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Figure 3: Norathyriol blocks the EGF/TPA-induced AP-1 transactivation in JB6 cells. For the luciferase assay, JB6 cells stably transfected with an AP-1 luciferase reporter plasmid were cultured in 5% FBS/MEM. Cells were starved in the serum-free medium for 24 h, and then treated with norathyriol (0– 25 μM), or its vehicle DMSO (control), in 5% FBS/ MEM for 2 h. Cells were then exposed to 10 ng/ml EGF (upper panel) or 20 ng/ml TPA (lower panel) and harvested at 12 h. The luciferase activity was assessed and the AP-1 activity was expressed relative to control cells without EGF or TPA treatment. Data are shown as means ± SE. The asterisk (*) indicates a signifi cant difference (P < 0.05) between groups treated with EGF/TPA and norathyriol compared to the group treated with EGF/TPA alone

Figure 3: Norathyriol blocks the EGF/TPA-induced AP-1 transactivation in JB6 cells. For the luciferase assay, JB6 cells stably transfected with an AP-1 luciferase reporter plasmid were cultured in 5% FBS/MEM. Cells were starved in the serum-free medium for 24 h, and then treated with norathyriol (0– 25 μM), or its vehicle DMSO (control), in 5% FBS/ MEM for 2 h. Cells were then exposed to 10 ng/ml EGF (upper panel) or 20 ng/ml TPA (lower panel) and harvested at 12 h. The luciferase activity was assessed and the AP-1 activity was expressed relative to control cells without EGF or TPA treatment. Data are shown as means ± SE. The asterisk (*) indicates a signifi cant difference (<i>P</i> < 0.05) between groups treated with EGF/TPA and norathyriol compared to the group treated with EGF/TPA alone