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 | 5-FU | ||
| 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, Luciferase reporter assay, in vitro knockdown, etc. |
| Sample | HCC tissues, HCC cell lines (Hep3B, HuH7, SNU398, SNU423, SNU429, Hep3G2, SK-HEP-1, and PLC/PRF/5) |
| Expression Pattern | down-regulated |
| Function Description | SNHG16 levels were markedly downregulated in both HCC cell lines and HCC tissues. Lentivirus-mediated SNHG16 overexpression inhibited HCC cell proliferation, 5-FU chemoresistance, and in vivo tumor growth. Hsa-miR-93 was confirmed to be directly sponging on SNHG16. Its upregulation in HCC cells reversed SNHG16 overexpression and induced tumor-suppressing effects in HCC cells. |
| Pubmed ID | 30573973 |
| Year | 2018 |
| Title | Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93 |
External Links
| Links for SNHG16 | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |