Autophagy and Novel Therapeutic Strategies in Neuroblastoma

Abstract In the cell, autophagy is the major regulatory catabolic mechanism responsible for the maintenance of cellular homeostasis. It is active at a basal level in all cell types, and it is highly inducible through a plethora of stress stimuli, including the cytotoxic ones caused by anticancer drugs. In this milieu, autophagy is an effective mechanism that, by promoting therapeutic resistance in tumor cells, may impede the complete drug activity and bring to question the patient's cure. In neuroblastoma, an increasing number of reports sustain intense activation of cytoprotective autophagy upon drug administration. However, autophagy can be easily found along with apoptosis activation and a proper balance between these two processes is crucial in determining the final fate of treated neuroblastoma cells. Defects in any one of them might have an important impact on the regulation of the other. In this chapter, we discuss the current state-of-the-art regarding the role of autophagy in neuroblastoma. It is a relatively new biological process for this field. We delineate the conditions where different kind of treatments can provoke autophagy activation in neuroblastoma cells. Moreover, we debate the chemical regulation of autophagy as a possible breakthrough therapy that might bring advantageous results in the cure of patients with neuroblastoma.