Source:http://linkedlifedata.com/resource/pubmed/id/15001536
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2004-6-18
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pubmed:abstractText |
Akt signaling is involved in tumorigenesis via a number of different mechanisms that result in increased proliferation and decreased apoptosis. Previous data have demonstrated that Akt-mediated signaling is functionally involved in keratinocyte transformation. This work investigates the involvement of angiogenesis as a mediator of tumorigenesis in Akt-transformed keratinocytes. Tumors produced by subcutaneous injection of the latter showed increased angiogenic profiles associated with increased vascular endothelial growth factor (VEGF) protein levels. However, in contrast to v-ras(Ha)-transformed keratinocytes, VEGF mRNA levels were not increased. The induction of VEGF protein by Akt is associated with increased phosphorylation and thus activation of p70S6K and eIF4E-binding protein 1, leading to increased VEGF translation. In addition, we observed increased metaloproteinases 2 and 9 expression, but not thrombospondin 1, in tumors derived from Akt-transformed keratinocytes. Collectively, these results demonstrate that Akt is an important mediator of angiogenesis in malignant keratinocytes through a post-transcriptional mechanism.
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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/Matrix Metalloproteinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0143-3334
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1137-47
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15001536-Animals,
pubmed-meshheading:15001536-Cell Differentiation,
pubmed-meshheading:15001536-Keratinocytes,
pubmed-meshheading:15001536-Matrix Metalloproteinase 2,
pubmed-meshheading:15001536-Matrix Metalloproteinase 9,
pubmed-meshheading:15001536-Mice,
pubmed-meshheading:15001536-Neovascularization, Pathologic,
pubmed-meshheading:15001536-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15001536-Proto-Oncogene Proteins,
pubmed-meshheading:15001536-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:15001536-Skin Neoplasms,
pubmed-meshheading:15001536-Time Factors,
pubmed-meshheading:15001536-Up-Regulation,
pubmed-meshheading:15001536-Vascular Endothelial Growth Factor A
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pubmed:year |
2004
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pubmed:articleTitle |
Akt mediates an angiogenic switch in transformed keratinocytes.
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pubmed:affiliation |
Department of Cell and Molecular Biology, CIEMAT, Av. Complutense 22, E-28040 Madrid, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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