Fig. 8. GREB1 is required for estrogen-dependent action in endometriosis.

a Representative images of ectopic lesions from wild type and Greb1 KO (n = 5) mice stained with anti-Cyclin D1. Red arrow, Cyclin D1-positive cells. E epithelium, S stroma. b Graph displays percentage of Cyclin D1-positive cells in endometriotic lesion epithelium. Paired, two-tailed, t-test. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 and ns, non-significant. c-d Representative MTT proliferation assays of Immortalized Human Endometriotic Epithelial Cells. c, and primary stromal cells isolated from human endometriotic lesions (HEnSCs) d from the indicated groups and time points. Data are presented as the mean ± SEM from triplicate samples from one experiment (three experiments were conducted in total). *P < 0.05, **P < 0.01, ***P < 0.001 and ns, non-significant. e Relative abundance of GREB1, CCND1, IGF1, and ESR1 transcripts in Human Endometriotic Epithelial Cells transfected with control or GREB1 siRNA and treated with estrogen or vehicle for 6 h. Data are presented as the mean ± SEM from triplicate samples from one experiment (three experiments were conducted in total). Analyzed by one-way ANOVA with Tukey’s multiple comparisons post-test, *P < 0.05, **P < 0.01, ***P < 0.001 and ns non-significant. f Schematic illustration (created with in association with InPrint at Washington University in St. Louis) of the hypothesis that GREB1 participates in both endometrial physiology and pathology.