Department of Chest Surgery, Yantaishan Hospital, Yantai, Shandong 264000, P.R. China.
Department of Biochemistry and Molecular Biology, Key Laboratory of Tumor Molecular Biology in Binzhou Medical University, Binzhou Medical University, Yantai, Shandong 264003, P.R. China.
Mol Med Rep. 2019 Oct;20(4):3355-3362. doi: 10.3892/mmr.2019.10566. Epub 2019 Aug 6.
MicroRNAs (miRNAs/miRs) serve important roles in the chemotherapeutic effect of anticancer drugs. To investigate the roles of miRNAs in cisplatin‑induced suppression of lung adenocarcinoma cell proliferation, A549 cells were treated with different concentrations of cisplatin. An MTT assay demonstrated that cisplatin inhibited A549 cell proliferation in a dose‑dependent manner. Cisplatin induced cell apoptosis and inhibited cell migration by increasing the levels of miR‑93, miR‑26a and miR‑26b. Furthermore, as an upstream factor, miR‑93 was proposed to regulate cyclin D2 expression in miR‑93‑transfected A549 cells. Cisplatin also induced Bcl‑2‑associated X protein expression, and decreased that of Bcl‑2 and c‑Myc in lung adenocarcinoma cells. In vivo analysis further supported that cisplatin inhibited lung adenocarcinoma cell growth by regulating cyclin D2 and miR‑93 expression. In conclusion, our findings demonstrated that cisplatin could effectively inhibit lung adenocarcinoma cell proliferation by decreasing cyclin D2 expression via miR‑93.
微小 RNA(miRNAs/miRs)在抗癌药物的化疗效果中发挥着重要作用。为了研究 miRNAs 在顺铂诱导的肺腺癌细胞增殖抑制中的作用,用不同浓度的顺铂处理 A549 细胞。MTT 分析表明,顺铂呈剂量依赖性抑制 A549 细胞增殖。顺铂通过增加 miR-93、miR-26a 和 miR-26b 的水平诱导细胞凋亡和抑制细胞迁移。此外,作为上游因子,miR-93 被提议调节 miR-93 转染的 A549 细胞中环蛋白 D2 的表达。顺铂还诱导 Bcl-2 相关 X 蛋白的表达,并降低肺腺癌细胞中 Bcl-2 和 c-Myc 的表达。体内分析进一步支持顺铂通过调节 cyclin D2 和 miR-93 的表达来抑制肺腺癌细胞的生长。总之,我们的研究结果表明,顺铂通过降低 miR-93 表达有效抑制肺腺癌细胞增殖。