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Originally published In Press as doi:10.1074/jbc.M101241200 on September 6, 2001

J. Biol. Chem., Vol. 276, Issue 45, 41717-41724, November 9, 2001
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p53 Homologue p63 Represses Epidermal Growth Factor Receptor Expression*

Hirotaka NishiDagger , Makoto Senoo§, Katsura H. NishiDagger , Barbara MurphyDagger , Toshiki RikiyamaDagger , Yasuko Matsumura§, Sonoko Habu§, and Alfred C. JohnsonDagger

From the Dagger  Laboratory of Molecular Biology, CCR, NCI, National Institutes of Health, Bethesda, Maryland 20892-4255 and the § Department of Immunology, Tokai University School of Medicine, Boseidai, Isehara, Kanagawa 259-1193, Japan

Tumor suppressor p53 has been shown to transactivate epidermal growth factor receptor (EGFR) expression through binding to a putative p53 responsive element in the EGFR promoter between nucleotides -265 and -239 (EGFRp53RE). Isotypes of p63 gene products, recently identified as p53 relatives, have a similar function to transactivate several p53 target gene promoters. However, our results indicate that TAp63gamma has a very low ability to bind to the EGFRp53RE and surprisingly represses both basal EGFR promoter activity and endogenous EGFR expression. Transient transfection assays show that the EGFR promoter region between -348 and -293, containing two Sp1 sites, is crucial for the repression of the EGFR expression by TAp63gamma . Mutations in these Sp1 sites in the reporter constructs result in loss of the TAp63gamma repression effect. We further show that TAp63gamma directly interacts with Sp1 by immunoprecipitation analysis and that TAp63gamma impairs Sp1 binding to the target DNA site in electrophoretic mobility shift assays. These results suggest that TAp63gamma is involved in the regulation of the EGFR gene expression through interactions with basal transcription factors.

* 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.

To whom correspondence should be addressed: Laboratory of Molecular Biology, CCR, NCI, National Institutes of Health, Bldg. 37, Rm. 2D18, 37 Convent Dr., MSC 4255, Bethesda, MD 20892-4255. Tel.: 301-496-3224; Fax: 301-496-2212; E-mail: acjohnson@nih.gov.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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