S100A9参与乙型肝炎病毒X蛋白介导的HepG2细胞增殖与迁移  

S100A9 is Involved in Hepatitis B Virus X-induced Proliferation and Migration of Human Hepatocellular Carcinoma Cell HepG2

作　　者：张秀瑜 王玎 杜燕娥 武睿 段亮 ZHANG Xiu-yu;WANG Ding;DU Yan-e;WU Rui;DUAN Liang(The Second Affiliated Hospital of Chongqing Medical University,Chongqing 400016,China;The First Affiliated Hospital of Chongqing Medical University,Chongqing 400016,China)

机构地区：[1]重庆医科大学附属第二医院,重庆400016 [2]重庆医科大学附属第一医院,重庆400016

出　　处：《中国生物工程杂志》2018年第10期108-114,共7页China Biotechnology

基　　金：国家自然科学基金(81601837)资助项目

摘　　要：目的：探讨S100A9在乙型肝炎病毒X（HBx）介导的HepG2细胞增殖及迁移中的作用。方法：用表达HBx蛋白的重组腺病毒AdHBx感染HepG2细胞后,用CCK-8实验检测细胞增殖能力及划痕愈合实验检测细胞迁移能力;在HepG2/AdHBx细胞中转染S100A9-siRNA及其对照si RNA后,检测HepG2细胞增殖及迁移能力;在HepG2/AdHBx和对照组HepG2/Ad GFP细胞中,采用Real-time PCR及Western Blot检测S100A9基因及蛋白的表达情况;在HepG2/AdHBx细胞中,加入不同剂量的NF-κB抑制剂BAY11-7082后,检测各组中S100A9的基因及蛋白表达情况。结果：HBx促进HepG2细胞的增殖与迁移; S100A9-siRNA抑制S100A9的表达后,HBx促进HepG2细胞的增殖与迁移的作用降低,HBx介导的HepG2细胞的增殖与迁移部分依赖于S100A9; S100A9基因及蛋白表达在HepG2/AdHBx中较对照组HepG2/Ad GFP显著升高,HBx可致S100A9表达增加;抑制NF-κB转录活性后,AdHBx＋BAY11-7082组S100A9基因及蛋白表达较对照组显著降低,阻断NF-κB转录活性可部分抑制HBx调控的S100A9表达。结论：HBx可调控S100A9的表达且与NF-κB活化有关,S100A9参与HBx介导的HepG2细胞的增殖与迁移。Objective：To investigate the effect of S100A9 on hepatocellular carcinoma cell HepG2 and the relevant mechanism.Methods：CCK-8 assay and cell migration assay were used to study HepG2 growth and migration mediated by Hepatitis B virus X（HBx）respectively.Transfected S100A9-siRNA into cells for silencing S100A9 expression,then the growth and migration of HepG2 infected with Ad HBx were analyzed.Realtime PCR and Western blot were used to detect S100A9 m RNA levels and expression in HepG2 cells infected with Ad HBx or AdGFP.After the treatment with or without NF-κB inhibitor BAY11-7082,S100A9 m RNA levels and expression in AdHBx-infected HepG2 cells were detected again.Result：HBx enhances the growth and migration of HepG2 cells.Silencing S100A9 expression partially blocked HBx-induced growth and migration of HepG2cells.The m RNA level and protein expression of S100A9 were significantly higher in HepG2 cells infected with AdHBx than with AdGFP,and that suggests S100A9 expression can be modulated by HBx.NF-κB inhibitor treatment efficiently suppressed the increase of S100A9 levels caused by HBx.Conclusion：Expression of S100A9is regulated by HBx-mediated NF-κB activation,and S100A9 plays an important role in HBx-induced growth and migration of hepatocellular carcinoma cell HepG2.

关 键 词：S100A9 HEPG2细胞 乙型肝炎病毒X蛋白 NF-κB 

分 类 号：R73[医药卫生—肿瘤]