Fig. 8

Silencing of PES1 inhibits the progression of prostate cancer in vivo and in vitro by activating the ERβ signaling pathway. The cells were transfected with both si-PES1 and DMSO or both si-PES1 and PHTPP. a mRNA and protein expression of PES1, ERα and ERβ in PC-3 cells detected by RT-qPCR and Western blot analysis. b Images of EdU assay (200×), positive rate of cells and the expression of Ki67 and PCNA in PC-3 cells determined using EdU assay and Western blot analysis. c PC-3 cell apoptosis and protein expression of c-caspase-3/caspase-3 and c-caspase-9/caspase-9 in PC-3 cells tested by flow cytometry and Western blot analysis. d Images (200×) and quantitative analysis of cell migration and invasion and protein expression of MMP-2 and MMP-9 in PC-3 cells evaluated by Transwell assay and Western blot analysis. e mRNA and protein expression of PES1, ERα and ERβ in mouse tumors detected by RT-qPCR and Western blot analysis. f Representative tumors and tumor growth rate of mice bearing human prostate cancer cell xenografts in response to co-treatment of sh-PES1 and DMSO or co-treatment of sh-PES1 and PHTPP (n = 6 for each group). *p < 0.05, vs. co-treatment of sh-NC and DMSO or co-treatment of sh-NC and DMSO; #p < 0.05, vs. co-treatment of sh-PES1 and DMSO or co-treatment of sh-PES1 and DMSO. Data obtained from three independent experiments were presented as mean ± standard deviation and tested using one-way ANOVA among multiple groups. Tumor size over indicated time points was compared using two-way ANOVA