ArticleMolecular biology reports2026
Vitexin inhibits renal cell carcinoma progression by targeting Galectin-1-mediated glycolytic metabolism.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
backgroundVitexin, a natural flavonoid compound, has shown anti-tumor effects, but its mechanism in Renal cell carcinoma (RCC) remains unclear. Galectin-1, a β-galactoside-binding lectin, promotes tumor progression through metabolic reprogramming.
objectiveThis study examined whether vitexin has antitumor activity against RCC by targeting Galectin-1 and its downstream metabolic pathways.
methodsHuman RCC cell lines (A498 and ACHN) were treated with vitexin to assess cell viability, apoptosis, cell cycle, migration, and invasion. Galectin-1 expression was manipulated through overexpression and knockdown approaches. Transcriptomic and metabolomic profiling were performed to identify pathway alterations. Glycolytic metabolism was evaluated using ATP measurements, glucose consumption, lactate production assays. The in vivo efficacy was validated using A498 xenograft models in nude mice.
resultsVitexin inhibited RCC cell proliferation, while significantly downregulating Galectin-1 expression. Furthermore, vitexin treatment caused cell cycle arrest, promoted apoptosis, and suppressed colony formation, migration, and invasion. Galectin-1 overexpression rescued vitexin-induced growth inhibition and reduced apoptosis. Transcriptomic analysis revealed that Galectin-1 modulation affected PI3K-AKT pathways, with significant alterations in glycolytic genes (SLC2A1, HK1, HK2, PFKM, PFKP, LDHB). Metabolomic profiling showed Galectin-1-dependent reprogramming of oxidative phosphorylation and energy metabolism. In addition, galectin-1 knockdown impaired glycolytic flux, reduced ATP production, glucose consumption, and lactate secretion. Conversely, Galectin-1 overexpression enhanced these metabolic parameters and activated PI3K/AKT signaling, counteracting vitexin's metabolic suppression. In vivo, vitexin significantly inhibited tumor growth, downregulated Galectin-1 and PI3K/AKT signaling, reduced cell proliferation, and increased TUNEL-positive apoptotic cells.
conclusionsVitexin exerts anti-tumor effects in RCC by targeting Galectin-1, which disrupts glycolytic metabolism through PI3K/AKT signaling inhibition. These findings suggest that the vitexin targeting Galectin-1 represents a potential therapeutic strategy for treating RCC.
Indexed as
Identifiers
42113369What OpenQuestion holds
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.