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Figure 6. The role of NETs in tumor chemotherapy, immunotherapy, and radiation resistance. (A) Chemotherapy-induced tumor cell death induces NETosis in two ways: by secreting chemokines that directly induce NETosis or by releasing ATP, which prompts surviving tumor cells to secrete cytokines that further trigger NETosis. The NETs contain ITGαvβ1 and MMP-9, which can induce EMT and confer chemoresistance to tumor cells; (B) Th17 cells secrete IL-17, which induces tumor cells to release chemokines and cytokines, subsequently promoting NETosis. The components of NETs can inhibit immune-mediated cytotoxicity by disrupting the contact between effectors and their targets, leading to resistance to immunotherapy; (C) Radiation can induce NETosis, and inhibiting NETs can enhance CD8⁺ T cell infiltration. Created with BioRender.com (accessed on 30 June 2022). NETs: Neutrophils extracellular traps; ATP: adenosine triphosphate; ITGαvβ1: integrins αvβ1; MMP-9: matrix metalloproteinases-9; EMT: epithelial-mesenchymal transition; Th17: T helper 17; IL-17: interleukin-17.