression was higher in PDAC tissue compared to adjacent normal tissues by qRT-PCR analysis.Upregulation of SNHG14 expression promoted cell invasion by affecting E-cadherin expression via interacting with EZH2.	Higher SNHG14 expression was significantly associated with advanced TNM stage and positive lymph node metastasis in PDAC patients.	Yes	Moreover, we showed that higher SNHG14 expression promoted cell proliferation, cell colony formation and cell invasion ability in PDAC.	31929143
Snhg15	LncRNA	Mus musculus	Reperfusion Injury	 infarcted area tissues of I/R mice and I/R-stimulated AC16 cells	Interaction(miR-335-3p/TLR4/NF-κB Pathway)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	SNHG15 was overexpressed in the infarcted area tissues of I/R mice and I/R-stimulated AC16 cells. Mechanistically, SNHG15 directly targeted miR-335-3p, and miR-335-3p was a functional mediator of SNHG15. MiR-335-3p inhibited TLR4 expression by targeting TLR4, and miR-335-3p-mediated inhibition of TLR4 alleviated I/R-induced injury in AC16 cells. Moreover, SNHG15 regulated the TLR4/nuclear factor-κB (NF-κB) signaling pathway through miR-335-3p.		Yes	SNHG15 knockdown alleviated I/R injury in AC16 cells.	35650158
circSirt1	CircRNA	Homo sapiens	Arthritis, Rheumatoid	RA-FLS MH7A cell line	Regulation	Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//ELISA//Colony Formation Assay	This study showed circ-Sirt1 inhibited the proliferation and induced apoptosis of MH7A cells. 		Yes	Overexpression of circ-Sirt1 decreased of the levels of interleukin (IL)-1β and IL-6, tumour necrosis factor (TNF)-α, and matrix matalloproteinases (MMP)-1 and MMP-3 in MH7A cells. In addition, overexpression of circ-Sirt1 increased the expression of Sirt1, Nrf2, HO-1, IκBα, GCLC and GCLM, and decreased the ratio of acetylated NF-κB to normal NF-κB, and the expression of AP-1, COX-2 and HMGB1. 	34431434
SNHG12	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues 	regulation[AKT pathway ]	Flow Cytometry//MTT//Colony Formation Assay//Transwell Assay	We found that the expression of SNHG12 in PCa tissues was significantly higher than that in matched normal adjacent tissues (P < 0.05) (Figure 1(a)). We found that SNHG12 was significantly upregulated in the DU145 cell line compared with the normal human prostate stromal cell line (WPMY-1) and the other two human prostate carcinoma cell lines, LNCAP and PC-3 (Figure 1(b)). Our results indicated that the AKT pathway was positively regulated by SNHG12, as found in studies of renal cell carcinoma [30]. 		Yes	We found that SNHG12 promoted cell proliferation and suppressed apoptosis in PCa cells, which suggests that SNHG12 is probably a novel PCa biomarker and therapy target of PCa.	33426070
circPTTG1IP	CircRNA	Homo sapiens	Arthritis, Rheumatoid	 RA patients and RA-FLSs	Interaction( miR-671-5p/TLR4 axis)	Western Blot//Transfection//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//ELISA//Transwell Assay	The results uncovered that circ-PTTG1IP was overexpressed in RA patients and RA-FLSs, and circ-PTTG1IP knockdown suppressed cell proliferation, migration, invasion and inflammatory response in RA-FLSs. Thus, circ-PTTG1IP knockdown repressed cell proliferation, migration, invasion and inflammatory response in RA-FLSs by regulating the miR-671-5p/TLR4 axis.		Yes	The results uncovered that circ-PTTG1IP was overexpressed in RA patients and RA-FLSs, and circ-PTTG1IP knockdown suppressed cell proliferation, migration, invasion and inflammatory response in RA-FLSs.	34100377
circFBXW7	CircRNA	Homo sapiens	Arthritis, Rheumatoid	RA-FLSs and  RA model	Interaction(miR-216a-3p/HDAC4)	RNA Pull-Down//Western Blot//Transfection//FISH//qRT-PCR//Luciferase Report Assay	 CircFBXW7 could directly sponge miR-216a-3p to upregulate the expression of HDAC4. Inhibition of HDAC4 or upregulation of miR-216a-3p abolished the therapeutic function of exosomal circFBXW7.		Yes	 Exosomal circFBXW7 treatment suppressed proliferation, migration and inflammatory response of RA-FLSs and damage of RA model. 	34853524
SNHG15	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cells and tissue	Interaction[sponging miR-141-3p]	Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Invasion Assay	SNHG15 expression was markedly increased, whereas miR-141-3p expression was substantially reduced in HCC cells and tissue samples relative to normal controls. These finding suggested that SNHG15 promoted HCC progression via negative regulation of miR-141-3p, thus identifying a potential novel HCC treatment pathway.		Yes	When SNHG15 was knocked down, this resulted in a significant disruption to the proliferation, as well as the invasive and migratory ability of these HCC cells.	31310393
SNHG15	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Regulation[miR-490-3p/ histone deacetylase 2 axis ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our research showed that up-regulation of SNHG15 was found in HCC and was related to aggressive behaviors in HCC patients.In conclusion, long noncoding RNA SNHG15 promotes HCC progression by mediating the miR-490-3p/HDAC2 axis in HCC.		Yes	Moreover, knockdown of SNHG15 restrained HCC cell proliferation, migration and invasion. 	31636472
SNHG15	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian tissues and cells	regulation[SNHG15/miR-18a-5p axis]	qRT-PCR	We found that the messenger RNA expression level of SNHG15 was significantly higher and miR-18 was decreased in ovarian cancer tissues and in OC cells.  SNHG15/miR-18a promoted the progression of OC cells via the protein kinase B/mammalian target of rapamycin signaling pathway.		Yes	Functional experiments showed that SNHG15 overexpression potentiated the migration and invasion of OC cells, while SNHG15 inhibition reduced the tumor proliferation, which was restored via overexpression of miR-18a. 	33135285
SNHG15	LncRNA	Homo sapiens	Ovarian Neoplasms	tumor tissues and the cell line	Interaction(miR-370-3p/CDK6)	qRT-PCR//Western Blot	SNHG15 was initially identified by using GEO datasets (GSE135886 and GSE119054) and validated by tumor tissues and the cell line, identifying that SNHG15 was upregulated in ovarian cancer. Mechanistically, SNHG15 promotes proliferation through upregulated CDK6 via sponging miR-370-3p.	 Besides, high SNHG15 indicated poor prognosis in ovarian cancer. 	Yes	 Furthermore, knockdown SNHG15 suppresses ovarian cancer proliferation and promotes apoptosis. 	34734088
SNHG15	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	 5637, UMUC3 and T24 cell lines	Expression(highly expressed)	CCK8//qRT-PCR	 The expression of lncRNA-SNHG15 was up regulated in 5637, UMUC3 and T24 cell lines compared with corresponding normal controls (P < 0.05).  Up regulation was positively related to tumor stage (P = 0.015). And tumor size (P = 0.0465). 	 Up regulation was positively related to tumor stage (P = 0.015). And tumor size (P = 0.0465). 	Yes	The down-regulation of lncRNA-SNHG15 with siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion.	34016097
SNHG15	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	Human OSCC cell lines (SCC-15, SCC-9, SCC-25, and HSC-2)	Interaction(miR-188-5p/DAAM1)	qRT-PCR//Luciferase Report Assay//RIP	SNHG15 presented a high expression in OSCC cells. Through the search of bioinformatics and RNA pull down assays, we confirmed that miR-188-5p was one target of SNHG15 in OSCC cells. Additionally, miR-188-5p could hamper the growth of OSCC cells. Moreover, it was manifested that DAAM1 was down-regulated by miR-188-5p.		Yes	Moreover, inhibition of SNHG15 exhibited repressive influence on proliferative, migrated, and invasive abilities but induce apoptosis of OSCC cells. 	33742497
SNHG15	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	regulation[miR-346/TRAF4 axis]	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 The expression of SNHG15 and TRAF4 was promoted in OS tissues opposite for that of miR-346. 		Yes	The silencing of SNHG15 limited the proliferation, invasion, and enhanced apoptosis of SaoS2 and HOS cells.	33817231
SNHG15	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tumor tissues and cells	Interaction(miR-4735-3p/HIF1a Pathway)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//ChIP	Using qRT-PCR, we determined that lncRNA SNHG15 is highly expressed in CC tumor tissues and cells. Using bioinformatics analysis, RNA pull-down, ChIP, and luciferase reporter assays, we verified the molecular mechanisms of lncRNA SNHG15 in CC progression and found that lncRNA SNHG15 expression in CC cells is transcriptionally regulated by SOX12; moreover, lncRNA SNHG15 promotes CC progression via the miR-4735-3p/HIF1a axis.		Yes	lncRNA SNHG15 knockdown also reduces the tumorigenic properties of CC in vitro, as determined using the MTT, EdU, flow cytometry, and transwell assays. 	35069980
hsa_circ_0088194	CircRNA	Homo sapiens	Arthritis, Rheumatoid	 RA fibroblast-like synoviocytes 	Interaction(miR-766-3p/MMP2 Axis)	Western Blot//Transfection//Migration Assay//qRT-PCR//FISH//RIP//Luciferase Report Assay//Invasion Assay	In the present study, we identified a novel circRNA, Circ_0088194, which was upregulated in RA fibroblast-like synoviocytes (RA-FLSs) and correlated with the disease activity score in 28 joints. Mechanistically, Circ_0088194 acted as a miR-766-3p sponge to relieve the repressive effect of miR-766-3p on its target, MMP2 (encoding matrix metalloproteinase 2), thereby promoting migration and invasion. Collectively, this study identified a novel circRNA Circ_0088194 that promotes RA-FLS invasion and migration via the miR-766-3p/MMP2 axis.		Yes	Overexpression of Circ_0088194 promoted RA-FLS migration and invasion, while inhibition of Circ_0088194 had the opposite effect.	33692802
SNHG15	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	regulation[miR-141-3p,KLF9]	qRT-PCR//Luciferase Report Assay//Western Blot	 SNHG15 was upregulated in NPC tissues and cells.  SNHG15 is upregulated in NPC tissues, and this aggravates the progression of NPC by absorbing miR-141-3p to upregulate KLF9.	High level of SNHG15 indicated worse survival in NPC patients. 	Yes	 Knockdown of SNHG15 markedly suppressed proliferative ability and induced apoptosis in SUNE1 and CNE1 cells. 	32633365
SNHG15	LncRNA	Homo sapiens	Thyroid Neoplasms	 thyroid cancer tissues and cell lines	Expression[lower expressed]	qRT-PCR	 In results, SNHG15 expression was downregulated in thyroid cancer tissues and cells	In results, SNHG15 expression was downregulated in thyroid cancer tissues and cells, and correlated with age, pathology classification, clinical stage, tumor size, distant metastasis, and disease-free survival.	Yes	The in vitro studies suggested SNHG15 overexpression suppressed cell proliferation, migration, and invasion in thyroid cancer.	30623483
SNHG15	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and cells.	Interaction(microRNA-345-5p/RAB27B axis)	In Vivo Experiment//Transfection//Wound Healing Assay//qRT-PCR//MTT//Transwell Assay	The relative expression level of lncRNA SNHG15 and RAB27B was elevated, but that of miR-345-5p was decreased in PC. miR-345-5p was the target gene of SNHG15 and suppressed cell proliferation, migration and invasion in PC. Furthermore, miR-345-5p targeted RAB27B. 		Yes	Silencing of SNHG15 suppressed the proliferation, invasion and migration of PC cells in vitro and suppressed tumour growth in xenograft mice in vivo. 	34594410
SNHG15	LncRNA	Homo sapiens	Prostatic Neoplasms	 cell lines	Regulation[regulating miR-338-3p/FKBP1A axis]	Western Blot//qRT-PCR//RIP//MTT//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Using qRT-PCR analysis, we identified the upregulation of SNHG15 in PCa cell lines.  Finally, the involvement of miR-338-3p and FKBP1A in SNHG15-mediated biological function was demonstrated by performing rescue assays. In summary, our study revealed the function of a novel pathway in PCa.		Yes	Loss-of function assays were conducted to determine the regulatory effect of SNHG15 on PCa cell proliferation, migration and epithelial-mesenchymal transition (EMT).	30981837
SNHG15	LncRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues and cells	regulation[microRNA-18b-5p/LIM-only 4 axis]	qRT-PCR	 SNHG15 and LMO4 were overexpressed while miR-18b-5p was downregulated in liver cancer tissues and cells. The work has illuminated that silencing SNHG15 represses liver cancer progression by modulating miR-18b-5p and LMO4, indicating the therapeutic potency of SNHG15/miR-18b-5p/LMO4 axis in liver cancer.	Up-regulated SNHG15 was connected with inferior prognosis and aggressive behaviors of liver cancer patients.	Yes	SNHG15 knockdown or miR-18b-5p restoration depressed SMMC-7721 cell growth in vivo and in vitro.	33372376
SNHG15	LncRNA	Homo sapiens	Diabetic Nephropathies	 pediatric DN tissues and HG-induced HGMCs	Interaction(miR-141/ICAM-1 axis in vitro)	qRT-PCR//ELISA//MTT//Western Blot	 The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. T		Yes	Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. 	33506255
SNHG15	LncRNA	Homo sapiens	Ischemic Stroke	 nerve cells	Interaction(miR-141/SIRT1 Axis)	Western Blot//Transfection//qPCR//Luciferase Report Assay//Bioinformatics Analysis	SNHG15 expression increased during the process of oxygen-glucose-deprived reoxygenation, and the oxidative stress process was reduced by miR-141/SIRT1.		Yes	In the SNHG15-siRNA-transfected oxygen-glucose-deprived reoxygenation cell model group, miR-141 expression increased, SIRT1 expression decreased, and the expressions of p65, TNF-α, and IL-6 increased compared with the si-NC group. In the miR-141-mimic-transfected oxygen-glucose-deprived reoxygenation cell model, SNHG15 expression decreased, SIRT1 expression decreased, and the expressions of p65, TNF-α, IL-1β, and IL-6 increased. 	34868528
SNHG14	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Expression[highly expressed]	CCK8//Flow Cytometry//EdU Staining//qRT-PCR	Compared with normal cervical tissues, the expression of SNHG14 was significantly higher in cervical cancer tissues.Subsequently, we investigated the possible underlying mechanism. The results found that the knockdown of SNHG14 enhanced the activation of caspases-3, and increased the protein expression of Bax, JAK2 and STAT3, whereas decreased the expression of Bal-2 and Bid.	The prognosis of patients with higher expression of SNHG14 was worse than those with a lower level.  The results demonstrated that a higher expression level of SNHG14 indicated later tumor stage and higher incidence of lymph node metastasis.	Yes	After knocking down SNHG14, the viability and proliferation ability of SW756 and SiHa cells were remarkably decreased, while cell apoptosis was increased.	31114991
SNHG14	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 CC tissues and cell lines	Interaction[miR-206/YWHAZ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In this study, we discovered that the relative expression of SNHG14 was significantly upregulated in CC tissues and cells, and associated with the overall survival of CC patients.Molecular mechanism explorations revealed that SNHG14 acted as a sponge of miR-206 and that YWHAZ was a downstream target gene of miR-206 in CC. Spearman's correlation analysis uncovered a significantly negative correlation between SNHG14 (or YWHAZ) and miR-206 expression, while a significantly positive correlation between SNHG14 and YWHAZ expression in CC tissues. We also found that the effect of SNHG14 knockdown on the CC progression could be partly rescued by overexpression of YWHAZ at the same time. Our findings revealed that SNHG14 acted as a sponge of miR-206 to regulate the expression of YWHAZ in CC, hinting the promising therapeutic target role of SNHG4 for CC patients.	 In this study, we discovered that the relative expression of SNHG14 was significantly upregulated in CC tissues and cells, and associated with the overall survival of CC patients.	Yes	Moreover, knockdown of SNHG14 significantly inhibited cell proliferation, migration and invasion, and promoted cell apoptosis in CC. 	30611620
SNHG14	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	 NPC tissues	Interaction(miR-5590- 3p-ZEB1 /PD-L1)	Bioinformatics Analysis//Western Blot	SNHG14 was upregulated in NPC tissues. Additionally, the expression of ZEB1 was positively related to that of the SNHG14, while it was inversely correlated with that of miR-5590-3p. Moreover, ZEB1 transcription upregulated PD-L1 and promoted the EMT, while SNHG14 could accelerate the EMT of NPC in vivo by regulating the PD-1 and PD-L1.		Yes	 Knocking down SNHG14 markedly inhibited the EMT of NPC.	34706799
SNHG12	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cells	regulation[SNHG12/miR-326/E2F1 feedback loop ]	qRT-PCR	In present study, qRT-PCR manifested the upregulation of SNHG12 expression in OSCC tissues and cells. This research unveiled that SNHG12/miR-326/E2F1 feedback loop facilitated OSCC progression, which shed new light on therapeutic methods in OSCC.		Yes	Suppression of SNHG12 inhibited cell proliferation, migration, invasion, and EMT process in OSCC. Additionally, SNHG12 depletion also attenuated OSCC tumor growth in vivo.	32506729
SNHG12	LncRNA	Homo sapiens	Colonic Neoplasms	colon cancer samples compared to normal adjacent tissues	Interaction(miR-485-3p/FGF3 axis)	In Vivo Experiment//IHC//Western Blot//Migration Assay//qRT-PCR//MTT//Luciferase Report Assay//cell invasion assay//Colony Formation Assay	Here, we found that the expression of lncRNA small nucleolar RNA host gene 12 (SNHG12) was markedly upregulated in colon cancer samples compared to normal adjacent tissues. 	Notably, patients with low expression of SNHG12 displayed higher survival rate than those with high expression of SNHG12. 	Yes	Further researches revealed that knockdown of SNHG12 suppressed the malignant phenotype of colon cancer cells. Interestingly, SNHG12 could function as a sponge to specifically bind to microRNA-15a (miR-15a). Moreover, we confirmed that pyruvate dehydrogenase kinase 4 (PDK4) is a direct target gene of miR-15a. 	34650693
SNHG12	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	PTC tissues	Interaction[ targeting miR-16-5p]	qRT-PCR	In this study, SNHG12 was found to be increased in PTC tissues and cell lines using quantitative real-time PCR. Mechanistic investigations revealed that SNHG12 functions as a competing endogenous RNA (ceRNA) to sponge miR-16-5p, which was downregulated in PTC tissues.		Yes	 Knockdown of SNHG12 significantly inhibited PTC cell proliferation, migration and invasion and induced apoptosis in vitro. 	31355416
hsa_circ_0088036	CircRNA	Homo sapiens	Arthritis, Rheumatoid	blood	regulation[circ0088036/miR-140-3p/SIRT 1 axis]	qRT-PCR	Our previous study verified that hsa_circ_0088036 (circ0088036) is significantly elevated in peripheral blood mononuclear cells from patients with RA. In conclusion, this study revealed that circ0088036 may play an essential role in promoting synovial pathogenesis via the circ0088036/miR-140-3p/SIRT 1 axis in RA, providing new insight into circRNAs during RA progression.		Yes	Functionally, upregulated circ0088036 promoted the proliferation and migration of RA-FLSs. 	32673817
SNHG12	LncRNA	Homo sapiens	Carcinoma, Renal Cell	renal tissue,cell lines	Interaction[HIF1α]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	SNHG12 was aberrantly up-regulated in renal carcinoma both in vivo and in vitro.Mechanistically, SNHG12 modulated HIF1α expression via competing with miR-199a-5p, which consequently contributed to its oncogenic potential. MiR-199a-5p inhibition severely compromised SNHG12 silencing-elicited tumor repressive effects.		Yes	 Deficiency of SNHG12 significantly suppressed cell viability, anchorage-independent growth and induced apoptosis. In addition, SNHG12 silencing inhibited migrative and invasive in vitro and xenograft tumor growth in vivo. 	31114448
SNHG12	LncRNA	Homo sapiens	Carcinoma, Renal Cell	RCC tumor tissues	regulation[SNHG12/miR-200c-5p/COL11A1 axis ]	qRT-PCR//Western Blot	"Reverse transcription?quantitative PCR, demonstrated that SNHG12 expression levels were upregulated in RCC tumor tissues, but not in normal kidney tissues. In conclusion, the results of the present study suggested that the SNHG12/miR‑200c‑5p/COL11A1 axis may be crucial for RCC progression, which provided an insight into potential therapeutic strategies for RCC treatment.
"		Yes	 SNHG12 knockdown markedly inhibited cell viability and invasion, while increasing apoptosis in both A498 and 786O cell lines.	32901847
SNHG12	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 RCC tissues and cells	Regulation(CEP55 )	qRT-PCR//Luciferase Report Assay//Genotyping	SNHG12 was highly expressed in RCC tissues and cells, and it was related to the poor prognosis of RCC patients. KMT2B up-regulated SNHG12 expression through modifying H3K4me3 in its promoter region. In addition, SNHG12 promoted CEP55 expression by recruiting the transcription factor E2F1. Knockdown of SNHG12 blocked E2F1 recruitment and down-regulated the expression of CEP55, thereby inhibiting tumor formation and angiogenesis in nude mice.		Yes	 SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. 	35597996
SNHG12	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell lines	Interaction(miR-516a-5p)	qRT-PCR//IHC//RIP	SNHG12 and HEG1 were upregulated, miR-516a-5p was downregulated in HCC cell lines. SNHG12 could interact with and inhibit miR-516a-5p. MiR-516a-5p could interact with HEG1 and inhibit HEG1 expression.		Yes	Knock down SNHG12 inhibited proliferation, migration, invasion, EMT and promoted apoptosis of HCC cells. Such effects were antagonized by inhibiting miR-516a-5p. SNHG12 overexpression lead to opposite results. Similar results were observed in mice. 	33774129
SNHG12	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues	Interaction[absorbing miRNA-129 to Expression[Expression[highly expressed]-expression]regulate SOX4]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	SNHG12 was Expression[Expression[up-expression]-expression]regulated in OC tissues relative to adjacent normal ones. We observed the binding between SNHG12 and miRNA-129, and the latter was lowly expressed in OC. The miRNA-129 overexpression partially reversed the promotive effects of SNHG12 on proliferative and migratory abilities of OC cells. Subsequently, SOX4 was proved to be the target gene of miRNA-129. The SOX4 overexpression was further confirmed to reverse the inhibitory effects of miRNA-129 on proliferative and migratory abilities of OC cells.	Patients with metastatic OC or those in stage III-IV had a higher level of SNHG12 compared with non-metastatic or stage I-II patients.The 5-year survival was markedly worse in OC patients with high-level SNHG12 than those in the low-level groExpression[Expression[up-expression]-expression].	Yes	Overexpression of SNHG12 accelerated A2780 and HO8910 cells to proliferate and migrate. 	30964158
SNHG12	LncRNA	Homo sapiens	Osteosarcoma	cell lines	Interaction[targeting miR-195-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results show that lncSNHG12 was upregulated in OS cell lines. Also, lncSNHG12 downregulation suppressed the expression of insulin growth factor 1 receptor (IGF1R) expression through sponging miR-195-5p, which was verified with the luciferase reporter assay and rescue experiments.		Yes	Downregulation lncSNHG12 suppressed the metastasis and proliferation both in vitro and in vivo. 	31743769
SNHG14	LncRNA	Homo sapiens	Pancreatic Neoplasms	cancerous tissues	Interaction[miR-613]	CCK8//qRT-PCR//Western Blot//Transwell Assay	SNHG14 expression was up-regulated in cancerous tissues from pancreatic cancer patients. Mechanistic studies revealed that miR-613 was targeted by SNHG14, and Annexin A2 (ANXA2) was targeted and inversely regulated by miR-613 in pancreatic cancer cells. In vivo studies showed that SNHG14 knockdown attenuated tumour growth. MiR-613 was down-regulated and ANXA2 was up-regulated in the pancreatic cancer tissues, and SNHG14 expression levels were inversely correlated with miR-613 expression levels and positively correlated with the ANXA2 mRNA expression levels	High expression of SNHG14 was associated with poor tumour differentiation, advanced TNM stage and nodal metastasis. 	Yes	SNHG14 overexpression enhanced cell proliferative, growth and invasive abilities, and suppressed apoptotic rates and caspase-3 activity in pancreatic cancer cells, while SNHG14 knockdown exerted opposite effects. 	31513352
SNHG12	LncRNA	Homo sapiens	Parkinson Disease	 SH-SY5Y cells	Interaction( miR-138-5p)	qRT-PCR	 Transfection of the lncRNA SNHG12-plasmid reduced neuronal apoptosis, inflammation, and oxidative stress in MPP+-stimulated SH-SY5Y cells that were rescued by adding the miR-138-5p mimic.  These results showed that lncRNA SNHG12 could affect neuronal apoptosis, inflammation, and oxidative stress in a PD cell model by regulating miR-138-5p expression. TargetScan and dual-luciferase reporter analysis suggested that miR-138-5p targeted nuclear factor I/B (NFIB). Furthermore, the expression level of NFIB was downregulated after MPP+ stimulation in SH-SY5Y cells. 		Yes	 Transfection of the lncRNA SNHG12-plasmid reduced neuronal apoptosis, inflammation, and oxidative stress in MPP+-stimulated SH-SY5Y cells that were rescued by adding the miR-138-5p mimic. 	34783303
SNHG12	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cell lines	Regulation[miR-125b/STAT3 axis]	qRT-PCR	Meanwhile, the expression of SNHG12 was obviously upregulated in cervical cancer cell lines (HeLa, SiHa, Caski, C4-1, and C33A) compared with the immortalized cervical epithelial cells.  Meanwhile, miR-125b mimics repressed the expression of signal transducer and activator of transcription 3 (STAT3). The further assay showed that STAT3 was a target of miR-125b in cervical cancer. In addition, sh-STAT3 repressed the migration and invasion of cervical cancer cells. Furthermore, it showed that miR-125b inhibitors reversed STAT3 expression restrained by the reduction of SNHG12 expression. In general, SNHG12 modulated STAT3 by sponging miR-125b in cervical cancer and played an important role in the development of cervical cancer.		Yes	In addition, SNHG12 inhibition restrained the proliferation, migration, and invasion of cervical cancer cells. 	30246459
SNHG12	LncRNA	Homo sapiens	Glioma	glioma tissues and cells	Regulation[miR-101-3p/FOXP1 axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	SNHG12 expression was enhanced and high-expressed in the glioma clinical tissue samples and cell lines, especially in the advanced clinical grade. Overall, we confirmed a functional regulatory pathway that SNHG12 and miR-101-3p regulated the expression of FOXP1 in glioma cells, forming the SNHG12/miR-101-3p/FOXP1 pathway. 	SNHG12 expression was enhanced and high-expressed in the glioma clinical tissue samples and cell lines, especially in the advanced clinical grade.	Yes	In functional study, knockdown of SNHG12 impaired the proliferation, induced the apoptosis in vitro and, meanwhile, inhibited the tumor growth in vivo. 	30098431
SNHG12	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	interaction[HuR]	qRT-PCR//RNA Pull-Down//RIP	The results revealed that SNHG12 was significantly upregulated in glioma tissues and cell lines. 	 High levels of SNHG12 were associated with the deterioration of patients with glioma. Patients with high levels of SNHG12 exhibited a reduced 5-year overall survival rate (compared to those with lower levels), particularly in cohorts with high-grade carcinoma (III-IV). 	Yes	 The silencing of SNHG12 expression by RNA interference led to a reduced viability and mobility, and in an increased apoptosis of human glioma cells.	30015836
SNHG12	LncRNA	Homo sapiens	Atherosclerosis	 AS patients and  HUVECs	Interaction(miR-218-5p/IGF2 axis)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA//Bioinformatics Analysis	 We found that SNHG12 and IGF2 expression levels were high and miR-218-5p expression levels were low in AS patients and ox-LDL-treated HUVECs. Overall, SNHG12 promotes the development of AS by the miR-218-5p/IGF2 axis.		Yes	SNHG12 depletion attenuated ox-LDL-induced injury in HUVECs, whereas miR-218-5p suppression partially abated this effect. Moreover, IGF2 overexpression prevented the alleviative role of miR-218-5p in ox-LDL-treated HUVECs. SNHG12 upregulated IGF2 expression by sponging miR-218-5p. More importantly, SNHG12 increased proinflammatory cytokine production and augmented atherosclerotic lesions in vivo. 	34313533
SNHG12	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	LSCC tissues	Interaction[sponging miR-129-5p and potentiating WWP1]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	SNHG12 was significantly overexpressed in LSCC tissues compared with adjacent normal tissues. 	The expression level of SNHG12 was significantly associated with T classification, lymph node metastasis, and cancer stage of LSCC. High expression of SNHG12 predicted shorter disease-free survival. 	Yes	Our study demonstrated that SNHG12 promoted LSCC cells progression via sponging miR-129-5p and potentiating WWP1 expression.	31348766
SNHG12	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cell lines	Interaction[sponging microRNA-195]	qRT-PCR	In the present study, we found that SNHG12 was highly expressed in human PCa tissues and cell lines. Further in-depth mechanistic studies showed that SNHG12 might serve as a competing endogenous RNA for miR-195 in PCa cells, and miR-195 expression level was negatively associated with the expression of SNHG12 in PCa tissues. Finally, we found that the activity of Wnt/β-catenin signaling is enhanced by SNHG12 overexpression and rescued by co-transfection with miR-195 mimics in PCa cells. Collectively, the present study indicated the oncogenic function of SNHG12 in PCa and our findings might provide a new target in the treatment of PCa.		Yes	 In addition, gain-of-function and loss-of-function studies showed that overexpression of SNHG12 promoted, while downregulation suppressed the proliferation, invasion, and migration of PCa cells in vitro. Knockdown of SNHG12 also repressed PCa xenograft tumor growth in vivo. 	30945357
SNHG12	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa cells and tissues	Interaction[sponging miR-133b]	Flow Cytometry//qRT-PCR//CCK8//Colony Formation Assay//Transwell Assay	"Results
showed that SNHG12 was overexpressed, which indicated a high
expression level of SNHG12 in PCa (Figure 1g,h; Table S3). Direct interactions between miR-133b and SNHG12 have been found and SNHG12 acts as an oncogene to promote tumorigenesis of PCa by sponging tumor suppressor gene miR-133b.
