Activated β-catenin forces N2A cell-derived neurons back to tumor-like neuroblasts and positively correlates with a risk for human neuroblastoma.

ABSTRACT: 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-3β inhibitor, promoted N2A cells-derived neurons to become tumor-like neuroblasts. Moreover, constitutively activated β-catenin (S33Y) also promoted this process, whereas, silencing endogenous expression of β-catenin abolished BIO-induced effects. These results implicated the potential relationship between the Wnt/β-catenin signaling and neuroblastoma formation. Indeed, we found that the amount of β-catenin in nucleus, which indicated the activation of Wnt/β-catnin signaling, was accumulated in human neuroblastoma specimens and positively correlated with clin

SUBMITTER: Zhi F 

PROVIDER: S-EPMC3269611 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature