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Model depicting the mechanism by which selective targeting of PARP-2 attenuates AR signaling and inhibits PCa growth. PARP-2 enhances AR transcriptional activity via physically interacting with the pioneer factor FOXA1. Selective PARP-2 inhibitor UPF-1069 blocks this interaction, diminishes the genomic occupancies of FOXA1 and H3K27Ac at AR binding sites, and, thereby, inhibits AR-mediated gene expression and PCa growth.
