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

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

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Gastric cancer is one of the leading causes of cancerrelated 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.

Original languageEnglish
Pages (from-to)298-306
Number of pages9
JournalInternational Journal of Oncology
Volume51
Issue number1
DOIs
StatePublished - 2017

Keywords

  • Epithelial-mesenchymal transition
  • Gastric cancer
  • Peroxiredoxin 5
  • Reactive oxygen species
  • Tumorigenicity

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