"	"That is, higher SNHG12
expression level was positively correlated with new tumor events after
treatment (p < .0001; Figure 3a), positive lymph nodes (p = .0036; Figure
3b), Gleason score 8–10 (p < .0001; Figure 3c) and advanced residual
tumor grade R1+R2 (p = .0027; Figure 3d)."	Yes	" All mentioned above have
elucidated that SNHG12 regulates proliferation, migration, invasion,
and cell cycle of PCa, thus promoting the development of Pca."	31267540
SNHG12	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues,cell lines	Interaction[sponging microRNA-16]	CCK8//qRT-PCR//Transwell Assay	It was observed that SNHG12 was markedly upregulated in CRC tissues when compared with that in adjacent non-tumour tissues, and its high expression was associated with CRC progression, as well as poor prognosis of patients.In addition, the expression of SNHG12 was higher in CRC cell lines when compared with that in a normal intestinal epithelial cell line.A Bioinformatics analysis predicted that SNHG12 and miR-16 have complementary binding sites, which was confirmed by a luciferase reporter gene assay. The expression levels of miR-16 were markedly decreased in CRC tissues and cell lines compared with those in normal tissues or cells, and were inversely correlated with the expression levels of SNHG12 in CRC tissues. Furthermore, silencing of miR-16 eliminated the suppressive effects of SNHG12 knockdown on CRC cell proliferation and invasion. In conclusion, the present study demonstrated that SNHG12 promotes CRC cell proliferation and invasion, at least in part, by acting as a molecular sponge of miR-16, suggesting that SNHG12 may be a promising therapeutic target for CRC.	 It was observed that SNHG12 was markedly upregulated in CRC tissues when compared with that in adjacent non-tumour tissues, and its high expression was associated with CRC progression, as well as poor prognosis of patients. 	Yes	Knockdown of SNHG12 significantly inhibited CRC cell proliferation and invasion, while ectopic overexpression of SNHG12 had the opposite effect.	31316616
SNHG12	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCA tissues	regulation[SNHG12/miRNA-195-5p/BCL9 network]	qRT-PCR	SNHG12 was downregulated in human ESCA tissues compared to control tissues. 	The expression of SNHG12 was strongly associated with T stage, N stage, and TNM stage. Low SNHG12 expression in esophageal tumor tissues was significantly correlated with poor prognosis.	Yes	 Furthermore, knockdown of SNHG12 not only promoted proliferation, colony formation, migration, and invasion and inhibited apoptosis in ESCC cells in vitro, but also increased tumor growth in vivo. 	32086782
SNHG12	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC specimens and CD133 cells	regulation[BMI1 and CTNNB1]	RNA Pull-Down//IHC//Western Blot//Flow Cytometry//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	In this study, lncRNA small nucleolar RNA host gene 12 (SNHG12), mainly distributed in ESCC cell cytoplasm, was overexpressed in ESCC specimens and CD133 cells. In summary, SNHG12 induces proliferation, migration, EMT, and stemness of ESCC cells via post-transcriptional regulation of BMI1 and CTNNB1, indicating that targeting SNHG12 might be a novel target for ESCC treatment. +-		Yes	In CD133 ESCC cells, SNHG12 overexpression promoted cell proliferation, migration, epithelial-mesenchymal transition (EMT), and stemness and SNHG12 silencing led to opposite results.	32239639
SNHG12	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(HuR/PD-L1/USP8 axis)	CCK8//qRT-PCR//Colony Formation Assay//RIP	 LncRNA SNHG12 was found to be prominently expressed in NSCLC tissues and cells, which was associated with a poor prognosis. Mechanically, the binding of lncRNA SNHG12 to HuR improved mRNA stability and expression of PD-L1 and USP8, and USP8-mediated deubiquitination stabilized the protein level of PD-L1. Overexpression of USP8 or PD-L1 weakened the inhibition of silencing lncRNA SNHG12 on the immune escape of NSCLC.	 LncRNA SNHG12 was found to be prominently expressed in NSCLC tissues and cells, which was associated with a poor prognosis.	Yes	 Silencing lncRNA SNHG12 resulted in the reduction in proliferation and the promotion of apoptosis of NSCLC cells, while simultaneously increasing PBMC proliferation and the ratio of CD8+ T cells. Silencing lncRNA SNHG12 restricted tumor growth and upregulated the ratio of CD8+ T cells by decreasing USP8 and PD-L1.	35658874
SNHG14	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tumor tissues	regulation[microRNA-655-3p]	CCK8//qRT-PCR//Flow Cytometry//EdU Staining	qPCR results indicated that SHHG14 expression in EC tumor tissues was remarkably higher than that in adjacent tissues. Additionally, lncRNA SNHG14 is capable of accelerating malignant progression of EC by regulating microRNA-655-3P expression.	Compared with patients with low expression of SNHG14, patients with high expression of SNHG14 had larger tumor size, lower overall survival, and more advanced pathological stage. 	Yes	In vitro, compared with those in the control group, the overexpression of SNHG14 markedly enhanced EC cell proliferation while inhibited cell apoptosis, and the opposite result was observed in SNHG14 silencing group.	33155197
SNHG14	LncRNA	Homo sapiens	Arthritis, Rheumatoid	RA patients	Interaction(miR-17-5p/MINK1-JNK pathway)	Western Blot//Transfection//qRT-PCR//FISH//Luciferase Report Assay//ELISA//Colony Formation Assay//EdU Staining	 Here, we found that high expression of SNHG14 in RA was closely related to the disease activity.  In mechanism, SNHG14 served as a sponge of microRNA-17-5p (miR-17-5p), and misshapen like kinase 1 (MINK1) was a target of miR-17-5p. 	 Here, we found that high expression of SNHG14 in RA was closely related to the disease activity. 	Yes	 Functional assays indicated that SNHG14 knockdown obviously hampered phorbol myristate acetate-activated THP-1 (pTHP-1) cell proliferation and proinflammatory cytokines production. 	34529319
SNHG14	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cell lines	Interaction[SNHG14/miR-5590-3p/ZEB1 ]	CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Results depicted that SNHG14 was upregulated in DLBCL and its depletion retarded proliferation, migration and epithelial-to-mesenchymal transition (EMT). In conclusion, we firstly showed that SNHG14/miR-5590-3p/ZEB1 positive feedback loop promoted diffuse large B cell lymphoma progression and immune evasion through regulating PD-1/PD-L1 checkpoint, indicating that targeting SNHG14 was a potential approach to improve the efficacy of immunotherapy in DLBCL.		Yes	 Results depicted that SNHG14 was upregulated in DLBCL and its depletion retarded proliferation, migration and epithelial-to-mesenchymal transition (EMT). 	31570691
SNHG14	LncRNA	Homo sapiens	Pre-Eclampsia	PE patients	Interaction(miR-330-5p)	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//IF//Luciferase Report Assay//Cell Cycle Assay//Invasion Assay//Transwell Assay	lncRNA SNHG14 was downregulated in PE patients; it was involved in trophoblast proliferation and regulated cell proliferation during G1/S transition.  Luciferase reporter assay indicated that lncRNA SNHG14 served as a molecular sponge for miR-330-5p and negatively regulated miR-330-5p expression in PE. Furthermore, the effects of silenced SNHG14 on trophoblast proliferation, migration, invasion and EMT were reversed by addition of miR-330-5p inhibitor, suggesting that in PE lncRNA SNHG14 functions by competitively binding to miR-330-5p. 		Yes	lncRNA SNHG14 was downregulated in PE patients; it was involved in trophoblast proliferation and regulated cell proliferation during G1/S transition.  In addition, lncRNA SNHG14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) in HTR-8/SVneo cells.	33161910
SNHG14	LncRNA	Homo sapiens	Acute Kidney Injury	 HK-2 cells	Interaction(miR-93/IRAK4 and IL-6R/NF-κB and STAT3 signaling)	Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//ChIP	Increased expression of SNHG14 was observed in LPS-induced HK-2 cells, and this was due to the activation of the TLR4/NF-κB pathway. Further investigations confirmed that SNHG14 exerted the functions via miR-93 which could regulate the activation of NF-κB and STAT3 signaling by targeting IRAK4 and IL-6R. 		Yes	 In vitro studies showed that SNHG14 was involved in the oxidative stress, inflammation, and apoptosis of LPS-induced HK-2 cells. 	33505213
SNHG14	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid tumour cells 	Interaction(miR-93-5p)	In Vivo Experiment//Transwell Assay//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//IHC//IF	SNHG14 was upregulated in thyroid tumour cells compared with normal cells. Moreover, SNHG14 directly targeted miR-93-5p and there was a negative correlation between them. Further functional experiments illustrated that miR-93-5p overexpression dramatically reversed the promoting role of SNHG14 in proliferation, migration and invasion of TPC-1 cells. 		Yes	Downregulation of SNHG14 effectively reduced the proliferation, migration and invasion of TPC-1 cells, and induced cell apoptosis.	34380584
SNHG14	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	 DLBCL tissues and cell line	Interaction(miR-152-3p)	Western Blot//Transfection//Migration Assay//CCK8//qRT-PCR//RIP//Transwell Assay	The results showed that SNHG14 expression increased and miR-152-3p expression decreased in DLBCL tissues and cell lines, indicating a negative correlation between miR-152-3p and SNHG14 expression.Furthermore, both the immune escape and progression of DLBCL are advanced by SNHG14 expression via its interactions with miR-152-3p. 		Yes	Moreover, SNHG14 was found to promote DLBCL growth, migration, and EMT-like processes in vitro, and directly inhibits miR-152-3p gene expression via sequestration of the miR-152-3p transcripts in DLBCL. Additionally, SNHG14/miR-152-3p inhibits apoptosis and promotes cell proliferation on cytotoxic T lymphocytes (CTLs) in DLBCL via the PD-1/PD-L1 checkpoint.	33682607
Snhg14	LncRNA	Mus musculus	Parkinson Disease	brain tissues	Interaction[miR-133b/ α-synuclein pathway]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//IHC//ChIP	 Firstly, we found that the expression level of SNHG14 was elevated in brain tissues of PD mice. Further study showed that miR-133b down-regulated α-syn expression by targeting its 3'-UTR of mRNA and SNHG14 could reverse the negative effect of miR-133b on α-syn expression. Interference of SNHG14 reduced rotenone-induced DA neuron damage through miR-133b in MN9D cells and α-syn was responsible for the protective effect of miR-133b. Similarly, interference of SNHG14 mitigated neuron injury in PD mouse model. All in all, silence of SNHG14 mitigates dopaminergic neuron injury by down-regulating α-syn via targeting miR-133b, which contributes to improving PD.		Yes	Similarly, interference of SNHG14 mitigated neuron injury in PD mouse model. All in all, silence of SNHG14 mitigates dopaminergic neuron injury by down-regulating α-syn via targeting miR-133b, which contributes to improving PD.	31683259
Snhg14	LncRNA	Mus musculus	Parkinson Disease	brain tissues	regulation[miR-214-3p/KLF4 Axis ]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry//Luciferase Report Assay//ELISA	Our data indicated that SNHG14 was upregulated and miR-214-3p was downregulated in PD models.Our current study first demonstrated the protective effect of SNHG14 knockdown on MPP-stimulated cytotoxicity in SK-N-SH cells at least partially by targeting the miR-214-3p/KLF4 axis, illuminating a promising target for PD intervention and treatment. +		Yes	SNHG14 knockdown ameliorated MPP-stimulated damage in SK-N-SH cells, as evidenced by the enhancement in cell viability and the suppression in cell apoptosis and pro-inflammatory cytokine production.	33071725
Snhg14	LncRNA	Mus musculus	Plaque, Atherosclerotic	atherosclerotic plaque tissues	interaction[Sponge miR-19a-3p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay	In this study, we found a significant decrease in the expression of lncRNA-SNHG14 in atherosclerotic plaque tissues of ApoE-/- mice.The results of qRT-PCR showed that the level of RORα mRNA was significantly increased in the aortas treated with miR-19a-3p and SNHG14 compared with that treated with miR-19a-3p alone.		Yes	Overexpression of lncRNA-SNHG14 can inhibit VSMC proliferation while promoting apoptosis. 	32908577
SNHG12	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	Interaction[phosphatidylinositol 3-kinase/AKT pathway ]	RNA Pull-Down//Western Blot//Wound Healing Assay//CCK8//FISH//qRT-PCR//Microarray//Transwell Assay	Long non-coding RNAs contribute to the development of human cancers. We compared the long non-coding RNA levels in gastric cancer (GC) and para-cancerous tissues in the Gene Expression Omnibus, and found that small nucleolar RNA host gene 12 (SNHG12) was upregulated in GC tissues.Fluorescence in situ hybridization confirmed that SNHG12 is overexpressed in GC tissues.Taken together, cancer pathway microarray and bioinformatics analyses, RNA pulldown assays, Western blotting and immunohistochemistry revealed that SNHG12 induces GC tumorigenesis by activating the phosphatidylinositol 3-kinase/AKT pathway. SNHG12 may thus be a useful marker for predicting poor survival in GC patients.		Yes	In vitro, silencing SNHG12 suppressed GC cell proliferation, migration and invasion, but induced apoptosis and cell cycle arrest. Overexpressing SNHG12 had the opposite effects. In xenografted mice, knocking down SNHG12 reduced GC tumor growth. 	31808752
SNHG12	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines,blood	Interaction[targeting miR-16]	CCK8//qRT-PCR//Luciferase Report Assay//Migration Assay	In the present study, it was observed that SNHG12 was significantly upregulated in GC tissues and cell lines. In conclusion, the present study demonstrates that inhibition of SNHG12 suppresses GC cell proliferation and migration by modulation of miR-16 expression, and thus suggests that the SNHG12/miR-16 interaction may be used as a promising target for GC treatment.	High expression of SNHG12 was associated with GC progression and poor prognosis of patients.	Yes	 Knockdown of SNHG12 markedly inhibited the proliferation and migration of the BGC823 and HGC27 GC cell lines. 	31258654
SNHG12	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	 Interaction(miR-218-5p/YWHAZ axis)	Western Blot//ISH//Co-IP//Migration Assay//qRT-PCR//FISH//Luciferase Report Assay//IHC//ChIP	 In the present study, we demonstrated that SNHG12 was upregulated in GC tissues and cell lines.	the expression level of SNHG12 in GC samples was significantly related to tumor invasion depth, TNM stage and lymph node metastasis and was associated with disease-free survival (DFS) and overall survival (OS) in GC patients.	Yes	In vivo and in vitro assays indicated that SNHG12 promotes GC metastasis and epithelial-mesenchymal transition (EMT). Bioinformatics and mechanistic analyses revealed that SNHG12 can directly target miR-218-5p to regulate YWHAZ mRNA, forming an SNHG12/miR-218-5p/YWHAZ axis and decreasing the ubiquitination of β-catenin. 	33994849
SNHG12	LncRNA	Homo sapiens	Stomach Neoplasms	 GC cells and tissues	Regulation(YWHAZ /AKT/GSK-3β Pathway)	In Vivo Experiment//Western Blot//ISH//CCK8//qRT-PCR//RIP//FISH//PCR//IHC	" SNHG12 was highly expressed in GC cells and tissues, and predicted poor survival.  Bioinformatics analysis predicted that YWHAZ was the common target of SNHG12 and HuR, and that the ""SNHG12-HuR"" complex enhanced the stability of YWHAZ mRNA. Furthermore, YWHAZ, which was highly expressed in GC, predicted poor survival and promoted GC proliferation by phosphorylating AKT. Rescue assays verified that SNHG12 promoted GC proliferation by activating the AKT/GSK-3β pathway."		Yes	In vitro and in vivo assays showed that SNHG12 knockdown inhibited GC proliferation, while SNHG12 overexpression promoted GC proliferation. 	34195070
SNHG12	LncRNA	Homo sapiens	Breast Neoplasms	BC tumors	interaction[SALL4,miR-15a-5p]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	SNHG12 and SALL4 expressions were upregulated whereas miR-15a-5p was downregulated in BC tumors compared with normal tissues.  SNHG12 promotes cell proliferation, migration, and invasion but suppresses apoptosis in BC by upregulating SALL4 expression via sponging miR-15a-5p, representing potential targets for the development of novel diagnosis and treatment methods.		Yes	 More importantly, SNHG12 knockdown attenuated BC tumor growth in vitro and in vivo. 	32386479
SNHG12	LncRNA	Homo sapiens	Breast Neoplasms	BC tissues and cells	regulation[AKT/mTOR pathway]	Western Blot//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 In this study, we found that SNHG12 was significantly increased in BC tissues and cells. Knockdown of SNHG12 inhibited cell proliferation, invasion, and migration by regulating miR-451a through suppression of AKT/mTOR pathway in BC.		Yes	Knockdown of SNHG12 inhibited BC cell proliferation, invasion, and migration in vitro as well as suppressed tumor growth in vivo.	32269676
SNHG12	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	 NSCLC tumor tissues and NSCLC cell lines	Interaction(miR-101-3p/CUL4B axis )	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	Our data indicated that SNHG12 targeted and negatively regulated miR-101-3p, and this depletion reversed the inhibitory effect of si-SNHG12 on NSCLC cells. Furthermore, CUL4B was confirmed as a functional target of miR-101-3p, and its knockdown resulted in a strong alleviation of the NSLCL cell phenotype, which was enhanced by the silencing of miR-101-3p.  Mechanistically, we found that SNHG12 regulated miR-101-3p to modulate the PI3K/AKT pathway mediated by CUL4B.		Yes	This study clarified that SNHG12 knockdown significantly reduced proliferation, migration, invasion and EMT of NSCLC cells.	34002487
RP11-20B24.6	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//RNA-seq//FISH	By RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). 		Yes	 PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression.	33219721
hsa_circTPT1_003	CircRNA	Homo sapiens	bladder carcinoma	bladder cancer tissues	Interaction(has_circTPT1_003-has-miR-218-5p-CCNE2/SMC4 Signaling Axis )	qRT-PCR//Microarray	Further excavation analysis showed that seven differentially overexpressed circRNAs including hsa_circ_0000133, hsa_circ_0023610, hsa_circ_0005615, hsa_circ_0030162, hsa_circ_0077007, hsa_circ_0001140, and hsa_circ_0107031 were associated with bladder cancer invasiveness, and the cell cycle signal axis. has_circTPT1_003-has-miR-218-5p-CCNE2/SMC4 was finally clarified as a possible mechanism for bladder cancer progression. Based on results derived from multiple approaches, we identified that has_circTPT1_003-has-miR-218-5p-CCNE2/SMC4 signal axis may be involved in the invasion process of bladder cancer.		Yes	has_circTPT1_003-has-miR-218-5p-CCNE2/SMC4 was finally clarified as a possible mechanism for bladder cancer progression.	35005988
SNHG3	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 GEO (cervical cancer and adjacent normal tissues)	Expression [highly expressed]	Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	SNHG3 was over-expressed in cervical cancer tissues and SiHa cells.		Yes	 In SiHa cells, knocking down SNHG3 significantly inhibited the proliferation (P < 0.001), migration (P < 0.01) and invasion abilities (P < 0.001) of the cells, down-regulated the expression levels of N-cadherin, Snail and vimentin (P < 0.001) and up-regulated the expression of E-cadherin (P < 0.001).	34238747
PCGEM1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	cell lines	regulation[sponging miR-433-3p to upregulate WTAP]	RNA Pull-Down//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//EdU Staining//Transwell Assay	PCGEM1 was highly expressed in NSCLC cells, while miR-433-3p was lowly expressed in NSCLC cells. PCGEM1 accelerates NSCLC progression via sponging miR-433-3p to upregulate WTAP.		Yes	 PCGEM1 silencing or miR-433-3p overexpression inhibited cell proliferation, migration and invasion but accelerated cell apoptosis. 	32787827
PCNA-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC cell and tissues	Interaction(miR-2467-3p/PCNA axis)	Western Blot//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Invasion Assay	As a result, PCNA-AS1 was highly expressed in ESCC and was associated with patient prognosis. PCNA-AS1 and PCNA were positively correlated in ESCC. Bioinformatics analysis, RIP and luciferase reporter gene assays revealed that PCNA-AS1 could act as a competitive endogenous RNA to sponge miR-2467-3p, thus upregulating PCNA. 	As a result, PCNA-AS1 was highly expressed in ESCC and was associated with patient prognosis.	Yes	 PCNA-AS1 overexpression strongly contributed to ESCC cell proliferation, invasion and migration. 	36213440
PCNA-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	regulation[Upregulating CCND1]	CCK8//qRT-PCR//Cell Cycle Assay//Western Blot	Our results showed that PCNA-AS1 was upregulated in NSCLC tissues and cell lines, and correlated with TNM stages. Moreover, depletion of CCND1 abrogated the oncogenic roles of PCNA-AS1 in NSCLC. In conclusion, highly expressed PCNA-AS1 promotes NSCLC cell proliferation and oncogenic activity via upregulating CCND1.	Our results showed that PCNA-AS1 was upregulated in NSCLC tissues and cell lines, and correlated with TNM stages.	Yes	Functional experiments showed that overexpression of PCNA-AS1 promoted NSCLC cell proliferation and cell cycle progression. Depletion of PCNA-AS1 inhibited NSCLC cell proliferation and cell cycle progression, and also inhibited NSCLC tumor growth in vivo.	32194807
PCLN16	LncRNA	Homo sapiens	Prostatic Neoplasms	prostate cancer tissues	Expression[highly expressed]	qRT-PCR//Migration Assay	The AR-regulated PCLN16 was abundantly overexpressed in localized or metastatic prostate cancer tissues and AR-dependent cell lines.		Yes	PCLN16 silence suppressed AR signaling and tumor growth.	33387886
hsa_circ_0001742	CircRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues	Regulation[ miR-634/RAB1A pathway]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 In the present study, results reported that the expression of hsa_circ_0001742 was obviously increased and correlated with TSCC patients with advanced clinical stage, lymph-node metastasis.Thus, our study showed that hsa_circ_0001742 could promote TSCC progression by targeting miR-634/RAB1A pathway.	 In the present study, results reported that the expression of hsa_circ_0001742 was obviously increased and correlated with TSCC patients with advanced clinical stage, lymph-node metastasis.	Yes	 In vitro function assays revealed that hsa_circ_0001742 inhibition decreased the proliferation, invasion, and epithelial-mesenchymal transition (EMT) processes of TSCC cells.	30944081
PCGEM1	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues,cell lines	Interaction[regulating SNAI1]	qRT-PCR//Western Blot//Transwell Assay	 LncRNA PCGEM1 was overexpressed in GC cells and tissues, and was induced by hypoxia in GC cells.Our findings indicated that PCGEM1 is a hypoxia-responsive lncRNA, and contributes to the invasion and metastasis of GC. The potential mechanism is attributed to the regulation of EMT by PCGEM1 and its influence on the expression of SNAI1.		Yes	Additional experiments confirmed that the knockdown of PCGEM1 significantly repressed the invasion and metastasis of GC cells.	30690667
PCGEM1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	regulation[PCGEM1/miR-129-5p/P4HA2 axis]	ISH//qRT-PCR//Luciferase Report Assay//Western Blot	 GC cells expressed high levels of cytoplasmic PCGEM1.The PCGEM1/miR-129-5p/P4HA2 axis was confirmed to possess a crucial role in GC metastasis and invasion, suggesting its utility as a potential diagnostic and therapeutic biomarker.		Yes	 Loss-of-function experiments displayed that the silencing of PCGEM1 suppressed metastatic and invasive cell qualities.	32622013
PCGEM1	LncRNA	Homo sapiens	Stomach Neoplasms	 HGC exosomes	Regulation(SNAI1)	Western Blot//Wound Healing Assay//qRT-PCR//Invasion Assay//Transwell Assay	 Long non-coding RNA (lncRNA) prostate cancer gene expression marker 1 (PCGEM1) was specifically expressed in HGC exosomes. On the mechanism, PCGEM1 maintained stability and reduced the degradation of SNAI1, which could induce the epithelial-mesenchymal transition of GC.		Yes	. HGC-derived PCGEM1-riched exosomes could promote the invasion and migration of NGC.	32519176
PCGEM1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells 	Interaction(miR-152-3p)	qRT-PCR//Luciferase Report Assay	 Increased expression of PCGEM1 was observed in NSCLC tissues and cells compared with the corresponding controls (all P < 0.001). The further luciferase reporter assay and expression results showed that miR-152-3p might be a target gene of PCGEM1 and mediate the effects of PCGEM1 on cell proliferation, migration and invasion in NSCLC.	PCGEM1 expression was associated with NSCLC patients' lymph node metastasis and TNM stage (all P < 0.05), and the knockdown of PCGEM1 in NSCLC cells led to inhibited cell proliferation, migration and invasion. 	Yes	PCGEM1 expression was associated with NSCLC patients' lymph node metastasis and TNM stage (all P < 0.05), and the knockdown of PCGEM1 in NSCLC cells led to inhibited cell proliferation, migration and invasion. 	34455968
PCNAP1	LncRNA	Homo sapiens	Liver Neoplasms	 liver tissues	Regulation[miR-154/PCNA/HBV cccDNA signaling and the PCNAP1/PCNA signaling]	Southern Blot//Western Blot//qRT-PCR//RNA-seq//Luciferase Report Assay//Microarray//ChIP	Additionally, our data revealed that the levels of PCNAP1 were significantly elevated in 39 HBV-related HCC patients relative to those in their adjacent non-tumorous liver tissues (Figure ​(Figure1B),1B), supporting that PCNAP1 may be positively related to HBV-related HCC.		Yes	Functionally, PCNAP1 or PCNA remarkably enhanced HBV replication and accelerated the growth of HCC in vitro and in vivo. 	31410212
PCGEM1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC cells and tumors	Interaction(PCGEM1/miR-433-3p/CTCF axis)	RNA Pull-Down//Tunel//CCK8//qRT-PCR//RIP//Luciferase Report Assay	 PCGEM1 possessed a high expression level in CRC cells as well as tumors. CTCF transcriptionally activated PCGEM1 expression. Moreover, PCGEM1 bound miR-433-3p to prevent miR-433-3p from targeting CTCF. We first revealed PCGEM1/miR-433-3p/CTCF positive feedback loop as an oncogenic axis in CRC cells, which potentially provides new clues for the advancement of CRC treatment.		Yes	 Knockdown of PCGEM1 or CTCF impeded proliferation and migration and drove apoptosis of CRC cells.	35872368
PCGEM1	LncRNA	Homo sapiens	Colorectal Neoplasms	colorectal cancer cells and tissues	Interaction(miR-129-5p/SOX4)	qRT-PCR//Western Blot	We found that PCGEM1 is overexpressed in colorectal cancer cells and tissues, while miR-129-5p is underexpressed. SOX4 is overexpressed in colorectal cancer cells and tissues. Functionally, PCGEM1 silencing can significantly inhibit the proliferation, invasion, and migration of colorectal cancer cells. Mechanically, PCGEM1 acted as a sponge for miR-129-5p and absorbed its expression, and miR-129-5p was found to target SOX4, constructing the axis of PCGEM1/miR-129-5p/SOX4 in colorectal cancer. In conclusion, PCGEM1 mediates the proliferation, invasion, and migration of colorectal cancer cells by targeting miR-129-5p/SOX4 axis.		Yes	PCGEM1 silencing can significantly inhibit the proliferation, invasion, and migration of colorectal cancer cells.	36193492
