ArticleMolecular cancer research : MCR2014
Glucose-6-phosphatase is a key metabolic regulator of glioblastoma invasion.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
52 citing papers in PubMed, 79 citations in OpenAlex.
- A FOXO1-G6PC transcriptional axis restrains renal cell carcinoma progression: multi-omics, epigenetic, and mechanistic evidence.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Article
- The glucose-6-phosphatase system in cancer: from endoplasmic reticulum glucose-6-phosphate flux to stemness, immune escape, and therapeutic vulnerability.Frontiers in oncology · 2026Review
- Disulfidptosis in tumor progression.Cell death discovery · 2025Review
- G6PC1 expression as a prognostic biomarker associated with metabolic reprogramming and tumor microenvironment in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Revealing propionate metabolism-related genes in glioblastoma and investigating their underlying mechanisms.Frontiers in oncology · 2025Article
- Identifying G6PC3 as a Potential Key Molecule in Hypoxic Glucose Metabolism of Glioblastoma Derived from the Depiction ofBioMed research international · 2024Article
- Multiomic screening of invasive GBM cells reveals targetable transsulfuration pathway alterations.The Journal of clinical investigation · 2023Article
- The disulfidptosis-related signature predicts prognosis and immune features in glioma patients.Scientific reports · 2023Article
- Emerging roles of cytosolic phosphoenolpyruvate kinase 1 (PCK1) in cancer.Biochemistry and biophysics reports · 2023Review
- Perivascular invasion of primary human glioblastoma cells in organotypic human brain slices: human cells migrating in human brain.Journal of neuro-oncology · 2023Article
- MiR-494 induces metabolic changes through G6pc targeting and modulates sorafenib response in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- Integrated transcriptomics and metabolomics analysis reveals the biomolecular mechanisms associated to the antitumoral potential of a novel silver-based core@shell nanosystem.Mikrochimica acta · 2023Article
- Genetics of enzymatic dysfunctions in metabolic disorders and cancer.Frontiers in oncology · 2023Review
- A molecular signature for the G6PC3/SLC37A2/SLC37A4 interactors in glioblastoma disease progression and in the acquisition of a brain cancer stem cell phenotype.Frontiers in endocrinology · 2023Article
- G6PC indicated poor prognosis in cervical cancer and promoted cervical carcinogenesis in vitro and in vivo.Reproductive biology and endocrinology : RB&E · 2022Article
- [Glucose-6 phosphatase catalytic subunit inhibits the proliferation of liver cancer cells by inducing cell cycle arrest].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022Article
- Glucagon signaling via supraphysiologic GCGR can reduce cell viability without stimulating gluconeogenic gene expression in liver cancer cells.Cancer & metabolism · 2022Article
- Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma.International journal of molecular sciences · 2022Review
- Influence of supramarginal resection on survival outcomes after gross-total resection of IDH-wild-type glioblastoma.Journal of neurosurgery · 2022Observational
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledGlioblastoma (GBM) remains the most aggressive primary brain cancer in adults. Similar to other cancers, GBM cells undergo metabolic reprogramming to promote proliferation and survival. Glycolytic inhibition is widely used to target such reprogramming. However, the stability of glycolytic inhibition in GBM remains unclear especially in a hypoxic tumor microenvironment. In this study, it was determined that glucose-6-phosphatase (G6PC/G6Pase) expression is elevated in GBM when compared with normal brain. Human-derived brain tumor-initiating cells (BTIC) use this enzyme to counteract glycolytic inhibition induced by 2-deoxy-d-glucose (2DG) and sustain malignant progression. Downregulation of G6PC renders the majority of these cells unable to survive glycolytic inhibition, and promotes glycogen accumulation through the activation of glycogen synthase (GYS1) and inhibition of glycogen phosphorylase (PYGL). Moreover, BTICs that survive G6PC knockdown are less aggressive (reduced migration, invasion, proliferation, and increased astrocytic differentiation). Collectively, these findings establish G6PC as a key enzyme with promalignant functional consequences that has not been previously reported in GBM and identify it as a potential therapeutic target. IMPLICATIONS: This study is the first to demonstrate a functional relationship between the critical gluconeogenic and glycogenolytic enzyme G6PC with the metabolic adaptations during GBM invasion.
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