ArticleSignal transduction and targeted therapy2020
Hypoxia-induced GBE1 expression promotes tumor progression through metabolic reprogramming in lung adenocarcinoma.
Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 112 citations in OpenAlex.
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- Identification of Genes and Construction of Prognostic Model of Lung Adenocarcinoma Based on Propionate Metabolism-Related Genes.World journal of oncology · 2026Article
- circ-UBR5 in hypoxia-induced exosomes may mediate lung adenocarcinoma metastasis via the targeting of HNRNPR.Translational lung cancer research · 2026Article
- Idiopathic Pulmonary Fibrosis: Analysis of Predisposing Variants in Patients with Familial Forms.Biomedicines · 2026Article
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Metabolic reprogramming and immune evasion interaction in the tumor microenvironment promote tumor progression.Frontiers in oncology · 2026Review
- Body mass index and fasting insulin predict survival and EGFR-TKI benefit in Stage IV lung adenocarcinoma.Frontiers in oncology · 2026Article
- Exosomes in cancer metabolism and drug resistance: A review.Biomolecules & biomedicine · 2025Review
- Hypoxia-induced histone lactylation promotes pulmonary arterial smooth muscle cells proliferation in pulmonary hypertension.Molecular and cellular biochemistry · 2025Article
- Metabolic Plasticity and Cancer Stem Cell Metabolism: Exploring the Glycolysis-OXPHOS Switch as a Mechanism for Resistance and Tumorigenesis.Stem cell reviews and reports · 2025Review
- The origin patterns, admixture, and selection signatures of the global gamecock populations.Poultry science · 2025Article
- SIRT7 drives energy metabolic shifts in endometriosis via interaction with TUFM and Rhoa/Rock/Akt pathway activation.Cellular and molecular life sciences : CMLS · 2025Article
- Prediction of Lung Cancer Metastasis Risk Based on Single-Cell Metabolic Profiling of Circulating Tumor Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Tumor hypoxia: Classification, detection, and its critical role in cancer progression.Biomolecules & biomedicine · 2025Review
- Salmonella Typhi gut invasion drives hypoxic immune subsets associated with disease outcomes.Nature communications · 2025Article
- Machine learning-based integration develops a hypoxia-derived signature for improving outcomes in glioma.iScience · 2025Article
- The Emerging Roles of Metabolic Reprogramming in Non-Small Cell Lung Cancer Progression.Frontiers in bioscience (Landmark edition) · 2025Review
- LncRNAs in hypoxic microenvironment; insight in their impact in cancer biology.Functional & integrative genomics · 2025Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia mediates a metabolic switch from oxidative phosphorylation to glycolysis and increases glycogen synthesis. We previously found that glycogen branching enzyme (GBE1) is downstream of the hypoxia-inducible factor-1 (HIF1) signaling pathway in lung adenocarcinoma (LUAD) cells; however, the molecular mechanism underlying HIF1 regulation of GBE1 expression remains unknown. Herein, the effect of GBE1 on tumor progression via changes in metabolic signaling under hypoxia in vitro and in vivo was evaluated, and GBE1-related genes from human specimens and data sets were analyzed. Hypoxia induced GBE1 upregulation in LUAD cells. GBE1-knockdown A549 cells showed impaired cell proliferation, clone formation, cell migration and invasion, angiogenesis, tumor growth, and metastasis. GBE1 mediated the metabolic reprogramming of LUAD cells. The expression of gluconeogenesis pathway molecules, especially fructose-1,6-bisphosphatase (FBP1), was markedly higher in shGBE1 A549 cells than it was in the control cells. FBP1 inhibited the tumor progression of LUAD. GBE1-mediated FBP1 suppression via promoter methylation enhanced HIF1α levels through NF-κB signaling. GBE1 may be a negative prognostic biomarker for LUAD patients. Altogether, hypoxia-induced HIF1α mediated GBE1 upregulation, suppressing FBP1 expression by promoter methylation via NF-κB signaling in LUAD cells. FBP1 blockade upregulated HIF1α, triggered the switch to anaerobic glycolysis, and enhanced glucose uptake. Therefore, targeting HIF1α/GBE1/NF-κB/FBP1 signaling may be a potential therapeutic strategy for LUAD.
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