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Neuroblastoma is an embryonic malignancy arising from neuroblasts.The mechanisms that regulate the origination of neuroblastoma are still not very clear.In this study, we revealed that 6-bromoindirubin 3'-oxime (BIO), a specific GSK-3 inhibitor, promoted N2A cells-derived neurons to become tumor-like neuroblasts.Moreover, constitutively activated-catenin (S33Y) also promoted this process, whereas, silencing endogenous expression of-catenin abolished BIO-induced effects.These results implicated the potential relationship between the Wnt/-catenin signaling and neuroblastoma formation.Indeed, we found that the amount of-catenin in nucleus, which indicated the activation of Wnt/-catnin signaling, was accumulated in human neuroblastoma specimens and positively correlated with clinical risk of neuroblastoma.These results give us a new sight into the neuroblastoma initiation and progression, and provide a potential drug target for neuroblastoma treatment.