Source:http://linkedlifedata.com/resource/pubmed/id/14707726
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2004-1-6
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pubmed:abstractText |
Pancreatic ductal adenocarcinomas (PDACs) overexpress several members of the fibroblast growth factor (FGF) family of ligands and the type I FGF receptor (FGFR-1), and enhanced FGF-2 protein levels correlate with shorter postoperative survival of patients with PDAC. In this study, we investigated the effects of FGF-2 on cell proliferation and mitogen-activated protein kinase (MAPK) activation before and after abrogation of FGFR-1-dependent signaling in 4 pancreatic cancer cell lines (ASPC-1, COLO-357, MIA-PaCa-2, and PANC-1). Signaling was blocked by infecting the cells with an adenoviral vector encoding for a truncated FGFR-1 (AdtrFGFR-1). FGF-2 enhanced the growth of all 4 cell lines and activated MAPK in 3 of these cell lines. Infection with the AdtrFGFR-1 virus resulted in abundant expression of the truncated FGFR-1 at the RNA and protein level, markedly attenuated FGF-2-induced proliferation in all 4 tested cell lines, and decreased FGF-2-dependent MAPK activation in the 3 cell lines in which FGF-2 activated this pathway. These findings suggest that FGFR-1-mediated mitogenesis in multiple pancreatic cancer cells can be efficiently blocked with an adenoviral vector encoding a truncated FGFR-1, raising the possibility that AdtrFGFR-1 may ultimately have a therapeutic role in PDAC.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/FGFR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Fibroblast Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fibroblast Growth Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1536-4828
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-30
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pubmed:dateRevised |
2010-5-26
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pubmed:meshHeading |
pubmed-meshheading:14707726-Adenoviridae,
pubmed-meshheading:14707726-Cell Division,
pubmed-meshheading:14707726-Cell Line,
pubmed-meshheading:14707726-Cell Line, Tumor,
pubmed-meshheading:14707726-Dose-Response Relationship, Drug,
pubmed-meshheading:14707726-Enzyme Activation,
pubmed-meshheading:14707726-Fibroblast Growth Factor 2,
pubmed-meshheading:14707726-Gene Expression,
pubmed-meshheading:14707726-Humans,
pubmed-meshheading:14707726-Mitogen-Activated Protein Kinases,
pubmed-meshheading:14707726-Mutation,
pubmed-meshheading:14707726-Pancreatic Neoplasms,
pubmed-meshheading:14707726-RNA, Messenger,
pubmed-meshheading:14707726-Receptor, Fibroblast Growth Factor, Type 1,
pubmed-meshheading:14707726-Receptor Protein-Tyrosine Kinases,
pubmed-meshheading:14707726-Receptors, Fibroblast Growth Factor,
pubmed-meshheading:14707726-Signal Transduction,
pubmed-meshheading:14707726-Transfection
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pubmed:year |
2004
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pubmed:articleTitle |
Adenovirus-mediated transfer of a truncated fibroblast growth factor (FGF) type I receptor blocks FGF-2 signaling in multiple pancreatic cancer cell lines.
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pubmed:affiliation |
Division of Endocrinology, Department of Medicine, University of Heidelberg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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