Regulating SLC7A11/GSH/GPX4 axis by glucose dyshomeostasis to simultaneously promote disulfidptosis, cuproptosis and ferroptosis.

ABSTRACT: As one of the key targets of tumor metabolic therapy, glucose dyshomeostasis by disrupting glucose metabolism possesses the potential to reverse therapeutic resistance of a variety of regulated cell deaths (RCDs), but the functional pathways are not fully revealed and employed. Herein, we demonstrate that the intervention on SLC7A11/GSH/GPX4 antioxidant axis by glucose dyshomeostasis can simultaneously promote disulfidptosis, cuproptosis and ferroptosis, which is verified by employing glucose oxidase (GOx)-modified copper-apigenin (CuAp) network nanoshuttles (CuAp@GOx NSs) in ovarian tumor therapy. Ap and GOx can jointly induce glucose dyshomeostasis respectively by inhibiting glucose transporter 1-mediated glucose uptake upstream, and consuming massive glucose downstream. As a result of g

SUBMITTER: Zhang M 

PROVIDER: S-EPMC12628065 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature