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Notch and Senescence.

Authors
  • Hoare, Matthew1, 2
  • Narita, Masashi3
  • 1 Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK. [email protected]
  • 2 Department of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK. [email protected]
  • 3 Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK. [email protected]
Type
Published Article
Journal
Advances in experimental medicine and biology
Publication Date
Jan 01, 2018
Volume
1066
Pages
299–318
Identifiers
DOI: 10.1007/978-3-319-89512-3_15
PMID: 30030833
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Cellular senescence, previously thought of as an autonomous tumour suppressor mechanism, is emerging as a phenotype and effector present throughout the life of an organism from embryogenesis to senile decline. Senescent cells have powerful non-autonomous effects upon multiple players within their microenvironment mainly through their secretory phenotype. How senescent cells co-ordinate numerous, sometimes functionally contrasting outputs through their secretome had previously been unclear. The Notch pathway, originally identified for its involvement in Drosophila wing development, has more recently been found to underpin diverse effects in human cancer. Here we discuss recent findings that suggest that Notch is intimately involved in the development of senescence and how it acts to co-ordinate the composition and functional effects of the senescence secretome. We also highlight the complex physical and functional interplay between Notch and p53, critical to both senescence and cancer. Understanding the interplay between Notch, p53 and senescence could allow us develop the therapeutics of the future for cancer and ageing.

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