Prostate cancer is a common cause of death among men. Current treatment includes hormone therapy that targets the androgen receptor (AR). The AR promotes the growth of prostate cancer. Unfortunately, prostate cancer cells remain resistant to current therapy. This is partly due to the formation of active forms of AR. We need to understand how active forms of AR arise. Thus, we can discover therapies that will not become resistant to treatment. The JMJD1A protein plays an important role in this process. In this study we will look at how JMJD1A promotes the generation of active AR forms. JMJD1A may regulate several other proteins (e.g. HUWE1, c-Myc and HNRNPA1) to do this. We will block the expression of these proteins to see if prostate cancer cells become sensitive to hormone therapy. Our experiments include cell culture and mouse tumor models. Our study will stimulate the interest to develop inhibitors that block the activity of JMJD1A or the proteins it regulates. The inhibitors will serve as effective therapies for prostate cancer.
Location: University of Maryland School of Medicine Greenebaum Cancer Center - MD
Proposal: JMJD√A promotes the activity of androgen receptor splice variants in castration-resistant prostate cancer