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Cancer Research 67, 6477, July 1, 2007. doi: 10.1158/0008-5472.CAN-07-0746
© 2007 American Association for Cancer Research
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Endocrinology

Positive Cross-Regulatory Loop Ties GATA-3 to Estrogen Receptor {alpha} Expression in Breast Cancer

Jérôme Eeckhoute, Erika Krasnickas Keeton, Mathieu Lupien, Susan A. Krum, Jason S. Carroll and Myles Brown

Division of Molecular and Cellular Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts

Requests for reprints: Myles Brown, Division of Molecular and Cellular Oncology, Dana-Farber Cancer Institute, Boston, MA 02115. Phone: 617-632-4738; Fax: 617-582-8501; E-mail: myles_brown{at}dfci.harvard.edu.

The transcription factor GATA-3 is required for normal mammary gland development, and its expression is highly correlated with estrogen receptor {alpha} (ER{alpha}) in human breast tumors. However, the functional role of GATA-3 in ER{alpha}-positive breast cancers is yet to be established. Here, we show that GATA-3 is required for estradiol stimulation of cell cycle progression in breast cancer cells. The role of GATA-3 in estradiol signaling requires the direct positive regulation of the expression of the ER{alpha} gene itself by GATA-3. GATA-3 binds to two cis-regulatory elements located within the ER{alpha} gene, and this is required for RNA polymerase II recruitment to ER{alpha} promoters. Reciprocally, ER{alpha} directly stimulates the transcription of the GATA-3 gene, indicating that these two factors are involved in a positive cross-regulatory loop. Moreover, GATA-3 and ER{alpha} regulate their own expression in breast cancer cells. Hence, this transcriptional coregulatory mechanism accounts for the robust coexpression of GATA-3 and ER{alpha} in human breast cancers. In addition, these results highlight the crucial role of GATA-3 for the response of ER{alpha}-positive breast cancers to estradiol. Moreover, they identify GATA-3 as a critical component of the master cell-type–specific transcriptional network including ER{alpha} and FoxA1 that dictates the phenotype of hormone-dependent breast cancer. [Cancer Res 2007;67(13):6477–83]




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cancer Prevention Research
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Copyright © 2007 by the American Association for Cancer Research.