Background: Eicosapentaenoic acid (EPA) suppresses the proliferation of cell lines derived from colon, pancreatic, breast and other cancers. Few reports have described the effect of EPA on esophageal cancer cell lines.
Materials And Methods: We investigated the effect of EPA on the proliferation of the esophageal squamous cell carcinoma cell lines TE11 and KYSE180 with a WST-1 assay. Apoptosis was evaluated with a DNA fragmentation assay. Levels of apoptosis-related proteins (caspase-3, -7, -9 and poly (ADP-ribose) polymerase (PARP)) and cleaved caspase-3, -7, -9 and PARP were evaluated by western blot analysis.
Results: After exposure to EPA for 24 h, KYSE180 and TE11 cell proliferation was suppressed in a dose-dependent manner (p<0.05). In addition, caspase -3, -7, -9 and PARP were activated. EPA (0.1 μM, 1 μM, 10 μM) induced apoptosis in a dose-dependent manner, as detected by the DNA fragmentation assay.
Conclusion: EPA shows potential as a new treatment for esophageal cancer.
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December 2024
Department of Medicine III, Division of Endocrinology and Metabolism, Medical University of Vienna, Austria; Department of Medicine III and Karl Landsteiner Institute for Metabolic Diseases and Nephrology, Clinic Hietzing, Vienna, Austria. Electronic address:
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Medical University of South Carolina, Charleston, SC, USA.
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University of Michigan, Department of Internal Medicine, Ann Arbor, MI, United States.
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December 2024
Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China. Electronic address:
Introduction: Inflammatory bowel disease (IBD) is often associated with impaired proliferation and differentiation of intestinal stem cells (ISCs). Eicosapentaenoic acid (EPA), which is predominantly found in fish oil, has been recognized for its intestinal health benefits, although the potential mechanisms are not well understood.
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