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Constitutive active STING signaling in MC38 tumor cells [RNA-Seq]

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

ORGANISM(S): Mus musculus

PROVIDER: GSE216896 | GEO | 2023/03/17

REPOSITORIES: GEO

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Constitutive active STING signaling in MC38 tumor cells [CITE-seq]

Project description:Parental MC38 tumor cells were transduced with the STING-N153S mutant

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Constitutive active STING signaling in MC38 tumor cells

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Constitutive active STING signaling in MC38 tumor cells [CITE-seq]

Project description:Constitutive active STING signaling in MC38 tumor cells [CITE-seq]

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Constitutive active STING signaling in MC38 tumor cells

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

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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.

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Single-cell RNA-seq of MC38 tumor model

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Single amino acid change in STING leads to constitutive active signaling.

Project description:The production of cytokines by the immune system in response to cytosolic DNA plays an important role in host defense, autoimmune disease, and cancer immunogenicity. Recently a cytosolic DNA signaling pathway that is dependent on the endoplasmic reticulum adaptor and cyclic dinucleotide sensor protein STING has been identified. Association of cytosolic DNA with cyclic-GMP-AMP synthase (cGAS) activates its enzymatic activity to synthesize the cyclic dinucleotide second messenger cGAMP from GTP and ATP. Direct detection of cGAMP by STING triggers the activation of IRF3 and NF-kB, and the production of type I interferons and proinflammatory cytokines. The mechanism of how STING is able to mediate downstream signaling remains incompletely understood although it has been shown that dimerization is a prerequisite. Here, we identify a single amino acid change in STING that confers constitutive active signaling. This mutation appears to both enhance ability of STING to both dimerize and associate with its downstream target TBK1.

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

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Cyclic-Di-Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling

Project description:Activation of the STING (Stimulator of Interferon Genes) pathway by microbial or self-DNA, as well as cyclic di nucleotides (CDN), results in the induction of numerous genes that suppress pathogen replication and facilitate adaptive immunity. However, sustained gene transcription is rigidly prevented to avoid lethal STING-dependent pro-inflammatory disease by mechanisms that remain unknown. We demonstrate here that after autophagy-dependent STING delivery of TBK1 (TANK-binding kinase 1) to endosomal/lysosomal compartments and activation of transcription factors IRF3 (interferon regulatory factors 3) and NF-κB (nuclear factor kappa beta), that STING is subsequently phosphorylated by serine/threonine UNC-51-like kinase (ULK1/ATG1) and IRF3 function is suppressed. ULK1 activation occurred following disassociation from its repressor adenine monophosphate activated protein kinase (AMPK), and was elicited by CDN’S generated by the cGAMP synthase, cGAS. Thus, while CDN’s may initially facilitate STING function, they subsequently trigger negative-feedback control of STING activity, thus preventing the persistent transcription of innate immune genes. Total RNA obtained from primary STING deficient mouse embryonic fibroblast reconstituted with mSTING (W), S365A variant (A), or S365D variant (D). These cells were transfected with dsDNA (ISD) for 3 hours.

2013-10-10 | E-GEOD-51199 | biostudies-arrayexpress

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