Celastrol promotes apoptotic cell death in children neuroblastoma cells through caspases dependent pathway

OBJECTIVE: To investigate the in-depth pharma-cological mechanisms of celastrol in children neuro-blastoma treatment. METHODS: In the current study, we examined the effects of celastrol on children neuroblastoma cells viability and proliferation by cell counting kit-8 assay and colony formation assay. Annexin V-FTIC and PI staining were applied to determine cell apoptosis after celastrol treatment. ROS generation levels were examined by 2 ', 7 '-dichloroflfluorescin diacetate.RESULTS: We found that celastrol could suppress the proliferation of children neuroblastoma cells with few effects on normal cell lines in vitro. Further mechanisms studies have shown that celastrol inhibited cell cycle progression and induced cell apoptosis in QDDQ-NM and SH-SY5Y cells. In addition, ROS production might involve in celastrol-mediated apoptotic cell death in children neuroblastoma cells by activating caspase death pathway.CONCLUSIONS: Our findings demonstrated that celastrol could promote ROS generation-induced apoptosis in neuroblastoma cell by activating caspase death pathway. These findings suggested that celastrol might be a potential novel anti-neuroblastoma agent with minor cytotoxicity.