ArticleNature communications2022
ATF4-dependent fructolysis fuels growth of glioblastoma multiforme.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- PCBP1 orchestrates amino acid metabolism burst during the naïve-to-primed pluripotency transition.Stem cell reports · 2026Article
- Transcription Factor ATF4 Deletion Reprograms Glucose Metabolism in Clear Cell Renal Cell Carcinoma.Cancers · 2026Article
- ATF4: Orchestrating Cellular Stress Adaptation, Metabolism, and Immune Regulation in Health and Disease.International journal of molecular sciences · 2026Review
- Elucidating the causal relationships between cerebrospinal fluid metabolites and glioblastoma insights from mendelian randomization study.Neurosurgical review · 2026Article
- Metabolic reprogramming is associated with symptomatic COVID-19: a serum proteomics and causal inference study identifying ALDOB and glycerol as candidate metabolic correlates.Frontiers in microbiology · 2026Article
- Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025Review
- TMEM166 negatively regulates unfolded protein response to affect hepatocellular carcinoma cell growth and sorafenib resistance.Cell death & disease · 2025Article
- ERK1-mediated GLYCTK2 phosphorylation promotes fructolysis to sustain glioblastoma survival under glucose deprivation.Cell death discovery · 2025Article
- Metabolic traits shape responses to LSD1-directed therapy in glioblastoma tumor-initiating cells.Science advances · 2025Article
- An Overview of Research Advances in Oncology Regarding the Transcription Factor ATF4.Current drug targets · 2025Review
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- Endoplasmic reticulum stress orchestrates tumor metabolism and immunity: new insights into immunometabolic therapeutics.Frontiers in immunology · 2025Review
- Metabolic reprogramming and epigenetic effects due to reducing sugars and glycation products in cancer.Frontiers in epigenetics and epigenomics · 2025Review
- Hyaluronic Acid Influences Amino Acid Metabolism via Differential L-Type Amino Acid Transporter 1 Expression in the U87-Malignant Glioma Cell Line.Advanced nanobiomed research · 2024Article
- GCN2 is a determinant of the response to WEE1 kinase inhibition in small-cell lung cancer.Cell reports · 2024Article
- ATF4 inhibits tumor development and mediates p-GCN2/ASNS upregulation in colon cancer.Scientific reports · 2024Article
- The Glucose Transporter 5 Enhances CAR-T Cell Metabolic Function and Anti-tumour Durability.Research square · 2024Article
- Article
- OGDH and Bcl-xL loss causes synthetic lethality in glioblastoma.JCI insight · 2024Article
- Activating transcription factor 4: a regulator of stress response in human cancers.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive consumption of fructose in the Western diet contributes to cancer development. However, it is still unclear how cancer cells coordinate glucose and fructose metabolism during tumor malignant progression. We demonstrate here that glioblastoma multiforme (GBM) cells switch their energy supply from glycolysis to fructolysis in response to glucose deprivation. Mechanistically, glucose deprivation induces expression of two essential fructolytic proteins GLUT5 and ALDOB through selectively activating translation of activating transcription factor 4 (ATF4). Functionally, genetic or pharmacological disruption of ATF4-dependent fructolysis significantly inhibits growth and colony formation of GBM cells in vitro and GBM growth in vivo. In addition, ATF4, GLUT5, and ALDOB levels positively correlate with each other in GBM specimens and are poor prognostic indicators in GBM patients. This work highlights ATF4-dependent fructolysis as a metabolic feature and a potential therapeutic target for GBM.
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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.