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目的探讨扶正抗癌方逆转H1650细胞对吉非替尼耐药的分子机制。方法 CCK8活力检测法分别观察吉非替尼、扶正抗癌方及两者联合给药对H1650细胞增殖的影响;蛋白质印迹法检测扶正抗癌方对p-c Met(Tyr1349)、c Met和pEGFR(Tyr1068)表达的影响。结果 H1650细胞对吉非替尼产生耐药;扶正抗癌方以浓度和时间依赖性抑制H1650细胞的增殖(P<0.05);扶正抗癌方联合吉非替尼抑制H1650细胞增殖效果优于扶正抗癌方单药(P<0.05);扶正抗癌方以时间依赖性下调p-c Met(Tyr1349)、c Met和p-EGFR(Tyr1068)的表达(P<0.05)。结论扶正抗癌方可通过抑制c Met通路逆转H1650细胞对吉非替尼的耐药。
Objective To investigate the molecular mechanism of Fuzheng Kangai Fang in reversing the resistance of Ge-Shi-Ni to H1650 cells. Methods CCK8 activity assay was used to observe the effects of gefitinib, Fuzheng anticancer drug and the combination of both on Proliferation of H1650 cells. Western blotting was used to detect the effect of Fuzheng Kangai Fang on the expression of pc Met (Tyr1349), c Met and pEGFR (Tyr1068 ) Expression. Results H1650 cells were resistant to gefitinib; Fuzheng Kangai Fang inhibited the proliferation of H1650 cells in a concentration- and time-dependent manner (P <0.05); Fuzheng Kangai Fang combined with Gefitinib inhibited H1650 cells proliferation better than Fuzheng Fuzheng anticancer drug down-regulated the expression of pc Met (Tyr1349), c Met and p-EGFR (Tyr1068) in a time-dependent manner (P <0.05). Conclusion Fuzheng Kangai Decoction can reverse the resistance of c-Fibronectin to H1650 cells by inhibiting the c Met pathway.