贝伐单抗对肝癌细胞株HepG2增殖的抑制作用  

Anti-proliferative effect of bevacizumab on liver cancer cell HepG2

作　　者：崔斐[1] 万骋[2] 郑航[1] 罗荣城[1] 陈斌[1] 陈锦章[1] 

机构地区：[1]南方医科大学南方医院肿瘤中心,广东广州510515 [2]南京大学医学院附属鼓楼医院,江苏南京210008

出　　处：《沈阳药科大学学报》2009年第6期483-487,共5页Journal of Shenyang Pharmaceutical University

基　　金：广东省科技计划资助项目(2008B030301144)

摘　　要：目的通过体外实验探讨贝伐单抗(bevacizumab)对人肝癌细胞HepG2增殖的抑制作用及可能的分子机制。方法MTT法检测贝伐单抗对肝癌细胞增殖的抑制作用;流式细胞仪检测细胞凋亡;RT-PCR分析肝癌细胞株VEGF、Flt-1、KDR mRNA表达量的变化。结果不同质量浓度的贝伐单抗对肝癌细胞株HepG2的增殖有抑制作用;贝伐单抗可诱导肝癌细胞株HepG2的凋亡;贝伐单抗作用于肝癌细胞株HepG2后,其VEGF、KDR mRNA表达量均减少。结论贝伐单抗可能通过阻断VEGF的促增殖作用而抑制HepG2细胞增殖。Objective To investigate the anti-proliferative effect of bevacizumab on human liver cancer cell HepG2 in vitro. Methods Cell proliferation and apoptosis were evaluated with MTT assays and flow cyto- metric analysis,respectively. The expression of VEGF,FIt-1 ,and KDR was measured by RT-PCR and Westere blot analysis. Results The results showed that bevacizumab inhibited HepG2 cell proliferation and induced cell apoptosis. After the treatment of bevacizumab on HepG2 cell, the expressions of VEGF and KDR were down-regulated. Conclusions Bevacizumab may inhibit HepG2 cell proliferation and induce apoptosis through blocking VEGF signal pathway.

关 键 词：肝癌 贝伐单抗 血管内皮生长因子受体 

分 类 号：R96[医药卫生—药理学]