ArticleDiscover oncology2025
Role of fructose in renal cell carcinoma progression.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Fructose induces PERK-dependent ER stress and mitochondrial dysfunction via nucleotide depletion in clear cell renal cell carcinoma.Cell death & disease · 2026Article
- CD31 regulates metabolic switch in Treg migration attenuates rheumatoid arthritis.Clinical and translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Renal cell carcinoma (RCC) is a highly malignant tumor with a poor prognosis, underscoring the urgent need for novel therapeutic strategies. RCC cells exhibit rapid proliferation and high metabolic demands, leading to hypoglycemic and hypoxic conditions within the tumor microenvironment (TME). Our study reveals that the fructose transporter Glut5 is prominently expressed in RCC, facilitating increased fructose uptake. This compensatory mechanism supports RCC survival under glucose deprivation and hypoxia. Fructose utilization sustains RCC proliferation, migration, and colony formation in vitro, significantly reduces apoptosis, and accelerates renal cancer growth in vivo. Mechanistically, fructose activates the cAMP/PKA signaling pathway, driving metabolic reprogramming and promoting tumor progression. Furthermore, 2,5-dehydro-D-mannitol (2,5-AM), a competitive inhibitor of fructose transport, significantly inhibits RCC growth both in vivo and in vitro. These findings provide new insights into the role of fructose metabolism in RCC progression and suggest potential therapeutic targets.
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Registered trials
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