Cell Senescence and the DNA Single-Strand ...
Document type :
Article dans une revue scientifique: Article de synthèse/Review paper
DOI :
Title :
Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway
Author(s) :
Sarma, Parvathy [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Physique - IEMN [PHYSIQUE - IEMN]
Abbadie, Corinne [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
De Launoit, Yvan [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Cleri, Fabrizio [Auteur]
Physique - IEMN [PHYSIQUE - IEMN]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Physique - IEMN [PHYSIQUE - IEMN]
Abbadie, Corinne [Auteur]

Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
De Launoit, Yvan [Auteur]

Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Cleri, Fabrizio [Auteur]

Physique - IEMN [PHYSIQUE - IEMN]
Journal title :
DNA
Pages :
530-552
Publisher :
MDPI
Publication date :
2024-12-04
ISSN :
2673-8856
English keyword(s) :
cell senescence
DNA damage
radiotherapy
DNA repair pathways
base-excision repair
single-strand breaks
radiation-induced stress
DNA damage
radiotherapy
DNA repair pathways
base-excision repair
single-strand breaks
radiation-induced stress
HAL domain(s) :
Sciences du Vivant [q-bio]/Biologie cellulaire/Organisation et fonctions cellulaires [q-bio.SC]
Sciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire/Génomique, Transcriptomique et Protéomique [q-bio.GN]
Sciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire/Génomique, Transcriptomique et Protéomique [q-bio.GN]
English abstract : [en]
Cellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation, and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond ...
Show more >Cellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation, and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond breaking in the DNA double-helix structure, which are treated by dedicated enzymatic repair pathways. In this review, we discuss the correlation between senescence and the accumulation of non-repaired single-strand breaks, as can occur during radiation therapy treatments. Recent in vitro cell irradiation experiments using high-energy photons have shown that single-strand breaks may be preferentially produced at the borders of the irradiated region, inducing senescence in competition with the apoptosis end-point typically induced by double-strand breaks. Such a particular response to radiation damage has been proposed as a possible cause of radiation-induced second primary cancer, as cells with an accumulation of non-repaired single-strand breaks might evade the senescent state at much later times. In addition, we highlight the peculiarities of strand-break repair pathways in relation to the base-excision pathway that repairs several different DNA oxidation defects.Show less >
Show more >Cellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation, and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond breaking in the DNA double-helix structure, which are treated by dedicated enzymatic repair pathways. In this review, we discuss the correlation between senescence and the accumulation of non-repaired single-strand breaks, as can occur during radiation therapy treatments. Recent in vitro cell irradiation experiments using high-energy photons have shown that single-strand breaks may be preferentially produced at the borders of the irradiated region, inducing senescence in competition with the apoptosis end-point typically induced by double-strand breaks. Such a particular response to radiation damage has been proposed as a possible cause of radiation-induced second primary cancer, as cells with an accumulation of non-repaired single-strand breaks might evade the senescent state at much later times. In addition, we highlight the peculiarities of strand-break repair pathways in relation to the base-excision pathway that repairs several different DNA oxidation defects.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Collections :
Source :
Files
- document
- Open access
- Access the document
- dna-3332141-english.pdf
- Open access
- Access the document