Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2018 Apr 3;27(4):710-711.
doi: 10.1016/j.cmet.2018.03.009.

Senescence Elicits Stemness: A Surprising Mechanism for Cancer Relapse

Affiliations
Comment

Senescence Elicits Stemness: A Surprising Mechanism for Cancer Relapse

Zhixun Dou et al. Cell Metab. .

Abstract

Cellular senescence is traditionally viewed as a permanent form of cell cycle arrest that restrains tumorigenesis. In a recent study in Nature, however, Milanovic et al. (2018) challenge this conventional view, showing that senescence can counterintuitively promote cancer stemness and tumor aggressiveness. This finding suggests that attacking senescence can be exploited in cancer therapy.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.. Therapy-Induced Senescence Can Promote Cancer Sternness and Cancer Aggressiveness
In response to cancer therapy, such as chemotherapy or radiation therapy, tumors regress by cell death (apoptosis or necrosis) and senescence. Senescence is traditionally viewed as an endpoint of cancer therapy, as senescent cells are non-dividing. However, Milanovic et al. (2018) report that senescent cells can acquire features of sternness, partly through activation of Wnt. This can give rise to tumor-initiating cells (e.g., cancer stem cells), which can eventually lead to cancer relapse and metastasis.

Comment on

  • Senescence-associated reprogramming promotes cancer stemness.
    Milanovic M, Fan DNY, Belenki D, Däbritz JHM, Zhao Z, Yu Y, Dörr JR, Dimitrova L, Lenze D, Monteiro Barbosa IA, Mendoza-Parra MA, Kanashova T, Metzner M, Pardon K, Reimann M, Trumpp A, Dörken B, Zuber J, Gronemeyer H, Hummel M, Dittmar G, Lee S, Schmitt CA. Milanovic M, et al. Nature. 2018 Jan 4;553(7686):96-100. doi: 10.1038/nature25167. Epub 2017 Dec 20. Nature. 2018. PMID: 29258294

References

    1. Cahu J, Bustany S, and Sola B (2012). Senescence-associated secretory phenotype favors the emergence of cancer stem-like cells. Cell Death Dis. 3, e446. - PMC - PubMed
    1. He S, and Sharpless NE (2017). Senescence in health and disease. Cell 169,1000–1011. - PMC - PubMed
    1. Maherali N, Sridharan R, Xie W, Utikal J, Eminli S, Arnold K, Stadtfeld M, Yachechko R, Tchieu J, Jaenisch R, et al. (2007). Directly reprogrammed fibroblasts show global epigenetic remodeling and widespread tissue contribution. Cell Stem Cell 1, 55–70. - PubMed
    1. Milanovic M, Fan DNY, Belenki D, Däbritz JHM, Zhao Z, Yu Y, Dörr JR, Dimitrova L, Lenze D, Monteiro Barbosa IA, et al. (2018). Senescence-associated reprogramming promotes cancer sternness. Nature 553, 96–100. - PubMed
    1. Mosteiro L, Pantoja C, Alcazar N, Marion RM, Chondronasiou D, Rovira M, Fernandez-Marcos PJ, Muñoz-Martin M, Blanco-Aparicio C, Pastor J, et al. (2016). Tissue damage and senescence provide critical signals for cellular reprogramming in vivo. Science 354, 354. - PubMed

Publication types

LinkOut - more resources