Basic Information
| LncRNA/CircRNA Name | SNHG14 |
| Synonyms | NA |
| Region | GRCh38_15:24978583-25419462 |
| Ensemble | ENSG00000224078 |
| Refseq | NR_146177 |
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 | gastric cancer |
| ICD-0-3 | C16 |
| Methods | qPCR, Western blot, Luciferase reporter assay etc. |
| Sample | gastric cancer tissues, cell lines (BGC-823, SGC-7901, and HGC-27) |
| Expression Pattern | up-regulated |
| Function Description | LncRNA SNHG14 was markedly up-regulated in gastric cancer tissues and cells. Knockdown of SNHG14 significantly inhibited SGC-7901 cell viability, migration, invasion, and promoted cell apoptosis.In addition, miR-145 was negatively regulated by SNHG14 and the effects of SNHG14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis-related proteins and EMT-markers were reversed by inhibition of miR-145 at the same time. Furthermore, SOX9 was verified as a functional target of miR-145, and miR-145 regulated tumor malignant behaviors through regulating SOX9. Besides, knockdown of SNHG14 inhibited the expression of p-PI3K, p-AKT, and p-mTOR and promoted PTEN expression, where miR-145 inhibition had opposite effects. Moreover, the activated PI3K/AKT/mTOR pathway caused by miR-145 inhibition was counteracted after knockdown of SOX9. |
| Pubmed ID | 29667771 |
| Year | 2018 |
| Title | Long non-coding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis. |
External Links
| Links for SNHG14 | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |