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 | ovarian cancer |
| ICD-0-3 | C56.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay, CCK-8 assay etc. |
| Sample | cell lines (EVs, A2780, A2780cp, OVCAR-3 and SKOV3) |
| Expression Pattern | up-regulated |
| Function Description | Curcumin weakened the EVs-N's capability to induce drug resistance and induced significant changes of lncRNAs in the EVs. MEG3 is one of the most upregulated lncRNAs. Curcumin led to demethylation in the promoter region of MEG3 and 5-AZA-dC treatment restored MEG3 expression in a dose dependent manner. MEG3 restoration by curcumin significantly reduced miR-214 in cells and in EVs. Functionally, miR-214 inhibition weakened the EVs-N's capability to enhance chemoresistance, while miR-214 overexpression increased the capability of EVs-CU in inducing chemoresistance. |
| Pubmed ID | 28175963 |
| Year | 2017 |
| Title | Curcumin suppresses cisplatin resistance development partly via modulating extracellular vesicle-mediated transfer of MEG3 and miR-214 in ovarian cancer. |
External Links
| Links for MEG3 | GenBank HGNC NONCODE |
| Links for ovarian cancer | OMIM COSMIC |