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Dichotomous metabolism of Enterococcus faecalis induced by haematin starvation modulates colonic gene expression.
Commensal bacteria drive endogenous transformation and tumour stem cell marker expression through a bystander effect.
Enterococcus faecalis induces aneuploidy and tetraploidy in colonic epithelial cells through a bystander effect.
TNF-a mediates macrophage-induced bystander effects through Netrin-1.
Cyclooxygenase-2 generates the endogenous mutagen trans-4-hydroxy-2-nonenal in Enterococcus faecalis-infected macrophages.
Colon Macrophages Polarized by Commensal Bacteria Cause Colitis and Cancer through the Bystander Effect.
Extracellular superoxide production by Enterococcus faecalis promotes chromosomal instability in mammalian cells.
4-hydroxy-2-nonenal mediates genotoxicity and bystander effects caused by Enterococcus faecalis-infected macrophages.
Commensal-infected macrophages induce dedifferentiation and reprogramming of epithelial cells during colorectal carcinogenesis.
Microbiome-triggered reprogramming and mutation of colon epithelial cells leading to tumor stem-like cells
Enterococcus faecalis, Colorectal Cancer, and Bystander Effects