ArticleCurrent pharmaceutical design2025
Crippled Hepatocarcinogenesis Inhibition of Quercetin in Glycolysis Pathway with Hepatic Farnesoid X Receptor Deficiency.
Article in Current pharmaceutical design, 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.
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Who cites it
2 citing papers in PubMed.
- Mechanism of FXR signaling: from liver inflammation to hepatocellular carcinoma.Biochemistry and biophysics reports · 2026Review
- Potential of Orally Administered Quercetin, Hesperidin, andInternational journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
aimQuercetin, a bioactive flavonoid extracted from traditional Chinese medicine, has antihepatocellular carcinoma effects. Farnesoid X receptor (FXR), a nuclear receptor highly expressed in the liver, plays important roles in maintaining hepatic glucose homeostasis, anti-inflammation, liver regeneration, and anti-cancer properties. Whether quercetin regulates the glycolysis/glycolysis pathway through FXR signaling remains unknown.
methodsKEGG Enrichment, GO Enrichment, Protein-Protein Interaction (PPI) Network, Molecular Docking, and RNA-Seq Analysis (Swiss Target Prediction, GeneCard databases, Kaplan-Meier Plotter, etc). Cell activity, cell proliferation, and cell cycles were separately analyzed by CCK-8 assay, clone formation assay, and flow cytometry. QRT-PCR determined the mRNA levels of related genes in response to quercetin. HPLCMS/ MSHPLC-MS/MS determined the metabolite profiles. FXR deficiency Hep3B cells were used for discriminating the quercetin's effects with or without FXR.
resultsQuercetin-related genes were significantly correlated with FXR in hepatocarcinogenesis, especially in glycolysis. The top 30 related genes between FXR, quercetin, and glycolysis were enriched and chosen to further study. Furthermore, the strongest binding energy determined by the molecular docking model of between quercetin and FXR was -6.55 kcal/mol. Quercetin inhibited cell proliferation by the accumulation of Hep3B cells in the S-phase. The differential expressed genes (C-MYC, PCNA, CYCLIN-D1, and P21) associated with glycolysis were observed. Furthermore, quercetin also inhibited the expression of HK2, GAPDH, and LDHA. Meanwhile, the levels of glycolysis/gluconeogenesis-related metabolites were regulated by quercetin.
conclusionQuercetin makes an essential anti-HCC effect by crippling the glycolysis/gluconeogenesis process via FXR signaling.
Indexed as
Identifiers
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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.