ArticlePPAR research2025
To Explore the Active Components, Targets, and Potential Effects of Emodin in the Treatment of Colorectal Cancer Based on Network Pharmacology.
Article in PPAR research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Plant-Derived Bioactive Compounds and Their Therapeutic Potential in Cancer.International journal of molecular sciences · 2026Review
- Mechanistic study of the role of emodin in targeting and inhibiting the Rap1 signaling pathway to regulate epithelial-mesenchymal transition and reverse cisplatin resistance in hepatocellular carcinoma.Translational cancer research · 2026Article
- Emodin-induced cell cycle arrest: A promising approach for cancer therapy (Review).Medicine internationalReview
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: The objective was to investigate the effects and potential molecular mechanisms of emodin on colorectal cancer via network pharmacology combined with experimental validation. Methods: The active components and targets of emodin were retrieved from TCMSP and BATMAN-TCM databases, while colorectal cancer (CRC)-related genes were screened via GeneCards, OMIM, and DisGeNET. The intersection targets were used to construct a compound-disease network and a protein-protein interaction (PPI) network. GO and KEGG enrichment analyses were conducted to reveal key biological functions and pathways. Molecular docking was used to assess binding affinities between core targets and active components. In vitro experiments (CCK-8, colony formation, and apoptosis assays) and in vivo xenograft models were performed to validate the antitumor effect of emodin. Quantitative real-time PCR and Western blot were used to evaluate the regulation of hub genes and signaling pathways. Results: A total of 37 active components and 235 targets of emodin were identified, of which 82 overlapped with CRC-related genes. Core targets (CASP3, MMP9, BCL2, PTGS2, and IL1B) were highlighted through network analysis. These targets were enriched in oxidative stress, apoptosis, inflammation, and metabolic pathways. Molecular docking showed strong interactions between emodin and hub targets. Emodin significantly suppressed proliferation, colony formation, and induced apoptosis in CRC cell lines in a dose-dependent manner. In vivo, emodin inhibited tumor growth and activated the PPAR Conclusion: Emodin exerts anti-CRC effects via a multitarget, multipathway mechanism, particularly through modulation of the PPAR
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Registered trials
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