Correlation of the nuclear β-catenin expression with the clinicopathological parameters of hepatocellular carcinoma

Background: Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the human liver. However, the molecular changes and mechanisms that regulate the development and progression of HCC remain unclear. Beta-catenin is known as a multi-functional protein that acts as a regulator of the cadherin-mediated cell-cell adhesion system and also in the Wingless/Wnt signal transduction pathway. The aim of this study was to investigate the expression of β-catenin and its possible role in HCC. Methods: We investigated the expression of β-catenin, Ki-67, TP53, α-smooth muscle actin and CD34 by performing immunohistochemical staining for 61 specimens of HCC and their adjacent non-tumorous tissue. We also examined the relationship between the nuclear expression of β-catenin and the clinicopathologic parameters. Results: The altered expression of β-catenin was not detected in the non-tumorous liver tissue. The nuclear expression of β-catenin was observed in approximately 16% (10/61) of the HCC specimens. Double immunohistochemical staining for β-catenin and E-cadherin showed a close relationship between nuclear translocation of β-catenin and the loss of the membranous E-cadherin expression. Significant correlation was found between the nuclear translocation of β-catenin and the tumor size, tumor necrosis and the presence of microvessel invasion and intrahepatic metastasis (p<0.05). Conclusions: This data indicates the nuclear translocation of β-catenin could play a role in the growth and progression of HCC.