MicroRNA-495 regulates human gastric cancer cell apoptosis and migration through Akt and mTOR signaling

In the present study, we investigated the expression and cellular distribution of microRNA-495 (miR-495) in human gastric cancer. Prominent downregulation of miR-495 activation was evident in patients with gastric cancer. Cell viability and Annexin V/PI apoptosis assays were used to assess cell proliferation and apoptosis. Then, western blot analysis was used to assess cyclin D1, PI3K, p-Akt and p-mTOR protein expression. Overexpression of miR-495 significantly inhibited cell proliferation, and promoted cell apoptosis of gastric cancer cells. Overexpression of miR-495 also promoted caspase-3/-9 and Bax protein expression, and suppressed cyclin D1 protein expression and the PI3K/Akt/mTOR pathway in gastric cancer cells. Downregulation of miR-495 increased cell proliferation and inhibited cell apoptosis of gastric cancer cells through activation of the PI3K/Akt/mTOR pathway. The PI3K inhibitor, was used to suppress the PI3K/Akt/mTOR pathway, inhibit cell proliferation, promote cell apoptosis, promote caspase-3/-9 and Bax protein expression, and suppress cyclin D1 protein expression of gastric cancer cells through miR-495 inhibition. In conclusion, miR-495 is an important regulator of human gastric cancer cells and may contribute to cell apoptosis through the PI3K/Akt/mTOR/Bax-caspase-3/-9 and cyclin D1 pathway.