Metabolic regulation of the mitochondrial immune checkpoint.

Autor: Montrose DC; Department of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY, USA.; Stony Brook Cancer Center, Stony Brook, NY, USA., Saha S; Department of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY, USA., Galluzzi L; Department of Radiation Oncology, Weill Cornell Medicine, New York, NY, USA.; Sandra and Edward Meyer Cancer Center, New York, NY, USA.; Caryl and Israel Englander Institute for Precision Medicine, New York, NY, USA.
Jazyk: angličtina
Zdroj: Oncoimmunology [Oncoimmunology] 2024 Aug 26; Vol. 13 (1), pp. 2394247. Date of Electronic Publication: 2024 Aug 26 (Print Publication: 2024).
DOI: 10.1080/2162402X.2024.2394247
Abstrakt: Disrupting mitochondrial function in malignant cells is a promising strategy to enhance anticancer immunity. We have recently demonstrated that depriving colorectal cancer cells of serine results in mitochondrial dysfunction coupled with the cytosolic accumulation of mitochondrial DNA and consequent activation of CGAS- and STING-dependent tumor-targeting immune responses.
Competing Interests: DCM has consulting arrangements with Gleipnar Medical. LG is/has been holding research contracts with Lytix Biopharma, Promontory and Onxeo, has received consulting/advisory honoraria from Boehringer Ingelheim, AstraZeneca, AbbVie, OmniSEQ, Onxeo, The Longevity Labs, Inzen, Imvax, Sotio, Promontory, Noxopharm, EduCom, and the Luke Heller TECPR2 Foundation, and holds Promontory stock options. SS has no conflicts to declare.
(© 2024 The Author(s). Published with license by Taylor & Francis Group, LLC.)
Databáze: MEDLINE