Abstract
Objective: BRCA mutations lead to defective homologous recombination (HR) repair that underpins the development and progression of epithelial ovarian cancer (EOC) and renders hypersensitivity to poly(ADP-ribose) polymerase (PARP) inhibitor and platinum therapy. The objective of this study was to investigate the mechanism by which defective HR repair perpetuated invasion and metastasis of EOC in vitro and in vivo, as well as its therapeutic implications.
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