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Osteosarcoma is the most common primary malignant bone tumor. Raddeanin A ( RA ) is an active oleanane‐type triterpenoid saponin extracted from the traditional Chinese herb  Anemone raddeana  Regel that exerts antitumor activity against several cancer types. However, the effect of  RA  on osteosarcoma remains unclear. In the present study, we showed that  RA  inhibited proliferation and induced apoptosis of osteosarcoma cells in a dose‐ and time‐dependent way in vitro and in vivo.  RA  treatment resulted in excessive reactive oxygen species ( ROS ) generation and  JNK  and  ERK 1/2 activation. Apoptosis induction was evaluated by the activation of caspase‐3, caspase‐8, and caspase‐9 and poly‐ADP ribose polymerase ( PARP ) cleavage.  RA ‐induced cell death was significantly restored by the  ROS  scavenger glutathione ( GSH ), the pharmacological inhibitor of  JNK SP 600125, or specific  JNK  knockdown by sh RNA . Additionally, signal transducer and activator of transcription 3 ( STAT 3) activation was suppressed by  RA  in human osteosarcoma, and this suppression was restored by  GSH ,  SP 600125, and  JNK ‐sh RNA . Further investigation showed that  STAT 3 phosphorylation was increased after  JNK  knockdown. In a tibial xenograft tumor model,  RA  induced osteosarcoma apoptosis and notably inhibited tumor growth. Taken together, our results show that  RA  suppresses proliferation and induces apoptosis by modulating the  JNK /c‐Jun and  STAT 3 signaling pathways in human osteosarcoma. Therefore,  RA  may be a promising candidate antitumor drug for osteosarcoma intervention.

cancer science

Antitumor activity of Raddeanin A is mediated by Jun amino‐terminal kinase activation and signal transducer and activator of transcription 3 inhibition in human osteosarcoma