Prostate cancer (PCa) is the most frequently diagnosed malignancies among men worldwide and the second leading cause of cancer related deaths in the United States. Cancer is a multifaceted condition in which a cell begins dividing in an irregular manner due to various factors including mutations in genes. Our lab recently demonstrated that JunD plays an essential role in the proliferation of PCa cells and genes involved in cell cycle progression. In this study, utilizing genomic and proteomic analyses, we identified several JunD dependent genes involved in cell proliferation with c-MYC as the key downstream regulator. We further investigated whether c-MYC is required for JunD-mediated proliferation by targeting c-MYC protein in cells overexpressing JunD (D1). DU145 and D1 cells were treated in the presence or absence of JQ1, a c-MYC inhibitor, at specific time points. c-MYC inhibition by JQ1 resulted in a decrease in cell proliferation, cell cycle arrest in the G1 phase concomitant with a decrease in several JunD dependent genes. Our data suggests there is an effective approach to block prostate carcinogenesis by inhibiting JunD dependent cell cycle genes.
