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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [RNA-seq]

ABSTRACT: Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [RNA-seq]

PROVIDER: PRJNA760933 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15724948_1.fastq.gz	Fastqsanger.gz
	SRR15724948_2.fastq.gz	Fastqsanger.gz
	SRR15724949_1.fastq.gz	Fastqsanger.gz
	SRR15724949_2.fastq.gz	Fastqsanger.gz
	SRR15724950_1.fastq.gz	Fastqsanger.gz

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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [ChIP-seq]

Project description:The process in which locally confined epithelial malignancies progressively evolve into invasive cancers is often promoted by unjamming, a phase transition from a solid-like to a liquid-like state that occurs in various tissues. Whether this tissue-level mechanical transition impact phenotypes during carcinoma progression remains unclear. We show, here that the large fluctuations in cell density that accompany unjamming result in repeated mechanical deformations of cells and nuclei. Cells react to these protracted mechanical stresses by mounting a mechano-protective response that includes enlarged nuclear size and rigidity, altered heterochromatin distribution, and the remodeling of the perinuclear actin architecture into actin rings. The chronic strains and stresses associated with unjamming together with the reduction of Lamin B1 levels eventually result in DNA damage and nuclear envelope ruptures, with the release of cytosolic DNA that activates a cGAS/STING-dependent cytosolic DNA response gene program. This mechanically-driven transcriptional rewiring ultimately results in a change in cell state, with the emergence of malignant traits, including epithelial-to-mesenchymal plasticity phenotypes and chemo-resistance in invasive breast carcinoma.

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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [RNA-seq]

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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [RNA-seq of Organoids]

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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [ChIP-seq]

Project description:Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [ChIP-seq]

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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [SAMMY-seq]

Project description:Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [SAMMY-seq]

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Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [RNA-seq of Organoids]

Project description:Tissue fluidification promotes a cGAS/STING-mediated cytosolic DNA response in invasive breast cancer [RNA-seq of Organoids]

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Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence

Project description:Cellular senescence is triggered by various distinct stresses and characterized by a permanent cell cycle arrest. Senescent cells secrete a variety of inflammatory factors, collectively referred to as the senescence-associated secretory phenotype (SASP). The mechanism(s) underlying the regulation of the SASP remains incompletely understood. Here we define a role for innate DNA sensing in the regulation of senescence and the SASP. We find that cyclic GMP-AMP synthase (cGAS) recognizes cytosolic chromatin fragments (CCFs) in senescent cells. The activation of cGAS, in turn triggers the production of SASP factors via Stimulator of interferon genes (STING), thereby promoting paracrine senescence. We demonstrate that diverse stimuli of cellular senescence engage the cGAS-STING pathway in vitro and we show cGAS-dependent regulation of senescence upon irradiation and oncogene activation in vivo. Our findings provide insights into the mechanisms underlying cellular senescence by establishing the cGAS-STING pathway as a crucial regulator of senescence and the SASP.

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Urolithin A is a potent modulator of cGAS-Sting signaling pathway

Project description:The innate immune cGAS-STING pathway has emerged as an important signaling system in the organismal defense against viral and bacterial infections, inflammatory responses to cellular damage, regulation of autophagy, as well as in tumor immunosurveillance. Such key functions of the cGAS-STING pathway make it an attractive target for pharmacological intervention in disease treatments and in controlling inflammation and immunity. Here, we show that urolithin A (UA), an ellagic acid metabolite, exerts a profound effect on the expression of STING and enhances cGAS-STING activation and STING-related autophagy in response to cytosolic DNA in human cell lines. Animal laboratory models and limited human trials have reported no obvious adverse effects of UA administration. Thus, the use of UA alone or in combination with other pharmacological compounds may present a potential therapeutic approach in the treatment of human diseases that involves aberrant activation of the cGAS-STING pathway or accumulation of cytosolic DNA and warrants further investigation in relevant transgenic animal models.

2025-09-04 | GSE224258 | GEO

Tissue fluidification promotes a cGAS-STING cytosolic DNA response in invasive breast cancer.

Project description:The process in which locally confined epithelial malignancies progressively evolve into invasive cancers is often promoted by unjamming, a phase transition from a solid-like to a liquid-like state, which occurs in various tissues. Whether this tissue-level mechanical transition impacts phenotypes during carcinoma progression remains unclear. Here we report that the large fluctuations in cell density that accompany unjamming result in repeated mechanical deformations of cells and nuclei. This triggers a cellular mechano-protective mechanism involving an increase in nuclear size and rigidity, heterochromatin redistribution and remodelling of the perinuclear actin architecture into actin rings. The chronic strains and stresses associated with unjamming together with the reduction of Lamin B1 levels eventually result in DNA damage and nuclear envelope ruptures, with the release of cytosolic DNA that activates a cGAS-STING (cyclic GMP-AMP synthase-signalling adaptor stimulator of interferon genes)-dependent cytosolic DNA response gene program. This mechanically driven transcriptional rewiring ultimately alters the cell state, with the emergence of malignant traits, including epithelial-to-mesenchymal plasticity phenotypes and chemoresistance in invasive breast carcinoma.

| S-EPMC10156599 | biostudies-literature

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