人肝癌HepG2细胞表达甲胎蛋白抑制AMD3100诱导凋亡的研究  

Research of Alpha Fetoprotein Inhibits AMD3100 Induced Apoptosis of Human Haptoma HepG2 Cells

作　　者：龙儒桃[1,2] 翁启芳[1] 朱明月[1,3] 李伟[1,3] 马兰[2] 谢协驹[1,2] 李孟森[1,3] 

机构地区：[1]海南省肿瘤发生和干预重点实验室 海南医学院,海口571199 [2]海南医学院病理生理学教研室 [3]海南医学院分子生物学重点实验室

出　　处：《肿瘤防治研究》2013年第12期1109-1113,共5页Cancer Research on Prevention and Treatment

基　　金：国家自然科学基金资助项目(81360307;81260306;81160261;31060164;30960153);教育部新世纪优秀人才支持计划资助项目(NCET-10-0124);教育部重点科学技术资助项目(211146);海南省重点科技资助项目(DZXM20110038);海南省自然科学基金资助项目(309034;310044)

摘　　要：目的研究CXCR4信号对人肝癌HepG2细胞增殖及甲胎蛋白(alpha fetoprotein,AFP)表达在肝癌细胞耐受诱导凋亡中的作用。方法 MTT法检测CXCR4信号的拮抗剂AMD3100对人肝癌细胞HepG2增殖的影响,并用Western blot分析AMD3100处理前后AFP、CXCR4的表达变化;用RNA干扰技术抑制AFP表达24 h后再给予AMD3100处理24 h,荧光显微镜观察HepG2细胞的形态学变化以及流式细胞术分析细胞的凋亡情况。结果 AMD3100对人肝癌HepG2细胞的增殖有明显的抑制作用;AMD3100处理后HepG2细胞的CXCR4和AFP表达明显受到抑制;干扰AFP表达可协同AMD3100诱导HepG2细胞凋亡。结论 HepG2细胞通过表达AFP导致癌细胞耐受AMD3100诱导的凋亡。Objective To investigate the role of CXC chemokine receptor 4（CXCR4） signal effects on the expression of alpha fetoprotein（AFP） in human hepatoma cells, HepG2, and effects of AFP on AMD3100 induced apoptosis of HepG2 cells.Methods The effects of AMD3100, an antagonistic agent of CXCR4 ligand, on proliferation of human hepatocellular carcinoma cells HepG2 was detected by MTT. Western blot was applied to identify the expression of AFP and CXCR4. Small interference RNA was used to suppress expression of AFP in HepG2 cells, and apoptosis of HepaG2 cells were analazed by fluorescent microscopy and flow cytometry. Results Here we demonstrated that high concentration （〉l.0gg/ml） of AMD3100 might inhibit proliferation of HepG2 cells. AMD3100 had a function to down-regulate the expression of CXCR4 and AFP in HepG2 cells.The results also indicated that the expression of AFP had synergies with AMD3100 in inducing apoptosis of HepG2 cells in vitro. Conclusion HepG2 cells were tolerant to apoptosis induced by AMD3100 through expressing AFP.

关 键 词：CXCR4信号 甲胎蛋白 肝癌细胞 癌细胞增殖 

分 类 号：R735.7[医药卫生—肿瘤]