白花蛇舌草总黄酮对TGF-β1诱导的肝癌MHCC97-H细胞EMT的逆转作用及其机制  

Effect and mechanism of total flavones of oldenlendia diffusa willd on epithelial-mesenchymal transition of cell line MHCC97-H induced by TGF-β1

作　　者：张彦兵[1] 朱娇[2] 肖菊香[2] 郭亚焕[1] 廖子君[1] 徐瑞[1] 

机构地区：[1]西安交通大学附属陕西省肿瘤医院肿瘤内科,陕西西安710061 [2]西安交通大学第一附属医院肿瘤内科,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2016年第2期279-282,306,共5页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：陕西省社会发展攻关计划项目(No.2013K12-07-12)~~

摘　　要：目的探讨白花蛇舌草总黄酮(FOD)对TGF-β1诱导肝癌细胞MHCC97-H上皮细胞间质转化(EMT)的逆转作用及其相关机制。方法用TGF-β1诱导MHCC97-H细胞建立EMT模型,再将其分为5组:正常对照组、TGF-β1组、TGF-β1+FOD组、TGF-β1+5-FU组及TGF-β1+FOD+5-FU组,分别干预48h,Transwell侵袭小室法检测细胞体外侵袭能力,Western blot法检测各组细胞中E-cadherin、vimentin蛋白的表达。结果与正常细胞形态相比,TGF-β1诱导后细胞呈现明显的长梭形,且侵袭能力增强(P=0.02);给予药物处理后,TGF-β1+FOD组、TGF-β1+5-FU组细胞的穿透能力较TGF-β1组减弱(P=0.03、P=0.02),且联合用药组减弱程度更加明显(P=0.01);Western blot结果显示,TGF-β1组细胞中E-cadherin蛋白表达显著降低(P=0.01),vimentin蛋白的表达显著增加(P=0.01),TGF-β1+FOD组、TGF-β1+5-FU组E-cadherin蛋白表达有所上调(P=0.03、P=0.02),vimentin蛋白的表达有所下调(P=0.04、P=0.03),且联合组变化更为显著(P=0.01)。结论 FOD能够逆转TGF-β1诱导的肝癌MHCC97-H细胞的上皮间质转化,其机制可能与其抑制TGF-β1诱导的E-cadherin蛋白下调及上皮细胞间质转化相关。Objective To investigate the effects of total flavones of oldenlandia diffusa （FOD） on epithelial- mesenchymal transition in hepatocellular cancer cell line MHCC97-H. Methods TGF-β1 induced EMT in routinely cultured liver cancer cell line MHCC97-H; then MHCC97-H cell was divided into 5 groups： normal control group, TGF-β1 group, TGF-β1 ＋ FOD group, TGF-β1 5-FU group, and TGF-β1 FOD＋ 5-FU group. After 48 h of treatment, the invasion ability of MHCC97-H cell was detected by Transwell the proteins of E-cadherin and vimentin were determined by Western blot. Results Compared with the normal form of MHCC97-H cell line, the cell had obvious long fusiform after TGF-91 induction, and the invasion ability enhanced （P = 0.02）. But after treatment, the invasion ability of MHCC97-H cell decreased in FOD group and 5-FU group compared with that in TGF-β1 group （P= 0.03, P = 0.02）, and decreased more significantly in FOD＋ 5-FU group （P = 0.01）. The expression of E-cadherin at the protein level decreased significantly （P = 0. 01） in TGF-β1 group, which was abolished in FOD group （P=0.03） and 5-FU group （P=0.02）. The expression of vimentin at the protein level increased significantly （P=0.01） in TGF-β1 group, which was abolished in FOD group （P=0.04） and 5-FU group （P=0.03） and more obviously in FOD＋5-FU group （P=0.01）. Conclusion FOD can reverse the invasion of MHCC97-H cells in EMT induced by TGF-β1 through decreasing the expression of E-cadherin protein and inhibiting the epithelial-mesenchymal transition of MHCC97-H cell.

关 键 词：MHCC97-H细胞 TGF-Β1 上皮间质转化 白花蛇舌草总黄酮 侵袭 E-CADHERIN VIMENTIN 

分 类 号：R735.7[医药卫生—肿瘤]