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[Cancer Research 59, 4864-4869, October 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 4864-4869, October 1, 1999]
© 1999 American Association for Cancer Research

Endocrinology

Adrenal Androgens Stimulate the Proliferation of Breast Cancer Cells as Direct Activators of Estrogen Receptor {alpha}1

Marcello Maggiolini, Olivier Donzé, Elisabeth Jeannin, Sebastiano Andò and Didier Picard2

Département de Biologie Cellulaire, Université de Genève, Sciences III, CH-1211 Genève 4, Switzerland [M. M., O. D., E. J., D. P.], and Health Center, Department of Cellular Biology, Faculty of Pharmacy, University of Calabria, I-87030 Rende-Cosenza, Italy [S. A.]

Estrogens stimulate the proliferation of many breast tumors and cell lines derived from them. Antiestrogens have therefore become a powerful therapeutic agent to treat breast tumors that express estrogen receptor (ER) {alpha}. In addition, aromatase inhibitors are now used in postmenopausal women to block the in situ conversion of adrenal androgens to estrogens. This approach can only be successful if ER-{alpha} in a particular tumor is not directly stimulated by adrenal androgens. We have examined this possibility using several different cell lines as model systems: (a) wild-type MCF7 cells, an ER-{alpha}-dependent human breast cancer cell line; (b) MCF7SH cells, an estrogen-independent MCF7 variant; (c) Ishikawa cells, an ER-{alpha}-containing human uterine cell line; (d) ER-negative HeLa cells; and (e) budding yeast. Transactivation assays with transfected ER-{alpha} reporter genes reveal a direct activation of ER-{alpha} by dehydroepiandrosterone (DHEA), 5{alpha}-androstene-3ß,17ß-diol, testosterone, and the two nonaromatizable androgens, dihydrotestosterone and 5{alpha}-androstane-3ß,17ß-diol. The involvement of other steroid receptors could be ruled out with specific antihormones. Moreover, the same set of ligands stimulates the proliferation of the two breast cancer cell lines. At subsaturating and physiologically relevant concentrations of DHEA, DHEA stimulates the proliferation of MCF7SH cells, which correlates with a substantial, albeit submaximal, transcriptional response. Thus, adrenal androgens must also be considered as risk factors in postmenopausal women.




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Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1999 by the American Association for Cancer Research.