ArticleCancer research2020
H2A Monoubiquitination Links Glucose Availability to Epigenetic Regulation of the Endoplasmic Reticulum Stress Response and Cancer Cell Death.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
- Identification of hsa-miR-144-3p as a novel immunotherapeutic target for glioblastoma based on disulfidptosis-related analysis.Discover oncology · 2026Article
- Enhanced WWP2 Exacerbates Podocyte Injury in Lupus Nephritis through Monoubiquitylating H2A at K119.International journal of biological sciences · 2026Article
- A disulfidptosis-related gene signature predicts prognosis and immune-metabolic landscape in multiple myeloma.British journal of haematology · 2025Article
- Radiotherapy promotes cuproptosis and synergizes with cuproptosis inducers to overcome tumor radioresistance.Cancer cell · 2025Article
- Molecular signatures of disulfidptosis: interplay with programmed cell death pathways and therapeutic implications in oncology.Cellular & molecular biology letters · 2025Review
- Review
- Inhibition of Endoplasmic Reticulum Stress Cooperates with SLC7A11 to Promote Disulfidptosis and Suppress Tumor Growth upon Glucose Limitation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Emerging roles of metabolic biomarkers in renal cell carcinoma: from molecular mechanisms to clinical implications.Frontiers in cell and developmental biology · 2025Review
- BRCA1-Mediated Dual Regulation of Ferroptosis Exposes a Vulnerability to GPX4 and PARP Co-Inhibition in BRCA1-Deficient Cancers.Cancer discovery · 2024Article
- Review
- LIMA1 links the E3 ubiquitin ligase RNF40 to lipid metabolism.Cell death discovery · 2024Article
- Unraveling ETC complex I function in ferroptosis reveals a potential ferroptosis-inducing therapeutic strategy for LKB1-deficient cancers.Molecular cell · 2024Article
- Cell cycle arrest induces lipid droplet formation and confers ferroptosis resistance.Nature communications · 2024Article
- Molecular landmarks of tumor disulfidptosis across cancer types to promote disulfidptosis-target therapy.Redox biology · 2023Article
- Article
- Disulfidptosis: a new form of regulated cell death for cancer treatment.Molecular biomedicine · 2023Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Epigenetic Modifications Induced by the Gut Microbiota May Result from What We Eat: Should We Talk aboutMetabolites · 2023Review
- Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis.Nature cell biology · 2023Article
- Identification of hepatocellular carcinoma subtypes based on PcG-related genes and biological relevance with cancer cells.Clinical epigenetics · 2022Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Epigenetic regulation of gene transcription has been shown to coordinate with nutrient availability, yet the mechanisms underlying this coordination remain incompletely understood. Here, we show that glucose starvation suppresses histone 2A K119 monoubiquitination (H2Aub), a histone modification that correlates with gene repression. Glucose starvation suppressed H2Aub levels independently of energy stress-mediated AMP-activated protein kinase activation and possibly through NADPH depletion and subsequent inhibition of BMI1, an integral component of polycomb-repressive complex 1 (PRC1) that catalyzes H2Aub on chromatin. Integrated transcriptomic and epigenomic analyses linked glucose starvation-mediated H2Aub repression to the activation of genes involved in the endoplasmic reticulum (ER) stress response. We further showed that this epigenetic mechanism has a role in glucose starvation-induced cell death and that pharmacologic inhibition of glucose transporter 1 and PRC1 synergistically promoted ER stress and suppressed tumor growth
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