首页> 中文期刊> 《实用临床医药杂志》 >阻断血管内皮生长因子与表皮生长因子受体协同信号影响HepG2肝癌细胞生长的实验研究

阻断血管内皮生长因子与表皮生长因子受体协同信号影响HepG2肝癌细胞生长的实验研究

         

摘要

Objective To investigate the effects of blocking vascular endothelial growth factor (VEGF) and epidermal growth factor receptor ( EGFR) signal pathway on proliferation of HepG2 cells. Methods HepG2 cells were cultured in vitro. After HepG2 cells were incubated with anti -VEGF or anti-EGFR at concentration of 10-2, 10 -3 10 -4 and 10-5 μg/μL for 12,24 and 48 h, the reduced proliferation rates of HepG2 cells were examined by using methyl thiazolyl tetrazolium (MTT) assay. A dose - response curve was established by plotting the reduced cell proliferation rates against the concentrations of antibody. Results Anti-VEGF and anti-EGFR induced inhibition of proliferation of HepG2 cells in a concentration - dependent manner. Conclusion Blocking VEGF and EGFR signal pathway can inhibit the proliferation and induce the apoptosis of HepG2 cells in a concentration-dependent manner.%目的 探讨阻断血管内皮生长因子(VEGF)与表皮生长因子受体(EGFR)协同信号对HepG2肝癌细胞生长的影响.方法 体外培养HepG2肝癌细胞株,分别将含不同浓度(10-2、10-3、10-4、10-5μg/μL)抗VEGF抗体与抗EGFR抗体的培养液与HepG2肝癌细胞共同培养12、24、48 h,采用四甲基偶氮唑盐微量酶反应比色法(MTT)比色法计算细胞生长抑制率.以抗体的不同浓度对HepG2肝癌细胞抑制率作图,得到剂量反应曲线.结果 抗VEGF抗体和抗EGFR抗体对HepG2肝癌细胞生长的抑制均呈浓度依赖性,并且有一定的量效关系.结论 阻断VEGF与EGFR协同信号可抑制HepG2抗体肝癌细胞的增殖,具有剂量依赖性,可诱导细胞凋亡.

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