The possibility of developing the next generation of prostate cancer therapies, which are targeted at metabolism, is being explored by a University of Houston (UH) scientist and his team.
With approximately one out of six American men being diagnosed and nearly a quarter of a million new cases expected this year, prostate cancer is the most common malignancy among men in the U.S. Since prostate cancer relies on androgens for growth and survival, androgen ablation therapies are the standard of care for late-stage disease. While patients initially respond favorably to this course of treatment, most experience a relapse within two years, at which time limited treatment options exist. At this stage, known as castration-resistant prostate cancer, androgen-deprivation therapies are no longer effective, but interestingly, androgen receptor signaling is still active and plays a large role in the progression of the cancer. Because of this, both androgen receptors and the processes downstream of the receptor remain viable targets for therapeutic intervention. Unfortunately, it is unclear which specific downstream processes actually drive the disease and, therefore, what should be targeted.
Daniel Frigo, an assistant professor with the UH Center for Nuclear Receptors and Cell Signaling (CNRCS), has set his sights on a particular cascade of biochemical reactions inside the cell. Focusing specifically on an enzyme known as AMPK, which is considered a master regulator of metabolism, Frigo and his team have demonstrated that androgens have the capacity to take control of this enzyme's molecular signals.