Abstract
In the present study, we evaluated the ability of 4-hydroxytamoxifen (OHT) and epidermal growth factor (EGF) to regulate homotypic adhesion in MCF7 breast cancer cells. Our results demonstrate that OHT and EGF activate the E-cadherin promoter, increase E-cadherin mRNA and protein expression and enhance homotypic aggregation of MCF7 cells. Interestingly, an ERalpha and EGFR cross-talk is involved in the E-cadherin expression by OHT and EGF, as demonstrated by knocking down either receptor. On the basis of our findings, the well-established cross-talk between ERalpha and EGFR could be extended to the modulation of E-cadherin expression by OHT and EGF. Thus, the potential ability of tamoxifen to induce cell-cell aggregation may contribute to the biologic response of pharmacologic intervention in patients with breast cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents, Hormonal / pharmacology*
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Blotting, Western
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism*
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Cadherins / genetics
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Cadherins / metabolism*
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Cell Adhesion / drug effects
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Cell Aggregation / drug effects
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Cell Line, Tumor
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Epidermal Growth Factor / metabolism*
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ErbB Receptors / metabolism
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Estrogen Receptor alpha / metabolism
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Female
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Gene Expression
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Gene Expression Profiling
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Gene Expression Regulation, Neoplastic*
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Humans
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Oligonucleotide Array Sequence Analysis
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Receptor Cross-Talk / drug effects
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Receptor Cross-Talk / physiology
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction / physiology
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Tamoxifen / analogs & derivatives*
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Tamoxifen / pharmacology
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Transcriptional Activation
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Transfection
Substances
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Antineoplastic Agents, Hormonal
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Cadherins
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Estrogen Receptor alpha
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Tamoxifen
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afimoxifene
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Epidermal Growth Factor
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ErbB Receptors