Relation among p130Cas, E-cadherin and beta-catenin expression, clinicopathologic significance and prognosis in human hepatocellular carcinoma

Abstract

Background: p130Cas (p130Crk-associated substance) is a junction protein that is important to the adhesion between cytoskeleton and extracellular matrix. Also, the adhesion molecules E-cadherin and beta-catenin play important roles in the invasiveness of carcinoma. This study was undertaken to investigate the effects of p130Cas, E-cadherin and beta-catenin on the invasion, metastasis and prognosis of hepatocellular carcinoma (HCC).

Methods: Immunohistochemistry was used to evaluate the expression of p130Cas, E-cadherin, and beta-catenin in 40 patients with HCC. All patients were followed up postoperatively, and the relationship between expression and clinicopathological prognostic parameters was analyzed.

Results: The positive expression rates of p130Cas and E-cadherin in HCC tissue (n=40) were 62.50% and 55.00%, but in normal liver tissue 10%, and 100%, respectively (P<0.05). The abnormal expression rate of beta-catenin in HCC tissue was 70%, while in normal liver tissue it was 13.33% (P<0.05). The positive rate of p130Cas was correlated with lymph node invasion, pathological stage, TNM stage, and a worse prognosis, but not with gender, age, HBV infection, hepatic cirrhosis, alpha-fetoprotein (AFP) level before operation, and tumor diameter. Similarly, the expression of E-cadherin and beta-catenin was correlated with lymph node invasion, pathological stage, TNM stage, and worse prognosis, but not with gender, age, HBV infection, hepatic cirrhosis, AFP level before operation, and tumor size. Correlations were found between p130Cas and abnormal E-cadherin/beta-catenin expression (P<0.001 and <0.05, respectively).

Conclusions: In HCC, there is a negative correlation between the positive expression of p130Cas and the normal expression of the adhesion molecules E-cadherin/beta-catenin, and p130Cas plays important roles in the invasion, metastasis and prognosis of HCC. p130Cas may be involved in alterating the structure and function of E-cadherin/beta-catenin, by regulating tyrosine phosphorylation via the p130Cas-Src signal pathway.