Nonsmall cell lung cancer (NSCLC) is one of the most common malignancies and needs novel and effective chemotherapy. In this study, our purpose is to explore the anticancer effects of 2-methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol (SQ) on human NSCLC (A549 and H460) cells. We found that SQ suppressed the proliferation of NSCLC cells in time- and dose-dependent manners, and blocked the cells at G2/M phase, which was relevant to microtubule depolymerization. Additionally, SQ induced A549 and H460 cell apoptosis by activating the mitochondrial apoptotic pathway. Further, we demonstrated that SQ enhanced the generation of reactive oxygen species (ROS), and pretreatment with N-acetyl- L-cysteine (NAC) attenuated SQ-induced cell apoptosis. Meanwhile, SQ mediated-ROS generation caused DNA damage in A549 and H460 cells. Our data also revealed that SQ-induced apoptosis was correlated with the inhibition of mouse double minute 2 (MDM2) in A549 and H460 cells. In summary, our research indicates that the novel compound SQ has great potential for therapeutic treatment of NSCLC in future.

中文翻译：

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2-Methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol 通过线粒体凋亡途径和 MDM2 抑制导致 NSCLC 细胞中 G2/M 细胞周期停滞和凋亡

非小细胞肺癌（NSCLC）是最常见的恶性肿瘤之一，需要新型有效的化疗。在这项研究中，我们的目的是探索 2-methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol (SQ) 对人 NSCLC（A549 和 H460）细胞的抗癌作用。我们发现 SQ 以时间和剂量依赖性方式抑制 NSCLC 细胞的增殖，并在 G2/M 期阻断细胞，这与微管解聚有关。此外，SQ 通过激活线粒体凋亡途径诱导 A549 和 H460 细胞凋亡。此外，我们证明了 SQ 增强了活性氧 (ROS) 的产生，并用 N-乙酰 -L预处理-半胱氨酸 (NAC) 减弱 SQ 诱导的细胞凋亡。同时，SQ 介导的 ROS 生成导致 A549 和 H460 细胞中的 DNA 损伤。我们的数据还显示，SQ 诱导的细胞凋亡与 A549 和 H460 细胞中小鼠双分钟 2 (MDM2) 的抑制相关。综上所述，我们的研究表明，新型化合物 SQ 在未来治疗 NSCLC 方面具有巨大潜力。