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 | apoptosis | Drug | Gefitinib | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | lung cancer |
| ICD-0-3 | C34 |
| Methods | RNA-seq, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP |
| Sample | lung cancer tissues, human lung cancer cell lines (PC9, HCC827, A549, H1870, H1048, and H1299U87) |
| Expression Pattern | up-regulated |
| Function Description | LncRNA MIAT expression was associated with tumor size, lymph node metastasis,distant metastasis and TNM stage.Univariate analysis and multivariate analysis revealed that the lncRNA MIAT to be an independent factor for predicating the prognosis of lung cancer patients.Low lncRNA MIAT have longer overall survival time and progression-free survival time than patients with high lncRNA MIAT expression. Moreover, the knockdown of MIAT significantly sensitized PC9 and gefitinib-resistant PC9 cells to gefitinib in vitro and in vivo, and increased the expression of miR-34a and inactivated PI3K/Akt signaling. MIAT interacted with miR-34a and epigenetically controlled the miR-34a expression by hyper-methylating its promotor. MiR-34a promoter methylation status was measured by MSP in tissues and BSP in cells. |
| Pubmed ID | 29487526 |
| Year | 2018 |
| Title | Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a. |
External Links
| Links for MIAT | GenBank HGNC NONCODE |
| Links for lung cancer | OMIM COSMIC |