MiR-196b regulates gastric cancer cell proliferation and invasion via PI3K/AKT/mTOR signaling pathway.

Abstract

miR-196b plays a significant role in the regulation of tumor pathogenesis and progression by promoting tumor cell proliferation, invasion and metastasis. In order to explore the effects of miR-196b on the proliferation and invasion ability of gastric cancer cells and the involved mechanisms, in the present study the lentivirus expression vector miR-196b was constructed and transfected into the human gastric cancer cell line MKN28. The cell proliferation and invasion ability were observed and the expression of PI3K/AKT/mTOR protein and mRNA were analyzed following upregulation of the expression of miR-196b. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) results revealed that the proliferation of MKN28 cells was notably increased following upregulation of the expression of miR-196b (P<0.01). Flow cytometry analysis demonstrated that miR-196b decreased the ratios of cells in the GO/G1 stage but increased the ratios in S and G2 stage (P<0.05). Furthermore, the cell clone formation and trans-membrane rates were increased following upregulation of the expression of miR-196b (P<0.01). The nude mouse tumor growth test revealed that tumor growth was more rapid following upregulation of the expression of miR-196b. The expression of PI3K/AKT/mTOR protein and mRNA were increased following upregulation of the expression of miR-196b. We concluded that upregulation of miR-196b promotes the proliferation and invasion ability of gastric cancer cells by regulating the PI3K/AKT/mTOR pathway.