ArticleAmerican journal of cancer research2025
Integrated network pharmacology and experimental validation reveal
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Integrating in silico modeling and experimental validation to determine the anti-breast cancer mechanisms of mulberry leaf bioactive compounds.American journal of cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo validate the anti-hepatocellular carcinoma (HCC) efficacy of
methodsPotential targets of CTFs were retrieved from Traditional Chinese Medicine Systems Pharmacology (TCMSP) Database, while HCC-related targets were collected from GeneCards, OMIM, and DrugBank. Common targets were identified using VENNY2.1, and protein-protein interaction (PPI) networks were constructed via STRING. Functional Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using DAVID. A "CTFs-HCC-target-pathway" network was built with Cytoscape to identify key components and core targets. Molecular docking was performed using Autodock Vina. The Differential expression of key targets between HCC and normal tissues was visualized using boxplots, and prognostic relevance was evaluated by Kaplan-Meier survival analysis. In vitro assays, including CCK-8, live/dead staining, colony formation, flow cytometry, qPCR, were used to evaluate proliferation, viability, reactive oxygen species (ROS) levels, cell cycle distribution, and gene expression. A zebrafish xenograft model was established to determine the minimum toxic concentration (MTC) and evaluate tumor inhibition through fluorescence imaging and HE staining.
resultsNetwork analysis identified 27 bioactive components and 318 putative targets of CTFs, with 32 associated with HCC. Core targets included Caspase-3, P53, MAPK1, Bcl-2 and Bax, primarily interacting with quercetin, (-)-Epigallocatechin (EGCG), fisetin, acacetin, luteolin, and kaempferol. Molecular docking confirmed strong binding affinities between these compounds and core targets. Pro-apoptotic genes (Bax, Caspase-3, P53) were upregulated in HCC tissues, and low expression of Bax/Caspase-3 correlated with poor survival. CTFs treatment further enhanced expression of Bax, p53 and Caspase-3, suppressed Bcl-2 while increased the Bax/Bcl-2 ratio. In vitro, CTFs inhibited HepG2 proliferation, promoted LO2 growth, induced ROS production, G
conclusionCTFs exert anti-HCC effects through multi-target regulation of apoptosis-related genes and multiple signaling pathways, effectively inhibiting cancer cell proliferation.
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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.