This article investigates the mechanism by which tumor-infiltrating bacteria, specifically Fusobacterium nucleatum (F. nucleatum), influence cancer progression within the tumor microenvironment (TME). The research, which employs spatial imaging, single-cell transcriptomics, and in vitro/in vivo models, challenges previous paradigms by demonstrating that high loads of extracellular bacteria disrupt cancer epithelial cell-to-cell contacts. This disruption leads to a quiescent state or G0-G1 cell-cycle arrest in the epithelial cells, resulting in reduced proliferation and a scattered cell distribution within the tumor. Crucially, this bacteria-induced quiescence is shown to confer chemoresistance against agents like 5-Fluorouracil (5-FU), offering a mechanistic explanation for the correlation between high intratumoral Fusobacterium levels and poor patient outcomes in colorectal cancer (CRC).

References:

• Niño, Jorge Luis Galeano, et al. "Tumor-infiltrating bacteria disrupt cancer epithelial cell interactions and induce cell-cycle arrest." Cancer Cell (2025).