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P53 and E2f: Partners in Life and Death

Overview
Journal Nat Rev Cancer
Specialty Oncology
Date 2009 Sep 25
PMID 19776743
Citations 262
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Abstract

During tumour development cells sustain mutations that disrupt normal mechanisms controlling proliferation. Remarkably, the Rb-E2f and MDM2-p53 pathways are both defective in most, if not all, human tumours, which underscores the crucial role of these pathways in regulating cell cycle progression and viability. A simple interpretation of the observation that both pathways are deregulated is that they function independently in the control of cell fate. However, a large body of evidence indicates that, in addition to their independent effects on cell fate, there is extensive crosstalk between these two pathways, and specifically between the transcription factors E2F1 and p53, which influences vital cellular decisions. This Review discusses the molecular mechanisms that underlie the intricate interactions between E2f and p53.

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References
1.
OConnor D, Lu X . Stress signals induce transcriptionally inactive E2F-1 independently of p53 and Rb. Oncogene. 2000; 19(20):2369-76. DOI: 10.1038/sj.onc.1203540. View

2.
Tolbert D, Lu X, Yin C, Tantama M, Van Dyke T . p19(ARF) is dispensable for oncogenic stress-induced p53-mediated apoptosis and tumor suppression in vivo. Mol Cell Biol. 2001; 22(1):370-7. PMC: 134227. DOI: 10.1128/MCB.22.1.370-377.2002. View

3.
OConnor D, Bergamaschi D, Trigiante G, Hsieh J, Zhong S, Campargue I . ASPP proteins specifically stimulate the apoptotic function of p53. Mol Cell. 2001; 8(4):781-94. DOI: 10.1016/s1097-2765(01)00367-7. View

4.
Donehower L, Harvey M, Slagle B, McArthur M, Montgomery Jr C, Butel J . Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature. 1992; 356(6366):215-21. DOI: 10.1038/356215a0. View

5.
Lin W, Lin F, Nevins J . Selective induction of E2F1 in response to DNA damage, mediated by ATM-dependent phosphorylation. Genes Dev. 2001; 15(14):1833-44. PMC: 312742. View