Tumor cell adhesion to endothelial cells is increased by endotoxin via an upregulation of beta-1 integrin expression.
Affiliation
Department of Surgery, Cork University Hospital, Cork, Ireland., emmetandrews@eircom.netIssue Date
2012-02-03T15:11:47ZMeSH
Antigens, CD29/*biosynthesisCell 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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J Surg Res. 2001 May 1;97(1):14-9.Journal
The Journal of surgical researchDOI
10.1006/jsre.2001.6090PubMed ID
11319874Abstract
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
engISSN
0022-4804 (Print)0022-4804 (Linking)
ae974a485f413a2113503eed53cd6c53
10.1006/jsre.2001.6090
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