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作 者:梁利波[1] 千新来[1] 马业伟[1] 王争[1] 刘玉英[1] 赵清正[1]
机构地区:[1]中国医学科学院中国协和医科大学肿瘤研究所,北京100021
出 处:《中华结核和呼吸杂志》2001年第11期663-665,共3页Chinese Journal of Tuberculosis and Respiratory Diseases
基 金:国家自然科学基金资助项目 ( 39770 82 2 )
摘 要: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 。Objective To investigate the effects of E1A gene on the proliferation rate and the cell cycle of human lung adenoma cell line. Methods The characteristics of human adenoma cells transfected and untransfected with E1A gene were studied including the cell growth rate in vitro, the tumorigenicity in nude mouse, and cell cycle analyzed by flow cytometry. The level of P16, P21, P53 and cyclinB1 was assayed using Western blot.Results The proliferation rate in vitro and the tumorigenicity in vivo of the human lung adenoma cells transfected with E1A gene (Anip973 E1A) were suppressed and cell cycle was retarded at G 2/M phase. There was no significant change in the level of P16, P21 and P53, however, the level of cyclinB1 diminished remarkedly. Conclusions E1A gene could suppress the proliferation of human adenoma cells in vitro and in vivo. The expression level of cyclinB1, one of the key G 2/M checkpoint modulators, was inhibited by E1A, resulting in retardation at G 2/M phase. It may be one of the mechanisms of E1A as a tumor suppressing gene.
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