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. 2017 Sep 28;9(4):4282–4300. doi: 10.18632/oncotarget.21378

Figure 4. PR isoforms appropriate similar motifs at distinct locations to differentially reprogram estrogen signaling.

Figure 4

A. - B. Heatmaps display intensity of sequencing obtained on anti-ER ChIP before (10 nM estrogen (E2) alone) and after (10 nM estrogen plus 10 nM R5020) remodeling by PRA A. or PRB B.. C. - D. Expression of estrogen and progestin-regulated genes in T47D cells expressing either PRA C. or PRB D.. Heatmaps are row-normalized and include the union of estrogen and progestin-regulated genes. E. Cellular pathways enriched in the genes that are differentially expressed in response to 10 nM R5020 treatment of T47D cells expressing PRA/PRB mixtures [1] or PRA and PRB individually. F. - G. Changes in F. matrigel invasion and G. cell confluence of ER+/PRA+ and ER+/PRB+ T47D cells in response to treatments with 10 nM estrogen or both 10 nM estrogen plus 10 nM R5020. * denotes P-value < 10-1, *** P-value < 10-3. Three biological replicates were performed and each of the experimental conditions had at least 12 technical replicates.