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Targeting Vdac2 enables IFN gamma-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [ATAC-seq 1]

ABSTRACT: ATAC-seq analysis of the functional effect of targeting Vdac2 in tumor cells under the condition of chronic IFNg stimulation that induces IFNg resistance.

ORGANISM(S): Mus musculus

PROVIDER: GSE280326 | 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 [microarray 5]

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

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

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Targeting Vdac2 enables IFN gamma-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [ATAC-seq 1]

Project description:Targeting Vdac2 enables IFN gamma-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [ATAC-seq 1]

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Multifactorial remodeling of the cancer immunopeptidome by interferon gamma

Project description:In this study we combined previous transcriptomics and immunopeptidomics data with new proteomics data from untreated and IFNg-treated CRC PDOs to dissect mechanisms that lead to remodeling of the immunopeptidome through IFNg treatment (this is from the paper introduction, let me know if it needs any stylistic changes). · Experiment description: The cells were grown in DMEM/F12 media with 20% fetal bovine serum, 1X Glutamax, 100 units/ml penicillin/streptomycin and 2% matrigel, and treated with 600ng/mL IFNg for 48 hours before harvesting. Cells were washed twice with ice-cold PBS then snap-frozen.

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STING governs RCC growth through mitochondrial regulation of VDAC2

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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