Every type of cell movement including invasion of tumour cells is powered by dynamic changes in actin cytoskeleton organization and supervised by a vast variety of actin binding proteins (ABP) among others cofilin and gelsolin. These proteins are both downstream effectors of EGF-initiated signalling preceeding their actin filament depolimeryzing or capping activity. Our recent experiments have shown that the correlation exist between redistribution of cofilin and gelsolin and metastatic ability of human colon adenocarcinoma cells. Parental cell line LS180 and selected highly metastatic variants were used to examine intracellular distribution of fluorescently labeled cofilin and gelsolin and their colocalization with rodamine–phalloidin labelled F-actin. We have observed a redistribution of cofilin and gelsolin to the cell periphery in highly invasive variants and a strong colocalization of these proteins with F-actin after EGF stimulation. These results clearly ilustrate the acquisition of a malignant phenotype by tumour cells as well as demonstrate the changes in the dynamics of actin cytoskeleton in examined cells. These results were followed by the dermination of statically significant decrease in gelsolin and P-cofilin (phosphorylated, inactive form of cofilin) expression level determined by the densitomentry of Western blots. In summary, our data demonstrate a clear correlation between the metastatic potential of human colon adenocarcinoma cells and rearengments of actin cytoskeleton and a distribution it’s binding proteins.

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