Source:http://linkedlifedata.com/resource/pubmed/id/16273386
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2006-3-9
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| pubmed:abstractText |
T-cadherin is a unique receptor of adiponectin, which plays a critical role in various angiogenesis. In the present study, T-cadherin expression in tumor vessels of hepatocellular carcinoma (HCC) and, subsequently, the molecular mechanism, which induced T-cadherin expression in sinusoidal endothelial cells were investigated. Sinusoidal endothelium in nontumorous liver, chronic hepatitis, or liver cirrhosis expressed little or no T-cadherin. By contrast, T-cadherin was found in intratumoral capillary endothelial cells of 34 out of 63 HCC specimens. In positive cases, focal T-cadherin expression was found in well-differentiated HCC, whereas diffuse and intense T-cadherin expression was observed in poorly differentiated HCC specimens. T-cadherin was much expressed in intratumoral capillary endothelial cells in a less differentiated HCC region than that in a well-differentiated region in five specimens, in which various differentiated HCC components were coexistent. In a double-cell chamber assay, fibroblast growth factor-2 appeared to have a critical role to induce T-cadherin in cultured liver sinusoidal endothelial cells. The present finding indicated that T-cadherin was selectively expressed in intratumoral capillary endothelial cells of many HCCs, increasingly expressed as tumor progression, and T-cadherin may have a positive role in angiogenesis of HCC. In addition, cross talk between the signal pathways mediated by fibroblast growth factor-2 and adiponectin was suggested.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
0945-6317
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
448
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
311-8
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| pubmed:meshHeading |
pubmed-meshheading:16273386-Cadherins,
pubmed-meshheading:16273386-Capillaries,
pubmed-meshheading:16273386-Carcinoma, Hepatocellular,
pubmed-meshheading:16273386-Endothelium, Vascular,
pubmed-meshheading:16273386-Fibroblast Growth Factor 2,
pubmed-meshheading:16273386-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16273386-Genes, Tumor Suppressor,
pubmed-meshheading:16273386-Hepatitis,
pubmed-meshheading:16273386-Humans,
pubmed-meshheading:16273386-In Situ Hybridization,
pubmed-meshheading:16273386-Liver,
pubmed-meshheading:16273386-Liver Cirrhosis,
pubmed-meshheading:16273386-Liver Neoplasms,
pubmed-meshheading:16273386-Neovascularization, Pathologic,
pubmed-meshheading:16273386-Receptor Cross-Talk,
pubmed-meshheading:16273386-Receptors, Adiponectin,
pubmed-meshheading:16273386-Tumor Cells, Cultured
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| pubmed:year |
2006
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| pubmed:articleTitle |
An adiponectin receptor, T-cadherin, was selectively expressed in intratumoral capillary endothelial cells in hepatocellular carcinoma: possible cross talk between T-cadherin and FGF-2 pathways.
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| pubmed:affiliation |
Department of Pathology, Kochi Medical School, Nankoku, Kochi, Japan.
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| pubmed:publicationType |
Journal Article
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