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 | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | oral squamous cell carcinoma |
| ICD-0-3 | C06.9 |
| Methods | qPCR, Western blot, in vitro knockdown, etc. |
| Sample | OSCC tissues, SCC-25, CAL-27 cells and normal human oral keratinocyte (NHOK) |
| Expression Pattern | up-regulated |
| Function Description | c-Myc and SNHG16 were overexpressed in OSCC tissues and cell lines compared with normal tissues and normal human oral keratinocytes cells. There was a notable positive correlation between SNHG16 and c-Myc expression in OSCC tissues. c-Myc silencing by either shRNA c-Myc or by 10058-F4 (c-Myc inhibitor) resulted in a dose-dependent reduction in SNHG16 levels in CAL-27 and TSCCA cells; conversely, upregulation of c-Myc by pcDNA c-Myc markedly increased SNHG16 expression. Depletion of SNHG16 in CAL-27 cells strikingly inhibited cell proliferation, migration and invasion, as indicated by downregulation of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, depletion of SNHG16 induced cell apoptosis and inhibited epithelial-to-mesenchymal transition as indicated by induction of cleaved caspase-3 and epithelial cadherin (E-cadherin) along with reduction of N-cadherin and Snail. Intriguingly, c-Myc knockdown led to the similar functional effects as that of SNHG16 knockdown in TSCCA cells. However, these changes caused by c-Myc knockdown were abrogated by SNHG16 overexpression. Knockdown of SNHG16 conspicuously repressed tumor growth in nude mice. Similarly, silencing of c-Myc markedly inhibited tumor growth and reduced SNHG16 expression in nude mice. Moreover, overexpression of SNHG16 blocked the inhibitory effect of c-Myc silencing on tumor growth in vivo. Thus, we conclude that c-Myc-induced upregulation of SNHG16 enhances progression and carcinogenesis in OSCC. |
| Pubmed ID | 30607006 |
| Year | 2019 |
| Title | c-Myc induced upregulation of long non-coding RNA SNHG16 enhances progression and carcinogenesis in oral squamous cell carcinoma |
External Links
| Links for SNHG16 | GenBank HGNC NONCODE |
| Links for oral squamous cell carcinoma | OMIM COSMIC |