Fig. 9

ER-dependent FGF1 signaling emerges with endocrine resistance. A Venn diagrams comparing the genes that were up- or down-regulated by FGF1, and reversed by co-treatment with fulvestrant (ICI) in MCF7 cells (left) or MCF7 TAMR cells (right), all FDR p < 0.05. B Hallmark gene set analysis of the 603 genes in MCF7 TAMR cells induced or repressed by FGF1 treatment and reversed by co-treatment with fulvestrant (ICI). Glycolysis is emphasized. C Heatmap of relative expression of 8 genes associated with glycolysis, expressed as fold change compared to vehicle (Veh) within each cell line. Genes include Slc2a1 (Glut1), Aldoc, Pgk1, Eno1, Eno2, Pfkp, Ldha, and Slc16a3 (MCT4). D Kaplan–Meier curves of recurrence-free survival % (left) and distant metastasis-free survival % (right) of patients with ER-positive breast cancer expressing high levels of glycolytic genes indicated in the heatmap in panel I. (K) GSEA analysis of dataset GSE24185 comparing ER-positive tumors from patients with obesity versus those without. Normalized enrichment scores (NES) of p < 0.05 gene sets are plotted. Glycolysis is emphasized in the bar graph (left) and in the GSEA plot (right). E GSEA analysis of datasets GSE24185 and GSE78958 comparing ER-positive tumors from patients with obesity versus those without. Normalized enrichment scores (NES) of adjusted p < 0.05 gene sets are plotted. Glycolysis is emphasized in the bar graphs and in the GSEA plots