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.