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Purpose <p>Metastatic colorectal cancer (CRC; Stage IV/M1) remains the second most prevalent malignancy worldwide, largely due to its high metastatic potential. Targeting molecular mechanisms that drive epithelial–mesenchymal transition (EMT) is essential to prevent disease progression. This study evaluates the flavanol Morin as an inhibitor of EMT in TGF-β–induced HCT 116 colorectal cancer cells.</p> Methods <p>Cytotoxicity was determined using a tetrazolium-based assay. Apoptosis was confirmed through acridine orange/ethidium bromide staining, while cell aggregation and clonogenic assays demonstrated suppression of tumorigenic progression. Scratch and migration assays were employed to assess anti-invasive effects. Furthermore, cell cycle distribution, immunofluorescence assay, quantitative real-time PCR, and western blotting were conducted to elucidate molecular mechanisms underlying Morin’s activity.</p> Results <p>Morin exhibited dose-dependent cytotoxicity in TGF-β–stimulated HCT116 cells (IC₅₀ = 82.48&#xa0;µg/mL) and induced apoptosis. Morin markedly suppressed EMT-associated behaviors, reducing colony formation, inhibiting cell aggregation, wound closure, and transwell migration. Cell-cycle analysis indicated that TGF-β treatment increased G0/G1 phase accumulation, whereas Morin treatment partially restored the distribution of cells in other phases of the cell cycle. Mechanistically, Morin downregulated β-catenin at both mRNA and protein levels while upregulating NUMB, and significantly reduced TGF-β–induced nuclear localization of β-catenin, indicating inhibition of canonical Wnt signaling.</p> Conclusion <p>Collectively, these findings demonstrate Morin’s anti-proliferative and anti-metastatic properties in the HCT 116 cell line, suggesting its promise as a therapeutic candidate for targeting EMT via Wnt/β-catenin signaling in CRC.</p> Graphical Abstract <p></p>

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Morin Suppresses Invasion and Migration in TGF-β–stimulated Colorectal Cancer Cells Via Modulation of the Wnt/β-catenin Signaling Pathway: An In vitro Study

  • 期刊论文

  • 发表日期：

    2026年4月30日

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  • Lu Huang,
  • Chao Wang,
  • Amirah Albaqami,
  • Wedad Mawkili,
  • Faten F. Bin Dayel,
  • Tahera Waheed Alnassfan

摘要

Purpose

Metastatic colorectal cancer (CRC; Stage IV/M1) remains the second most prevalent malignancy worldwide, largely due to its high metastatic potential. Targeting molecular mechanisms that drive epithelial–mesenchymal transition (EMT) is essential to prevent disease progression. This study evaluates the flavanol Morin as an inhibitor of EMT in TGF-β–induced HCT 116 colorectal cancer cells.

Methods

Cytotoxicity was determined using a tetrazolium-based assay. Apoptosis was confirmed through acridine orange/ethidium bromide staining, while cell aggregation and clonogenic assays demonstrated suppression of tumorigenic progression. Scratch and migration assays were employed to assess anti-invasive effects. Furthermore, cell cycle distribution, immunofluorescence assay, quantitative real-time PCR, and western blotting were conducted to elucidate molecular mechanisms underlying Morin’s activity.

Results

Morin exhibited dose-dependent cytotoxicity in TGF-β–stimulated HCT116 cells (IC₅₀ = 82.48 µg/mL) and induced apoptosis. Morin markedly suppressed EMT-associated behaviors, reducing colony formation, inhibiting cell aggregation, wound closure, and transwell migration. Cell-cycle analysis indicated that TGF-β treatment increased G0/G1 phase accumulation, whereas Morin treatment partially restored the distribution of cells in other phases of the cell cycle. Mechanistically, Morin downregulated β-catenin at both mRNA and protein levels while upregulating NUMB, and significantly reduced TGF-β–induced nuclear localization of β-catenin, indicating inhibition of canonical Wnt signaling.

Conclusion

Collectively, these findings demonstrate Morin’s anti-proliferative and anti-metastatic properties in the HCT 116 cell line, suggesting its promise as a therapeutic candidate for targeting EMT via Wnt/β-catenin signaling in CRC.

Graphical Abstract