Nuclear softening is essential for protease-independent migration.

摘要: During amoeboidal migration, cancer cells migrate in a protease-independent manner by squeezing through pre-existing gaps the extracellular matrix (ECM). However, extent to which alter their physical properties order sustain this mode of migration remains unclear. Here, we address question documenting biophysical changes highly invasive MDA-MB-231 and HT-1080 upon inhibition pericellular proteolysis. Remarkably, treatment with broad spectrum MMP inhibitor GM6001 not only induces cell rounding loss actomyosin contractility, but also nuclear softening via increased phosphorylation membrane protein lamin A/C. Though is necessary for sustaining sub-nuclear sized transwell pores, it sufficient. In addition, baseline levels contractility mediating pore entry peri-nuclear actin inside pores are required. Taken together, our results suggest that tracks enabled deformation softened nucleus network.