| [1] PubMed ID: | 30481748 |
| Disease Name: | Osteosarcoma |
| Sample: | osteosarcoma tissues |
| Dysfunction Pattern: | Regulation[PI3K-Akt Signaling Pathway] |
| Validated Method: | Wound Healing Assay//CCK8//qRT-PCR//Colony Formation Assay//Transwell Assay |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | Overexpression of MALAT1 promoted osteosarcoma cell proliferation, migration, and invasion in vitro and enhanced tumor growth in a tumor xenograft mouse model. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 30365098 |
| Disease Name: | Osteosarcoma |
| Sample: | OS tissues and cell lines |
| Dysfunction Pattern: | Regulation[miR‑34a/cyclin D1 axis] |
| Validated Method: | qRT-PCR//RIP//MTT//Luciferase Report Assay//Transwell Assay |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | In addition, MALAT1 promoted OS cell viability, invasion and migration, while MALAT1 silencing exhibited opposing effects. |
| Clinical-realted Application: | Additionally, MALAT1 expression was correlated with tumor size, clinical stage and distant metastasis in patients with OS. |
| [3] PubMed ID: | 30793707 |
| Disease Name: | Osteosarcoma |
| Sample: | osteosarcoma tissues and cell lines |
| Dysfunction Pattern: | Interaction[binding to miR-34a/c-5p and miR-449a/b] |
| Validated Method: | Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Luciferase Report Assay |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | Knockdown of MALAT1 inhibited proliferation, migration, and invasion of osteosarcoma cells. |
| Clinical-realted Application: | 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. |
| [4] PubMed ID: | 34692524 |
| Disease Name: | Osteosarcoma |
| Sample: | OS cell |
| Dysfunction Pattern: | Interaction(miR-150-5p/VEGFA signaling ) |
| Validated Method: | qRT-PCR//ELISA//Western Blot |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | 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. |
| Clinical-realted Application: | |
| [5] PubMed ID: | 33358903 |
| Disease Name: | Osteosarcoma |
| Sample: | OS tissues and cells |
| Dysfunction Pattern: | Interaction(miR-485-3p/AKT3/mTOR signalling) |
| Validated Method: | qRT-PCR//Western Blot |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | Knockdown MALAT1 or overexpression of miR-485-3p restrained OS tumour growth and lung metastasis in vivo. |
| Clinical-realted Application: | |
| [6] PubMed ID: | 34373692 |
| Disease Name: | Osteosarcoma |
| Sample: | OS cell lines and tissue specimens |
| Dysfunction Pattern: | Interaction(miR-124-3p/SphK1 signaling pathway ) |
| Validated Method: | CCK8//qRT-PCR |
| Description: | 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). |
| Causality: | Yes |
| Causal Description: | 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. |
| Clinical-realted Application: | |
| [7] PubMed ID: | 36277152 |
| Disease Name: | Osteosarcoma |
| Sample: | OS tissues and cell lines |
| Dysfunction Pattern: | Interaction(miR-590-3p) |
| Validated Method: | RNA Pull-Down//Western Blot//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Transwell Assay |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | 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. |
| Clinical-realted Application: | |
| [8] PubMed ID: | 32728178 |
| Disease Name: | Osteosarcoma |
| Sample: | osteosarcoma tissues |
| Dysfunction Pattern: | regulation[miR-202 ] |
| Validated Method: | qRT-PCR |
| Description: | Comparison of different lncRNAs in tumor samples from osteosarcoma with and without lung metastasis led to identification of MALAT1 as the most differentially upregulated lncRNA in the osteosarcoma patients with lung metastasis.In conclusion, MALAT1-miR-202 represents a potential lncRNA-miRNA signature that affects lung metastasis of osteosarcomas and could potentially be targeted for therapy. |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | |
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