Emerging Role of Ubiquitination in the Regulation of PD-1/PD-L1 in Cancer Immunotherapy.
PD-1
PD-L1
deubiquitination
immunotherapy
ubiquitination
Journal
Molecular therapy : the journal of the American Society of Gene Therapy
ISSN: 1525-0024
Titre abrégé: Mol Ther
Pays: United States
ID NLM: 100890581
Informations de publication
Date de publication:
03 03 2021
03 03 2021
Historique:
received:
28
09
2020
revised:
09
12
2020
accepted:
22
12
2020
pubmed:
4
1
2021
medline:
19
11
2021
entrez:
3
1
2021
Statut:
ppublish
Résumé
A growing amount of evidence suggests that ubiquitination and deubiquitination of programmed death 1 (PD-1)/programmed death-ligand 1 (PD-L1) play crucial roles in the regulation of PD-1 and PD-L1 protein stabilization and dynamics. PD-1/PD-L1 is a major coinhibitory checkpoint pathway that modulates immune escape in cancer patients, and its engagement and inhibition has significantly reshaped the landscape of tumor clearance. The abnormal ubiquitination and deubiquitination of PD-1/PD-L1 influence PD-1/PD-L1-mediated immunosuppression. In this review, we describe the ubiquitination- and deubiquitination-mediated modulation of PD-1/PD-L1 signaling through a variety of E3 ligases and deubiquitinating enzymes (DUBs). Moreover, we briefly expound on the anticancer potential of some agents that target related E3 ligases, which further modulate the ubiquitination of PD-1/PD-L1 in cancers. Therefore, this review reveals the development of a highly promising therapeutic approach for cancer immunotherapy by targeting PD-1/PD-L1 ubiquitination.
Identifiants
pubmed: 33388422
pii: S1525-0016(20)30725-5
doi: 10.1016/j.ymthe.2020.12.032
pmc: PMC7934629
pii:
doi:
Substances chimiques
B7-H1 Antigen
0
CD274 protein, human
0
PDCD1 protein, human
0
Programmed Cell Death 1 Receptor
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
908-919Informations de copyright
Copyright © 2020 The American Society of Gene and Cell Therapy. Published by Elsevier Inc. All rights reserved.
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