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E-cadherin mediates the aggregation of breast cancer cells induced by tamoxifen and epidermal growth factor

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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 ERα 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 ERα 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.

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Acknowledgments

This work was supported by MURST, Ex 60%, AIRC grants 2007, 2008, MFAG 2008.

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Correspondence to Sebastiano Andò.

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Loredana Mauro and Michele Pellegrino have contributed equally to this work.

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Mauro, L., Pellegrino, M., Lappano, R. et al. E-cadherin mediates the aggregation of breast cancer cells induced by tamoxifen and epidermal growth factor. Breast Cancer Res Treat 121, 79–89 (2010). https://doi.org/10.1007/s10549-009-0456-4

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