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      The role of neutrophil extracellular traps in cancer progression, metastasis and therapy

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          Abstract

          Neutrophil extracellular traps (NETs) released by activated neutrophils typically consist of DNA-histone complexes and granule proteins. NETs were originally identified as a host defense system against foreign pathogens and are strongly associated with autoimmune diseases. However, a novel and predominant role of NETs in cancer is emerging. Increasing evidence has confirmed that many stimuli can facilitate NET formation in an NADPH oxidase (NOX)-dependent/NOX-independent manner. In cancer, NETs have been linked to cancer progression, metastasis, and cancer-associated thrombosis. In this review, we aimed to summarize the current available knowledge regarding NET formation and focused on the role of NETs in cancer biological behaviors. The potential target for cancer therapy will be further discussed.

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          Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

          Lorenzo Galluzzi, Ilio Vitale, Stuart A. Aaronson … (2018)
          Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.
          Article 0 comments Cited 1830 times – based on 0 reviews     Review now
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            Matrix metalloproteinases: regulators of the tumor microenvironment.

            Kai Kessenbrock, Vicki Plaks, Zena Werb (2010)
            Extracellular proteolysis mediates tissue homeostasis. In cancer, altered proteolysis leads to unregulated tumor growth, tissue remodeling, inflammation, tissue invasion, and metastasis. The matrix metalloproteinases (MMPs) represent the most prominent family of proteinases associated with tumorigenesis. Recent technological developments have markedly advanced our understanding of MMPs as modulators of the tumor microenvironment. In addition to their role in extracellular matrix turnover and cancer cell migration, MMPs regulate signaling pathways that control cell growth, inflammation, or angiogenesis and may even work in a nonproteolytic manner. These aspects of MMP function are reorienting our approaches to cancer therapy. Copyright 2010 Elsevier Inc. All rights reserved.
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              Polarization of tumor-associated neutrophil phenotype by TGF-beta: "N1" versus "N2" TAN.

              Zvi Fridlender, Jing Sun, Samuel Kim … (2009)
              TGF-beta blockade significantly slows tumor growth through many mechanisms, including activation of CD8(+) T cells and macrophages. Here, we show that TGF-beta blockade also increases neutrophil-attracting chemokines, resulting in an influx of CD11b(+)/Ly6G(+) tumor-associated neutrophils (TANs) that are hypersegmented, more cytotoxic to tumor cells, and express higher levels of proinflammatory cytokines. Accordingly, following TGF-beta blockade, depletion of these neutrophils significantly blunts antitumor effects of treatment and reduces CD8(+) T cell activation. In contrast, in control tumors, neutrophil depletion decreases tumor growth and results in more activated CD8(+) T cells intratumorally. Together, these data suggest that TGF-beta within the tumor microenvironment induces a population of TAN with a protumor phenotype. TGF-beta blockade results in the recruitment and activation of TANs with an antitumor phenotype.
              Article 0 comments Cited 699 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jun He: he-001jun@163.com
                Journal
                Journal ID (nlm-ta): Exp Hematol Oncol
                Journal ID (iso-abbrev): Exp Hematol Oncol
                Title: Experimental Hematology & Oncology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2162-3619
                Publication date (Electronic): 16 November 2022
                Publication date PMC-release: 16 November 2022
                Publication date Collection: 2022
                Volume: 11
                Electronic Location Identifier: 99
                Affiliations
                [1 ]GRID grid.414367.3, Department of Pathology, , Beijing Shijitan Hospital, Capital Medical University, ; Beijing, 100038 China
                [2 ]GRID grid.54549.39, ISNI 0000 0004 0369 4060, Department of Medical Oncology, , Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, Medicine School of University of Electronic Science and Technology, ; Chengdu, 610041 China
                [3 ]GRID grid.13291.38, ISNI 0000 0001 0807 1581, West China School of Medicine, Sichuan University, ; Chengdu, 610041 China
                [4 ]Southeast Medical University, Luzhou, 646099 China
                [5 ]GRID grid.284723.8, ISNI 0000 0000 8877 7471, Southern Medical University, ; Guangzhou, 510515 China
                [6 ]GRID grid.452803.8, Department of Oncology, , The Third Hospital of Mianyang (Sichuan Mental Health Center), ; Mianyang, 621015 China
                Article
                Publisher ID: 345
                DOI: 10.1186/s40164-022-00345-3
                PMC ID: 9667637
                PubMed ID: 36384979
                SO-VID: b8b3a76a-e397-4a88-991e-d80ebf18e13d
                Copyright © © The Author(s) 2022
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 18 August 2022
                Date accepted : 15 October 2022
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2022

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: neutrophil,neutrophil extracellular traps,cancer,metastasis,targeted therapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: neutrophil, neutrophil extracellular traps, cancer, metastasis, targeted therapy

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