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P-Cadherin Is Up-Regulated by the Antiestrogen ICI 182,780 and Promotes Invasion of Human Breast Cancer Cells

¹ Institute of Pathology and Molecular Immunology of Porto University and ² Medical Faculty, Porto University, Porto, Portugal; and ³ Laboratory of Experimental Cancerology, Department of Radiotherapy and Nuclear Medicine, ⁴ Department of Clinical Chemistry, Microbiology and Immunology, Ghent University Hospital, and ⁵ Units of Molecular and Cellular Oncology and Molecular Cell Biology, Department of Molecular Biomedical Research, VIB-Ghent University, Ghent, Belgium

P-cadherin expression in breast carcinomas has been associated with tumors of high histologic grade and lacking estrogen receptor-, suggesting a link between these proteins. In the MCF-7/AZ breast cancer cell line, blocking estrogen receptor- signaling with the antiestrogen ICI 182,780 induced an increase of P-cadherin, which coincided with induction of in vitro invasion. Retroviral transduction of MCF-7/AZ cells, as well as HEK 293T cells, showed the proinvasive activity of P-cadherin, which requires the juxtamembrane domain of its cytoplasmic tail. This study establishes a direct link between P-cadherin expression and the lack of estrogen receptor- signaling in breast cancer cells and suggests a role for P-cadherin in invasion, through its interaction with proteins bound to the juxtamembrane domain.

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