Functional analysis of these genes revealed progestin-mediated increases in genes involved in cell cycle progression, suggesting that the proliferative effects of progestin may not require FOXA1. As FOXA1 appeared to have an effect on PR transcription distinct from that observed for ER, we compared the density of FOXA1 ChIP-seq interactions around PR Nutlin-3 Mdm2 inhibitor binding regions in T-47D cells, with those observed at FOXA1 or ER binding regions . Binding of FOXA1 around ER binding regions was very high, confirming the absolute requirement for this factor in estrogen signalling. In contrast, although a peak of FOXA1 interaction was seen near PR binding regions, sequence enrichment was significantly lower suggesting that while FOXA1 may be involved in PR binding at some regions, this may represent a subset of binding events. This was supported by the finding that FOXA1 binding was much stronger at PR binding regions in which a FOXA1 motif had been predicted, than in regions where no motif was found, and was similar to the density of binding observed overall in ER binding regions . In order to test whether PR binding site numbers were different near genes that Rapamycin mTOR inhibitor gained progestin-regulation upon FOXA1 expression, we compared the number of PR binding peaks in FOXA1 negative AB32 cells that were near to genes that lost, gained or retained progestin regulation when FOXA1 was expressed. Although there were slightly fewer PR binding regions near genes that gained regulation , the difference was not significant. This suggested that the capacity of FOXA1 to influence PR binding and transcriptional regulation of target genes was not inherently related to PR binding site density; PR may form weak associations near to the ����gained���� subset of genes, but FOXA1 was required for the interaction to become productive. We also examined the level of enrichment of motifs for NF1 and AP-1 in PR binding regions associated with genes that lost, gained or conserved progestin regulation when FOXA1 was expressed and found no difference between the groups . FOXA1 influences transcription factor activity via its DNA bending activity . We speculated that PR binding regions that require FOXA1 to affect transcription may be further from the target gene than those that do not, and that binding of FOXA1 near those regions results in DNA bending, which brings the PR transcriptional complex closer to the target gene. Examination of the distance from PR binding regions to genes that gained regulation by FOXA1 revealed that this was the case and that this subset of regions was significantly further from the regulated gene than binding regions near genes regulated in the absence of FOXA1 . In summary, ChIP-seq profiling in two different cell lines has revealed remarkably distinct patterns of PR binding.