Relationships between DNA repair and RTK-mediated signaling pathways.
Apoptosis
/ drug effects
Cell Survival
/ drug effects
DNA Repair
/ drug effects
Gene Expression Regulation, Neoplastic
/ drug effects
Humans
Neoplasms
/ drug therapy
Protein Kinase Inhibitors
/ therapeutic use
Receptor Protein-Tyrosine Kinases
/ antagonists & inhibitors
Signal Transduction
/ drug effects
Cancer
DNA repair
Inhibition
Receptor tyrosine kinase
Journal
Biochimica et biophysica acta. Reviews on cancer
ISSN: 1879-2561
Titre abrégé: Biochim Biophys Acta Rev Cancer
Pays: Netherlands
ID NLM: 9806362
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
25
08
2020
revised:
06
12
2020
accepted:
13
12
2020
pubmed:
22
12
2020
medline:
15
4
2021
entrez:
21
12
2020
Statut:
ppublish
Résumé
Receptor Tyrosine Kinases (RTK) are an important family involved in numerous signaling pathways essential for proliferation, cell survival, transcription or cell-cycle regulation. Their role and involvement in cancer cell survival have been widely described in the literature, and are generally associated with overexpression and/or excessive activity in the cancer pathology. Because of these characteristics, RTKs are relevant targets in the fight against cancer. In the last decade, increasingly numerous works describe the role of RTK signaling in the modulation of DNA repair, thus providing evidence of the relationship between RTKs and the protein actors in the repair pathways. In this review, we propose a summary of RTKs described as potential modulators of double-stranded DNA repair pathways in order to put forward new lines of research aimed at the implementation of new therapeutic strategies targeting both DNA repair pathways and RTK-mediated signaling pathways.
Identifiants
pubmed: 33346130
pii: S0304-419X(20)30214-6
doi: 10.1016/j.bbcan.2020.188495
pii:
doi:
Substances chimiques
Protein Kinase Inhibitors
0
Receptor Protein-Tyrosine Kinases
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
188495Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.