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J. Biol. Chem., Vol. 280, Issue 1, 347-354, January 7, 2005

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Cell- and Ligand-specific Regulation of Promoters Containing Activator Protein-1 and Sp1 Sites by Estrogen Receptors and ^*

Jennifer R. Schultz, Larry N. Petz, and Ann M. Nardulli¶

From the Department of Molecular and Integrative Physiology, University of Illinois, Urbana, Illinois 61801

Estrogen plays a critical role in development and maintenance of female reproductive and mammary tissues, but is also involved in maintenance of cardiovascular, skeletal, and neural function. Although it is widely accepted that the estrogen-occupied receptor mediates its effects by interacting with estrogen response elements (EREs) residing in target genes, a number of estrogen-responsive genes contain no identifiable ERE. To understand how estrogen-responsive genes lacking EREs but containing activator protein 1 (AP-1) and Sp1 sites respond to hormone treatment, we have identified four discrete regions of the human progesterone receptor gene that contain AP-1 or Sp1 sites and examined their abilities to modulate transcription in the presence of 17-estradiol, ICI 182,780, tamoxifen, raloxifene, genistein, or daidzein. Transient cotransfection assays demonstrated that ER was a more potent activator of transcription than ER in bone, uterine, and mammary cells. The Sp1-containing promoters were substantially more potent transcriptional enhancers than the AP-1-containing promoters, but a 1.5-kb region of the human progesterone receptor gene containing both AP-1 and Sp1 sites was the most hormone-responsive promoter tested. The ability of ligands to modulate transcription of AP-1- or Sp1-containing promoters was dependent on cell context, but the expression of AP-1 or Sp1 proteins was not necessarily related to transcriptional response. Taken together, these studies have helped to delineate the roles of ER and ER in modulating transcription of genes containing AP-1 and Sp1 sites and define the effects of widely used, pharmacologic agents in target cells with distinct cellular environments.

Received for publication, July 13, 2004 , and in revised form, October 22, 2004.

^* This work was supported in part by National Institutes of Health Grants DK 53884 and DK 61463 (to A. M. N). 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 predoctoral National Institutes of Health Cell and Molecular Biology Training Program Grant T32 GM07283, National Institutes of Health Reproductive Biology Training Program Grant PHS 5T32 HD07028, and a Susan G. Komen Breast Cancer Foundation Dissertation Fellowship.

Supported by postdoctoral National Institutes of Health NIEHS Training Program Grant ES07326.

^¶ To whom correspondence should be addressed: Dept. of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, 524 Burrill Hall, 407 South Goodwin Ave., Urbana, IL 61801. Tel.: 217-244-5679; Fax: 217-333-1133; E-mail: anardull{at}life.uiuc.edu.

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