Role for the p53 homologue p73 in E2F-1-induced apoptosis

Meredith Irwin, Maria Carmen Marin, Andrew C. Phillips, Ratnam S. Seelan, David I. Smith, Wanguo Liu, Elsa R. Flores, Kenneth Y. Tsai, Tyler Jacks, Karen H. Vousden and William G. Kaelin ()
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Meredith Irwin: Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School
Maria Carmen Marin: Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School
Andrew C. Phillips: Regulation of Cell Growth Laboratory, NCI-FCRDC
Ratnam S. Seelan: Mayo Clinic/ Mayo Medical School
David I. Smith: Mayo Clinic/ Mayo Medical School
Wanguo Liu: Mayo Clinic/ Mayo Medical School
Elsa R. Flores: Massachusetts Institute of Technology
Kenneth Y. Tsai: Massachusetts Institute of Technology
Tyler Jacks: Massachusetts Institute of Technology
Karen H. Vousden: Regulation of Cell Growth Laboratory, NCI-FCRDC
William G. Kaelin: Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School

Nature, 2000, vol. 407, issue 6804, 645-648

Abstract: Abstract The transcription factor E2F-1 induces both cell-cycle progression and, in certain settings, apoptosis. E2F-1 uses both p53-dependent and p53-independent pathways to kill cells1,2,3,4,5,6,7,8. The p53-dependent pathway involves the induction by E2F-1 of the human tumour-suppressor protein p14ARF, which neutralizes HDM2 (human homologue of MDM2) and thereby stabilizes the p53 protein9. Here we show that E2F-1 induces the transcription of the p53 homologue p73. Disruption of p73 function inhibited E2F-1-induced apoptosis in p53-defective tumour cells and in p53-/- mouse embryo fibroblasts. We conclude that activation of p73 provides a means for E2F-1 to induce death in the absence of p53.

Date: 2000
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DOI: 10.1038/35036614

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