At specific loci, the histone methyltransferase enhancer of zeste homolog 2 (EZH2), a subunit of PRC2, catalyzes H3K27 trimethylation, leading to chromatin compaction and subsequently silencing of genes in prostate cancer . Abnormal functions of PcGs are one of the main factors involved in the initiation and progression phases in many cancers, including prostate cancer . EZH2 is highly overexpressed in prostate cancer and strongly associated with epigenetic silencing in cancer. EZH2 is so prominently involved in aggressive cell growth, metastasis, drug resistance and stem cell maintenance that it has become an attractive therapeutic target in prostate cancer [13–15]. Previous studies show that EZH2 up-regulation is correlated with H3K27me3 deregulation and poor-prognosis prostate tumor . The H3K27me3 repressive mark has been found on many gene promoters that are silenced , and genome-wide profiling studies of the H3K27me3 mark in metastatic and prostate cancer cells suggest a silencing function of EZH2 in prostate cancer [18, 19].