Abstract
Coexpression of epidermal growth factor receptor (EGFR) and c-erbB-2 in 47-68% of ovarian cancer cells indicate their strong association with tumor formation. We examined the effects of simultaneous antisense- or immunosuppression of EGFR and c-erbB-2 expression on the invasive phenotype, aneuploidy, and genotype of cultured human ovarian carcinoma cells (NIH:OVCAR-8). We report here that suppression of both EGFR and c-erbB-2 results in regression of aneuploidy and genomic imbalances in NIH:OVCAR-8 cells, restores a more normal phenotype, and results in a more normal gene expression profile. Combined with cytogenetic analysis, our data demonstrate that the regression of aneuploidy is due to the selective apoptosis of double antisense transfected cells with highly abnormal karyotype.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Aneuploidy*
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal, Humanized
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Cell Line, Tumor
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DNA, Antisense / genetics
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Dinoprostone / pharmacology
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ErbB Receptors / antagonists & inhibitors*
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ErbB Receptors / biosynthesis
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ErbB Receptors / genetics
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Female
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Humans
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Immunosuppressive Agents / pharmacology
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Oligonucleotide Array Sequence Analysis
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Ovarian Neoplasms / genetics*
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Ovarian Neoplasms / metabolism
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Ovarian Neoplasms / pathology
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Ovarian Neoplasms / therapy
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Receptor, ErbB-2 / antagonists & inhibitors*
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Receptor, ErbB-2 / biosynthesis
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Receptor, ErbB-2 / genetics
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Transfection
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Trastuzumab
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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DNA, Antisense
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Immunosuppressive Agents
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ErbB Receptors
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Receptor, ErbB-2
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Dinoprostone
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Trastuzumab