The extracellular matrix is a gel. That is to say a solid network of macromolecuiles linked together, here mainly proteins like collagen. This matrix surrounds and delimits organs. So that, cell invasion and tumor vascularization necessarily imply its crossing by cells, which for this produce proteolytic enzymes (proteinases) which break the links of this network. Uderstanding how they work is therefore important to fight against the spread of cancer cells.
Cellular displacements are sensitive to certain physical properties of the matrix which imply scale lengths much larger than that of macromolecules. This is why cell motions are controlled by the mecanism of phase transition induced by proteinases, which by liquefying the matrix allow the cells to make their way through it. Our work has highlighted that this mechanism is controlled by the diffusion of enzymes in the gel which introduces correlations between broken links. In particular, measurements of the degradation kinetics have enabled us to propose a universal behavior law (called “scaling law”) and to demonstrate that the random walk of enzymes in these systems is self-attracting (the walker is “timid” and preferentially returns to areas already visited) leading to a “continuum percolation” model for the phase transition (like the percolation of holes in emmental).
Two different kinds of random walker representing an enzyme (in red) munching a gel (in blue). Left side : an ordinary random walker. Right side : a timid walker.
Read more :
- Scaling and continuum percolation model for enzyme-catalyzed gel degradation, Phys. Rev. Lett. 98: 228302, 2007 , PDF
- Percolation model for enzyme gel degradation, Phys. Rev. Lett. 93: 228301, 2004 , PDF
- Enzyme catalyzed gel proteolysis: an anomalous diffusion-controlled mechanism, Biophys. J. 85: 2808, 2003 , PDF