Basic Information
| LncRNA/CircRNA Name | CCAT1 |
| Synonyms | NA |
| Region | NA |
| Ensemble | ENSG00000247844 |
| Refseq | NR_108049 |
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 | colorectal cancer |
| ICD-0-3 | C19.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, etc. |
| Sample | IBD tissues, Human colorectal cancer cell line Caco-2 |
| Expression Pattern | up-regulated |
| Function Description | Gene set enrichment analysis revealed that several inflammation-related genes were enriched in the CCAT1 high-expressed group of CRC patients. The relationship between CCAT1 and inflammation activation in IBD patients was further confirmed. CCAT1 expression positively correlated with MLCK, which acts as a protein kinase to phosphorylate myosin light chain and induces tight junction protein distribution, whereas it was negatively correlated with miR-185-3p in IBD tissues. We also determined that CCAT1 overexpression increased Caco-2 monolayer permeability and upregulated MLCK. Furthermore, CCAT1-induced MLCK overexpression and IBD disease progression were significantly attenuated by miR-185-3p. |
| Pubmed ID | 30615124 |
| Year | 2019 |
| Title | CCAT1 lncRNA Promotes Inflammatory Bowel Disease Malignancy by Destroying Intestinal Barrier via Downregulating miR-185-3p |
External Links
| Links for CCAT1 | GenBank HGNC NONCODE |
| Links for colorectal cancer | OMIM COSMIC |