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Clinical Cancer Research Vol. 5, 2971-2977, October 1999
© 1999 American Association for Cancer Research

Cancer Biology, Immunology, Cytokines

Tamoxifen-induced Apoptosis in Breast Cancer Cells Relates to Down-Regulation of bcl-2, but not bax and bcl-XL, without Alteration of p53 Protein Levels1

Guo-Jun Zhang2, Izo Kimijima, Masamitsu Onda, Masahiko Kanno, Hisayoshi Sato, Takanori Watanabe, Atsuo Tsuchiya, Rikiya Abe and Seiichi Takenoshita

Department of Surgery II [G. J. Z., I. K., M. O., M. K., H. S., T. W., A. T., S. T.], Fukushima Medical University School of Medicine, Ohara Research Institute [R. A.], Ohara General Hospital, Fukushima 960-1295, Japan

Tamoxifen (TAM) has been shown to induce apoptosis in breast cancer cells. bcl-2 family genes, which can interact with each other, have been shown to interfere with apoptosis after various stimuli. In this study, we investigated the effects of TAM on bcl-2 family gene products bcl-2, bax, and bcl-XL and on p53 levels in estrogen receptor-positive MCF-7 breast cancer cells. We found that TAM induced time- and concentration-dependent down-regulation of bcl-2 at both the mRNA and protein level. Down-regulation of bcl-2 correlated with TAM-induced apoptosis. In addition, estradiol treatment significantly increased bcl-2 protein expression and blocked the reduction of bcl-2 by TAM. TAM did not, however, affect bax, bcl-XL, or p53 expression at the mRNA or protein level. Our results demonstrate that TAM can induce apoptosis in a time- and dose-dependent manner by modulating bcl-2 levels in breast cancer cells, and down-regulation of bcl-2 induced by TAM was not accompanied by alterations in p53 levels.




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