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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adenocarcinoma, Antineoplastic Agents, Apoptosis, Atorvastatin, Blotting, Western, Cell Line, Tumor, Cell Proliferation, Cell Survival, Dose-Response Relationship, Drug, Esophageal Neoplasms, Flow Cytometry, Heptanoic Acids, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Intercellular Adhesion Molecule-1, NF-kappa B, Pravastatin, Pyrroles, Simvastatin.
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Does statin therapy attenuate growth and malignant potential of human esophageal adenocarcinoma cells? Context: Esophageal adenocarcinoma is an aggressive malignancy generally diagnosed after metastatic spread and currently lacks effective medical therapy. Expression of intracellular adhesion molecule-1 (ICAM-1) is an adverse prognostic indicator in various human tumor cells and contributes significantly to their metastatic potential. Statin therapy reduces circulating ICAM-1 levels in patients with coronary heart disease and is associated with reduction in progression from Barrett esophagus to esophageal adenocarcinoma. We hypothesize that statin therapy may attenuate growth and malignant potential via ICAM-1 expression and nuclear factor-kappa beta activation in human esophageal adenocarcinoma cells. Verified human esophageal adenocarcinoma cells (FLO-1) were treated with simvastatin, atorvastatin, or pravastatin (10-, 30-, and 50-μmol/L concentrations). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide viability, 5-bromo-2'-deoxyuridine proliferation, or annexin V apoptosis assays were performed, or cells were stimulated with tumor necrosis factor-alpha and collected for immunoblotting and flow cytometry. Simvastatin decreased cell viability and proliferation while increasing apoptosis in a dose-dependent manner (P < .05). Simvastatin attenuated total cellular and cell-surface ICAM-1 expression as well as nuclear factor-kappa beta activation (P < .05). Atorvastatin had mild effects and pravastatin had essentially no effect on growth and metastatic potential of these cells.
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We demonstrate that treatment of human esophageal adenocarcinoma cells with simvastatin attenuates growth, by decreasing cell viability, decreasing cell proliferation, and increasing apoptosis, and attenuates metastatic potential, by decreasing expression of key metastatic markers. These findings identify simvastatin as a potential therapeutic and chemopreventive modality to thwart the progression of esophageal adenocarcinoma. Final Decision: yes