GRP78在肝癌细胞抵抗棕榈酸诱导凋亡中的作用

被引：7

作者：

王进举 ^{[1
]}

张春燕 ^{[2
]}

肖斌 ^{[2
]}

李洪 ^{[2
]}

敬健雄 ^{[1
]}

冯春红 ^{[1
]}

夏先明 ^{[1
]}

代荣阳 ^{[2
]}

机构：

[1] 泸州医学院附属医院肝胆外科

[2] 泸州医学院生物化学教研室

来源：

中国老年学杂志 | 2016年 / 36卷 / 09期

关键词：

内质网应激; 葡萄糖调节蛋白78; 棕榈酸; 凋亡; 肝癌细胞;

D O I：

暂无

中图分类号：

R735.7 [肝肿瘤];

学科分类号：

100112 [医学生物化学与分子生物学];

摘要：

目的探讨内质网应激(ER stress)信号调控对棕榈酸(PA)诱导肝癌细胞凋亡的影响及其机制。方法培养人肝癌细胞SMMC-7721,在采用ER stress抑制剂4-苯丁酸(PBA)和过表达葡萄糖调节蛋白(GRP)78的基础上,利用流式细胞和免疫印迹技术分析ER stress以及GRP78对PA诱导肝癌细胞凋亡的影响。结果 PA诱导肝癌细胞发生ER stress,PBA抑制ER stress并减弱了PA诱导的肝癌细胞凋亡(P<0.05)。PA和ER stress诱导剂衣霉素(Tun)对ER stress分子标志的诱导水平差异显著(P<0.05),其中PA诱导的GRP78远低于Tun的诱导作用。过表达GRP78明显抑制了PA诱导的肝癌细胞凋亡(P<0.05)。结论 GRP78的诱导表达不足在PA介导的肝癌细胞凋亡中起重要作用。

引用

页码：2056 / 2059

页数：4

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