三七皂苷R1调控PI3K/AKT/mTOR信号通路诱导人下咽鳞状细胞癌FaDu细胞凋亡和自噬

目的:探讨三七皂苷R1(notoginsenoside R1,NGR1)对人下咽鳞状细胞癌(hypopharyngeal squamous cell carcinoma,HSCC)FaDu细胞凋亡以及自噬的影响,并对其涉及的信号通路进行研究。方法:75μmol/L、150μmol/L、300μmol/L NGR1作用于FaDu细胞24 h后,采用MTT检测细胞增殖能力;流式细胞术检测细胞凋亡;自噬双标腺病毒检测自噬流;Western blot检测自噬相关蛋白LC3Ⅱ/LC3Ⅰ以及PI3K/AKT/mTOR信号通路相关蛋白表达水平。结果:NGR1能够抑制FaDu细胞的增殖并促进细胞凋亡;NGR1可诱导FaDu细胞自噬,并呈一定浓度依赖性;Western blot结果显示,NGR1作用于Fa Du细胞24 h后,LC3Ⅱ表达明显增加,而p-PI3K、p-AKT、p-m TOR表达相较于Control组明显下降。结论:NGR1可抑制Fa Du细胞增殖,诱导细胞凋亡与自噬,其机制可能与抑制PI3K/AKT/m TOR信号通路有关。

Notoginsenoside R1 induces apoptosis and autophagy of FaDu cell via PI3K/AKT/mTOR signaling pathway

Objective:To investigate the effect of notoginsenoside R1（NGR1） on apoptosis and autophagy of FaDu cell,and to explore the possible signaling pathway in these processes.Methods:The FaDu cell were treated with 75 μmol/L,150 μmol/L,300 μmol/L NGR1,and the cell viability was detected by MTT assy.The apoptosis was detected by flow cytometry.The autophagy was detected by double-labeled adenoviruses.Western blot was used to detect the expression levels of autophagy specific protein LC3Ⅱ/LC3Ⅰ and PI3K/AKT/mTOR signaling proteins.Results:NGR1 significantly inhibited the viability and induced the apoptosis of FaDu cell.And NGR1 can induce autophagy to form autophagy flow in FaDu cell,and it had a certain concentration dependence.Western blot results showed that after NGR1 treated FaDu cells for 24 h,the expression of LC3Ⅱ increased significantly,and the expression of p-PI3K,p-AKT and p-mTOR in FaDu cells were significantly lower than those in Control group.Conclusion:NGR1 can inhibit FaDu cell proliferation and induce cell apoptosis and autophagy,the mechanism of which may be related to the inhibition of PI3K/AKT/mTOR signaling pathway.