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. 2017 May 15;8(27):44295–44311. doi: 10.18632/oncotarget.17869

Figure 2. VS-5584 treatment causes activation of ERK in PDAC cells.

Figure 2

(A and B) BxPC-3 and HPAC cells were treated with vehicle control or variable concentrations of VS-5584 for 48 h. Whole cell lysates were subjected to Western blotting and probed with the indicated antibody. The fold changes for the densitometry measurements, normalized to β-actin and then compared to vehicle control, are indicated. (C and D) BxPC-3 and HPAC cells were treated with vehicle control or 2 μM VS-5584 for 4, 8, 12, 24, or 48 h. Whole cell lysates were subjected to Western blotting and probed with anti-p-AKT(S473), -p-AKT(T308), -AKT, -p-S6, or -β-actin antibody. The fold changes for the densitometry measurements, normalized to β-actin and then compared to no drug treatment control, are indicated. (E and F) BxPC-3 and HPAC cells were treated with vehicle control or variable concentrations of VS-5584 for 48 h. Whole cell lysates were subjected to Western blotting and probed with anti-p-ERK, -ERK, or -β-actin antibody. The fold changes for the densitometry measurements, normalized to β-actin and then compared to no drug treatment control, are indicated. (G and H) BxPC-3 and HPAC cells were treated with vehicle control or 2 μM VS-5584 for 4, 8, 12, 24, or 48 h. Whole cell lysates were subjected to Western blotting and probed with anti-p-ERK, -ERK, or -β-actin antibody. The fold changes for the densitometry measurements, normalized to β-actin and then compared to no drug treatment control, are indicated.