ArticleJournal of experimental & clinical cancer research : CR2022
UBR7 inhibits HCC tumorigenesis by targeting Keap1/Nrf2/Bach1/HK2 and glycolysis.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 69 citations in OpenAlex.
- Epigenetic Factor Dysregulation and Distinct Expression Signatures in Retinoblastoma: A Transcriptomic Analysis.Investigative ophthalmology & visual science · 2026Article
- Ubiquitination and NOncology letters · 2026Review
- BACH1 stabilization by antioxidants facilitates hepatocellular carcinoma metastasis.Cell death & disease · 2026Article
- OTUD4 regulates pancreatic cancer progression via Hippo/YAP axis.Neoplasia (New York, N.Y.) · 2026Article
- TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SERPINA4 facilitates colorectal cancer progression through m⁶A-dependent stabilization.Journal of translational medicine · 2026Article
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- Bidirectional regulation of the ubiquitin-RNA modification axis in cancer.Frontiers in oncology · 2026Review
- Comparative Efficacy of Triamcinolone versus Dexamethasone in Local Injection for Stenosing Tenosynovitis of the Metacarpophalangeal Joint: A Retrospective Cohort Study.Drug design, development and therapy · 2026Article
- Glycolytic reprogramming in cancer: immune crosstalk, nutrient competition, and supportive care perspectives.Frontiers in immunology · 2026Review
- IGF2BP1 orchestrates glycolytic reprogramming via HK2 to accelerate hepatocellular carcinoma malignancy.American journal of cancer research · 2026Article
- mFrontiers in cell and developmental biology · 2026Review
- Baicalin suppresses colorectal cancer proliferation and induces M1 polarization of tumor-associated macrophages by promoting proteasomal degradation of HK2.Frontiers in immunology · 2026Article
- The dual roles of ferroptosis in digestive tract tumors: mechanisms, microenvironment regulation, and therapeutic integration with emphasis on immune interactions.Frontiers in immunology · 2026Review
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- The NRF2 signaling pathway in hepatocellular carcinoma: dual roles, epigenetic reprogramming, and therapeutic opportunities in metabolic vulnerability.Frontiers in oncology · 2026Review
- ALKBH5 deficiency suppresses hepatocarcinogenesis in mice via mActa pharmacologica Sinica · 2026Article
- Demethoxycurcumin suppresses HK2-mediated glycolysis by targeting PTEN/Akt signaling.Cancer gene therapy · 2025Article
- Hyperosmolarity-Induced Oxidative Stress Leads to Senescence in Human Corneal Epithelial Cells (HCEPC) via DNA Damage, Metabolic Disturbance and Mitophagy Decline.Antioxidants (Basel, Switzerland) · 2025Article
- The upregulation of GDF15 is controlled epigenetically by oncogenic TCF19 signaling in human hepatocellular carcinoma.iScience · 2025Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundGlycolysis metabolism is an attractive target for cancer therapy. Reprogramming metabolic pathways could improve the ability of metabolic inhibitors to suppress cancers with limited treatment options. The ubiquitin-proteasome system facilitates the turnover of most intracellular proteins with E3 ligase conferring the target selection and specificity. Ubiquitin protein ligase E3 component N-recognin 7 (UBR7), among the least studied E3 ligases, recognizes its substrate through a plant homeodomain (PHD) finger. Here, we bring into focus on its suppressive role in glycolysis and HCC tumorigenesis, dependent on its E3 ubiquitin ligase activity toward monoubiquitination of histone H2B at lysine 120 (H2BK120ub).
methodsIn this study, we carried out high-throughput RNAi screening to identify epigenetic candidates in regulating lactic acid and investigated its possible roles in HCC progression.
resultsUBR7 loss promotes HCC tumorigenesis both in vitro and in vivo. UBR7 inhibits glycolysis by indirectly suppressing HK2 expression, a downstream target of Nrf2/Bach1 axis. Mechanically, UBR7 regulates H2BK120ub to bind to Keap1 promoter through H2BK120ub monoubiquitination, thereby modulating Keap1 expression and downstream Nrf2/Bach1/HK2 signaling. Pharmaceutical and genetic inhibition of glycolytic enzymes attenuate the promoting effect of UBR7 deficiency on tumor growth. In addition, methyltransferase ALKBH5, downregulated in HCC, regulated UBR7 expression in an m6A-dependent manner.
conclusionsThese results collectively establish UBR7 as a critical negative regulator of aerobic glycolysis and HCC tumorigenesis through regulation of the Keap1/Nrf2/Bach1/HK2 axis, providing a potential clinical and therapeutic target for the HCC treatment.
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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 OpenQuestion graph.