罗格列酮通过PTEN/PI3K/Akt通路影响人肝癌细胞QGY-7701的增殖及凋亡  

Rosiglitazone Affects Proliferation and Apoptosis of Human Liver Cancer Cell Line QGY-7701 through PTEN/PI3K/Akt Pathway

作　　者：万春梅 胡雪莲[1] 陈欢[1] 王武 余瑜[1] Wan Chunmei;Hu Xuelian;Chen Huan;Wang Wu;Yu Yu(Chongqing Medical University,Chongqing,400016)

机构地区：[1]重庆医科大学,重庆400016

出　　处：《基因组学与应用生物学》2020年第5期2418-2423,共6页Genomics and Applied Biology

基　　金：国家科技重大计划(2010ZX09401-306-1-1);国家自然科学研究基金项目(81172097,30772595,30171070和30371632);重庆市科学技术项目(cstc2002-14-25和cstc2017jcyjAX0228)共同资助。

摘　　要：本研究为了探讨罗格列酮对人肝癌细胞QGY-7701增殖凋亡的影响,阐明其作用机制,以罗格列酮和人肝癌细胞QGY-7701为材料,通过结晶紫染色及CCK8方法,发现罗格列酮对人肝癌细胞QGY-7701有明显的抑制作用,其IC50为83.24μmol/L;通过RT-PCR,发现罗格列酮上调PTEN基因;通过Western blotting,发现罗格列酮能使PCNA、Bcl-2和p-Akt蛋白表达下调,使Bad、PPARγ和PTEN的蛋白表达上调,经PPARγ抑制剂处理后,PTEN和p-Akt表达下调。结果表明,罗格列酮可能通过调节PTEN/PI3K/AKT基因的途径,诱导人肝癌细胞QGY-7701凋亡,并抑制癌细胞的进一步增殖。本研究为临床肝癌研究提供理论基础。In order to investigate the effect of rosiglitazone on the proliferation and apoptosis of human hepatoma cell QGY-7701,and to elucidate its mechanism of action,using rosiglitazone and human hepatoma cell QGY-7701 as materials,through crystal violet staining and CCK8 method,we found Rosiglitazone has a significant inhibitory effect on human hepatoma cells QGY-7701 with IC50 of 83.24μmol/L;by RT-PCR,rosiglitazone was found to upregulate the PTEN gene;by Western blotting,rosiglitazone was found to downregulate the protein expression of PCNA,Bcl-2 and p-Akt,upregulate the protein expression of Bad,PPARγand PTEN.After treatment with PPARγinhibitors,the expression of PTEN and p-Akt was down-regulated.The results showed that rosiglitazone may induce apoptosis of human hepatoma cell QGY-7701 by regulating the PTEN/PI3K/AKT gene pathway and inhibit the further proliferation of cancer cells.This study provides a theoretical basis for clinical liver cancer research.

关 键 词：罗格列酮 PTEN/PI3K/AKT QGY-7701 增值 凋亡 

分 类 号：R735.7[医药卫生—肿瘤]