非小细胞肺癌中PI3K/Akt信号通路通过Cdh1调控Skp2表达的机制研究  

Regulative mechanism of PI3K/Akt signal pathway on Skp2 via Cdh1 in non-small cell lung cancer

作　　者：孙秀华[1] 张洪开[1] 李玉[1] 于爱鸣[1] 

机构地区：[1]中国医科大学,沈阳110001

出　　处：《山东医药》2011年第12期30-32,118,共4页Shandong Medical Journal

基　　金：辽宁省教育厅资助项目(2004D225)

摘　　要：目的探讨非小细胞肺癌(NSCLC)中Cdc20同源蛋白1(Cdh1)参与磷脂酰肌醇三羟基激酶(PI3K)/Akt信号通路对S期激酶相关蛋白2(Skp2)表达调控的机制。方法体外培养NSCLC细胞系A549、LK2和H460,LY294002特异性阻断PI3K/Akt信号通路后,Western blot检测Skp2、Cdh1及p-Akt蛋白表达的变化,免疫荧光(IF)检测Cdh1在NSCLC中的定位变化。结果 LY294002处理后,与对照组相比3种细胞中Skp2蛋白表达和Akt磷酸化水平均降低(P<0.01),Cdh1在3种细胞的核内表达均增多。结论 NSCLC中PI3K/Akt信号通路抑制剂LY294002使Skp2蛋白表达下调与Cdh1由细胞质向细胞核转位有关。Objective To investigate the regulative mechanism of phosphatidylinositol 3 kinase（PI3K）/Akt signaling pathway on S-phase kinase-associated protein 2（Skp2） via Cdc20 homolog 1（Cdh1） in non-small cell lung cancer（NSCLC）.Methods NSCLC cell lines A549,LK2 and H460 were cultured in vitro and treated with LY294002 to block the PI3K/Akt pathway.Western blot method was used to detect the expression of Skp2,Cdh1 and p-Akt proteins.Immunofluorescence（IF） analysis was used to examine the localization of Cdh1 in NSCLC.Results Compared with control cells,the protein expression of Skp2 and p-Akt decreased（P0.01）.IF result showed a redistribution of Cdh1 to the nucleus.Conclusion The inhibitor of PI3K/Akt signaling pathway LY294002 down-regulated the expression of Skp2,which might correlated with the nuclear localization of Cdh1.

关 键 词：肺肿瘤 磷脂酰肌醇三羟基激酶 S期激酶相关蛋白2 Cdc20同源蛋白1 

分 类 号：R735.7[医药卫生—肿瘤] Q78[医药卫生—临床医学]