Conclusion
Prior inhibition of Wnt/β-catenin pathway abolished the antitumor effects induced by β-asarone. β-asarone exerted antitumor effects in RB cells by inactivating the Wnt/β-catenin signaling pathway.
Methods
RB cell lines SO-Rb50 and HXO-Rb44 were treated with different doses of β-asarone. Then, CCK8 and BrdU experiments were adopted to examine the RB cell proliferation. Wound healing test and Transwell assay were employed to detect cell migration and invasion. RB cell apoptosis was tested by flow cytometry and Western blot. An RB cell xenograft model was constructed on nude mice for testing the role of β-asarone on RB cell growth in vivo. RT-PCR and Western blot were used to determine the effect of β-asarone on Wnt/β-catenin signaling pathway. Furthermore, the Wnt/β-catenin pathway inhibitor PNU-74654 and activator HLY78 were administered to RB cells for confirming the effects of β-asarone in Wnt/β-catenin pathway.
Purpose
β-asarone is the prime component of essential oil extracted from Acori graminei Rhizoma, which plays an inhibitory role in various tumors. Here, we aim to investigate the functions as well as the mechanism of β-asarone in retinoblastoma (RB).
Results
In vivo experiment showed that β-asarone attenuated SO-Rb50 cell growth in nude mice. Further research found that β-asarone significantly repressed Wnt/β-catenin canonical pathway activation.