Source:http://linkedlifedata.com/resource/pubmed/id/15809749
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2005-4-5
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| pubmed:abstractText |
It has been shown that the interaction between the potent angiogenic factor; the vascular endothelial growth factor (VEGF) and its receptors (VEGFR-1 and VEGFR-2), plays a pivotal role in tumor development, including hepatocellular carcinoma (HCC). However, the properties of the respective VEGF receptor in the signaling transduction pathway of VEGF-mediated effects in HCC have not been elucidated yet. The aim of this study was to examine the respective signaling pathway of two VEGFRs in the VEGF-mediated murine HCC development and angiogenesis. We examined the signaling cascades of VEGFR-1 and VEGFR-2 in the VEGF-mediated HCC development in combination with a retroviral tetracycline (tet)-regulated (Retro-Tet) gene expression system, which can manipulate the gene expression in vivo by providing tet in the drinking water, as well as VEGFR-1 and VEGFR-2 specific neutralizing monoclonal antibodies (R-1mAb and R-2mAb, respectively). Both R-1mAb and R-2mAb significantly suppressed the VEGF-mediated tumor growth associated with reduction of the tumoral neovascularization, and the combination treatment with both mAbs almost completely attenuated the tumor development and angiogenesis. The protein kinase-C (PKC) and MEK1/2 activities in the tumor were markedly attenuated by treatment with R-2mAb, whereas R-1mAb did not alter these activities. These results suggested that both VEGFR-1 and VEGFR-2 play important roles, and lie in the different signaling cascades by which VEGF augments HCC development and angiogenesis.
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD31,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor...
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1021-335X
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| pubmed:author |
pubmed-author:FukuiHiroshiH,
pubmed-author:IkenakaYasuhideY,
pubmed-author:KitadeMitsuteruM,
pubmed-author:KuriyamaShigekiS,
pubmed-author:NamisakiTadashiT,
pubmed-author:NoguchiRyuichiR,
pubmed-author:UemuraMasahitoM,
pubmed-author:YamazakiMasaharuM,
pubmed-author:YanaseKojiK,
pubmed-author:YoshiiJunichiJ,
pubmed-author:YoshijiHitoshiH
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| pubmed:issnType |
Print
|
| pubmed:volume |
13
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
853-7
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:15809749-Animals,
pubmed-meshheading:15809749-Antibodies, Monoclonal,
pubmed-meshheading:15809749-Antigens, CD31,
pubmed-meshheading:15809749-Carcinoma, Hepatocellular,
pubmed-meshheading:15809749-Cell Division,
pubmed-meshheading:15809749-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15809749-Humans,
pubmed-meshheading:15809749-Liver Neoplasms,
pubmed-meshheading:15809749-Mice,
pubmed-meshheading:15809749-Mice, Inbred BALB C,
pubmed-meshheading:15809749-Mice, Transgenic,
pubmed-meshheading:15809749-Neovascularization, Pathologic,
pubmed-meshheading:15809749-Polymerase Chain Reaction,
pubmed-meshheading:15809749-RNA, Messenger,
pubmed-meshheading:15809749-Signal Transduction,
pubmed-meshheading:15809749-Vascular Endothelial Growth Factor A,
pubmed-meshheading:15809749-Vascular Endothelial Growth Factor Receptor-1,
pubmed-meshheading:15809749-Vascular Endothelial Growth Factor Receptor-2
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| pubmed:year |
2005
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| pubmed:articleTitle |
Different cascades in the signaling pathway of two vascular endothelial growth factor (VEGF) receptors for the VEGF-mediated murine hepatocellular carcinoma development.
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| pubmed:affiliation |
The Third Department of Internal Medicine, Nara Medical University, Shijo-cho 840, Kashihara, Nara 634-8522, Japan. yoshijih@naramed-u.ac.jp
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| pubmed:publicationType |
Journal Article
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