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 | gastric cancer |
| ICD-0-3 | C16 |
| Methods | qPCR, RIP, Western blot, Luciferase reporter assayin vitro knockdown etc. |
| Sample | cell line (BGC-823, MGC-803), gastric cancer tissues |
| Expression Pattern | up-regulated |
| Function Description | MIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis.MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo.MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression.In BGC-823 and MGC-803 cells with si-MIAT,DDX5 overexpression resulted in an increase of cell proliferation,migration and invasion.Our data indicated that MIAT played an oncogenic role in GC growth and metastasis,and could serve as a novel molecular target for treating GC. |
| Pubmed ID | 29540201 |
| Year | 2018 |
| Title | Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway. |
External Links
| Links for MIAT | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |