Neutrophil extracellular traps promote metastasis in gastric cancer patients with postoperative abdominal infectious complications

Xia, Xiang; Zhang, Zizhen; Zhu, Chunchao; Ni, Bo; Wang, Shuchang; Yang, Shuofei; Yu, Fengrong; Zhao, Enyue; Li, Qing; Zhao, Gang

doi:10.1038/s41467-022-28492-5

Cited by 98 publications

(61 citation statements)

References 57 publications

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“…Moreover, we should highlight the contribution of TGF-β to breast cancer metastasis because breast cancer can quickly metastasize to the lung, brain, bone, and liver, which is lethal [ 200 ]. In addition to breast cancer, TGF-β is also critical in the metastasis of other cancers including bone, and gastric cancer [ 201 – 203 ]. TGF-β participates in breast cancer metastasis by up-regulating CXCR4 in monocytes.…”

Section: Introductionmentioning

confidence: 99%

Targeting TGF-β signal transduction for fibrosis and cancer therapy

et al. 2022

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Transforming growth factor β (TGF-β) has long been identified with its intensive involvement in early embryonic development and organogenesis, immune supervision, tissue repair, and adult homeostasis. The role of TGF-β in fibrosis and cancer is complex and sometimes even contradictory, exhibiting either inhibitory or promoting effects depending on the stage of the disease. Under pathological conditions, overexpressed TGF-β causes epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) deposition, cancer-associated fibroblast (CAF) formation, which leads to fibrotic disease, and cancer. Given the critical role of TGF-β and its downstream molecules in the progression of fibrosis and cancers, therapeutics targeting TGF-β signaling appears to be a promising strategy. However, due to potential systemic cytotoxicity, the development of TGF-β therapeutics has lagged. In this review, we summarized the biological process of TGF-β, with its dual role in fibrosis and tumorigenesis, and the clinical application of TGF-β-targeting therapies.

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Section: Introductionmentioning

confidence: 99%

Targeting TGF-β signal transduction for fibrosis and cancer therapy

et al. 2022

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“…Notably, for the NET smear assay, 1 ul plasma stained with Sytox Green and DAPI for 15 min provided clear NET structures ( Figure 3 ) that correlated with brightfield images taken immediately after smearing ( Figure 5 ). Like immunofluorescence staining of neutrophils on poly-L-lysine-coated plates ( 32 , 38 ), specificity for NETs was increased by staining with anti-MPO(Abcam) and -CitH3(Abcam) antibodies along with DAPI ( Figure 4 ). While data from both methods of NET detection revealed significant and comparable differences between healthy donor and SLE patient plasma, results from healthy donor GaP samples indicate that the ELISA is more sensitive and has a wider range for detecting low levels of plasma NETs, than smear assay.…”

Section: Discussionmentioning

confidence: 99%

“…To the best of our knowledge, this is the first study to visualize and quantify NET levels in only 1 ul of patient plasma. Notably, the method requires minimal time, reagents, specialized equipment and/or costs ( 22 , 34 , 36 – 38 ).…”

Section: Discussionmentioning

confidence: 99%

Detection of neutrophil extracellular traps in patient plasma: method development and validation in systemic lupus erythematosus and healthy donors that carry IRF5 genetic risk

2022

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Neutrophil extracellular traps (NETs) are web-like structures extruded by neutrophils after activation or in response to microorganisms. These extracellular structures are decondensed chromatin fibers loaded with antimicrobial granular proteins, peptides, and enzymes. NETs clear microorganisms, thus keeping a check on infections at an early stage, but if dysregulated, may be self-destructive to the body. Indeed, NETs have been associated with autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), antiphospholipid syndrome (APS), psoriasis, and gout. More recently, increased NETs associate with COVID-19 disease severity. While there are rigorous and reliable methods to quantify NETs from neutrophils via flow cytometry and immunofluorescence, the accurate quantification of NETs in patient plasma or serum remains a challenge. Here, we developed new methodologies for the quantification of NETs in patient plasma using multiplex ELISA and immunofluorescence methodology. Plasma from patients with SLE, non-genotyped healthy controls, and genotyped healthy controls that carry either the homozygous risk or non-risk IRF5-SLE haplotype were used in this study. The multiplex ELISA using antibodies detecting myeloperoxidase (MPO), citrullinated histone H3 (CitH3) and DNA provided reliable detection of NETs in plasma samples from SLE patients and healthy donors that carry IRF5 genetic risk. An immunofluorescence smear assay that utilizes only 1 µl of patient plasma provided similar results and data correlate to multiplex ELISA findings. The immunofluorescence smear assay is a relatively simple, inexpensive, and quantifiable method of NET detection for small volumes of patient plasma.

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“…Rather than promoting anti-tumor immune responses, NETs support neoplastic growth and metastatic processes by multiple mechanisms (189). Indeed, NETs can provide a physical shield that protects tumor cells from T and NK cell-mediated immune attack (190), or directly support tumor cell proliferation and invasiveness by activating the CCDC25integrin linked kinase-b-parvin pathway (191) or TGF-b signaling cascade (192). NETs have been shown to promote proliferation and invasiveness of glioma cells via HMGB1-mediated stimulation of RAGE and activation of the NF-kB signaling in vitro (193).…”

Section: Extracellular Traps In Brain Tumorsmentioning

confidence: 99%

Unveiling Leukocyte Extracellular Traps in Inflammatory Responses of the Central Nervous System

Colciaghi

Costanza

2022

Front. Immunol.

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Over the past nearly two decades, increasing evidence has uncovered how immune cells can actively extrude genetic material to entrap invading pathogens or convey sterile inflammatory signals that contribute to shaping immune responses. Originally identified in neutrophils, the release of decondensed chromatin fibers decorated with antimicrobial proteins, called extracellular traps (ETs), has been recognized as a specific form of programmed inflammatory cell death, which is now known to occur in several other leukocytes. Subsequent reports have shown that self-DNA can be extruded from immune cells even in the absence of cell death phenomena. More recent data suggest that ETs formation could exacerbate neuroinflammation in several disorders of the central nervous system (CNS). This review article provides an overview of the varied types, sources, and potential functions of extracellular DNA released by immune cells. Key evidence suggesting the involvement of ETs in neurodegenerative, traumatic, autoimmune, and oncological disorders of the CNS will be discussed, outlining ongoing challenges and drawing potentially novel lines of investigation.

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Neutrophil extracellular traps promote metastasis in gastric cancer patients with postoperative abdominal infectious complications

Cited by 98 publications

References 57 publications

Targeting TGF-β signal transduction for fibrosis and cancer therapy

Targeting TGF-β signal transduction for fibrosis and cancer therapy

Detection of neutrophil extracellular traps in patient plasma: method development and validation in systemic lupus erythematosus and healthy donors that carry IRF5 genetic risk

Unveiling Leukocyte Extracellular Traps in Inflammatory Responses of the Central Nervous System

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