Moniliformediquinone Induces In Vitro and In Vivo Antitumor Activity through Glutathione Involved DNA Damage Response and Mitochondrial Stress in Human Hormone Refractory Prostate Cancer

Abstract

Our data suggest that moniliformediquinone is a potential anticancer agent for hormone refractory metastatic prostate cancer by decreasing cellular glutathione, leading to a DNA damage response and cell cycle arrest at the S-phase. Mitochondrial stress also occurs due to moniliformediquinone action through loss of mitochondrial membrane potential and cytochrome c release, which in turn induce the activation of caspase cascades and apoptotic cell death.