Synthetic Lethal Interactions of RECQ Helicases.
Animals
Antineoplastic Agents
/ pharmacology
Cell Line, Tumor
DNA Repair
/ drug effects
DNA Replication
/ drug effects
Gene Knockdown Techniques
Genomic Instability
/ drug effects
Humans
Medical Oncology
/ methods
Mice
Mutation
Neoplasms
/ drug therapy
Precision Medicine
/ methods
RecQ Helicases
/ antagonists & inhibitors
Synthetic Lethal Mutations
/ drug effects
Xenograft Model Antitumor Assays
Bloom’s syndrome
RECQ
Rothmund–Thomson Syndrome
Werner syndrome
cancer
genetic disease
genomic stability
helicase
synthetic lethality
Journal
Trends in cancer
ISSN: 2405-8025
Titre abrégé: Trends Cancer
Pays: United States
ID NLM: 101665956
Informations de publication
Date de publication:
02 2021
02 2021
Historique:
received:
22
05
2020
revised:
20
08
2020
accepted:
04
09
2020
pubmed:
13
10
2020
medline:
1
10
2021
entrez:
12
10
2020
Statut:
ppublish
Résumé
DNA helicases have risen to the forefront as genome caretakers. Their prominent roles in chromosomal stability are demonstrated by the linkage of mutations in helicase genes to hereditary disorders with defects in DNA repair, the replication stress response, and/or transcriptional activation. Conversely, accumulating evidence suggests that DNA helicases in cancer cells have a network of pathway interactions such that codeficiency of some helicases and their genetically interacting proteins results in synthetic lethality (SL). Such genetic interactions may potentially be exploited for cancer therapies. We discuss the roles of RECQ DNA helicases in cancer, emphasizing some of the more recent developments in SL.
Identifiants
pubmed: 33041245
pii: S2405-8033(20)30255-7
doi: 10.1016/j.trecan.2020.09.001
pmc: PMC7855770
mid: NIHMS1628108
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
RecQ Helicases
EC 3.6.4.12
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
146-161Subventions
Organisme : Intramural NIH HHS
ID : Z01 AG000741
Pays : United States
Informations de copyright
Published by Elsevier Inc.
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