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PI3K/Akt抑制剂对内质网应激下肝癌细胞MEK/ERK途径的影响 被引量：2

The effect of PI3K inhibitor on MEK/ERK pathway under endoplasmic reticulum stress in hepatocellular carcinoma
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摘要 目的:研究内质网应激介导的PI3K/Akt抑制剂对肝癌细胞MEK/ERK途径的影响。方法:采用PI3K抑制剂LY294002/激活型突变载体myr-Akt分别阻断/激活内质网应激介导的Akt和ERK活化,并利用Western blot ting技术分析内质网应激条件下PI3K/Akt和MEK/ERK途径间的关系。结果:阻断PI3K/Akt促进内质网应激介导的MEK/ERK活化,过度激活PI3K/Akt则抑制内质网应激介导的MEK/ERK活化。结论:PI3K/Akt和MEK/ERK信号途径间在内质网应激肝癌细胞中可能存在信号交流。 Objective：To research the effect of PI3K/Akt inhibitor on MEK/ERK pathway under endoplasmic reticulum stress in human hepatocellular carcinoma cells.Methods： PI3K inhibitor LY294002/constitutively activated Akt mutant construct were used to block/activate the PI3K/Akt pathway respectively.Then,Western blot ting was used to study the relation between the PI3K/Akt and MEK/ERK pathway under endoplasmic reticulum stress in human hepatocellular carcinoma cells.Results： PI3K inhibitor not only efficiently blocked Akt activation but also markedly increased ERK phosphorylation under endoplasmic reticulum stress.Furthermore,myr-Akt inhibited endoplasmic reticulum stress-mediated ERK phosphorylation.Conclusion： There is probably a cross-talk between the PI3K/Akt and MEK/ERK pathway under endoplasmic reticulum stress in human hepatocellular carcinoma cells.
作者 严冬梅 邓莉 张春燕 段春燕
机构地区 泸州医学院生物化学教研室 泸州医学院医学基础研究中心
出处 《泸州医学院学报》 2012年第2期127-129,共3页 Journal of Luzhou Medical College
基金 四川省卫生厅项目(100220)
关键词 PI3K/AKT MEK/ERK 内质网应激 肝癌细胞 PI3K/Akt MEK/ERK Endoplasmic reticulum stress Hepatocellular carcinoma cells
分类号 R735.7 [医药卫生—肿瘤] Q255 [生物学—细胞生物学]
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参考文献11

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泸州医学院学报
2012年 第2期

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