Project description:Parental MC38 tumor cells were transduced with the STING-N153S mutant and RNA-seq for differential gene expression analysis was performed

2023-03-17 | GSE216896 | GEO

Constitutive active STING signaling in MC38 tumor cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-17 | GSE216898 | GEO

Gene expression in STING-/- MEF cells expressing STING R284S variant

Project description:STING R284S variant is constitutively active and induces inflammatory genes even in absence of STING ligand cGAMP.

2019-02-27 | GSE111196 | GEO

Tissue-specific inflammation induced by constitutively active STING is mediated by enhanced TNF signaling

Project description:Constitutive activation of STING by gain-of-function mutations triggers manifestation of the systemic autoinflammatory disease STING-associated vasculopathy with onset in infancy (SAVI) in humans and in mice. Murine SAVI is characterized by T cell lymphopenia, severe inflammatory interstitial lung disease, neuroinflammation and neurodegeneration with only limited contribution of type I interferon signaling. Here, we show that pharmacologic inhibition of TNF signaling in SAVI mice improved T cell lymphopenia, but had no effect on interstitial lung disease. However, complete blocking of TNF receptor signaling by knocking out TNFR1 and TNFR2 in SAVI mice rescued both, loss of thymocytes as well as interstitial lung disease. Furthermore, chronic STING signaling in lung endothelial cells of diseased mice enhanced transcription of cytokines, chemokines and adhesions proteins resulting in increased transendothelial migration of neutrophils across the endothelial barrier that could be reverted by genetic inactivation of TNFR1 and 2. Thus, our results demonstrate a pivotal role of TNFR-signaling in the development of SAVI-associated lung disease and suggest this pathway as promising target to ameliorate human SAVI

2024-04-16 | GSE244062 | GEO

RNA-seq of parental MC38 and anti-PD-1 resistant MC38 subcutaneous tumors

Project description:MC38 tumors resistant to anti-PD-1 treatment (MC38-resistant) were generated through serial in vivo passaging, and global gene expression analysis was used to compare resistant and parental tumors. MC38 and MC38-resistant tumors exhibited widespread changes in global gene expression.

2021-07-22 | GSE180309 | GEO

Immunopeptidome on MC38 Cell line

Project description:PTM – driven antigenicity – immunopeptidome of MC38 cell line

2022-10-12 | PXD017448 | Pride

Inflammation-Driven Carcinogenesis is Mediated through STING [MEFs]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.

2014-05-31 | E-GEOD-57603 | biostudies-arrayexpress

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