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VDAC2 brake release: unleashing inflammation via IFNγ. | LitMetric

VDAC2 brake release: unleashing inflammation via IFNγ.

Trends Pharmacol Sci

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX, USA; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. El

Published: August 2025


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Article Abstract

Identification of therapeutic vulnerabilities in cancer remains a high priority for cancer research. A recent CRISPR/Cas9 screen identified that VDAC2 deletion in tumors enhanced their sensitivity to interferon-γ (IFNγ) through the release of mitochondrial DNA (mtDNA) and activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. These data suggest that VDAC2 inhibition could enhance antitumor therapies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352517PMC
http://dx.doi.org/10.1016/j.tips.2025.07.001DOI Listing

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