Peroxiredoxin VI regulates the epithelial‐mesenchymal transition in colorectal cancer

Abstract

In energy metabolism, organisms that use oxygen are exposed to reactive oxygen species (ROS) as their product or byproduct. Excessive ROS can cause damage to DNA, lipids, and proteins, and these damages accumulate and cause a variety of diseases. To prevent such damage, antioxidant enzymes such as NRF2, catalase, and peroxiredoxin are present in cells to maintain redox balance with ROS. Recent studies have shown that the expression of antioxidant enzymes is greatly increased in cancer cells compared to normal cells due to increased vulnerability of cancer cells to ROS. Because cancer cells grow and multiply faster than normal cells, they produce large amounts of ROS. It has also been reported that the expression of antioxidant enzymes is increased to eliminate them. Since the human colon, the large intestine, is particularly exposed to ROS, it was thought to be of great significance to study cancer cell development in the colon. Peroxiredoxin VI, which removes H2O2, is well known as an antioxidant enzyme that effectively reduces ROS, and its expression has been reported to be increased in cancer cells. However, there are not many studies on the precise mechanism and effect of how peroxiredoxin VI helps cancer cells grow. A peroxiredoxin VI overexpression cell line was constructed using a colon cancer cell line. Silencing of peroxiredoxin VI was performed in the same cell line using the RNA gene silencing technique, and the increase and decrease of EMT was confirmed. Overexpressed peroxiredoxin VI increased both EMT transcription factors snail and twist1, and changes in EMT markers Vimentin and E-cadherin were confirmed. Both snail and twist1 were decreased in the peroxiredoxin VI silenced colon cancer cell line, and the EMT marker change was observed in contrast to the peroxiredoxin VI overexpression. In addition, for in vivo mouse xenografts, tumor formation was increased in peroxiredoxin VI overexpressing cells and decreased in peroxiredoxin VI silenced cells. In conclusion, this study confirms that regulation of peroxiredoxin VI expression can slow the proliferation and metastasis of cancer cells and provides a clue to future cancer treatment studies. Peroxiredoxin 6 regulation of p38-mediated epithelial-mesenchymal transition in HCT-116 cells This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.