摘要
CTNNB1 （or beta-catenin） is regarded as a central effecter in molecules of the wingless/Wnt signalling pathway, It is cadherin mediated cell to forms a complex with a key component of the cell adhesion system and the protein product of adenomatous polyposis coil （APC）, glycogen synthase kinase 3β （GSK3β） and conductin. 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.
CTNNB1 （or beta-catenin） is regarded as a central effecter in molecules of the wingless/Wnt signalling pathway, It is cadherin mediated cell to forms a complex with a key component of the cell adhesion system and the protein product of adenomatous polyposis coil （APC）, glycogen synthase kinase 3β （GSK3β） and conductin. 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.
