Gorospe M, Holbrook N J
Section on Gene Expression and Aging, National Institute on Aging, NIH, Baltimore, Maryland 21224, USA.
Cancer Res. 1996 Feb 1;56(3):475-9.
Prostaglandin A2 (PGA2) treatment induces growth arrest of most cells, and we have recently shown that, for breast carcinoma MCF-7 cells, this is correlated with an induction of the cyclin-dependent kinase inhibitor p21 and reduced cyclin-dependent kinase 2 activity. In this study, we demonstrate that, in RKO cells, PGA2 treatment fails to induce growth arrest, but rather results in significant cell death. These effects are correlated with lack of p21 induction and enhanced cyclin-dependent kinase 2 activity. Reduction of endogenous p21 expression in MCF-7 cells through expression of antisense p21 resulted in a response pattern approaching that seen in RKO cells, characterized by diminished growth arrest and increased death. These findings support a role for p21 in PGA2-mediated growth arrest, which we propose serves to prevent cell death caused by inappropriate cell cycle progression.
前列腺素A2(PGA2)处理可诱导大多数细胞生长停滞,我们最近发现,对于乳腺癌MCF-7细胞而言,这与细胞周期蛋白依赖性激酶抑制剂p21的诱导及细胞周期蛋白依赖性激酶2活性降低相关。在本研究中,我们证明,在RKO细胞中,PGA2处理未能诱导生长停滞,反而导致显著的细胞死亡。这些效应与p21诱导缺失及细胞周期蛋白依赖性激酶2活性增强相关。通过反义p21表达降低MCF-7细胞内源性p21表达,导致其反应模式接近RKO细胞,其特征为生长停滞减弱及死亡增加。这些发现支持p21在PGA2介导的生长停滞中发挥作用,我们认为这一作用是为了防止因不适当的细胞周期进程导致的细胞死亡。