Aryl Hydrocarbon Receptor Ligands Inhibit IGF-II and Adipokine Stimulated Breast Cancer Cell Proliferation
Figure 3
AHR ligand-stimulated inhibition of IGF-2 requires the AHR. (a, c) MCF-7 (a) or T-47D (c) cells transiently transfected with con-siRNA or AHR-siRNA for 36 hr, followed by isolation of total cellular extract and western blot analysis with AHR and GAPDH antibody. GAPDH was used to normalize between samples. Data shown are the means ± S.E. of three experiments. A significant () decrease in AHR by AHR-siRNA (*) is indicated. (b, d) The total number of MCF-7 (b) or T-47D (d) cells transfected with nontargeting control short interfering RNA (con-siRNA) or aryl hydrocarbon receptor siRNA (AHR-siRNA) for 36 hr and then treated with DMSO, vehicle control (con), IGF2 (100 ng/mL) plus DMSO or IGF2 plus TCDD (MCF-7; 10 nM, T-47D; 100 nM) for three additional days in culture was determined and is displayed relative to the number of live cells in the DMSO con-siRNA group, which was assigned a value of 1. Data shown are the means ± S.E. of three experiments. (e) The total number of MCF-7 cells transfected with con-siRNA or AHR-siRNA for 36 hr and then treated with DMSO vehicle control (con), IGF2 (100 ng/mL) plus DMSO, or IGF2 plus SU5416 (100 nM) for three additional days in culture was determined and is displayed relative to the number of live cells in the DMSO con-siRNA group, which was assigned a value of 1. Data shown are the means ± S.E. of three experiments.
