Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation

Gastric carcinoma is one of the most frequently diagnosed gastrointestinal tumors. Long non‑coding RNAs (lncRNAs) are broadly defined as endogenous cellular non‑coding RNA molecules. Studies have demonstrated that they may be associated with human cancer progression. In the present study, the role of lncRNA‑maternally expressed gene 3 (MEG3) in the progression of gastric carcinoma cells was investigated in vitro and in vivo. It was demonstrated that lncRNA‑MEG3 expression was downregulated in gastric carcinoma cells compared with normal gastric cells. lncRNA‑MEG3 transfection increased E‑cadherin expression and markedly inhibited gastric carcinoma cell growth, migration and invasion. Flow cytometric analysis revealed that lncRNA‑MEG3 transfection promoted the apoptosis of gastric carcinoma 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 upregulated 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 suppressed 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.