ArticleFrontiers in microbiology2025
Gut microbiota dysbiosis impairs TGF-β/Smad4 signaling to drive postoperative metastasis in colorectal cancer.
Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
Background: After surgical intervention, metastasis remains the primary contributor of mortality rates in colorectal cancer (CRC). While compelling evidence implicates gut microbiota dysbiosis as a key driver of CRC progression, its role in postoperative metastasis remains unclear. Methods: A total of 97 participants were recruited, comprising 21 postoperative CRC patients with metastasis (M group), 37 postoperative CRC patients without metastasis (C group), and 39 healthy individuals (H group). Fecal microbiota composition, short-chain fatty acid (SCFA) concentrations, and serum cytokines were quantified. Spearman correlation was used to assess the relationship between microbiota and SCFAs. Fecal microbiota transplantation (FMT) was performed by transferring patient specimens into antibiotic-pretreated orthotopic CRC mice models. Epithelial-mesenchymal transition (EMT) markers and TGF-β/Smad4 signaling were subsequently analyzed. Results: In humans, M group patients exhibited significant gut dysbiosis, characterized by enriched Conclusion: Gut microbiota dysbiosis and SCFA depletion exert profound regulatory effects on postoperative CRC metastasis, potentially by promoting EMT through mechanisms involving the TGF-β/Smad4 signaling axis. Thus, targeting gut microbiota may offer promising therapeutic strategies to mitigate CRC metastasis.
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