Fig. 6

Tumorigenic assessment of two Luminal-A breast cancer cell lines under mPR-specific PRG actions. Two Luminal-A breast cancer cell lines, T47D and MCF7, were treated in triplicates in FBS-free medium containing vehicle control (EtOH, DMSO), MIF (20 µM), PRG (20 µM), or mPR-specific PRG treatment (MIF + PRG, 20 µM each). A T47D cell migration was measured with all hormone treatments when plated on Collagen-I coated plates, (top left panel). T47D cells were also cultured on non-coated plates (top middle panel). MCF7 cell migration was measured with all hormone treatments on non-coated plates (top right panel). Similar trends in wound healing experiments were observed. T47D wound closure was measured with all hormone treatments, when plated on Collagen-I coated plates (bottom left panel). T47D cells were also cultured on non-coated plates (bottom middle panel). MCF7 cells wound closure was also measured on non-coated plates (Bottom right panel). B Cell invasion assays for T47D cells under combined mPR-specific PRG actions (left panel) and MCF7 under mPR-specific PRG actions (right panel). C Temporal RNA expression patterns of 5 key CmPn network genes, CCM1, CCM3, nPRs, mPRα (PAQR7) and mPRβ (PAQR8) genes, were demonstrated in a time course analysis of the response to mPR-specific PRG treatment for T47D cells (top panel) and MCF7 cells (bottom panel). RNA expression of both nPR and mPRs (PAQR7/PAQR8) genes in T47D cells (top panel) and MCF7 cells (bottom panel). Statistical significance for migration and wound healing was performed using two-way ANOVA or with students t-test for invasion assay. All experiments were performed with triplicates per experiment (n = 3); for all panels, * above bars indicate P ≤ 0.05