紫杉醇提高胃癌MGC803细胞对TRAIL的敏感性  

Paclitaxel increases the senisitivity of gastric cancer MGC803 cells to TRAIL

作　　者：徐玲[1] 曲秀娟[1] 刘云鹏[1] 刘静[1] 侯科佐[1] 张晔[1] 

机构地区：[1]中国医科大学附属第一医院肿瘤内科,辽宁沈阳110001

出　　处：《现代肿瘤医学》2011年第4期650-653,共4页Journal of Modern Oncology

基　　金：国家自然科学基金(No.30770993)

摘　　要：目的:研究紫杉醇对TRAIL诱导胃癌细胞凋亡的影响,探讨死亡受体5(DR5)在TRAIL诱导细胞凋亡中的作用。方法:采用MTT法测定细胞活力,流式细胞仪检测细胞凋亡,western blot检测蛋白表达。结果:在MGC803细胞中,100ng/ml的TRAIL导致轻度的增殖抑制和细胞凋亡,TRAIL(100ng/ml)联合紫杉醇(3.41g/ml)引起明显的增殖抑制和细胞凋亡(P<0.05)。TRAIL单药没有改变死亡受体5(DR5)的表达,而3.41g/ml紫杉醇作用MGC803细胞后明显上调了DR5的表达。结论:紫杉醇通过上调DR5的表达增强TRAIL诱导的胃癌MGC803细胞凋亡。Objective：To assess the effect of paclitaxel on TRAIL-induced apoptosis in gastric cancer cells,and the action of death receptor 5（DR5） in TRAIL-induced apoptosis.Methods：Cell proliferation was measured using MTT assay.Cell apoptosis was determined by flow cytometry.Expression of proteins was analyzed by western blot.Results：Treatment with 100 ng/ml TRAIL for 24 h resulted in a slight reduction in cell viability and a little increase in cell apoptosis in MGC803 cells.Treatment with TRAIL（100 ng/ml） and paclitaxel（3.41 g/ml） leaded to a significant reduction in cell viability and a dramatic increase in cell apoptosis（P0.05）.TRAIL alone did not change the expression of death receptor 5（DR5）,while 3.41 g/ml paclitaxel significantly upregulated the expression of DR5 in MGC803 cells.Conclusion：Paclitaxel enhanced TRAIL-induced apoptosis in gastric cancer MGC803 cells by upregulating the expression of DR5.

关 键 词：TRAIL 紫杉醇 胃癌 凋亡 死亡受体 

分 类 号：R735.2[医药卫生—肿瘤]