Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle

Neutrophil extracellular traps (NETs) are a neutrophil-generated extracellular network of chromatin and chromatin-bound molecules with antimicrobial potency. Recent data suggest that NETs are associated with cancer progression and cancer-associated hypercoagulability. Pancreatic adenocarcinoma (PDAC...

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Main Authors: Michail Mitsis, Panagiota Drosou, Vasileios Tatsis, Georgios S. Markopoulos
Format: Article
Language:English
Published: MDPI AG 2022-07-01
Series:Cancers
Subjects:
Online Access:https://www.mdpi.com/2072-6694/14/14/3339
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author Michail Mitsis
Panagiota Drosou
Vasileios Tatsis
Georgios S. Markopoulos
author_facet Michail Mitsis
Panagiota Drosou
Vasileios Tatsis
Georgios S. Markopoulos
author_sort Michail Mitsis
collection DOAJ
description Neutrophil extracellular traps (NETs) are a neutrophil-generated extracellular network of chromatin and chromatin-bound molecules with antimicrobial potency. Recent data suggest that NETs are associated with cancer progression and cancer-associated hypercoagulability. Pancreatic adenocarcinoma (PDAC) is a lethal type of cancer in which hypercoagulability and cancer-related thrombosis are among the main complications. In the current report, we summarize the available data on the interplay between NET formation and PDAC development. We conclude that NETs support a dual role during PDAC progression and metastasis. Their formation is on the one hand an important event that shapes the cancer microenvironment to support cancer cell proliferation, invasion and metastasis. On the other hand, NETs may lead to cancer-associated thrombosis. Both mechanisms seem to be dependent on distinct molecular mechanisms that link inflammation to cancer progression. Collectively, NET formation may contribute to the pathogenesis of PDAC, while during cancer development, the proinflammatory environment enables the induction of new NETs and thrombi, forming a vicious cycle. We suggest that targeting NET formation may be an effective mechanism to inhibit both PDAC development and the accompanying hypercoagulability.
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spelling doaj.art-1081fe7277524414b06738a555929dc42023-12-01T21:59:08ZengMDPI AGCancers2072-66942022-07-011414333910.3390/cancers14143339Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious CycleMichail Mitsis0Panagiota Drosou1Vasileios Tatsis2Georgios S. Markopoulos3Department of Surgery, School of Health Sciences, Faculty of Medicine, University Hospital of Ioannina, University of Ioannina, 455 00 Ioannina, GreeceDepartment of Surgery, School of Health Sciences, Faculty of Medicine, University Hospital of Ioannina, University of Ioannina, 455 00 Ioannina, GreeceDepartment of Surgery, School of Health Sciences, Faculty of Medicine, University Hospital of Ioannina, University of Ioannina, 455 00 Ioannina, GreeceDepartment of Surgery, School of Health Sciences, Faculty of Medicine, University Hospital of Ioannina, University of Ioannina, 455 00 Ioannina, GreeceNeutrophil extracellular traps (NETs) are a neutrophil-generated extracellular network of chromatin and chromatin-bound molecules with antimicrobial potency. Recent data suggest that NETs are associated with cancer progression and cancer-associated hypercoagulability. Pancreatic adenocarcinoma (PDAC) is a lethal type of cancer in which hypercoagulability and cancer-related thrombosis are among the main complications. In the current report, we summarize the available data on the interplay between NET formation and PDAC development. We conclude that NETs support a dual role during PDAC progression and metastasis. Their formation is on the one hand an important event that shapes the cancer microenvironment to support cancer cell proliferation, invasion and metastasis. On the other hand, NETs may lead to cancer-associated thrombosis. Both mechanisms seem to be dependent on distinct molecular mechanisms that link inflammation to cancer progression. Collectively, NET formation may contribute to the pathogenesis of PDAC, while during cancer development, the proinflammatory environment enables the induction of new NETs and thrombi, forming a vicious cycle. We suggest that targeting NET formation may be an effective mechanism to inhibit both PDAC development and the accompanying hypercoagulability.https://www.mdpi.com/2072-6694/14/14/3339NETsNETosishypercoagulabilitypancreatic adenocarcinomainflammationcancer
spellingShingle Michail Mitsis
Panagiota Drosou
Vasileios Tatsis
Georgios S. Markopoulos
Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle
Cancers
NETs
NETosis
hypercoagulability
pancreatic adenocarcinoma
inflammation
cancer
title Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle
title_full Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle
title_fullStr Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle
title_full_unstemmed Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle
title_short Neutrophil Extracellular Traps and Pancreatic Cancer Development: A Vicious Cycle
title_sort neutrophil extracellular traps and pancreatic cancer development a vicious cycle
topic NETs
NETosis
hypercoagulability
pancreatic adenocarcinoma
inflammation
cancer
url https://www.mdpi.com/2072-6694/14/14/3339
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AT panagiotadrosou neutrophilextracellulartrapsandpancreaticcancerdevelopmentaviciouscycle
AT vasileiostatsis neutrophilextracellulartrapsandpancreaticcancerdevelopmentaviciouscycle
AT georgiossmarkopoulos neutrophilextracellulartrapsandpancreaticcancerdevelopmentaviciouscycle