DNA-dependent protein kinase: Epigenetic alterations and the role in genomic stability of cancer.
Cancer
DNA damage
DNA repair
DNA-PK
Epigenetic alternations
Genomic stability
Journal
Mutation research. Reviews in mutation research
ISSN: 1388-2139
Titre abrégé: Mutat Res Rev Mutat Res
Pays: Netherlands
ID NLM: 101632211
Informations de publication
Date de publication:
Historique:
received:
22
02
2018
accepted:
13
06
2018
entrez:
10
8
2019
pubmed:
10
8
2019
medline:
3
3
2020
Statut:
ppublish
Résumé
DNA-dependent protein kinase (DNA-PK), a member of phosphatidylinositol-kinase family, is a key protein in mammalian DNA double-strand break (DSB) repair that helps to maintain genomic integrity. DNA-PK also plays a central role in immune cell development and protects telomerase during cellular aging. Epigenetic deregulation due to endogenous and exogenous factors may affect the normal function of DNA-PK, which in turn could impair DNA repair and contribute to genomic instability. Recent studies implicate a role for epigenetics in the regulation of DNA-PK expression in normal and cancer cells, which may impact cancer progression and metastasis as well as provide opportunities for treatment and use of DNA-PK as a novel cancer biomarker. In addition, several small molecules and biological agents have been recently identified that can inhibit DNA-PK function or expression, and thus hold promise for cancer treatments. This review discusses the impact of epigenetic alterations and the expression of DNA-PK in relation to the DNA repair mechanisms with a focus on its differential levels in normal and cancer cells.
Identifiants
pubmed: 31395353
pii: S1383-5742(18)30013-9
doi: 10.1016/j.mrrev.2018.06.001
pii:
doi:
Substances chimiques
DNA-Activated Protein Kinase
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
92-105Informations de copyright
Copyright © 2018. Published by Elsevier B.V.