科研之友
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摘要
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 beta inhibitor, promoted N2A cells-derived neurons to become tumor-like neuroblasts. Moreover, constitutively activated beta-catenin (S33Y) also promoted this process, whereas, silencing endogenous expression of beta-catenin abolished BIO-induced effects. These results implicated the potential relationship between the Wnt/beta-catenin signaling and neuroblastoma formation. Indeed, we found that the amount of beta-catenin in nucleus, which indicated the activation of Wnt/beta-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.
