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Gene expression changes of intraperitoneal tumor microenvironment after STING activation

ABSTRACT: The results revealed dramatic differences between the STING-activated and Control tumors

ORGANISM(S): Mus musculus

PROVIDER: GSE159825 | GEO | 2020/10/23

REPOSITORIES: GEO

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Gene expression changes of tumor microenvironment (TME) after STING activation

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Gene expression changes of intraperitoneal tumor microenvironment after STING activation

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Project description:Activation of Stimulator of interferon genes (STING) is well known to upregulate inflammation through canonical TBK1 signaling. STING is recently found to activate noncanonical functions through its transmembrane proton channel. Whether STING stimulates any transcription programs through its channel is unknown. In this study, we identified the transcription factor EB (TFEB) as a downstream effector of the STING channel. TFEB is a transcriptional regulator of lysosomal biogenesis and autophagy. Using RNA sequencing approaches, we confirmed that STING activated transcriptional upregulation of lysosomal biogenesis and autophagy independently of TBK1.

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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.

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| S-EPMC8900217 | biostudies-literature

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