The present study investigated the role of microRNA-137-regulated AKT serine/threonine kinase 2 (AKT2) on tumor growth and cisplatin sensitivity in patients with non-small cell lung cancer (NSCLC). The results demonstrated that the expression of microRNA-137 in cisplatin-treated NSCLC patient tissue samples was markedly lower than that in healthy tissue samples. The disease-free survival and overall survival rates of patients with NSCLC exhibiting a high microRNA-137 expression were higher than the survival rates of patients with NSCLC exhibiting a low expression of microRNA-137. Overexpression of microRNA-137 inhibited the proliferation of A549 and H520 cells treated with cisplatin. Overexpression of miR-137 suppressed the protein expression of AKT2, increased caspase-3 activity, increased Bax protein expression and suppressed Cyclin D1 protein expression in A549 and H520 cells treated with cisplatin. MK2206, an AKT2 inhibitor, inhibited AKT2 protein expression and suppressed the proliferation of A549 and H520 cells treated with cisplatin following overexpression of miR-137. The inhibition of AKT2 also increased caspase-3 activity and Bax protein expression, and suppressed Cyclin D1 protein expression in A549 and H520 cells treated with cisplatin following overexpression of miR-137. Taken together, the results of the present study suggested that microRNA-137-regulated AKT2 inhibits tumor growth and sensitizes cisplatin in patients with NSCLC.
Keywords: AKT serine-/threonine kinase 2; cisplatin; microRNA-137; non-small cell lung cancer.