摘要
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 discuss the molecular mechanism of FZKA decoction in reversing the resistance of H1650 cells to ge- fitinib. Methods Effects of gefitinib, FZKA decoction and the two combination on H1650 cells proliferation were detected by CCK8 assay. Effects of FZKA decoction on the expression of p -cMet（Tyr1349） , cMet and p- EGFR（Tyr1068） were detected by western blot assay. Results H1650 cells was resistant to gefitinib. However, proliferation of H1650 cells was inhibited by FZ- KA decoction in concentration - dependent and time - dependent manners （P 〈 0.05 ）. And the inhibiting effect of combination between FZKA decoction and gefitinib was better than FZKA decoction alone （P 〈 0.05 ）. Expression of p - cMet（ Tyr1349）, cMet and p - EGFR（Tyr1068 ） were reduced in time - dependent manner （P 〈 0.05）. Conclusion FZKA decoction reverses the resistance of H1650 cells to gefitinib via cMet.
出处
《时珍国医国药》
CAS
CSCD
北大核心
2016年第10期2318-2321,共4页
Lishizhen Medicine and Materia Medica Research
基金
国家自然科学基金(No.81273965
No.81503507)
广东省自然科学基金(No.2015A030310245)
广东省建设中医药强省科研课题(No.20141104)
