AI Article Synopsis
- Prx6 is an antioxidant enzyme that plays a crucial role in protecting cells from oxidative stress and regulating signaling pathways linked to cancer progression, specifically in colon cancer.
- Prx6 influences the epithelial-mesenchymal transition (EMT) process by affecting the expression of certain genes and proteins, which can enhance cancer cell proliferation and migration.
- Experimental results demonstrated that overexpression of Prx6 in HCT116 colon cancer cells led to increased tumor growth in mice, indicating its significant role in tumorigenesis through modulation of EMT signaling pathways.
Article Abstract
Background: 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. 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.
Methods: We 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.
Results: We 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.
Conclusion: We suggested that Prx6 regulates EMT signaling pathway through p38 phosphorylation modulation in HCT116 colon cancer cells.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8609821 | PMC |
| http://dx.doi.org/10.1186/s40709-021-00153-6 | DOI Listing |
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