ArticleJournal of Cancer2025
Isoliquiritigenin inhibits colorectal cancer progression by targeting the FGFR4/FASN mediated lipid metabolism pathway.
Article in Journal of Cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Investigation of Fatty Acid Metabolism-Associated Molecular CPOX and the Underlying Mechanism in Follicular Lymphoma.Biochemical genetics · 2026Article
- ATP2C2-PLA2R1 axis underlies lipid metabolism modulation and invasion in papillary thyroid carcinoma mediated by a VGIC signature.Discover oncology · 2026Article
- ELOVL6 Promotes the Proliferation and Migration of Oral Squamous Cell Carcinoma Cells Through Fatty Acid Remodelling and ROS Modulation in vitro.OncoTargets and therapy · 2026Article
- HO-1 Up-regulation and PINK1/Parkin-Mediated Mitophagy Contribute to the Anti-tumor Effects of Metochalcone in Colorectal Cancer.Research (Washington, D.C.) · 2026Article
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Authors and funding
7 authors.
Funding
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Abstract
Colorectal cancer (CRC) is one of the most common malignant tumors. Isoliquiritigenin (ISL), a natural chalcone compound extracted from the roots of licorice and other plants, has demonstrated significant anti-tumor activity in various cancers. However, its specific mechanisms of action against CRC remain unclear. In this study, we investigated the molecular mechanisms underlying the effects of ISL targeting Fibroblast Growth Factor Receptor 4 (FGFR4) in CRC. Our findings revealed that FGFR4 is highly expressed in CRC cell lines, and functional assays demonstrated that silencing FGFR4 significantly inhibits cellular proliferation and migration. Further mechanistic studies showed that FGFR4 regulates fatty acid biosynthesis and the PI3K/Akt signaling pathway, as evidenced by the downregulation of Fatty Acid Synthase (FASN) and PI3K/Akt pathway proteins upon FGFR4 knockdown. Moreover, ISL significantly suppresses CRC cell proliferation and migration while disrupting tumor cell fatty acid metabolism. This study suggests that ISL may inhibit CRC progression by downregulating FGFR4 and suppressing PI3K/Akt-mediated fatty acid metabolism reprogramming.
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