Abstract
Cell migration and invasion is driven by turnover of the actin cytoskeleton, a process initiated by cofilin activation. Active cofilin concentrations correlate with the grade of primary brain tumors, tumor cell migration and brain invasion (Nagai S, Moreno O, Smith CA, Ivanchuk S, Romagnuolo R, Golbourn B, Weeks A, Seol HJ, and Rutka JT. 2011, Genes Cancer. Sep;2(9):859-69). To investigate how cell migration and invasion is enhanced in high grade brain tumors by cofilin we have developed a physical model based on the molecular mechanisms for actin turnover already known to be enhanced by cofilin. The model is then used to fit actin distributions in eGFP-actin transfected U251 brain tumor cells using model convolution microscopy. The best fits of the model yield estimates for the kinetic parameters for actin turnover in high grade brain tumor cells. These parameters are similar to isolated in vitro measurements made in the presence of cofilin and suggest that actin turnover is stimulated throughout the cell by cofilin. Further analysis of the model is used to elucidate potential mechanisms to regulate brain tumor cell motility.
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