c‐Met inhibitor upregulates E‐cadherin, which is lost in portal vein tumor thrombus of hepatocellular carcinoma.

Aim Methods Results Conclusions Portal vein tumor thrombus (PVTT) in hepatocellular carcinoma (HCC) is an essential therapeutic and prognostic factor. E‐cadherin plays a crucial role in adhesive properties and intercellular interaction in various cancer tissues, including HCC, but the expression profile and functional contribution of E‐cadherin in PVTT remain unknown. This study aimed to analyze the expression of E‐cadherin in the main tumor tissue and PVTT tissue of HCC, and evaluate the functional roles of E‐cadherin in PVTT formation.A retrospective analysis was performed using the medical records of patients who underwent liver resection for HCC with PVTT, analyzing tissue specimens from 1995 to 2016. E‐cadherin expression is evaluated using immunohistochemistry and western blot. The study also uses a c‐Met inhibitor to explore its impact on E‐cadherin expression in vitro and in vivo using cell lines and a tumor xenograft mouse model.The results revealed a reduced E‐cadherin expression in PVTT tissue than in the main tumor tissue. The inhibition of c‐Met activation, frequently detected in HCC, upregulated E‐cadherin expression in HCC cell lines. Furthermore, treatment with c‐Met inhibitors induced changes in epithelial morphology, and inhibited migration and invasion of HCC cell lines.This study demonstrates the downregulation of E‐cadherin in PVTT, and underscores the potential of c‐Met inhibition in upregulating E‐cadherin and inhibiting metastatic behavior. Understanding the significance of E‐cadherin and c‐Met in HCC progression provides a foundation for future clinical investigations into the therapeutic effects of c‐Met inhibitors on PVTT in HCC patients. [ABSTRACT FROM AUTHOR]