Ferulic acid in combination with PARP inhibitor sensitizes breast cancer cells as chemotherapeutic strategy.

Abstract	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 chemotherapeutic modality. We previously showed that knockdown of the WD40-repeat containing protein, Uaf1, causes an HR repair defect in mouse embryo fibroblast cells and therefore, increases sensitivity to PARP inhibitor, ABT-888. Similarly, here, we show that ferulic acid reduces HR repair, inhibits RAD 51 foci formation, and accumulates γ-H2AX in breast cancer cells. Moreover, ferulic acid, when combined with ABT-888, renders breast cancer cells become hypersensitive to ABT-888. Our study indicates that ferulic acid in combination with ABT-888 treatment may serve as an effective combination chemotherapeutic agent as a natural bioactive compound.
Authors	Young Eun Choi, Eunmi Park
Journal	Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 458 Issue 3 Pg. 520-524 (Mar 13 2015) ISSN: 1090-2104 [Electronic] United States
PMID	25677620 (Publication Type: Journal Article)
Copyright	Copyright © 2015 Elsevier Inc. All rights reserved.
Chemical References	Antineoplastic Agents Antioxidants Benzimidazoles Coumaric Acids Enzyme Inhibitors Poly(ADP-ribose) Polymerase Inhibitors veliparib ferulic acid Poly(ADP-ribose) Polymerases Rad51 Recombinase
Topics	Antineoplastic Agents (administration & dosage, pharmacology) Antineoplastic Combined Chemotherapy Protocols Antioxidants (administration & dosage, pharmacology) Benzimidazoles (administration & dosage, pharmacology) Breast (drug effects, metabolism, pathology) Breast Neoplasms (drug therapy, genetics, metabolism, pathology) Cell Line, Tumor Coumaric Acids (administration & dosage, pharmacology) DNA Damage (drug effects) Enzyme Inhibitors (administration & dosage, pharmacology) Female Humans Poly(ADP-ribose) Polymerase Inhibitors Poly(ADP-ribose) Polymerases (metabolism) Rad51 Recombinase (metabolism) Recombinational DNA Repair (drug effects)

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