Wnt signaling and colon tumorigenesis - A view from the periphery

被引：72

作者：

Burgess, Antony W. ^{[1
]}

Faux, Maree C. ^{[1
]}

Layton, Meredith J. ^{[2
]}

Ramsay, Robert G. ^{[3
,4
]}

机构：

[1] Ludwig Inst Canc Res, Parkville Branch, Melbourne, Vic 3050, Australia

[2] Monash Univ, Dept Biochem & Mol Biol, Melbourne, Vic 3800, Australia

[3] Peter MacCallum Canc Ctr, Melbourne, Vic 3002, Australia

[4] Univ Melbourne, Dept Pathol, Parkville, Vic 3050, Australia

来源：

EXPERIMENTAL CELL RESEARCH | 2011年 / 317卷 / 19期

基金：

英国医学研究理事会;

关键词：

Apc; Phospho-beta-catenin; E-cadherin; Myb; Myc; ADENOMATOUS POLYPOSIS-COLI; TUMOR-SUPPRESSOR PROTEIN; CATENIN DESTRUCTION COMPLEX; PHOSPHORYLATED BETA-CATENIN; COLORECTAL-CANCER CELLS; TRCP-UBIQUITIN LIGASE; APC GENE-PRODUCT; LGR5; STEM-CELLS; EPITHELIAL-CELLS; IN-VITRO;

D O I：

10.1016/j.yexcr.2011.08.010

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

In this brief overview we discuss the association between Wnt signaling and colon cell biology and tumorigenesis. Our current understanding of the role of Apc in the beta-catenin destruction complex is compared with potential roles for Apc in cell adhesion and migration. The requirement for phosphorylation in the proteasomal-mediated degradation of beta-catenin is contrasted with roles for phospho-beta-catenin in the activation of transcription, cell adhesion and migration. The synergy between Myb and beta-catenin regulation of transcription in crypt stem cells during Wnt signaling is discussed. Finally, potential effects of growth factor regulatory systems, Apc or truncated-Apc on crypt morphogenesis, stem cell localization and crypt fission are considered. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：2748 / 2758

页数：11

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