IFN-I signaling in cancer: the connection with dysregulated Insulin/IGF axis
Affiliation
Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Catania, Garibaldi-Nesima Hospital, 95122 Catania, ItalyIssue Date
2022
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Show full item recordAbstract
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.Citation
Vella V, De Francesco EM, Bonavita E, Lappano R, Belfiore A. IFN-I signaling in cancer: the connection with dysregulated Insulin/IGF axis. Vol. 33, Trends in Endocrinology & Metabolism. Elsevier BV; 2022. p. 569–86.Journal
Trends in Endocrinology and MetabolismDOI
10.1016/j.tem.2022.04.009PubMed ID
35691786Additional Links
https://dx.doi.org/10.1016/j.tem.2022.04.009Type
ArticleLanguage
enae974a485f413a2113503eed53cd6c53
10.1016/j.tem.2022.04.009
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