Fig. 3

NETs as potential therapeutic targets. Inhibition of NETs formation via targeting crucial players, such as NE, MPO, or PAD4 in the formation pathway. Another way to inhibit NETs is by blocking CXCR1/2 and IL-8, key mediators of neutrophil chemotactic recruitment. Blockage of NETs-cancer cells interaction via targeting the TLR4/9 and CCDC25 can prevent the effect of NETs on cancer cells. As the core component of NETs, DNA can cause targeted destruction using DNAse. In addition, N2 neutrophils (pro-tumorigenic) can be converted to N1 neutrophils (anti-tumorigenic) by TGF-β inhibitors. Therapeutics used to target NETs may be a potential beneficial approach in combination with immunotherapy.