曲格列酮对肝癌细胞株HepG2侵袭潜能的抑制作用  

THE INHIBITORY EFFECT OF TROGLITAZONE ON INVASION POTENTIAL OF HUMAN LIVER CANCER CELL LINE HepG2

作　　者：李殿启[1] 杨甲梅[2] 张瑞秀[1] 殷正丰[1] 

机构地区：[1]第二军医大学东方肝胆外科医院分子肿瘤实验室,上海200438 [2]第二军医大学东方肝胆外科医院特需科,上海200438

出　　处：《肝胆外科杂志》2010年第5期381-382,共2页Journal of Hepatobiliary Surgery

摘　　要：目的观察过氧化物酶体增长因子活化受体γ激动剂曲格列酮对人肝癌细胞株HepG2侵袭潜能的抑制作用及其机制。方法以曲格列酮处理体外培养的HepG2细胞,Transwell小室检测细胞侵袭能力,RT-PCR检测尿激酶型纤溶酶原激活剂(urokinase-type plasminogen activator,u-PA)和血管内皮生长因子(vascular endothelial growth factor,VEGF)mRNA表达。结果经曲格列酮作用后,HepG2细胞侵袭潜能受到明显抑制,u-PA和VEGF mRNA的表达水平下降。结论曲格列酮可抑制肝癌细胞的侵袭潜能,其机制涉及下调u-PA、VEGF的表达。Objective To examine the effect of a peroxisome proliferator-activated receptor（PPAR） γ ligand troglitazone on invasiveness in human hepatic cancer cell line HepG2 and its mechanism.Methods HepG2 cell line was used in the experiments.Invasiveness assay was performed in Transwell chambers.Urokinase-type plasminogen activator（u-PA） and vascular endothelial growth factor（VEGF） mRNA were measured by RT-PCR.Results HepG2 cell invasiveness was significantly suppressed after treatment with troglitazone,which was associated with a reduction of mRNA levels of u-PA and VEGF.Conclusion Troglitazone inhibits invasion of human liver cancer cells,these effects involving down-regulation of u-PA and VEGF.

关 键 词：过氧化物酶体增长因子活化受体γ 癌 肝细胞 侵袭 

分 类 号：R735.7[医药卫生—肿瘤]