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Originally published In Press as doi:10.1074/jbc.M208447200 on September 15, 2002

J. Biol. Chem., Vol. 277, Issue 47, 45611-45618, November 22, 2002
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Human Papilloma Virus 16 E6 Oncoprotein Inhibits Retinoic X Receptor-mediated Transactivation by Targeting Human ADA3 Coactivator*

Musheng ZengDagger , Ajay KumarDagger §, Gaoyuan MengDagger §, Qingshen GaoDagger , Goberdhan DimriDagger , David WazerDagger , Hamid Band, and Vimla BandDagger ||**

From the Dagger  Division of Radiation and Cancer Biology, Department of Radiation Oncology, New England Medical Center and the || Department of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts 02111 and the  Division of Rheumatology, Immunology, and Allergy, Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115

The expression of human papillomavirus (HPV) E6 oncoprotein is causally linked to high-risk HPV-associated human cancers. We have recently isolated hADA3, the human homologue of yeast transcriptional co-activator yADA3, as a novel E6 target. Human ADA3 binds to the high-risk (cancer-associated) but not the low-risk HPV E6 proteins and to immortalization-competent but not to immortalization-defective HPV16 E6 mutants, suggesting a role for the perturbation of hADA3 function in E6-mediated oncogenesis. We demonstrate here that hADA3 directly binds to the retinoic X receptor (RXR)alpha in vitro and in vivo. Using chromatin immunoprecipitation, we show that hADA3 is part of activator complexes bound to the native RXR response elements within the promoter of the cyclin-dependent kinase inhibitor gene p21. We show that hADA3 enhances the RXRalpha -mediated sequence-specific transactivation of retinoid target genes, cellular retinoic acid-binding protein II and p21. Significantly, we demonstrate that E6 inhibits the RXRalpha -mediated transactivation of target genes, implying that perturbation of RXR-mediated transactivation by E6 could contribute to HPV oncogenesis.

* This work was supported by National Institutes of Health Grants CA81076 and CA70195 (to V. B.) and CA87986, CA75075, and CA76118 (to H. B.).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.

§ Recipients of fellowships from the Massachusetts Department of Public Health.

** To whom correspondence should be addressed: Dept. of Radiation Oncology, Box 824, New England Medical Center, 750 Washington St., Boston, MA 02111. Tel.: 617-636-4776; Fax: 617-636-6205; E-mail: VBAND@lifespan.org.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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