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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-10-21
pubmed:abstractText
In this experimental study, the influence of surgery-induced proinflammatory cytokines on tumor recurrence in the lung was investigated. A reproducible human in vitro assay was developed to study the adhesion of HT29 colon carcinoma cells to monolayers of microvascular endothelial cells of the lung (HMVECs-L) or human umbilical venous endothelial cells (HUVECs). Preincubation of HMVECs-L with maximally active concentrations of IL-1beta and TNF-alpha, but not with IL-6, resulted in at least 250% adhesion compared to control adhesion (p <or= 0.01). The effect of IL-1beta and TNF-alpha was concentration- and time-dependent. Comparable results were found for HUVECs. Tumor cell adhesion was not increased after preincubation of HT29 with TNF-alpha. Enzyme immunoassays of cytokine-preincubated HUVECs and HMVECs-L showed concentration- and time-dependent upregulation of E-selectin, ICAM-1 and VCAM-1 expression. In addition, LFA-1 and VLA-4 were only expressed on HMVECs-L, creating more binding possibilities for HMVECs-L compared to HUVECs. Inhibition assays with anti-E-selectin monoclonal antibody significantly decreased tumor cell adhesion to HUVECs; however, it did not affect tumor cell adhesion to HMVECs-L. Furthermore, anti-ICAM-1 and anti-VCAM-1 antibodies did not affect adhesion. Our results prove IL-1beta and TNF-alpha promote tumor cell adhesion to HMVECs-L in vitro and may therefore account for enhanced tumor recurrence in the lung seen after major surgical trauma. The adhesion of HT29 to HUVEC is inhibitable by E-selectin antibodies, whereas the adhesion to HMVEC-L is not inhibitable by these antibodies. Probably not one but a complex of adhesion molecules is responsible for enhanced adhesion to HMVECs-L.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
(c) 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
112
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
943-50
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed-meshheading:15386356-Carcinoma, pubmed-meshheading:15386356-Cell Adhesion, pubmed-meshheading:15386356-Cell Adhesion Molecules, pubmed-meshheading:15386356-Cell Line, Tumor, pubmed-meshheading:15386356-Cell Proliferation, pubmed-meshheading:15386356-Colonic Neoplasms, pubmed-meshheading:15386356-Dose-Response Relationship, Drug, pubmed-meshheading:15386356-E-Selectin, pubmed-meshheading:15386356-Endothelial Cells, pubmed-meshheading:15386356-Gene Expression Regulation, Neoplastic, pubmed-meshheading:15386356-Humans, pubmed-meshheading:15386356-Immunoenzyme Techniques, pubmed-meshheading:15386356-Immunohistochemistry, pubmed-meshheading:15386356-Inflammation, pubmed-meshheading:15386356-Intercellular Adhesion Molecule-1, pubmed-meshheading:15386356-Interleukin-1, pubmed-meshheading:15386356-Interleukin-1beta, pubmed-meshheading:15386356-Interleukin-6, pubmed-meshheading:15386356-Peptide Fragments, pubmed-meshheading:15386356-Time Factors, pubmed-meshheading:15386356-Tumor Necrosis Factor-alpha, pubmed-meshheading:15386356-Vascular Cell Adhesion Molecule-1
pubmed:year
2004
pubmed:articleTitle
Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium.
pubmed:affiliation
Department of Surgery, Erasmus Medical Center, Rotterdam, The Netherlands.
pubmed:publicationType
Journal Article, In Vitro