Microbiome and host interaction in CRC. (IMAGE)

China Anti-Cancer Association

Microbiome and host interaction in CRC.

Caption

Microbiome and host interaction in CRC. pks+ Escherichia coli: Produces the genotoxin colibactin, which induces DNA double-strand breaks and genomic instability. Enterotoxigenic Bacteroides fragilis (ETBF): Secretes BFT, which contributes to ROS generation and induces DNA damage; BFT also disrupts E-cadherin-mediated cell adhesion, activating β-catenin signaling. ETBF downregulates the tumor-suppressive microRNA, miR-149-3p. Fusobacterium nucleatum: Utilizes virulence factors (FadA and Fap2) to bind host E-cadherin and Gal-GalNAc, respectively. F. nucleatum promotes TNFSF9 gene expression, upregulates the lncRNA ENO1-IT1, and suppresses the m6A “writer” enzyme (METTL3) via the YAP signaling pathway. Other bacteria promote cholesterol biosynthesis. Commensal-derived metabolites, such as butyrate, function as HDAC inhibitors, while microbial LPS activates TLR4 and NF-κB signaling, collectively fostering an inflammatory and pro-tumorigenic microenvironment. BTF, Bacteroides fragilis toxin; CRC, colorectal cancer; Gal-GalNAc, galactose-N-acetyl-d-galactosamine; HDAC, histone deacetylase; LPS, lipopolysaccharide; ROS, reactive oxygen species; TLR4, Toll-like receptor 4.

Credit

Cancer Biology & Medicine

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