The transition of a tumor to malignancy is associated with many genetic and epigenetic modifications of its cells. For some cancers, it is established that part of these modifications corresponds to changes in the expression level of some proteins implicated in the regulation of the actin cytoskeleton. As a consequence, cancer cells have altered motile and biomechanical properties, but these properties are also well adapted for their propagation during the formation of metastasis.
The actin cytoskeleton is composed of dense filamentous networks. These networks are essential for a large number of cellular processes implicating the generation of forces, or the resistance to mechanical constraints, such as cell motility, adhesion or division. The reason why actin-based structures, all composed of filaments assembled from identical subunits, are able to perform many different functions is due to the fact that cells are able to organize actin filaments in a wide variety of structures. Each of these structures has specific geometrical, dynamical and rheological properties that are adapted for a given cellular process. These properties are constantly remodeled by specific sets of actin binding proteins (ABPs).
Our objective is to determine how cells can generate a variety of structures of actin filaments with defined properties, and with appropriate protein composition, from a common pool of cytoplasmic components. This global understanding will enable us to predict how misbalancing the equilibrium of the cell affects actin networks properties.
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