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Originally published In Press as doi:10.1074/jbc.M005737200 on December 13, 2000

J. Biol. Chem., Vol. 276, Issue 14, 11310-11316, April 6, 2001
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Oncogenes Induce and Activate Endogenous p73 Protein*

Alexander Zaika, Meredith IrwinDagger , Christine Sansome, and Ute M. Moll§

From the Department of Pathology, State University of New York at Stony Brook, Stony Brook, New York 11794-8691 and Dagger  Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115

The identification of upstream pathways that signal to TP73 is crucial for understanding the biological role of this gene. Since some evidence suggests that TP73 might play a role in tumorigenesis, we asked whether oncogenes can induce and activate endogenous TP73. Here, we show that endogenous p73 alpha  and beta  proteins are up-regulated in p53-deficient tumor cells in response to overexpressed E2F1, c-Myc, and E1A. E2F1, c-Myc, and E1A-mediated p73 up-regulation leads to activation of the p73 transcription function, as shown by p73-responsive reporter activity and by induction of known endogenous p73 target gene products such as p21 and HDM2. Importantly, E2F1-, c-Myc-, and E1A-mediated activation of endogenous p73 induces apoptosis in SaOs-2 cells. Conversely, inactivation of p73 by a dominant negative p73 inhibitor (p73DD), but not by a mutant p73DD, inhibits oncogene-induced apoptosis. These data show that oncogenes can signal to TP73 in vivo. Moreover, in the absence of p53, oncogenes may enlist p73 to induce apoptosis in tumor cells.

* This work was supported by the United States Army Medical Research Command United States Army Grant BC971469 and a grant from the Carol Baldwin Breast Cancer Research Fund.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. E-mail: umoll@ path.som.sunysb.edu.

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


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