Abstract
Collective migration of eukaryotic cells plays a fundamental role in tissue growth, wound healing and immune response. The motion, arising spontaneously or in response to chemical and mechanical stimuli, is also important for understanding life-threatening pathologies, such as cancer and metastasis formation. We present a phase-field model to describe the movement of many self-organized, interacting cells. The model takes into account the main mechanisms of cell motility – acto-myosin dynamics, as well as substrate-mediated and cell-cell adhesion. It predicts that collective cell migration emerges spontaneously as a result of inelastic collisions between neighboring cells: collisions lead to a mutual alignment of the cell velocities and to the formation of coherently-moving multi-cellular clusters. Small cell-to-cell adhesion, in turn, reduces the propensity for large-scale collective migration, while higher adhesion leads to the formation of moving bands. Our study provides valuable insight into biological processes associated with collective cell motility.
Highlights
Collective migration of eukaryotic cells plays a fundamental role in tissue growth, wound healing and immune response
It predicts that collective cell migration emerges spontaneously as a result of inelastic collisions between neighboring cells: collisions lead to a mutual alignment of the cell velocities and to the formation of coherently-moving multi-cellular clusters
W hile a significant effort was focused on understanding the mechanics, dynamics and motility of individual cells, the processes determining collective cell migration remain elusive to a large extent
Summary
Collective migration of eukaryotic cells plays a fundamental role in tissue growth, wound healing and immune response. There is a variety of modeling approaches to collective cell migration, including Vicsek-type models of selfpropelled particles without[24] or with inter-particle adhesion[25,26,27,28], particle-based approaches[29], lattice models[5,30] and elastic spring models[31] of epithelial spreading/wound healing, as well as phenomenological continuum theories focusing on various aspects[32,33,34,35,36,37,38,39] All these approaches neglect the crucial dynamics associated with individual cell deformations Intermediate cell adhesion leads to transient multi-cell clusters and to an overall suppression of collective migration
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