JS-K对口腔鳞状细胞癌H157和CAL-27细胞增殖与凋亡的影响及机制实验研究

Effects and mechanism of JS-K on proliferation and apoptosis of oral squamous cell carcinoma H157 and CAL-27 cells

目的:探讨一氧化氮(NO)前体化合物(JS-K)对口腔鳞状细胞癌(OSCC)H157和CAL-27细胞增殖与凋亡的影响,并分析相关机制。方法:采用细胞活力与平板克隆实验检测JS-K对OSCC细胞增殖能力的影响。采用流式细胞术检测细胞周期与细胞凋亡,以及半胱氨酸蛋白酶3/7(Caspase-3/7)活性测定评估JS-K对OSCC细胞周期与凋亡的影响。检测JS-K干预后OSCC细胞中ROS生成情况。采用亚细胞分离技术与Western blot探索JS-K诱导OSCC细胞周期停滞与细胞凋亡的机制。结果:JS-K通过p38丝裂原活化蛋白激酶(MAPK)信号通路抑制OSCC细胞的增殖,诱导细胞凋亡和细胞周期阻滞。此外,JS-K激活的p38 MAPK信号通路导致OSCC细胞中ROS增加,并诱导细胞周期阻滞在G_(2)/M期。结论:JS-K通过p38 MAPK信号通路调控ROS,诱导OSCC细胞周期阻滞在G_(2)/M期并凋亡,最终抑制OSCC细胞增殖。JS-K可能为一种治疗OSCC的潜在药物。

Objective:To investigate the effects of nitric oxide(NO)precursor compounds(JS-K)on the proliferation and apoptosis of oral squamous cell carcinoma(OSCC)H157 and CAL-27 cells,and to explore the related mechanisms.Methods:The effect of JS-K on OSCC cell proliferation was determined by cell viability and colony formation assay.The cell cycle and apoptosis were detected by flow cytometry,and the effect of JS-K on OSCC cell cycle and apoptosis was evaluated by Caspase-3/7 activity.ROS detection was used to detect ROS production in OSCC cells after JS-K application.Subcell separation techniques and Western blot were used to explore the mechanism of JS-K induced OSCC cell cycle arrest and cell apoptosis.Results:JS-K inhibited OSCC cell proliferation,induced cell apoptosis and cell cycle arrest through p38 MAPK signaling pathway.In addition,the JS-K-activated p38 MAPK signaling pathway leads to an increase in ROS in OSCC cells and induces cell cycle arrest in the G_(2)/M phase.Conclusion:JS-K regulates ROS through p38 MAPK signaling pathway,inducing cell cycle arrest in G_(2)/M phase and apoptosis,and finally inhibiting OSCC cell proliferation.JS-K may be a potential treatment for OSCC.