Anthony Williams, PhD

Washington University in St. Louis (WU)

The development of androgen receptor (AR)-targeted drug resistance in prostate cancer (PC) remains therapeutically challenging, and mechanisms of resistance owing to this challenge are likely to involve both AR-dependent and -independent signaling nodes. Genomic analyses performed by our group in ARSI-resistant PC cells reveals FOXP1, a transcription factor and tumor suppressor that negatively regulates AR signaling, as a dysregulated gene in this context. Loss of FOXP1 expression has been associated with poor survival in PC, and interestingly, an increased risk of aggressive PC disease particularly for African-American men. Through a comprehensive investigation of FOXP1-mediated biology in PC, the overarching objectives of our studies are to: 1) delineate the basis of irregular FOXP1 biology for AR-dependent and -independent transcriptional programming, 2) discover new drug targets that mitigate FOXP1 loss-mediated behavior, and 3) determine the extent to which FOXP1 loss drives ethnicity-dependent, aggressive PC.