PCGEM1	LncRNA	Homo sapiens	Endometrial Neoplasms	EC tissues	Expression[highly expressed]	qRT-PCR	We found that PCGEM1 expression was significantly higher in EC tissues than in normal endometrial tissues via quantitative reverse transcription (qRT)-PCR. 		Yes	The upregulation of PCGEM1 promoted the proliferation, migration, and invasive ability of EC cells while inhibiting apoptosis. The silencing of PCGEM1 had the opposite effects. Nude mouse xenograft assay showed that PCGEM1 overexpression could promote tumor growth in vivo.	30257404
PCGEM1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Regulation[miR-182/FBXW11 axis]	qRT-PCR//Luciferase Report Assay//RNA Pull-Down//RIP	Our present study showed that PCGEM1 was significantly upregulated in CC tissues and cell lines.  In conclusion, our findings demonstrated that PCGEM1-miR-182-FBXW11 axis play an important role in CC progression, and indicated a promising therapeutic target for CC patients.	Overexpression of PCGEM1 was correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node, distant metastasis and poor prognosis in CC patients. 	Yes	Functionally, PCGEM1 promoted cell proliferation, cell cycle progression, migration and invasion, while suppressed cell apoptosis in CC cells.	31832017
PCGEM1	LncRNA	Homo sapiens	Glioma	glioma tissues and tumor cell lines	Interaction(miR-539-5p/CDK6 axis)	In Vivo Experiment//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//Transwell Assay	 LncRNA PCGEM1 was upregulated in glioma tissues and tumor cell lines. PCGEM1 played as a competing endogenous RNA (ceRNA) for miR-539-5p to promote CDK6 expression. MiR-539-5p mimics repressed glioma progression while CDK6 overexpression reversed the roles of PCGEM1 knockdown.	PCGEM1 upregulation predicted unsatisfactory prognosis. 	Yes	PCGEM1 knockdown inhibited proliferation, colony formation, migration and invasion.  PCGEM1 knockdown delayed tumor growth in vivo. 	33589577
PCGEM1	LncRNA	Homo sapiens	Prostatic Neoplasms	PCa tissues and cells	Interaction(miR-129-5p/CDT1)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay	Both PCGEM1 and CDT1 were upregulated in PCa, while miR-129-5p was downregulated and negatively correlated with PCGEM1 and CDT1.  PCGEM1 plays a crucial role in the progression of PCa by sponging miR-129-5p as a ceRNA of CDT1. 		Yes	Downregulation of PCGEM1 or CDT1 inhibited the viability, promoted apoptosis and cycle arrest of PCa cells in vitro, and controlled tumor growth in vivo.	35412947
PCGEM1	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissues and cells	Interaction(miR-506/TRIAP1)	RNA Pull-Down//Western Blot//qRT-PCR//RIP//Cell Proliferation Assay//Transwell Assay	PCGEM1 expression was increased in PCa tissues and cells. In PCa tissues, High PCGEM1 expression was associated with high Gleason score, distant metastasis and extracapsular extension. miR-506-3p may interact with PCGEM1 or TRIAP1, and the suppressive effect of PCGEM1 knockdown was reversed when TRIAP1 or a miR-506-3p inhibitor was cotransfected.		Yes	 In addition, PCGEM1 knockdown inhibited PCa cell (C4-2B and PC-3) proliferation, invasion and migration. 	35109849
PCGEM1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	renal carcinoma cells	interaction[miR-433-3p,FGF2 ]	qRT-PCR//Luciferase Report Assay//RIP//FISH	 In this study, PCGEM1 was observed to be lifted in renal carcinoma cells.MiR-433-3p inhibitor could reverse the cell growth and migration caused by PCGEM1 downregulation.		Yes	Loss-of-function experiments displayed that silencing of PCGEM1 repressed cell proliferation and migration, and activated apoptosis in renal carcinoma.	31958075
PCNAP1	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	regulation[miR-340-5p,SOX4]	Western Blot//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Transwell Assay	 lncRNA PCNAP1 was found to be upregulated in human breast cancer tissues, and high lncRNA PCNAP1 levels predicted poor overall survival.Overall, we found that lncRNA PCNAP1 predicted a poor prognosis in breast cancer and promoted cancer metastasis via miR‑340‑5p‑dependent upregulation of SOX4 expression.	 lncRNA PCNAP1 was found to be upregulated in human breast cancer tissues, and high lncRNA PCNAP1 levels predicted poor overall survival.	Yes	Function assays showed that knockdown of lncRNA PCNAP1 suppressed the migration and invasion of breast cancer cells in vitro and in vivo.	32945462
hsa_circ_0001742	CircRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cells	Regulation[miR-431-5p/ATF3 axis]	RNA Pull-Down//Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	The expression of circ_0001742 was upregulated in TSCC tissues and cells.Our results demonstrated that circ_0001742 plays a tumor-promoting effect in TSCC cells by serving as a competing endogenous RNA (ceRNA) to regulate miR-431-5p/ATF3 axis, which might provide a potential therapeutic target for TSCC.		Yes	Knockdown of circ_0001742 inhibited proliferation, migration, invasion and EMT and induced apoptosis in TSCC cells. 	31841185
PELATON	LncRNA	Homo sapiens	Crohn Disease	CD patient and cell line	Interaction(miR-153-5p)	In Vivo Experiment//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//H&E Staining//Transwell Assay//IF	 LINC01272 was highly expressed in patients with CD. Knockdown of LINC01272 inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT). Additionally, LINC01272 regulated TGF-β1-induced EMT through the miR-153-5p axis, and knockdown of LINC01272 inhibited EMT in CD mice in vivo.		Yes	Knockdown of LINC01272 inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT). Additionally, LINC01272 regulated TGF-β1-induced EMT through the miR-153-5p axis, and knockdown of LINC01272 inhibited EMT in CD mice in vivo.	35559411
PGM5-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	Interaction(miR-484)	CCK8//qRT-PCR	pgm5-as1 was upregulated in CRC tissues and cell lines; however, its downregulation contributed to the decreasing of cell viability, growth, migration, and invasion of SW480 and HCT116 cells. Moreover, miR-484 was predicted as the target of pgm5-as1, and the downregulation of pgm5-as1 partially restored the elevated cell viability, growth, migration, and invasion that were induced by the inhibition of miR-484 expression in SW480 and HCT116 cells. 		Yes	pgm5-as1 was upregulated in CRC tissues and cell lines; however, its downregulation contributed to the decreasing of cell viability, growth, migration, and invasion of SW480 and HCT116 cells.	32354224
PGM5-AS1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cells	Regulation(miR-587/SLIT3 Axis)	qRT-PCR//Western Blot	PGM5-AS1 and SLIT3 were expressed at low levels in BC, whereas miR-587 exhibited the opposite trend. PGM5-AS1 overexpression significantly inhibited BC cell proliferation and migration, promoted apoptosis in vitro, and alleviated tumor growth in vivo. miR-587 has been shown to be a target of PGM5-AS1, and miR-587 overexpression can reverse the inhibitory effect of PGM5-AS1 upregulation on BC cell growth. Furthermore, miR-587 directly targeted SLIT3 and negatively regulated its expression. PGM5-AS1 inhibited BC cell proliferation and migration while facilitating apoptosis through the miR-587/SLIT3 pathway. PGM5-AS1 represses BC development via the miR-587/SLIT3 axis, indicating that PGM5-AS1 may be a candidate biomarker and target for BC treatment.		Yes	 PGM5-AS1 overexpression significantly inhibited BC cell proliferation and migration, promoted apoptosis in vitro, and alleviated tumor growth in vivo.	36017912
PGM5-AS1	LncRNA	Homo sapiens	Osteosarcoma	osteosarcoma tissues	regulation[miR-140-5p-mediated FBN1]	qRT-PCR//RNA Pull-Down//Luciferase Report Assay//RIP	 Expression of PGM5-AS1, miR-140-5p, and FBN1 was altered by overexpression, shRNA, mimic, or inhibitors in order to investigate how they regulated migration, invasion, and EMT of osteosarcoma cells in vitro. Taken together, PGM5-AS1 depletion causes FBN1 reduction to retard osteosarcoma processes by negatively modulating miR-140-5p.		Yes	Loss- and gain-of-function approaches were employed in nude mice to detect their roles in tumorigenesis in vivo. 	32412676
PGM5-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cells	Interaction(miR-4284/DCN)	RNA Pull-Down//Western Blot//Bioinformatics Analysis//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//EdU Staining//Transwell Assay	Using real-time quantitative polymerase chain reaction or western blotting, PGM5-AS1 and decorin (DCN) were downregulated in CC tissues and cells, whereas miR-4284 was upregulated.Luciferase assay, RNA pull-down assay, and western blotting showed that PGM5-AS1 could sponge miR-4284 to upregulate DCN expression in CC cells. In summary, this study identified that PGM5-AS1 negatively regulates CC cell malignancy by targeting miR-4284/DCN.		Yes	Additionally, cell functional experiments showed that PGM5-AS1 overexpression led to decreased proliferation, migration, and invasion of CC cells. However, the inhibitory effect of PGM5-AS1 overexpression on CC cells was partly relieved by DCN knockdown because of the targeting interaction between PGM5-AS1, miR-4284, and DCN.	35420507
PFL	LncRNA	Mus musculus	Cardiac Fibrosis	 hearts of mice	Interaction [let-7d/Ptafr]	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//EdU Staining//IF	Using a combination of in vitro and in vivo studies, we identified a lncRNA NONMMUT022555, which is designated as a pro-fibrotic lncRNA (PFL), and revealed that PFL is up-regulated in the hearts of mice in response to myocardial infarction (MI) as well as in the fibrotic cardiac fibroblasts (CFs).  More importantly, PFL acted as a competitive endogenous RNA (ceRNA) of let-7d, as forced expression of PFL reduced the expression and activity of let-7d. Moreover, let-7d levels were decreased in the MI mice and in fibrotic CFs. Inhibition of let-7d resulted in fibrogenesis in CFs, whereas forced expression of let-7d abated fibrogenesis through targeting platelet-activating factor receptor (Ptafr). Furthermore, overexpression of let-7d by adenoviruses carrying let-7d precursor impeded cardiac fibrosis and improved cardiac function in MI mice.		Yes	We found that knockdown of PFL by adenoviruses carrying shRNA attenuated cardiac interstitial fibrosis and improved ejection fraction (EF) and fractional shortening (FS) in MI mice. Further study showed that forced expression of PFL promoted proliferation, fibroblast-myofibroblast transition and fibrogenesis in mice CFs by regulating let-7d, whereas silencing PFL mitigated TGF-β1-induced myofibroblast generation and fibrogenesis. 	29464008
PELATON	LncRNA	Homo sapiens	Stomach Neoplasms	GC cell lines, GC tissues	Expression[highly expressed]	qRT-PCR//Wound Healing Assay//Transwell Assay	We found that LINC01272 was upregulated in GC and was associated with GC staging and lymph node metastasis. 	We found that LINC01272 was upregulated in GC and was associated with GC staging and lymph node metastasis. 	Yes	 The results of wound-healing and Transwell assays revealed that the LINC01272 was closely related to GC cell migration and invasion.LINC01272 knockdown inhibited the migration and invasion ability of GC cells by reducing the expression of EMT-related proteins. Overexpression of LINC01272 had the opposite effect.	32368096
PELATON	LncRNA	Homo sapiens	Lung Neoplasms	LUAD tissues	Interaction(MiR-7-5p/CRLS1 Axis)	Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay	 LINC01272 was downregulated in LC and low LINC01272 expression had poor prognosis.  LINC01272 negatively regulated miR-7-5p and CRLS1 was a target of miR-7-5p. LINC01272 suppressed cell multiplication and induced apoptosis via regulating the miR-7-5p/CRLS1 axis in LC.		Yes	 In A549 and PC-9 cells, LINC01272 inhibited cell viability and multiplication and induced apoptosis.	34099597
PELATON	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues	Interaction(miR-876/ITGB2 axis )	qRT-PCR//Luciferase Report Assay	 qRT-PCR revealed that LINC01272 was highly expressed and negatively associated with miR-876 in CRC. Moreover, LINC01272 potentially targeted miR-876, and miR-876 potentially targeted ITGB2. 	We found that LINC01272 was highly expressed in multiple cancers and closely related to core epithelial-mesenchymal transition (EMT) factors and that high levels of LINC01272 are associated with a poor prognosis in CRC patients.	Yes	 Additionally, LINC01272 or ITGB2 silencing reduced, while miR-876 overexpression promoted, the invasiveness and metastatic capacity of CRC cells in vitro.	34093798
PELATON	LncRNA	Homo sapiens	glioblastoma	GBM cells	Interaction(p53 )	Western Blot//Transfection//Wound Healing Assay//Co-IP//qRT-PCR//RIP//FISH//Transwell Assay	PELATON can inhibit the expression of p53 in p53 wild-type GBM cells and regulate the expression of BACH1 and CD44, but it has no effect on p53, BACH1 and CD44 in p53 mutant GBM cells. PELATON and p53 can form a complex through the RNA binding protein EIF4A3.		Yes	Knockdown of PELATON resulted in smaller mitochondria, increased mitochondrial membrane density, and enhanced sensitivity to ferroptosis inducers to inhibit GBM cell proliferation and invasion. 	35574340
PCTST	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues	Regulation[TACC-3]	qRT-PCR	Briefly, our data demonstrated that lnc-PCTST expression is down-regulated in PC tissues.In conclusion, lnc-PCTST is a potential tumor suppressor in PC, which inhibits cell proliferation, invasion, tumorigenesis and EMT by modulating TACC-3.		Yes	Furthermore, lnc-PCTST overexpression in PC cell lines inhibited cell proliferation and invasion in vitro, and tumorigenesis in vivo (using nude mice as animal model), but did not altered cell migration. 	29978472
PEG10	LncRNA	Homo sapiens	Glioma		Interaction[JAK1/STAT3 signal pathway]	CCK8//qRT-PCR//Western Blot//Transwell Assay	Meanwhile, PEG10 silence upregulated the expression of p16 and p53, Bax, cleaved-Caspase-3/9 expression, and downregulated Bcl-2 expression. PEG10 silence upregulated miR-506 expression. Co-transfection with sh-PEG10 and miR-506 inhibitor impaired the tumor suppressive effects. PEG10 knockdown decreased the phosphorylation of Raf/MEK/ERK and JAK1/STAT3-related proteins Raf, MEK, ERK, JAK1 and STAT3. PEG10 knockdown inhibited cell viability, migration and invasion, induced cell apoptosis through miR-506 upregulation, as well as inactivation of Raf/MEK/ERK and JAK1/STAT3 signal pathways.		Yes	Transfection with sh-PEG10 inhibited cell viability, migration and invasion, and increased cell apoptosis. 	31241046
PEG10	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues and cells	interaction[sponging miR-101-3p]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	 PEG10 and KIF2A level were significantly upregulated, while miR-101-3p was downregulated in DLBCL tissues and cells. Besides, miR-101-3p was a target of PEG10 and miR-101-3p could directly target KIF2A. PEG10 promoted KIF2A level by sponging miR-101-3p. 		Yes	PEG10, or KIF2A deletion significantly inhibited the proliferative, migratory, and invasive abilities of DLBCL cells and elevated cell apoptosis in DLBCL cells.	32976381
PDS5B-DT	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell line	Interaction(miR-206)	qRT-PCR	Our results showed that Linc1749808 was highly expressed in both HCC tissues and cell lines. Furthermore, Linc1749808 was found to act as a sponge of miR-206. Inhibition of miR-206 counteracted the effect of Linc1749808 knockdown in 97H cells by regulating YAP1 and epithelial-mesenchymal transition (EMT).		Yes	 Linc1749808 expression was significantly correlated with microvascular invasion, metastasis, and prognosis. After the knockdown of Linc1749808, the metastatic potential of 97H and HepG2 cells was attenuated in vitro and in vivo, but the proliferative capacity did not significantly change. 	34196215
PD-L1-lnc	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD tissues	Interaction(c-Myc )	In Vivo Experiment//Western Blot//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//Cell Apoptosis Assay//cell invasion assay	Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ.   Mechanistically, PD-L1-lnc promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity.		Yes	Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells.	33849634
PDIA3P1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and the adjacent normal tissues	Regulation[Wnt/β-catenin signaling ]	CCK8//qRT-PCR//Invasion Assay//Western Blot	In the present study, PDIA3P expression in NSCLC tissues was examined. RT-qPCR analysis showed that PDIA3P expression was significantly higher in NSCLC tissues (Fig. 1A; P<0.05) compared with the control. The present study showed that lncRNA PDIA3P promoted NSCLC progression by regulating Wnt/β-catenin signaling, highlighting a potential therapeutic target for treating patients with NSCLC treatment.	 In the present study, it was demonstrated that lncRNA PDIAP3 expression was significantly increased in patients with NSCLC, particularly in patients with an advanced Tumor-Node-Metastasis stages and lymph-node metastasis. The Gene Expression Profiling Interactive Analysis database revealed that patients with NSCLC with high lncRNA PDIA3P expression had a poorer disease-free survival rate.	Yes	Furthermore, functional assays suggested that PDIA3P inhibition significantly suppressed the proliferation and invasion of NSCLC cells in vitro and reduced tumor growth in vivo. 	31572559
PDE3B	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	Interaction(miR-136-5p/MAP3K2 axis)	Western Blot//Flow Cytometry//qRT-PCR//MTT//PCR//Transwell Assay	 The results showed that circ_PDE3B was highly expressed in ESCC tissues and cells.Circ_PDE3B served as a sponge for miR-136-5p, and miR-136-5p inhibition reversed the roles of circ_PDE3B knockdown in ESCC cells. MAP3K2 was a direct target of miR-136-5p, and miR-136-5p targeted MAP3K2 to inhibit the malignant behaviors of ESCC cells. Furthermore, circ_PDE3B regulated MAP3K2 expression by sponging miR-136-5p. 		Yes	Downregulated circ_PDE3B expression in ESCC cells significantly reduced cell proliferation, migration and invasion. Importantly, circ_PDE3B knockdown inhibited tumor growth in vivo.	36533720
PDCD4-AS1	LncRNA	Homo sapiens	Breast Neoplasms	TNBC tissues and cells	regulation[increasing expression of IQGAP2 via miR-10b-5p]	Wound Healing Assay//Tunel//qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	 In this work, PDCD4-AS1 and IQGAP2 were lowly expressed while miR-10b-5p was strongly expressed in TNBC tissues and cells.Our findings identified lncRNA PDCD4-AS1 as a tumor suppressor in TNBC by regulating IQGAP2 expression via miR-10b-5p, giving a novel insight into the regulatory mechanism of PDCD4-AS1 in the pathogenesis of TNBC.		Yes	PDCD4-AS1 or IQGAP2 overexpression effectively attenuated TNBC cell proliferation, migration and invasion, and increased the apoptosis rate, while this effect was abandoned in response to miR-10b-5p mimics transfection.	33248413
PDCD4-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	42 fresh tissue samples of TNBC and adjacent normal tissues 	Interaction(IQGAP2 via miR-10b-5p)	Western Blot//Transfection//Wound Healing Assay//Tunel//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	In this work, PDCD4-AS1 and IQGAP2 were lowly expressed while miR-10b-5p was strongly expressed in TNBC tissues and cells. miR-10b-5p bound to IQGAP2 and acted as a downstream target of PDCD4-AS1.		Yes	PDCD4-AS1 or IQGAP2 overexpression effectively attenuated TNBC cell proliferation, migration and invasion, and increased the apoptosis rate, while this effect was abandoned in response to miR-10b-5p mimics transfection. 	33248413
PCGEM1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cell lines	regulation[miR-642a-5p/LGMN axis]	qRT-PCR//Luciferase Report Assay	In the present study, PCGEM1 was over-expressed in cervical carcinoma cells as evidenced by real-time quantitative polymerase chain reaction (RT-qPCR) assay.  Taken together, our data indicated that knockdown of PCGEM1 inhibited proliferation, migration and invasion in cervical carcinoma by modulating the miR-642a-5p/ LGMN axis.		Yes	Knockdown of PCGEM1 significantly repressed proliferation, migration, and invasion, while induced G1 arrest in cervical carcinoma cells. 	33121976
PCED1B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissue samples and cell line	Interaction(miR-10a/BCL6 Axis)	CCK8//qRT-PCR	PCED1B-AS1 is upregulated in HCC, and its upregulation correlates with poor survival. Across HCC tissues, PCED1B-AS1 expression inversely correlates with miR-10a but positively correlates with BCL6. In HCC cells, overexpression of PCED1B-AS1 decreases miR-10a expression and increases BCL6 expression. Moreover, PCED1B-AS1 overexpression reduces the inhibitory effects of miR-10a overexpression on BCL6 expression and cell proliferation. PCED1B-AS1 is upregulated in HCC and regulates the miR-10a/BCL6 axis to promote cell proliferation.	PCED1B-AS1 is upregulated in HCC, and its upregulation correlates with poor survival. 	Yes	Moreover, PCED1B-AS1 overexpression reduces the inhibitory effects of miR-10a overexpression on BCL6 expression and cell proliferation. PCED1B-AS1 is upregulated in HCC and regulates the miR-10a/BCL6 axis to promote cell proliferation.	35997114
PGM5-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissue	Expression[lower expressed]	Western Blot//Colony Formation Assay//CCK8//qRT-PCR//RNA-seq//IHC	Then, we showed that the expression levels of PGM5-AS1, B3GALT5-AS1 and PGM5 were significantly downregulated in CRC tissues compared with corresponding normal tissues.		Yes	Functionally, overexpression of PGM5-AS1 could induce cell apoptosis and cell cycle arrest in CRC. Animal study indicated that PGM5-AS1 overexpression inhibited CRC growth in vivo.	31619123
PCAT6	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues 	Interaction(miR-143-3p)	qRT-PCR//Western Blot	PCAT6 expression was significantly increased in OC tissues and positively correlated with advanced stages and with poor overall survival, progression-free survival and post-progression survival.Notably, PCAT6 bound to miR-143-3p and affected the expression of transforming growth factor (TGF)-β-activated kinase 1 (TAK1). Subsequent rescue assays confirmed that upregulation of miR-143-3p decreased the PCAT6 overexpression-induced promotion of proliferation, migration and invasion. Moreover, downregulation of miR-143-3p reversed the PCAT6 knockdown-induced inhibition of proliferation, migration, and invasion.	PCAT6 expression was significantly increased in OC tissues and positively correlated with advanced stages and with poor overall survival, progression-free survival and post-progression survival.	Yes	Knockdown of PCAT6 in A2780 and SKOV3 cells inhibited OC cell proliferation, migration and invasion.  In contrast, Overexpression of PCAT6 exerted the opposite effects on OC cells. 	33634115
PCAT6	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells and tissues	regulation[RB/E2F and Wnt/β-catenin pathways]	qRT-PCR//Luciferase Report Assay	 PCAT6 was highly expressed in GC cells and tissues.Finally, PCAT6 was a target of miR-15a. Silencing of lncRNA PCAT6 restrained proliferation and EMT of GC cells by targeting miR-15a via RB/E2F and Wnt/β-catenin pathways.		Yes	 Silencing of PCAT6 restrained the relate-proteins of cell proliferation and EMT.	32039820
PCAT6	LncRNA	Homo sapiens	Breast Neoplasms	 breast cancer tissues and cell lines.	Interaction(miR-326/LRRC8E axis)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	Our findings revealed that PCAT6 was overexpressed in breast cancer tissues and cell lines.We also found that the transcription factor SP1 could bind to the PCAT6 promoter and promoted its expression. Subsequently, it was verified that PCAT6 was a molecular sponge for microRNA-326 (miR-326), and the leucine-rich repeat containing the eight family member E (LRRC8E) was a direct target of miR-326. Rescue assays revealed that LRRC8E overexpression attenuated the suppressive effect of PCAT6 knockdown on cellular progression of breast cancer. 	Furthermore, elevation of PCAT6 reflected an adverse prognosis of patients. 	Yes	Functional experiments indicated that PCAT6 knockdown hampered cell proliferation, facilitated apoptosis and cell cycle arrest in vitro, and inhibited tumor growth in vivo. 	34620745
PCAT6	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues,cell lines  	Expression[Expression[highly expressed]-expression]	CCK8//qRT-PCR//ELISA	We found that KDM5BAS1 was significantly overexpressed in tumor specimens and selected cancerous cell lines.	Meanwhile, higher KDM5BAS1 expression predicted poor overall survival. 	Yes	 Increased KDM5BAS1 expression can promote proliferation or migration and inhibit apoptosis in H1838 and H1299 cells. Furthermore, knocking Expression[down-expression] of KDM5BAS1 levels can also reduce tumor growth in in vivo implantation experiments.	31562647
PCAT6	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cells	Interaction(miR-326/KLF1 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ELISA//Transwell Assay	In addition, dual-luciferase reporter assay illustrated that miR-326 was the target of PCAT6 and KLF1 was the target of miR-326 in NSCLC cells. Moreover, NSCLC cells-derived exosomes could promote macrophages M2 polarization by transporting PCAT6. Meanwhile, macrophages M2 polarization was able to promote the metastasis and epithelial-mesenchymal transition (EMT) process of NSCLC cells via regulating PCAT6/miR-326/KLF1 axis. 		Yes	We found knockdown of PCAT6 significantly inhibited the viability, migration, and invasion of NSCLC cells.	35609331
PCAT6	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tumor tissues and cell lines	Expression(highly expressed)	CCK8//qRT-PCR//Western Blot	In the current study, we discovered that lncRNA PCAT6, which was aberrantly upregulated in ESCC tumor tissues, significantly promoted cell proliferation and migration in ESCC cell lines Eca-109 and Kyse-30 cells. Flow cytometry assays showed that PCAT6 knockdown promoted the apoptosis of ESCC cells. Furthermore, real-time PCR and western blot assays validated that knockdown of PCAT6 could increase the levels of GDF15 and DUSP4 in Eca-109 and Kyse-30 cells. 		Yes	In the current study, we discovered that lncRNA PCAT6, which was aberrantly upregulated in ESCC tumor tissues, significantly promoted cell proliferation and migration in ESCC cell lines Eca-109 and Kyse-30 cells. Flow cytometry assays showed that PCAT6 knockdown promoted the apoptosis of ESCC cells.  Mechanistically, RNA-seq and Gene Ontology analyses indicated that PCAT6 knockdown influenced the expression of genes that participated in cell proliferation and migration.	35069911
