Skip to main content
. 2016 May 10;7(25):37693–37713. doi: 10.18632/oncotarget.9264

Figure 2. Entinostat reduces both the protein and mRNA levels of Survivin in NSCLC cells without disturbing the PI-3K/Akt and MEK/MAPK signaling pathways.

Figure 2

(A) A549 and H460 cells were treated with either entinostat (3 μmol/L and 0.5 μmol/L for A549 and H460, respectively) for 24 or 48 h (left panel), or indicated concentrations of entinostat for 24 h (right panel). Cells were collected and subjected to western blot analyses of Bcl-xL, Mcl-1, Survivin, Acetyl-Histone H3 (Ac-H H3), Histone H3 (H H3), or β-actin. The densitometry analyses of Survivin signals were shown underneath, and the arbitrary numbers indicate the intensities of each cell line relative to controls, defined as 1.0. (B) A549 and H460 cells were treated with either indicated concentrations of entinostat for 24 h (left panel), or a fixed concentration of entinostat for 12, 24, or 48 h (right panel). Cells were collected and subjected to total RNA extraction. The mRNA levels of Survivin were measured by qRT-PCR. All results were normalized with the internal control β-actin. Bars, S.D. Data show the representative of three independent experiments. (C) Cells treated with entinostat (3 mmol/L and 0.5 mmol/L for A549 and H460, respectively) for 24 h were collected and subjected to western blot analyses of P-Akt, Akt, P-MAPK (Erk1/2), MAPK (Erk1/2), or β-actin. (D) A549 and H460 cells treated with LY294002 (LY, 10 μmol/L), Akt inhibitor VIII (Akti, 1 μmol/L), or Rapamycin (Rapa, 100 nmol/L) for 24 h were subjected to western blot analyses of Survivin, P-Akt, Akt, P-mTOR, mTOR, or β-actin.