ReviewMolecular oncology2026
An outer membrane vesicle-associated two-track model for enterotoxigenic Bacteroides fragilis oncogenesis.
Review in Molecular oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Enterotoxigenic Bacteroides fragilis (ETBF) is a pro-carcinogenic pathobiont thought to drive oncogenesis solely through E-cadherin cleavage by its metalloprotease toxin, Bacteroides fragilis toxin (BFT). This canonical framework leaves three paradoxes unresolved: the cell type selectivity of BFT, the cytosolic engagement of NOD1 by an extracellularly secreted toxin, and the divergent epidemiology of BFT isoforms. The recent identification of claudin-4 as the obligate BFT receptor resolves the first but sharpens the others. Here we propose an outer membrane vesicle (OMV)-associated two-track model. In Track 1, the surface program, claudin-4-dependent docking drives E-cadherin ectodomain cleavage, junctional disruption and β-catenin/Th17-driven inflammation. In Track 2, the proposed intracellular program, OMV-mediated endocytosis delivers OMV-anchored BFT-1 into the endocytic compartment, where endosomal escape would permit cytosolic NOD1 engagement and activation of a GAK-NUMB-NOTCH1-HEY1 axis linked to cancer stem cell expansion and chemoresistance-an axis so far demonstrated in breast cancer cells, not in colonic epithelium. We further hypothesize an intrinsic isoform bias: BFT-2 toward surface cleavage, BFT-1 toward intracellular NOD1 engagement. This spatially resolved model unifies recent mechanistic advances with unexplained epidemiological patterns.
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