Basic Information
| LncRNA/CircRNA Name | MEG3 |
| Synonyms | MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 |
| Region | GRCh38_14:100779410-100861031 |
| Ensemble | ENSG00000214548 |
| Refseq | NR_002766 |
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 | acute myeloid leukemia |
| ICD-0-3 | NA |
| Methods | qPCR, Luciferase reporter assay, Western blot |
| Sample | AML tissues, cell lines (TF-1, U937, NB4, KG-1, Kasumi-1, HL-60 and K562) |
| Expression Pattern | down-regulated |
| Function Description | MEG3 is significantly downregulated in AML and suppresses leukemogenesis not only in a p53-dependent, but also a p53-independent manner.MEG3 is proven to be transcriptionally activated by Wilms' tumor 1 (WT1), dysregulation of which by epigenetic silencing or mutations is causally involved in AML.Therefore MEG3 is identified as a novel target of the WT1 molecule. Ten-eleven translocation-2 (TET2) mutations frequently occur in AML and significantly promote leukemogenesis of this disorder.TET2, acting as a cofactor of WT1, increases MEG3 expression. |
| Pubmed ID | 28400619 |
| Year | 2017 |
| Title | Dysfunction of the WT1-MEG3 signaling promotes AML leukemogenesis via p53-dependent and -independent pathways. |
External Links
| Links for MEG3 | GenBank HGNC NONCODE |
| Links for acute myeloid leukemia | OMIM COSMIC |