Miral R. Sadaria, MD, Amy E. Reppert, MD, Jessica A

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Presentation transcript:

Statin therapy attenuates growth and malignant potential of human esophageal adenocarcinoma cells Miral R. Sadaria, MD, Amy E. Reppert, MD, Jessica A. Yu, MD, Xianzhong Meng, MD, PhD, David A. Fullerton, MD, T. Brett Reece, MD, Michael J. Weyant, MD The Journal of Thoracic and Cardiovascular Surgery Volume 142, Issue 5, Pages 1152-1160 (November 2011) DOI: 10.1016/j.jtcvs.2011.08.004 Copyright © 2011 The American Association for Thoracic Surgery Terms and Conditions

Figure 1 Proliferation of human esophageal adenocarcinoma cells (FLO-1) after statin therapy. Simvastatin treatment attenuated FLO-1 cell proliferation at all concentrations (A). Atorvastatin decreased cell proliferation at the 30- and 50-μmol/L concentrations (B), and pravastatin attenuated proliferation of FLO-1 cells at the 10- and 50-μmol/L concentrations (C). ∗P < .0001 compared with vehicle control and all concentrations; ∗∗P < .005 compared with vehicle control; ∗∗∗P < .01 compared with vehicle control and 10-μmol/L concentration; n = 6. The Journal of Thoracic and Cardiovascular Surgery 2011 142, 1152-1160DOI: (10.1016/j.jtcvs.2011.08.004) Copyright © 2011 The American Association for Thoracic Surgery Terms and Conditions

Figure 2 Apoptosis of human esophageal adenocarcinoma cells (FLO-1) after statin therapy. Simvastatin treatment increased the total percentage of FLO-1 cells undergoing early and late apoptosis at the 30- and 50-μmol/L concentrations (A), whereas atorvastatin (B) and pravastatin (C) had no effect on the total percentage of cells undergoing apoptosis. ∗P < .05 compared with vehicle control and 10-μmol/L concentration; n = 6. The Journal of Thoracic and Cardiovascular Surgery 2011 142, 1152-1160DOI: (10.1016/j.jtcvs.2011.08.004) Copyright © 2011 The American Association for Thoracic Surgery Terms and Conditions

Figure 3 Total cellular ICAM-1 expression after statin therapy in human esophageal adenocarcinoma cells (FLO-1). Representative Western blots demonstrate a dose-dependent attenuation of total cellular ICAM-1 expression in FLO-1 cells when treated with simvastatin (A) and atorvastatin (B), whereas treatment with pravastatin demonstrates no significant attenuation (C and F). The 30- and 50-μmol/L concentrations of simvastatin reduced total cellular ICAM-1 expression compared with vehicle control (D), whereas all concentrations of atorvastatin reduced total cellular ICAM-1 expression compared with vehicle control (E). ∗P < .01 compared with vehicle control; ∗∗P < .01 compared with vehicle control and 10-μmol/L concentration ∗∗∗P < .05 compared with vehicle control and all concentrations; n = 6. ICAM-1, Intracellular adhesion molecule-1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. The Journal of Thoracic and Cardiovascular Surgery 2011 142, 1152-1160DOI: (10.1016/j.jtcvs.2011.08.004) Copyright © 2011 The American Association for Thoracic Surgery Terms and Conditions

Figure 4 Cell-surface ICAM-1 expression after statin therapy in human esophageal adenocarcinoma cells (FLO-1). Representative flow cytometry histograms demonstrate a reduction in mean intensity fluorescence and, thus, cell-surface ICAM-1 expression after treatment of FLO-1 cells with simvastatin (A), atorvastatin (B), and pravastatin (C). Cell-surface ICAM-1 expression decreased with all concentrations of simvastatin (D), 30 and 50 μmol/L of atorvastatin (E), and 10 and 30 μmol/L of pravastatin (F). ∗P < .05 compared with vehicle control; ∗∗P < .05 compared with vehicle control and 10-μmol/L concentration; n = 6. ICAM-1, Intracellular adhesion molecule-1. The Journal of Thoracic and Cardiovascular Surgery 2011 142, 1152-1160DOI: (10.1016/j.jtcvs.2011.08.004) Copyright © 2011 The American Association for Thoracic Surgery Terms and Conditions

Figure 5 NF-κB activation after statin therapy in human esophageal adenocarcinoma cells (FLO-1). Representative Western blots demonstrate a dose-dependent attenuation in NF- κB activation in FLO-1 cells when treated with simvastatin (A), whereas treatment with atorvastatin (B and E) and pravastatin (C and F) demonstrate no significant attenuation when compared with vehicle control. A decrease in NF-κB activation was demonstrated at all concentrations of simvastatin treatment (D). ∗P < .05 compared with vehicle control; n = 6. NF-κB, Nuclear factor kappa beta. The Journal of Thoracic and Cardiovascular Surgery 2011 142, 1152-1160DOI: (10.1016/j.jtcvs.2011.08.004) Copyright © 2011 The American Association for Thoracic Surgery Terms and Conditions