ArticleMicrobiome2025
Lipid accumulation inhibition strategies alleviate Fusobacterium nucleatum-infected colorectal cancer.
Article in Microbiome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Host-Microbe Mechanisms of Fusobacterium nucleatum in Colorectal Cancer.Molecular oral microbiology · 2026Review
- Dietary Terpenoids in Advancing Biofilm-Mediated Cancer Prevention: Antibiofilm Cascade, Molecular Crosstalk, and Nano-Facilitated Functional Delivery.Cell biochemistry and function · 2026Review
- Identification of the CYP19A1-GPER1 axis as a critical oncogenic driver in hepatocellular carcinoma via AKT activation.Journal of translational medicine · 2026Article
- Engineered live bacteria for liver diseases and gut-liver axis disorders: from genetic modification to advanced delivery systems.Journal of nanobiotechnology · 2026Review
- Intratumoral microbiome: the double-edged sword in remodeling cancer immunotherapy.Molecular cancer · 2026Review
- GMrepo v3: a curated human gut microbiome database with expanded disease coverage and enhanced cross-dataset biomarker analysis.Nucleic acids research · 2026Article
- Crosstalk between mFrontiers in immunology · 2026Review
- Orlistat: a comprehensive review of a lipase inhibitor from obesity management to emerging oncological applications.Frontiers in pharmacology · 2026Review
- The microbiota-metabolite-immune axis in colorectal cancer: mechanistic insights and emerging clinical applications.Frontiers in immunology · 2026Review
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFusobacterium nucleatum (F. nucleatum) is prevalent in colorectal cancer (CRC), and it can promote proliferation and induce chemoresistance via multiple pathways. The development of treatment strategies for F. nucleatum-infected CRC is of great importance.
methodsShotgun metagenomic and metabolomic analyses of human feces, as well as metabolomic analysis of human blood, were performed to reveal the dysbiosis and metabolic dysregulation in CRC. Furthermore, the effects of Bifidobacterium animalis (B. animalis) on F. nucleatum and CRC were assessed in vitro and in vivo. Using a mouse CRC model, the function of bile salt hydrolase (BSH) in B. animalis was verified through heterologous expression in Escherichia coli (E. coli). Bile acids and drug library screening experiments were performed to inhibit F. nucleatum and tumor proliferation.
resultsWe identified an increase in F. nucleatum, enrichment of lipid metabolites, and depletion of Bifidobacterium in CRC patients. Furthermore, B. animalis inhibited F. nucleatum and CRC cells growth in an acid-dependent manner and reduced F. nucleatum-induced tumor increasement in mice. Mechanistically, F. nucleatum caused lipid accumulation, exacerbated inflammation, and intestinal barrier disruption, whereas B. animalis alleviated these changes, increased the Simpson diversity index, reduced lipid metabolites, and altered secondary bile acid composition in mice. Moreover, E. coli-BSH and ursodeoxycholic acid (UDCA) inhibited F. nucleatum-induced lipid accumulation and FASN/CPT1/NF-κB upregulation. Additionally, they alleviated F. nucleatum-related intestinal tumorigenesis in vivo. Targeting F. nucleatum-infected CRC cells and subcutaneous tumors in mice, penfluridol or the combination of orlistat and 5-FU exhibited superior inhibitory effects compared to 5-FU alone.
conclusionsF. nucleatum and lipid metabolites are enriched in CRC patients. Furthermore, BSH-expressing E. coli, UDCA, and penfluridol can alleviate F. nucleatum-induced lipid accumulation and tumor growth in mice. Video Abstract.
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