ArticleNature communications2024
Hexosaminidase B-driven cancer cell-macrophage co-dependency promotes glycolysis addiction and tumorigenesis in glioblastoma.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed.
- Lipocalin 2 promotes papillary thyroid cancer progression through activation of glycolysis via Hippo/YAP1/HIF1α axis.Journal of endocrinological investigation · 2026Article
- Aging disrupts spatiotemporal coordination in the cycling murine ovary.Nature aging · 2026Article
- Microglia-specificity of different markers is overridden in glioblastoma specimens.Scientific reports · 2026Article
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Metabolic profiling defines glioblastoma subtypes with distinct prognoses and therapeutic vulnerabilities.Neuro-oncology · 2026Article
- Prognostic value of palmitoylation-regulated mechanisms in glioblastoma: integrated multi-omics analysis via least absolute shrinkage and selection operator (LASSO) regression and single-cell sequencing.Translational cancer research · 2026Article
- Lactate transmission from hypoxic tumor cells promotes macrophage senescence and M2 polarization via the DNMT1-NHE7 axis to accelerate endometrial cancer progression.Cell death & disease · 2026Article
- Current Pharmacotherapeutic Strategies in Diffuse Gliomas: Focus on Glioblastoma, IDH-Wildtype, and Emerging Targeted Therapies for IDH-Mutant Tumors.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Spatiotemporal and metabolic heterogeneity of tumor-associated macrophages in glioblastoma: from single-cell insights to therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Mn-MIL-100@AKG alleviates intervertebral disc degeneration by regulating mitophagy.Materials today. Bio · 2025Article
- Therapeutic potential of targeting macrophages and microglia in glioblastoma.Trends in pharmacological sciences · 2025Review
- scCOSMIX: A Mixed-Effects Framework for Differential Coexpression and Transcriptional Interactions Modeling in Single-Cell RNA-Seq.Statistics in medicine · 2025Article
- ncRNA-mediated ITGB1 upregulation correlates with poor prognosis and tumor-immune infiltration in gastric cancer.European journal of medical research · 2025Article
- Proteomic analysis of Buffalo milk somatic cells reveals metabolomic and immunological transitions during early lactation.Scientific reports · 2025Article
- Glycosylation Gene Signatures as Prognostic Biomarkers in Glioblastoma.Annals of clinical and translational neurology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Glycolytic metabolic reprogramming in cancer is regulated by both cancer intrinsic variations like isocitrate dehydrogenase 1 (IDH1) status and non-cancerous microenvironment components like tumor associated macrophages (TAMs). However, the detailed mechanism remains elusive. Here, we identify hexosaminidase B (HEXB) as a key regulator for glycolysis in glioblastoma (GBM). HEXB intercellularly manipulates TAMs to promote glycolysis in GBM cells, while intrinsically enhancing cancer cell glycolysis. Mechanistically, HEXB elevation augments tumor HIF1α protein stability through activating ITGB1/ILK/YAP1; Subsequently, HIF1α promotes HEXB and multiple glycolytic gene transcription in GBM cells. Genetic ablation and pharmacological inhibition of HEXB elicits substantial therapeutic effects in preclinical GBM models, while targeting HEXB doesn't induce significant reduction in IDH1 mutant glioma and inhibiting IDH1 mutation-derived 2-hydroxyglutaric acid (2-HG) significantly restores HEXB expression in glioma cells. Our work highlights a HEXB driven TAMs-associated glycolysis-promoting network in GBM and provides clues for developing more effective therapies against it.
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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 OpenQuestion graph.