熊佳易;陈蕾;魏燕;圣娟娟;钱桂兰;

• 1:中国人民解放军总医院第六医学中心妇产科

摘要(Abstract)：

目的探讨程序性细胞死亡因子4(programmed cell death protein 4,PDCD4)对卵巢癌细胞生长、凋亡及磷酸化信号转导和转录激活因子3(phosphorylated signal transducer and activator of transcription 3,p-STAT3)、磷酸化p38丝裂原激活蛋白激酶(phosphorylated p38 mitogen activation protein kinase,p-p38MAPK)表达的影响。方法卵巢癌细胞SKO-V3转染PDCD4过表达载体(pDsRes2-N1-PDCD4)和对照载体(pDsRes2-N1),分别记为过表达组和阴性组,同时以不转染的细胞作为对照组。以下列方法对三组细胞进行检测和比较:以实时逆转录聚合酶链反应和蛋白质印迹法检测细胞PDCD4蛋白和mRNA表达水平,以噻唑蓝比色法和细胞克隆实验检测细胞增殖能力,以流式细胞术检测细胞凋亡情况,以蛋白质印迹法检测p-p38MAPK、p-STAT3水平。结果阴性组和对照组细胞中PDCD4 mRNA和蛋白表达水平、光密度(optical density,OD)、细胞克隆形成数目、凋亡率、p-p38MAPK和p-STAT3表达水平比较均无显著差异(P_均> 0.05)。过表达组细胞中PDCD4mRNA和蛋白表达水平及细胞凋亡率均明显高于对照组和阴性组(P_均<0.01),细胞OD和克隆形成数目均明显低于对照组和阴性组(P_均<0.01)。过表达组细胞p-STAT3/STAT3比值明显低于对照组(P <0.01),p-p38MAPK/p38MAPK比值明显高于对照组(P <0.01)。结论 PDCD4抑制卵巢癌细胞生长,促进卵巢癌细胞凋亡,这可能与其抑制STAT3信号通路激活和促进p38MAPK信号通路激活有关。

关键词(KeyWords)： 卵巢癌;程序性细胞死亡因子4;凋亡;生长

Abstract:

Keywords:

基金项目(Foundation):

作者(Authors): 熊佳易;陈蕾;魏燕;圣娟娟;钱桂兰;

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