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  3. Neutrophil extracellular traps in cancer.

Neutrophil extracellular traps in cancer.

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DOI
10.48350/158317
Publisher DOI
10.1016/j.semcancer.2021.07.011
PubMed ID
34280576
Abstract
Beyond their well-known functions in the acute phases of the immune response, neutrophils play important roles in the various phases of tumor initiation and progression, through the release of their stored or newly synthesized mediators. In addition to reactive oxygen species, cytokines, chemokines, granule proteins and lipid mediators, neutrophil extracellular traps (NETs) can also be released upon neutrophil activation. NET formation can be achieved through a cell-death process or in association with the release of mitochondrial DNA from viable neutrophils. NETs are described as extracellular fibers of DNA and decorating proteins responsible for trapping and killing extracellular pathogens, playing a protective role in the antimicrobial defense. There is increasing evidence, however, that NETs play multiple roles in the scenario of cancer-related inflammation. For instance, NETs directly or indirectly promote tumor growth and progression, fostering tumor spread at distant sites and shielding cancer cells thus preventing the effects of cytotoxic lymphocytes. NETs can also promote tumor angiogenesis and cancer-associated thrombosis. On the other hand, there is some evidence that NETs may play anti-inflammatory and anti-tumorigenic roles. In this review, we focus on the main mechanisms underlying the emerging effects of NETs in cancer initiation and progression.
Date Issued
2022-02
Publication Type
Article
Subject(s)
600 Technology > 610 Medicine & health
Subjects
Angiogenesis Cancer Inflammation Neutrophil Neutrophil extracellular trap
Language(s)
en
Author(s)
Cristinziano, Leonardo
Modestino, Luca
Antonelli, Alessandro
Marone, Gianni
Simon, Hans-Uwe  orcid-logo
Institut für Pharmakologie  
Varricchi, Gilda
Galdiero, Maria Rosaria
Additional Credits
Institut für Pharmakologie  
Journal
Seminars in cancer biology
Publisher
Elsevier
ISSN
1096-3650
Access(Rights)
restricted
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