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Interplay of cadherin-mediated cell adhesion and canonical wnt signaling

Item Type:Article
Title:Interplay of cadherin-mediated cell adhesion and canonical wnt signaling
Creators Name:Heuberger, J. and Birchmeier, W.
Abstract:The epithelial-mesenchymal transition is essential in both embryonic development and the progression of carcinomas. Wnt signaling and cadherin-mediated adhesion have been implicated in both processes; clarifying their role will depend on linking them to rearrangements of cellular structure and behavior. beta-Catenin is an essential molecule both in cadherin-mediated cell adhesion and in canonical Wnt signaling. Numerous experiments have shown that the loss of cadherin-mediated cell adhesion can promote beta-catenin release and signaling; this is accomplished by proteases, protein kinases and other molecules. Cadherin loss can also signal to several other regulatory pathways. Additionally, many target genes of Wnt signaling influence cadherin adhesion. The most conspicuous of these Wnt target genes encode the transcription factors Twist and Slug, which directly inhibit the E-cadherin gene promoter. Other Wnt/beta-catenin target genes encode metalloproteases or the cell adhesion molecule L1, which favor the degradation of E-cadherin. These factors provide a mechanism whereby cadherin loss and increased Wnt signaling induce epithelial-mesenchymal transition in both carcinomas and development.
Keywords:Cadherins, Cell Adhesion, Epithelium, Developmental Gene Expression Regulation, Enzymologic Gene Expression Regulation, Mesoderm, Biological Models, Genetic Promoter Regions, Wnt Proteins, Beta Catenin, Animals
Source:Cold Spring Harbor Perspectives in Biology
Publisher:Cold Spring Harbor Laboratory Press
Page Range:a002915
Date:February 2010
Official Publication:https://doi.org/10.1101/cshperspect.a002915
PubMed:View item in PubMed

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