Basic Information
| LncRNA/CircRNA Name | CCAT1 |
| Synonyms | CCAT1, CARLo-5, onco-lncRNA-40 |
| Region | GRCh38_8:127207382-127219268 |
| Ensemble | ENSG00000247844 |
| Refseq | NR_108049 |
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 | acute myeloid leukemia |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay etc. |
| Sample | blood, cell line (HL-60) |
| Expression Pattern | up-regulated |
| Function Description | the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients. By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155. Accordingly, a significant decrease in miR-155 level was detected in AML patients. Re-introduction of miR-155 into HL-60 cells restored monocytic maturation and repressed cell proliferation. Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155. In conclusion, these results revealed new mechanism of lncRNA CCAT1 in AML development, and suggested that the manipulation of CCAT1 expression could serve as a potential strategy in AML therapy. |
| Pubmed ID | 26923190 |
| Year | 2016 |
| Title | Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia |
External Links
| Links for CCAT1 | GenBank HGNC NONCODE |
| Links for acute myeloid leukemia | OMIM COSMIC |