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 | breast cancer |
| ICD-0-3 | C50 |
| Methods | qPCR, Western blot, in vitro knockdown, RNAi |
| Sample | breast tumor tissues, human breast cancer cells (MCF7, SKBR-3), human prostate cancer cells (PC-3, LNCaP), human brain cancer cells (A-172, U-87), neuroblastoma cell line (SH-SY5Y), human colon cancer cell lines (HT-29, SW48, SW480, SW1116), human stomach cancer cell (AGS), human cervix cell (HELA) and human liver hepatocellular carcinoma cell line (Hep G2) |
| Expression Pattern | up-regulated |
| Function Description | MIAT expression was much higher in high-grade tumors compared to low-grade ones. Unlike P53 positive tumors, MIAT expression was upregulated in ER, PR, Her2 positive tumor tissues. An increase in the expression of mir-302, mir-150, and a decrease in the expression of mir-29c were detected following MIAT silencing. More importantly, knockdown MIAT significantly elevated the expression of p16Ink4A and Cox2, which commitment cellular senescence in breast cancer cells. |
| Pubmed ID | 29345338 |
| Year | 2018 |
| Title | MIAT lncRNA is overexpressed in breast cancer and its inhibition triggers senescence and G1 arrest in MCF7 cell line. |
External Links
| Links for MIAT | GenBank HGNC NONCODE |
| Links for breast cancer | OMIM COSMIC |