PT - JOURNAL ARTICLE AU - YONG-ZHE JIN AU - YI-XI GONG AU - YUE LIU AU - DAN-PING XIE AU - CHEN-XI REN AU - SEUNG-JAE LEE AU - HU-NAN SUN AU - TAEHO KWON AU - DONG-YUAN XU TI - Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis <em>via</em> ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells AID - 10.21873/anticanres.14949 DP - 2021 Apr 01 TA - Anticancer Research PG - 1831--1840 VI - 41 IP - 4 4099 - http://ar.iiarjournals.org/content/41/4/1831.short 4100 - http://ar.iiarjournals.org/content/41/4/1831.full SO - Anticancer Res2021 Apr 01; 41 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.