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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2000-12-8
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pubmed:abstractText |
Over-expression of epidermal growth factor receptor (EGFR) in ovarian cancer has been well documented. Human NIH:OVCAR-8 ovarian carcinoma cells were transfected with an expression vector containing the anti-sense orientation of truncated human EGFR cDNA. EGFR anti-sense over-expression resulted in decreased EGFR protein and mRNA expression, cell proliferation and tumor formation in nude mice. In accordance with the reduced levels of EGFR in EGFR anti-sense-expressing cells, tyrosine phosphorylation of EGFR was decreased compared to untransfected parental cells treated with EGF. In EGFR anti-sense-transfected cells, expression of erbB-3, but not erbB-2, was increased. In addition, basal and heregulin-beta 1-stimulated tyrosine phosphorylation of erbB-3 was higher in EGFR anti-sense vector-transfected cells. A morphological alteration in EGFR anti-sense gene-expressing cells was correlated with a decrease in the expression of E-cadherin, alpha-catenin and, to a lesser extent, beta-catenin. Changes in the expression of these proteins were associated with a reduction in complex formation among E-cadherin, beta-catenin and alpha-catenin and between beta-catenin and EGFR in EGFR anti-sense-expressing cells compared to sense-transfected control cells. These results demonstrate that EGFR expression in ovarian carcinoma cells regulates expression of cell adhesion proteins that may enhance cell growth and invasiveness.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CTNNA1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CTNNB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/Catna1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Catnb protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytoskeletal Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Antisense,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-3,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/alpha Catenin,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0020-7136
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2000 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
88
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
566-74
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11058872-Animals,
pubmed-meshheading:11058872-Cadherins,
pubmed-meshheading:11058872-Cell Adhesion,
pubmed-meshheading:11058872-Cell Division,
pubmed-meshheading:11058872-Cytoskeletal Proteins,
pubmed-meshheading:11058872-DNA, Antisense,
pubmed-meshheading:11058872-Female,
pubmed-meshheading:11058872-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:11058872-Genetic Vectors,
pubmed-meshheading:11058872-Humans,
pubmed-meshheading:11058872-Mice,
pubmed-meshheading:11058872-Mice, Nude,
pubmed-meshheading:11058872-Ovarian Neoplasms,
pubmed-meshheading:11058872-Receptor, Epidermal Growth Factor,
pubmed-meshheading:11058872-Receptor, erbB-3,
pubmed-meshheading:11058872-Trans-Activators,
pubmed-meshheading:11058872-Transcription, Genetic,
pubmed-meshheading:11058872-Transfection,
pubmed-meshheading:11058872-Tumor Cells, Cultured,
pubmed-meshheading:11058872-Xenograft Model Antitumor Assays,
pubmed-meshheading:11058872-alpha Catenin,
pubmed-meshheading:11058872-beta Catenin
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pubmed:year |
2000
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pubmed:articleTitle |
Anti-sense suppression of epidermal growth factor receptor expression alters cellular proliferation, cell-adhesion and tumorigenicity in ovarian cancer cells.
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pubmed:affiliation |
Cellular Biochemistry Section, Laboratory of Tumor Immunology and Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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