Prostate cancer (PCa) is the most commonly diagnosed cancer and the second leading cause of cancer deaths in American men. PCa begin to form when healthy prostate cells undergo mutations in various genes that regulate the cell cycle. Our lab recently demonstrated that JunD, a transcription factor, controls cell proliferation of PCa cells and JunD-dependent genes required for cell cycle regulation. We also showed that JunD-mediated cell proliferation is mediated through cMYC, an oncogene and a critical player in cell cycle regulation. Many of JunD-dependent genes act upstream and downstream of c-MYC. In this present study, we investigated the effect of c-MYC inhibition on JunD-mediated cell proliferation, cell cycle regulation, and on JunD-dependent genes’ protein levels in PCa cells. JunD overexpressing cells (D1) and DU145 control cells were treated with c-MYC siRNA or control siRNA for 72 hrs. We analyzed cell proliferation using manual cell counting, cell cycle analysis using Flow Cytometry, and the protein levels of JunD-dependent genes using western blot analysis. Based on our results, JunD is a key regulator of cell cycle progression and is mediated through c-MYC signaling pathway. Understanding these mechanisms involved in PCa initiation may provide discoveries of therapeutics to combat this disease.
