The Wnt signaling pathways and cell adhesion

被引:67
作者
Amin, Nancy [1 ]
Vincan, Elizabeth [1 ]
机构
[1] Univ Melbourne, Dept Anat & Cell Biol, Canc Biol Lab, Parkville, Vic 3010, Australia
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2012年 / 17卷
基金
英国医学研究理事会;
关键词
Wnt; Frizzled; cell-adhesion; polarity; PCP; EMT; MET; beta-Catenin; Cadherin; Review; ADENOMATOUS POLYPOSIS-COLI; EPITHELIAL-MESENCHYMAL TRANSITIONS; NF2; TUMOR-SUPPRESSOR; SRC FAMILY KINASES; BETA-CATENIN; CANCER-CELLS; E-CADHERIN; COLORECTAL-CANCER; RHO-GTPASES; ADHERENS JUNCTIONS;
D O I
10.2741/3957
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
In multicellular organisms, the processes of tissue and organ formation are governed by morphogenetic signaling pathways. The Wnt pathways regulate morphogenesis by controlling cell adhesion and migration; processes that when corrupted, lead to tumorgenesis. It is well known that the Wnt signaling pathways affect adhesion and migration via downstream effectors. Canonical Wnt signaling regulates cell adhesion by regulating the stability of beta-Catenin, a component of the adherens junction. Whereas, non-canonical signaling modulates cytoskeletal dynamics by regulating the activity of downstream effectors that function to organize the cytoskeleton. Recent studies have uncovered a multitude of points of crosstalk between the Wnt pathways and the mechanisms that control cellular architecture, from the level of receptors to the level of transcription. At the same time, cellular mechanisms that are responsible for the regulation of adhesion and migration also function to modulate the activity of several Wnt pathway components. Uncovering these points of crosstalk may lead to better understanding and treatment of the processes that can lead to tumorgenesis.
引用
收藏
页码:784 / 804
页数:21
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