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目的:探讨白血病阿霉素耐药与磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)信号转导通路的相关性。方法:选择磷脂酰肌醇3-激酶特异性抑制剂LY294002,将白血病敏感株K562/S和白血病阿霉素耐药株K562/ADM细胞分别给予LY294002和ADM干预,评价LY294002作用前后阿霉素对白血病细胞的抑制作用,检测K562/S和K562/ADM各组细胞PI3K和Akt表达水平。结果:LY294002干预前后不同浓度阿霉素对白血病K562/S和K562/ADM细胞抑制作用具有非常显著性差异(P<0.05);不同浓度LY294002可降低K562/S和K562/ADM细胞中PI3K和Akt表达,LY294002各浓度组与ADM组及对照组组间比较具有非常显著性差异(P<0.05)。结论:磷脂酰肌醇3-激酶/蛋白激酶B信号通路异常与白血病阿霉素耐药有关,抑制磷脂酰肌醇3-激酶/蛋白激酶B信号通路能增强白血病阿霉素敏感性。
Objective: To investigate the relationship between doxorubicin resistance and phosphatidylinositol 3-kinase / protein kinase B (PI3K / Akt) signal transduction pathway in leukemia. Methods: LY294002, a specific inhibitor of phosphatidylinositol 3-kinase, was used to infect leukemia cell line K562 / S and leukemia adriamycin resistant cell line K562 / ADM to LY294002 and ADM respectively to evaluate the effect of doxorubicin on LY294002 The inhibitory effect of leukemia cells on K562 / S and K562 / ADM cells PI3K and Akt expression levels. Results: The inhibitory effect of doxorubicin on K562 / S and K562 / ADM cells was significantly different (P <0.05) before and after LY294002 treatment. LY294002 decreased the expression of PI3K and Akt in K562 / S and K562 / ADM cells Expression, LY294002 concentrations of ADM group and control group compared with the significant difference (P <0.05). CONCLUSION: The abnormality of phosphatidylinositol 3-kinase / protein kinase B signaling pathway is related to doxorubicin resistance in leukemia, and inhibition of phosphatidylinositol 3-kinase / protein kinase B signaling pathway may enhance the doxorubicin sensitivity of leukemia.