Yong-Zhe Jin1,2, Hu-Nan Sun3, Yue Liu3, Dong-Ho Lee4, Ji-Su Kim4, Sun-Uk Kim5, Bing-Yang Jiao3, Ying-Hao Han3, Mei-Hua Jin3, Gui-Nan Shen3, Dong-Seok Lee6, Taeho Kwon7, Dong-Yuan Xu8,2, Y U Jin8,2. 1. School of Nursing, Yanbian University, Yanji, P.R. China. 2. College of Medicine, Yanbian University, Yanji, P.R. China. 3. College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China. 4. Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea. 5. Futuristic Animal Resource & Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungcheongbuk-do, Republic of Korea. 6. School of Life Sciences, KNU Creative BioResearch Group (BK21 plus project), Kyungpook National University, Daegu, Republic of Korea. 7. Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea kwon@kribb.re.kr dyxu@ybu.edu.cn jinyu@ybu.edu.cn. 8. School of Nursing, Yanbian University, Yanji, P.R. China kwon@kribb.re.kr dyxu@ybu.edu.cn jinyu@ybu.edu.cn.
Abstract
BACKGROUND/AIM: Peroxiredoxin (Prx) protein family is aberrantly expressed in various cancers including gastric cancer. Among the six family members, Prx V has been known as an antioxidant enzyme which scavenges intracellular reactive oxygen species (ROS) and modulates cellular apoptosis. This study aimed at investigating the role of Prx V in apoptosis of gastric cancer cells. MATERIALS AND METHODS: Stably constructed Prx V knockdown, over-expression and mock AGS cells (a human gastric adenocarcinoma cell line) were used to study the effect of Prx V on emodin-induced apoptosis by western blotting, cell viability, apoptosis and ROS detection assays. RESULTS: Overexpression of Prx V significantly decreased emodin-induced cellular apoptosis and ROS levels compared to Mock and Prx V knockdown AGS cells. Also, overexpression of Prx V down-regulated the expression of pro-apoptotic proteins, Bad and cleaved PARP, and increased the expression of anti-apoptotic protein, Bcl2. CONCLUSION: Prx V suppresses AGS cell apoptosis via scavenging intracellular ROS and modulating apoptosis-related markers. Copyright
BACKGROUND/AIM: Peroxiredoxin (Prx) protein family is aberrantly expressed in various cancers including gastric cancer. Among the six family members, Prx V has been known as an antioxidant enzyme which scavenges intracellular reactive oxygen species (ROS) and modulates cellular apoptosis. This study aimed at investigating the role of Prx V in apoptosis of gastric cancer cells. MATERIALS AND METHODS: Stably constructed Prx V knockdown, over-expression and mock AGS cells (a humangastric adenocarcinoma cell line) were used to study the effect of Prx V on emodin-induced apoptosis by western blotting, cell viability, apoptosis and ROS detection assays. RESULTS: Overexpression of Prx V significantly decreased emodin-induced cellular apoptosis and ROS levels compared to Mock and Prx V knockdown AGS cells. Also, overexpression of Prx V down-regulated the expression of pro-apoptotic proteins, Bad and cleaved PARP, and increased the expression of anti-apoptotic protein, Bcl2. CONCLUSION:Prx V suppresses AGS cell apoptosis via scavenging intracellular ROS and modulating apoptosis-related markers. Copyright