The MYCN transcription factor drives neuroblastoma progression by directly up-regulating downstream genes involved in a variety of metabolic processes including protein translation (1). One such gene, ABCE1 (2), encodes a translation factor and a member of the ABC superfamily of transporters. In yeast, ABCE1 supports protein synthesis by catalysing the dissociation of the 80S ribosomes, leading to the re-initiation of the translation cycle (3). We have previously shown that high expression of ABCE1 is associated with reduced neuroblastoma patient survival (2); however, the biological role of ABCE1 in neuroblastoma is currently unknown. In order to determine how ABCE1 influences neuroblastoma cell biology, we undertook siRNA-mediated suppression of this gene, migration, invasion and colony formation assays, and polysomal profiling using the MYCN-amplified neuroblastoma cell lines, SK-N-BE(2) and CHP134. The results demonstrated that ABCE1 suppression severely impaired migration (SK-N-BE(2) P=0.0007; CHP134 P<0.0001) and the invasion of extracellular matrix by the neuroblastoma cells (SK-N-BE(2) P=0.0002), and significantly reduced the number of colonies (SK-N-BE(2) P=0.0007, CHP134 P<0.0001). At the molecular level, suppression of ABCE1 reduced the proportion of heavy polysomes (i.e. translating ribosomes), leading to impaired global protein synthesis. In addition, ABCE1 suppression was associated with reduced expression of vimentin, an intermediate filament protein involved in neuroblastoma cell migration (4). These results show that by enhancing global protein synthesis, ABCE1 supports survival and motility of MYCN-amplified neuroblastoma cells and highlights, together with recent evidence demonstrating the clinical potential of inhibiting mRNA translation in Myc-driven malignance (5), the importance of ABCE1 as a therapeutic target for this disease.