The multifaceted functions of homologous recombination in dealing with replication-associated DNA damages.

Autor: Chakraborty S; Institut Curie, Université PSL, CNRS UMR3348, 91400 Orsay, France; Université Paris-Saclay, CNRS UMR3348, 91400 Orsay, France; Equipe Labelisée Ligue Nationale Contre le Cancer, France., Schirmeisen K; Institut Curie, Université PSL, CNRS UMR3348, 91400 Orsay, France; Université Paris-Saclay, CNRS UMR3348, 91400 Orsay, France; Equipe Labelisée Ligue Nationale Contre le Cancer, France., Lambert SA; Institut Curie, Université PSL, CNRS UMR3348, 91400 Orsay, France; Université Paris-Saclay, CNRS UMR3348, 91400 Orsay, France; Equipe Labelisée Ligue Nationale Contre le Cancer, France. Electronic address: sarah.lambert@curie.fr.
Jazyk: angličtina
Zdroj: DNA repair [DNA Repair (Amst)] 2023 Sep; Vol. 129, pp. 103548. Date of Electronic Publication: 2023 Aug 01.
DOI: 10.1016/j.dnarep.2023.103548
Abstrakt: The perturbation of DNA replication, a phenomena termed "replication stress", is a driving force of genome instability and a hallmark of cancer cells. Among the DNA repair mechanisms that contribute to tolerating replication stress, the homologous recombination pathway is central to the alteration of replication fork progression. In many organisms, defects in the homologous recombination machinery result in increased cell sensitivity to replication-blocking agents and a higher risk of cancer in humans. Moreover, the status of homologous recombination in cancer cells often correlates with the efficacy of anti-cancer treatment. In this review, we discuss our current understanding of the different functions of homologous recombination in fixing replication-associated DNA damage and contributing to complete genome duplication. We also examine which functions are pivotal in preventing cancer and genome instability.
Competing Interests: Declaration of Competing Interest The authors declare no competing interests.
(Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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