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

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、4-8h，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。

Preliminary studies of blocking VEGF and EGFR signal pathway on proliferation of HepG2 cells

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 （MTr） 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 sig- nal pathway can inhibit the proliferation and induce the apoptosis of HepG2 cells in a concentration-de- pendent manner.