作者
CheukMan C. Au,Seaho Kim,Prerna Vatsa,Mohd Azrin Bin Jamalruddin,Michael Miller,Peter T. Meinke,Paraskevi Giannakakou
摘要
Abstract Castration resistance prostate cancer (CRPC) is a lethal disease in which the expression of ligand-independent androgen receptor (AR) splice variants (AR-Vs) is associated with worse clinical outcomes. AR-V7 is the most prevalent variant in CRPC, it lacks the ligand binding domain and is constitutively active in the nucleus. We and others have showed that, AR-V7 expression confers resistance to the AR signaling inhibitors (abiraterone/enzalutamide) and to taxanes in vivo and in patients with metastatic CRPC. Since abiraterone/enzalutamide and taxanes represent the two most effective therapeutic modalities for men with CRPC, the development of selective AR-V7 inhibitors is a high priority, clinically unmet need. AR-V7 shares with full-length AR (AR-fl), high sequence homology, largely overlapping cistromes and gene transactivation profiles. To develop selective AR-V7 inhibitors, we sought to identify unique biological features of AR-V7, that differentiate it from AR-fl and therapeutically exploit them. Mechanistic studies showed that AR-V7 utilizes a unique nuclear import pathway, not shared by AR-fl. Using fluorescently tagged-AR-fl or AR-V7 proteins in conjunction with live cell imaging, FRAP assays and pathway inhibitors, we showed that AR-V7 exhibits fast nuclear import kinetics partially mediated by the dimerization D-box domain, independently of microtubules and importin α/β. Taken together, these data suggest that AR-V7 nuclear import mechanism is distinct providing a window of therapeutic opportunity to selectively target it. To identify AR-V7 selective inhibitors, we designed and performed a high throughput enzyme complementation screening (HTS) assay using nuclear AR-V7 as a surrogate for AR-V7 activity. We screened a chemical library of ~170K compounds and identified hit compounds inhibiting AR-V7 by proteasomal degradation. Among the degraders, we observed 2 main modes of action: I. compounds selectively degrading AR-V7 and II. compounds degrading both AR-fl and AR-V7. Ongoing efforts include medicinal chemistry for lead compound optimization and target validation experiments.In conclusion, we identified first-in-class selective AR-V7 inhibitors, with the potential to be clinically combined with existing, but mechanistically unrelated AR signaling inhibitors. Further mechanistic studies will elucidate their potential for future clinical development. Citation Format: CheukMan Cherie Au, Seaho Kim, Prerna Vatsa, Mohd Azrin Bin Jamalruddin, Michael Miller, Peter T. Meinke, Paraskevi Giannakakou. Development of selective small molecule AR-V7 inhibitors for prostate cancer treatment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3946.