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 | gastric cancer |
| ICD-0-3 | C16 |
| Methods | qPCR, Western blot, RNAi etc. |
| Sample | cell lines (AGS, NCI-N87, SGC7901, MKN45, TMK1 and GES1) |
| Expression Pattern | down-regulated |
| Function Description | MEG3 was downregulated while miR-21 was upregulated in gastric cancer tissues and cell lines by qRT-PCR.Overexpression of MEG3 suppressed cell mobility of gastric cancer cells (AGS) by downregulating the expression of MMP-3, MMP-9 and VEGF. overexpression of MEG3 also suppressed epithelial mesenchymal transition (EMT) by increasing the expression of an epithelial marker (E-cadherin) and downregulating the expression of mesenchymal markers, indicating that MEG3 suppressed cell mobility through the inhibition of EMT in gastric cancer. The expression of miR-21 was negatively regulated by MEG3 and overexpression of miR-21 promoted cell mobility of AGS through activation of EMT.Co-transfection of lncRNA-MEG3 and miR-21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3, suggesting that the MEG3/miR-21 axis affects cell mobility by suppressing EMT in gastric cancer. |
| Pubmed ID | 29749532 |
| Year | 2018 |
| Title | MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer. |
External Links
| Links for MEG3 | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |