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    Human neutrophils facilitate tumor cell transendothelial migration.

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    Authors
    Wu, Q D
    Wang, J H
    Condron, C
    Bouchier-Hayes, D
    Redmond, H P
    Affiliation
    Department of Surgery, Cork University Hospital, University College Cork, Wilton,, Cork, Ireland.
    Issue Date
    2012-02-03T15:12:02Z
    MeSH
    *Adenocarcinoma
    Adult
    Antibodies, Monoclonal
    Antigens, CD29/immunology/metabolism
    Apoptosis/physiology
    *Breast Neoplasms
    Capillaries/cytology
    Carcinogens/pharmacology
    Cell Division/physiology
    Cell Movement/drug effects/*physiology
    Culture Media, Conditioned/pharmacology
    Endothelium, Vascular/*cytology
    Female
    Flow Cytometry
    Humans
    Intercellular Adhesion Molecule-1/immunology/metabolism
    Lipopolysaccharides/pharmacology
    Neoplasm Metastasis/*physiopathology
    Neutralization Tests
    Neutrophils/*physiology
    Tetradecanoylphorbol Acetate/pharmacology
    Tumor Cells, Cultured/cytology
    Umbilical Veins/cytology
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    Citation
    Am J Physiol Cell Physiol. 2001 Apr;280(4):C814-22.
    Journal
    American journal of physiology. Cell physiology
    URI
    http://hdl.handle.net/10147/209091
    PubMed ID
    11245598
    Abstract
    Tumor cell extravasation plays a key role in tumor metastasis. However, the precise mechanisms by which tumor cells migrate through normal vascular endothelium remain unclear. In this study, using an in vitro transendothelial migration model, we show that human polymorphonuclear neutrophils (PMN) assist the human breast tumor cell line MDA-MB-231 to cross the endothelial barrier. We found that tumor-conditioned medium (TCM) downregulated PMN cytocidal function, delayed PMN apoptosis, and concomitantly upregulated PMN adhesion molecule expression. These PMN treated with TCM attached to tumor cells and facilitated tumor cell migration through different endothelial monolayers. In contrast, MDA-MB-231 cells alone did not transmigrate. FACScan analysis revealed that these tumor cells expressed high levels of intercellular adhesion molecule-1 (ICAM-1) but did not express CD11a, CD11b, or CD18. Blockage of CD11b and CD18 on PMN and of ICAM-1 on MDA-MB-231 cells significantly attenuated TCM-treated, PMN-mediated tumor cell migration. These tumor cells still possessed the ability to proliferate after PMN-assisted transmigration. These results indicate that TCM-treated PMN may serve as a carrier to assist tumor cell transendothelial migration and suggest that tumor cells can exploit PMN and alter their function to facilitate their extravasation.
    Language
    eng
    ISSN
    0363-6143 (Print)
    0363-6143 (Linking)
    Collections
    Cork University Hospital

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