cerivastatin and Glioblastoma

To investigate the biological effect of cerivastatin on glioblastoma cells, we exposed them to various concentrations of cerivastatin. Cerivastatin exhibited dual effects on glioblastoma cells in a dose-dependent manner. Immunofluorescence microscopy showed disruption of actin stress fibers and focal adhesion plaques even at nanomolar concentrations. Matrigel assay demonstrated marked inhibition of glioblastoma cell invasion. Immunoblot analysis using a phosphospecific antibody against focal adhesion kinase (FAK) showed that inhibition of migration was associated with the down-regulation of tyrosine phosphorylation of FAK. Our data suggest that cerivastatin may be beneficial for combination therapy with conventional anti-cancer drugs by inhibiting the invasion of glioblastoma.

Topics: Brain Neoplasms; Cell Adhesion; Cell Movement; Collagen; Depression, Chemical; Dose-Response Relationship, Drug; Drug Combinations; Drug Screening Assays, Antitumor; Enzyme Induction; Focal Adhesion Kinase 1; Focal Adhesion Protein-Tyrosine Kinases; Focal Adhesions; Glioblastoma; Humans; Laminin; Microscopy, Fluorescence; Neoplasm Invasiveness; Neoplasm Proteins; Phosphorylation; Protein Processing, Post-Translational; Protein-Tyrosine Kinases; Proteoglycans; Pyridines; Signal Transduction; Stress Fibers; Tumor Cells, Cultured