Mechanisms of Immune Sensing of DNA Damage.

DNA Damage Immune sensing RNA sensing Sensors of replication-associated DNA damage cGAS-STING cytosolic DNA sensing

Journal

Journal of molecular biology
ISSN: 1089-8638
Titre abrégé: J Mol Biol
Pays: Netherlands
ID NLM: 2985088R

Informations de publication

Date de publication:
28 Dec 2023
Historique:
received: 13 10 2023
revised: 22 12 2023
accepted: 26 12 2023
medline: 2 1 2024
pubmed: 2 1 2024
entrez: 30 12 2023
Statut: aheadofprint

Résumé

Genomic stability relies on a multifaceted and evolutionarily conserved DNA damage response (DDR). In multicellular organisms, an integral facet of the DDR involves the activation of the immune system to eliminate cells with persistent DNA damage. Recent research has shed light on a complex array of nucleic acid sensors crucial for innate immune activation in response to oncogenic stress-associated DNA damage, a process vital for suppressing tumor formation. Yet, these immune sensing pathways may also be co-opted to foster tolerance of chromosomal instability, thereby driving cancer progression. This review aims to provide an updated overview of how the innate immune system detects and responds to DNA damage. An improved understanding of the regulatory intricacies governing this immune response may uncover new avenues for cancer prevention and therapeutic intervention.

Identifiants

pubmed: 38159716
pii: S0022-2836(23)00541-7
doi: 10.1016/j.jmb.2023.168424
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

168424

Informations de copyright

Copyright © 2023. Published by Elsevier Ltd.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: G.P.G. is a co-inventor on a patent held by the University of North Carolina at Chapel Hill on methods for detecting tumor-derived viral DNA in blood (U.S. Patent 11,168,373), receives patent licensing fees from and has equity in Naveris, Inc, and is the recipient of research funding from Breakpoint Therapeutics and Merck.A.M.G, M.G.C, and L.M.L. have no competing interests.

Auteurs

Anna M Goddard (AM)

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Min-Guk Cho (MG)

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Lynn M Lerner (LM)

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Genetics and Molecular Biology Curriculum, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Gaorav P Gupta (GP)

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Radiation Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Classifications MeSH