ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2023
Fructose utilization enhanced by GLUT5 promotes lung cancer cell migration via activating glycolysis/AKT pathway.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- The metabolic code of pulmonary disease: from mechanisms to therapeutic opportunities.Breathe (Sheffield, England) · 2026Review
- Unraveling the αVβ5-GLUT5 axis in breast cancer: linking extracellular matrix signaling to fructose metabolism: a scoping review.Molecular biology reports · 2026Article
- [Advances in Lactate Metabolic Reprogramming in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Epigenetic and metabolic rewiring in metastatic pheochromocytomas and paragangliomas driven by SDHB mutations.Communications biology · 2026Article
- ZNF473 as a biomarker and potential therapeutic target in cancer: integrated bioinformatics and experimental evidence with a focus on hepatocellular carcinoma.Frontiers in oncology · 2026Article
- Lactylation modification in lung cancer: A review of current research and future directions (Review).Oncology reports · 2025Review
- CCDC137/DGCR8 axis promotes aerobic glycolysis in hepatocellular carcinoma via activation of the AKT/mTOR signaling pathway.European journal of medical research · 2025Article
- Role of fructose in renal cell carcinoma progression.Discover oncology · 2025Article
- Sweet regulation - The emerging immunoregulatory roles of hexoses.Journal of advanced research · 2025Review
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- Fructose-Induced mTORC1 Activation Promotes Pancreatic Cancer Progression through Inhibition of Autophagy.Cancer research · 2023Article
- Come, Sweet Death: Why Endothelial Cells Die in Fructose.American journal of respiratory cell and molecular biology · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeLung cancer is the leading cause of cancer-related mortalities worldwide, and metastasis contributes to a large number of deaths in lung carcinoma patients. New approaches for anti-metastatic treatment are urgently needed. Enhanced fructose metabolism mediated by GLUT5 directly contributes to cancer metastasis. However, the underlying mechanism remains to be elucidated, which we aimed to explore in this study.
methodsThe overexpression and knockdown of SLC2A5, the encoding gene of GLUT5, were established by retrovirus system and CRISPR/Cas9 technology, respectively. Cell migration was conducted by trans-well assay. Western blotting assay was carried out to detect the expression of GLUT5, total AKT, phosphorylated AKT (pAKT-S473 and pAKT-T308) and LDHA. Lactate production was measured by colorimetric assay. Experimental lung metastasis model by tail vein injection was constructed to evaluate the metastatic potential of GLUT5 in vivo.
resultsOverexpression of SLC2A5 promoted migration of lung cancer cells both in vitro and in vivo, and shortened the overall survival of mice. While, SLC2A5 deletion blocked the migration of lung cancer cells. GLUT5-mediated fructose utilization upregulated phosphorylated AKT, which was responsible for enhanced migration of lung cancer cells. Additionally, GLUT5-mediated fructose utilization boosted glycolysis with overproduction of lactate, resulting in upregulation of phosphorylated AKT. Moreover, lung cancer cell migration and AKT activation were restrained by glycolysis inhibitor 2-deoxy-D-glucose (2-DG) or GLUT5-specific inhibitor 2,5-anhydro-D-mannitol (2,5-AM).
conclusionOur study unveils glycolysis/lactate/AKT pathway is responsible for lung cancer cell migration induced by GLUT5-mediated fructose metabolism, providing a potential therapeutic avenue for lung cancer metastasis.
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