Basic Information
| LncRNA/CircRNA Name | DUXAP10 |
| Synonyms | PCAN-3 |
| Region | GRCh38_14:19294785-19337674 |
| Ensemble | NA |
| Refseq | NA |
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 | hepatocellular carcinoma |
| ICD-0-3 | C22.0 |
| Methods | qRT-PCR, Western blotting etc. |
| Sample | HCC specimens and corresponding neighbouring non-tumour samples, normal immortalized human hepatocyte LO2 cells and HCC cell lines (Hep3B, HepG2, Huh7, MHCC-97L and HCCLM3) |
| Expression Pattern | up-regulated |
| Function Description | MiR-1914 inhibition in HCC cell lines and tumour specimens correlates with tumour size and histological grade. MiR-1914 inhibited tumour proliferation and colony formation, resulting in cell cycle arrest and increased apoptosis. Moreover, miR-1914 mediated its functional effects by directly targeting GPR39 in HCC cells, leading to PI3K/AKT/mTOR repression. Restoring GPR39 expression incompletely counteracted the physiological roles of miR-1914 in HCC cells. In addition, down-regulation of AKT phosphorylation inhibited the effects of miR-1914 in HCC. Furthermore, the overexpression of lncRNA DUXAP10 negatively correlated with the expression of miR-1914 in HCC; thus, lncRNA DUXAP10 regulated miR-1914 expression and modulated the GPR39/PI3K/AKT-mediated cellular behaviours. |
| Pubmed ID | 31576658 |
| Year | 2019 |
| Title | microRNA-1914, Which Is Regulated by lncRNA DUXAP10, Inhibits Cell Proliferation by Targeting the GPR39-mediated PI3K/AKT/mTOR Pathway in HCC |
External Links
| Links for DUXAP10 | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |