ArticleFrontiers in oncology2025
Fruquintinib inhibits the migration and invasion of colorectal cancer cells by modulating epithelial-mesenchymal transition via TGF-β/Smad signaling pathway.
Article in Frontiers in oncology, 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.
- Sphingomonas paucimobilis-Driven Epithelial-Endothelial Transition in Adenomyosis Pathogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cytokine and chemokine networks in colorectal cancer.Frontiers in immunology · 2026Review
- A Real-World Pharmacovigilance Study of Fruquintinib Based on the FDA Adverse Event Reporting System (FAERS) Database.Cancer medicine · 2025Article
- New strategies to enhance the efficacy of PD-1/PD-L1 inhibitors in treating microsatellite stable colorectal cancer.Future oncology (London, England) · 2025Review
- Eurycomanone Blocks TGF-β1-Induced Epithelial-to-Mesenchymal Transition, Migration, and Invasion Pathways in Human Non-Small Cell Lung Cancer Cells by Targeting Smad and Non-Smad Signaling.International journal of molecular sciences · 2025Article
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Abstract
Background: Fruquintinib, a selective vascular endothelial growth factor receptor (VEGFR) inhibitor, has shown considerable efficacy in colorectal cancer (CRC) treatment. Despite its promising therapeutic effects, the precise molecular mechanisms underlying its therapeutic effects remain incompletely understood. In this study, we explored the functional roles and molecular mechanisms of fruquintinib in CRC therapy. Material and methods: Human CRC cells (HCT-116 and LOVO) were cultured and treated with fruquintinib. Cell counting kit-8 assay kit (CCK-8) and colony formation assays were performed to investigate the effects of fruquintinib on cell proliferation. Wound healing and transwell assays were conducted to explore the role of fruquintinib on migration and invasion. RNA sequencing and bioinformatics analysis was used to investigate the potential mechanism of fruquintinib in the development of CRC. Western blot was used to measure the protein level. Results: Fruquintinib significantly inhibited the proliferation, migration, and invasion of colorectal cancer cells. Bioinformatics analysis indicated that fruquintinib modulated the epithelial-mesenchymal transition (EMT) pathway, and experimental validation confirmed its regulatory effects on core EMT-associated protein biomarkers. Notably, fruquintinib treatment resulted in the upregulation of E-cadherin and the downregulation of N-cadherin, vimentin, and MMP9. Western blot analysis revealed that fruquintinib dose-dependently suppressed SMAD2/3 expression. Notably, treatment with the TGF-β receptor agonist KRFK TFA attenuated fruquintinib's effect, reversing the upregulation of E-cadherin as well as the downregulatin of N-cadherin and SMAD2/3. Additionally, KRFK TFA partially restored CRC cell migration and invasion in transwell assays, counteracting fruquintinib's inhibitory impact. Conclusion: These findings indicate that Fruquintinib effectively hampers the migration and invasion of CRC cells by disrupting the EMT process via the TGF-β/Smad signaling pathway. This study sheds light on the mechanisms by which fruquintinib inhibits CRC progression and underscores its potential for further clinical investigation.
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