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J. Biol. Chem., Vol. 281, Issue 32, 22656-22664, August 11, 2006

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The SWI/SNF Chromatin Remodeling Subunit BAF57 Is a Critical Regulator of Estrogen Receptor Function in Breast Cancer Cells^*

Juana M. García-Pedrero, Evangelos Kiskinis, Malcolm G. Parker, and Borja Belandia¹

From the Institute of Reproductive and Developmental Biology, Imperial College London, London W12 ONN, United Kingdom and Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Biomédicas and Universidad Autónoma de Madrid, 28029 Madrid, Spain

Estrogen receptors (ERs) play critical roles in both normal mammary gland development and in the formation and progression of breast tumors, constituting a major therapeutic target for breast cancer treatment. We have previously described that ER transcriptional activity is potentiated by BAF57, a core subunit of the mammalian SWI/SNF chromatin remodeling complex. Here we provide evidence demonstrating an important role for BAF57 as regulator of ER functions in breast cancer cells. Different experimental manipulations leading to the abrogation of BAF57 expression and/or function severely reduced the expression of various endogenous ER target genes and blocked estrogen-stimulated proliferation in ZR-75-1 breast cancer cells. Moreover, using a structure-function analysis, we have defined the protein domains required for the functional interaction between ER and BAF57, including a key region within the hinge of ER that is essential for BAF57 recruitment and its function on ER-mediated transcription. Interestingly, we found that BAF57 is an ER subtype-selective modulator that specifically regulates ER-mediated transcription. Taken together, our results suggest that targeting BAF57 could represent a new way to effectively inhibit the action of ER.

Received for publication, March 20, 2006 , and in revised form, June 9, 2006.

^* This work was supported by Wellcome Trust Grant 061930, Association for International Cancer Research Grant 03-098, and Ministerio de Educacióny Ciencia Grant SAF2004-02549. 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.

¹ To whom correspondence should be addressed: Instituto de Investigaciones Biomédicas, CSIC-UAM, Arturo Duperier 4, 28029 Madrid, Spain. Tel.: 34-91-585-4453; Fax: 34-91-585-4401; E-mail: bbelandia{at}iib.uam.es.

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