ArticleFrontiers in pharmacology2025
Reversal of sorafenib resistance in hepatocellular carcinoma by curcumol: insights from network pharmacology, molecular docking, and experimental validation.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrated transcriptomic and molecular docking analysis identifies Rhotekin 2 as a promising therapeutic target for overcoming gemcitabine resistance in cholangiocarcinoma.Biomedical reports · 2026Article
- Lysosome-dependent cell death in hepatocellular carcinoma: unlocking the therapeutic potential of natural products.Frontiers in pharmacology · 2026Review
- Network Pharmacology-Based Identification of Potential Targets and Mechanisms of Isoginkgetin in Gastric Cancer.BioMed research international · 2026Article
- Molecular targets and therapeutic implications of curcumin in hepatocellular carcinoma: a comprehensive literature review.Cancer cell international · 2025Review
- Transcription factor YBX1 orchestrates drug resistance and tumor progression in HCC.Drug discovery today · 2025Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Curcumol, a bioactive sesquiterpenoid extracted from traditional Chinese medicine (TCM), has demonstrated potential in overcoming tumor drug resistance. However, its mechanisms in reversing drug resistance, particularly in hepatocellular carcinoma (HCC) resistant to sorafenib, are not yet fully elucidated. This study aims to explore the molecular mechanisms by which curcumol reverses sorafenib resistance in HCC using a combination of network pharmacology, molecular docking, and Methods: We identified curcumol targets and genes associated with sorafenib-resistant HCC, resulting in a set of overlapping targets. These intersection targets underwent enrichment analysis using DAVID, and a protein-protein interaction (PPI) network was constructed via the STRING database and Cytoscape. Molecular docking confirmed the binding of curcumol to core targets. Results: We identified 117 potential targets for curcumol in reversing sorafenib resistance in HCC. Among them, five core targets-ALB, STAT3, HSP90AA1, HSP90AB1, and SRC-showed strong binding affinity with curcumol. KEGG pathway analysis of the intersecting genes highlighted significant involvement of the PI3K/AKT, JAK/STAT3, Ras, Rap1, HIF-1, FoxO, and mTOR signaling pathways. Conclusion: This study provides compelling evidence that curcumol can reverse sorafenib resistance in HCC by modulating multiple signaling pathways, including PI3K/AKT and JAK/STAT3 pathways. Our findings suggest that curcumol holds promise as a novel therapeutic agent for overcoming drug resistance in HCC, offering a new avenue for clinical intervention.
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