E-cadherin is a marker for epithelial cells which expressed at the cell surface and adherens junctions. b-catenin is a partner for E-cadherin and binds to its cytoplasmic domain. Lack of E-cadherin expression in malignant epithelial tumors and invasive cancer cell lines such as PC-3 (prostate cancer cell), has been reported. Also it has been reported that PC-3 cells are negative for E-Cadherin. We showed that the E-cadherin protein does not appear to be localized at the cell membranes and it has a diffuse staining pattern inside the PC-3 cells. We demonstrated that treatment of PC-3 cells leads to restoration of this protein and also translocation of b -catenin protein from the nucleus to the cell membrane, formation of E-cadherin/catenin complex and adherens junction strengthening. In this study, we showed that increasing the cellular levels of E-cadherin and b -catenin proteins in PC-3 cells induces a mesenchymal to epithelial transition (MET). This led to inhibition of cell invasion capability of PC-3 cells. We also indicated that formation of E-cadherin/catenin complex leads to changing the expression of its target genes. Taken together, this study shows that E-cadherin is an appropriate diagnostic marker for epithelial cancers and inducing the translocation of E-cadherin induces the formation of E-cadherin/ b -catenin complex. We found that inducing the expression of Ecadherin could be a strategy to inhibit invasive cancer cells.
