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. 2012 Aug 29;287(42):35161–35169. doi: 10.1074/jbc.M112.367367

FIGURE 2.

FIGURE 2.

Clofibrate suppresses hypoxia-induced HIF-1α expression and activity in a concentration-dependent manner. A, MCF-7 cells were transfected with the pGL3-HRE-luciferase reporter construct. Cells were treated with different concentrations of clofibrate for 4 h prior to placement in a hypoxia chamber for 16 h. Cell lysates were prepared, and luciferase activity was assayed. Data (mean ± S.E., n = 3) are expressed as percentages of the luciferase activity detected in untreated cells under normoxia. *, p < 0.05; **, p < 0.01 compared with untreated cells using one-way ANOVA, followed by Dunnett's analysis. B, MCF-7 cells were treated with different concentrations of clofibrate for 4 h prior to placement in a hypoxia chamber for 16 h. Cell lysates were prepared, and Western blotting was performed using antibodies against HIF-1α and β-actin. Shown are representative images of three individual experiments. C, A2780 cells were transfected with the pGL3-HRE-luciferase reporter construct. Cells were treated with different concentrations of clofibrate for 4 h prior to placement in a hypoxia chamber for 16 h. Cell lysates were prepared, and luciferase activity was assayed. Data (mean ± S.E., n = 3) are expressed as percentages of the luciferase activity detected in untreated cells under normoxia. *, p < 0.05; **, p < 0.01 compared with untreated cells using one-way ANOVA, followed by Dunnett's analysis. D, A2780 cells were treated with different concentrations of clofibrate for 4 h prior to placement in a hypoxia chamber for 16 h. Cell lysates were prepared, and Western blotting was performed using antibodies against HIF-1α and β-actin. Shown are representative images of three individual experiments.