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. Author manuscript; available in PMC: 2015 Apr 13.
Published in final edited form as: Oncogene. 2005 Jan 20;24(4):616–626. doi: 10.1038/sj.onc.1208125

Figure 2.

Figure 2

Arsenite increases the apoptotic response of WM793 melanoma (vertical growth phase) cells to the EGFR inhibitor. (a) Additive effects of AG1478 (20 μM) and arsenite (10 μM) for the induction of apoptosis of WM793 melanoma cells 24 and 48 h after treatment. (b) Effects of LY294002 (50 μM), rapamycin (100 nM) or herbimycin (10 and 20 μM) on arsenite-induced apoptosis. Cell-cycle apoptosis analysis was 24 h after treatment performed using flow cytometry. (c) Western blot analysis of total and phospho-EGFR, phospho-ERK and phospho-AKT levels following treatment with AG1478 (20 μM), arsenite (10 μM) or their combination. Induction of HO-1 was used as a demonstration of arsenite-induced oxidative stress. β-Actin served as an internal standard. (d) PARP cleavage was determined by Western blot analysis 18 h after treatment with AG1478 (20 μM), PD153035 (20 μM), arsenite (10 μM) and indicated combinations of inhibitors with arsenite. (e) Effects of caspase inhibitors, Ac-IETD-CHO (50 μM), Ac-LEHD-CHO (50 μM) and zVAD-fmk (50 μM), on induction of apoptosis of WM793 cells by AG1478 or PD153035 (20 μM) treatment