ArticleCancer research2025
The Microbial Bile Acid Metabolite 3-Oxo-LCA Inhibits Colorectal Cancer Progression.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The gut microbiome-bile acid-FXR interplay: a pivotal axis in metabolic and gastrointestinal diseases.Gut microbes · 2026Review
- Gut microbiota in health and disease.Molecular biomedicine · 2026Review
- Gut Microbiota in Colorectal Cancer: Mechanisms of Carcinogenesis, Biomarkers, and Therapeutic Perspectives.Journal of clinical medicine · 2026Review
- Gut microbiota and its metabolites: Key factors of drug resistance in the treatment of advanced prostate cancer (Review).Molecular medicine reports · 2026Review
- Cholecystectomy-associated gut microbiota dysbiosis promotes colorectal carcinogenesis: from epidemiological controversy to FXR-centered mechanistic insights.Journal of the Egyptian National Cancer Institute · 2026Review
- Indole-3-Carbaldehyde fromResearch (Washington, D.C.) · 2026Article
- The microbiota-metabolite-immune axis in colorectal cancer: mechanistic insights and emerging clinical applications.Frontiers in immunology · 2026Review
- Minimum Dietary Fat Threshold for Effective Ketogenesis and Obesity Control in Mice.Nutrients · 2025Article
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Authors and funding
15 authors.
Funding
Abstract
Bile acids (BA) not only influence the gut microbiome composition but are also metabolized by gut bacteria to form various microbial BAs. Among these, 3-oxo-lithocholic acid (3-oxo-LCA) and isoallo-LCA have been reported to modulate host immunity, suppress intestinal pathogens, and provide antiaging benefits, suggesting that they could also affect intestinal epithelial cells and colorectal cancer progression. To investigate the impact of 3-oxo-LCA on intestinal tumorigenesis, we evaluated its activity in vitro on mouse and human colorectal cancer cell lines, as well as primary mouse intestinal organoids and patient-derived colorectal cancer organoids, and in vivo using a genetically engineered mouse model, cell line-derived syngeneic and xenograft tumors, and patient-derived xenografts. 3-Oxo-LCA functioned as a potent FXR agonist that restored FXR signaling both in vitro and in vivo. Activation of FXR signaling reduced the growth of colorectal cancer cell lines and suppressed the proliferation of intestinal stem cells in both mouse organoids and patient-derived colorectal cancer organoids. In the APCMin/+ genetically engineered mouse model, 3-oxo-LCA reduced BA levels, enhanced gut barrier function, decreased tumor burden, and suppressed tumor initiation. Furthermore, 3-oxo-LCA significantly inhibited tumor progression in syngeneic and xenograft mouse models and promoted apoptosis within the tumors. Together, these results underscore the function of 3-oxo-LCA as an FXR agonist with the ability to inhibit colorectal cancer tumorigenesis and progression by modulating epithelial cell growth and death. SIGNIFICANCE: The microbial bile acid 3-oxo-LCA activates FXR signaling in intestinal epithelial cells that inhibits cancer stem cell proliferation and induces apoptosis, highlighting the potential of 3-oxo-LCA for treating intestinal tumorigenesis.
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