Abstract

As the predominant host defense against pathogens, neutrophil extracellular traps (NETs) have attracted increasing attention due to their vital roles in infectious inflammation in the past few years. Interestingly, NETs also play important roles in noninfectious conditions, such as rheumatism and cancer. The process of NETs formation can be regulated and the form of cell death accompanied by the formation of NETs is regarded as “NETosis”. A large amount of evidence has confirmed that many stimuli can facilitate the release of NETs from neutrophils. Furthermore, it has been illustrated that NETs promote tumor growth and progression via many molecular pathways. Meanwhile, NETs also can promote metastasis in many kinds of cancers based on multiple studies. In addition, some researchs have found that NETs can promote coagulation and cancer-associated thrombosis. In the present review, it will highlight how NETosis, which is stimulated by various stimuli and signaling pathways, affects cancer biological behaviors via NETs. Given their crucial roles in cancer, NETs will become possible therapeutic targets for inhibiting proliferation, metastasis and thrombosis in cancer patients.

Highlights

  • Neutrophil extracellular traps (NETs) are net-like structures composed of granule proteins and nuclear components [1]

  • The regulatory mechanism of NETs in cancer biological behavior is discussed in detail

  • NETs regulate tumor biological behaviors through interaction with tumor microenvironment, which is different from traditional molecule targets

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Summary

Introduction

Neutrophil extracellular traps (NETs) are net-like structures composed of granule proteins and nuclear components (such as DNA and histones) [1]. Some studies have shown increased generation of NETs in tumors induced by G-CSF [43, 44]. Some studies have confirmed that PMA can promote the release of NETs from neutrophils in both healthy donors and cancer patients [48–50]. LPS promotes the activation of platelets through platelet TLR4, inducing the interaction of platelets with neutrophils and the generation of NETs [69, 70].

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