Inhibition of migration of human glioblastoma cells by cerivastatin in association with focal adhesion kinase (FAK)
Copyright policy )Inhibition of migration of human glioblastoma cells by cerivastatin in association with focal adhesion kinase (FAK)
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.
- Kagoshima University Japan
- University of Toyama Japan
Focal Adhesions, Dose-Response Relationship, Drug, Brain Neoplasms, Neoplasm Proteins, Drug Combinations, Microscopy, Fluorescence, Cell Movement, Depression, Chemical, Enzyme Induction, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Cell Adhesion, Humans, Neoplasm Invasiveness, Collagen, Laminin, Drug Screening Assays, Antitumor, Phosphorylation, Glioblastoma, Protein Processing, Post-Translational
Focal Adhesions, Dose-Response Relationship, Drug, Brain Neoplasms, Neoplasm Proteins, Drug Combinations, Microscopy, Fluorescence, Cell Movement, Depression, Chemical, Enzyme Induction, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Cell Adhesion, Humans, Neoplasm Invasiveness, Collagen, Laminin, Drug Screening Assays, Antitumor, Phosphorylation, Glioblastoma, Protein Processing, Post-Translational
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