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Biophys J. 2008 Jul;95(1):155-65. doi: 10.1529/biophysj.107.114678. Epub 2008 Mar 13.

Modeling the influence of the E-cadherin-beta-catenin pathway in cancer cell invasion: a multiscale approach.

Author information

1
French National Institute for Research in Computer Science and Control (INRIA), Domaine de Voluceau-Rocquencourt, Le Chesnay, France. ignacio.ramis_conde@inria.fr

Abstract

In this article, we show, using a mathematical multiscale model, how cell adhesion may be regulated by interactions between E-cadherin and beta-catenin and how the control of cell adhesion may be related to cell migration, to the epithelial-mesenchymal transition and to invasion in populations of eukaryotic cells. E-cadherin mediates cell-cell adhesion and plays a critical role in the formation and maintenance of junctional contacts between cells. Loss of E-cadherin-mediated adhesion is a key feature of the epithelial-mesenchymal transition. beta-catenin is an intracellular protein associated with the actin cytoskeleton of a cell. E-cadherins bind to beta-catenin to form a complex which can interact both with neighboring cells to form bonds, and with the cytoskeleton of the cell. When cells detach from one another, beta-catenin is released into the cytoplasm, targeted for degradation, and downregulated. In this process there are multiple protein-complexes involved which interact with beta-catenin and E-cadherin. Within a mathematical individual-based multiscale model, we are able to explain experimentally observed patterns solely by a variation of cell-cell adhesive interactions. Implications for cell migration and cancer invasion are also discussed.

PMID:
18339758
PMCID:
PMC2426623
DOI:
10.1529/biophysj.107.114678
[Indexed for MEDLINE]
Free PMC Article

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