Indeed, the analyzed prostate cancer cells do not use E-cadherin for cell-cell adhesion but, instead, the production of the soluble 80 KD isoform is positively correlated to the increased migratory capability of these cells. Furthermore, the above described data reported in this Special Issue also highlight that not only the cadherin-mediated adhesion but cell-cell and cell-matrix communications in general are fundamental mechanisms underlying the neoplastic transformation as well as the processes that occur during the onset of metastases. In cancer cells, as a result of the binding with other cadherins and the 2 1-collagen IV complex, CDH17 might contribute to both cell-cell and cell-matrix interactions but also to cell proliferation and invasion. Since 1991 [[2]], the E-cadherin has been proposed as a tumor suppressor gene and by in vitro and in vivo models the loss of strong E-cadherin-mediated cell-cell adhesion in cancer cells was proven to be the cause of the acquisition of mesenchymal features, thus leading to metastasis formation. [Extracted from the article]