Nitidine chloride (NC) has significant anti-tumor properties; however, the precise mechanism related to NC still needs further investigation. This study intends to investigate the anti-tumor functions and the feasible molecular basis of NC in NSCLC cells. Therefore, we determined the mechanism of NC-mediated anti-tumor function through various methods. Cell proliferation ability and migration and invasion were detected by CCK-8, colony formation assay and Transwell assay, respectively. Furthermore, flow cytometry was used to detect apoptosis, cell cycle and ROS. Moreover, protein expression level was measured by western blot. Our results showed that NC can inhibit the growth, motility of NSCLC cells, induce apoptosis and arrest cell cycle. Meanwhile, NC increased the level of ROS in NSCLC cells. Moreover, western blot data showed that NC suppressed the expression of Lats1, Mob1, and YAP, and enhanced the expression of p-Lats1, p-Mob1, p-YAP1 (ser127). Overall, our research reveals that NC exerts anticancer activity by activating and modulating the Hippo signaling pathway.

氯化两面针碱（NC）具有显着的抗肿瘤特性；然而，与NC相关的确切机制仍需进一步研究。本研究旨在探讨NC在NSCLC细胞中的抗肿瘤功能及其可行的分子基础。因此，我们通过多种方法确定了NC介导的抗肿瘤功能的机制。分别采用CCK-8、集落形成实验和Transwell实验检测细胞增殖能力以及迁移和侵袭能力。此外，使用流式细胞术检测细胞凋亡、细胞周期和ROS。此外，通过蛋白质印迹测量蛋白质表达水平。我们的结果表明NC可以抑制NSCLC细胞的生长、运动、诱导细胞凋亡和阻滞细胞周期。同时，NC增加了NSCLC细胞中ROS的水平。此外，蛋白质印迹数据显示，NC 抑制 Lats1、Mob1 和 YAP 的表达，并增强 p-Lats1、p-Mob1、p-YAP1 (ser127) 的表达。总体而言，我们的研究表明 NC 通过激活和调节 Hippo 信号通路发挥抗癌活性。