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.