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

ABSTRACT: Microarray analysis of WT, Vdac2 KO, Bim/Bid dKO and Vdac2/Bim/Bid TKO B16-OVA tumor cells after IFNg treatment for 24 hours.

ORGANISM(S): Mus musculus

PROVIDER: GSE280185 | 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 [ATAC-seq2]

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

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Targeting VDAC2 enables IFNg-mediated destruction and inflammatory remodeling of tumors to overcome immune evasion [microarray 5]

Project description:Microarray analysis of WT and VDAC2 KO LOVO tumor cells without or with IFNg treatment for 48 hours.

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

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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 5]

Project description: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 [microarray 6]

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

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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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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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Gene expression data from murine CAR T cells

Project description:Compare the gene expression profile among Mouse m19delta.GFP and m1928z.GFP T cells and examine the differential upregulation of Bim, Bid, FasL and Apaf1 in m1928z T cells.

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Gene Expression patterns in mouse B16-OVA melanoma tumors

Project description:This laboratory focuses on selectin mediated recruitment during adoptive immunotherapy for metastatic cancer. This study seeks to determine changes in the expression levels of Fucosyltransferases, Selectins, and cytokines in normal and inflamed mouse skin, melanoma tumor tissue of different sizes, and tumor cells grown in culture. Since the ability to treat the tumor effectively is directly related to the size of the tumor, differences in glyco-expression patterns may be of interest. In this study, five groups were hybridized and analyzed using the GLYCOv2 array. Each group was analyzed in triplicate. The groups were: Normal mouse skin, normal mouse skin inflamed by treatment with Oxazolone, B16-OVA melanoma tissue from 6 day tumors, B16-OVA melanoma tissue from 11 day tumors, and B16-OVA grown in cell culture.

2011-02-17 | E-GEOD-27355 | biostudies-arrayexpress

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