RT Journal Article
SR Electronic
T1 Peroxiredoxin V Reduces β-Lapachone-induced Apoptosis of Colon Cancer Cells
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3677
OP 3686
DO 10.21873/anticanres.13516
VO 39
IS 7
A1 YUE LIU
A1 TAEHO KWON
A1 JI-SU KIM
A1 NISANSALA CHANDIMALI
A1 YING-HUA JIN
A1 YI-XI GONG
A1 DAN-PING XIE
A1 YING-HAO HAN
A1 MEI-HUA JIN
A1 GUI-NAN SHEN
A1 DONG KEE JEONG
A1 DONG-SUN LEE
A1 YU-DONG CUI
A1 HU-NAN SUN
YR 2019
UL http://ar.iiarjournals.org/content/39/7/3677.abstract
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.