Overexpression of Fyn Induces Formation of filopodia and lamellipodia in CHO Cells via Rearrangement of F-Actin

As a main ancillary molecule involved in the regulation of proliferation, differentiation and migration of cortical neurons, fyn has also been identified as a signal factor in motility and growth involved with cytoskeleton. however, the molecular mechanism of fyn on cytoskeleton remains unclear. the results showed that the morphology of the cho cells transfected with the recombination vector changed remarkably. the numbers of stress fibers may be crunched to transformation for generating and supporting the formation of filopodia and lamellipodia, but the changes of vinculin and tubulin are unremarkable. in addition, high concentrations of fyn cause formation of lamellipodia as well as filopodia. from this research we can draw a conclusion that overexpression of mouse fyn induces the f-actin cytoskeleton rearrangement and both vinculin and tubulin are absent in the process of fyn-mediated f-actin reorganization.