Lu Zhuming, Wang Minghui, Wu Shuoyun, Ye Min, Lin Zhichao, Shun Tao, Duan Chuxiao
Department of Thoracic Surgery, Jiangmen Central Hospital, Sun Yat-Sen University, Jiangmen, Guangdong 529030, P.R. China.
Department of Thoracic Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 520120, P.R. China.
Oncol Lett. 2018 Aug;16(2):1876-1884. doi: 10.3892/ol.2018.8823. Epub 2018 May 29.
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.
本研究调查了微小RNA-137调控的AKT丝氨酸/苏氨酸激酶2（AKT2）在非小细胞肺癌（NSCLC）患者肿瘤生长和顺铂敏感性中的作用。结果表明，顺铂处理的NSCLC患者组织样本中微小RNA-137的表达明显低于健康组织样本。微小RNA-137高表达的NSCLC患者的无病生存率和总生存率高于微小RNA-137低表达的NSCLC患者。微小RNA-137的过表达抑制了顺铂处理的A549和H520细胞的增殖。miR-137的过表达抑制了A549和H520细胞中AKT2的蛋白表达，增加了caspase-3活性，增加了Bax蛋白表达，并抑制了顺铂处理的A549和H520细胞中细胞周期蛋白D1的蛋白表达。AKT2抑制剂MK2206抑制了AKT2蛋白表达，并在miR-137过表达后抑制了顺铂处理的A549和H520细胞的增殖。在miR-137过表达后，对AKT2的抑制也增加了顺铂处理的A549和H520细胞中caspase-3活性和Bax蛋白表达，并抑制了细胞周期蛋白D1的蛋白表达。综上所述，本研究结果表明，微小RNA-137调控的AKT2抑制NSCLC患者的肿瘤生长并使顺铂敏感。
