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J. Biol. Chem., Vol. 279, Issue 26, 27008-27016, June 25, 2004
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-Estradiol and Phytoestrogens in Breast Cancer Cells*
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¶
From the
Departments of Pharmaco-Biology and Cellular Biology, University of Calabria, 87030 Rende (CS), Italy and the Département de Biologie Cellulaire, Université de Genève, Sciences III, CH-1211 Genève 4, Switzerland
A growing body of evidence concerning estrogen effects cannot be explained by the classic model of hormone action, which involves the binding to estrogen receptors (ERs) 
and ER
and the interaction of the steroid-receptor complex with specific DNA sequences associated with target genes. Using c-fos proto-oncogene expression as an early molecular sensor of estrogen action in ER-positive MCF7 and ER-negative SKBR3 breast cancer cells, we have discovered that 17-estradiol (E2), and the two major phytoestrogens, genistein and quercetin, stimulate c-fos expression through ER as well as through an ER-independent manner via the G protein-coupled receptor homologue GPR30. The c-fos response is repressed in GPR30-expressing SKBR3 cells transfected with an antisense oligonucleotide against GPR30 and reconstituted in GPR30-deficient MDA-MB 231 and BT-20 breast cancer cells transfected with a GPR30 expression vector. GPR30-dependent activation of ERK1/2 by E2 and phytoestrogens occurs via a G
-associated pertussis toxin-sensitive pathway that requires both Src-related and EGF receptor tyrosine kinase activities. The ability of E2 and phytoestrogens to regulate the expression of growth-related genes such as c-fos even in the absence of ER has interesting implications for understanding breast cancer progression.
Received for publication, March 31, 2004 , and in revised form, April 15, 2004.
* This research was supported by grants from the Associazione Italiana per la Ricerca sul Cancro (AIRC, 2003) and the Ministero dell'Università e Ricerca Scientifica e Tecnologica (PRIN, 2003). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
|| Supported by the Swiss National Science Foundation, Krebsforschung Schweiz, and the Canton de Genève.
¶ To whom correspondence should be addressed. Tel.: 39-0984496201; Fax: 39-0984493271; E-mail: sebastiano.ando{at}unical.it.
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