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Originally published In Press as doi:10.1074/jbc.C000324200 on June 29, 2000

J. Biol. Chem., Vol. 275, Issue 34, 26551-26555, August 25, 2000
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HOXA5 Regulates Expression of the Progesterone Receptor*

Venu RamanDagger §, Akihiro TamoriDagger §, Mustafa ValiDagger , Karen ZellerDagger , Dorian KorzDagger , and Saraswati SukumarDagger ||

From the Dagger  Breast Cancer Program, Johns Hopkins Oncology Center, Baltimore, Maryland 21231

The majority of breast carcinomas show reduced or no expression of the transcription factor, HOXA5. Recently, we have shown that HOXA5 is a potent transactivator of p53 in breast cells and thus may affect the response of breast cancer cells to DNA damage. To determine whether HOXA5 played a role in growth and homeostasis in breast cells, we studied its interaction with the progesterone receptor. The progesterone receptor (PR) belongs to the superfamily of nuclear receptors whose members co-ordinate morphogenesis of the mammary gland in response to binding to their cognate ligands. An increased expression of the endogenous PR gene was seen in MCF-7 cells following induced expression of an exogenously transfected HOXA5 gene. HOXA5, but not HOXB4, -B5, or -B7 activated the PR promoter in two breast cancer cell lines, MCF-7 and Hs578T. Deletion and mutation analysis of the promoter identified a single HOXA5-binding site required for transactivation of the PR gene by HOXA5. HOXA5 binds directly to this site in the PR promoter. Thus, HOXA5 may behave as a transcriptional regulator of multiple target genes, two among which are p53 and the progesterone receptor.

* This work was supported by National Institutes of Health Grants RO1 C48943 (to S. S.) and T32 CA09630 (to M. V.).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.

§ These two authors contributed equally to this work.

Present address: Osaka City University Medical School, Osaka 545, Japan.

|| To whom correspondence should be addressed: Johns Hopkins Oncology Center, 1650 Orleans St., Baltimore, MD 21231-1000. Tel.: 410-614-2479; Fax: 410-614-4073; E-mail: saras@jhmi.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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