Inhibition of Endoplasmic Reticulum Stress Cooperates with SLC7A11 to Promote Disulfidptosis and Suppress Tumor Growth upon Glucose Limitation.

ABSTRACT: Disulfidptosis is a newly discovered type of regulated cell death triggered by disulfide bond accumulation and NADPH (nicotinamide adenine dinucleotide phosphate) depletion due to glucose deprivation. However, the regulatory mechanisms involving additional cellular circuits remain unclear. Excessive disulfide bond accumulation can impair endoplasmic reticulum (ER) homeostasis and activate the ER stress response. In this study, we found that SLC7A11-mediated disulfidptosis upon glucose deprivation is accompanied by ER stress induction. Pharmacological inhibition of SLC7A11-mediated cystine uptake or cystine withdrawal not only blocks disulfidptosis under glucose starvation but also suppresses the ER stress response, indicating a close link between these processes. Moreover, inhibitors targe

SUBMITTER: Wang J 

PROVIDER: S-EPMC11831432 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature