| pubmed-article:17132227 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17132227 | lifeskim:mentions | umls-concept:C0279628 | lld:lifeskim |
| pubmed-article:17132227 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:17132227 | lifeskim:mentions | umls-concept:C0679199 | lld:lifeskim |
| pubmed-article:17132227 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:17132227 | lifeskim:mentions | umls-concept:C0302350 | lld:lifeskim |
| pubmed-article:17132227 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:17132227 | pubmed:dateCreated | 2006-11-29 | lld:pubmed |
| pubmed-article:17132227 | pubmed:abstractText | The hepatocyte growth factor (HGF) receptor c-Met is a tyrosine kinase receptor with established oncogenic properties. We have previously shown that c-Met is usually overexpressed in esophageal adenocarcinoma (EA), yet the implications of c-Met inhibition in EA remain unknown. Three c-Met-overexpressing EA cell lines (Seg-1, Bic-1, and Flo-1) were used to examine the effects of a c-Met-specific small molecule inhibitor (PHA665752) on cell viability, apoptosis, motility, invasion, and downstream signaling pathways. PHA665752 demonstrated dose-dependent inhibition of constitutive and/or HGF-induced phosphorylation of c-Met, which correlated with reduced cell viability and inhibition of extracellular regulated kinase 1/2 phosphorylation in all three EA cell lines. In contrast, PHA665752 induced apoptosis and reduced motility and invasion in only one EA cell line, Flo-1. Interestingly, Flo-1 was the only cell line in which phosphatidylinositol 3-kinase (PI3K)/Akt was induced following HGF stimulation. The PI3K inhibitor LY294002 produced effects equivalent to those of PHA665752 in these cells. We conclude that inhibition of c-Met may be a useful therapeutic strategy for EA. Factors other than receptor overexpression, such as c-Met-dependent PI3K/Akt signaling, may be predictive of an individual tumor's response to c-Met inhibition. | lld:pubmed |
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| pubmed-article:17132227 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17132227 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17132227 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17132227 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17132227 | pubmed:issn | 1476-5586 | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:GoodingWillia... | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:HughesSteven... | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:ChristensenJa... | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:StangMichael... | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:Queiroz de... | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:LevyRyan MRM | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:WatsonGregory... | lld:pubmed |
| pubmed-article:17132227 | pubmed:author | pubmed-author:ZhangXingluX | lld:pubmed |
| pubmed-article:17132227 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17132227 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:17132227 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17132227 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17132227 | pubmed:pagination | 949-55 | lld:pubmed |
| pubmed-article:17132227 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:17132227 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:17132227 | pubmed:articleTitle | Inhibition of c-Met as a therapeutic strategy for esophageal adenocarcinoma. | lld:pubmed |
