IFN-I signaling in cancer: the connection with dysregulated Insulin/IGF axis.
IGF axis
insulin receptor isoform A
insulin receptor isoforms
interferon signaling
Journal
Trends in endocrinology and metabolism: TEM
ISSN: 1879-3061
Titre abrégé: Trends Endocrinol Metab
Pays: United States
ID NLM: 9001516
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
received:
23
03
2022
revised:
15
04
2022
accepted:
26
04
2022
pubmed:
13
6
2022
medline:
16
7
2022
entrez:
12
6
2022
Statut:
ppublish
Résumé
Type I interferons (IFN-Is) are prototypical inflammatory cytokines produced in response to stress. IFN-Is have a critical role in antitumor immunity by driving the activation of leukocytes and favoring the elimination of malignant cells. However, IFN-I signaling in cancer, specifically in the tumor microenvironment (TME), can have opposing roles. Sustained IFN-I stimulation can promote immune exhaustion or enable tumor cell-intrinsic malignant features. Herein, we discuss the potential impact of the insulin/insulin-like growth factor system (I/IGFs) and of metabolic disorders in aberrant IFN-I signaling in cancer. We consider the possibility that targeting I/IGFs, especially in patients with cancer affected by metabolic disorders, contributes to an effective strategy to inhibit deleterious IFN-I signaling, thereby restoring sensitivity to various cancer therapies, including immunotherapy.
Identifiants
pubmed: 35691786
pii: S1043-2760(22)00082-0
doi: 10.1016/j.tem.2022.04.009
pii:
doi:
Substances chimiques
Insulin
0
Insulin-Like Growth Factor I
67763-96-6
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
569-586Informations de copyright
Copyright © 2022 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare that there are no conflicts of interest.