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J. Biol. Chem., Vol. 280, Issue 3, 2294-2299, January 21, 2005

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HOXA5-Twist Interaction Alters p53 Homeostasis in Breast Cancer Cells^*

Ioannis A. Stasinopoulos, Yelena Mironchik, Ana Raman, Flonne Wildes, Paul Winnard, Jr., and Venu Raman¶

From the Department of Radiology, Johns Hopkins University School of Medicine, Baltimore 21205, Maryland and the Department of Biological Sciences, University of Maryland at Baltimore County, Baltimore, Maryland 21250

The homeotic gene HOXA5 has been shown to play an important role in breast tumorigenesis. We have shown that loss of p53 correlated with loss of a developmentally regulated transcription factor, HOXA5, in primary breast cancer. Searching for potential protein interacting partners we found that HOXA5 binds to an anti-apoptotic protein, Twist. Furthermore, Twist-overexpressing MCF-7 cells displayed a deregulated p53 response to -radiation and decreased regulation of downstream target genes. Using a p53-promoter-reporter system, we demonstrated that HOXA5 could partially restore the inhibitory effects of Twist on p53 target genes. These effects are likely mediated through both the transcriptional up-regulation of p53 and the protein-protein interaction between HOXA5 and Twist. Thus, the loss of HOXA5 expression could lead to the functional activation of Twist resulting in aberrant cell cycle regulation and promoting breast carcinogenesis.

Received for publication, September 24, 2004

^* This work was supported by National Institutes of Health Grant 1RO1 CA097226 (to V. R.). 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.

^¶ To whom correspondence should be addressed: Dept. of Radiology, Johns Hopkins University School of Medicine, 340 Traylor Bldg., 720 Rutland Ave., Baltimore, MD 21205. Tel.: 410-955-7492; Fax: 410-614-1948; E-mail: vraman2{at}jhmi.edu.

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