Modeling the Influence of the E-Cadherin-?-Catenin Pathway in Cancer Cell Invasion: a multiscale approach

Ignacio Ramis-Conde, Dirk Drasdo, Alexander R. A. Anderson, Mark A. J. Chaplain

Research output: Contribution to journalArticlepeer-review

173 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)155-165
Number of pages11
JournalBiophysical Journal
Issue number1
Publication statusPublished - 1 Jul 2008


  • Tumor growth
  • In vitro
  • Adhesion
  • Micropheology
  • Progression
  • Expression
  • Mechanism
  • Dynamics
  • Systems


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