胶质瘤细胞U251中RNA干扰敲低wnt2的表达下调PI3K/AKT信号通路的体内外研究  

Study of downregulating PI3K/AKT pathway after knocking down Wnt2 by RNAi in U251 cell line in vitro and in vivo

作　　者：张志勇[1] 张晋霞[2] 李绍彩[3] 秦丽娟[4] 浦佩玉[5] 裘明哲[5] 江荣才[5] 

机构地区：[1]河北联合大学附属医院神经外科,河北唐山063000 [2]河北联合大学附属医院神经内一科,河北唐山063000 [3]遵化市人民医院心内科,河北遵化064200 [4]河北联合大学基础医学院生理学教研室,河北唐山063000 [5]天津医科大学总医院神经外科,天津市神经病学研究所神经肿瘤实验室,天津300000

出　　处：《海南医学院学报》2013年第6期721-724,727,共5页Journal of Hainan Medical University

基　　金：国家自然科学基金:Wnt与notch信号通路在脑胶质瘤中的表达调控机制研究(30300365);key project of Health Department of Hebei Province(grant No.20110170)~~

摘　　要：目的:研究人脑胶质瘤细胞U251中RNA干扰敲低wnt2的表达对PI3K/AKT信号通路的影响。方法:向U251细胞转染靶向Wnt2的siRNA后,免疫印记及免疫荧光检测转染后,Wnt2、Frizzled2、β-catenin、PI3K、磷酸化AKT的表达变化。建立裸鼠胶质瘤皮下动物模型,瘤内注射Wnt2siRNA观察以上指标的表达变化。结果:体外应用RNA干扰敲低Wnt2的表达后,frizzled2、β-catenin、PI3K、p-AKT的表达均下调。结论:胶质瘤细胞U251中RNA干扰敲低Wnt2的表达后,PI3K/AKT信号通路活性受到抑制。Objective： To study the effects of down regulating wnt2 expression by RNAi on the PI3K/AKT pathway in the human glioma cell U251.Methods： Animal glioma models were established by Wnt2 siRNA injection,the expression of Wnt2,frizzled2,β-catenin,PI3K and phosphorylated-AKT（p-AKT） was focused after knocking down of Wnt2 with RNAi in vitro and in vivo by Western blot analysis and immunohistochemistry methods.Results： The expression of Wnt2,frizzled2,β-catenin in Wnt pathway was positively correlated with PI3K and p-AKT expression either in vitro or in vivo study.Conclusion： The activation of PI3K/AKT was inhibited in the human gliomas cell U251 after wnt2 expressionwas knocked down with RNAi.

关 键 词：胶质瘤 Wnt2 FRIZZLED 2 β-catenin PI3K 磷酸化AKT 

分 类 号：R739.41[医药卫生—肿瘤]