| [1] PubMed ID: | 33787057 |
| Disease Name: | Carcinoma, Renal Cell |
| Sample: | ccRCC tissues and cells |
| Dysfunction Pattern: | Interaction( miR-30a-3p) |
| Validated Method: | In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Luciferase Report Assay//IHC//EdU Staining//Transwell Assay |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | SNHG12 knockdown notably inhibited proliferation and migration of RCC cells. |
| Clinical-realted Application: | 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. |
| [2] PubMed ID: | 31824846 |
| Disease Name: | Carcinoma, Renal Cell |
| Sample: | ccRCC tissues and cell lines |
| Dysfunction Pattern: | Interaction[Sponging miR-129-5p] |
| Validated Method: | qRT-PCR//Luciferase Report Assay//RIP |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | Functional inhibition of SNHG12 suppressed the viability and mobility of ccRCC cells. |
| Clinical-realted Application: | |
| [3] PubMed ID: | 31114448 |
| Disease Name: | Carcinoma, Renal Cell |
| Sample: | renal tissue,cell lines |
| Dysfunction Pattern: | Interaction[HIF1α] |
| Validated Method: | Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Transwell Assay |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | 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. |
| Clinical-realted Application: | |
| [4] PubMed ID: | 32901847 |
| Disease Name: | Carcinoma, Renal Cell |
| Sample: | RCC tumor tissues |
| Dysfunction Pattern: | regulation[SNHG12/miR-200c-5p/COL11A1 axis ] |
| Validated Method: | qRT-PCR//Western Blot |
| Description: | 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.
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| Causality: | Yes |
| Causal Description: | SNHG12 knockdown markedly inhibited cell viability and invasion, while increasing apoptosis in both A498 and 786O cell lines. |
| Clinical-realted Application: | |
| [5] PubMed ID: | 35597996 |
| Disease Name: | Carcinoma, Renal Cell |
| Sample: | RCC tissues and cells |
| Dysfunction Pattern: | Regulation(CEP55 ) |
| Validated Method: | qRT-PCR//Luciferase Report Assay//Genotyping |
| Description: | 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. |
| Causality: | Yes |
| Causal Description: | SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. |
| Clinical-realted Application: | |
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