PT - JOURNAL ARTICLE AU - YUE LIU AU - TAEHO KWON AU - JI-SU KIM AU - NISANSALA CHANDIMALI AU - YING-HUA JIN AU - YI-XI GONG AU - DAN-PING XIE AU - YING-HAO HAN AU - MEI-HUA JIN AU - GUI-NAN SHEN AU - DONG KEE JEONG AU - DONG-SUN LEE AU - YU-DONG CUI AU - HU-NAN SUN TI - Peroxiredoxin V Reduces β-Lapachone-induced Apoptosis of Colon Cancer Cells AID - 10.21873/anticanres.13516 DP - 2019 Jul 01 TA - Anticancer Research PG - 3677--3686 VI - 39 IP - 7 4099 - http://ar.iiarjournals.org/content/39/7/3677.short 4100 - http://ar.iiarjournals.org/content/39/7/3677.full SO - Anticancer Res2019 Jul 01; 39 AB - 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 β-lapachone-induced apoptosis in SW480 human colon cancer cells. Materials and Methods: β-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 β-lapachone-induced cellular apoptosis and Prx V silencing increased β-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 β-lapachone-induced SW480 cells apoptosis, the Wnt/β-catenin signaling was studied. The Wnt/ β-catenin signaling pathway was found to be induced by β-lapachone. Conclusion: Prx V regulates SW480 cell apoptosis via scavenging ROS cellular levels and mediating the Wnt/β-catenin signaling pathway, which was induced by β-lapachone.