摘要
目的探讨磷酸化c-JUN氨基末端激酶(p-JNK)参与胃癌顺铂的耐药机制。方法应用四氮唑炎酶还原法(MTT)检测药物的敏感性,免疫组化检测122例胃癌和35例正常胃组织中P-gp、p-JNK表达情况及关系。结果 SP600125抑制p-JNK表达,敏感株SGC7901及耐药菌株SGC7901-DDP的药物敏感性及细胞的凋亡率均明显增加(P <0.05);P-gp、p-JNK在胃癌中的表达率分别为53.28%、45.08%,显著高于正常胃组织中22.86%、11.43%的表达率(P <0.05)。结论 JNK通路参与了DDP所致胃癌耐药,高表达预示化疗的效果不佳,抑制通路可成为逆转耐药的新靶点。
Objective To investigate the mechanism of phosphorylation of c-JUN amino terminal kinase(p-JNK) in the resistance of cisplatin in gastric cancer. Methods The sensitivity of the drug was detected by mitrazolase reduction(MTT). The expression and relationship of P-gp and p-JNK in 122 cases of gastric cancer and 35 cases of normal gastric tissue were detected by immunohistochemistry. Results The expression of p-JNK was inhibited by SP600125. The drug sensitivity and apoptosis rate of the sensitive strains SGC7901 and SGC7901-DDP were significantly increased(P<0.05). The expression rates of P-gp and p-JNK in gastric cancer They were significantly increased. They were 53.28% and 45.08%,respectively,which were significantly higher than those in normal gastric tissues(22.86% and 11.43%,P<0.05). Conclusion The JNK pathway is involved in DDP-induced gastric cancer drug resistance. The high expression of the JNK pathway predicts that the chemotherapy is not effective. The inhibition pathway may become a new target for reversing drug resistance.
出处
《大医生》
2018年第9期56-57,共2页
Doctor
关键词
胃癌
氨基末端激酶
顺铂
耐药机制
gastric cancer
amino terminal kinase
cisplatin
drug resistance mechanism
