正常乳腺上皮细胞通过p53介导的途径诱导MCF-7乳腺癌细胞凋亡

Robert-Alain Toillon , Eric Adriaenssens , Danièle Wouters , Severine Lottin , Bénoni Boilly , Hubert Hondermarck , Xuefen Le Bourhis
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引用次数: 7

摘要

癌症的发展不仅取决于肿瘤细胞本身的性质,还取决于各种正常细胞的调节作用。本研究旨在更好地了解正常乳腺上皮细胞(NBEC)控制MCF-7乳腺癌细胞生长的机制。当MCF-7细胞用NBEC条件培养基处理时,细胞生长受到浓度依赖性的抑制。这种抑制是由于诱导细胞凋亡而不改变细胞周期进程。细胞凋亡的诱导与p53、p21waf1水平升高和bcl-2水平降低有关。用两种p53 cDNA构建的MCF-7细胞的瞬时转染表明,内源性p53介导了细胞凋亡的诱导。综上所述,我们的研究结果表明,NBEC通过内源性p53诱导MCF-7乳腺癌细胞凋亡,从而抑制MCF-7乳腺癌细胞的生长。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Normal Breast Epithelial Cells Induce Apoptosis of MCF-7 Breast Cancer Cells through a p53-Mediated Pathway

Cancer development depends not only on the nature of the tumor cells themselves but also on the regulatory effects of various normal cells. The present study was performed to better understand the mechanism by which normal breast epithelial cells (NBEC) can control the growth of MCF-7 breast cancer cells. When MCF-7 cells were treated with NBEC conditioned medium, cell growth was inhibited in a concentration-dependent manner. This inhibition was due to an induction of apoptosis without any change in cell cycle progression. The induction of apoptosis was correlated with increased levels of p53, p21waf1 and decreased levels of bcl-2. Transient transfections of MCF-7 cells with two p53 cDNA constructs demonstrated the induction of apoptosis was mediated by endogenous p53. Taken together, our results indicate that NBEC inhibit the growth of MCF-7 breast cancer cells by inducing apoptosis in them via endogenous p53.

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