Peroxiredoxin V Inhibits Emodin-induced Gastric Cancer Cell Apoptosis via the ROS/Bcl2 Pathway

In Vivo. 2019 Jul-Aug;33(4):1183-1192. doi: 10.21873/invivo.11589.

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.

Keywords: Peroxiredoxin V; ROS; apoptosis; emodin; gastric cancer.

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / genetics*
  • Cell Line, Tumor
  • Emodin / pharmacology*
  • Fluorescent Antibody Technique
  • Gene Expression
  • Humans
  • Peroxiredoxins / genetics*
  • Peroxiredoxins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction / drug effects*
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / metabolism

Substances

  • BCL2 protein, human
  • Proto-Oncogene Proteins c-bcl-2
  • Reactive Oxygen Species
  • Peroxiredoxins
  • Emodin