DNA Damage Stress: Cui Prodest?
G2-arrest
adaptation
cell cycle checkpoints
cell death
genomic instability
repair of DNA damage
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
01 Mar 2019
01 Mar 2019
Historique:
received:
18
01
2019
revised:
18
02
2019
accepted:
26
02
2019
entrez:
6
3
2019
pubmed:
6
3
2019
medline:
5
6
2019
Statut:
epublish
Résumé
DNA is an entity shielded by mechanisms that maintain genomic stability and are essential for living cells; however, DNA is constantly subject to assaults from the environment throughout the cellular life span, making the genome susceptible to mutation and irreparable damage. Cells are prepared to mend such events through cell death as an extrema ratio to solve those threats from a multicellular perspective. However, in cells under various stress conditions, checkpoint mechanisms are activated to allow cells to have enough time to repair the damaged DNA. In yeast, entry into the cell cycle when damage is not completely repaired represents an adaptive mechanism to cope with stressful conditions. In multicellular organisms, entry into cell cycle with damaged DNA is strictly forbidden. However, in cancer development, individual cells undergo checkpoint adaptation, in which most cells die, but some survive acquiring advantageous mutations and selfishly evolve a conflictual behavior. In this review, we focus on how, in cancer development, cells rely on checkpoint adaptation to escape DNA stress and ultimately to cell death.
Identifiants
pubmed: 30832234
pii: ijms20051073
doi: 10.3390/ijms20051073
pmc: PMC6429504
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Associazione Italiana per la Ricerca sul Cancro
ID : AIRC15218
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