槲皮素通过Stat3/Mcl-1途径介导肺癌PC9/GR细胞凋亡的研究

目的 探究槲皮素(Que)对人非小细胞肺癌(NSCLC)获得性耐药细胞株PC9/Gefitinib-Resisitant (GR)细胞的凋亡的影响及作用机制.方法 MTT法检测不同浓度Que对PC9/GR细胞增殖的影响,计算其半数抑制浓度(IC50)值.光镜下观察细胞形态学改变.流式细胞术检测Que介导的细胞凋亡.Western blot法检测Stat3/Mcl-1信号途径相关蛋白水平的改变.结果 MTT显示Que可明显抑制PC9/GR细胞增殖,并呈浓度依赖性,IC50值为(74.83±4.83)μmol/L.流式细胞学结果表明,与对照组相比,Que 可呈浓度依赖性地促进细胞凋亡(P＜0.05).Western blot 表明Que可减弱Stat3蛋白的活化水平,其下游的凋亡相关蛋白Mcl-1表达亦减弱(P＜0.05).结论 Que对获得性耐药NSCLC细胞PC9/GR具有较强的抗肿瘤作用,作用机制可能与Stat3/Mcl-1途径介导的细胞凋亡密切相关.

Quercetin promotes apoptosis of lung cancer PC9/GR cell via Stat3/Mcl-1 pathway

Objective To investigate the effect of Que on the apoptosis of acquired resisitant NSCLC PC9 / GR cells and to explore its potential mechanism.Methods The anti-proliferative effect of Que on PC9/GR cells was assessed by MTT assay and the half inhibitory concentration (IC50) was calculated.The morphological alterations about groups of different concentrations of Que were observed by microscope.The apoptosis ratios were detected by flow cytometry analysis.And the protein expression of Stat3 / Mcl-1 signal pathway was detected by Western blot.Results MTT assay showed that Que could significantly inhibit the proliferation of PC9 / GR cells in a dose-dependent manner with an IC50 of (74.83 ± 4.83) μmol/L.Flow cytometry showed that Que could promote the apoptosis in a dose-dependent manner compared with the control group (P ＜ 0.05).Western blot showed that Que could decrease the activation level of Stat3 protein,and the expression of apoptosis-related protein Mcl-1 was also decreased (P ＜ 0.05).Conclusion Que has a strong antitumor effect on acquired resisitant NSCLC PC9 / GR cells,and the mechanism may be closely related to Stat3/Mcl-1 pathway mediated apoptosis.