ArticleInternational journal of oncology2010
Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells.
Article in International journal of oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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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Who cites it
38 citing papers in PubMed, 76 citations in OpenAlex.
- Large-scale serum N-glycomics tracks N-glycosylation dynamics in hepatocellular carcinoma progression and enables early diagnosis.Nature communications · 2026Article
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- KLC3 drives gastric cancer progression by stabilizing SLC2A5 to activate MAPK signaling and promote epithelial-mesenchymal transition.BMC cancer · 2025Article
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- GLUT5-overexpression-related tumorigenic implications.Molecular medicine (Cambridge, Mass.) · 2024Review
- Review
- Review
- Fructose-induced metabolic reprogramming of cancer cells.Frontiers in immunology · 2024Review
- Fructose-Induced mTORC1 Activation Promotes Pancreatic Cancer Progression through Inhibition of Autophagy.Cancer research · 2023Article
- GLUT5, GLUT7, and GLUT11 expression and Bcl-2/Bax ratio on Breast Cancer Cell Line MCF-7 Treated with Fructose and Glucose.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- GLUT5: structure, functions, diseases and potential applications.Acta biochimica et biophysica Sinica · 2023Review
- Article
- Fructose promotes angiogenesis by improving vascular endothelial cell function and upregulating VEGF expression in cancer cells.Journal of experimental & clinical cancer research : CR · 2023Article
- Spatial metabolomics for evaluating response to neoadjuvant therapy in non-small cell lung cancer patients.Cancer communications (London, England) · 2022Article
- Fructose Induces Pulmonary Fibrotic Phenotype Through Promoting Epithelial-Mesenchymal Transition Mediated by ROS-Activated Latent TGF-β1.Frontiers in nutrition · 2022Article
- Increased Proliferation of Neuroblastoma Cells under Fructose Metabolism Can Be Measured by Isothermal Microcalorimetry.Children (Basel, Switzerland) · 2021Article
- Fructose and Mannose in Inborn Errors of Metabolism and Cancer.Metabolites · 2021Review
- Mechanoresponsive metabolism in cancer cell migration and metastasis.Cell metabolism · 2021Review
- Ketohexokinase-A acts as a nuclear protein kinase that mediates fructose-induced metastasis in breast cancer.Nature communications · 2020Article
- Fructose contributes to the Warburg effect for cancer growth.Cancer & metabolism · 2020Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant glycosylation is a universal feature of cancer cells, and certain glycan structures are well-known markers for tumor progression. Availability and composition of sugars in the microenvironment may affect cell glycosylation. Recent studies of human breast tumor cell lines indicate their ability to take up and utilize fructose. Here we tested the hypothesis that adding fructose to culture as a carbon source induces phenotypic changes in cultured human breast tumor cells that are associated with metastatic disease. MDA-MB-468 cells were adapted to culture media in which fructose was substituted for glucose. Changes in cell surface glycan structures, expression of genes related to glycan assembly, cytoskeleton F-actin, migration, adhesion and invasion were determined. Cells cultured in fructose expressed distinct cell-surface glycans. The addition of fructose affected sialylation and fucosylation patterns. Fructose feeding also increased binding of leukoagglutinating Phaseolus vulgaris isolectin, suggesting a possible rise in expression of branching beta-1, 6 GlcNAc structures. Rhodamine-phalloidin staining revealed an altered F-actin cytoskeletal system. Fructose accelerated cellular migration and increased invasion. These data suggest that changing the carbon source of the less aggressive MDA-MB-468 cell line induced characteristics associated with more aggressive phenotypes. These data could be of fundamental importance due to the markedly increased consumption of sweeteners containing free fructose in recent years, as they suggest that the presence of fructose in nutritional microenvironment of tumor cells may negatively affect the outcome for some breast cancer patients.
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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.