Figure 4 Tumour-induced neutrophil extracellular trap

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Figure 4 Tumour-induced neutrophil extracellular trap formation facilitates tumorigenesis and thrombus formation Figure 4 | Tumour-induced neutrophil extracellular trap formation facilitates tumorigenesis and thrombus formation. a | Neutrophils show an N2 phenotype around invasive cancer. N2 neutrophils contribute to cancer progression via the reconstruction of extracellular matrix, promotion of angiogenesis and lymphangiogenesis and production of pro-tumorigenic cytokines. Some types of cancer cells produce granulocyte colony-stimulating factor (G-CSF) and CXC-chemokine ligand 8 (CXCL8), which induce neutrophil extracellular trap (NET) formation. NETs are assumed to be sources of tissue factor and promote angiogenic activity in the cancer microenvironment. b | NET formation owing to cancer-mediated signals, systemic infection or inflammation facilitates cancer metastasis. The DNA mesh component of NETs traps circulating cancer cells via interactions with β1 integrins. Furthermore, excessive NET formation increases vascular permeability, which promotes the extravasation of cancer cells. c | Tumour-induced NET formation is associated with thrombus formation in patients with cancer. Gastrointestinal and lung cancers are known to carry the highest rates of venous thromboembolism. NETs promote thrombus formation by providing a scaffold for platelet activation, generating thrombin and fibrin and releasing von Willebrand factor (vWF). Neutrophil elastase included in NETs also increases thrombosis by participating in the local proteolysis of tissue factor pathway inhibitors. Factor XII, coagulation factor XII. Honda, M. & Kubes, P. (2018) Neutrophils and neutrophil extracellular traps in the liver and gastrointestinal system Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.183