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Abstract
Simple SummaryTumor-associated neutrophils constitute an important portion of the infiltrating immune cells in the tumor microenvironment. One of the abilities of neutrophils is forming neutrophil extracellular traps. Recent studies on tumor-associated neutrophils have drawn increasing attention to the role of neutrophil extracellular traps in the tumor microenvironment. There were also some reviews summarize the pro-tumorigenic activity of NETs in tumors. The specific novelty of this article is the specific summarization on the pivotal roles of NETs in tumor invasion-metastasis cascade and the recapitulation on the potential of NETs in clinical applications. Neutrophil extracellular trap (NET) formation is an ability of neutrophils to capture and kill pathogens by releasing chromatin scaffolds, along with associated cytotoxic enzymes and proteases, into the extracellular space. NETs are usually stimulated by pathogenic microorganisms and their products, surgical pressure or hypoxia. Interestingly, a number of recent studies suggest that tumor cells can induce NET formation, which in turn confers tumor cell malignancy. Notably, emerging studies indicate that NETs are involved in enhancing local invasion, increasing vascular permeability and facilitating immune escape and colonization, thus promoting tumor metastasis. In this article, we review the pivotal roles of NETs in the tumor metastasis cascade. We also recapitulate the potential of NETs as a cancer prognostic biomarker and therapeutic target.
Highlights
Neutrophils are abundant and heterogeneous leukocytes in mammals that mediate against infection or injury
Metastasis involves a series of events [69]: (1) local invasion, which is facilitated by breakdown of the extracellular matrix (ECM); at the same time, the release of cytokines embedded in the ECM further promotes the growth and survival of tumor cells; (2) intravasation into the tumor vasculature; (3) escape of circulating tumor cells from the immune system; (4) arrest in capillaries at the distant site and extravasation into the Metastasis is the major cause of cancer-related mortality
Metastasis involves a series of events [69]: (1) local invasion, which is facilitated by breakdown of the extracellular matrix (ECM); at the same time7,otfh1e9 release of cytokines embedded in the ECM further promotes the growth and survival of tumor cells; (2) intravasation into the tumor vasculature; (3) escape of circulating tumor cells from the immune system; (4) arrest in capillaries at the distant site and extravasation ipnatroetnhcehpymaraenocfhtyamrgaetoofrtgaargnest; (o5r)geanntsr;y(5in) etontdroyrimntaondt oturmaonrtcteullms oanr dcerlelsacatnivdarteioanct;ivanatdio(n6); acnoldon(6iz) actoiloonnaiznadtidonevaenlodpdmeveneltoopfmmeanctroomf metaacsrtoamseest.astases
Summary
Neutrophils are abundant and heterogeneous leukocytes in mammals that mediate against infection or injury. The mechanism behind NET formation depends on the properties of the stimulation [3,33] Stimuli such as PMA, LPS and various types of bacteria result in reactive oxygen species (ROS) production through activation of NADPH oxidase via the Raf-MEKERK pathway [34,35]. Neutrophils with excessive cytoplasmic ROS are more prone to form NETs [36] Many other stimuli such as calcium ionophores, nigericin, certain microbes, UV light and some crystals lead to NET formation without NADPH oxide but requiring mitochondrial reactive oxygen species (mROS) [37]. Neutrophils do not need to pay the price of cell death or cytolysis to form NETs [6] They can squeeze out nuclear DNA through vesicle transport mechanisms [17]. The main mechanisms of NET formation have already been well studied, but there are numerous interesting scientific problems in the intracellular process of NET formation waiting to be formulated and replenished
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