ArticleDiscover oncology2025
Liraglutide inhibits the development of colorectal cancer by regulating TGF-β/Smad3 signaling pathway and affecting epithelial-mesenchymal transition.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pharmacological mechanisms and clinical impacts of antidiabetic drugs on colorectal cancer risk: a systematic review.Frontiers in pharmacology · 2026Review
- The central role of IL-6 in the differential effects of GLP-1 receptor agonists and metformin across multiple health conditions.Frontiers in immunology · 2026Review
- Glucagon-like Peptide-1 Receptor Agonists and Colorectal Cancer Risk.AACE endocrinology and diabetesReview
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Authors and funding
5 authors.
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Abstract
backgroundLiraglutide, a glucagon-like peptide-1 receptor agonist commonly used in diabetes management, has shown potential anti-cancer effects across various malignancies. However, its role and underlying mechanisms in colorectal cancer (CRC) remain unclear.
methodWe investigated the effects of Liraglutide on human normal colon epithelial (NCM-460) and colorectal cancer (CRC) cells (LoVo and HCT116) using varying concentrations. Cell viability, proliferation, apoptosis, cell cycle progression, migration, invasion, and the expression of TGF-β/Smad3 and EMT-related markers were assessed. Additionally, we explored the effects of TGF-β agonists on the TGF-β/Smad3 signaling pathway. Tumor growth was evaluated in a nude mouse model.
resultLiraglutide reduced CRC cell proliferation in a dose-dependent manner, with the high-concentration treatment (Liraglutide-H) showing the most potent effect (p < 0.01 for Liraglutide-L, p < 0.0001 for Liraglutide-H). High-dose Liraglutide (Liraglutide-H) promoted apoptosis and induced G1-S phase arrest (p < 0.05). Migration and invasion of CRC cells were significantly reduced in both treatment groups (p < 0.05), with Liraglutide-H showing the strongest inhibitory effect. Liraglutide also modulated the TGF-β/Smad3 pathway: it decreased TGF-β, p-Smad3/Smad3 and N-cadherin levels while increasing E-cadherin levels (p < 0.05). These effects were reversed by the addition of a TGF-β agonist (p < 0.05).
conclusionLiraglutide inhibits CRC progression by modulating the TGF-β/Smad3 signaling pathway, which affects EMT, cell migration, and invasion. These findings suggest a potential therapeutic role for Liraglutide in CRC treatment.
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