Toillon R A, Adriaenssens E, Wouters D, Lottin S, Boilly B, Hondermarck H, Bourhis X L
Laboratoire de Biologie du Développement, Equipe Facteurs de Croissance (UPRES 1033), Villeneuve d'Ascq Cedex, 59655, France.
Mol Cell Biol Res Commun. 2000 Jun;3(6):338-44. doi: 10.1006/mcbr.2000.0236.
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, p21(waf1) 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.
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。本研究旨在更好地理解正常乳腺上皮细胞（NBEC）控制MCF-7乳腺癌细胞生长的机制。当用NBEC条件培养基处理MCF-7细胞时，细胞生长以浓度依赖的方式受到抑制。这种抑制是由于诱导细胞凋亡，而细胞周期进程没有任何变化。细胞凋亡的诱导与p53、p21（waf1）水平的升高以及bcl-2水平的降低相关。用两种p53 cDNA构建体对MCF-7细胞进行瞬时转染表明，细胞凋亡的诱导是由内源性p53介导的。综上所述，我们的结果表明，NBEC通过内源性p53诱导MCF-7乳腺癌细胞凋亡来抑制其生长。