PCAT6	LncRNA	Homo sapiens	Carcinoma, Hepatocellular		Expression[highly expressed]	qRT-PCR//MTT//Migration Assay	The result revealed that the expression of PCAT6 was significantly higher in LIHC samples than adjacent samples 		Yes	 Knockdown of PCAT6 could inhibit cell proliferation and migration in hepatocellular carcinoma (LIHC) cells. 	30968586
PCAT6	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues 	Expression[highly expressed]	qRT-PCR	And we found that PCAT6 was significantly upregulated in HCC tissues and correlated with poor overall survival and disease-free survival in HCC patients.	And we found that PCAT6 was significantly upregulated in HCC tissues and correlated with poor overall survival and disease-free survival in HCC patients.	Yes	Furthermore, elevated PCAT6 promoted cell proliferation, inhibited cell cycle arrest and cell apoptosis while deficiency of PCAT6 impaired cell proliferation, caused cell cycle arrest and induced cell apoptosis of HCC.	32064636
PCAT6	LncRNA	Homo sapiens	Ovarian Neoplasms	ovarian cancer tissues	Interaction[PTEN]	CCK8//qRT-PCR//Wound Healing Assay	QRT-PCR results showed that the expression level of PCAT6 in ovarian cancer was higher than that in the adjacent normal tissues.QRT-PCR results demonstrated that the PTEN expression was increased after the knockdown of PCAT6. In addition, the recovery experiment also revealed that PCAT6 and PTEN have a mutual regulation, which can jointly regulate the development of ovarian cancer.	The incidence of distant metastasis and lymph node metastasis in patients with high expression of PCAT6 was higher than those with low PCAT6 expression.	Yes	The overexpression of GAS5 suppressed the protein level of COX-2, and inhibited cell proliferation of LPS-induced RWPE-1 cells and HPECs, which was rescued by the co-transfection with pcDNA-GAS5 and pcDNA-COX-2. 	31646553
PCAT6	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissue	Expression[highly expressed]	qRT-PCR	 We identified that the expression level of PCAT6 in BC tissue was higher than that in adjacent normal tissues.	In addition, the expression level of PCAT6 was correlated with tumor size (p = 0.005), differentiation (p = 0.018), TNM stage (p = 0.04), lymph nodes metastasis (p = 0.019), and distant metastasis (p = 0.028). Kaplan-Meier analysis showed that BC patients with high PCAT6 expression had shorter overall survival (OS) and progression-free survival (PFS). 	Yes	The loss-of-function results revealed that the proliferation and viability of BC cells in PCAT6 knockdown groups decreased significantly, compared with the negative control groups.	33142195
PCAT7	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell line	Interaction(miR-486-5p/CDK4 axis)	CCK8//qRT-PCR	GEPIA combined ENCORI database illustrated that LncRNA PCAT7 was upregulated dramatically in NSCLC. The mRNA level of PCAT7 cells was higher than that in normal cells. Data from ENCORI website showed that miR-486-5p was the target of PCAT7 and was negatively controlled by it. The data also showed that CDK4 could be bound and negatively regulated by miR-486-5p. MiR-486-5p inhibitor or CDK4 could partly restore the inhibitory effect of PCAT7 in NSCLC cells. In addition, silencing PCAT7 could arrest cell cycle to S in addition to G2 stage while transfecting miR-486-5p inhibitor or CDK4 could partially eliminate the retarding effects.		Yes	Silencing PCAT7 inhibited the progression of NSCLC cells significantly. 	35702078
PCAT6	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues and cell lines	interaction[targeting miR-513a-5p]	CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	PCAT6 expression was upregulated, while miR-513a was downregulated in BC tissues and cell lines.Our study illustrated that PCAT6 knockdown inhibited cell progression of BC by regulating miR-513a, suggesting that PCAT6 might act as a prognostic biomarker and therapeutic target for BC patients.	BC patients with high expression of PCAT6 exhibited a shorter overall survival time compared with those patients with low expression of PCAT6.	Yes	Moreover, PCAT6 knockdown notably suppressed cell progression. 	33090394
PCAT6	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction(microRNA-143-3p/PDIA6 axis)	qRT-PCR//Wound Healing Assay	The results demonstrated that the expression levels of PCAT6 were upregulated in bladder cancer tissues relative to those in adjacent normal bladder tissues. Collectively, the results of the present study demonstrated that PCAT6 may serve an oncogenic role in bladder cancer via the miR-143-3p/PDIA6 axis. 		Yes	Knockdown of PCAT6 served a role in suppressing the proliferation, migration and invasion of T24T and EJ bladder cancer cells. PCAT6 knockdown contributed to a reduction of PDIA6 expression at the mRNA and protein levels compared with that in negative control-transfected cells, whilst the miR-143-3p inhibitor partially mitigated this reduction effect. 	34335889
PCAT6	LncRNA	Homo sapiens	Osteosarcoma	OS tissues	Regulation[PCAT6-miR-185-5p-TGFBR1/2-TGF-β signaling axis  ]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that PCAT6 was elevated in OS tissues relative to that in their adjacent normal tissues.  This study uncovers a novel underlying molecular mechanism of PCAT6-miR-185-5p-TGFBR1/2-TGF-β signaling axis in promoting tumor progression in OS, which indicates that PCAT6 may serve as a promising prognostic factor and therapeutic target again OS.	The upregulation of PCAT6 was positively associated with metastasis status and advanced stages and predicted poor overall and progression-free survivals in patients with OS. 	Yes	Functionally, silencing PCAT6 inhibited the proliferation, migration and invasion abilities of OS cells. 	31676070
PCAT6	LncRNA	Homo sapiens	Osteosarcoma		regulation[MDM2 , P53 ,P21]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Transwell Assay	To conclude, lncRNA PCAT6 promoted the proliferation, migration and invasion of osteosarcoma cells by promoting the expression of MDM2 and suppressing the expression of P53 and P21.		Yes	The present study found that the proliferation, migration and invasion of osteosarcoma cells increased following overexpression of lncRNA PCAT6. 	33125146
PCAT6	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	PDAC tissues	regulation[miR-185-5p/CBX2 axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	 Our study confirmed that PCAT6 expression was upregulated in PDAC and the expression of PCAT6 was related to TNM stage, lymph node invasion and overall survival of PDAC patients.The results above suggested that PCAT6/miR-185-5p/CBX2 exerted crucial functions in tumorigenesis and progression of PDAC.	 Our study confirmed that PCAT6 expression was upregulated in PDAC and the expression of PCAT6 was related to TNM stage, lymph node invasion and overall survival of PDAC patients.	Yes	 Moreover, knockdown of PCAT6 inhibited cell proliferation, migration and invasion of PDAC in vitro.	32825947
PCAT6	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	Regulation[Wnt/β-catenin signaling pathway]	Western Blot//CCK8//qRT-PCR//EdU Staining//Transwell Assay	We found that PCAT6 expression was significantly up-regulated in human CC tissues and cell lines compared with their normal counterparts, and its high levels were associated with advanced FIGO stage, depth of cervical invasion and positively lymph node metastasis.Mechanistic investigation showed PCAT6 activates Wnt/β-catenin signaling in CC cell lines by promoting the expression of β-catenin, cyclin D1 and c-myc.	We found that PCAT6 expression was significantly up-regulated in human CC tissues and cell lines compared with their normal counterparts, and its high levels were associated with advanced FIGO stage, depth of cervical invasion and positively lymph node metastasis. Survival assays indicated that high PCAT6 expression had a negative influence on overall survival and disease-free survival. 	Yes	Functionally, knockdown of PCAT6 significantly suppressed CC cells proliferation, migration and invasion, and promoted apoptosis. 	30915737
PCAT6	LncRNA	Homo sapiens	Prostatic Neoplasms	 PCa tissue	Regulation(IGF2BP2/IGF1R RNA-protein three-dimensional complex)	In Vivo Experiment//ISH//qRT-PCR//Cell Proliferation Assay//IHC	PCAT6 was upregulated in PCa tissues with bone metastasis and increased PCAT6 expression predicted poor prognosis in PCa patients. Mechanistically, METTL3-mediated m6 A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated IGF1R expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex.  Importantly, PCAT6 inhibition by ASO in vivo showed therapeutic potential against bone metastasis in PCa. Finally, the clinical correlation of METTL3, IGF2BP2, IGF1R, and PCAT6 was further demonstrated in PCa tissues and cells.		Yes	Functional experiments found that PCAT6 knockdown significantly inhibited PCa cell invasion, migration, and proliferation in vitro, as well as bone metastasis and tumor growth in vivo.  Importantly, PCAT6 inhibition by ASO in vivo showed therapeutic potential against bone metastasis in PCa. Finally, the clinical correlation of METTL3, IGF2BP2, IGF1R, and PCAT6 was further demonstrated in PCa tissues and cells.	34185427
PCAT6	LncRNA	Homo sapiens	Liver Neoplasms	 liver cancer tissues 	Interaction(miR-326/hnRNPA2B1 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Bioinformatics Analysis//Transwell Assay	The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. A dual-luciferase reporter gene assay demonstrated that PCAT6 could bind to miR-326 and that hnRNPA2B1 was a direct target gene of miR-326. 	The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. 	Yes	Moreover, knockdown of PCAT6 significantly inhibited the proliferation and invasion of liver cancer cells in vitro and in vivo. 	33907581
PCAT6	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues	interaction[microRNA-30]	CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 PCAT6 was overexpressed in gastric cancer tissues than those of paracancerous tissues.PCAT6 is overexpressed in gastric cancer, which promotes the development of gastric cancer by endogenously competition with microRNA-30 via targeting MKRN3.	 PCAT6 expression was negatively correlated to prognosis, tumor size, TNM (tumor node metastasis) stage and metastasis of gastric cancer.	Yes	For in vitro experiments, overexpression of PCAT6 increased proliferation, migration, and invasion, whereas decreased apoptosis of gastric cancer cells. 	30178843
circMACF1	CircRNA	Homo sapiens	acute myocardial infarction	MI patients	Interaction(miR-500b-5p-EMP1 Axis)	qRT-PCR//Tunel//Western Blot	 In the MI group, the expression levels of circMACF1 and EMP1 were decreased with the increasing expression level of miR-500b-5p.CircMACF1 upregulated the expression of EMP1 as a sponge of miR-500b-5p, and circMACF1 was a direct target of miR-500b-5p. CircMACF1 impaired the progression of AMI by modulating the miR-500b-5p/EMP1 axis. 		Yes	CircMACF1 upregulated the expression of EMP1 as a sponge of miR-500b-5p, and circMACF1 was a direct target of miR-500b-5p. CircMACF1 impaired the progression of AMI by modulating the miR-500b-5p/EMP1 axis. 	32162171
PCED1B-AS1	LncRNA	Homo sapiens	colorectal adenocarcinoma	colorectal adenocarcinoma tissues and corresponding cell lines	Regulation(miR-633/HOXA9 axis)	Transfection	We found that PCED1B-AS1 was upregulated and miR-633 was downregulated in colorectal adenocarcinoma tissues and corresponding cell lines. Knockdown of PCED1B-AS1 inhibited cell proliferation and promoted apoptosis, while miR-633 inhibitor elevated proliferation and reduced apoptosis of cancer cell lines. In addition, overexpression of HOXA9 obviously attenuated the protective role of knockdown of PCED1B-AS1 or miR-633 mimics in colorectal adenocarcinoma progression. PCED1B-AS1 could negatively regulate the expression of HOXA9 by sponging miR-633. The in vivo experiments confirmed the role of PCED1B-AS1 and miR-633 in colorectal adenocarcinoma, as well as the regulatory relationship of this axis. Our results demonstrated that knockdown of PCED1B-AS1 inhibited the progression of colorectal adenocarcinoma by regulating the miR-633/HOXA9 axis.		Yes	Our results demonstrated that knockdown of PCED1B-AS1 inhibited the progression of colorectal adenocarcinoma by regulating the miR-633/HOXA9 axis.	35176937
PCBP2-OT1	LncRNA	Homo sapiens	Esophageal Neoplasms	esophageal malignancy tissues 	Regulation	CCK8//qRT-PCR//Western Blot	Fluorescence reckonable PCR exhibit that TUC338 was exceptionally communicated in esophageal cancer tissues, and was significantly related with metastasis and TNM stage in tolerant.		Yes	Functional experiments showed that in esophageal disease cell lines, knocking down the declaration of TUC338 significantly inhibited cell multiplication, clone development, and intrusion and movement. Further experiments on molecular mechanisms showed that knocking down TUC338 inhibited statement of N-cadherin and vimentin in cells.	34164197
PCED1B-AS1	LncRNA	Homo sapiens	Osteosarcoma	 tissues from OS patients and cell lines 	Interaction(miR-10a)	qRT-PCR//Transwell Assay	 PCED1B-AS1 level was increased in OS and positively correlated with miR-10a level. In OS cells, PCED1B-AS1 siRNA silencing downregulated miR-10a. Methylation-specific PCR analysis showed that PCED1B-AS1 siRNA silencing decreased the methylation of miR-10a gene promoter. Moreover, PCED1B-AS1 siRNA silencing suppressed OS cell proliferation, invasion, and migration. In addition, miR-10a overexpression attenuated the effects of PCED1B-AS1 siRNA silencing.		Yes	Moreover, PCED1B-AS1 siRNA silencing suppressed OS cell proliferation, invasion, and migration. 	36274134
PCED1B-AS1	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	 PDAC tumor tissues	Interaction(miR‑411‑3p/HIF‑1α axis)	CCK8//qRT-PCR//EdU Staining	We demonstrated that PCED1B‑AS1 was significantly upregulated in PDAC tumor tissues, and its expression was associated with advanced Tumor‑Node‑Metastasis stage and lymph node metastasis. Mechanistically, PCED1B‑AS1 was shown to target miR‑411‑3p, resulting in the upregulation of HIF‑1α.	We demonstrated that PCED1B‑AS1 was significantly upregulated in PDAC tumor tissues, and its expression was associated with advanced Tumor‑Node‑Metastasis stage and lymph node metastasis.	Yes	PCED1B‑AS1 knockdown inhibited PDAC cell proliferation, invasion as well as epithelial‑mesenchymal transition (EMT) in vitro. 	34036383
PCED1B-AS1	LncRNA	Homo sapiens	Glioma		Regulation[miR-194-5p/PCED1B axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay	The modulation mechanism of the PCED1B-AS1/miR-194-5p/PCED1B axis in glioma was investigated and affirmed, which supports researchers with a new insight into the therapy of patients with glioma.		Yes	Loss-of-function experiments depicted that the proliferation ability was restrained and apoptosis ability was induced in glioma cells by PCED1B-AS1 silencing and this phenomenon was also observed when PCED1B was knocked down.	31680313
PCED1B-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM tissues and cell lines 	regulation[Upregulating HIF-1α]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//IHC	 PCED1B-AS1 was notably upregulated in GBM tissues and cell lines and closely associated with larger tumor size and higher grade. Taken together, our findings demonstrate that PCED1B-AS1 is a novel oncogenic lncRNA in GBM and functions in a HIF-1α-dependent manner, which provides a promising prognostic biomarker and druggable target for GBM.	 Patients with high PCED1B-AS1 had shorter survival time than those with low PCED1B-AS1. 	Yes	 Functional experiments showed that depletion of PCED1B-AS1 significantly inhibited, while overexpression of PCED1B-AS1 promoted cell proliferation, glucose uptake, and lactate release. 	32326742
PCED1B	LncRNA	Homo sapiens	Stomach Neoplasms	 GC tissues and cell lines	Interaction(microRNA-215-3p / C-X-C motif chemokine receptor 1 axis)	Western Blot//EdU Staining//Migration Assay//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Invasion Assay	We demonstrated that, PCED1B-AS1 expression level was raised in GC tissues and cell lines, and increased expression of PCED1B-AS1 was in association with tumor size, TNM stage and lymph node metastasis in GC patients. Mechanistically, PCED1B-AS1 specifically inhibited miR-215-3p expressions, thus up-regulating CXCR1 expressions.	We demonstrated that, PCED1B-AS1 expression level was raised in GC tissues and cell lines, and increased expression of PCED1B-AS1 was in association with tumor size, TNM stage and lymph node metastasis in GC patients. 	Yes	Additionally, PCED1B-AS1 overexpression promoted GC cells proliferation, migration, invasion and EMT, and miR-215-3p overexpression counteracted the biological effects of PCED1B-AS1.	34516330
PCDHB17P	LncRNA	Homo sapiens	Breast Neoplasms	human breast cancer tissues and cell lines	Interaction(miR-145-3p/MELK/NF-κB Feedback Loop)	Western Blot//Wound Healing Assay//FISH//RIP//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	 Here, we demonstrated that lncRNA PCDHB17P was up-expressed in human breast cancer tissues and cell lines. MiR-145-3p was significantly decreased in breast cancer samples, which was negatively correlated to the expression of PCDHB17P. Mechanistic investigation indicated that PCDHB17P acted as a cancer-promoting competing endogenous RNA (ceRNA) by binding miR-145-3p and upregulating MELK.Interestingly, MELK could in turn increase the promoter activity and expression of PCDHB17P via NF-κB, thus forming a positive feedback loop that drives the metastasis and angiogenesis of breast cancer. 		Yes	Knockdown of PCDHB17P remarkably suppressed migration and invasion, as well as tube formation ability of breast cancer cells. 	34350110
PCDH10	CircRNA	Homo sapiens	Pancreatic Neoplasms	PC cells	Interaction(miR-338-3p/hTERT axis)	colony Formation Assay//Wound Healing Assay//Transfection//RIP//IF//PCR//IP//Colony Formation Assay//Transwell Assay	 Our research found that the PCDH10 gene could be transcribed into linear mRNA or circular RNA, and FUS could bind to the introns flanking the circularized exons, inducing the PCDH10 linear mRNA to shift to circPCDH10 in PC cells. Mechanistically, circPCDH10 acted as a sponge of miR-338-3p, which could negatively regulate hTERT expression in PC cells. 		Yes	Knockdown of circPCDH10 significantly inhibited PC progression.	34017382
PCBP2-OT1	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer tissues	Interaction[upregulating miR-10b]	qRT-PCR	We found that TUC338 was upregulated in early-stage bladder cancer patients and showed early diagnostic values. After surgical resection, plasma levels of TUC338 were significantly downregulated. Bladder cancer cells with TUC338 overexpression showed upregulated miR-10b, while miR-10b overexpression failed to significantly affect TUC338. 		Yes	TUC338 and miR-10b overexpression significantly promoted bladder cancer cell invasion and migration. 	31162712
PCBP2-OT1	LncRNA	Homo sapiens	prostate carcinoma	PC tissues	Interaction[downregulatingmiR-466]	qRT-PCR//Transwell Assay	It was observed that TUC338 was Expression[up-expression]regulated in tumor tissues comparing to adjacent healthy tissues of prostate carcinoma patients. TUC338 and miR-466 were inversely correlated in tumor tissues. miR-466 overexpression failed to affect TUC338 expression, while TUC338 overexpression led to downregulated miR-466 expression. 	Plasma levels of TUC338 were also higher in prostate carcinoma patients than in healthy controls. A 5-year follow-Expression[up-expression] study showed that high plasma level of TUC338 was correlated with poor survival.	Yes	TUC338 overexpression failed to significantly affect cancer cell proliferation, but promoted cancer cell migration and invasion. 	31085276
PCBP1-AS1	LncRNA	Homo sapiens	vulva squamous cell carcinoma	VSCC tissues and cells 	Interaction[TRAF5 and NF-κB]	CCK8//qRT-PCR//Wound Healing Assay//Transwell Assay	 PCBP1-AS1 and TRAF5 mRNA expression were downregulated in VSCC tissues and were correlated with patient clinicopathological characteristics.  As a tumor suppressor gene, PCBP1-AS1 regulates the proliferation and apoptosis of VSCC via TRAF5-mediated expression of the NF-κB.		Yes	Increase of PCBP1-AS1 significantly inhibited proliferation and enhanced apoptosis via TRAF5-mediated regulation of the NF-κB signaling pathway.	35116901
PCBP2-OT1	LncRNA	Homo sapiens	Nasopharyngeal Neoplasms	NPC cells	Interaction(miR-1226-3p/FGF2 axis)	In Vivo Experiment//RNA Pull-Down//IP//Western Blot//qPCR//Luciferase Report Assay//Cell Proliferation Assay//Cell Cycle Assay	 Higher level of TUC338 was also observed in NPC cells.  Mechanistically, TUC338 acted as molecular sponge of miR-1226-3p and attenuated the negative regulation of miR-1226-3p on the expression of fibroblast growth factor 2 (FGF2). 	Interestingly, NPC patients harboring overexpressed TUC338 have worse prognosis. 	Yes	Functional study indicated that down-regulated TUC338 remarkably suppressed the NPC cell proliferation and cell migration. Notably, depletion of TUC338 significantly inhibited the in vivo tumor growth.	36224455
PCBP2-OT1	LncRNA	Homo sapiens	Lymphoma, Large B-Cell, Diffuse	DLBCL tissues	Interaction( miR-28-5p/EGFR/PI3K/AKT Signaling Pathway)	In Vivo Experiment//RNA Pull-Down//Transfection//Immunoblotting//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay	In this study, we found that TUC338 was remarkably upregulated in DLBCL tissues as compared to matched normal tissues. Further, we found that TUC338 was able to directly bind to miR-28-5p and increased EGFR level, resulting in activating carcinogenic PI3K/AKT signaling, thereby facilitating DLBCL uncontrolled growth.	High TUC338 was closely related to advanced Ann Arbor stage, resistance to CHOP-like treatment, and high IPI (International Prognostic Index). 	Yes	Stable knockdown of TUC338 evidently inhibited cell proliferation and chemotherapy resistance to Adriamycin and induced apoptosis. 	33986803
hsa_circ_0119872	CircRNA	Homo sapiens	Melanoma	MM tissues and cell lines	Interaction(miR-582-3p/E2F3 axis)	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	Circ_0119872 was remarkably upregulated in MM tissues and cell lines. In addition, miR-582-3p was identified as a downstream target of circ_0119872. The target genes of miR-193a-3p are involved in melanogenesis and cancer-related signaling pathways. Mechanistically, circ_0119872 facilitated MM progression by adsorbing miR-582-3p and upregulating E2F3 expression.		Yes	Circ_0119872 knockdown suppressed the cell proliferation and metastasis	34644734
hsa_circ_0079593	CircRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction(miR-573/ABHD2 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Luciferase Report Assay//Cell Cycle Assay//Colony Formation Assay	Our data showed that circ_0079593 level was up-regulated in melanoma tissues and cells.Mechanistically, circ_0079593 directly targeted miR-573, and circ_0079593 controlled ABHD2 expression by miR-573. MiR-573 mediated the regulation of circ_0079593 on melanoma cell progression in vitro. 		Yes	The knockdown of circ_0079593 suppressed cell proliferation, cell cycle progression, migration, invasion, and enhanced apoptosis in vitro and inhibited tumor growth in vivo. 	33648800
hsa_circ_0084043	CircRNA	Homo sapiens	Melanoma	melanoma tissue	Regulation[miR-153-3p/Snail axis]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	We found that circRNA_0084043 was significantly up-regulated in melanoma tissue, and the result was replicated in a larger sample size. Bioinformatics and luciferase reporter assays confirmed that circRNA_0084043 directly binds to miR-153-3p, and Snail is directly targeted by miR-153-3p. We also demonstrated that circRNA_0084043 may act as the sponge of miR-153-3p to up-regulate Snail expression, and consequently function as an oncogene in melanoma. 	High circRNA_0084043 expression was an independent risk factor of overall survival in melanoma patients. 	Yes	circRNA_0084043 promotes melanoma cell proliferation, invasion and migration. 	29777697
PCBP1-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissues	Expression [highly expressed]	Western Blot//Transfection//Wound Healing Assay//qPCR//Survival Analysis//Microarray//Cell Proliferation Assay//Bioinformatics Analysis//Transwell Assay	 PCBP1-AS1 had significantly higher expression levels in cervical cancer tissues than in their normal counterparts (p < 0.001). 	Moreover, univariate analysis revealed that PCBP1-AS1 expression, tumor stage, pathologic T stage, and lymph vascular invasion were significantly correlated with the OS of cervical cancer patients	Yes	Collectively, these results suggest that the expression level of PCBP1-AS1 affected the proliferation, migration, and invasion of cervical cancer cells.	33833992
PCBP1-AS1	LncRNA	Homo sapiens	Glioma	 glioma cells	Epigenetics [methylation ]	Transfection//Migration Assay//qRT-PCR//Cell Proliferation Assay//Colony Formation Assay//Invasion Assay	Furthermore, we identified two lncRNAs termed PCBP1-AS1 and LINC02875 that may be involved in the malignant progression of glioma cells by using the TCGA database.		Yes	 Loss-of-function assays confirmed that knockdown of PCBP1-AS1 and LINC02875 inhibited the proliferation, migration, and invasion of glioma cells. 	33828990
PCBP1-AS1	LncRNA	Homo sapiens	Adenocarcinoma of Lung	LUAD cells and tumor tissues	Expression(lower expressed)	qRT-PCR//Western Blot//Invasion Assay//Migration Assay	 ScRNA-seq analysis showed that PCBP1-AS1 and ZSCAN16-AS1 were significantly negatively correlated with most of the functional states of LUAD cells, especially with metastasis. Functionally, PCBP1-AS1 was aberrantly downregulated in LUAD cells and tumor tissues. 		Yes	 Knockdown of PCBP1-AS1 significantly promoted the migration and invasion of LUAD cells. Consistently, PCBP1-AS1 overexpression suppressed the metastasis of LUAD in vitro and in vivo.Besides, PCBP1-AS1 inhibition induced decreased E-cadherin expression and increased N-cadherin, Vimentin and Snail expression. 	34107009
PGM5-AS1	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC and adjacent normal tissues	Regulation[ miR-466/PTEN axis]	Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//ChIP	we collected 113 pairs of ESCC and adjacent normal tissues to conduct qRT-PCR analysis. The result showed that PGM5-AS1 was significantly downregulated in ESCC.Mechanistically, PGM5-AS1 was transcriptionally activated by p53 and it could directly interact with and sequester miR-466 to elevate PTEN expression, thereby inhibiting ESCC progression.	 In the present study, we found that PGM5-AS1 was frequently downregulated in ESCC tissues, plasma, and cell lines, and low PGM5-AS1 expression was positively correlated with poor differentiation, advanced tumor node metastasis (TNM) stage, and lymph node metastasis. Importantly, PGM5-AS1 was identified to be an effective diagnostic and prognostic biomarker for ESCC patients.	Yes	Functional experiments revealed that exogenous expression of PGM5-AS1 significantly suppressed the proliferation, migration, and invasion of ESCC cells in vitro as well as tumor growth in vivo.	31185143
