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Targeting Vdac2 enables IFNg-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [ATAC-seq2]

ABSTRACT: ATAC-seq analysis of intratumoral CD8+ T cells in Vdac2-deficient and control B16-OVA tumors.

ORGANISM(S): Mus musculus

PROVIDER: GSE280328 | GEO | 2025/03/19

REPOSITORIES: GEO

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Targeting Vdac2 enables IFNg-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [microarray 6]

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Targeting Vdac2 enables IFNg-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [ATAC-seq2]

Project description:Targeting Vdac2 enables IFNg-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [ATAC-seq2]

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Project description:STING is an innate immune sensor for immune surveillance of viral or bacterial infection and maintenance of an immune-friendly microenvironment to unfavored tumorigenesis. Whether and how STING exerts any innate immunity independent function remains elusive. Here, we report that STING expression is increased in RCC patients and STING governs RCC growth through non-canonical innate immune signaling by maintaining mitochondrial ROS and calcium homeostasis. Mechanistically, we identify mitochondrial calcium transporter VDAC2 as a new STING binding partner and downstream effector, through suppression of which STING controls proper mitochondrial ROS/calcium levels. We also find palmitoylation of STING-C88/C91 residues is critical to mediate STING interaction with VDAC2 and inhibiting STING palmitoyl-transferases ZDHHCs by 2-BP significantly impedes RCC cell growth. Together, our studies reveal an innate immunity-independent function of STING in regulating RCC mitochondrial function and growth. We hope our study provides a rationale to apply palmitoylation inhibitors to treating RCC.

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