Abstract
Objective: PEO1 epithelial ovarian cancer (EOC) cells contain a mutated BRCA2 gene, a tumor suppressor gene that functions to repair DNA double-strand breaks (DSBs) through the homologous recombination (HR) repair pathway. While this type of cancer has been treated by poly(ADP-ribose) polymerase (PARP) inhibitors, such as olaparib, novel targets are needed to develop therapeutic strategies to enhance the efficacy of these inhibitors. Our objective was to investigate the role of AKT signaling and nonhomologous end joining (NHEJ) repair pathways in promoting the survival of BRCA2-mutated EOC cells following olaparib-induced DNA damage.
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