Also, knockdown- or pharmacological agent-based attenuation of EGFR, FAK or Graf (ARHGAP26)/small GTPase-mediated pathways markedly mitigated the aggressiveness of glioblastoma cells.
A recent study showed that a combination of Y15 (a FAK autophosphorylation inhibitor) with temozolomide (TMZ) treatment was effective in glioblastoma (GBM) therapy.
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.
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.