Human neutrophils facilitate tumor cell transendothelial migration.

Hdl Handle:
http://hdl.handle.net/10147/209091
Title:
Human neutrophils facilitate tumor cell transendothelial migration.
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.
Citation:
Am J Physiol Cell Physiol. 2001 Apr;280(4):C814-22.
Journal:
American journal of physiology. Cell physiology
Issue Date:
3-Feb-2012
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
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
ISSN:
0363-6143 (Print); 0363-6143 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorWu, Q Den_GB
dc.contributor.authorWang, J Hen_GB
dc.contributor.authorCondron, Cen_GB
dc.contributor.authorBouchier-Hayes, Den_GB
dc.contributor.authorRedmond, H Pen_GB
dc.date.accessioned2012-02-03T15:12:02Z-
dc.date.available2012-02-03T15:12:02Z-
dc.date.issued2012-02-03T15:12:02Z-
dc.identifier.citationAm J Physiol Cell Physiol. 2001 Apr;280(4):C814-22.en_GB
dc.identifier.issn0363-6143 (Print)en_GB
dc.identifier.issn0363-6143 (Linking)en_GB
dc.identifier.pmid11245598en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209091-
dc.description.abstractTumor 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.en_GB
dc.language.isoengen_GB
dc.subject.mesh*Adenocarcinomaen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAntibodies, Monoclonalen_GB
dc.subject.meshAntigens, CD29/immunology/metabolismen_GB
dc.subject.meshApoptosis/physiologyen_GB
dc.subject.mesh*Breast Neoplasmsen_GB
dc.subject.meshCapillaries/cytologyen_GB
dc.subject.meshCarcinogens/pharmacologyen_GB
dc.subject.meshCell Division/physiologyen_GB
dc.subject.meshCell Movement/drug effects/*physiologyen_GB
dc.subject.meshCulture Media, Conditioned/pharmacologyen_GB
dc.subject.meshEndothelium, Vascular/*cytologyen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshFlow Cytometryen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntercellular Adhesion Molecule-1/immunology/metabolismen_GB
dc.subject.meshLipopolysaccharides/pharmacologyen_GB
dc.subject.meshNeoplasm Metastasis/*physiopathologyen_GB
dc.subject.meshNeutralization Testsen_GB
dc.subject.meshNeutrophils/*physiologyen_GB
dc.subject.meshTetradecanoylphorbol Acetate/pharmacologyen_GB
dc.subject.meshTumor Cells, Cultured/cytologyen_GB
dc.subject.meshUmbilical Veins/cytologyen_GB
dc.titleHuman neutrophils facilitate tumor cell transendothelial migration.en_GB
dc.contributor.departmentDepartment of Surgery, Cork University Hospital, University College Cork, Wilton,, Cork, Ireland.en_GB
dc.identifier.journalAmerican journal of physiology. Cell physiologyen_GB
dc.description.provinceMunster-
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