Anti–sense suppression of epidermal growth factor receptor expression alters cellular proliferation, cell–adhesion and tumorigenicity in ovarian cancer cells
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...
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Veröffentlicht in: | International journal of cancer 2000-11, Vol.88 (4), p.566-574 |
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Zusammenfassung: | 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‐β1–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, α‐catenin and, to a lesser extent, β‐catenin. Changes in the expression of these proteins were associated with a reduction in complex formation among E‐cadherin, β‐catenin and α‐catenin and between β‐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. Int. J. Cancer 88:566–574, 2000. © 2000 Wiley‐Liss, Inc. |
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ISSN: | 0020-7136 1097-0215 |
DOI: | 10.1002/1097-0215(20001115)88:4<566::AID-IJC8>3.0.CO;2-D |