Peroxiredoxin V Reduces β-Lapachone-induced Apoptosis of Colon Cancer Cells

Background/Aim: Peroxiredoxin (Prx) V has been known as an antioxidant enzyme which scavenges intracellular reactive oxygen species (ROS). Also, Prx V has been shown to mediate cell apoptosis in various cancers. However, the mechanism of Prx V-induced apoptosis in colon cancer cells remains unknown. Thus, in this study we analyzed the effects of Prx V in beta-lapachone-induced apoptosis in SW480 human colon cancer cells. Materials and Methods: beta-lapachone-induced apoptosis was analyzed by the MTT assay, western blotting, fluorescence microscopy, Annexin V staining and flow cytometry. Results: Overexpression of Prx V, significantly decreased beta-lapachone-induced cellular apoptosis and Prx V silencing increased beta-lapachone-induced cellular apoptosis via modulating ROS scavenging activity compared to mock SW480 cells. In addition, to further explore the mechanism of Prx V regulated beta-lapachone-induced SW480 cells apoptosis, the Wnt/beta-catenin signaling was studied. The Wnt/beta-catenin signaling pathway was found to be induced by beta-lapachone. Conclusion: Prx V regulates SW480 cell apoptosis via scavenging ROS cellular levels and mediating the Wnt/beta-catenin signaling pathway, which was induced by beta-lapachone.