【摘要】 目的研究VEGF-C对体外培养的宫颈癌Hela细胞增殖和凋亡的分子机制。方法应用重组人VEGF-C蛋白体外刺激宫颈癌Hela细胞,MTT法检测细胞增殖、流式细胞仪检测细胞周期和凋亡、Western Blotting检测增殖凋亡相关基因Bcl-2、cyclin D1蛋白水平的变化。结果 10、20、50 ng/μl VEGF-C处理后,细胞增殖指数分别为(1.00±0.03)、(1.25±0.05)、(1.55±0.08)、(2.13±0.08),呈剂量依赖性升高(P<0.05)。细胞周期S期比率呈剂量依赖性升高(P<0.05),分别为(30.91±0.09)%、(37.95±0.27)%、(45.05±0.40)%、(64.26±0.20)%;细胞凋亡率呈剂量依赖性降低(P<0.05),分别为(12.4±0.3)、(11.4±0.2)、(9.6±0.15)、(5.5±0.25)。Bcl-2、cyclin D1蛋白表达呈剂量依赖性升高。结论外源性VEGF-C通过细胞内信号的传递,诱导cyclin D1的表达,使肿瘤细胞S期加快,促进细胞周期的进程,来促进Hela细胞增殖;诱导Bcl-2的表达,抑制凋亡。更多还原

【Abstract】 Objective To investigate the molecular mechanisms of cell proliferation and apoptosis induced by VEGF-C in human cervical cancer Hela cells. Methods Hela cells were stimulated by recombinant VEGF-C in vitro. Cell proliferation was detected by MTT assay. Cell cycle and cell apoptosis were detected by flow cytometry(FCM). The expression of proliferation and apoptosis related genes, Bcl-2 and cyclin D1, were determined by western blotting. Results VEGF-C of 10 ng/ μl, 20 ng/μl and 50 ng/μl was found to increase the cell proliferation to 1.25± 0.05,1.55± 0.08 and 2.13± 0.08 when compared to the control 1.00± 0.03. And the cell number in S phase was increased to(37.95± 0.27)%,(45.05± 0.40)% and(64.26± 0.20)% from the control(30.91± 0.09)%. The cell apoptosis was inhibited in a dose-dependent manner, with the apoptosis index decreasing to 11.4± 0.2, 9.6± 0.15 and 5.5± 0.25 from the control 12.4± 0.3(P< 0.05). The expression levels of Bcl-2 and cyclin D1 were increased in a dose-dependent manner after being stimulated by VEGF-C(P< 0.05). Conclusions Exogenous VEGF-C induces the expression of cyclin D1, which accelerates cell cycle phase S and promotes cell proliferation. It also inhibits cell apoptosis by inducing the expression of Bcl-2.更多还原