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

@article{citeulike:2909311, 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.}, address = {French National Institute for Research in Computer Science and Control (INRIA), Domaine de Voluceau-Rocquencourt, Le Chesnay, France. ignacio.ramis\_conde@inria.fr}, author = {Ramis-Conde, I. and Drasdo, D. and Anderson, A. R. and Chaplain, M. A. }, citeulike-article-id = {2909311}, doi = {http://dx.doi.org/10.1529/biophysj.107.114678}, issn = {1542-0086}, journal = {Biophysical journal}, keywords = {cell-adhesion, multi-scale}, month = {July}, number = {1}, pages = {155--165}, posted-at = {2008-06-20 04:06:00}, priority = {3}, title = {Modeling the influence of the E-cadherin-beta-catenin pathway in cancer cell invasion: a multiscale approach.}, url = {http://dx.doi.org/10.1529/biophysj.107.114678}, volume = {95}, year = {2008} }

TY - JOUR ID - citeulike:2909311 L3 - citeulike-article-id:2909311 TI - Modeling the influence of the E-cadherin-beta-catenin pathway in cancer cell invasion: a multiscale approach. JF - Biophysical journal VL - 95 IS - 1 SP - 155 EP - 165 AD - French National Institute for Research in Computer Science and Control (INRIA), Domaine de Voluceau-Rocquencourt, Le Chesnay, France. ignacio.ramis_conde@inria.fr SN - 1542-0086 N2 - 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. KW - cell-adhesion KW - multi-scale AU - Ramis-Conde, I AU - Drasdo, D AU - Anderson, AR AU - Chaplain, MA PY - 2008/07// UR - http://dx.doi.org/10.1529/biophysj.107.114678 ER -