RT Journal Article SR Electronic T1 Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis via ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 1831 OP 1840 DO 10.21873/anticanres.14949 VO 41 IS 4 A1 YONG-ZHE JIN A1 YI-XI GONG A1 YUE LIU A1 DAN-PING XIE A1 CHEN-XI REN A1 SEUNG-JAE LEE A1 HU-NAN SUN A1 TAEHO KWON A1 DONG-YUAN XU YR 2021 UL http://ar.iiarjournals.org/content/41/4/1831.abstract AB Background/Aim: Peroxiredoxin V (Prx V) plays crucial roles in cellular apoptosis and proliferation in various cancer cells by regulating the cellular reactive oxygen species (ROS) levels. Materials and Methods: Here, we examined the possible regulatory effects of Prx V on doxorubicin (DOX)-induced cellular apoptosis and its mechanisms in the human gastric adenocarcinoma cell line (AGS cells). Results: Our findings suggest that Prx V knockdown may significantly increase the DOX-induced apoptosis by aggravating intracellular ROS accumulation. We also found that DOX-induced mitochondrial ROS levels and membrane permeability were significantly higher in short hairpin Prx V cells than in mock cells, and these phenomena were dramatically reversed by ROS scavenger treatment. Prx V knockdown also significantly upregulated the cleaved caspase 9, 3, and B-cell lymphoma 2 (Bcl2)-associated agonist of cell death/Bcl2 protein expression levels, suggesting that Prx V knockdown activates mitochondria-dependent apoptotic signaling pathways. Conclusion: Taken together, this study suggests that Prx V may be a strong molecular target for gastric cancer (GC) chemotherapy, and further elucidates the role of Prx V in oxidative stress-induced cell apoptosis.