A recent study showed that a combination of Y15 (a FAK autophosphorylation inhibitor) with temozolomide (TMZ) treatment was effective in glioblastoma (GBM) therapy.
In this report, we found that naringin can specifically inhibit the kinase activity of FAK and suppress the FAK<sup>p-Try397</sup>and its downstream pathway in glioblastoma cells.
Also, knockdown- or pharmacological agent-based attenuation of EGFR, FAK or Graf (ARHGAP26)/small GTPase-mediated pathways markedly mitigated the aggressiveness of glioblastoma cells.
Thus, microarray gene expression analysis can be effective in establishing genes affected in response to FAK inhibitor alone and in response to combination of Y15 with temozolomide that is important for glioblastoma therapy.
p27Kip1 and cyclin D1 are necessary for focal adhesion kinase regulation of cell cycle progression in glioblastoma cells propagated in vitro and in vivo in the scid mouse brain.