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Microbial metabolite trimethylamine-N-oxide induces intestinal carcinogenesis through inhibiting farnesoid X receptor signaling
Microbial molecule trimethylamine-N-oxide may promote intestinal cancer by blocking a key cell signaling pathway
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Abstract
TMAO administration increased tumor cell and stem cell proliferation while decreasing apoptosis.
- TMAO is associated with DNA damage and gut barrier impairment.
- Changes in the intestinal microbial community structure were observed, with a reduction in beneficial bacteria.
- TMAO may bind to the farnesoid X receptor (FXR), inhibiting the FXR-fibroblast growth factor 15 (FGF15) axis.
- Activation of the Wnt/β-catenin signaling pathway was induced by TMAO.
- The FXR agonist GW4064 could reduce TMAO-induced activation of the Wnt/β-catenin pathway.
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