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We present a generic model of cell motility generated by acto-myosin contraction of the cell cortex. We identify analytically dynamical instabilities of the cortex and show that they trigger spontaneous cortical flows which in turn can induce cell migration in 3-dimensional (3D) environments as well as bleb formation. This contractility--based mechanism, widely independent of actin treadmilling, appears as an alternative to the classical picture of lamellipodial motility on flat substrates. Theoretical predictions are compared to experimental data of tumor cells migrating in 3D matrigel and suggest that this mechanism could be a general mode of cell migration in 3D environments.
Cell proliferation is typically incorporated into stochastic mathematical models of cell migration by assuming that cell divisions occur after an exponentially distributed waiting time. Experimental observations, however, show that this assumption is
The dynamic interplay between collective cell movement and the various molecules involved in the accompanying cell signalling mechanisms plays a crucial role in many biological processes including normal tissue development and pathological scenarios
Cells crawling through tissues migrate inside a complex fibrous environment called the extracellular matrix (ECM), which provides signals regulating motility. Here we investigate one such well-known pathway, involving mutually antagonistic signalling
The phenomenological model for cell shape deformation and cell migration (Chen et.al. 2018; Vermolen and Gefen 2012) is extended with the incorporation of cell traction forces and the evolution of cell equilibrium shapes as a result of cell different
A theory of fractional kinetics of glial cancer cells is presented. A role of the migration-proliferation dichotomy in the fractional cancer cell dynamics in the outer-invasive zone is discussed an explained in the framework of a continuous time rand