Normal cells can respond to expression of activated oncogenes by initiating cellular senescence, a permanent state of proliferative arrest. But whether this process reflects a relevant anticancer mechanism has been debated. Several studies now show that oncogene-induced senescence can occur in vivo and provides a bona fide barrier to tumorigenesis.
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
EndoBind detects endogenous protein-protein interactions in real time
Communications Biology Open Access 15 September 2021
-
Combined treatment with emodin and a telomerase inhibitor induces significant telomere damage/dysfunction and cell death
Cell Death & Disease Open Access 11 July 2019
Access options
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Hayflick, L. Exp. Cell Res. 37, 614–636 (1965).
Lowe, S.W., Cepero, E. & Evan, G. Nature 432, 307–315 (2004).
Campisi, J. Cell 120, 513–522 (2005).
Braig, M. et al. Nature 436, 660–665 (2005).
Chen, Z. et al. Nature 436, 725–730 (2005).
Collado, M. et al. Nature 436, 642 (2005).
Michaloglou, C. et al. Nature 436, 720–724 (2005).
Lazzerini Denchi, E., Attwooll, C., Pasini, D. & Helin, K. Mol. Cell. Biol. 25, 2660–2672 (2005).
Franza, B.R., Jr., Maruyama, K., Garrels, J.I. & Ruley, H.E. Cell 44, 409–418 (1986).
Serrano, M., Lin, A.W., McCurrach, M.E., Beach, D. & Lowe, S.W. Cell 88, 593–602 (1997).
Serrano, M. & Blasco, M.A. Curr. Opin. Cell Biol. 13, 748–753 (2001).
Narita, M. et al. Cell 113, 703–716 (2003).
Deng, Q., Liao, R., Wu, B.L. & Sun, P. J. Biol. Chem. 279, 1050–1059 (2004).
Benanti, J.A. & Galloway, D.A. Mol. Cell. Biol. 24, 2842–2852 (2004).
Guerra, C. et al. Cancer Cell 4, 111–120 (2003).
Tuveson, D.A. et al. Cancer Cell 5, 375–387 (2004).
Dimri, G.P. et al. Proc. Natl. Acad. Sci. USA 92, 9363–9367 (1995).
Lachner, M. & Jenuwein, T. Curr. Opin. Cell Biol. 14, 286–298 (2002).
Lin, A.W. & Lowe, S.W. Proc. Natl. Acad. Sci. USA 98, 5025–5030 (2001).
Kelly-Spratt, K.S., Gurley, K.E., Yasui, Y. & Kemp, C.J. PLoS Biol. 2, E242 (2004).
Kim, C.F. et al. Cell 121, 823–835 (2005).
Schmitt, C.A. et al. Cell 109, 335–346 (2002).
te Poele, R.H., Okorokov, A.L., Jardine, L., Cummings, J. & Joel, S.P. Cancer Res. 62, 1876–1883 (2002).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Narita, M., Lowe, S. Senescence comes of age. Nat Med 11, 920–922 (2005). https://doi.org/10.1038/nm0905-920
Issue Date:
DOI: https://doi.org/10.1038/nm0905-920
This article is cited by
-
EndoBind detects endogenous protein-protein interactions in real time
Communications Biology (2021)
-
Combined treatment with emodin and a telomerase inhibitor induces significant telomere damage/dysfunction and cell death
Cell Death & Disease (2019)
-
Cellular senescence causes ageing
Nature Reviews Molecular Cell Biology (2019)
-
Induction of p53-mediated senescence is essential for the eventual anticancer therapeutic effect of RH1
Archives of Pharmacal Research (2019)
-
miR-30 disrupts senescence and promotes cancer by targeting both p16INK4A and DNA damage pathways
Oncogene (2018)