Resumen
Here, we examined the functional role of Ezin-radixin-moesin-binding phosphoprotein 50 (EBP50) during colorectal carcinoma (CRC) progression. EBP50 depletion was frequently found in the outer areas of tumor lesions and was significantly associated with several unfavorable prognostic factors including depressive tumor growth, deep invasions, high tumor budding (BD), and the presence of neural invasion in CRC cases. EBP50-knockout CRC cells disrupted the interaction between EBP50 and ß-catenin at the plasma membrane, leading to epithelial?mesenchymal transition (EMT)-like features, decreased proliferation, accelerated migration capability, and stabilized nuclear ß-catenin. In addition, Slug expression was positively correlated with nuclear ß-catenin status in tumor outer lesions including BD areas, consistent with ß-catenin-driven transactivation of the Slug promoter. These findings suggest that EBP50 depletion is due to nuclear ß-catenin accumulation, allowing transactivation of the Slug gene to promote EMT. This in turn contributes to the progression of CRC to a more aggressive phase through the induction of tumor budding.