KU60019 induced ATM blockage regulates GPR91/has-miR-576-3p to inhibit ovarian cancer progression

Abstract

Abstract Ataxia telangiectasia mutated (ATM) protein play a key role in the DNA damage response and sustain genomic stability, targeting which has been widely studied in different types of cancer as a potential therapeutic strategy for antitumor therapies. However, the mechanism of targeting ATM in ovarian cancer has not been fully elaborated. In the current study, we explore the influence of GPR91 on ovarian cancer cells in the context of ATM blockage in vitro. We identified that GPR91 might be a potential target of miR-576-3p in ovarian cancer cells upon KU60019 treatment. KU60019 induced cell apoptosis by downregulating GPR91 level. Inhibition of miR-576-3p reversed KU60019 induced cell apoptosis by upregulating GPR91 in vitro. Our results revealed cellular and molecular pathways in KU60019 induced cell death as well as identified a novel potential target for antitumor research.