E2F-1 is a critical modulator of cellular senescence in human cancer

  • Authors:
    • Chaehwa Park
    • Inkyoung Lee
    • Won Ki Kang
  • View Affiliations

  • Published online on: May 1, 2006     https://doi.org/10.3892/ijmm.17.5.715
  • Pages: 715-720
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Abstract

Senescence limits cellular proliferation, and therefore might be a mechanism which could suppress the progression of cancer. Herein we show that E2F1, a transcription factor essential to a cell cycle progress and a main target of tumor suppressor Rb, is a critical barrier for the induction of senescence. Human cancer cells transfected with siE2F1 were shown to express replicative senescence markers, in addition to yielding positive results upon SA-β-Gal staining. Consistent with the notion of the critical role in senescence of E2F1, cells which overexpressed E2F1 proved to be immune to the induction of senescence. Importantly, it appears that E2F1 depletion-induced cancer cell senescence is not reliant on the integrity of either Rb or p53. Our results provide a molecular explanation for the selectivity with which senescence induction occurs, and also provides insights into the possibility of using E2F1 as a therapeutic target in the treatment of cancer.

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May 2006
Volume 17 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Park C, Lee I and Kang WK: E2F-1 is a critical modulator of cellular senescence in human cancer. Int J Mol Med 17: 715-720, 2006
APA
Park, C., Lee, I., & Kang, W.K. (2006). E2F-1 is a critical modulator of cellular senescence in human cancer. International Journal of Molecular Medicine, 17, 715-720. https://doi.org/10.3892/ijmm.17.5.715
MLA
Park, C., Lee, I., Kang, W. K."E2F-1 is a critical modulator of cellular senescence in human cancer". International Journal of Molecular Medicine 17.5 (2006): 715-720.
Chicago
Park, C., Lee, I., Kang, W. K."E2F-1 is a critical modulator of cellular senescence in human cancer". International Journal of Molecular Medicine 17, no. 5 (2006): 715-720. https://doi.org/10.3892/ijmm.17.5.715