Role of p53 in the Regulation of Cellular Senescence.
DNA damage
cell cycle arrest
microenvironment
p53
senescence
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
08 03 2020
08 03 2020
Historique:
received:
31
01
2020
revised:
04
03
2020
accepted:
05
03
2020
entrez:
19
3
2020
pubmed:
19
3
2020
medline:
19
3
2021
Statut:
epublish
Résumé
The p53 transcription factor plays a critical role in cellular responses to stress. Its activation in response to DNA damage leads to cell growth arrest, allowing for DNA repair, or directs cellular senescence or apoptosis, thereby maintaining genome integrity. Senescence is a permanent cell-cycle arrest that has a crucial role in aging, and it also represents a robust physiological antitumor response, which counteracts oncogenic insults. In addition, senescent cells can also negatively impact the surrounding tissue microenvironment and the neighboring cells by secreting pro-inflammatory cytokines, ultimately triggering tissue dysfunction and/or unfavorable outcomes. This review focuses on the characteristics of senescence and on the recent advances in the contribution of p53 to cellular senescence. Moreover, we also discuss the p53-mediated regulation of several pathophysiological microenvironments that could be associated with senescence and its development.
Identifiants
pubmed: 32182711
pii: biom10030420
doi: 10.3390/biom10030420
pmc: PMC7175209
pii:
doi:
Substances chimiques
TP53 protein, human
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : H2020 Marie Skłodowska-Curie Actions
ID : 713714
Pays : International
Organisme : Commonwealth of Pennsylvania, Department of Health
ID : 290228/13650
Pays : International
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