Basic Information
| LncRNA/CircRNA Name | MIAT |
| Synonyms | NA |
| Region | GRCh38_22:26646428-26676475 |
| Ensemble | ENSG00000225783 |
| Refseq | NR_003491 |
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 | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc. |
| Sample | HCC tissues, human HCC cell lines (Huh-6, Huh-7, BEL-7402, MHCC97-H) and L02 cells |
| Expression Pattern | up-regulated |
| Function Description | the long non-coding RNA, myocardial infarction associated transcript (MIAT) was up-regulated in both HCC tissues and cell lines. MIAT suppressed the expression and function of miR-520d-3p. Moreover, erythropoietin-producing hepatocellular A2 (EPHA2) was speculated and confirmed as a direct target of miR-520d-3p. We also demonstrated that MIAT may function as a sponge competitive endogenous RNA for miR-520d-3p, and thus regulate the molecular expression of EPHA2. In summary, our study has identified a novel signaling pathway through which miR-520d-3p exerts its anticarcinogenic roles and suggested that the MIAT/miR-520d-3p/EPHA2 may be a new target for HCC therapy. |
| Pubmed ID | 30551417 |
| Year | 2019 |
| Title | Deregulation of miR-520d-3p promotes hepatocellular carcinoma development via lncRNA MIAT regulation and EPHA2 signaling activation |
External Links
| Links for MIAT | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |