Correlation of the nuclear accumulation of CTNNB1 and colonic tumorigenesis

摘要： <正>CTNNB1 (or beta-catenin) is regarded as a central effecter in molecules of the wingless/Wnt signalling pathway. It is a key component of the cadherin mediated cell to cell adhesion system and forms a complex with the protein product of adenomatous polyposis coli (APC), glycogen synthase kinase 3β(GSK3β) and conductin.1 One mutation of APC is also responsible for activation of wingless/Wnt signalling pathway and accumulation of free beta-catenin in the cell. Beta-catenin upregulates oncogenes, such as cyclin D1 and c-myc. Beta-catenin expression in cytoplasm and nuclei was reported to increase in many cases of intestinal tumorigenesis. In addition, the hyperexpression of integrin linked kinase (ILK) in colonic polyposis has been demonstrated. （共5頁）