Basic Information
LncRNA/CircRNA Name | SOX2OT |
Synonyms | SOX2-OT, NCRNA00043, SOX2OT |
Region | GRCh38_3:180989762-181836880 |
Ensemble | ENSG00000242808 |
Refseq | NR_004053 |
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 | gastric cancer |
ICD-0-3 | C16 |
Methods | qPCR, Luciferase reporter assay, Western blot etc. |
Sample | gastric cancer tissues, cell line (MGC-803, SGC-7901, MKN-28 and TMK-1) |
Expression Pattern | up-regulated |
Function Description | We observed that SOX2OT was overexpressed in GC tissues and cell lines. Overexpressed SOX2OT promoted cell proliferation and metastasis of GC cells (SGC-7901, TMK-1) and the phosphorylation of AKT2 as well, while knockdown of SOX2OT reversed these effects. Besides that, miR-194-5p was predicted to be a target of SOX2OT and decreased expression of miR-194-5p was observed in GC tissues and cell lines. Overexpressed miR-194-5p counteracted the promoting role of SOX2OT on cell proliferation and invasion of GC cells. Moreover, AKT2 was predicted to be a target of miR-194-5p. The expression of AKT2 was negatively regulated by miR-194-5p while positively regulated by SOX2OT. Overexpressed AKT2 also promoted GC cell proliferation and invasion. Our in vitro experiments suggested that SOX2OT promoted cell proliferation and metastasis of GC cells via sponging miR-194-5p from AKT2. Finally, our in vivo experiments indicated that overexpressed SOX2OT promoted GC tumor growth and metastasis in nude mice. |
Pubmed ID | 29782828 |
Year | 2018 |
Title | Long noncoding RNA SOX2OT contributes to gastric cancer progression by sponging miR-194-5p from AKT2. |
External Links
Links for SOX2OT | GenBank HGNC NONCODE |
Links for gastric cancer | OMIM COSMIC |