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      Neutrophil extracellular DNA traps promote pancreatic cancer cells migration and invasion by activating EGFR/ERK pathway

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          Abstract

          Neutrophil extracellular DNA traps (NETs) are newly discovered forms of activated neutrophils. Increasing researches have shown that NETs play important roles in cancer progression. Our previous study has proved that tumour‐infiltrating NETs could predict postsurgical survival in patients with pancreatic ductal adenocarcinoma (PDAC). However, the roles of NETs on the progression of pancreatic cancer are unknown. Here, we investigated the effects of NETs on pancreatic cancer cells. Results showed that both PDAC patients’ and normal individuals’ neutrophils‐derived NETs could promote migration and invasion of pancreatic cancer cells with epithelial‐mesenchymal transition. Further, study confirmed that EGFR/ERK pathway played an important role in this progression. The addition of neutralizing antibodies for IL‐1β could effectively block the activation of EGFR/ERK companied with reduction of EMT, migration and invasion. Taken together, NETs facilitated EMT, migration and invasion via IL‐1β/EGFR/ERK pathway in pancreatic cancer cells. Our study suggests that NETs may provide promising therapeutic targets for pancreatic cancer.

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          Most cited references56

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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.
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            Cancer-related inflammation and treatment effectiveness.

            Connie I. Diakos, Kellie A. Charles, Donald C. McMillan … (2014)
            Inflammation is a recognised hallmark of cancer that substantially contributes to the development and progression of malignancies. In established cancers, there is increasing evidence for the roles that local immune response and systemic inflammation have in progression of tumours and survival of patients with cancer. This knowledge provides an opportunity to target these inflammatory responses to improve patient outcomes. In this Review, we examine the complex interplay between local immune responses and systemic inflammation, and their influence on clinical outcomes, and propose potential anti-inflammatory interventions for patients with cancer.
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              Neutrophil: A Cell with Many Roles in Inflammation or Several Cell Types?

              Carlos Rosales (2018)
              Neutrophils are the most abundant leukocytes in the circulation, and have been regarded as first line of defense in the innate arm of the immune system. They capture and destroy invading microorganisms, through phagocytosis and intracellular degradation, release of granules, and formation of neutrophil extracellular traps after detecting pathogens. Neutrophils also participate as mediators of inflammation. The classical view for these leukocytes is that neutrophils constitute a homogenous population of terminally differentiated cells with a unique function. However, evidence accumulated in recent years, has revealed that neutrophils present a large phenotypic heterogeneity and functional versatility, which place neutrophils as important modulators of both inflammation and immune responses. Indeed, the roles played by neutrophils in homeostatic conditions as well as in pathological inflammation and immune processes are the focus of a renovated interest in neutrophil biology. In this review, I present the concept of neutrophil phenotypic and functional heterogeneity and describe several neutrophil subpopulations reported to date. I also discuss the role these subpopulations seem to play in homeostasis and disease.
              Article 0 comments Cited 446 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Wei Jin:
                ORCID: https://orcid.org/0000-0002-3639-1547
                woshijinweia@126.com
                Hua‐Xiang Xu: xuhuaxiang@fudanpci.org
                Liang Liu: liuliang@fudanpci.org
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J Cell Mol Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 06 May 2021
                Publication date (Print): June 2021
                Volume: 25
                Issue: 12 ( doiID: 10.1111/jcmm.v25.12 )
                Pages: 5443-5456
                Affiliations
                [ 1 ] Shanghai Institute of Immunology Department of Immunology and Microbiology Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education Shanghai Jiao Tong University School of Medicine Shanghai China
                [ 2 ] Department of Pancreatic Surgery Pancreatic Cancer Institute Fudan University Shanghai Cancer Center Department of Oncology Shanghai Medical College Shanghai China
                [ 3 ] Translational Medicine Center Shanghai General Hospital Shanghai Jiao Tong University School of Medicine Shanghai China
                Author notes
                [*] [* ] Correspondence

                Liang Liu and Hua‐Xiang Xu, Pancreatic Cancer Institute, Pancreatic Cancer Institute, Department of Pancreatic Surgery, Fudan University, Shanghai Cancer Center, 270 Dong An Road, Shanghai 200032, China.

                Email: liuliang@ 123456fudanpci.org (LL); xuhuaxiang@ 123456fudanpci.org (HX)

                Wei Jin, Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China.

                Email: woshijinweia@ 123456126.com

                Author information
                https://orcid.org/0000-0002-3639-1547
                Article
                Publisher ID: JCMM16555
                DOI: 10.1111/jcmm.16555
                PMC ID: 8184670
                PubMed ID: 33955688
                SO-VID: efc77c18-1e8a-4d63-bff7-75efa1a771c0
                Copyright © © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date revision received : 25 March 2021
                Date received : 19 October 2020
                Date accepted : 01 April 2021
                Page count
                Figures: 6, Tables: 1, Pages: 14, Words: 7084
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81601985
                Award ID: 81802380
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date June 2021
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.2 mode:remove_FC converted:07.06.2021

                ScienceOpen disciplines: Molecular medicine
                Keywords: emt,il‐1β,nets,pancreatic cancer
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: emt, il‐1β, nets, pancreatic cancer

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