PCAT29	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer tissues,cell lines	Expression[lower expressed]	qRT-PCR//MTT//Colony Formation Assay//Transwell Assay	The expression of LncRNA PCAT29 was significantly suppressed in the breast cancer tissues and the triple-negative breast cancer cell lines.		Yes	PCAT29 overexpression caused inhibition of the proliferation rate and colony formation of the MDA-MB-231 cells.	32521844
hsa_circ_0039459	CircRNA	Homo sapiens	Liver Neoplasms	hepatocellular carcinoma cells and tissues	Interaction(miR-432/SYVN1)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 We found that circ-0039459 and SYVN1 mRNA were highly expressed, whereas miR-432 was lowly expressed in hepatocellular carcinoma cells and tissues.circ-0039459 targeted and regulated miR-432, which targeted and regulated SYVN1. The decreased miR-432 expression reversed the effects of circ-0039459 knockout in cancer cells. Furthermore, SYVN1 overexpression reversed the effect of miR-432 overexpression in hepatoma cells. Hence, circ-0039459 can affect the proliferation, apoptosis, migration, and invasion of hepatocellular carcinoma cells through the adsorption of miR-432, thereby regulating the expression of SYVN1.		Yes	After treatment with ribonuclease R or actinomycin D, the expression of linear RNA was reduced, whereas that of circular RNA was not significantly changed. circ-0039459 knockdown or miR-432 overexpression can inhibit cell proliferation, invasion, and migration and the expression of N-cadherin and vimentin proteins in carcinoma cells as well as promote apoptosis and increase the E-cadherin level. 	35543347
circLRP6	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues	regulation[ circ-LRP6/miR-182/Myc signaling ]	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 Circ-LRP6 was significantly upregulated in ESCC tissues and correlated with malignant clinicopathological characteristics and poor prognosis. Therefore, our data indicate that circ-LRP6 is a novel oncogenic circRNA in ESCC, targeting the circ-LRP6/miR-182/Myc signaling may be a promising therapeutic approach for ESCC patients.	 Circ-LRP6 was significantly upregulated in ESCC tissues and correlated with malignant clinicopathological characteristics and poor prognosis.	Yes	Knockdown of circ-LRP6 evidently reduced ESCC cell viability, colony formation and invasion.	32867570
hsa_circ_0072088	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues and cells	interaction[Absorbing miR-377]	qRT-PCR//FISH	As a result, circ_0072088 was significantly overexpressed in ESCC tissues and cells, which was closely associated with tumor size, invasion depth, clinical stage, and lymph node metastasis of esophageal cancer.Mechanistically, circ_0072088 upregulated VEGF gene expression by acting as the sponge of miRNA-377.	As a result, circ_0072088 was significantly overexpressed in ESCC tissues and cells, which was closely associated with tumor size, invasion depth, clinical stage, and lymph node metastasis of esophageal cancer.	Yes	circ_0072088 promoted ESCC cell proliferation, migration and invasion in vitro, and cell proliferation in vivo.	33061973
PMSB8-AS1	LncRNA	Homo sapiens	Pancreatic Neoplasms	PC tissues and PC cell lines	regulation[miR-382-3p/STAT1/PD-L1 axis]	colony Formation Assay//Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	 PMSB8-AS1 expression was upregulated in PC tissues and cell lines and positively associated with the worst survival in patients with PC. lncRNA PMSB8-AS1 promotes pancreatic cancer progression via STAT1 by sponging miR-382-3p involving regulation PD-L1.	 PMSB8-AS1 expression was upregulated in PC tissues and cell lines and positively associated with the worst survival in patients with PC. 	Yes	The in vitro and in vivo assays demonstrated that overexpression of PMSB8-AS1 significantly promoted pancreatic cancer cell proliferation, migration, and invasion, whereas knockdown of PMSB8-AS1 suppressed cell proliferation, migration, invasion, and EMT, and decreased apoptosis of PC cells. 	32891166
PMS2P2	LncRNA	Homo sapiens	Osteoarthritis	OA patient synovial fluid 	Interaction(miR-34a)	CCK8//qRT-PCR//BrdU//MTT	The results showed that PMS2L2 expression in OA patient synovial fluid was lower compared to that in control group fluid, and the extent of this reduction was related to disease stage. It was found that PMS2L2 over-expression caused increased miR-34a expression in OA patient chondrocytes but not in cells from healthy controls. In contrast, miR-34a over-expression in either cell population did not affect PMS2L2 expression.	The results showed that PMS2L2 expression in OA patient synovial fluid was lower compared to that in control group fluid, and the extent of this reduction was related to disease stage.	Yes	 Lastly, over-expression of both PMS2L2 and miR-34a led to inhibited chondrocyte proliferation. Of note, a combined over-expression of PMS2L2 and miR-34a resulted in stronger effects on proliferation compared to that from either single over-expression. 	35930398
PMS2P2	LncRNA	Homo sapiens	gastric adenocarcinoma	cancer tissues 	Expression[lower expressed]	qRT-PCR//Transwell Assay	The results revealed that PMS2L2 expression was downregulated in cancer tissues obtained from patients with GA compared with healthy adjacent tissues and was not significantly affected by clinical stage. Therefore, PMS2L2 may downregulate miR-25 expression to inhibit GA.	 Furthermore, low levels of PMS2L2 in cancer tissues were closely associated with a low overall 5-year survival rate in patients. 	Yes	Furthermore, PMS2L2 overexpression inhibited the migration and invasion of GA cells.	32565974
circFoxo3	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cell lines,ESCC tissues	Regulation[miR-23a/PTEN axis]	CCK8//qRT-PCR//Luciferase Report Assay//Western Blot	"In this study, circ-Foxo3 was lowly expressed in cell lines and ESCC tissues. Mechanically, we found a potential miRNA target, miR-23a, which negatively correlated with circ-Foxo3 in ESCC. Then, a luciferase assay confirmed the relationship between the circ-Foxo3 and miRNA. Moreover, circ-Foxo3 upregulation of PTEN occurred through ""sponging"" miR-23a."		Yes	Meanwhile, overexpression of circ-Foxo3 inhibited cell growth, migration, and invasion, whether in vivo or in vitro. 	31680314
hsa_circ_0075829	CircRNA	Homo sapiens	Pancreatic Carcinoma	 PC clinical specimens and cell lines	regulation[ circ_0075829/miR-1287-5p/LAMTOR3 axis]	qRT-PCR//Luciferase Report Assay//FISH	Compared with paracancerous tissues, the expression of circ_0075829 was increased in PC tissues, which was positively correlated with the clinical features of PC.		Yes	 Knockdown of circ_0075829 significantly suppressed the proliferative, migratory and invasive rates of SW1990 and BxPC-3 cells both in vitro and in vivo. 	33184989
circFOXO3	CircRNA	Homo sapiens	Liver Neoplasms	liver cancer cells	Regulation(PI3K/Akt Pathway)	Transfection//Invasion Assay//Migration Assay	circFOXO3 showed low expression in liver cancer cells; compared with the control group, the circFOXO3 expression and apoptosis rate of HuH-7 liver cancer cells in the circFOXO3 mimic group were significantly increased (P < 0.05) and the PI3K/Akt pathway-related protein expression, cell viability, invasion, and migration abilities were significantly reduced (P < 0.05); the apoptosis rate of HuH-7 liver cancer cells in the PI3K activator group was significantly reduced (P < 0.05) and the PI3K/Akt pathway related protein expression, cell viability, invasion and migration abilities were significantly increased (P < 0.05). Compared with the circFOXO3 mimic group, the apoptosis rate of HuH-7 liver cancer cells in the circFOXO3 mimic + PI3K activator group was significantly reduced (P < 0.05) and the PI3K/Akt pathway-related protein expression, cell viability, invasion and migration abilities were significantly increased (P < 0.05).		Yes	circFOXO3 showed low expression in liver cancer cells; compared with the control group, the circFOXO3 expression and apoptosis rate of HuH-7 liver cancer cells in the circFOXO3 mimic group were significantly increased (P < 0.05) and the PI3K/Akt pathway-related protein expression, cell viability, invasion, and migration abilities were significantly reduced (P < 0.05); the apoptosis rate of HuH-7 liver cancer cells in the PI3K activator group was significantly reduced (P < 0.05) and the PI3K/Akt pathway related protein expression, cell viability, invasion and migration abilities were significantly increased (P < 0.05). Compared with the circFOXO3 mimic group, the apoptosis rate of HuH-7 liver cancer cells in the circFOXO3 mimic + PI3K activator group was significantly reduced (P < 0.05) and the PI3K/Akt pathway-related protein expression, cell viability, invasion and migration abilities were significantly increased (P < 0.05).	35909586
hsa_circ_0066966	CircRNA	Homo sapiens	Liver Neoplasms	HBV-positive liver cancer cells	Expression(highly expressed)	qRT-PCR//Transfection//MTT//migration assay	 Among them, hsa_circ_0066966 had the highest absolute Log2FC value and was abnormally increased in HBV-positive liver cancer cells. 		Yes	 Functional experiments further verified that knockdown of hsa_circ_0066966 had a significant inhibitory effect on the proliferation and migration of HBV-positive liver cancer cells. By contrast, overexpression of hsa_circ_0066966 in HBV-negative liver cancer cells resulted in the opposite effect.	34976133
circSIRT1	CircRNA	Homo sapiens	Cardiomegaly	 hiPSC-CMs	Regulation(SIRT1 )	In Vivo Experiment//RNA Pull-Down//Western Blot//Co-IP//qRT-PCR//FISH//RIP//Luciferase Report Assay//ELISA//IF	Our results showed that circ-SIRT1 (hsa_circ_0093884) expression was downregulated in Ang II-treated hiPSC-CMs, and confirmed that its conserved mouse homolog circ-Sirt1 (mmu_circ_0002354) was expressed at low levels in Ang II-treated H9c2 cells and TAC-induced mice model. Mechanistically, circ-SIRT1 could upregulate its host gene SIRT1 at the post-transcriptional level by sponging miR-3681-3p/miR-5195-3p and stabilized SIRT1 protein at the post-translational level by recruiting USP22 to induce deubiquitination on SIRT1 protein. 		Yes	 Functionally, circ-SIRT1/circ-Sirt1 attenuated Ang II-induced CH and induced autophagy in hiPSC-CMs and H9c2 cardiomyocytes. Further, SIRT1 knockdown could rescue the effect of circ-SIRT1 upregulation on Ang II-induced CH and autophagy in vitro and in vivo. 	34759275
hsa_circ_0078710	CircRNA	Homo sapiens	Liver Neoplasms	 liver cancer tissues and cells.	Interaction(miR-431-5p/TXNDC5 )	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 Circ_0078710 and TXNDC5 were notably expressed in liver cancer tissues and cells.MiR-431-5p is the target of circ_0078710, and silence circ_0078710 can inhibit the malignant behavior and glycolysis of hepatocellular carcinoma (HCC) cells by releasing miR-431-5p. In addition, TXNDC5 was a target of miR-431-5p, and overexpression of TXNDC5 restored cell proliferation and glycolysis inhibition due to miR-431-5p.		Yes	Circ_0078710 knockdown diminished proliferation, migration, invasion and glycolytic metabolism of huh7 and Hep3B cells, and accelerated cell apoptosis. Animal experiments made clear the anti-tumor effect of circ_0078710 knockdown.	34606982
circDLC1	CircRNA	Homo sapiens	Liver Neoplasms	HCC tissues	Interaction(HuR and MMP1)	In Vivo Experiment//RNA Pull-Down	 Our data demonstrated that circDLC1 was downregulated in HCC tissues and closely relevant to favorable prognosis. Mechanistic investigations revealed that circDLC1 could bind to RNA-binding protein HuR, which subsequently reduced the interaction between HuR and MMP1 mRNAs, and thus inhibited the expression of MMP1, ultimately contributing to inhibition of HCC progression. 		Yes	Overexpression of circDLC1 inhibited the proliferation and motility of hepatoma cells in vitro and in vivo, while silencing of circDLC1 played the opposite role. 	33391541
PLOD2	CircRNA	Homo sapiens	Colonic Neoplasms	 colon cancer tissue and cell lines	Interaction(miR-513a-5p/SIX1/LDHA axis)	colony Formation Assay//RNA Pull-Down//IHC//ChIP//Western Blot//ISH//Transfection//Colony Formation Assay//qRT-PCR//RIP//FISH//PCR//IP//Transwell Assay//IF	Here, we found circPLOD2 was dramatically upregulated in colon cancer tissue and cell lines. Moreover, based on the analysis of RNA pull-down, RNA immunoprecipitation, luciferase and rescued assays, we confirmed that the interactions between circPLOD2, miR-513a-5p and SIX1. It suggested that circPLOD2 acted as a sponge of miR-513a-5p to regulate the activation of the target gene SIX1.		Yes	In vitro CCK-8, colony formation and transwell assays, and in vivo tumor transplantation assay were performed and explored that circPLOD2 might promote tumor proliferation, migration and invasion in vitro and in vivo. 	36071678
PLIC11	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues	Interaction(YY1/PIWIL4 axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	In our study, we found that PLIC11 was upregulated in lung cancer, particularly in metastatic lung cancer tissues. Mechanically, PLIC11 could interact with YY1 and promote PIWIL4 expression by transcription activation. Therefore, PLIC11 upregulation is a potential indicator of aggressive lung cancer, Silencing of PLIC11 has great potential therapeutic strategy in NSCLC.		Yes	Overexpression of PLIC11 enhanced cell proliferation, migration, and metastasis in vitro and in vivo. 	36537719
circMEG3	CircRNA	Homo sapiens	Liver Neoplasms	human liver cancer line Huh7 	Expression [lower expressed]	qRT-PCR//Colony Formation Assay//ChIP//Western Blot	Herein, our results indicate that CircMEG3 is downregulated expression and negatively correlated with the expression of telomerase-related gene Cbf5 in human liver cancer. Moreover, CircMEG3 inhibits the expression of Cbf5, a component of telomere synthetase H/ACA ribonucleoprotein (RNP; catalyst RNA pseudouracil modification) through METTL3 dependent on HULC. 		Yes	Moreover, CircMEG3 inhibits the growth of human liver cancer stem cells in vivo and in vitro. CircMEG3 inhibits the expression of m6A methyltransferase METTL3 dependent on HULC. Strikingly, increased Cbf5 abrogates the ability of CircMEG3 to inhibit malignant differentiation of human liver cancer stem cells.	33425489
hsa_circ_G004213	CircRNA	Homo sapiens	Liver Neoplasms	Hepatic artery blood 	Interaction(miR‑513b‑5p/PRPF39)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay	A novel gene was screened out; hsa‑circRNA‑G004213 (circ‑G004213) was significantly upregulated following TACE (fold change >10, P < 0.01). Further analysis found circ‑G004213 significantly increased the cisplatin sensitivity of HepG2 cells and positively associated with the prognosis of tumor‑bearing mice. It was demonstrated that circ‑G004213 regulated cisplatin resistance via the miR‑513b‑5p/PRPF39 axis. 		Yes	Further analysis found circ‑G004213 significantly increased the cisplatin sensitivity of HepG2 cells and positively associated with the prognosis of tumor‑bearing mice. 	33864660
PLEKHA8P1	LncRNA	Homo sapiens	Liver Neoplasms	TCGA(418 samples including 369 primary tumor and 49 solid tissue normal samples)	Expression [highly expressed]	Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//Cell Proliferation Assay//Cell Cycle Assay//Colony Formation Assay	PLEKHA8P1 Is Up-Regulated in HCC Samples and Predicts Unfavorable Prognosis in Patients from the TCGA-LIHC Dataset		Yes	 PLEKHA8P1 Promotes Proliferation, Invasion and Migration in HCC Cells	34299245
PLCD3-OT1	LncRNA	Homo sapiens	Cataract	lens capsule	Interaction[miR-224-5p]	Tunel//qRT-PCR//FISH//Luciferase Report Assay//RNA-seq	 The expression of lncRNA PLCD3-OT1 and PLCD3 were significantly decreased in ARC.In addition, PLCD3-OT1 may act as a ceRNA to regulate the expression of PLCD3 through competition for miR-224-5p.		Yes	PLCD3-OT1 overexpression promoted the expression of PLCD3, cell viability, proliferation, and inhibited cell apoptosis upon oxidative stress, while knockdown of PLCD3 showed the opposite results. 	31725166
hsa_circ_0004771	CircRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	cancer tissues	regulation[miR-339-5p/CDC25A axis]	qRT-PCR	 Here we profiled six pair plasma circRNA in ESCC based on RNA sequencing, and then verified the elevation of hsa_circ_0004771 in 20 cancer tissues and 105 pair case-control plasma samples by quantitative reverse transcriptase PCR.Mechanistically, hsa_circ_0004771 positively regulated CDC25A by acting as a molecular sponge of miR-339-5p and rescue assay confirmed this regulatory relationship.	 The upregulation of hsa_circ_0004771 was correlated with heavier tumor burden and poor prognosis, knockdown of it inhibited the ESCC cells proliferation both in vitro and in vivo. 	Yes	 The upregulation of hsa_circ_0004771 was correlated with heavier tumor burden and poor prognosis, knockdown of it inhibited the ESCC cells proliferation both in vitro and in vivo. 	32050790
POLR1HASP	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	NPC tissues and cells	regulation[ miR-335-ROCK1 Axis]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	 ZNRD1-AS1 expression was elevated in the NPC tissues and cells, and ZNRD1-AS1 overexpression was positively correlated with advanced TNM stage and the presence of lymph node metastasis. We provided evidence that ZNRD1-AS1 facilitates the invasion and metastasis of NPC cells via the miR-335-ROCK1 axis.	 ZNRD1-AS1 expression was elevated in the NPC tissues and cells, and ZNRD1-AS1 overexpression was positively correlated with advanced TNM stage and the presence of lymph node metastasis. 	Yes	Our biological experiments indicated that ZNRD1-AS1 knockdown reduces NPC cell invasion and metastasis. 	32547105
Platr4	LncRNA	Mus musculus	Non-alcoholic Fatty Liver Disease	mouse liver	Interaction(Nlrp3/ NF-κB signaling)	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//qPCR//Co-IP//FISH//RIP//RNA-seq//Luciferase Report Assay//IF	Cyclic expression of Platr4 is generated by the core clock component Rev-erbα via two RevRE elements (i.e., -1354/-1345 and -462/-453 bp). NF-κB transcriptionally drives Platr4 through direct binding to two κB sites (i.e., -1066/-1056 and -526/-516 bp), potentially accounting for up-regulation of Platr4 in experimental steatohepatitis.Platr4 functions to inactivate Nlrp3 inflammasome via intercepting NF-κB signaling. 		Yes	 Loss of Platr4 down-regulates Nlrp3 inflammasome activity in the liver, blunts its diurnal rhythm, and sensitizes mice to experimental steatohepatitis, whereas overexpression of Platr4 ameliorates the pathological conditions in an Nlrp3-dependent manner. 	33391484
POU3F3	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	breast cancer tissues	Interaction[inactivating caspase 9]	CCK8//qRT-PCR//ELISA//Western Blot	In the present study we found that expression levels of lncRNA POU3F3 were higher in tumor tissues than in adjacent healthy tissues of triple negative breast cancer (TNBC) patients and were significantly and inversely correlated with levels of cleaved caspase 9 only in tumor tissues.  In addition, plasma levels of lncRNA POU3F3 were higher in TNBC patients than in healthy controls and were significantly and inversely correlated with levels of cleaved caspase 9 only in TNBC patients. In addition, treatment of exogenous Cleaved Caspase-9 significantly attenuated the effects of lncRNA POU3F3 overexpression on cancer cell proliferation and apoptosis. lncRNA POU3F3 may promote proliferation and inhibit apoptosis of cancer cells in triple-negative breast cancer.		Yes	 In addition, treatment of exogenous Cleaved Caspase-9 significantly attenuated the effects of lncRNA POU3F3 overexpression on cancer cell proliferation and apoptosis.	30843771
circTP63	CircRNA	Homo sapiens	lung squamous cell carcinoma	 LUSC tissues and adjacent nontumorous tissues	Interaction[upregulating FOXM1]	Western Blot//CCK8//qRT-PCR//RIP//Microarray	By analyzing the co-expression network of differentially expressed circRNAs and dysregulated mRNAs, we identify that a cell cycle-related circRNA, circTP63, is upregulated in LUSC tissues and its upregulation is correlated with larger tumor size and higher TNM stage in LUSC patients.	By analyzing the co-expression network of differentially expressed circRNAs and dysregulated mRNAs, we identify that a cell cycle-related circRNA, circTP63, is upregulated in LUSC tissues and its upregulation is correlated with larger tumor size and higher TNM stage in LUSC patients.	Yes	Elevated circTP63 promotes cell proliferation both in vitro and in vivo. 	31324812
circLDLR	CircRNA	Homo sapiens	Coronary Artery Disease	 coronary artery disease tissues	Interaction(miR-26-5p/KDM6A Axis)	qRT-PCR//Transfection//Cell Apoptosis Assay//Western Blot	Downregulation of circLDLR was associated with increased miR-26-5p in coronary artery disease tissues. Moreover, the overexpression of KDM6A reduced VSMCs proliferation and increased apoptosis in an miR-26-5p/circLDLR axis-dependent manner. CircLDLR modulates the proliferation and apoptosis of VSMCs through miR-26-5p/KDM6A axis.		Yes	In addition, circLDLR could inhibit cell proliferation and promote cell apoptosis by regulating miR-26-5p. 	35384910
POU6F2-AS1	LncRNA	Homo sapiens	Lung Neoplasms	 LADC tissues	Interaction(miR-34c-5p/KCNJ4)	Western Blot//Migration Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay//Transwell Assay	High-regulation of POU6F2-AS1 was presented in LADC tissues compared with adjacent normal tissues, which was correlated with poor outcome of LADC patients. Collectively, POU6F2-AS1 might function as a ceRNA through sponging miR-34c-5p to high-regulate KCNJ4 in LADC, which indicates that POU6F2-AS1 might be a promising therapeutic target with significant prognostic value for LADC treatment.	High-regulation of POU6F2-AS1 was presented in LADC tissues compared with adjacent normal tissues, which was correlated with poor outcome of LADC patients. 	Yes	 Functional experiments in Calu-3 and NCI-H460 cells showed that POU6F2-AS1 significantly promoted LADC cell proliferation, colony formation, invasion and migration. 	33999092
POU3F3	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC  tissues 	regulation[downregulating microRNA-30d-5p]	qRT-PCR//Transwell Assay	POU3F3 was upregulated, while miR-30d-5p was downregulated in cancer tissues than in adjacent healthy tissues of NSCLC patients.  POU3F3 might positively regulate NSCLC cell proliferation, migration and invasion through downregulation of miR-30d-5p.		Yes	Overexpression of POU3F3 mediated enhanced proliferation, migration and invasion of NSCLC cells. 	32615948
POU3F3	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 tumor tissues	Regulation(LncRNA GAS5)	RNA Pull-Down//Western Blot//CCK8//qRT-PCR//FISH//RIP//Luciferase Report Assay//Transwell Assay//IF	In the present study, we found that POU3F3 was upregulated while GAS5 was downregulated in tumor tissues than that in adjacent healthy tissues of patients with RCC. In situ hybridization analysis showed that POU3F3 was mostly expressed in tumor tissues, while GAS5 was mostly expressed in adjacent healthy tissues.  Overexpression of POU3F3 mediated the downregulation of GAS5 in RCC cells, while GAS5 overexpression failed to significantly affect POU3F3 expression. Overexpression of POU3F3 led to promoted, while GAS5 overexpression led to inhibited proliferation, migration, and invasion of RCC cells. In addition, GAS5 overexpression attenuated the enhancing effects of POU3F3 overexpression on cancer cell proliferation, migration, and invasion.	High level of POU3F3 and low level of GAS5 were closely correlated with poor prognosis of RCC patients. Expression levels of POU3F3 and GAS5 were significantly and inversely correlated in tumor tissues but not in adjacent healthy tissues of RCC patients. 	Yes	 Overexpression of POU3F3 mediated the downregulation of GAS5 in RCC cells, while GAS5 overexpression failed to significantly affect POU3F3 expression. Overexpression of POU3F3 led to promoted, while GAS5 overexpression led to inhibited proliferation, migration, and invasion of RCC cells. In addition, GAS5 overexpression attenuated the enhancing effects of POU3F3 overexpression on cancer cell proliferation, migration, and invasion.	34352801
POU3F3	LncRNA	Homo sapiens	Osteoarthritis	OA patients/animal cartilage tissues, chondrocyte model	Interaction(miR-29a- 3p/FOXO3 Axis)	Western Blot//CCK8//qRT-PCR//Flow Cytometry//ELISA	The expression level of POU3F3 was decreased in OA patients/animal cartilage tissues and IL-1β-stimulated in vitro chondrocyte model. Mechanistically, Luciferase reporter and RNA immunoprecipitation (RIP) assays indicated that miR-29a-3p could directly bind to POU3F3, and FOXO3 was a target gene of miR-29a-3p. Functional rescue assays confirmed this POU3F3/miR-29a-3p/FOXO3 axis in chondrocytes during OA occurrence. 		Yes	POU3F3 overexpression inhibited IL-1β-induced injury of chondrocytes, enhancing cell viability, suppressing apoptosis and inflammatory cytokine secretion, rescuing metabolic dysfunction, and restraining autophagy in vitro. Furthermore, intraarticularly delivery of lentivirus containing POU3F3 alleviates the damage in mouse OA model in vivo.	35264092
POU3F3	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues and cell lines	Expression[highly expressed]	qRT-PCR	Our results suggested that levels of linc-POU3F3 were dramatically increased in hepatocellular carcinoma tissues and cell lines compared with paired normal hepatic tissues and normal hepatic cell line, respectively. 	 Levels of linc-POU3F3 were positively correlated with clinical stage, tumor size, vascular invasion and metastasis. 	Yes	The gain- and loss-of-function experiments showed that linc-POU3F3 expression significantly promoted tumor cell proliferation, migration and invasion.	29906746
POU3F3	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	cervical cancer tissue,cell line	Interaction[miR-127-5p/FOXD1]	ChIP//Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	POU3 F3 was validated to be up-regulated in the cervical cancer tissue specimens and cells comparing with normal controls. The transcriptional expression of POU3 F3 was activated by the transcription factor SP1. Mechanically, POU3 F3 acted as the sponge to target miR-127-5p, while miR-127-5p bind with the 3'-UTR of FOXD1 gene. In conclusion, our data verifies that lncRNA POU3 F3, induced by transcription factor SP1, acts as an oncogene in the cervical cancer tumorigenesis via regulating miR-127-5p/FOXD1 axis, providing a possible therapeutic target for cervical cancer.		Yes	In vitro, POU3 F3 promoted the proliferation, invasion of cervical cancer cells. In vivo, POU3 F3 knockdown repressed the tumor growth of cervical cancer cells.	31252264
POU3F3	LncRNA	Homo sapiens	Nasopharyngeal carcinoma	blood	Interaction[TGF-β1]	Western Blot//Migration Assay//qRT-PCR//ELISA//Invasion Assay	Our study showed that plasma levels of lncRNA POU3F3 and TGF-β1 (transforming growth factor-β) were both increased in nasopharyngeal carcinoma patients than in healthy controls.TGF-β1 inhibitor partially rescued the inhibited cancer cell migration and invasion caused by lncRNA POU3F3 overexpression. LncRNA POU3F3 overexpression led to down-regulated TGF-β1 expression, while exogenous TGF-β1 and TGF-β1 inhibitor treatment did not significantly change the expression level of lncRNA POU3F3. Therefore, lncRNA POU3F3 may promote cancer cell migration and invasion in nasopharyngeal carcinoma by up-regulating TGF-β1.	 Plasma levels of lncRNA POU3F3 were not affected by the diameter of primary tumors but increased in patients with tumor metastasis. Follow-up study showed that high plasma levels of lncRNA POU3F3 were significantly correlated with poor overall survival.	Yes	 LncRNA POU3F3 overexpression and exogenous TGF-β1 treatment led to promoted, while TGF-β1 inhibitor led to inhibited migration and invasion of nasopharyngeal carcinoma cells.	30602452
