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Prevention of Irradiation-induced Glioma Cell Invasion by Temozolomide Involves Caspase 3 Activity and Cleavage of Focal Adhesion Kinase¹

Laboratories of Molecular Neuro-Oncology [W. W., J. D., M. W.] and Neurodegeneration [A. W., J. B. S., J. D.] and Department of Radiation Oncology [H. P. R.], University of Tübingen, Medical School, D-72076 Tübingen, Germany

Sublethal doses of irradiation enhance the invasiveness of human malignantglioma cells. This can be inhibited by subtoxic concentrations of temozolomide (TMZ) but not by lomustine. Antagonism of irradiation-induced motility by TMZ is associated with the prevention of irradiation-induced _vß₃-integrin, matrix metalloproteinase-2 and MT1-matrix metalloproteinase-expression. Irradiation induces focal adhesion kinase (FAK) activation by phosphorylation, whereas TMZ promotes FAK cleavage. Inhibition of caspases prevents TMZ-induced FAK processing and restores the promigratory effect of irradiation, suggesting that the resistance of glioma cells to irradiation-induced caspase processing may determine the invasive responses of glioma cells to irradiation. In contrast, DAOY medulloblastoma cells, which respond with caspase activation to irradiation alone, do not show enhanced invasiveness when irradiated.

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