Background: prostatic cancer antigen 3 was firstly identified the DD3 (later called PCA3) gene, functioning as non-coding RNA.Using a reverse transcriptase polymerase chain reaction (RT-PCR) method, they detected that PCA3 was overexpressed in cancerous tissue and low expressed in benign prostatic tissue and not measurable in the normal tissue of numerous organs such as the testis, bladder, kidney, seminal vesicles, brain and lung. PCA3 is highly prostate specific and was overexpressed in 95 % of tumor lesions, but in only 1 of 7 human PCa cell lines (lymph node carcinoma of the prostate) and in none of 18 non-malignant prostate samples. A multitude of studies further implicated significantly higher PCA3-mRNA expression in prostatic tumors in comparison to non-malignant prostatic tissue. These findings promoted the idea of developing a PCA3 diagnostic test. It was reported that transient knockdown of PCA3 transcripts reduced cell growth and viability, in addition to inducing apoptotic cell death .These data reinforced the hypothesis that PCA3 could modulate PCa cell survival. It was also reported an association between PCA3 and the androgen-receptor (AR) signaling pathway,and it was found that cells treated with AR agonist dihydrotestosterone (DHT) induced significant upregulation of PCA3 expression, which was reversed by AR antagonist flutamide. In addition, it was also observed upregulation of androgen-responsive genes (ARGs) (TMPRSS2, NDRG1, GREB1, PSA, AR, FGF8, CdK1, CdK2, and PMEPA1) in response to DHT treatment. Interestingly, these findings were reversed when silencing PCA3 using RNA interference