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    Bacterial endotoxin enhances colorectal cancer cell adhesion and invasion through TLR-4 and NF-kappaB-dependent activation of the urokinase plasminogen activator system.

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    Authors
    Killeen, S D
    Wang, J H
    Andrews, E J
    Redmond, H P
    Affiliation
    Department of Academic Surgery, Cork University Hospital and University College Cork, Cork, Ireland. sdfkilleen@eircom.net
    Issue Date
    2009-05-19
    MeSH
    Amiloride
    Antibodies
    Bacterial Toxins
    Caco-2 Cells
    Carcinoma
    Cell Adhesion
    Cell Movement
    Colorectal Neoplasms
    Humans
    Lipopolysaccharides
    NF-kappa B
    Neoplasm Invasiveness
    Receptors, Urokinase Plasminogen Activator
    Toll-Like Receptor 4
    Tumor Cells, Cultured
    Urokinase-Type Plasminogen Activator
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    Citation
    Bacterial endotoxin enhances colorectal cancer cell adhesion and invasion through TLR-4 and NF-kappaB-dependent activation of the urokinase plasminogen activator system. 2009, 100 (10):1589-602 Br. J. Cancer
    Journal
    British journal of cancer
    URI
    http://hdl.handle.net/10147/201209
    DOI
    10.1038/sj.bjc.6604942
    PubMed ID
    19436306
    Additional Links
    http://www.nature.com/bjc/journal/v100/n10/pdf/6604942a.pdf
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696751/pdf/6604942a.pdf
    Abstract
    Perioperative exposure to lipopolysaccharide (LPS) is associated with accelerated metastatic colorectal tumour growth. LPS directly affects cells through Toll-like receptor 4 (TLR-4) and the transcription factor NF-kappaB. The urokinase plasminogen activator (u-PA) system is intimately implicated in tumour cell extracellular matrix (ECM) interactions fundamental to tumour progression. Thus we sought to determine if LPS directly induces accelerated tumour cell ECM adhesion and invasion through activation of the u-PA system and to elucidate the cellular pathways involved. Human colorectal tumour cell lines were stimulated with LPS. u-PA concentration, u-PA activity, active u-PA, surface urokinase plasminogen activator receptor (u-PAR) and TLR-4 expression were assessed by ELISA, colorimetric assay, western blot analysis and flow cytometry respectively. In vitro tumour cell vitronectin adhesion and ECM invasion were analysed by vitronectin adhesion assay and ECM invasion chambers. u-PA and u-PAR function was inhibited with anti u-PA antibodies or the selective u-PA inhibitors amiloride or WXC-340, TLR-4 by TLR-4-blocking antibodies and NF-kappaB by the selective NF-kappaB inhibitor SN-50. LPS upregulates u-PA and u-PAR in a dose-dependent manner, enhancing in vitro tumour cell vitronectin adhesion and ECM invasion by >40% (P<0.01). These effects were ameliorated by u-PA and u-PAR inhibition. LPS activates NF-kappaB through TLR-4. TLR-4 and NF-kappaB inhibition ameliorated LPS-enhanced u-PA and u-PAR expression, tumour cell vitronectin adhesion and ECM invasion. LPS promotes tumour cell ECM adhesion and invasion through activation of the u-PA system in a TLR-4- and NF-kappaB-dependent manner.
    Item Type
    Article
    Language
    en
    ISSN
    1532-1827
    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.bjc.6604942
    Scopus Count
    Collections
    Cork University Hospital

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