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    Tumor cell adhesion to endothelial cells is increased by endotoxin via an upregulation of beta-1 integrin expression.

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    Authors
    Andrews, E J
    Wang, J H
    Winter, D C
    Laug, W E
    Redmond, H P
    Affiliation
    Department of Surgery, Cork University Hospital, Cork, Ireland., emmetandrews@eircom.net
    Issue Date
    2012-02-03T15:11:47Z
    MeSH
    Antigens, CD29/*biosynthesis
    Cell Adhesion/*drug effects
    Cells, Cultured
    Endothelium, Vascular/drug effects/*metabolism
    Humans
    Kinetics
    Laminin/biosynthesis
    Lipopolysaccharides/*pharmacology
    NF-kappa B/antagonists & inhibitors/metabolism
    Neoplasm Metastasis
    Neoplasms/*metabolism/pathology
    Peptides/pharmacology
    Tumor Cells, Cultured
    Up-Regulation
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    Citation
    J Surg Res. 2001 May 1;97(1):14-9.
    Journal
    The Journal of surgical research
    URI
    http://hdl.handle.net/10147/209082
    DOI
    10.1006/jsre.2001.6090
    PubMed ID
    11319874
    Abstract
    BACKGROUND: Recent studies have demonstrated that metastatic disease develops from tumor cells that adhere to endothelial cells and proliferate intravascularly. The beta-1 integrin family and its ligand laminin have been shown to be important in tumor-to-endothelial cell adhesion. Lipopolysaccharide (LPS) has been implicated in the increased metastatic tumor growth that is seen postoperatively. We postulated that LPS increases tumor cell expression of beta-1 integrins and that this leads to increased adhesion. METHODS: The human metastatic colon cancer cell line LS174T was labeled with an enhanced green fluorescent protein (eGFP) using retroviral transfection. Cell cultures were treated with LPS for 1, 2, and 4 h (n = 6 each) and were subsequently cocultured for 30 or 120 min with confluent human umbilical vein endothelial cells (HUVECs), to allow adherence. Adherent tumor cells were counted using fluorescence microscopy. These experiments were carried out in the presence or absence of a functional blocking beta-1 integrin monoclonal antibody (4B4). Expression of beta-1 integrin and laminin on tumor and HUVECs was assessed using flow cytometric analysis. Tumor cell NF-kappaB activation after incubation with LPS was measured. RESULTS: Tumor cell and HUVEC beta-1 integrin expression and HUVEC expression of laminin were significantly (P < 0.05) enhanced after incubation with LPS. Tumor cell adhesion to HUVECs was significantly increased. Addition of the beta-1 integrin blocking antibody reduced tumor cell adhesion to control levels. LPS increased tumor cell NF-kappaB activation. CONCLUSIONS: Exposure to LPS increases tumor cell adhesion to the endothelium through a beta-1 integrin-mediated pathway that is NF-kappaB dependent. This may provide a target for immunotherapy directed at reducing postoperative metastatic tumor growth.
    Language
    eng
    ISSN
    0022-4804 (Print)
    0022-4804 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1006/jsre.2001.6090
    Scopus Count
    Collections
    Cork University Hospital

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