P-cadherin is a cell-cell adhesion molecule, whose expression is highly 
associated with undifferentiated cells in normal adult epithelial tissues, as 
well as with poorly differentiated carcinomas. Its expression has been already 
reported in human embryonic stem cells and it is presumed to be a marker of stem 
or progenitor cells of some epithelial tissues. In normal breast, P-cadherin has 
an essential role during ductal mammary branching, being expressed by the 
monolayer of epithelial cap cells at the end buds. In mature mammary tissue, its 
expression is restricted to the myoepithelium; it has been postulated that it 
may also be present in early luminal progenitor cells. In breast cancer, 
P-cadherin is frequently overexpressed in high-grade tumours, being a 
well-established indicator of poor patient prognosis. It has been reported as an 
important inducer of cancer cell migration and invasion, with underlying 
molecular mechanisms involving the signalling mediated by its juxtamembrane 
domain, the secretion of matrix metalloproteases to the extracellular media, and 
the cleavage of a P-cadherin soluble form with pro-invasive activity. 
Intracellularly, this protein interferes with the endogenous cadherin/catenin 
complex, inducing p120-catenin delocalization to the cytoplasm, and the 
consequent activation of Rac1/Cdc42 and associated alterations in the actin 
cytoskeleton. Considering P-cadherin's role in cancer cell invasion and 
metastasis formation, a humanized monoclonal antibody was recently produced to 
antagonize P-cadherin-associated signalling pathways, which is currently under 
Phase I clinical trials. In this review, the most important findings about the 
role of P-cadherin in normal breast development and cancer will be illustrated 
and discussed, with emphasis on the most recent data.