Basic Information
| LncRNA/CircRNA Name | KCNKI5-ASI |
| Synonyms | NA |
| Region | NA |
| 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 | gastric cancer |
| ICD-0-3 | C16 |
| Methods | qRT-PCR, Western blotting, Methylation-specific PCR, in vitro knockdown, RIP etc. |
| Sample | tumor tissues and the adjacent noncancerous tissues,human gastric cancer cell lines (BGC-823 and SGC7901) |
| Expression Pattern | down-regulated |
| Function Description | The expression of KCNK15-AS1 was lower in the tumor tissue compared to the normal tissue. KCNK15-AS1 interacted with miR-21. Both the overexpression of KCNK15-AS1 and the knockdown of the expression of miR-21 inhibited proliferation and promoted apoptosis and decreased the level of MMP-9, bcl-2, and MMP-2 but increased the level of Bax. In addition, the methylation of KCNK15-AS1 was detected in the tumor tissue but was not detected in the normal tissue. Treatment with 5-azacytidine and chidamide decreased the level of DNMT1 and HDAC1 and increased the level of KCNK15-AS1. The RNA pull-down and RNA immunoprecipitation results showed that KCNK15-AS1 interacted with DNMT1 and HDAC1. The ChIP-seq result showed that the promoter of MAPK interacted with DNMT1, and the promoter of AKT and STAT5 interacted with HDAC1. |
| Pubmed ID | 31572012 |
| Year | 2019 |
| Title | Epigenetic Regulation of IncRNA KCNKI5-ASI in Gastric Cancer |
External Links
| Links for KCNKI5-ASI | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |