Fig. 3: MPA regulated the expression of RANKL via its receptor PR.

A Analysis of the expression of PR in different tumors by TIMER2 database. B The expression and survival analysis of PR in endometrial tissues and breast tissues by GEPIA, respectively. C Western blotting showing the levels of RANKL in Ishikawa and T47D cells treated with RU486 or in combination with MPA. D Silencing of PR attenuated the effect of MPA on RANKL expression by Western blotting analysis. E Potential PR binding site in the promoter of RANKL examined with dual-luciferase reporter assay by transfecting the wild-type (WT) or mutated (MUT1, MUT2) plasmids. F Binding of PR to the predicted site was confirmed by ChIP-PCR using primers specific to the binding site in Ishikawa and T47D cells. *p < 0.05, **p < 0.01, ***p < 0.001.