Resumen
MYC proteins are essential regulators which could affect more than 15% of all genes through an interaction with other transcription factors. High-risk neuroblastoma associated with treatment failure is characterized by amplification of the MYCN proto-oncogene. Here, we show for the first time that the iron chelator VLX600 inhibits mitochondrial activity and induces cell death, regardless of MYCN status in neuroblastoma cells. Blocking glucose uptake enhances the effect of VLX600, indicating that targeting pathways or cellular activities related to energy supply/metabolism may help to find better therapeutic strategy for neuroblastoma.