Abstract
BackgroundPeroxiredoxins (Prxs) are antioxidant enzymes that protect cells from oxidative stress induced by several factors. They regulate several signaling pathways, such as metabolism, immune response, and intracellular reactive oxygen species (ROS) homeostasis. Epithelial–mesenchymal transition (EMT) is a transforming process that induces the loss of epithelial features of cancer cells and the gain of the mesenchymal phenotype. The EMT promotes metastasis and cancer cell progression mediated by several pathways, such as mitogen-activated protein kinases (MAPKs) and epigenetic regulators.MethodsWe used Prx6 overexpressed and downregulated HCT116 cells to study the mechanism between Prx6 and colon cancer. The expression of Prx6, GAPDH, Snail, Twist1, E-cadherin, Vimentin, N-cadherin, ERK, p-ERK, p38, p-p38, JNK, and p-JNK were detected by Western blotting. Additionally, an animal study for xenograft assay was conducted to explore the function of Prx6 on tumorigenesis. Cell proliferation and migration were determined by IncuCyte Cell Proliferation and colony formation assays.ResultsWe confirmed that the expression of Prx6 and EMT signaling highly occurs in HCT116 compared with that in other colon cancer cell lines. Prx6 regulates the EMT signaling pathway by modulating EMT-related transcriptional repressors and mesenchymal genes in HCT116 colon cancer cells. Under the Prx6-overexpressed condition, HCT116 cells proliferation increased significantly. Moreover, the HCT116 cells proliferation decreased in the siPrx6-treated cells. Eleven days after HCT116 cell injection, Prx6 was overexpressed in the HCT116-injected mice, and the tumor volume increased significantly compared with that of the control mice. Furthermore, Prx6 regulates EMT signaling through p38 phosphorylation in colon cancer cells.ConclusionWe suggested that Prx6 regulates EMT signaling pathway through p38 phosphorylation modulation in HCT116 colon cancer cells.
Highlights
Peroxiredoxins (Prxs) are antioxidant enzymes that protect cells from oxidative stress induced by several factors
Peroxiredoxin 6 and Epithelial–mesenchymal transition (EMT)‐related genes are highly expressed in HCT116_siPrx6 E-cadherin (HCT116) cells First, Prx series in four colon cancer cell lines were screened for detecting Prxs effect on colorectal cancer cell growth (Fig. 1A)
We confirmed that the expression of Peroxiredoxin 6 (Prx6) and EMT signaling occurs highly in HCT116 compared with that in other colon cancer cell lines
Summary
Peroxiredoxins (Prxs) are antioxidant enzymes that protect cells from oxidative stress induced by several factors They regulate several signaling pathways, such as metabolism, immune response, and intracellular reactive oxygen species (ROS) homeostasis. Chae et al Journal of Biological Research-Thessaloniki (2021) 28:22 for maintaining the balance between ROS and antioxidant enzymes [2] If ROS overwhelms the capacity of the cellular antioxidant defense system, excessive oxidative stress would destroy DNA, lipids, and proteins [8] It promotes abnormal cell growth and proliferation, in case ROS level is out of control due to antioxidants. The regulation of antioxidants is closely related to cancer cell growth and proliferation
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