蛋白酶体抑制剂MG132对肝癌细胞生长的影响及其机制  

Effect of proteasome inhibitor MG132 on growth of hepatoma carcinoma cells and relevant mechanism

作　　者：钱冠华[1,2] 段昌柱[1,3] 彭惠民[1,4] 

机构地区：[1]重庆医科大学细胞生物学与遗传学教研室,重庆400016 [2]重庆医科大学附属第二医院妇产科,重庆400010 [3]重庆医科大学检验系临床检验诊断学教育部重点实验室,重庆400016 [4]重庆医科大学基础医学实验教学中心,重庆400016

出　　处：《中国生物制品学杂志》2012年第6期714-717,共4页Chinese Journal of Biologicals

基　　金：重庆医科大学重点科研课题(XBZD201001);国家自然科学基金资助项目(30872248)

摘　　要：目的探讨蛋白酶体抑制剂MG132对肝癌细胞HepG2和HepG2.2.15生长的影响及其机制。方法用不同浓度的MG132(0、250、500、1 000 nmol/L)处理HepG2和HepG2.2.15细胞,采用MTT法、流式细胞术和Western blot法检测其对两种细胞增殖、细胞周期和细胞中相关蛋白GSK-3β、pGSK-3β、β-catenin表达的影响。结果经MG132处理后,两种细胞的增殖均受到明显抑制,致使细胞周期阻滞在G1期,细胞中pGSK-3β和β-catenin蛋白的表达量上升,且均呈剂量依赖性,其对HepG2.2.15细胞的影响更为显著。结论 MG132可通过使肝癌细胞中GSK-3β失活和细胞周期阻滞抑制细胞增殖,为MG132成为一种新型HCC治疗药物提供了实验依据。Objective To investigate the effect of proteasome inhibitor MG132 on the growth of hepatoma carcinoma（HCC） HepG2 and HepG2.2.15 cells as well as the relevant mechanism.Methods HepG2 and HepG2.2.15 cells were treated with MG132 at various concentrations（0,250,500 and 1 000 nmol / L）,and determined for growth by MTT method,for proliferation and cell cycle by flow cytometry,and for expressions of relevant proteins GSK-3β,pGSK-3β and β-catenin by Western blot.Results Both the proliferations of HepG2 and HepG2.2.15 cells were inhibited after treatment with MG132,while the cell cycles were arrested at G1 phase,and the expression levels of pGSK-3β and β-catenin increased,each in a dose-dependent mode.However,the effect on HepG2.2.15 cells was more significant as compared with that on HepG2 cells.Conclusion MG132 inhibited the proliferations of HepG2 and HepG2.2.15 cells by inactivating the GSK-3β in cells and arresting the cell cycle,which provided an experimental basis for development of MG132 as a novel drug for HCC.

关 键 词：HEPG2细胞 HEPG2.2.15细胞 三肽基乙醛 原发性肝细胞癌 

分 类 号：R735.7[医药卫生—肿瘤]