| Literature DB >> 32169849 |
Roni F Rayes1, Phil Vourtzoumis1, Marianne Bou Rjeily1, Rashmi Seth1, France Bourdeau1, Betty Giannias1, Julie Berube2, Yu-Hwa Huang3, Simon Rousseau2, Sophie Camilleri-Broet4, Richard S Blumberg3, Nicole Beauchemin5, Sara Najmeh1, Jonathan Cools-Lartigue1, Jonathan D Spicer1, Lorenzo E Ferri6.
Abstract
Neutrophils promote tumor growth and metastasis at multiple stages of cancer progression. One mechanism through which this occurs is via release of neutrophil extracellular traps (NETs). We have previously shown that NETs trap tumor cells in both the liver and the lung, increasing their adhesion and metastasis following postoperative complications. Multiple studies have since shown that NETs play a role in tumor progression and metastasis. NETs are composed of nuclear DNA-derived web-like structures decorated with neutrophil-derived proteins. However, it is unknown which, if any, of these NET-affiliated proteins is responsible for inducing the metastatic phenotype. In this study, we identify the NET-associated carcinoembryonic Ag cell adhesion molecule 1 (CEACAM1) as an essential element for this interaction. Indeed, blocking CEACAM1 on NETs, or knocking it out in a murine model, leads to a significant decrease in colon carcinoma cell adhesion, migration and metastasis. Thus, this work identifies NET-associated CEACAM1 as a putative therapeutic target to prevent the metastatic progression of colon carcinoma.Entities:
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Year: 2020 PMID: 32169849 PMCID: PMC7534954 DOI: 10.4049/jimmunol.1900240
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422