Mutation and Expression of APC/β-Catenin/E-cadherin in Colorectal Adenocarcinoma

Abstract

The pathogenesis of colorectal adenocarcinoma is described as a sequential multistep accumulation of genetic alterations. Most research into the development of colorectal cancer has focused on the detection of mutation of particular gene, but the elucidation for the interaction of these mutated genes with cell adhesion molecules is also important to understand the colorectal tumorigenesis. To elucidate the role of APC/β-catenin/E-cadherin in the colorectal adenocarcinoma, we identified APC/β-catenin/E-cadherin mutation and expression in 42 colorectal adenocarcinomas. Mutations of APC exon 15 and β-catenin exon 3 were detected in 11 cases (26.2%) and 1 case (2.4%), but there was no evidence of aberrant shift in E-cadherin exon 6-9. APC and E-cadherin promoter methylations were found in 5 cases (11.9%) and 25 cases (59.5%). The membranous staining of APC and E-cadherin was decreased in 30 cases (71.4%) and 37 cases (88.1%). The β-catenin expression was increased in the membranes in 34 cases (81.0%), cytoplasms in 17 cases (40.0%) and nuclei in 21 cases (50.0%) . At the invasive areas of tumor growth, nuclear expression of β-catenin was common. Down-regul, β-catenin has comprehensive influence with APC and E-cadherin on tumorigenesis of colorectal adenocarcinoma. Therefore, β-catenin has comprehensive influence with APC and E-cadherin on tumorigenesis of colorectal adenocarcinoma.