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Originally published In Press as doi:10.1074/jbc.M100953200 on February 21, 2001

J. Biol. Chem., Vol. 276, Issue 21, 17808-17814, May 25, 2001
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Estrogen Receptor beta -Selective Transcriptional Activity and Recruitment of Coregulators by Phytoestrogens*

Jinping AnDagger , Christina Tzagarakis-FosterDagger , Tiffany C. ScharschmidtDagger , Noureddine Lomri§, and Dale C. LeitmanDagger

From the Dagger  Department of Obstetrics, Gynecology, and Reproductive Sciences, Center for Reproductive Sciences and § Department of Medicine, Gastroenterology Division and Liver Center, University of California, San Francisco, California 94143

Estrogens used in hormone replacement therapy regimens may increase the risk of developing breast cancer. Paradoxically, high consumption of plant-derived phytoestrogens, particularly soybean isoflavones, is associated with a low incidence of breast cancer. To explore the molecular basis for these potential different clinical outcomes, we investigated whether soybean isoflavones elicit distinct transcriptional actions from estrogens. Our results demonstrate that the estrogen 17beta -estradiol effectively triggers the transcriptional activation and repression pathways with both estrogen receptors (ERs) ERalpha and ERbeta . In contrast, soybean isoflavones (genistein, daidzein, and biochanin A) are ERbeta -selective agonists of transcriptional repression and activation at physiological levels. The molecular mechanism for ERbeta selectivity by isoflavones involves their capacity to create an activation function-2 surface of ERbeta that has a greater affinity for coregulators than ERalpha . Phytoestrogens may act as natural selective estrogen receptor modulators that elicit distinct clinical effects from estrogens used for hormone replacement by selectively recruiting coregulatory proteins to ERbeta that trigger transcriptional pathways.

* This work was supported by a National Institutes of Health postdoctoral training grant and a Bank of America Giannini postdoctoral fellowship (to C. T.-F.) and grants from the Paul Beeson Physician Faculty Scholars in Aging Research Program (funded by the Alliance for Aging Research, John A. Hartford Foundation, Commonwealth Fund and Starr Foundation), NICHD Women's Reproductive Health Research Program, National Institutes of Health, and the Susan B. Komen Foundation (to D. C. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: University of California, San Francisco, Center for Reproductive Sciences, HSE 1619 P. O. Box 0556, San Francisco, CA 94143-0556. Tel.: 415-502-5261; Fax: 415-753-3271; E-mail: leitmand@obgyn.ucsf.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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