摘要
目的探讨B7-H1(B7-homolog 1)在乙型肝炎病毒(HBV)感染导致的肝细胞癌(HCC)中的作用机制。方法通过慢病毒lentivirus-B7-H1转染人正常肝细胞系L02、人肝癌细胞系HepG2、HepG2.2.15后,应用MTT法观察细胞活性,流式细胞仪检测细胞的凋亡情况,Western blot技术检测蛋白B7-H1、Survivin蛋白的变化情况。结果抑制B7-H1表达水平后,通过MTT检测表明细胞系HepG2.2.15细胞活性比HepG2细胞、L02细胞活性降低,流式细胞仪检测凋亡增加,同时Western blot显示Survivin蛋白的表达减少。结论通过慢病毒转染抑制B7-H1的表达可以促进细胞系HepG2.2.15凋亡,B7-H1可能是通过调控Survivin的变化影响HBV感染的肿瘤细胞的增殖与凋亡。
Objective To study the effect and mechanism of B7-H1 in the course that hepatitis B virus （HBV） caused hepatocelhlar carcinoma （HCC）. Methods This study employed lentivirus mediated knockdown of B7- H1 to elucidate the oncogenic role of B7-H1 in human hepatocelhlar carcinoma HepG2 and HepG2.2.15 cell, MTT assay and flow cytometry that B7-H1 knockdown induced decreased cell proliferation and increased apoptosis, Western blot used to test the expression of B7-H1 and Survivin. Results The transfected lentivirus- B7-H1 HepG2 and HepG2.2.15 cells induced decreased cell proliferation and increased apoptosis, and at the same time the expression of Survivin protein also decreased. Conclusions Knockdown of B7-H1 induced decreased cell proliferation and increased apoptosis of HepG2.2.15 cell, B7-H1 effected on proliferation and apoptosis of that HBV causes HCC which may have role in Survivin ways.
出处
《中国肝脏病杂志（电子版）》
CAS
2013年第4期6-9,共4页
Chinese Journal of Liver Diseases：Electronic Version
基金
国家"十二五"传染病重大专项(No.2012ZX10002003)
建立HBV相关肝脏纤维化无创诊断标准/模型的研究(2013ZX10002005)
