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From the Italian Foundation for Cancer Research Institute of Molecular Oncology,* Milan, Italy; Mario Negri Institute of Pharmacological Research, Milan, Italy; the Medical University of South Carolina, the Department of Cell Biology and The Cardiovascular Developmental Biology Center, Charleston, South Carolina; the National Cancer Institute,¶ Milan, Italy; the Department of Biomolecular Sciences and Biotechnology, University of Milan, Milan, Italy; Unitat de Biologia Cellular i Molecular,|| Instituto Municipal de Investigacio Medica, Barcelona, Spain; Departamento de Bioquímica, Universidad Autonoma de Madrid,** Madrid, Spain; and the University Vita-Salute San Raffaele School of Medicine and Department of Biological and Technological Research, Milan, Italy
Survivin is strongly expressed in embryonic organs and in tumor cells but is low or absent in differentiated normal tissues. Resting endothelium expresses low levels of survivin but can up-regulate its synthesis on activation to proliferate. The mechanisms responsible for survivin down-regulation in resting conditions are still unknown. We report here that confluence and vascular endothelial-cadherin (VE-cadherin) expression induce contact inhibition of cell growth and survivin down-regulation in the endothelium. Using ß-catenin null and positive isogenic endothelial cell lines we found that the effect requires ß-catenin expression and its association to VE-cadherin cytoplasmic tail. Furthermore, in allantois organ cultures, survivin expression is up-regulated in areas of growing vessels where VE-cadherin is partially dismantled from junctions or in VE-cadherin –/– specimens. Overall, these data indicate that VE-cadherin and ß-catenin may negatively regulate survivin synthesis in endothelial cells. Consistently, in epidermal and pancreatic cell lines or ovarian tumors, epithelial-cadherin (E-cadherin) and survivin expression is inversely related, suggesting a non-cell-specific role of cadherins in reducing survivin synthesis.
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