Peroxiredoxin 5 overexpression enhances tumorigenicity and correlates with poor prognosis in gastric cancer

Kim,Bokyung; Kim,Yeon Soo; Ahn,Hye-Mi; Lee,Hyo Jin; Jung,Min Kyu; Jeong,Hyun Yong; Choi,Dong Kyu; Lee,Jun Hyeog; Lee,Sang-Rae; Kim,Jin Man; Lee,Dong-Seok

doi:10.3892/ijo.2017.4013

Peroxiredoxin 5 overexpression enhances tumorigenicity and correlates with poor prognosis in gastric cancer

Authors:
- Bokyung Kim
- Yeon Soo Kim
- Hye-Mi Ahn
- Hyo Jin Lee
- Min Kyu Jung
- Hyun Yong Jeong
- Dong Kyu Choi
- Jun Hyeog Lee
- Sang-Rae Lee
- Jin Man Kim
- Dong-Seok Lee
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Affiliations: School of Life Sciences and Biotechnology, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea, Department of Internal Medicine, Daejeon St. Mary's Hospital, The Catholic University, Daejeon, Republic of Korea, Department of Internal Medicine, College of Medicine, Chungnam National University, Daejeon, Republic of Korea, Department of Pathology and Medical Science, College of Medicine, Chungnam National University, Daejeon, Republic of Korea, New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation (DGMIF), Daegu, Republic of Korea, The National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Ochang, Republic of Korea
Published online on: May 19, 2017 https://doi.org/10.3892/ijo.2017.4013
Pages: 298-306

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Abstract

Gastric cancer is one of the leading causes of cancer-related deaths worldwide. Despite the advanced surgical resection techniques and anticancer drugs currently available to treat early stage gastric cancer, the prognosis of patients with gastric cancer remains poor. The epithelial to mesenchymal transition (EMT) is an important process for the initiation of tumorigenesis. Recent studies suggested that reactive oxygen species (ROS) can promote cell migration and invasion. Thus, an imbalance of redox homeostasis can result in cancer cells exhibiting EMT properties. PRXs are upregulated in various tumors in the breast, bladder, lung, cervical, ovarian, prostate, esophageal, and hepatocellular. However, PRX expression and its impact on disease prognosis, patient survival rate, and EMT are rarely studied in the context of human gastric cancer. The expression of PRX5 was significantly correlated with tumor size, depth of tumor, lymphatic invasion in patients of gastric cancer. In addition, overexpression of PRX5 enhanced carcinogenicity by increasing the proliferation and invasiveness of gastric cancer cells via upregulation of Snail. Taken together, we suggest that PRX5 may be a potential factor that may contribute to poor prognosis of gastric cancer through enhancing the mesenchymal phenotype. Finally, PRX5 is a putative therapeutic target and clinical strategy for various cancers overexpressing PRX5.

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