Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer
Related Experiment Video
Updated: Aug 5, 2026
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Guodong Zang1, Ying Liu2, Xingyu Mu3
1Department of Respiratory and Critical Care Medicine, Shandong University of Traditional Chinese Medicine Affiliated Hospital, Jinan, Shandong, China.
Background:
Fibrosis and cancer share epithelial-mesenchymal transition (EMT) as a core pathological driver, making EMT-targeted therapy a promising dual strategy. The natural flavonoid luteolin shows preliminary anti-fibrotic and anti-tumour activities, but its translational potential remains poorly systematized.
Methods:
We conducted a ConPhyMP compliant systematic review, searching PubMed for 2008-2026 studies on luteolin and its derivatives, EMT, fibrosis and cancer, to synthesize evidence on their mechanisms, efficacy and translational prospects.
Results:
Luteolin inhibits EMT via multi-target regulation of core pathways (TGF-β1/Smad, PI3K/Akt, Hippo/YAP), exerting consistent dose-dependent efficacy in suppressing cancer metastasis and multi-organ fibrosis. Structural modifications and nanodelivery systems resolved its bioavailability limitations, and rigorous validation ruled out pan-assay interference compounds (PAINS).
Conclusion:
Luteolin and its derivatives are promising dual-effect EMT-targeted therapeutics. Optimized formulations lay the groundwork for clinical translation, and future large-scale trials are needed to validate their clinical efficacy.
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