AntagomiR-103协同阿霉素对TGF-β1诱导的HepG2细胞转化及生长的影响  

Effects of AntagomiR-103 and ADM on TGF-β1 Induced EMT and Growth of Hep G2 Cell

作　　者：王金利 张敏[2] 

机构地区：[1]无锡市惠山区人民医院,江苏无锡214187 [2]贵州医科大学,贵州贵阳550004

出　　处：《贵州医科大学学报》2016年第12期1424-1429,共6页Journal of Guizhou Medical University

基　　金：贵阳市科技局基金项目[(2011103)17号]

摘　　要：目的:探讨antagomiR-103协同阿霉素(ADM)对TGF-β1诱导肝癌细胞(HepG2)发生上皮-间质细胞转化(EMT)及HepG2细胞存活率的影响。方法:HepG2细胞体外培养,设为control组、TGF-β1组、TGF-β1+ADM组、TGF-β1+microRNA inhibitor N.C组、TGF-β1+ADM+microRNA inhibitor N.C组、TGF-β1+antagomiR-103组、TGF-β1+ADM+antagomiR-103组及使用western-blot检测EMT标志蛋白N-Cadherin、E-Cadherin、vimentin的表达水平;设control组、TGF-β1组、antagomiR-103组、TGF-β1+antagomiR-103组,用不同浓度的ADM作用于各组细胞24 h,使用MTT法检测细胞存活率,并计算IC50。结果:与control组相比,antagomiR-103+ADM组E-Cadherin表达上调,N-Cadherin、Vimentin表达下调;细胞存活率随ADM浓度的增高而逐渐降低;在ADM浓度相同的条件下,不同药物预处理组之间进行比较,当ADM浓度为25 mg/L时,antagomiR-103+ADM组的细胞存活率明显低于其他组。结论:antagomiR-103联合ADM可抑制TGF-β1诱导发生EMT的HepG2细胞存活。Objective： To investigate the effect of antagomir-103 synergized by ADM on epithelial mesenchymal transition （EMT） in Hep G2 induced by TGF-β1 and on the cell survival rate of and Hep G2 cells. Methods ： Hep G2 ceils were cultivated in DMEM with 10% fetal calf serum and divid- ed into the control group, the TGF-β1 group, TGF-β1 ＋ADM group, TGF-β1 ＋ microRNA inhibitor N. C group, TGF-β1 ＋ ADM ＋ microRNA inhibitor N. C group, the TGF-β1 ＋ antagomiR-103 group, and the TGF-β1 ＋ ADM ＋ antagomiR-103 group. Western-blot was adopted to detect the expression level of EMT, E-cadherin, vimentin and N-cadherin in all these groups. On the other hand, the Hep G2 cells were also divided into the control group, TGF-β1group, antagomiR-103 group, TGF-β1 ＋ an- tagomiR-103. With different concentrations of ADM on each above group for 24 h, MTF method was used to detect cell survival rate, and IC 50 was calculated. Results： Compared with control group, the expression of E-cadherin was up-regulated in antagomiR-103 ＋ ADM group, while N-cadherin, vimen- tin expression was down regulated. The cell survival rate decreased with the increase of ADM concen- tration. The cell survival rate of antagomiR-103 ＋ ADM group was significantly lower than that of theother groups at the same ADM concentration and when the ADM concentration was 25 mg/L. Conclu- sion： antagomiR-103 combined with ADM can inhibit transformation of TGF-β1 induced EMT and growth of Hep G2 cell.

关 键 词：药物疗法 联合 肝肿瘤 细胞 antagomiR-103 阿霉素 上皮细胞一间充质细胞转换 TGFΒ-1 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R575.2[医药卫生—基础医学]