Correlation of the nuclear accumulation of CTNNB1 and colonic tumorigenesis

作     者：QIU Zhe-fu Maruyama Keiji HAN De-min Nakamura Satoshi 

作者机构：Second Department of Surgery Hamamatsu University School of Medicine 1-20-1 Handayama Hamamatsu 431-3192 Japan Beijing Otolaryngology-Head and Neck Surgery Research Centre Affiliated Beijing Tongren Hospital of Capital University of Medical Sciences Beijing 100005 China 

出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)

年 卷 期：2006年第119卷第13期

页      面：1113-1117页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1002[医学-临床医学] 10[医学] 

主　　题：beta catenin colonic polyps integrin-linked kinase piroxicam mice 

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.