RNA干扰敲除Smac基因的表达促进人肺癌细胞的生长及增强顺铂耐药性  

Knockdown of Smac expression by RNAi enhances growth and cisplatin resistance of human lung cancer cells

作　　者：曾辉[1] 黄绪群[2] 蔡煜[1] 胡作为[1] 王刚胜 

机构地区：[1]武汉市第一医院肿瘤科 [2]黄石市第一医院肿瘤内1科

出　　处：《中华临床医师杂志（电子版）》2012年第11期39-42,共4页Chinese Journal of Clinicians(Electronic Edition)

摘　　要：目的探讨RNA干扰敲除Smac基因的表达对肺癌细胞的生长及顺铂(cDDP)耐药性的影响。方法通过转染含有以人Smac基因为靶基因的慢病毒载体系统,即含有小分子干扰RNA序列的pGC-FU载体,分别在A549和95D细胞中实施Smac基因敲除。通过转染含有Smac全长编码序列的pGC-FU载体来实现Smac的高表达。细胞生长、细胞周期及凋亡采用四甲基偶氮唑盐(MTT)法、克隆形成实验及流式细胞仪测定。药物耐药用10μg/ml顺铂检测。结果 Smac下调表达促进A549和95D细胞中肺癌细胞的生长及增强顺铂耐药性;Smac高表达抑制A549细胞生长并且增强其对顺铂的敏感性。结论 Smac抑制肺癌细胞生长并且增强其对顺铂的敏感性。Objective Smac is a mitochondrial protein that promotes apoptosis in many kinds of cancers.Here we investigate for the first time the effects of Smac RNAi on growth and drug resistance to cisplatin（cDDP）of lung cancer cells.Methods Knockdown of Smac expression in A549 and 95D cells was mediated by transfection with pGC-FU vector containing siRNA sequences targeting human Smac with the lentivirus vector system.Smac was also overexpressed by transfection with pOE vector containing full-length coding region of Smac.Cell growth,cell cycle and apoptosis were measured by methyl-thiazol tetrazolium（MTT）assay,colony-formation assay,and flow cytometry.Drug resistance was performed by treatment with 10 μg/ml cisplatin.Results Down-regulation of Smac enhanced cell growth and drug resistance to cisplatin of A549 and 95D cells,whereas Smac over-expression did reversely.Conclusions Smac helps inhibit cell growth and potentiate drug sensitivity to cisplatin of lung cancer cells.

关 键 词：RNA干扰 肺肿瘤 顺铂 SMAC 

分 类 号：R734.2[医药卫生—肿瘤]