Perampanel Inhibits Neuroblastoma Cell Proliferation through Down-regulation of AKT and ERK Pathways

Abstract

Background/Aim: Activation of AKT serine/ threonine kinase (AKT) predicts poor outcome in neuroblastoma, which highlights the potential of the AKT pathway as a promising target for neuroblastoma treatment. Several studies reported that blockade of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptors (AMPARs) reduces proliferation in glioblastoma or lung cancer by inhibiting AKT and extracellular signal-related kinase (ERK) pathways. In this study, we examined the effect of the AMPAR antagonist perampanel on human neuroblastoma cells. Materials and Methods: Cell proliferation, caspase activity, and western blot assays were performed to determine the effect of perampanel on the KP-N-SI9s human neuroblastoma cell line. Results: Perampanel inhibited cell proliferation without triggering apoptosis in neuroblastoma cells. Down-regulation of AKT protein levels, AKT phosphorylation, and ERK1/2 phosphorylation were also observed in neuroblastoma cells with perampanel treatment. Conclusion: Perampanel inhibits neuroblastoma cell proliferation through down-regulation of AKT and ERK pathways and has potential for the treatment of neuroblastoma.