Stable intraepithelial adhesion complexes are essential for the maintenance of epithelial integrity. Alterations in these complexes are key events in the development and progression of many diseases. One of the major proteins involved in maintaining epithelial cell-cell adhesion is the cell-adhesion junction protein E-cadherin, a member of the cadherin family of transmembrane adhesion proteins. E-cadherin is involved in many cellular processes including morphogenesis, adhesion, recognition, communication and oncogenesis. Inactivation of its adhesive properties is often a key step in tumour progression and metastasis, leading to its recent description as a tumour suppressor gene. Mutations of the Ecadherin gene CDH1 in gastric and mammary cancers have been well documented and reports of transcriptional repression during tumour progression are increasing. This review examines the role of posttranslational truncation of Ecadherin in cancer cells focusing on implications for tumour progression. The various proteins involved in the directed cleavage of E-cadherin and consequences of these truncations are discussed.