Basic Information
| LncRNA/CircRNA Name | MIAT |
| Synonyms | MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT |
| Region | GRCh38_22:26646428-26676475 |
| Ensemble | ENSG00000225783 |
| Refseq | NR_003491 |
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 | colorectal cancer tissues, cell lines (HcoEpic, HT-29, SW480, and LOVO) |
| Expression Pattern | up-regulated |
| Function Description | MIAT was highly expressed in CRC tissues and cells.MIAT knockdown inhibited proliferation,migration and invasion and enhanced apoptosis of CRC cells.Further,we demonstrated that MIAT acted as a competing endogenous RNA for miR-132, antagonized its functions,and resulted in the de-repression of its target gene Derlin-1,which acted as an oncogene in promoting growth and metastasis of CRC cells.In LOVO and SW480 cells with si-MIAT, miR-132 inhibitor resulted in an increase of cell proliferation, migration and invasion and a decrease of cell apoptosis, which was partially abolished by transfection of Derlin-1 shRNA.Our data indicated that highly expressed MIAT was an oncogenic lncRNA that promoted the growth and metastasis of CRC through miR-132/Derlin-1 axis. |
| Pubmed ID | 29686537 |
| Year | 2018 |
| Title | Long non-coding RNA MIAT promotes growth and metastasis of colorectal cancer cells through regulation of miR-132/Derlin-1 pathway. |
External Links
| Links for MIAT | GenBank HGNC NONCODE |
| Links for colorectal cancer | OMIM COSMIC |