ArticleCellular oncology (Dordrecht, Netherlands)2024
Microbial metabolite trimethylamine-N-oxide induces intestinal carcinogenesis through inhibiting farnesoid X receptor signaling.
Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- Targeting FMO3 suppresses the malignant phenotype of colorectal cancer: evidence from bioinformatics to functional experiments.Future science OA · 2026Article
- Trimethylamine-N-oxide: the microbial cue in immune-mediated disorders.Trends in endocrinology and metabolism: TEM · 2026Review
- Intratumoral microbiota in the growth of CRC and lung cancer: Comprehensive insights from etiology to therapy.iScience · 2026Review
- The multifaceted role of SOCS3 in colorectal cancer: molecular mechanisms and clinical implications.Molecular biology reports · 2026Review
- Gut Microbiota in Colorectal Cancer: Mechanisms of Carcinogenesis, Biomarkers, and Therapeutic Perspectives.Journal of clinical medicine · 2026Review
- Integrating bile acid metabolism into precision nutrition strategies for improved swine performance.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Review
- The microbiota-metabolite-immune axis in colorectal cancer: mechanistic insights and emerging clinical applications.Frontiers in immunology · 2026Review
- Chenodeoxycholic acid suppresses colorectal cancer by activating Farnesoid X receptor.American journal of cancer research · 2026Article
- Microbial metabolite trimethylamine-N-oxide facilitates colorectal inflammation-cancer transformation by blocking lysosomal degradation of Wnt signaling.Gut microbes · 2025Article
- Gut microbial metabolites in cancer immunomodulation.Molecular cancer · 2025Review
- Lower Thyroid Function and Higher Plasma Choline: Effect Modification by Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Article
- The Microbiota-Diet-Immunity Axis in Cancer Care: From Prevention to Treatment Modulation and Survivorship.Nutrients · 2025Review
- Crosstalk Between Bile Acids and Intestinal Epithelium: Multidimensional Roles of Farnesoid X Receptor and Takeda G Protein Receptor 5.International journal of molecular sciences · 2025Review
- Intratumoral microbiota: implications for cancer progression and treatment.Frontiers in microbiology · 2025Review
- Microbial metabolite-driven immune reprogramming in tumor immunotherapy: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Gut microbiota dysbiosis in people living with HIV who have cancer: novel insights and diagnostic potential.Frontiers in immunology · 2025Article
- Emerging roles of intratumor microbiota in cancer: tumorigenesis and management strategies.Journal of translational medicine · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
purposeMicrobial dysbiosis is considered as a hallmark of colorectal cancer (CRC). Trimethylamine-N-oxide (TMAO) as a gut microbiota-dependent metabolite has recently been implicated in CRC development. Nevertheless, evidence relating TMAO to intestinal carcinogenesis remains largely unexplored. Herein, we aimed to examine the crucial role of TMAO in CRC progression.
methodsApc
resultsTMAO administration increased tumor cell and stem cell proliferation, and decreased apoptosis, accompanied by DNA damage and gut barrier impairment. Gut microbiota analysis revealed that TMAO induced changes in the intestinal microbial community structure, manifested as reduced beneficial bacteria. Mechanistically, TMAO bound to farnesoid X receptor (FXR), thereby inhibiting the FXR-fibroblast growth factor 15 (FGF15) axis and activating the Wnt/β-catenin signaling pathway, whereas the FXR agonist GW4064 could blunt TMAO-induced Wnt/β-catenin pathway activation.
conclusionThe microbial metabolite TMAO can enhance intestinal carcinogenesis by inhibiting the FXR-FGF15 pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.