Basic Information
| LncRNA/CircRNA Name | EPIC1 |
| 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 | cholangiocarcinoma |
| ICD-0-3 | NA |
| Methods | qPCR, RIP, other |
| Sample | CCA tissues and cell lines (KKU-055, KKU-100, KKU-213, KKU-214 CCA) |
| Expression Pattern | up-regulated |
| Function Description | And also, its expression also increased in several CCA cancer cell lines than that in human normal immortalized cholangiocyte cell. Loss-and-gain of Lnc-EPIC1 contributes to the CCA cell growth, colony formation, cell apoptosis and also cell cycle. Myc has been reported to directly interact with Lnc-EPIC1 in several cancer cells. Myc targets, including Cyclin A/D and CDK9 were downregulated by Lnc-EPIC1 siRNA. Myc knockout also suppresses the CCA cell growth, colony formation and cell apoptosis. However, Lnc-EPIC1 knockdown failed to enhance the Myc-KO-induced suppression of CCA tumor progression. RNA immunoprecipitation (RIP) results showed the direct interaction between Lnc-EPIC1 and Myc. |
| Pubmed ID | 30205958 |
| Year | 2018 |
| Title | Long Non-Coding RNA EPIC1 Promotes Cholangiocarcinoma Cell Growth |
External Links
| Links for EPIC1 | GenBank HGNC NONCODE |
| Links for cholangiocarcinoma | OMIM COSMIC |