POLR1HASP	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	BC tissues,cell lines	regulation[regulating miR-194 and ZEB1]	CCK8//qRT-PCR//Transwell Assay//Western Blot	Zinc ribbon domain containing 1 antisense RNA 1level was upregulated in BC. Knockdown of ZNRD1-AS1 suppressed BC cell development in vitro and in vivo via targeting miR-194 to regulate ZEB1, indicating a novel avenue for treatment of BC.		Yes	ZNRD1-AS1 silence repressed proliferation, migration, invasion and EMT in BC cells. 	32862492
POU3F3	LncRNA	Homo sapiens	Melanoma	melanoma tissues	Regulation(lncRNA MEG3)	qRT-PCR//Invasion Assay	We found that POU3F3 was upregulated, while lncRNA MEG3 was downregulated in melanoma. Expression levels of POU3F3 and MEG3 were inversely correlated across tumor tissues. 		Yes	In vitro experiments showed that POU3F3 overexpression decreased MEG3 expression in melanoma cells, while MEG3 overexpression failed to affect POU3F3.  POU3F3 overexpression increased melanoma cell proliferation, while MEG3 overexpression decreased melanoma cell proliferation.  In addition, rescue experiments showed that MEG3 overexpression attenuated the enhancing effects of POU3F3 overexpression.	35201451
POU3F3	LncRNA	Homo sapiens	prostate carcinoma	prostate carcinoma tissues	Interaction[upregulating rho-associated protein kinase 1 ]	CCK8//qRT-PCR//Western Blot	Expression levels of POU3F3 increased with increase in the diameter of tumor but were not significantly affected by lymph node metastasis or distant metastasis.Expression levels of POU3F3 and ROCK1 were positive correlated in tumor tissues but not in adjacent healthy tissues. POU3F3 and ROCK1 overexpression promoted, while ROCK1 knockdown inhibited the proliferation of prostate carcinoma cells. ROCK1 knockdown reduced the enhancing effect of POU3F3 overexpression on cancer cell proliferation. POU3F3 overexpression led to ROCK1 overexpression in prostate carcinoma cells, while ROCK1 overexpression did not significantly affect POU3F3 expression. 		Yes	POU3F3 and ROCK1 overexpression promoted, while ROCK1 knockdown inhibited the proliferation of prostate carcinoma cells. ROCK1 knockdown reduced the enhancing effect of POU3F3 overexpression on cancer cell proliferation. 	30474879
POT1-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC cells	Interaction(miR-497-5p/PDK3 axis)	Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	In this study, high POT1-AS1 expression in GC cells was confirmed, and its elevated expression was linked to patients’ negative clinicopathological characteristics, as well as shorter disease-free survival (DFS) and overall survival (OS).  POT1-AS1 was shown to serve as a competing endogenous RNA (ceRNA) by sponging miR-497-5p to increase PDK3 expression. 	In this study, high POT1-AS1 expression in GC cells was confirmed, and its elevated expression was linked to patients’ negative clinicopathological characteristics, as well as shorter disease-free survival (DFS) and overall survival (OS). 	Yes	The impact of POT1-AS1 silencing on GC malignant phenotypes could be reversed by suppressing miR-497-5p or restoring PDK3, according to rescue experiments.	35070402
circROBO2	CircRNA	Homo sapiens	Coronary Artery Disease	HASMCs	Interaction(Circ_ROBO2/miR-149 Axis)	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Transwell Assay	The expression patterns of circ_ROBO2 and miR-149 in CAD patients and PDGF-BB-treated human aortic smooth muscle cells (HASMCs) were upregulated and downregulated, respectively. Knockdown of circ_ROBO2 could markedly inhibit the capabilities of proliferation and migration, enhance the apoptotic rate, and suppress NF-κB signaling in PDGF-BB-treated HASMCs. Mechanistically, circ_ROBO2 acted as a sponge of miR-149 to activate TRAF6/NF-κB signaling. Rescue studies demonstrated that neither silencing miR-149 nor activation of NF-κB signaling obviously abolished the biological roles of circ_ROBO2 knockdown in PDGF-BB treated-HASMCs.		Yes	Knockdown of circ_ROBO2 could markedly inhibit the capabilities of proliferation and migration, enhance the apoptotic rate, and suppress NF-κB signaling in PDGF-BB-treated HASMCs. 	34649241
POSTN	CircRNA	Homo sapiens	Myocardial Infarction	blood	regulation[miR-96-5p/BNIP3 Axis]	qRT-PCR//Western Blot//PCR//IF	We identified that the expression of circPostn was elevated in the plasma of MI patients, MI mouse model, and hypoxia and reoxygenation (H/R)-treated human cardiomyocytes.Thus, we conclude that circPostn contributes to MI-induced myocardial injury and cardiac remodeling by regulating miR-96-5p/BNIP3 axis.		Yes	The depletion of circPostn significantly attenuated MI-related myocardium injury and reduced the infarct size in MI mouse model. 	33681183
Postn	CircRNA	Mus musculus	Myocardial Infarction	ventricular tissues of mice	Regulation(miR-96-5p/BNIP3 Axis)	Western Blot//RIP//PCR//IP//IF	The depletion of circPostn was able to decrease MI-induced expression of collagen 1α1 and collagen 3α1 in the ventricular tissues of mice. The protein expression of collagen and α-smooth muscle actin (SMA) was up-regulated in MI mice and was inhibited by circPostn knockdown. Meanwhile, the expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was repressed by circPostn depletion in the ventricular tissues of MI mice. Besides, the circPostn depletion attenuated cardiomyocyte apoptosis in mice. Mechanically, circPostn served as a miR-96-5p sponge and miR-96-5p-targeted BNIP3 in human cardiomyocytes, in which circPostn up-regulated BNIP3 expression by targeting miR-96-5p. circPostn promoted H/R-induced cardiomyocyte injury by modulating miR-96-5p/BNIP3 axis. Thus, we conclude that circPostn contributes to MI-induced myocardial injury and cardiac remodeling by regulating miR-96-5p/BNIP3 axis. Our finding provides new insight into the mechanism by which circPostn regulates MI-related cardiac dysfunction. circPostn, miR-96-5p, and BNIP3 are potential targets for the treatment of MI-caused heart injury.		Yes	The circPostn knockdown obviously enhanced left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) and inhibited left ventricular anterior wall thickness at diastole (LVAWd) and left ventricular posterior wall thickness at diastole (LVPWd).	33681183
hsa_circ_0001006	CircRNA	Homo sapiens	Cardiomegaly	cardiac hypertrophy mice and cardiomyocytes 	Interaction(miR-214-3p/PAK6 axis)	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Microarray	In this report, we found that circular RNA hsa_circ_0001006 (circ_0001006) was upregulated in cardiac hypertrophy mice and cardiomyocytes treated with angiotensin II (Ang II).Our data demonstrated that circRNA_0001006 exacerbates cardiac hypertrophy via suppressing miR-214-3p leading to enhanced PAK6 levels.		Yes	Next, we noticed that gain of function circ_0001006 could induce cardiomyocyte hypertrophy; oppositely, knockdown of circ_0001006 remitted Ang II-induced cardiomyocyte hypertrophy. 	35306484
POLR1HASP	LncRNA	Homo sapiens	Stomach Neoplasms	gastric cancer tissues 	Interaction( miR-9-5p/HSP90AA1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//CCK8//FISH//qRT-PCR//migration assay//Luciferase Report Assay//H&E Staining	 In this study, we found that ZNRD1-AS1 levels were significantly upregulated in gastric cancer tissues compared to those in adjacent healthy gastric tissues.  ZNRD1-AS1 knockdown suppressed tumor growth and pulmonary metastasis in a nude mouse model ZNRD1-AS1 can bind to miR-9-5p and ZNRD1-AS1 knockdown can decrease the protein level of heat shock protein 90 alpha family class A member 1 (HSP90AA1), which is the target of miR-9-5p. 	ZNRD1-AS1 levels were correlated with lymph node metastasis, distal metastasis, and TNM stage, but were not correlated with age and sex.	Yes	ZNRD1-AS1 knockdown suppressed cell proliferation, migration, and invasion, and promoted apoptosis. ZNRD1-AS1 overexpression had the opposite effect. 	34226297
circCSPP1	CircRNA	Homo sapiens	Liver Neoplasms	cell lines	Interaction(miR-1182)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//CCK8//FISH//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	CircCSPP1 knockdown inhibited the proliferation, migration and invasion while promoted apoptosis of liver cancer cells. Mechanically, we predicted and verified the target miR of circCSPP1 which is miR-1182. miR-1182 was capable of reversing the effect of circCSPP1 on liver cancer cells.		Yes	CircCSPP1 knockdown inhibited the proliferation, migration and invasion while promoted apoptosis of liver cancer cells. Mechanically, we predicted and verified the target miR of circCSPP1 which is miR-1182. miR-1182 was capable of reversing the effect of circCSPP1 on liver cancer cells.	33935503
hsa_circ_0000105	CircRNA	Homo sapiens	Liver Neoplasms	liver cancer tissues and cell lines	regulation[miR-498/PIK3R1]	Western Blot//CCK8//qRT-PCR//RIP//Flow Cytometry	 Circ_0000105 was highly expressed in liver cancer tissues and cell lines.Circ_0000105 plays a cancer-promoting role in liver cancer by regulating the miR-498/PIK3R1 axis.	Moreover, its high expression was associated with an increase in the T stage of liver cancer patients and a low degree of tumor differentiation. 	Yes	Circ_0000105 overexpression promoted liver cancer cell proliferation and inhibited apoptosis, whereas knocking down circ_0000105 triggered the opposite effect.	32729955
PGM5P4-AS1	LncRNA	Homo sapiens	Lung Neoplasms	 Lung cancer tissues 	Expression [lower expressed]	Wound Healing Assay//qRT-PCR//MTT//Cell Cycle Assay//Transwell Assay	In this work, we found that a newly discovered lncRNA, lncRNA PGM5P4-AS1, was lower expressed in lung cancer tissues than adjacent tissues. Then, the lncRNA PGM5P4-AS1 was overexpressed or knocked-down in different lung cancer cells, and its effects on the malignant phenotypes were measured by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, cell cycle assay, wound healing assay, and transwell assay.  Further, the growth of lung cancer tumors in nude mice was also inhibited by PGM5P4-AS1 overexpression. In mechanism, PGM5P4-AS1 has the binding site of miR-1275 and could positively regulate the expression of LZTS3 via sponging miR-1275.		Yes	The results showed that the overexpression of PGM5P4-AS1 inhibited lung cancer cell proliferation, migration, and invasion activities, while these abilities were prominently promoted by the interference of PGM5P4-AS1.	33315502
PICSAR	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	cell lines	regulation[RelA/p65]	qRT-PCR//RNA-seq	 These data were validated in several PDAC cell lines, and significant upregulation of LINC00162 was found in all of them. Furthermore, the result of Chromatin immunoprecipitation assay revealed that RelA/p65 directly bound to LINC00162, and the expression of LINC00162 in PDAC decreased after RelA/p65 knock-down, the proliferation ability of AsPc-1 also significantly inhibited after knocking down LINC00162 and RelA/p65 simultaneously, indicating that RelA/p65 directly involve in the transcriptional regulation of LINC00162.		Yes	Knock-down of LINC00162 significantly inhibited the proliferation, colony formation and migration of PATC cells in vitro and suppressed the growth of PATC xenografts in vivo.	32364285
hsa_circ_0043265	CircRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cell lines (SCC25, SCC15, SCC9 and Cal27)	Interaction(miR-1243/SALL1 Axis)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Transwell Assay	the current study demonstrated that circ_0043265 was downmodulated in TSCC and was identified as a ceRNA that restrained the cell proliferation, migration and invasion of SCC25 and Cal27 cells via modulating the miR-1243/SALL1 axis.		Yes	Functionally, circ_0043265 overexpression led to an attenuation of cell proliferation, migration and invasion of SCC25 and Cal27 cells.	34257535
PINK1-AS	LncRNA	Homo sapiens	Small Cell Lung Carcinoma	SCLC tissues	Expression(highly expressed)	Transfection//qPCR//Transwell Assay	We found that PINK1-AS was upregulated in SCLC tissues compared to that in non-cancer tissues. Plasma expression levels of PINK1-AS were increased in SCLC patients compared to that in the controls. 	High plasma expression levels of PINK1-AS were closely associated with worse survival. Plasma expression of PINK1-AS was only closely correlated with distant tumor metastasis, but not other factors. High plasma expression levels of PINK1-AS effectively separated patients with distant metastasis from non-metastatic patients. 	Yes	Moreover, PINK1-AS positively regulated the migration and invasion of SCLC cells.	35764723
PILAR1	LncRNA	Homo sapiens	Adenocarcinoma of Lung		Expression[Expression[highly expressed]-expression]	qRT-PCR	The expression of PILAR1 in Dhanasekaran et al. and TCGA cohorts is shown in Fig. 1 D and E. Further, to examine the diagnostic ability of PILAR1 in discriminating LUAD patients from normal lung samples, ROC analysis was performed. The Area Under Curve (AUC) obtained for samples from the TCGA cohort was 0.95, and Dhanasekaran et al. cohort was 0.89, suggesting its potential in diagnosis of LUAD patients (Fig. 1 F). We utilised GTEx data to explore the expression of PILAR1 in normal human tissues. Interestingly, expression of PILAR1 was limited to skin, and testis (Fig. 1 G). Further, we explored the expression of PILAR1 in human cancer using MiPanda database. Interestingly, PILAR1 was overexpressed in almost all the cancer types compared to the normal counterpart (SExpression[up-expression]plementary Fig. S1 D). These results suggest that PILAR1 is a cancer-specific LncRNA with very restricted expression in normal samples.	Further, we performed the Kaplan-Meier analysis of PILAR1 in Dhanasekaran et al. and TCGA cohorts. As expected, in both the cohorts, patients with high PILAR1 expression showed significantly poor survival (Dhanasekaran et al. cohort: HR = 2.29, p-value = 0.017 and TCGA cohort: HR = 1.51 and p-value = 0.017) (Fig. 1H and I). Furthermore, we utilised microarray datasets available on KM Plotter database to perform the Kaplan-Meier analysis in lung cancer samples (Affy id- 237563_s_at). Interestingly, PILAR1 significantly predicted the survival in KM-plotter datasets as well (HR = 2.67, p-value < 0.0001) (Fig. 1 J). In a multivariate analysis, PILAR1 predicted the survival independent of all clinical factors (SExpression[up-expression]plementary Fig. S1 E).	Yes	In vitro, we showed that lncRNA AK001796 knockdown markedly sExpression[up-expression]pressed cell proliferation and cell invasion abilities.	30639423
hsa_circ_0000003	CircRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues and cell lines,	Interaction(miR‑330‑3p/GLS axis)	RNA Pull-Down//Western Blot//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis	Here, we found that circ_0000003 expression was upregulated in TSCC tissues and cell lines, and high circ_0000003 expression was correlated with advanced TNM stage, increased tumor size and poor patient survival. Mechanistically, we found that circ_0000003 acted as a competing endogenous RNA (ceRNA) that sponged miR‑330‑3p, thereby elevating glutaminase (GLS) expression. Accordingly, cell invasion, migration, glutamine consumption, α‑ketoglutarate (α‑KG) production and ATP production were significantly decreased by circ_0000003 knockdown in TSCC cells, and these effects were reversed by miR‑330‑3p inhibition. 	Here, we found that circ_0000003 expression was upregulated in TSCC tissues and cell lines, and high circ_0000003 expression was correlated with advanced TNM stage, increased tumor size and poor patient survival.	Yes	Circ_0000003 was revealed to facilitate cell proliferation, migration and invasion of TSCC cells. 	33649795
PIK3CD-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues,cell lines	Interaction[binding with microRNA-566]	RNA Pull-Down//Western Blot//Transwell Assay//CCK8//FISH//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//IF	 LncRNA PIK3CD-AS1 was downregulated in HCC tissues and cells, and mainly located in cytoplasm.Collectively, our study suggests that the expression of PIK3CD-AS1 was down-regulated in HCC, and overexpression of PIK3CD-AS1 promoted the expression of LATS1 by competitive binding of miR-566 to inhibit the growth, invasion and metastasis of HCC cells.		Yes	Overexpression of PIK3CD-AS1 inhibited proliferation, colony formation, invasion, migration, epithelial-mesenchymal transition (EMT) and cell cycle progression and promoted apoptosis of HCC cells. Overexpression of PIK3CD-AS1 decreased the growth rate and weight of xenograft tumor in nude mice PIK3CD-AS1 competitively combined with miR-566 to regulate expression of LAST1.	31624469
circCLK3	CircRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues and cell lines	Interaction(miR-455-5p/PARVA axis)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//EdU Staining//Transwell Assay	 In the present study, our findings revealed the upregulated expression of circCLK3 in TSCC tissues and cell lines.Moreover, circCLK3 acted as a molecular sponge for miR-455-5p. PARVA was the target gene of miR-455-5p. Furthermore, the negative correlation between expression of miR-455-5p and circCLK3 or PARVA in TSCC tissues was discovered. Rescue assays indicated that PARVA overexpression reversed the circCLK3 knockdown-mediated inhibitory effects on the progression of TSCC.		Yes	CircCLK3 knockdown suppressed cell proliferation, migration invasion, and induced cell cycle arrest at G0/G1 phase in TSCC.	33655541
PICSAR	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cells	regulation[PI3K/AKT/mTOR signaling pathway]	IHC//Western Blot//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	 In the present study, we found that PICSAR was upregulated in HCC tissues and cells and correlated with progression and poor prognosis in HCC patients.PICSAR played an oncogenic role by targeting miR-588 and subsequently promoted EIF6 expression and PI3K/AKT/mTOR activation in HCC. 	 In the present study, we found that PICSAR was upregulated in HCC tissues and cells and correlated with progression and poor prognosis in HCC patients.	Yes	Gain- and loss-of-function experiments indicated that PICSAR enhanced cell proliferation, colony formation, and cell cycle progression and inhibited apoptosis of HCC cells. 	32860321
PICSAR	LncRNA	Homo sapiens	Urinary Bladder Neoplasms	bladder cancer cells and tissues	interaction[binding THRAP3]	Flow Cytometry//qRT-PCR//RNA Pull-Down//RIP	Here, we reported that LINC00162, a super-enhancer long noncoding RNA, was highly expressed in bladder cancer cells and tissues.Finally, we demonstrated a mechanism that LINC00162 could regulate PTTG1IP expression through binding THRAP3.		Yes	 Knocking down LINC00162 expression can inhibit the proliferative activity of bladder cancer cells and the growth of transplanted tumors in vivo, while knocking down the expression of PTTG1IP could restore the proliferative activity of bladder cancer cells. 	33344916
PICSAR	LncRNA	Homo sapiens	Skin Neoplasms	CSCC tissues and cells	regulation[miR-125b/YAP1 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Transwell Assay	PICSAR was upregulated in CSCC tissues and cells.PICSAR knockdown suppressed cell proliferation and invasion and promoted apoptosis in CSCC cells by regulating miR-125b/YAP1 axis, providing new sights for treatment of CSCC.		Yes	PICSAR knockdown inhibited cell proliferation and invasion and induced apoptosis in CSCC cells.	32841663
PINK1-AS	LncRNA	Homo sapiens	Stomach Neoplasms	 human GC	Interaction(microRNA-200a)	In Vivo Experiment//ISH//FISH//Luciferase Report Assay//IHC	The expression of miR-200a was downregulated in human GC, correlating with upregulation of a novel miR-200a-targeting long non-coding RNA (LncRNA), PINK1 (PTEN Induced Kinase 1)-AS.RNA immunoprecipitation, RNA-pull down, and RNA fluorescence in situ hybridization assays confirmed that PINK1-AS directly binds to miR-200a. 		Yes	Silencing PINK1-AS in GC cells led to miR-200a accumulation, Gαi1 downregulation, and inhibition of GC cell progression in vitro, whereas PINK1-AS upregulation produced the converse results. Significantly, anti-GC cell activity induced by PINK1-AS shRNA was ameliorated by the expression of miR-200a antisense or the 3'-UTR (untranslated region)-depleted Gαi1. In vivo, the growth of subcutaneous MGC-803 xenografts in nude mice was inhibited by PINK1-AS shRNA, but accelerated by PINK1-AS overexpression. Patient-derived GC xenograft growth in nude mice was largely inhibited after intratumoral injection of PINK1-AS shRNA lentivirus.	33958720
PICART1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and normal tissues,cell lines (HGC27, BGC823, SGC7901, MGC803)	Regulation[PI3K/AKT and ERK/MAPK signaling pathways]	CCK8//qRT-PCR//Western Blot	 LncRNA-PICART1 was lowly expressed in both GC tissues and cell lines.The regulation of the PI3K/AKT and ERK/MAPK signaling pathways might be the underlying mechanism of the tumor suppressor role of lncRNA-PICART1.	 	Yes	lncRNA-PICART1 significantly suppressed cell proliferation, whereas promoted cell apoptosis. 	30720166
PICART1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell 	Regulation[AKT1 signaling pathway]	qRT-PCR//MTT//Western Blot	In addition, PICART1 expression was down-regulated in NSCLC cell lines.  These results suggested that overexpression of PICART1 suppressed cell growth and invasion partly through regulating AKT signaling pathway in NSCLC.		Yes	Overexpression of PICART1 inhibited NSCLC cell growth and induced cell cycle arrest at G2/M phase. Elevated expression of PICART1 suppressed NSCLC cell colony formation and cell invasion.	30662662
PICART1	LncRNA	Homo sapiens	Lung Neoplasms	 lung cancer tissues and cell lines	Regulation[ JAK2/STAT3 signaling]	Flow Cytometry//qRT-PCR//MTT//Transwell Assay	PICART1 expression was down-regulated in human lung cancer tissues and cell lines. Additionally, PICART1 acts as a tumor suppressor may be via regulation of JAK2/STAT3 pathway.		Yes	Knockdown of PICART1 increased cell viability of lung cancer cell lines.	29940776
PICART1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	CC tissues and cell lines	regulation[upregulating TCF21]	qRT-PCR//RIP//ChIP	PICART1 was downregulated in CC tissues and cell lines.lncRNA PICART1 recruits ARID1A to activate TCF21 expression, thus alleviating the malignant progression of CC.	CC patients with worse TNM staging and larger tumor size presented lower level of PICART1. Low level of PICART1 in CC patients predicted a worse prognosis. 	Yes	Silence of PICART1 stimulated the proliferative, migratory and invasive abilities of HeLa and SiHa cells. 	32382324
PHAROH	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma and mouse embryonic stem cells	Regulation(TIAR)	qRT-PCR	 We identified a long non-coding RNA, Gm19705, that is overexpressed in hepatocellular carcinoma and mouse embryonic stem cells. RNA-seq analysis of PHAROH knockouts revealed that a large number of genes with decreased expression contain a Myc motif in their promoter. 		Yes	We named this RNA Pluripotency and Hepatocyte Associated RNA Overexpressed in HCC, or PHAROH. Depletion of PHAROH impacts cell proliferation and migration, which can be rescued by ectopic expression of PHAROH. 	34002693
PHACTR2-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[ERK- and AKT/GSK-3β-Signaling Pathways]	RNA Pull-Down//Western Blot//Wound Healing Assay//Migration Assay//qRT-PCR//FISH//RIP//MTT//Cell Cycle Assay//Colony Formation Assay//Invasion Assay//Transwell Assay	 lncIHS was overexpressed in HCC and decreased the survival rate of HCC patients.Moreover, results from transcriptome-sequencing analysis and mass spectrometry showed that lncIHS regulated multiple genes that were the upstream molecules of the ERK- and AKT-signaling pathways.	 lncIHS was overexpressed in HCC and decreased the survival rate of HCC patients.	Yes	 Knockdown of lncIHS inhibited HCC cell migration, invasion, and proliferation, and vice versa.	31128422
PHACTR2-AS1	LncRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC tissues	Expression[highly expressed]	qRT-PCR	 In the present study, we investigated the biological role of PHACTR2-AS1 in tongue squamous cell carcinoma (TSCC). PHACTR2-AS1 was preferentially localized in the cytoplasm, and was notably upregulated in TSCC tissues. 	 High PHACTR2-AS1 was correlated with tumour differentiation, metastatic clinical features, relapse and shortened survival time.	Yes	Depletion of PHACTR2-AS1 did not affect TSCC cell viability and colony formation ability, whereas substantially inhibited cell migration and invasion in vitro and lung metastasis in vivo. 	32702100
hsa_circ_0002162	CircRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC cell lines & SCC-9 cells	Interaction(miR-33a-5p)	Transfection//qRT-PCR//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay	Hsa_circ_0002162 expression was increased in human TSCC cell lines SCC-9, CAL-27, HSC-4, and SCC-25 compared with HOK. In CAL-27 cells, hsa_circ_0002162 knockdown inhibited cell proliferation and invasion and promoted apoptosis. In SCC-9 cells, hsa_circ_0002162 overexpression enhanced cell proliferation and invasion and suppressed apoptosis. Furthermore, a negative regulation of hsa_circ_0002162 on miR-33a-5p (but not miR-302b-5p and miR-545-5p) was observed. In the rescue experiment, miR-33a-5p knockdown increased cell proliferation and invasion, and decreased apoptosis in hsa_circ_0002162 knockdown-treated CAL-27 cells, whereas miR-33a-5p overexpression decreased cell proliferation and invasion, but increased apoptosis in hsa_circ_0002162 overexpression-treated SCC-9 cells. The luciferase reporter assay showed the direct binding of hsa_circ_0002162 to miR-33a-5p.		Yes	In CAL-27 cells, hsa_circ_0002162 knockdown inhibited cell proliferation and invasion and promoted apoptosis. In SCC-9 cells, hsa_circ_0002162 overexpression enhanced cell proliferation and invasion and suppressed apoptosis. Furthermore, a negative regulation of hsa_circ_0002162 on miR-33a-5p (but not miR-302b-5p and miR-545-5p) was observed.	33729388
PINT87aa	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC cell 	Interaction(FOXM1/PHB2)	qRT-PCR	PINT87aa was significantly increased in the hydrogen peroxide-induced HCC cell senescence model.  In contrast, FOXM1 gain-of-function could partially reduce the proportion of senescent HCC cells and enhance mitophagy. PINT87aa overexpression did not affect the expression of FOXM1 itself but reduced that of its target genes involved in cell cycle and proliferation, especially PHB2, which was involved in mitophagy and transcribed by FOXM1. Structural analysis indicated that PINT87aa could bind to the DNA-binding domain of FOXM1, which was confirmed by co-immunoprecipitation and immunofluorescence co-localization. 		Yes	Overexpression of PINT87aa induced growth inhibition, cellular senescence, and decreased mitophagy in vitro and in vivo.	33754036
PLACT1	LncRNA	Homo sapiens	Pancreatic Neoplasms	tumor tissues 	regulation[NF-κB signaling pathway]	ISH//qRT-PCR	 We identified a novel lncRNA-PLACT1, which was significantly upregulated in tumor tissues and correlated with progression and poor survival in PDAC patients.Our findings suggest that PLACT1 provides a novel epigenetic mechanism involved in constitutive activation of NF-κB signaling pathway and may represent a new therapeutic target of PDAC.	 We identified a novel lncRNA-PLACT1, which was significantly upregulated in tumor tissues and correlated with progression and poor survival in PDAC patients.	Yes	Moreover, PLACT1 promoted the proliferation and invasion of PDAC cells in vitro.	32085715
PITPNA-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues	Interaction(miR-92a-3p)	In Vivo Experiment//Western Blot//Wound Healing Assay//CCK8//Flow Cytometry//Transwell Assay	The results of high throughput chip analysis identified that PITPNA-AS1 was up-regulated in GC tissues. Meanwhile, PITPNA-AS1 could regulate SOX4 expression via targeting miR-92a-3p.		Yes	 Our data revealed that knockdown of PITPNA-AS1 was able to inhibit tumor development of GC cells. Meanwhile, PITPNA-AS1 could regulate SOX4 expression via targeting miR-92a-3p.	34496348
PLAC45	LncRNA	Homo sapiens	Stomach Neoplasms	gastric tissues,GC cells	regulation[down-regulating C-Myc]	Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//Transwell Assay	The expression level of PLAC2 was downregulated in 38 out of 45 cases of GC tissues compared with that in normal gastric tissues, and it also declined in GC cells.  LncRNA PLAC2 affects the biological behaviors of GC cells by regulating the expression of c-Myc gene.		Yes	The results of flow cytometry showed that after overexpression of PLAC2, the cell cycle was arrested in the G1/G0 phase, and the apoptosis rate was increased.	33336736
PLA2G2C	LncRNA	Homo sapiens	Colonic Neoplasms	COAD tissues	Interaction(miR-515-5p/SLIT3 axis)	In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//migration assay//Luciferase Report Assay//Cell Proliferation Assay	 The results showed that UBXN10-AS1 and SLIT3 were expressed at low levels in COAD tissues, while miR-515-5p was expressed at high levels.  The luciferase reporter and RNA RIP assays demonstrated that UBXN10-AS1 targeted miR-515-5p, which in turn targeted SLIT3. Functionally, miR-515-5p overexpression reversed the inhibition of COAD cell proliferation and migration by UBXN10-AS1 overexpression, and SLIT3 overexpression counteracted the oncogenicity of miR-515-5p. 		Yes	 UBXN10-AS1 overexpression suppressed tumor growth in vitro and in vivo.	35034539
hsa_circ_0091579	CircRNA	Homo sapiens	Liver Neoplasms	 LCa tissues,cell lines	Interaction[regulating microRNA-490-3p ]	CCK8//qPCR//Luciferase Report Assay//Transwell Assay	circ_0091579 was highly expressed in HCC and HCC cells. Bioinformatics software predicted the binding sites between circ_0091579 and microRNA-490-3p, and dual-luciferase reporter gene assay confirmed the binding relationship between circ_0091579 and microRNA-490-3p. qPCR results showed that microRNA-490-3p was remarkably down-regulated in LCa tissues. In vitro experiments confirmed that overexpression of microRNA-490-3p inhibited the proliferative ability and metastasis of HCC cells.		Yes	In vitro experiments showed that down-regulation of circ_0091579 expression could remarkably inhibit the proliferative ability and metastasis of HCC cells. 	31841181
hsa_circ_100395	CircRNA	Homo sapiens	Liver Neoplasms	Liver Cancer tissues	Interaction[miR-1228]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Transwell Assay	 We found that circ_100395 was Expression[down-expression]regulated in cancerous liver tissues relative to the adjacent normal tissues.	The overexpression of circ_100395 was negatively associated with tumor differentiation, microvascular invasion, and portal vein tumor thrombosis. Moreover, Expression[Expression[up-expression]-expression]regulation of circ_100395 in liver cancer cells inhibited cell proliferation, induced apoptosis, then silenced the EMT pathway and reduced migration and invasion abilities, while this anti-tumor effect was significantly reversed by the Expression[down-expression]stream target, miR-1228. 	Yes	The FACS showed that the numbers of apoptotic cells significantly increased after overexpression of circ_10039 in Huh7 and HepG2 cell lines (Figure 2F, 2G). The above experiments indicate that circ_10039 exerts an anti-growth effect in liver cancer cell lines.	31421050
hsa_circ_0000231	CircRNA	Homo sapiens	tongue squamous cell carcinoma	TSCC patients and cell lines CAL-27, Tca-8113 and HN-4	Regulation(Wnt/β-catenin signaling pathway)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay//Transwell Assay	hsa_circ_0000231 was highly expressed in the tissue and saliva samples of TSCC patients and cell lines CAL-27, Tca-8113 and HN-4, but lowly expressed in paired para-carcinoma tissues, saliva samples of healthy people and normal human oral keratinocytes (all P<0.05). 	Log-rank univariate analysis showed that hsa_circ_0000231 expression level, tumor differentiation degree and T stage were related to the survival of TSCC patients (all P<0.05).	Yes	The knockdown of hsa_circ_0000231 reduced the proliferation, invasion and metastasis abilities of CAL-27 and Tca-8113 cells, which were reversed after TSCC cells were co-cultured with LiCl. The growth rate and volume of the tumors grafted subcutaneously in interference group using LiCl were greater than those in negative control group. 	36319130
hsa_circ_0081069	CircRNA	Homo sapiens	tongue squamous cell carcinoma	 TSCC tissues and cells	Interaction( miR-634/MAP2K4 axis)	In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay//Cell Cycle Assay//EdU Staining//Transwell Assay	Circ_0081069 was highly expressed in TSCC tissues and cells.  Mechanistically, circ_0081069 targeted miR-634 to negatively regulate miR-634 expression, and inhibition of miR-634 was able to weaken the inhibitory effect of circ_0081069 knockdown on proliferation, migration, and invasion of TSCC cells. MiR-634 targeted MAP2K4 and negatively regulated MAP2K4 expression, and overexpression of miR-634 inhibited TSCC cell proliferation, migration, and invasion, while co-overexpression of MAP2K4 was able to reverse the effects of miR-634 in TSCC cells.		Yes	 Silencing of circ_0081069 inhibited cell proliferation, cell cycle progress, cell migration and invasion in vitro, as well as hindered tumor growth in vivo.	36181561
PITX1	LncRNA	Homo sapiens	Melanoma	melanoma cells	Regulation	In Vivo Experiment//Western Blot//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//ChIP	Overexpression of PITX1 in melanoma cell lines resulted in a reduction in cell proliferation and an increase in apoptosis. Additionally, analysis of protein levels revealed an antagonistic cross-regulation between SOX9 and SOX10. Interestingly, PITX1 binds to the SOX9 promoter region as a positive regulatory transcription factor; PITX1 mRNA expression levels were positively correlated with SOX9 expression, and negatively correlated with SOX10 expression in melanoma tissues. Furthermore, transcription of the long noncoding RNA (lncRNA), survival-associated mitochondrial melanoma-specific oncogenic noncoding RNA (SAMMSON), was decreased in PITX1-overexpressing cells. 		Yes	Overexpression of PITX1 in melanoma cell lines resulted in a reduction in cell proliferation and an increase in apoptosis. 	34526609
PITPNA-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(microRNA-32-5p)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results demonstrated that PITPNA-AS1 was highly expressed in NSCLC tissues and cell lines. The luciferase reporter assay confirmed that miR-32-5p was a direct target of PITPNA-AS1. The rescue experiments suggested that a miR-32-5p inhibitor significantly reversed the inhibitory effects of PITPNA-AS1 silencing on proliferation, invasion, migration and EMT in NSCLC cells. 		Yes	 It was found that PITPNA-AS1 silencing inhibited the proliferation, invasion and migration of NSCLC cells. Furthermore, the protein expression of E-cadherin was upregulated, while the expression levels N-cadherin and vimentin were downregulated. 	33495838
PIP5K1A	CircRNA	Homo sapiens	Glioma	 glioma tissues	Interaction(miR-515-5p/TCF12/PI3K/AKT pathway)	RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//RIP//IF//PCR//BrdU//IP//Transwell Assay	The results manifested that CircPIP5K1A was upregulated in glioma tissues (compared with that in normal adjacent tissues), and overexpressed CircPIP5K1A was related to glioma volume and histopathological grade.  Besides, CircPIP5K1A upregulated TCF12 and PI3K/AKT activation. Bioinformatics analysis testified that miR-515-5p was a common target of CircPIP5K1A and TCF12, while the dual-luciferase reporter assay and RNA immunoprecipitation (RIP) experiment further confirmed that CircPIP5K1A targeted miR-515-5p, which bound the 3'-untranslated region (UTR) of TCF12.		Yes	 Functionally, overexpressing CircPIP5K1A notably elevated glioma cell proliferation, invasion, and EMT and inhibited apoptosis both in vivo and in vitro. 	33413401
PITPNA-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	CRC tissues and cell lines	regulation[miR-129-5p/ HMGB1 Axis]	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining	PITPNA-AS1 and HMGB1 mRNA expressions were observably elevated in CRC tissues and cell lines. PITPNA-AS1 can expedite CRC cell proliferation and migration, and inhibit apoptosis through miR-129-5p/HMGB1 axis.		Yes	Knocking down PITPNA-AS1 could significantly inhibit cell proliferation and migration, and promote apoptosis of CRC cells. 	33312000
PITPNA-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues	Regulation[PITPNA-AS1/miR-876-5p/WNT5A axis]	RNA Pull-Down//Northern Blot//Western Blot//Wound Healing Assay//Tunel//CCK8//qRT-PCR//FISH//IF//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	Firstly, PITPNA-AS1 was observed to be heightened in HCC tissues.Moreover, mechanism experiments validated that PITPNA-AS1 modulated WNT5A expression by targeting miR-876-5p. Rescue experiments affirmed that WNT5A silencing rescued the miR-876-5p suppression-induced cellular processes in PITPNA-AS1-silenced Hep3B cells. And in vivo experiments determined that PITPNA-AS1 regulated HCC progression in vivo via miR-876-5p/WNT5A pathway. 		Yes	Then function assays proved that overexpressing or silencing PITPNA-AS1 could manipulate the proliferation and motility of HCC cells. 	31700026
PITPNA-AS1	LncRNA	Homo sapiens	Uterine Cervical Neoplasms	 cervical cancer tissues and cell lines	regulation[miR-876-5p/c-MET axis]	qRT-PCR	In the study, we found that PITPNA-AS1 was markedly increased in human cervical cancer tissues and cell lines. PITPNA-AS1 meditated the effects of c-MET on the proliferation, apoptosis and cell cycle in cervical cancer cells by adsorbing miR-876-5p. 		Yes	PITPNA-AS1 over-expression elevated the proliferation of cervical cancer cells, whereas PITPNA-AS1 knockdown reduced the cell proliferation.	32460193
PITPNA-AS1	LncRNA	Homo sapiens	Triple Negative Breast Neoplasms	TNBC tissues and cells	Interaction(miR-520d-5p and DDX54)	In Vivo Experiment//RNA Pull-Down//IHC//ChIP//Western Blot//Transfection//Wound Healing Assay//CCK8//qRT-PCR//FISH//Flow Cytometry//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	PITPNA-AS1 showed high expression levels in TNBC tissues and cells.  Mechanistically, PITPNA-AS1 upregulated SIK2 expression by sponging miR-520d-5p and recruiting DDX54 protein. Results of rescue assays suggested that the inhibitive effects of silenced PITPNA-AS1 on TNBC cellular processes were partially rescued by overexpressing SIK2 or combination of miR-520d-5p inhibition and DDX54 overexpression. More importantly, we found that the upregulation of PITPNA-AS1 in TNBC cells was attributed to transcription factor MYBL2.		Yes	PITPNA-AS1 knockdown suppressed TNBC cell viability, proliferation, migration, invasion in vitro and inhibited xenograft tumor growth in mice. 	34353336
PITPNA-AS1	LncRNA	Homo sapiens	Glioblastoma	glioblastoma tissues	Interaction(miR-223-3p/EGFR axis/PI3K/AKT signaling pathway)	RNA Pull-Down//Western Blot//Transfection//qRT-PCR//FISH//RIP//Luciferase Report Assay//Colony Formation Assay//EdU Staining	Firstly, RT-qPCR examined that PITPNA-AS1 was highly expressed in glioblastoma. After confirming that PITPNA-AS1 mainly existed in cell cytoplasm, we conducted mechanism assays which disclosed that PITPNA-AS1 sequestered microRNA-223-3p (miR-223-3p) and modulated epidermal growth factor receptor (EGFR) expression, thereby participating in the activation of PI3K/AKT signaling pathway. 		Yes	The results demonstrated that depletion of PITPNA-AS1 inhibited the proliferation and promoted the apoptosis of glioblastoma cells. 	34470587
PITPNA-AS1	LncRNA	Homo sapiens	Thyroid Cancer, Papillary	papillary thyroid cancer tissues and cell lines	Interaction( miR-129-5p/UNC5B axis)	Western Blot//Transfection//Wound Healing Assay//Flow Cytometry//qRT-PCR//Luciferase Report Assay//EdU Staining	PITPNA-AS1 and UNC5B expressions were markedly increased in papillary thyroid cancer tissues and cell lines while miR-129-5p expression was down-regulated. PITPNA-AS1 targeted miR-129-5p to repress its expression and miR-129-5p targeted UNC5B to repress its expression. Silencing PITPNA-AS1 reduced the expression of UNC5B via regulating miR-129-5p expression.		Yes	Knockdown of PITPNA-AS1 could significantly inhibit papillary thyroid cancer cell growth and migration and promote cell apoptosis while UNC5B overexpression plasmids or miR-129-5p inhibitors counteracted the knockdown effect of PITPNA-AS1 on papillary thyroid cancer cells. 	33706585
PITPNA-AS1	LncRNA	Homo sapiens	lung squamous cell carcinoma	LUSC samples,LUSC cells	regulation[stabilizing HMGB3 by TAF15]	RNA Pull-Down//Western Blot//Tunel//Flow Cytometry//qRT-PCR//FISH//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Through online database GEPIA, lncRNA PITPNA antisense RNA 1 (PITPNA-AS1) was highly expressed in LUSC samples, and these tendency was further affirmed in LUSC cells. All in all, PITPNA-AS1 promoted the proliferation and migration of LUSC cells via stabilizing HMGB3 by TAF15. 		Yes	Functional experiments verified that depletion of PITPNA-AS1 hampered the proliferative and migratory abilities, but accelerated apoptosis of LUSC cells. 	32871048
PITPNA-AS1	LncRNA	Homo sapiens	lung squamous cell carcinoma	LUSC tissues and cells	Interaction(LncRNA PITPNA-AS1/miR-223-3p/PTN axis )	RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Luciferase Report Assay// In Vivo Experiment//Colony Formation Assay//Transwell Assay	The lncRNA PITPNA-AS1 had increased expression in LUSC and was linked to a poor prognosis. This mechanistic investigation showed that PITPNA-AS1 absorbed miR-223-3p and that miR-223-3p targeted PTN. MiR-223-3p inhibition or PTN overexpression might reverse the inhibitory effects of PITPNA-AS1 suppression on LUSC progression, as demonstrated by rescue experiments. In addition, the PITPNA-AS1/miR-223-3p/PTN axis accelerated tumor development in vivo.	The lncRNA PITPNA-AS1 had increased expression in LUSC and was linked to a poor prognosis.	Yes	In LUSC, PITPNA-AS1 also enhanced cell proliferation, migration, invasion, and stemness.	35588441
PCAT6	LncRNA	Homo sapiens	Pituitary Neoplasms	PA tissues	Interaction(miR-139-3p/BRD4 axis)	In Vivo Experiment//IHC//Western Blot//Wound Healing Assay//Tunel//CCK8//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	PCAT6 and BRD4 were high-expressed but miR-139-3p was low-expressed in PA. Both the 3'-untranslated regions of PCAT6 and BRD4 mRNAs were demonstrated to contain a potential binding site for miR-139-3p. PCAT6 was positively correlated to BRD4, and miR-139-3p was negatively correlated to PCAT6 and BRD4. 		Yes	MiR-139-3p mimic, shPCAT6 and siBRD4 inhibited the viability, migration, invasion, and proliferation of PA cells while inducing apoptosis. MiR-139-3p mimic and shPCAT6 inhibited the cell cycle progression of PA cells, decreased the weight and volume of the xenotransplanted tumor, and reduced the levels of Bcl-2 and BRD4 while enhancing the levels of Bax, miR-139-3p, and Cleaved caspase-3. 	33407504
PCAT29	LncRNA	Homo sapiens	Neuroblastoma	NB tissues and cells	Interaction(miR-21 )	qRT-PCR	The results showed that PCAT29 was downregulated and miR-21 was upregulated in NB. MiR-21 was inversely correlated with PCAT29. RNA-RNA interaction prediction revealed that miR-21 might target PCAT29.MiR-21 overexpression reduced PCAT29 expression and increased NB cell proliferation, whereas PCAT29 overexpression inhibited NB cell proliferation. PCAT29 overexpression promoted NB cell apoptosis, while miR-21 overexpression inhibited NB cell apoptosis and attenuated PCAT29 overexpression-mediated NB cell apoptosis. 		Yes	MiR-21 overexpression reduced PCAT29 expression and increased NB cell proliferation, whereas PCAT29 overexpression inhibited NB cell proliferation. PCAT29 overexpression promoted NB cell apoptosis, while miR-21 overexpression inhibited NB cell apoptosis and attenuated PCAT29 overexpression-mediated NB cell apoptosis. 	36017911
circFLNA	CircRNA	Homo sapiens	bladder carcinoma	BCa tissues and cell lines	Interaction(miR-216a-3p/BTG2 axis)	RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	Our study confirmed that downregulated circFLNA and BTG2 expression and upregulated miR-216a-3p were found in both BCa tissues and cell lines. MiR-216a-3p was a target gene of circFLNA and could target BTG2. Further analysis finally demonstrated that circFLNA sponged miR-216a-3p and indirectly promoted BTG2 expression, ultimately regulating proliferation, migration, invasion and EMT of BCa cells. 		Yes	Meanwhile, upregulated circFLNA inhibited proliferation, invasion and migration, EMT and stemness of BCa cells.	34852712
OXP4-AS	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-3184-5p/EIF5A axis)	qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Western Blot	The results showed that FOXP4-AS1 was upregulated and miR-3184-5p was downregulated in NSCLC tissues and cell lines. FOXP4-AS1 could regulated the expression of EIF5A by binding to miR-3184-5p. Rescue experiments showed that downregulation of miR-3184-5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si-FOXP4-AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis.		Yes	Downregulation of FOXP4-AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro.  Moreover, knockdown of FOXP4-AS1 could efficiently inhibited tumor development of NSCLC in vivo.	34921595
circFOXM1	CircRNA	Homo sapiens	Melanoma	melanoma tissues and cells	regulation[miR-143-3p/FLOT2 axis]	Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Circ-FOXM1 was elevated and miR-143-3p was reduced in melanoma tissues and cells. Circ-FOXM1 facilitated the development of melanoma by upregulating FLOT2 through miR-143-3p.		Yes	Circ-FOXM1 deficiency impeded cell proliferation, invasion, and glycolysis and facilitated cell apoptosis in melanoma in vitro and tumorigenesis in vivo.	32183822
hsa_circ_0002770	CircRNA	Homo sapiens	Melanoma	Melanoma tissues 	interaction[targeting miR-331-3p]	RNA Pull-Down//Western Blot//Wound Healing Assay//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 In the present study, we identified a circular RNA, circ_0002770, which is produced from the well-known oncogene MDM2, and was sharply increased in melanoma and correlated with a poor prognosis. Mechanistically, circ_0002770 acted as a sponge of miR-331-3p and could indirectly regulate DUSP5 and TGFBR1. Inhibition of miR-331-3p reversed the inhibitory effect of si-circ_0002770 on melanoma cell proliferation and invasion. 		Yes	 Knockdown of circ_0002770 suppressed melanoma cell invasion, migration and proliferation. 	32327630
P5848	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	hepatocellular carcinoma tissues	Regulation[LncRNA P5848-ENO1 axis]	Western Blot//qRT-PCR//FISH//MTT//Luciferase Report Assay	We identified an LncRNA P5848, whose expression level was Expression[Expression[up-expression]-expression]-regulated in tumor samples from HCC patients after radiofrequency ablation.Mechanistically, we have found that ENO1 was the target of LncRNA P5848. LncRNA P5848 Expression[Expression[up-expression]-expression]-regulated the gene and protein expression level of ENO1, promoting tumor growth and cell survival. However, siRNA-mediated knockExpression[down-expression] of ENO1 counteracted the effects of LncRNA P5848 on cancer cell growth, cell survival, and migration. Taken together, LncRNA P5848 promotes HCC development by Expression[Expression[up-expression]-expression]-regulating ENO1, indicating that LncRNA P5848-ENO1 axis is a potential therapeutic target for the treatment of HCC.		Yes	As such, we speculated that LncRNA P5848 may play a role in tumor growth. Here we showed that LncRNA P5848, whose Expression[Expression[up-expression]-expression]-regulation can lead to HCC cancer cell proliferation and migration. In vitro and in vivo overexpression of LncRNA P5848 promoted cell growth, cell survival, and cell invasion, whereas LncRNA P5848 depletion exerts opposite effects.	30541900
hsa_circ_0020710	CircRNA	Homo sapiens	Melanoma	melanoma tissues	regulation[miR-370-3p/CXCL12 axis]	Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	Our findings indicated that circ_0020710 was generally overexpressed in melanoma tissues, and high level of circ_0020710 was positively correlated with malignant phenotype and poor prognosis of melanoma patients. Elevated circ_0020710 drives tumor progression via the miR-370-3p/CXCL12 axis, and circ_0020710 is a potential target for melanoma treatment.	Our findings indicated that circ_0020710 was generally overexpressed in melanoma tissues, and high level of circ_0020710 was positively correlated with malignant phenotype and poor prognosis of melanoma patients.	Yes	 Elevated circ_0020710 promoted melanoma cell proliferation, migration and invasion in vitro as well as tumor growth in vivo.	32381016
circHIPK3	CircRNA	Homo sapiens	Melanoma	melanoma tissues and cell lines	regulation[miR-215-5p/YY1 axis]	qRT-PCR//Luciferase Report Assay//RIP//Western Blot	CircHIPK3 expression was strikingly upregulated while miR-215-5p was downregulated in melanoma tissues and cell lines.Our study corroborated that circHIPK3 regulated melanoma cell behaviors via the miR-215-5p/YY1 axis, which might provide a novel insight for the treatment of melanoma patients.		Yes	Moreover, we confirmed that overexpression of circHIPK3 could facilitate cell proliferation and depress cell apoptosis in melanoma while overexpression of miR-215-5p exerted opposite effects.	32800940
p4516	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	Expression[highly expressed]	FISH//IHC//Western Blot//qRT-PCR	LncRNA p4516 was mainly localized in the nucleus of GC cells and p4516 tended to have higher expression levels in GC cells compared to the normal gastric mucosa-derived cells GES-1.		Yes	Functional analysis revealed that p4516 participated in the regulation of GC cell proliferation, invasion and migration both in vivo and in vitro.	31354346
hsa_circ_0001591	CircRNA	Homo sapiens	Melanoma	blood	regulation[ROCK1/PI3K/AKT signal pathway,miR-431-5p]	qRT-PCR//MTT	The expression of circ 0001591 in serum of patients with melanoma was increased. Our findings demonstrated that circ 0001591 inhibits the progression of human melanoma through ROCK1/PI3K/AKT signal pathway by targeting ROCK1 by miR-431-5p.		Yes	Up-regulation of circ 0001591 promoted cell growth and cell invasion, and reduced apoptotic rate of melanoma. Down-regulation of circ 0001591 reduced cell growth and cell invasion, and promoted apoptotic rate of melanoma.	32830578
hsa_circ_0079593	CircRNA	Homo sapiens	Melanoma	melanoma tumor tissues	regulation[miR-516b/GRM3 axis]	RNA Pull-Down//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	Our results discovered that circ_0079593 was highly expressed in melanoma,Our study concluded that circ_0079593 accelerated melanoma progression via upregulating GRM3 by sponging miR-516b, which suggested that circ_0079593 had the potential to be a new therapeutic biomarker for melanoma.		Yes	Our results discovered that circ_0079593 was highly expressed in melanoma, and its silencing suppressed melanoma cell proliferation, migration, invasion, glucose metabolism and promoted apoptosis. 	32839935
OXCT1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cell lines	Interaction(miR-195/CCNE1 axis)	qRT-PCR//Colony Formation Assay//Luciferase Report Assay//Western Blot	 LncRNA OXCT1-AS1 was highly expressed and miR-195 was lowly expressed in NSCLC tissues and cell lines. LncBase predicted v.2.0 reported a high-scoring binding between OXCT1-AS1 and miR-195. The luciferase reporter assay defined the regulatory relationship between OXTC1-AS1 and miR-195.Furthermore, according to the results of the dual-luciferase activity assay, miR-195 targeted the 3' untranslated regions (3' UTRs) of CCNE1, validating that CCNE1 is a direct target of miR-195. Overexpression of CCNE1 restored the role of OXCR1-AS1 in NSCLC cells.		Yes	 In NSCLC cells, knockdown of OXCT1-AS1 significantly increased the expression of miR-195, decreased the proliferation and colony formation number of cancer cells, and reduced the expression of CCND1 and CCNE1. Meanwhile, overexpression of miR-195 significantly inhibited the cell proliferation and colony formation number, and reduced the expression of CCND1 and CCNE1.	35706791
PACERR	LncRNA	Homo sapiens	pancreatic ductal adenocarcinoma	TAMs	Interaction(miR-671-3p/KLF12/p-AKT/c-myc pathway)	In Vivo Experiment//qRT-PCR//Luciferase Report Assay//Western Blot	 LncRNA-PACERR was high expression in TAMs and associated with poor prognosis in PDAC patients.Mechanistically, LncRNA-PACERR activate KLF12/p-AKT/c-myc pathway by binding to miR-671-3p. And LncRNA-PACERR which bound to IGF2BP2 acts as an m6A-dependent manner to enhance the stability of KLF12 and c-myc in cytoplasm. In addition, the promoter of LncRNA-PACERR was a target of KLF12 and LncRNA-PACERR recruited EP300 to increase the acetylation of histone by interacting with KLF12 in nucleus.		Yes	 Our finding validated that LncRNA-PACERR increased the number of M2-polarized cells and facilized cell proliferation, invasion and migration in vitro and in vivo. 	35526050
OXCT1-AS1	LncRNA	Homo sapiens	Osteosarcoma	OS cells	Interaction(miR-886)	qRT-PCR//RNA Pull-Down	The expression of OXCT1-AS1 and miR-886 (mature and premature) in osteosarcoma and paired non-tumor tissues from 66 OS patients was negatively correlated. Overexpression and silencing assays showed that OXCT1-AS1 suppresses miR-886 maturation. RNA-RNA pulldown and subcellular fractionation assays demonstrated the direct interaction between OXCT1-AS1 and miR-886. 		Yes	BrdU proliferation assays revealed that OXCT1-AS1 promoted OS cell proliferation, and miR-886 reduced the enhancing effects of OXCT1-AS1 on OS cell proliferation. 	35191809
OXCT1-AS1	LncRNA	Homo sapiens	Glioblastoma	GBM tissue samples	Interaction(miR-195/CDC25A axis)	IHC//Western Blot//Transwell Assay//Transfection//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay//IF	In this study, it was found that the expression of lncRNA OXCT1-AS1 was upregulated in both The Cancer Genome Atlas (TCGA) GBM patients and GBM tissue samples, and high expression of OXCT1-AS1 predicted a poor prognosis. We further investigated the potential mechanism and found that OXCT1-AS1 may act as a ceRNA of miR-195 to enhance CDC25A expression and promote glioma cell progression. 	In this study, it was found that the expression of lncRNA OXCT1-AS1 was upregulated in both The Cancer Genome Atlas (TCGA) GBM patients and GBM tissue samples, and high expression of OXCT1-AS1 predicted a poor prognosis. 	Yes	Suppressing OXCT1-AS1 expression significantly decreased GBM cell proliferation and inhibited cell migration and invasion.Finally, knocking down OXCT1-AS1 notably attenuated the severity of glioma in vivo.	33832517
OXCT1-AS1	LncRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC cell lines	Regulation(LEF1)	In Vivo Experiment//RNA Pull-Down//Western Blot//qRT-PCR//RIP//Cell Proliferation Assay//Transwell Assay	Results indicated that lncRNA OXCT1-AS1 expression was significantly increased in NSCLC cell lines. Mechanistically, through direct interaction, lncRNA OXCT1-AS1 maintained LEF1 stability by blocking NARF-mediated ubiquitination. Furthermore, LEF1 knockdown impaired invasion and migration of NSCLC in vitro and in vivo. 		Yes	 Functional analysis revealed that knockdown of lncRNA OXCT1-AS1 impaired invasion and migration in vitro.Additionally, the ability of lncRNA OXCT1-AS1 to promote NSCLC metastasis was also confirmed in vivo.	34337014
circRNF20	CircRNA	Homo sapiens	Retinoblastoma	RB tissues and cells	Interaction(miR-132-3p/PAX6 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Wound Healing Assay//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay//Colony Formation Assay//Transwell Assay	 It was found that ircRNF20 level was increased in RB tissues and linked to advanced tumor, nodes, metastases (TNM) stage and poor overall survival rate.  circRNF20 directly targeted miR-132-3p and miR-132-3p overexpression inhibited RB cell progression. PAX6 was the target gene of miR-132-3p. Moreover, miR-132-3p inhibition or PAX6 overexpression reversed circRNF20 deficiency-mediated effects on RB cell malignant behaviors. In addition, exosomal circRNF20 was able to promote RB cell progression. 	 It was found that ircRNF20 level was increased in RB tissues and linked to advanced tumor, nodes, metastases (TNM) stage and poor overall survival rate. 	Yes	Deficiency of circRNF20 suppressed cell proliferation, migration and invasion and induced apoptosis in vitro, as well as blocked tumor growth in vivo. 	35663593
OXCT1	CircRNA	Homo sapiens	Carcinoma, Non-Small-Cell Lung	NSCLC tissues and cells	Interaction(miR-516b-5p/SLC1A5)	Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay	Circ-OXCT1 and SLC1A5 were upregulated and miR-516b-5p was downregulated in NSCLC tissues and cells. Besides, miR-516b-5p was a target of circ-OXCT1, and miR-516b-5p inhibitor could relieve circ-OXCT1 absence-mediated effects in NSCLC cells. SLC1A5 was identified as a target of miR-516b-5p. Circ-OXCT1 promoted SLC1A5 expression by target binding with miR-516b-5p.Circ-OXCT1 facilitated NSCLC progression via miR-516b-5p-dependent regulation of SLC1A5, which provided a possible circRNA-targeted therapy for NSCLC.		Yes	Functional experiments revealed that circ-OXCT1 silencing suppressed cell proliferation, migration and invasion, but promoted cell apoptosis in vitro. Circ-OXCT1 knockdown repressed tumor formation in vivo. 	35482822
circCUL2	CircRNA	Homo sapiens	Retinoblastoma	retinoblastoma tumor tissues and cells	Interaction(miR-214-5p/E2F2 Axis)	Western Blot//Transfection//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	CircCUL2 and E2F2 were lowly expressed, while miR-214-5p was highly expressed in retinoblastoma tumor tissues and cells. CircCUL2 negatively regulated miR-214-5p, while miR-214-5p negatively regulated E2F2. Overexpression of miR-214-5p or silencing of E2F2 in SO-Rb50 cells partially reversed the inhibitory effect of circCUL2 on the proliferation, invasion and migration of retinoblastoma cells. CircCUL2 inhibited the proliferation, invasion and migration of retinoblastoma cells by regulating the miR-214-5p/E2F2 axis.		Yes	 Transfection with pcDNA3.1-CUL2 or miR-214-5p inhibitor inhibited the proliferation, invasion and migration of Y79 and SO-Rb50 cells compared with the negative control; while transfection with sh-CUL2 or miR-214-5p mimics promoted the proliferation, invasion and migration of Y79 and SO-Rb50 cells. 	34387590
OTUD6B-AS1	LncRNA	Homo sapiens	Colorectal Neoplasms	 CRC cells and tissues	Interaction(microRNA-3171)	Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay	The results demonstrated that OTUD6B-AS1 expression was low in CRC cells and tissues.Furthermore, miR-3171 was demonstrated to be a direct target of OTUD6B-AS1 using a luciferase reporter assay. The rescue assays revealed that miR-3171 mimics markedly reversed the inhibitory effects of OTUD6B-AS1 overexpression on proliferation, invasion and migration of CRC cells.		Yes	Overexpression of OTUD6B-AS1 inhibited the proliferation, invasion and migration of HCT116 cells. 	33574932
OTUD6B-AS1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	HCC tissues and cell lines	regulation[GSKIP/Wnt/β-catenin signalling]	qRT-PCR//Colony Formation Assay	We found that the expression of OTUD6B-AS1 was up-regulated in HCC tissues, and patients with high levels of OTUD6B-AS1 expression had shorter survival rates than those with low OTUD6B-AS1 expression. Overall, these findings indicate that the lncRNA OTUD6B-AS1 accelerates the proliferation and invasion of HCC cells by enhancing GSKIP/Wnt/β-catenin signalling via the sequestration of miR-664b-3p. 	We found that the expression of OTUD6B-AS1 was up-regulated in HCC tissues, and patients with high levels of OTUD6B-AS1 expression had shorter survival rates than those with low OTUD6B-AS1 expression.	Yes	Elevated expression of the lncRNA was also found in multiple HCC cell lines and the silencing of OTUD6B-AS1 significantly decreased proliferation, colony formation and invasion.	32682012
hsa_circ_0084043	CircRNA	Homo sapiens	Melanoma	melanoma tissues and cell lines	regulation[miR429/TRIB2 axis,Wnt/β-catenin signaling pathway]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay	Expression of circ_0084043 and TRIB2 was upregulated in human melanoma tissues and cell lines. Knockdown of circ_0084043 suppressed the malignant development of melanoma presumably through modulating miR429/TRIB2 axis and inactivating Wnt/β-catenin signaling pathway.		Yes	 Both circ_0084043 knockdown and TRIB2 silencing could decrease cell proliferation, migration and invasion, but facilitate apoptosis in A375 and SK-MEL-28 cells. 	31954160
PAGR1	LncRNA	Homo sapiens	Glioma	cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Transwell Assay//Western Blot	The expression of lncRNA GAS5 was significantly decreased in glioma cell lines U251 and U87 compared with normal glial cells HEB (p < 0.01). 		Yes	n addition, overexpression of lncRNA GAS5 inhibited the proliferation, migration and invasion of U251 and U87 cells, and promoted cell apoptosis as demonstrated by the increased activity of Caspase 3/7. 	31172354
OTUD6B-AS1	LncRNA	Homo sapiens	Carcinoma, Renal Cell	 ccRCC tissue	Regulation[Wnt/β-catenin signaling pathway]	IHC//Western Blot//Flow Cytometry//qRT-PCR//MTT//Colony Formation Assay//IF	In this study, we found that the expression of the lncRNA OTUD6B-AS1 was downregulated in ccRCC tissue samples.The overexpression of OTUD6B-AS1 decreased the activity of the Wnt/β-catenin pathway and suppressed the expression of epithelial-to-mesenchymal transition (EMT)-related proteins (E-cadherin, N-cadherin and Snail) in ccRCC cells.	 In this study, we found that the expression of the lncRNA OTUD6B-AS1 was downregulated in ccRCC tissue samples and that patients with low OTUD6B-AS1 expression had shorter overall survival than patients with high OTUD6B-AS1 expression, which showed that the different expression level of OTUD6B-AS1 indirectly correlated with survival of patients.	Yes	Furthermore, OTUD6B-AS1 overexpression partly inhibited cell migration and invasion.In addition, compared with the parental ACHN cells, OTUD6B-AS1-overexpressing ACHN cells injected into nude mice exhibited decreased tumor growth in vivo.	30670025
PANDAR	LncRNA	Homo sapiens	Glioma	glioma tissues and cell lines	Regulation(CDK4)	qRT-PCR	Here, we report that expression of PANDAR is significantly up-regulated in glioma tissues and cell lines. Furthermore, PANDAR knockdown suppressed cell proliferation, G1/S transition, migration and invasion, and promoted apoptosis in glioma cell lines (U251 and U87). PANDAR knockdown decreased expression of CDK4, Bcl-2, N-cadherin and Vimentin, but increased E-cadherin expression in glioma cells. 	 PANDAR expression was correlated with tumor size (p=0.044) and World Health Organization (WHO) grades (p=0.005), as shown by chi-squared test. Moreover, significant upregulation of PANDAR was found to correlate with poor prognosis in glioma, as shown using Kaplan-Meier method and Cox multivariate survival analysis.	Yes	Furthermore, PANDAR knockdown suppressed cell proliferation, G1/S transition, migration and invasion, and promoted apoptosis in glioma cell lines (U251 and U87). PANDAR knockdown decreased expression of CDK4, Bcl-2, N-cadherin and Vimentin, but increased E-cadherin expression in glioma cells. 	36073766
PAQR7	CircRNA	Homo sapiens	Osteoarthritis	OA tissues and cells	Interaction(miR-761/FBXO21 )	IP//Transfection//Western Blot//IF	 circRNA-MSR and FBXO21 levels were elevated in OA, but miR-761 level was inhibited.  Suppressing circRNA-MSR promoted the autophagy of LPS-treated cells. circRNA-MSR could bind to miR-761 and inhibit its expression. MiR-761 inhibition reversed the promoted autophagy caused by circRNA-MSR knockdown in LPS-treated C28/I2 cells. Moreover, miR-761 could target FBXO21 and inhibit its expression. FBXO21 overexpression reversed the increased autophagy caused by miR-761 overexpression in LPS-treated C28/I2 cells. 		Yes	 Suppressing circRNA-MSR promoted the autophagy of LPS-treated cells. 	36278814
hsa_circ_0001776	CircRNA	Homo sapiens	Endometrial Neoplasms	EC tissues and cells	regulation[miR-182/LRIG2 axis]	Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay	 Circ_0001776 and LRIG2 were downregulated, while miR-182 was upregulated in EC tissues and cells. Our results confirmed that circ_0001776 inhibited EC tumorigenesis and progression via miR-182/LRIG2 axis, providing a potential therapeutic target for EC.	 Low expression of circ_0001776 was correlated with the 5-year survival rate of EC patients.	Yes	 Upregulated circ_0001776 markedly attenuated cell proliferation and glycolysis, and enhanced cell apoptosis. 	32863771
PAPPA-AS1	LncRNA	Homo sapiens	Cicatrix, Hypertrophic	HTS tissues and hypertrophic scar fibroblast (HTsFb) cells	Interaction(TAF15/TLR4 )	In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Transfection//qRT-PCR//FISH//RIP//Luciferase Report Assay//H&E Staining//Cell Proliferation Assay//IF	 PAPPA-AS1 was significantly upregulated in both HTS tissues and hypertrophic scar fibroblast (HTsFb) cells.Positive correlation and interaction were observed between PAPPA-AS1 and TAF15 and between TAF15 and the promoter of TLR4, respectively. In conclusion, lncRNA PAPPA-AS1 might induce the development of HTS by upregulating TLR4 through interacting with TAF15.		Yes	By knocking down PAPPA-AS1, the proliferation of HTsFb cells, TLR4, and TGF-β1 signal pathway and the expression of fibrosis markers both in HTsFb cells and HTS tissues were suppressed. It was accompanied by the alleviated pathological state in the HTS tissues, which were significantly reversed by cotransfecting with the pcDNA3.1-TLR4 vector. 	34285657
PANTR1	LncRNA	Homo sapiens	Carcinoma, Hepatocellular	 HCC tumor tissues and HCC cell lines	Interaction(miR-587/BCL2A1 axis)	CCK8//qRT-PCR//RNA Pull-Down//FISH	Our study found that lncRNA PANTR1 was upregulated in HCC tumor tissues and abundantly expressed in HCC cell lines. PANTR1 acted as a competent sponge for miR-587 and downregulated miR-587 expression in HCC cells. Further, MiR-587 directly targets BCL2A1. lncRNA PANTR1 promotes HCC progression via mediating the miR-587-BCL2A1 axis. 		Yes	PANTR1 knockdown inhibited cell growth and migration, promoted cell apoptosis in vitro, and suppressed tumor cell growth in vivo. Moreover, our results suggest that downregulated PANTR1 inhibited the Warburg effect in HCC cells. 	34423048
PANDAR	LncRNA	Homo sapiens	Breast Neoplasms	breast cancer tissues	Interaction[EMT pathway]	Western Blot//CCK8//qRT-PCR//Colony Formation Assay//Invasion Assay	 We demonstrated that lncRNA PANDAR expression was higher in breast cancer tissues and cells compared with adjacent normal tissues and the normal mammary epithelial cell line, respectively.Furthermore, we verified that knockExpression[down-expression] of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by Expression[down-expression]regulating Vimentin, MMP2 and MMP9 expression, but Expression[Expression[up-expression]-expression]regulating E-cadherin expression in breast cancer.	Higher lncRNA PANDAR expression positively associated with lymph node metastasis and advanced clinical stage in patients. 	Yes	 In vitro, we demonstrated that knockExpression[down-expression] of lncRNA PANDAR significantly sExpression[Expression[up-expression]-expression]pressed cell proliferation, cell colony formation and cell invasion ability in breast cells.	31104011
PANDAR	LncRNA	Homo sapiens	Lung Neoplasms	lung cancer tissues and cell lines	Expression[lower expressed]	CCK8//qRT-PCR//Western Blot	PANDAR was found to downregulate both in lung cancer tissues and cell lines compared with corresponding controls (P < 0.05 for all), which was related to tumor stage (P < 0.05). 		Yes	So, the high expression of PANDAR increased BECN1 expression levels and impaired the proliferation of NSCLC cell lines in vitro.	32626525
PANDAR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC cells	Interaction(SRSF7/PIM1)	CCK8//qRT-PCR//RNA Pull-Down//Western Blot	First of all, PANDAR was highly expressed in OSCC cells and loss-of-function assays mediated by CRISPR-dCas9 observed that PANDAR silencing restrained cell proliferation and promoted cell apoptosis. Subsequently, serine/threonine-protein kinase pim-1 (PIM1) was proved to be regulated by PANDAR in SRSF7-dependant way. Rescue experiments validated that PANDAR modulated the proliferation and apoptosis in OSCC through PIM1.		Yes	First of all, PANDAR was highly expressed in OSCC cells and loss-of-function assays mediated by CRISPR-dCas9 observed that PANDAR silencing restrained cell proliferation and promoted cell apoptosis. 	33842552
PANDAR	LncRNA	Homo sapiens	Squamous Cell Carcinoma of Head and Neck	OSCC tissues and cell lines	Expression(highly expressed)	qRT-PCR//Invasion Assay//Migration Assay	 PANDAR was highly expressed in OSCC tissues and cell lines (P < 0.05) and its high expression level was found to be closely associated with advanced TNM stage (P = 0.004) and positive distant metastasis (P = 0.001). 	 PANDAR was highly expressed in OSCC tissues and cell lines (P < 0.05) and its high expression level was found to be closely associated with advanced TNM stage (P = 0.004) and positive distant metastasis (P = 0.001).  Furthermore, overall survival rate of OSCC patients with high PANDAR expression was poorer than patients with low PANDAR expression (P < 0.001). Cox proportional hazards model analysis showed that expression level of PANDAR can be used as an independent prognostic indicator for OSCC. 	Yes	Functionally, knockdown of PANDAR can inhibit proliferation, invasion, and migration of OSCC cells.	31938389
hsa_circ_0103232	CircRNA	Homo sapiens	Melanoma	 melanoma patients and cells	Interaction( miR-661/RAB3D)	In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//CCK8//FISH//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay	Hsa_circ_0103232 expression was increased in melanoma patients, indicating lower overall survival. Hsa_circ_0103232 functioned as a sponge of miR-661 to increase RAB3D expression. miR-661 overexpression partially reversed hsa_circ_0103232 promoting effect on melanoma cells viability, proliferation, migration, invasion, and EMT (P < 0.01). In melanoma patients, hsa_circ_0103232 expression was negatively correlated with miR-661 and positively correlated with RAB3D. 	Hsa_circ_0103232 expression was increased in melanoma patients, indicating lower overall survival.	Yes	Hsa_circ_0103232 was mainly expressed in the cytoplasm of melanoma cells. Silencing hsa_circ_0103232 suppressed melanoma cell viability, proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) (P < 0.01). Silencing hsa_circ_0103232 suppressed melanoma cell growth in vivo and Ki67 and RAB3D expression in xenograft tumors (P < 0.01). 	35549813
PAICC	LncRNA	Homo sapiens	Cholangiocarcinoma	human ICC tissues	Interaction( miR-141-3p and miR-27a-3p)	Bioinformatics Analysis	In the present work, we used bioinformatics analysis to identify the differentially expressed lncRNAs in human ICC tissues, among which lncRNA-PAICC was found to be an independent prognostic marker in ICC. Mechanistically, lncRNA-PAICC acted as a competitive endogenous RNA (ceRNA) that directly sponged the tumor suppressive microRNAs miR-141-3p and miR-27a-3p. The competitive binding property was essential for lncRNA-PAICC to promote tumor growth and metastasis through activating the Hippo pathway. 		Yes	Moreover, lncRNA-PAICC promoted the proliferation and invasion of ICC cells. 	33552968
circITCH	CircRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction(miR-660/TFCP2 pathway)	In Vivo Experiment//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay	Results revealed that circITCH expression was repressed in melanoma versus adjacent normal tissues.  The mechanism study showed that circITCH-sponged miR-660 to upregulate TFCP2 and suppress melanoma progression.		Yes	Function study showed that circITCH suppressed melanoma cell proliferation and metastasis. 	35274492
PANDAR	LncRNA	Homo sapiens	Thyroid Neoplasms	 thyroid gland carcinoma cells	Interaction(miR-637/KLK4)	In Vivo Experiment//Western Blot//Luciferase Report Assay//Transwell Assay	We identified Promoter Region of CDKN 1A antisense DNA damage-activated RNA (PANDAR), which was positively correlated with thyroid gland carcinoma risk.PANDAR negatively correlated with miR-637, and miR-637 overexpression suppressed thyroid gland carcinoma progression, which could be reversed by PANDAR. MiR-637 could target Kallikrein-related peptidases 4 (KLK4) to inhibit its expression, which was high in thyroid gland carcinoma.		Yes	PANDAR could promote thyroid gland carcinoma cell proliferation and metastasis. 	34476001
hsa_circ_0079593	CircRNA	Homo sapiens	Melanoma	melanoma tissue samples and cell lines	(microRNA-433 & EGFR)	CCK8//qRT-PCR//Luciferase Report Assay//Bioinformatics Analysis//Transwell Assay	It was found that, in comparison with the normal control group, circ-0079593 showed a significantly high expression in melanoma tissues and cell lines, which predicted a poor prognosis of melanoma patients. In vitro experiments showed that the overexpression of circ-0079593 remarkably enhanced proliferation rate, as well as invasion ability of melanoma cells. Moreover, bioinformatics data analysis revealed that there exist binding sites of microRNA-433 both in circ-0079593 and EGFR. Meanwhile, the results of the Luciferase assay confirmed that circ-0079593 probably bound to microRNA-433, as an endogenous competitive RNA (ceRNA), to regulate EGFR expression. At last, cell reverse experiments demonstrated that the overexpression of microRNA-433 could attenuate the capacity of melanoma cells to proliferate and migrate, while simultaneous overexpression of circ-0079593 partially restored those cell functions.	It was found that, in comparison with the normal control group, circ-0079593 showed a significantly high expression in melanoma tissues and cell lines, which predicted a poor prognosis of melanoma patients. 	Yes	In vitro experiments showed that the overexpression of circ-0079593 remarkably enhanced proliferation rate, as well as invasion ability of melanoma cells.	33577032
PANDAR	LncRNA	Homo sapiens	Esophageal Squamous Cell Carcinoma	ESCC tissues,cell lines	Regulation[ CyclinD1/2-Cyclin E1 and Bcl-2 pathways]	Western Blot//Flow Cytometry//qRT-PCR//RIP//MTT//Colony Formation Assay//EdU Staining	Quantitative real-time PCR (qRT-PCR) was carried out to detect the PANDA expression, which was up-regulated in matched cancerous tissues and adjacent noncancerous tissues from 134 patients and 9 ESCC cell lines.In addition, PANDA binds SAFA to switch on the tumor proliferation program through CyclinD1/2-Cyclin E1 and Bcl-2 pathways.	 Higher expression of PANDA in ESCC tissues was associated with TNM stage, advanced clinical stage, and shorter overall survival of ESCC patients by MTT, EDU, colony formation assay and flow cytometry in KYSE180 and KYSE450 cells.	Yes	Exogenous down-regulation of PANDA expression significantly suppressed ESCC cells proliferation and colony formation by arresting G1-S checkpoint transition in vitro, and retarded the development of tumors in vivo.	31495606
hsa_circ_0062270	CircRNA	Homo sapiens	Melanoma	melanoma tissues and cells	Interaction(miR-331-3p)	In Vivo Experiment//Western Blot//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//EdU Staining//Transwell Assay	The expression of circ_0062270 was increased in melanoma tissues and cells. 		Yes	Knockdown of circ_0062270 inhibited proliferation, promoted apoptosis, and repressed metastasis in melanoma. Moreover, circ_0062270 could serve as miR-331-3p sponge, and miR-331-3p could target EPHA2.	34454812
PAINT	LncRNA	Rattus norvegicus	Prostatic Neoplasms	cell lines	Expression(highly expressed)	In Vivo Experiment//qRT-PCR//Western Blot	Inhibition of PAINT decreased cell proliferation, S-phase progression, increased expression of apoptotic markers, and improved sensitivity to docetaxel and Aurora kinase inhibitor VX-680. Inhibition of PAINT decreased cell migration and reduced expression of Slug and Vimentin. Upregulation of PAINT was noted in advanced stage and metastatic PCa.	Upregulation of PAINT was noted in advanced stage and metastatic PCa.	Yes	Inhibition of PAINT decreased cell proliferation, S-phase progression, increased expression of apoptotic markers, and improved sensitivity to docetaxel and Aurora kinase inhibitor VX-680. Inhibition of PAINT decreased cell migration and reduced expression of Slug and Vimentin. Ectopic expression of PAINT suppressed E-cadherin, increased S-phase progression and cell migration. 	33729568
OTUD6B-AS1	LncRNA	Homo sapiens	Thyroid Neoplasms	thyroid carcinoma tissue	interaction[miR-183-5p and miR-21]	qRT-PCR//MTT//Luciferase Report Assay//Transwell Assay	 OTUD6B-AS1 was downregulated in thyroid carcinoma tissue samples. Taken together, our findings present in vitro evidence of lncRNA OTUD6B-AS1 as a tumor suppressor in thyroid carcinomas. OTUD6B-AS1 inhibits viability, migration, and invasion of thyroid carcinoma by targeting miR-183-5p and miR-21.	The expression of OTUD6B-AS1 correlated with tumor size, clinical stage, and lymphatic metastasis of thyroid carcinoma.	Yes	Overexpression of OTUD6B-AS1 significantly decreased the viability, migration, and invasion of thyroid carcinoma cells.	32256450
hsa_circ_0075804	CircRNA	Homo sapiens	Retinoblastoma	 RB tissues and cells	Interaction(MiR-1287-5p/LASP1)	In Vivo Experiment//IHC//Western Blot//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//EdU Staining//Transwell Assay	 Upregulation of circ_0075804 and LASP1, and downregulation of miR-1287-5p were shown in RB tissues and cells.MiR-1287-5p was targeted by circ_0075804, and its repression largely reversed the functional effects of circ_0075804 knockdown. LASP1 was a functional target of miR-1287-5p. The inhibition of miR-1287-5p upregulation on RB cell proliferation, survival and invasion was reversed by LASP1 overexpression. Moreover, circ_0075804 knockdown weakened LASP1 expression via increasing miR-1287-5p.		Yes	Circ_0075804 knockdown repressed RB cell growth, invasion and survival, and hindered tumor development in vivo. 	35285372
circPUM1	CircRNA	Homo sapiens	Endometrial Neoplasms	endometrial tissue	regulation[miR-136/NOTCH3 pathway]	Western Blot//Wound Healing Assay//qRT-PCR//MTT//Luciferase Report Assay//Cell Apoptosis Assay//Invasion Assay	Circ_PUM1 was expressed at significantly higher levels in endometrial cancer tissues than in normal tissues.Circ_PUM1 can compete with miR-136, leading to up-regulation of NOTCH3, and thereby promote the development of endometrial cancer.		Yes	Up-regulation of circ_PUM1 promoted the proliferation, migration and invasion of endometrial carcinoma cells. Opposite results were observed with circ_PUM1 knockdown, and the tumorigenic ability of endometrial cancer cells after circ_PUM1 knockdown was reduced compared to control cells.	32073729
OIP5-AS1	LncRNA	Homo sapiens	Stomach Neoplasms	GC tissues and cell lines	regulation[miR-367-3p/HMGA2 axis]	Western Blot//Flow Cytometry//qRT-PCR//Luciferase Report Assay//Colony Formation Assay	Here we demonstrate for the first time that OIP5-AS1 expression was up-regulated in GC tissues and cell lines, which significantly correlated with unfavorable clinical characteristics and shorter survival. OIP5-AS1 regulated the activities of the PI3K/AKT and Wnt/β-catenin pathways through HMGA2.	Here we demonstrate for the first time that OIP5-AS1 expression was up-regulated in GC tissues and cell lines, which significantly correlated with unfavorable clinical characteristics and shorter survival. 	Yes	The results of in vitro and in vivo gain- and loss-of-function experiments indicate that OIP5-AS1 promoted cell proliferation and colony formation while inhibiting apoptosis of GC cells.	31959478
OIS1	LncRNA	Homo sapiens	cervical squamous cell carcinoma	cervical squamous cell carcinoma tissues	Interaction[ upregulating MTK-1]	CCK8//qRT-PCR//Western Blot	It was established that a reduction in OIS1 expression level in tumor tissues was apparent only in HPV-positive patients. Serum levels of OIS1 were lower in HPV-positive patients compared with that in HPV-negative patients and healthy controls, and no significant differences were observed between HPV-negative patients and healthy controls.  OIS1 transfection also decreased the expression of MTK-1 in HPV-positive cancer cell lines, but not in any of the other cell lines. 		Yes	 OIS1 overexpression inhibited and MTK-1 overexpression promoted the proliferation of HPV-positive, but not HPV-negative cancer or normal cell lines.	30854069
OIP5‑AS1	LncRNA	Homo sapiens	Ovarian Neoplasms	OC tissues and cells	Interaction(miR‑128‑3p/CCNG1 axis)	In Vivo Experiment//RNA Pull-Down//Western Blot//Migration Assay//Flow Cytometry//qRT-PCR//RIP//MTT//Lucifer