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Mcl-1 siRNA对TRAIL诱导胃癌细胞凋亡的影响

金玮 吴萍

安徽医科大学学报2016,Vol.51Issue(1):47-51,5.
安徽医科大学学报2016,Vol.51Issue(1):47-51,5.

Mcl-1 siRNA对TRAIL诱导胃癌细胞凋亡的影响

Effect of Mcl-1 siRNA on TRAIL-induced apoptosis in gastric cancer cells

金玮 1吴萍2

作者信息

  • 1. 安徽医科大学附属巢湖医院耳鼻喉科,巢湖 238000
  • 2. 安徽医科大学免疫学教研室,合肥 230032
  • 折叠

摘要

Abstract

Objective To explore the effect of Mcl-1 small interference RNA ( siRNA) on tumor necrosis factor-re-lated apoptosis-inducing ligand ( TRAIL)-induced apoptosis in gastric cancer HGC-27 cells. Methods The apop-totic rates of cells treated with TRAIL and pan-caspase inhibitor ( z-VAD-fmk) alone or combination were measured by propidium iodide (PI) method using flow cytometry. The activation of caspase-3, cleavage of PARP-1, as well as the protein level of anti-apoptotic Bcl-2 proteins Bcl-2, Bcl-XL and Mcl-1 before and after TRAIL treatment were monitored by Western blot analysis. Transfection of Mcl-1 siRNA was performed using Lipofectamine 2000 reagent. The efficiency of gene silencing was quantified by Western blot and the effect of Mcl-1 siRNA on TRAIL-induced apoptosis was measured using PI method. Results HGC-27 cells were resistant to TRAIL-induced apoptosis, and z-VAD-fmk pretreatment could block apoptosis nearly completely. Activation of caspase-3 and cleavage of PARP-1 occurred in the late stage of apoptosis. The expression levels of Bcl-2, Bcl-XL and Mcl-1 were not altered after exposure to TRAIL. Transfection with Mcl-1 siRNA could obviously downregulate the expression evel of Mcl-1 in HGC-27 cells and enhanced the sensitivity of cells to TRAIL-induced apoptosis. Conclusion Overexpression of Mcl-1 may account for the resistance of HGC-27 cells to TRAIL.ownregulation of Mcl-1 by siRNA can effectively enhance the sensitivity of HGC-27 cells to TRAIL-induced apoptosis.

关键词

胃癌/细胞凋亡/小干扰RNA/Mcl-1

Key words

gastric cancer/apoptosis/siRNA/Mcl-1

分类

医药卫生

引用本文复制引用

金玮,吴萍..Mcl-1 siRNA对TRAIL诱导胃癌细胞凋亡的影响[J].安徽医科大学学报,2016,51(1):47-51,5.

基金项目

安徽高校省级自然科学研究项目(编号:KJ2014A113) (编号:KJ2014A113)

安徽医科大学学报

OA北大核心CSTPCD

1000-1492

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