糖原合酶激酶3β以细胞周期蛋白D1依赖性方式引发人肺腺癌细胞A549细胞周期阻滞  

Glycogen synthase kinase 3βinduces cell cycle arrest in a cyclin D1-dependent manner in human lung adenocarcinoma cell line A549

作　　者：李建莎[1] 朱敏[1] 田丹[1] 王满香[1] 王芳[1] 李娜萍[1] 吴人亮[1] 

机构地区：[1]华中科技大学同济医学院病理学系卫生部呼吸系统疾病重点实验室,武汉430030

出　　处：《生理学报》2007年第2期204-209,共6页Acta Physiologica Sinica

基　　金：This work was supported by the National Natural Science Foundation of China (No. 30470757).

摘　　要：对糖原合酶激酶3β(glycogen synthase kinase 3β,6SK3β)在细胞增殖中的作用研究,在不同细胞系和不同刺激因素作用下得出了不同结论,本文旨在探讨GSK3β在人肺腺癌细胞系A549细胞生长中的直接作用。A549细胞瞬时转染持续激活型S9A-GSK3β以及显性负突变型KM-GSK3β两种GSK3β突变型质粒,改变GSK3β活性。24 h后,分别进行细胞计数,流式细胞术及Western blot检测。结果显示,增强GSK3β活性可导致细胞数量下降,G．期细胞百分比升高。细胞周期蛋白D1表达水平被GSK3β下调。结果提示,GSK3β可能以细胞周期蛋白D1依赖性方式引发A549细胞的G,期阻滞,从而发挥生长抑制效应。The effect of glycogen synthase kinase 3β （GSK3β） has been repeatedly implicated in cell proliferation, but studies on the effect of GSK3β in different cell lines with different stimuli have drawn different conclusions. To investigate the direct effect of GSK3β on cell growth in human lung adenocarcinoma cell line A549, we changed its activity by transient transfection with two kinds of GSK3β mutant plasmids, constitutively active form S9A-GSK3β and dominant negative form KM-GSK3β. Twenty-four hours later, cell counting, flow cytometry and Western blot detection were made respectively. The results showed that enhancing GSK3β activity caused a decrease in cell number, as well as a higher percentage of cells at G, phase. Further, the expression of cyclin D1 was downregulated by GSK3β. Taken together, our observations suggest that GSK3β may induce G1 cell cycle arrest in a cyclin D 1-dependent fashion and therefore possibly plays a growth-inhibitory role in A549 cells.

关 键 词：糖原合酶激酶3Β 细胞增殖 细胞周期 细胞周期蛋白D1 

分 类 号：R734.2[医药卫生—肿瘤]