Homologous-recombination (HR)-dependent repair defective cells are hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors. Combinations of defective HR pathway and PARP inhibitors have been an effective chemotherapy strategy. We previously showed that knockdown of the WD40-repeat containing protein, Uaf1, is HR repair defect in mouse embryo fibroblast cells and is sensitive to ABT-888, a chemotherapy drug commonly used for inhibiting PARP. Consistent with the HR defective mouse genetic study, here, we show that ferulic acid inhibits Rad 51 foci formation and accumulates γ-H2AX in breast cancer cells. Ferulic acid treatment reduces HR repair and causes breast cancer cells to become hypersensitive to ABT-888 treatment. Our study indicates that ferulic acid with PARP inhibitor treatment may be useful for the combination chemotherapy as a natural bioactive compound.

Citation Format: Eunmi Park, Hyuna Lee. Ferulic acid as a natural bioactive compound enhances PARP inhibitor sensitivity in breast cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1338.