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Area of Science:

  • Microbiology
  • Cancer Biology
  • Metabolic Engineering

Background:

  • Bacteria within the tumor microenvironment significantly influence cancer development and progression.
  • Fusobacterium nucleatum enrichment in colorectal cancer (CRC) is linked to increased mortality.
  • The metabolic adaptability of F. nucleatum is crucial for its survival in dynamic environments, but its mechanistic link to virulence and cancer phenotypes remains unclear.

Purpose of the Study:

  • To characterize the basal physiology of F. nucleatum.
  • To develop a genome-scale metabolic model (GEM) for simulating F. nucleatum phenotypes under various nutritional conditions.
  • To investigate the metabolic adaptations of F. nucleatum during interactions with human cells using gene expression data.

Main Methods:

  • Reconstruction of an experimentally validated genome-scale metabolic model (GEM) for F. nucleatum.
  • Simulation of bacterial phenotypes under different nutritional conditions using the GEM.
  • Integration of in vitro gene expression data to contextualize the metabolic model and simulate cell-interaction phenotypes.

Main Results:

  • Bacterial adhesion to human cells induces metabolic rewiring, including suppressed branched-chain amino acid catabolism and increased methionine and serine uptake.
  • Bacterial invasion prompts partial reactivation of central carbon and nitrogen metabolic pathways.
  • Shifts in short-chain fatty acid production and redox balance were identified, potentially influencing bacterial persistence and the tumor microenvironment.

Conclusions:

  • F. nucleatum exhibits significant metabolic plasticity in response to host cell interactions.
  • Metabolic rewiring during adhesion and invasion suggests mechanisms for bacterial persistence and modulation of the tumor microenvironment.
  • This study provides a mechanistic framework for understanding F. nucleatum's role in CRC through its metabolic adaptations.