Figure 2. The combined treatment of MEK inhibitor with statins induces apoptosis with the suppression of Akt activation in MDA-MB-231 cells.

(A) The sub-G1 populations after the combined treatment of CH5126766 with fluvastatin. Cells were treated with CH5126766 (40 nM) and/or fluvastatin (0.3 μM) for 72 h. DNA contents of the cells were analyzed by flow cytometer. Columns, means of triplicate data; bars, SD; ^**, P < 0.01. (B) The sub-G1 populations after the combined treatment of CH5126766 with simvastatin. Cells were treated with CH5126766 (20 nM) and/or simvastatin (0.3 μM) for 72 h. DNA contents of the cells were analyzed by flow cytometer. Columns, means of triplicate data; bars, SD; ^**, P < 0.01. (C) The cleavage of PARP after the combined treatment of CH5126766 with fluvastatin. Cells were treated with CH5126766 (40 nM) and/or fluvastatin (0.3 μM) for 48 h, and cleaved PARP was analyzed by Western blotting. The arrow indicates the cleaved form of PARP. β-Actin was used as a loading control. (D) The cleavage of PARP after the combined treatment of CH5126766 with simvastatin. Cells were treated with CH5126766 (20 nM) and/or simvastatin (0.3 μM) for 48 h, and cleaved PARP was analyzed by Western blotting. The arrow indicates the cleaved form of PARP. β-Actin was used as a loading control. (E) The phosphorylation status of ERK and Akt after the treatment of CH5126766. Cells were treated with CH5126766 (20 nM) for 24 h, and phosphorylated ERK and Akt were analyzed by Western blotting. (F) The phosphorylation status of Akt after the combined treatment of CH5126766 with fluvastatin. Cells were treated with CH5126766 (40 nM) and/or fluvastatin (0.3 μM) for 48 h, and phosphorylated Akt was analyzed by Western blotting. (G) The phosphorylation status of Akt after the combined treatment of CH5126766 with simvastatin. Cells were treated with CH5126766 (20 nM) and simvastatin (0.3 μM) for 48 h, and phosphorylated Akt was analyzed by Western blotting.