Objectives: The key mechanism responsible for the progression of endometrial carcinoma (EC) is the activation of epithelial-mesenchymal transition (EMT) a process which helps epithelial cells to acquire mesenchymal phenotype. One of the hallmarks of EMT is the loss of the adhesion molecule E-cadherin, nuclear accumulation of β-catenin and the acquisition of N-cadherin. Such tumor cells enter the invasion-metastasis cascade; while through the process of mesenchymal-epithelial transition (MET) re-establish their epithelial phenotype at distant sites. Little is known about aberrant expression of these proteins at histological level in EC. Patients and Methods: The study included 86 patients. For the immunohistochemical analysis tissue samples of primary tumors and their metastases were selected and the expression of E-cadherin, N-cadherin and β-catenin on the basis of percentage of positive tumor cells and staining intensity assessed in the central area (CA) of the tumor, at the invasive front (IF), in lymphovascular spaces (LVS) and metastases. Results: We found a significantly reduced expression of E-cadherin at the IF when compared to CA (p <0.0001) and a simultaneous higher expression of N-cadherin (p=0.005) indicating the appearance of the EMT process. A less significant reduction of positive membrane β-catenin from CA to IF was observed, while nuclear β-catenin expression was not correlated to EMT. We confirmed a re-expression of E-cadherin in metastases when compared to the IF (p=0.049) and a simultaneous significant loss of N-cadherin (p=0.008) suggesting the activation of MET. Negative membrane β-catenin at the IF was associated with deep myometrial invasion (p=0.004) and significantly shorter patient survival (p=0.0439). Conclusion: The results of our research have contributed to a better understanding of the role of E-cadherin, N-cadherin and β-catenin in the EMT and MET processes in EC. The immunohistochemical analysis of these markers confirmed that there is great heterogeneity within tumor areas in their expression as well as in metastases and support the hypothesis that the IF is the main tumor region in which EMT occurs.