Abstract

Prostate cancer is one of the leading causes of cancer related deaths in men worldwide. Recently, it has been determined that epigenetics, a stage of regulation of gene expression consisting of modifications of chromatin and histone tails, could be playing a role in prostate cancer formation and progression. In this study, we have investigated the effect of decitabine on the control of Secretoglobin (SCGB3A1) and the SAP/JNK kinase that are critical for the pathogenesis of prostate cancer in PC-3 and LNCaP prostate cell lines. We demonstrated that decitabine reactivates the SCGB3A1 gene in both LNCaP and PC3 prostate cancer cell lines. The effect of decitabine on JNK-1 and JNK-2 expression in prostate resistant PC-3 cells p53 negative which contrasts to the p53 positive LNCaP cells showed that JNK-1 and JNK-2 mRNA levels were significantly increased in PC-3 cells following treatment with 1, 3, 6 and 9 μM decitabine. However, the increase in LNCaP cells was only marginal compared with PC-3. In addition, DNA methyltransferase (DNMT) activity was decreased after decitabine treatment in both, LNCaP and PC-3 cell lines. The sum of results obtained suggests that Decitabine treatments can induce regression of the features of prostatic adenocarcinoma and targeting epigenetic mechanisms represents a novel strategy in anticancer therapy.