G Protein-Coupled Estrogen Receptor-Selective Ligands Modulate Endometrial Tumor Growth
Figure 5
GPER-mediated activation of PI3K and ERK in Hec50 cells by SERMs, a SERD, and an ER-selective agonist. (a) PH-RFP-transfected Hec50 cells were stimulated for 15 minutes with the following ligands: 4-hydroxytamoxifen (100 nM, 4OH-tamoxifen), ICI182,780 (100 nM), Raloxifene (100 nM), genistein (100 nM), PPT (100 nM), or DPN (10 μM). Hec50 cells were also cotransfected with ER-GFP (shown in inset) and PH-RFP and stimulated with 100 nM DPN to verify the activity of DPN as an ER agonist in Hec50 cells (ER-GFP:DPN). (b) Hec50 cells were stimulated for 15 min with vehicle (0.05% DMSO), estrogen (10 nM, E2), G-1 (10 nM), 4-hydroxytamoxifen (100 nM, Tam), Raloxifene (100 nM, Ral), ICI182,780 (100 nM, ICI), genistein (100 nM, Gen), PPT (100 nM), DPN (10 μM), or EGF (1 nM) either in the presence or absence of 1 μM G15 (10 min pretreatment, with 0.05% DMSO in samples without G15). (c) Band intensities of pERK were normalized to total ERK and plotted with estrogen as 100%. Data represent mean s.e.m. from three experiments. * versus DMSO; ** versus paired stimulus without G15.
