Mechanism of the effects of progesterone and mifepristone on human prostate cancer PC-3 cells

Objective To explore the mechanism of the effects of progesterone and mifepristone onPC-3 prostate cancer cells. Methods Cell proliferation assays were performed to demonstrate the effectsof progesterone and mifepristone on PC-3 cells.Expression of progesterone receptor gene mRNA was detectedby reverse transcriptase-polymerase chain reaction (RT-PCR) in PC-3 cells.Western blot analysis was em-ployed to show the effects of progesterone and mifepristone on phosphorylation of extracellular signal-regula-ted kinase 1/2 (ERK1/2) in PC-3 cells. Results After 7-d culture, the cell proliferation were signifi-cantly different between normal culture group and drug treatment group (P0.05).The cell number was(1.9±0.2)×105,(3.2±0.3)×105and (1.3±0.2)×105,respectively,in normal culture group,proges-terone (100 nmol/L) group and mifepristone (10μmol/L) group.RT-PCR showed obvious expression ofprogesterone receptor mRNA in PC-3 cells.Western blot showed that phosphorylated (activated) form ofERK1/2 was improved shortly after progesterone added to PC-3 cells.This effect was blocked by mifepristone(10μmol/L) added 1 h before progesterone stimulation.The intensity of p-ERK1/2 band in progesteroneand mifepristone groups was 70752±16377 and 12493±3478,respectively (P0.05). Conclusions Progesterone can improve PC-3 cell proliferation by activation of ERK1/2 pathway;mifepristone can inhibitPC-3 cell proliferation by blockage of progesterone effects on ERK1/2 activation.