论文部分内容阅读
目的 探讨E1A基因对人肺腺癌细胞增殖的抑制作用与细胞周期的关系及作用机制。方法 利用细胞增殖曲线和裸小鼠体内致瘤性实验研究E1A基因对人肺腺癌细胞增殖的影响 ,采用流式细胞术分析人肺腺癌细胞周期 ,以蛋白印迹方法分析P16、P2 1、P5 3和cyclinB1水平变化。结果转染E1A基因后 ,人肺腺癌细胞 (Anip973 E1A)生长缓慢 ,体内致瘤性降低。Anip973 E1A细胞周期出现明显的S期抑制和G2 M阻滞 ,周期调控蛋白P16、P2 1、P5 3水平无明显变化 ,但cyclinB1表达明显下降。结论 E1A基因能显著抑制人肺腺癌细胞的体内外增殖 ,降低周期蛋白cyclinB1的表达 ,使细胞周期阻滞于G2 M ,这可能与E1A基因抑癌作用有关
Objective To investigate the relationship between the inhibitory effect of E1A gene on human lung adenocarcinoma cell proliferation and cell cycle and its mechanism. Methods The proliferation of human lung adenocarcinoma cell line E1A was studied by cell proliferation curve and in vivo tumorigenicity in nude mice. The cell cycle of human lung adenocarcinoma was analyzed by flow cytometry. The expression of P16, P2 1, P5 3 and cyclinB1 levels. Results After transfected with E1A gene, human lung adenocarcinoma cell line Anip973 E1A grew slowly and the in vivo tumorigenicity decreased. The cell cycle of Anip973 E1A showed obvious S phase inhibition and G2 M block. The expression of cyclinB1 was not significantly changed in P16, P2 1 and P5 3 cells. Conclusion E1A gene can significantly inhibit the proliferation of human lung adenocarcinoma cells in vitro and in vivo, reduce the expression of cyclinB1 and block the cell cycle in G2 M, which may be related to the tumor suppressor effect of E1A gene