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Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

ABSTRACT: In this study, cisplatin activated cGAS-STING signal pathway and deficiency of STING attenuated cisplatin-induced cardiotoxicity in vivo and in vitro. Mechanistically, STING-TNF-α-AP-1 axis contributed to cisplatin-induced cardiotoxicity by triggering cardiomyocyte apoptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE181749 | GEO | 2021/08/12

REPOSITORIES: GEO

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Activation of cGAS-STING signal to inhibit the proliferation of bladder cancer: the immune effect of cisplatin

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PIKfyve inhibition synergizes with Cisplatin to provoke antitumor immunogenicity in melanoma by alleviating lysosomal degradation of STING

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The Cardiac Endothelial Cell cGAS-STING Pathway Promotes Doxorubicin-Induced Cardiotoxicity via CD38-Mediated NAD Decline and Mitochondrial Dysfunction [human]

Project description:Doxorubicin is an effective chemotherapy drug for treating various types of cancer. However, lethal cardiotoxicity severely limits its clinical use. Recent evidence has indicated that aberrant activation of the cytosolic DNA-sensing cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a critical role in cardiovascular destruction. Here, we investigate the involvement of this mechanism in doxorubicin-induced cardiotoxicity (DIC).

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The Cardiac Endothelial Cell cGAS-STING Pathway Promotes Doxorubicin-Induced Cardiotoxicity via CD38-Mediated NAD Decline and Mitochondrial Dysfunction [mouse]

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Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

Project description:Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

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ARF1 prevents aberrant type I IFN induction by regulating STING activation and recycling

Project description:Type I interferon (IFN) signalling is tightly controlled. Upon recognition of DNA by cyclic GMP-AMP synthase (cGAS), stimulator of interferon genes (STING) translocates along the endoplasmic reticulum (ER)-Golgi axis to induce IFN signalling. Afterwards, signal termination is achieved through autophagic degradation of STING, or STING recycling by retrograde COPI-mediated transport. Here we identify the GTPase ARF1 as a negative regulator of cGAS-STING signaling. Heterozygous ARF1 missense mutations cause a novel type I interferonopathy associated with enhanced IFN stimulated gene production. Expression of patient-derived, GTPase-defective, ARF1 in cell lines and primary cells results in increased cGAS-STING dependent type I IFN signalling. Mechanistically, mutated ARF1 both induces activation of cGAS by aberrant mitochondrial DNA, and promotes accumulation of active STING at the Golgi/ERGIC due to defective COPI retrograde transport. Our data establish ARF1 as a key factor in cGAS-STING homeostasis, which is required to maintain mitochondrial integrity and promote STING recycling.

2022-06-23 | MSV000089711 | MassIVE

Sting

Project description:Drosophila melanogaster Sting, Sting, is differentially expressed in 23 experiment(s);

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Sting

Project description:Drosophila melanogaster Sting, Sting, is expressed in 4 baseline experiment(s);

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IFNλ1 is a STING-dependent mediator of DNA damage and induces Immune activation in lung cancer

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2025-03-05 | GSE288796 | GEO

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2025-04-16 | GSE294678 | GEO

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