Human achaete-scute homolog complex 1 (hASH1), a basic helix-loop-helix transcription factor, is responsible for determining neuronal cell fate. Aberrant expression of hASH1 is correlated with lung cancer as well as a variety of neuroendocrine tumors, however, factors controlling hASH1 expression are largely unknown. Polysomal gradient analysis of cell extracts from neuroblastoma cells cultured under low O₂ conditions (1-2 %) revealed a rapid shift of hASH1 from the polysomal to non-polysomal fractions, which was accompanied by a corresponding decrease in hASH1 protein levels. Luciferase reporter assays revealed a role for both UTRs in this post-transcriptional regulation of hASH1 expression. Using biotinylated 5’ and 3’ UTRs in a pull-down assay, we identified several RNA binding proteins that interact specifically with either or both of these UTRs. We further show that some of these have a direct effect on regulating hASH1 expression during hypoxia.