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Originally published In Press as doi:10.1074/jbc.M212050200 on December 13, 2002

J. Biol. Chem., Vol. 278, Issue 9, 7580-7590, February 28, 2003
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Human Growth Hormone-regulated HOXA1 Is a Human Mammary Epithelial Oncogene*

Xin ZhangDagger §, Tao ZhuDagger §, Yong ChenDagger , Hichem C. Mertani, Kok-Onn LeeDagger , and Peter E. LobieDagger ||

From the Dagger  Institute of Molecular and Cell Biology and Department of Medicine, National University of Singapore, 30 Medical Dr., Singapore 117609, Republic of Singapore and  CNRS Unité Mixte Recherche 5578, Physiologies Energetiques Cellulaires et Moléculaires, Université Claude Bernard, Lyon 1, France

Increased mammary epithelial expression of the human growth hormone (hGH) gene is associated with the acquisition of pathological proliferation. We report here that autocrine hGH production by human mammary carcinoma cells increased the expression and transcriptional activity of the homeobox domain containing protein HOXA1. Forced expression of HOXA1 in human mammary carcinoma cells resulted in increased total cell number primarily by the promotion of cell survival mediated by the transcriptional up-regulation of Bcl-2. HOXA1 also abrogated the apoptotic response of mammary carcinoma cells to doxorubicin. Forced expression of HOXA1 in mammary carcinoma cells, in a Bcl-2-dependent manner, resulted in dramatic enhancement of anchorage-independent proliferation and colony formation in soft agar. Finally, forced expression of HOXA1 was sufficient to result in the oncogenic transformation of immortalized human mammary epithelial cells with aggressive in vivo tumor formation. Herein, we have therefore provided a molecular mechanism by which autocrine hGH stimulation of human mammary epithelial cells may result in oncogenic transformation.

* This work was supported by grants from the Agency for Science, Technology and Research (A*STAR) of Singapore (to P. E. L.).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.

§ Both authors contributed equally to this work.

|| To whom correspondence should be addressed: Tel.: 65-6874-7847; Fax: 65-6779-1117; E-mail: mcbpel@imcb.nus.edu.sg.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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