ArticleJCI insight2020
GLUT5-mediated fructose utilization drives lung cancer growth by stimulating fatty acid synthesis and AMPK/mTORC1 signaling.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 102 citations in OpenAlex.
- Fibrillarin Resists Cellular Senescence Via SIRT1-Dependent Nicotinamide Metabolism and Its Inhibition Sensitizes Senolytic Therapy in Esophageal Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fructose induces PERK-dependent ER stress and mitochondrial dysfunction via nucleotide depletion in clear cell renal cell carcinoma.Cell death & disease · 2026Article
- Fructose: metabolic signal and modern hazard.Nature metabolism · 2026Review
- GLUT5-Mediated Disruption of the Gut-Testis Axis Deteriorates Olanzapine-Induced Testicular Fibrosis and is Ameliorated by Dapagliflozin.Drug design, development and therapy · 2026Article
- GLUT5-Driven Gut-Liver Axis Injury Mediating Olanzapine-Induced NAFLD and Dapagliflozin Intervention.Drug design, development and therapy · 2026Article
- Monocyte Preprogramming by Tobacco Carcinogens and Fructose Intake Accelerates Lung Cancer Progression via Metabolic and Epigenetic Pathways.International journal of biological sciences · 2026Article
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
- Role and mechanism of circ_001024 endogenous competition for miR-145-3p targeting to regulate GLUT5 in RCC.BMC cancer · 2025Article
- High fructose consumption aggravates inflammation by promoting effector T cell generation via inducing metabolic reprogramming.Signal transduction and targeted therapy · 2025Article
- Reversal of amino acid metabolism patterns between circulating blood and tumors as a new biomarker for the Zhengxu Xieshi syndrome in patients with esophageal squamous cell carcinoma.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Fructose metabolism and its roles in metabolic diseases, inflammatory diseases, and cancer.Molecular biomedicine · 2025Review
- Role of fructose in renal cell carcinoma progression.Discover oncology · 2025Article
- Polyol pathway-generated fructose is indispensable for growth and survival of non-small cell lung cancer.Cell death and differentiation · 2025Article
- Identification of IGF2BPs-related mRNA signature for predicting the overall survival of lung adenocarcinoma.Scientific reports · 2025Article
- Changes in tumor and cardiac metabolism upon immune checkpoint.Basic research in cardiology · 2025Review
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
- Metabolic reprogramming and epigenetic effects due to reducing sugars and glycation products in cancer.Frontiers in epigenetics and epigenomics · 2025Review
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- STC2+ Malignant Cell State Associated with EMT, Tumor Microenvironment Remodeling, and Poor Prognosis Revealed by Single-Cell and Spatial Transcriptomics in Colorectal Cancer.Oncology research · 2025Article
- Role of ATP citrate lyase and its complementary partner on fatty acid synthesis in gastric cancer.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer (LC) is a leading cause of cancer-related deaths worldwide. Its rapid growth requires hyperactive catabolism of principal metabolic fuels. It is unclear whether fructose, an abundant sugar in current diets, is essential for LC. We demonstrated that, under the condition of coexistence of metabolic fuels in the body, fructose was readily used by LC cells in vivo as a glucose alternative via upregulating GLUT5, a major fructose transporter encoded by solute carrier family 2 member 5 (SLC2A5). Metabolomic profiling coupled with isotope tracing demonstrated that incorporated fructose was catabolized to fuel fatty acid synthesis and palmitoleic acid generation in particular to expedite LC growth in vivo. Both in vitro and in vivo supplement of palmitoleic acid could restore impaired LC propagation caused by SLC2A5 deletion. Furthermore, molecular mechanism investigation revealed that GLUT5-mediated fructose utilization was required to suppress AMPK and consequently activate mTORC1 activity to promote LC growth. As such, pharmacological blockade of in vivo fructose utilization using a GLUT5 inhibitor remarkably curtailed LC growth. Together, this study underscores the importance of in vivo fructose utilization mediated by GLUT5 in governing LC growth and highlights a promising strategy to treat LC by targeting GLUT5 to eliminate those fructose-addicted neoplastic cells.
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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.