Basic Information
| LncRNA/CircRNA Name | SNHG6 |
| Synonyms | NA |
| Region | GRCh38_8:66921684-66926398 |
| Ensemble | ENSG00000245910 |
| Refseq | NR_002599 |
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, RNAi, RIP |
| Sample | hepatocellular carcinoma tissues, cell lines(Huh7, HCC-LM3, SK-Hep-1, and Hep3B) |
| Expression Pattern | differential expression |
| Function Description | SNHG6 leads to genome-wide hypomethylation in hepatoma cells and that SNHG6 negatively correlates with the steady-state SAMe concentration in vivo and in vitro SNHG6 suppressed MAT1A protein expression by activating the miR-1297/FUS pathway to regulate nucleocytoplasmic shuttling of MAT1A mRNA. In addition, SNHG6 promoted expression of MAT2A by suppressing direct binding of miR-1297 to the MAT2A 3'UTR. SNHG6 regulated steady-state SAMe levels via coupling of two miR-1297-mediated SAMe-dependent positive feedback loops. Interestingly, the effect of SNHG6 on genome-wide methylation was inhibited by exogenous SAMe within a certain concentration range. These results suggest that single lncRNA dysregulation can lead to aberrant genome-wide hypomethylation by inhibiting SAMe production in HCC and that exogenous SAMe may be beneficial in the treatment of HCC. |
| Pubmed ID | 29844127 |
| Year | 2018 |
| Title | SNHG6 Acts as a Genome-Wide Hypomethylation Trigger via Coupling of miR-1297-Mediated S-Adenosylmethionine-Dependent Positive Feedback Loops |
External Links
| Links for SNHG6 | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |