Correlation of the nuclear accumulation of CTNNB1 and colonic tumorigenesis

二维码有效期 120s

摘要篇首： 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.2 Beta-catenin expression in cytoplasm and nuclei was reported to increase in many cases of intestinal tumorigenesis.3,4 In addition, the hyperexpression of integrin linked kinase (ILK) in colonic polyposis has been demonstrated.5

作者单位 Second Department of Surgery, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hmamatsu 431-3192, Japan;Beijing Otolaryngology-Head and Neck Surgery Research Centre,Affiliated Beijing Tongren Hospital of Capital University of Medical Sciences, Beijing 100005, China ^[1] Second Department of Surgery, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hmamatsu 431-3192, Japan ^[2] Beijing Otolaryngology-Head and Neck Surgery Research Centre,Affiliated Beijing Tongren Hospital of Capital University of Medical Sciences, Beijing 100005, China ^[3]

关键词 beta catenin colonic polyps integrin-linked kinase piroxicam mice

分类号 R73

栏目名称

BRIEF REPORTS

发布时间 2006-08-11

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