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Lymphomagenesis and female-specific lethality in p53-deficient mice occur independently of E2f1

Nature Cell Biology volume 6, pages 565–567 (2004)Cite this article

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E2f1 represents an intriguing link between the pRB and p53 tumour-suppressor pathways because it can induce both proliferation and apoptosis, suggesting that p53 and E2f1 may be part of the same pathways regulating apoptosis and growth arrest1,2,3. Specifically, E2f1 induces apoptosis in cultured cells through p53-dependent and -independent mechanisms. In the p53-dependent mechanism, E2f1 functions upstream of p53, inducing p19Arf, which stabilizes p53. In the p53-independent mechanism, E2f1 stimulates apoptosis by activating other targets, such as the p53 family member p73 and the caspase activator Apaf1. However, p53 activates the cyclin-dependent kinase inhibitor, p21Cip1, which can potentiate pRB-mediated repression of E2f1. Therefore, E2f1 also functions downstream of p53 for imposing cell-cycle arrest.

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Figure 1: Survival of p53-deficient animals is unchanged by loss of E2f1.

References

  1. Sherr, C.J. & McCormick, F. Cancer Cell 2, 103–112 (2002).

    Article  CAS  PubMed  Google Scholar 

  2. Trimarchi, J.M. & Lees, J.A. Nature Rev. Mol. Cell Biol. 3, 11–20 (2002).

    Article  CAS  Google Scholar 

  3. Vousden, K.H. & Lu, X. Nature Rev. Cancer 2, 594–604 (2002).

    Article  CAS  Google Scholar 

  4. Donehower, L.A. et al. Nature 356, 215–221 (1992).

    Article  CAS  PubMed  Google Scholar 

  5. Jacks, T. et al. Curr. Biol. 4, 1–7 (1994).

    Article  CAS  PubMed  Google Scholar 

  6. Yamasaki, L. et al. Cell 85, 537–48 (1996).

    Article  CAS  PubMed  Google Scholar 

  7. Wikonkal, N.M. et al. Nature Cell Biol. 5, 655–660 (2003).

    Article  CAS  PubMed  Google Scholar 

  8. Clarke, A.R. et al. Nature 362, 849–852 (1993).

    Article  CAS  PubMed  Google Scholar 

  9. Lowe, S.W. et al. Nature 362, 847–849 (1993).

    Article  CAS  PubMed  Google Scholar 

  10. Armstrong, J.F. et al. Curr. Biol. 5, 931–936 (1995).

    Article  CAS  PubMed  Google Scholar 

  11. Sah, V.P. et al. Nature Genet. 10, 175–180 (1995).

    Article  CAS  PubMed  Google Scholar 

  12. Rotter, V. et al. Proc. Natl Acad. Sci. USA 90, 9075–9079 (1993).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. La Thangue, N.B. Nature Cell Biol. 5, 587–589 (2003).

    Article  CAS  PubMed  Google Scholar 

  14. Field, S.J. et al. Cell 85, 549–561 (1996).

    Article  CAS  PubMed  Google Scholar 

  15. Zhu, J.W. et al. Mol. Cell. Biol. 21, 8547–8564 (2001).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

The authors wish to thank the members of the Yamasaki laboratory for helpful discussions, and B. Andreson and the Experimental Molecular Pathology Core Facility in the Herbert Irving Comprehensive Cancer Center for technical assistance. L.Y. thanks M. Pagano and C. Prives for critical reading of this manuscript, and thanks M. Pagano and I. Pagano for their constant support throughout the course of this work. V.C. is supported by the American-Italian Cancer Foundation and L.Y. is supported by the Pew Scholars Program in the Biomedical Sciences and by the National Institutes of Health, National Cancer Institute (R01-CA79646).

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Authors and Affiliations

  1. Department of Biological Sciences, Columbia University, New York, 10027, NY, USA

    Elzbieta H Wloga, Vittoria Criniti & Lili Yamasaki

  2. Tufts University School of Veterinary Medicine, Boston, 02111, MA, USA

    Roderick T. Bronson

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  1. Elzbieta H Wloga
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  2. Vittoria Criniti
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Correspondence to Lili Yamasaki.

Supplementary information

Supplementary Table 1

Tumor Spectrum in p53-Deficient Animals with Loss of E2f1 (DOC 43 kb)

Supplementary methods (PDF 54 kb)

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Wloga, E., Criniti, V., Bronson, R. et al. Lymphomagenesis and female-specific lethality in p53-deficient mice occur independently of E2f1. Nat Cell Biol 6, 565–567 (2004). https://doi.org/10.1038/ncb0704-565

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