ArticleOncogenesis2024
Tumor suppressor BAP1 suppresses disulfidptosis through the regulation of SLC7A11 and NADPH levels.
Article in Oncogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed.
- OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.Cell cycle (Georgetown, Tex.) · 2026Article
- TWF1 inhibition overcomes cisplatin resistance in NSCLC by inducing ferroptosis via p53-dependent SLC7A11 repression and autophagy-mediated glutathione metabolism reprogramming.Cancer gene therapy · 2026Article
- Dual Compartmentalization of GSTA4 Suppresses Ferroptosis to Drive Antiandrogen Resistance in Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The SLC7A11 Thermostat: A Molecular Signaling Switch Between Ferroptosis and Disulfidptosis in Neurodegenerative Disease.Molecular neurobiology · 2026Review
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- Metabolic cell death: ferroptosis, cuproptosis, and disulfidptosis as a unified framework for targeting metabolic vulnerabilities in disease.Apoptosis : an international journal on programmed cell death · 2026Review
- Harnessing disulfidptosis-ferroptosis synergy to potentiate radiotherapy in triple-negative breast cancer.Mikrochimica acta · 2026Article
- The emerging role of disulfidptosis in metabolic synergistic death and cancer immunotherapy.Oncogenesis · 2026Review
- Disulfidptosis-related gene DSTN predicts prognosis and promotes malignant progression in head and neck squamous cell carcinoma.Molecular and cellular biochemistry · 2026Article
- Epigenetic regulation of ACSL4 via H2A monoubiquitylation connects lipid metabolism to BAP1-mediated ferroptosis.Cell death and differentiation · 2026Article
- Disulfidptosis in hepatocellular carcinoma: molecular mechanisms, therapeutic potential, and exploratory insights into chronic liver diseases.Apoptosis : an international journal on programmed cell death · 2026Review
- Disulfidptosis vs. Ferroptosis: A Comprehensive Review of SLC7A11-Mediated Metal Dyshomeostasis and Cell Death.Biomolecules · 2026Review
- The Mechanism and Regulation of Disulfidptosis and Its Role in Disease.Biomedicines · 2026Review
- Enhancing cancer susceptibility to disulfidptosis by inducing cell cycle arrest and impairing DNA repair.Theranostics · 2026Article
- Integrative oxidative stress-disulfidptosis analysis identifiesFrontiers in molecular biosciences · 2026Article
- Exploiting metabolic cell death for cancer therapy.Nature reviews. Cancer · 2026Review
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Unveiling the metal-driven death: ferroptosis and cuproptosis in leukemia.European journal of medical research · 2025Review
- Metabolic cell deaths in head and neck cancer: mechanisms, therapeutic potential, and challenges.Annals of medicine · 2025Review
- Comprehensive analysis of disulfidoptosis-related genes reveals molecular heterogeneity and key regulators in retinoblastoma progression.Translational pediatrics · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
BAP1, BRCA1-Associated Protein 1, serves as a novel tumor suppressor through the deubiquitination of monoubiquitination of H2A and subsequent gene transcriptional regulation. Regulated cell death like apoptosis or ferroptosis is considered an essential mechanism mediating tumor suppression. Previous reports, including ours, have demonstrated that BAP1 could promote apoptosis and ferroptosis to inhibit tumor development. Whether BAP1 regulated additional types of cell death remains unclear. Disulfidptosis is a recently identified novel cell death mode characterized by aberrant accumulation of intracellular disulfide (e.g., cystine) and depletion of NADPH. In this study, we first demonstrated that BAP1 could significantly protect disulfidptosis induced by glucose starvation, which is validated by various cell death inhibitors and the accumulation of disulfide bonds in the cytoskeleton proteins. BAP1 is known to inhibit SLC7A11 expression. We found that the protective effect of BAP1 against disulfidptosis was counteracted when overexpressing SLC7A11 or adding additional cystine. Conversely, BAP1-mediated suppression of disulfidptosis was largely abrogated when SLC7A11-mediated cystine uptake was inhibited by the knockout of SLC7A11 or erastin treatment. Besides, high BAP1 expression showed lower NADP
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.