AP-2 Inhibits c-MYC Induced Oxidative Stress and Apoptosis in HaCaT Human Keratinocytes
Figure 4
Wild type AP-2 attenuated apoptosis induced by c-MYC in HaCaT cells. HaCaT cells were infected with Ad-Bgl II 100 MOI (Control), 50 MOI Ad-Bgl II + 50 MOI Ad-AP-2 (AP-2), 50 MOI Ad-Bgl II + 50 MOI Ad-c-MYC (c-MYC), or 50 MOI Ad-AP-2 + 50 MOI Ad-c-MYC (AP-2 + c-MYC). Propidium iodide (PI) staining for sub-G1 and phycoerythrin (PE)-conjugated anti-caspase-3 antibody staining for active caspase-3 were performed as indicated in the Materials and Methods section. (a) AP-2 decreased the sub-G1 population induced by c-MYC. Upper panels: representative flow cytometry plots of PI-sub-G1 DNA content (M1) in the variously treated cells. Lower panel: quantitative determination of sub-G1 DNA content. Error bars represent standard deviations, 4. .01 compared to control, AP-2, and AP-2 + c-MYC groups. (b) AP-2 decreased the percentage of cells positive for active caspase-3 induced by c-MYC. Upper panels: representative flow cytometry plots of measurement of PE-active caspase-3. Lower panel: quantitative determination of active caspase-3. Error bars represent standard deviations, 4. .01 compared to control, .05 compared to control and c-MYC group.
