Source:http://linkedlifedata.com/resource/pubmed/id/17583578
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
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| pubmed:dateCreated |
2007-8-27
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| pubmed:abstractText |
The glycoantigen sialyl-Lewis x (sLex) and its isomer sialy-Lewis a (sLea) are frequently associated with advanced states of cancer and metastasis. In a previous work, we have shown that hepatocarcinoma cells (HCC) HepG2 interact with the endothelial E-selectin exclusively through sLe(x) oligosaccharides, the synthesis of which could be completely prevented by the alpha(1,2)-fucosyltransferase-I (FUT1), thus resulting in a strong inhibition of adhesion and rolling on activated endothelial cells. The purpose of the present study was to evaluate the impact of inhibiting sLex synthesis and the subsequent E-selectin adhesion, on HCC tumor growth in nude mice. Four weeks after subcutaneous transplantation of cells, no FUT1-derived tumor could be detected, whereas 75% of control animals developed large size tumor nodules. Between the 4th and the 8th week postinoculation, 33% tumors arose from FUT1-transduced cells but showed a slow growth (nodule volumes less than 500 mm(3)), while more than 50% of control tumors reached volumes between 1,500 and 3,000 mm(3). Several parameters were examined, including cell division and proliferation, apoptosis, adhesion to extracellular matrix components and angiogenesis/vasculogenesis. We provide evidence that among all, vasculogenesis was the most clearly affected by FUT1 expression, suggesting that tumor angiomorphogenesis may, at least partly, depend on E-selectin-mediated interaction between HCC and endothelial cells, the inhibition of which remarkably retards tumor growth.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/5-acetylneuraminyl-(2-3)-galactosyl-...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiogenesis Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Fucose,
http://linkedlifedata.com/resource/pubmed/chemical/Fucosyltransferases,
http://linkedlifedata.com/resource/pubmed/chemical/Oligosaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/galactoside...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0020-7136
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| pubmed:author | |
| pubmed:copyrightInfo |
(c) 2007 Wiley-Liss, Inc.
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| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
121
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1680-9
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| pubmed:meshHeading |
pubmed-meshheading:17583578-Angiogenesis Inhibitors,
pubmed-meshheading:17583578-Animals,
pubmed-meshheading:17583578-Antineoplastic Agents,
pubmed-meshheading:17583578-Apoptosis,
pubmed-meshheading:17583578-Blotting, Western,
pubmed-meshheading:17583578-Carcinoma, Hepatocellular,
pubmed-meshheading:17583578-Cell Division,
pubmed-meshheading:17583578-Cell Proliferation,
pubmed-meshheading:17583578-E-Selectin,
pubmed-meshheading:17583578-Extracellular Matrix,
pubmed-meshheading:17583578-Fucose,
pubmed-meshheading:17583578-Fucosyltransferases,
pubmed-meshheading:17583578-Immunohistochemistry,
pubmed-meshheading:17583578-Liver Neoplasms,
pubmed-meshheading:17583578-Mice,
pubmed-meshheading:17583578-Mice, Nude,
pubmed-meshheading:17583578-Neovascularization, Pathologic,
pubmed-meshheading:17583578-Oligosaccharides,
pubmed-meshheading:17583578-Time Factors,
pubmed-meshheading:17583578-Transduction, Genetic,
pubmed-meshheading:17583578-Transplantation, Heterologous
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| pubmed:year |
2007
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| pubmed:articleTitle |
Introducing alpha(1,2)-linked fucose into hepatocarcinoma cells inhibits vasculogenesis and tumor growth.
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| pubmed:affiliation |
Laboratories of INSERM UMR-777, Faculté de Médecine, 27 Bd. J. Moulin 13385 Marseille, France.
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| pubmed:publicationType |
Journal Article
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