Acrylamide has been known to have a neurotoxic effect which is associated with nerve damage in both the central and peripheral nervous systems. Since neural cell adhesion molecule (NCAM) plays an important role in the processes of neuronal development and synaptic plasticity, the down-regulation of NCAM may lead impaired spatial memory and reduced long-term potentiation. We examined the effect of acrylamide on NCAM expression and the mechanisms of its effect in human neuroblastoma cells. Treatment with acrylamide resulted in the decrease of NCAM expression, which was reversed by CK2 inhibitor, 4,5,6,7-tetrabromobenzotriazole (TBB). Moreover, Western blot analysis showed that acrylamide induced the expression of CK2. Acrylamide dose-dependently decreased the DNA binding affinity of the Ikaros transcription factor, which is a bifunctional differentiation factor. In addition, the cells treated with acrylamide and CK2 inhibitor showed increased Ikaros activity compared with the acrylamide treatment only. Small interfering RNA-mediated depletion of CK2-α also increased Ikaros activity in acrylamide-treated cells. Overall, these data suggest that acrylamide decreases the Ikaros DNA binding activity via the CK2 pathway, resulting in a decrease of NCAM expression and provide further insight into the mechanisms underlying acrylamide actions.
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