Basic Information
| LncRNA/CircRNA Name | SNHG16 |
| Synonyms | NA |
| Region | GRCh38_17:76557766-76565348 |
| Ensemble | ENSG00000163597 |
| Refseq | NR_038108 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | |||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | hepatocellular carcinoma |
| ICD-0-3 | C22.0 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP |
| Sample | Human HCC cell lines (HepG2, SMMC7721, Hep3B, Bel7402, Huh7) and normal liver cell line (LO2), HCC and adjacent non-tumor liver tissues |
| Expression Pattern | up-regulated |
| Function Description | the expression level of SNHG16 in HCC tissues and cell lines was upregulated compared with adjacent noncancerous tissues and normal cells. In vitro, loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation and weakened invasion of SMMC7721 and HepG2 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. |
| Pubmed ID | 31306653 |
| Year | 2019 |
| Title | Long intergenic noncoding RNA SNHG16 interacts with miR-195 to promote proliferation, invasion and tumorigenesis in hepatocellular carcinoma |
External Links
| Links for SNHG16 | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |