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A more recent version of this article appeared on March 30, 2001
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Papers In Press, published online ahead of print December 13, 2000
J. Biol. Chem, 10.1074/jbc.M005737200
Submitted on June 29, 2000
Revised on December 4, 2000
Accepted on December 12, 2000

Oncogenes induce and activate endogenous p73 protein

Alexander Zaika, Meredith Irwin, Christine Sansome, and Ute M. Moll

Pathology, State University of New York at Stony Brook, Stony Brook, NY 11794-8691

Corresponding Author: umoll{at}path.som.sunysb.edu

The identification of upstream pathways that signal to p73 is crucial for understanding the biological role of this gene. Since some evidence suggests that p73 might play a role in tumorigenesis, we asked whether oncogenes can induce and activate endogenous p73. Here, we show that endogenous p73 ? and ? proteins are upregulated in p53-deficient tumor cells in response to overexpressed E2F1, cMyc and E1A. E2F1, cMyc and E1A-mediated p73 upregulation 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-, cMyc- and E1A-mediated activation of endogenous p73 induces apoptosis in Saos2 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 p73 in vivo. Moreover, in the absence of p53, oncogenes may enlist p73 to induce apoptosis in tumor cells.


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