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Neutrophil Extracellular Traps induced by chemotherapy inhibit tumor growth in vivo

ABSTRACT: Neutrophil Extracellular Traps induced by chemotherapy inhibit tumor growth in vivo

PROVIDER: PRJNA1030052 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26446451_1.fastq.gz	Fastqsanger.gz
	SRR26446451_2.fastq.gz	Fastqsanger.gz
	SRR26446452_1.fastq.gz	Fastqsanger.gz
	SRR26446452_2.fastq.gz	Fastqsanger.gz
	SRR26446453_1.fastq.gz	Fastqsanger.gz

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Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

Project description:This SuperSeries is composed of the following subset Series: GSE32542: Murine serum reactivity to common autoantigens in response to immunization with neutrophil extracellular traps GSE32543: Human and murine serum reactivity to specific histone posttranslational modifications in neutrophil extracellular traps Refer to individual Series

2012-01-26 | E-GEOD-32544 | biostudies-arrayexpress

Neutrophil Extracellular Traps induced by chemotherapy inhibit tumor growth in vivo

Project description:Neutrophil Extracellular Traps (NETs), a web-like structure of cytosolic and granule proteins assembled on decondensed chromatin, kill pathogens and causes tissue damage in diseases. Whether NETs can kill cancer cells is unexplored. Here, we report that a combination of glutaminase inhibitor CB-839 and 5-FU inhibits the growth of PIK3CA mutant colorectal cancers (CRCs) in xenograft, syngeneic, and genetically engineered mouse models in part through NETs. Disruption of NETs by either DNase I treatment or depletion of neutrophils in CRCs attenuated the efficacy of the drug combination. Moreover, NETs were present in tumor biopsies taken from patients treated with the drug combination in a phase II clinical trial. Increased NET levels in tumors are associated with longer progression-free survival. Mechanistically, the drug combination induced the expression of IL-8 preferentially in PIK3CA mutant CRCs to attract neutrophils into the tumors. Further, the drug combination increased the levels of reactive oxygen species in neutrophils, thereby inducing NETs. Cathepsin G (CTSG), a serine protease localized in NETs, enters CRC cells through the RAGE cell surface protein. The internalized CTSG cleaves 14-3-3 proteins, releases Bax, and triggers apoptosis in CRC cells. Thus, our studies illuminate a previously unrecognized mechanism by which chemotherapy-induced NETs kill cancer cells.

2024-01-12 | GSE245839 | GEO

Piezo1 induces neutrophil extracellular traps formation directing M1 macrophage differentiation

Project description:To research the neutrophil extracellular traps in the regulation of macrophages differentiation, we performed gene expression profiling analysis using data obtained from RNA-seq of mice and control with virus infection.

2024-07-10 | GSE220198 | GEO

mRNA, ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

Project description:ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

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Neutrophil extracellular traps formed during chemotherapy confers TGFβ activation in breast metastatic cancer cells

Project description:Neutrophil extracellular traps formed during chemotherapy confers TGFβ activation in breast metastatic cancer cells

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Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

Project description:This study invesigates the effects of neutrophil extracellular traps (NETs) on articular cartilage degredation and resulting autoimmune responses in rheumatoid arthritis.

2020-08-10 | GSE150466 | GEO

Hydrogen gas inhibits the formation of neutrophil extracellular traps

Project description:Neutrophil extracellular traps (NETs) contribute to inflammatory pathogenesis, especially in infectious and cardiovascular diseases. H2 gas acts as an antioxidant and has been clinically and experimentally proven to ameliorate inflammation. Therefore, we investigated whether H2 gas could inhibit NET formation associated with excessive neutrophil activation. Phorbol-12-myristate-13-acetate (PMA)-stimulated human neutrophils exposed to H2 exhibited reduced citrullination of histones, membrane disruption by chromatin complexes, and release of NET components over controls. Mechanistically, H2 suppressed the phosphorylation of Ser-139 residue in H2AX, a marker of DNA damage, thereby reducing the expression of CXC-chemokine receptor 4 (CXCR4) in PMA-stimulated neutrophils. Along with the upregulation of CXCR4, the intracellular content of myeloperoxidase (MPO) and the production of MPO-derived hypochlorous acid (HOCl) was increased; however, these effects were markedly suppressed in H2-exposed cultures. Thus, H2 neutralized HOCl produced by the oxidative burst, inhibited DNA damage, and subsequently inhibited NET formation. We further confirmed that inhalation of H2 inhibited the formation and release of NET components in the blood and bronchoalveolar lavage of a lipopolysaccharide-induced sepsis model in mice and aged minipigs. Therefore, H2 therapy has the potential to be a new therapeutic agent for inflammatory diseases involving NETs associated with excessive neutrophil activation.

2022-02-23 | GSE178883 | GEO

Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

Project description:Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

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Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

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Hydrogen gas inhibits the formation of neutrophil extracellular traps

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