  Epithelization, the process whereby an epithelium covers a cell-free surface,
is not only central to wound healing but also pivotal in embryonic
morphogenesis, regeneration, and cancer. In the context of wound healing, the
epithelization mechanisms differ depending on the sizes and geometries of the
wounds as well as on the cell type while a unified theoretical decription is
still lacking. Here, we used a barrier-based protocol that allows for making
large arrays of well-controlled circular model wounds within an epithelium at
confluence, without injuring any cells. We propose a physical model that takes
into account border forces, friction with the substrate, and tissue rheology.
Despite the presence of a contractile actomyosin cable at the periphery of the
wound, epithelization was mostly driven by border protrusive activity. Closure
dynamics was quantified by an epithelization coefficient $D = \sigma_p/\xi$
defined as the ratio of the border protrusive stress $\sigma_p$ to the friction
coefficient $\xi$ between epithelium and substrate. The same assay and model
showed a high sensitivity to the RasV12 mutation on human epithelial cells,
demonstrating the general applicability of the approach and its potential to
quantitatively characterize metastatic transformations.
