| [1] PubMed ID: | 31524253 |
| Disease Name: | stomach carcinoma |
| Sample: | cell lines (HGC-27,BGC-823) |
| Dysfunction Pattern: | Interaction[EMT regulation] |
| Validated Method: | qRT-PCR//MTT//IHC//Western Blot |
| Description: | It was demonstrated that lncRNA‑MEG3 expression was Expression[down-expression]regulated in gastric carcinoma cells compared with normal gastric cells. Western blot analysis demonstrated that lncRNA‑MEG3 transfection inhibited the expression of anti‑apoptotic proteins B cell lymphoma-2 (Bcl‑2) and Bcl‑2‑like protein 2 and increased the expression of pro‑-apoptotic proteins caspase‑3 and caspase‑9 in gastric carcinoma cells. lncRNA‑MEG3 transfection Expression[Expression[up-expression]-expression]regulated the expression of epithelial marker E‑cadherin and inhibited the expression of mesenchymal markers vimentin and fibronectin in gastric carcinoma cells, which suggested that lncRNA‑MEG3 inhibited epithelial‑mesenchymal transition (EMT), which may subsequently inhibit progression in gastric carcinoma cells. The present study also revealed that lncRNA‑MEG3 transfection sExpression[Expression[up-expression]-expression]pressed tumor growth mainly by decreasing the expression of vascular endothelial growth factor and increasing the expression of Bcl‑2 in vivo. In conclusion, these results indicated that lncRNA‑MEG3 may regulate EMT‑associated signaling pathways and has the potential as a therapeutic target in gastric carcinoma. |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | |