Related Experiment Video For CRC
Updated: Jul 9, 2026
Non-invasive Assessment of the Efficacy of New Therapeutics for Intestinal Pathologies Using Serial Endoscopic Imaging of Live Mice
Published on: March 10, 2015
High-fat diet promotes colorectal tumorigenesis through gut microbiota-mediated metabolic reprogramming and M2
Liangfei Xu1, Jiajia Zhang2, Yuhan Xiao3
1Department of Laboratory Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Background:
High-fat diet (HFD) drives colorectal cancer (CRC) progression through gut microbiota dysbiosis and M2 macrophage polarization, yet the microbiota-immunity crosstalk remains mechanistically unresolved.
Methods:
APCmin/+ (CRC model, n = 8) and wild-type controls (n = 7) received 12-weeks HFD. We employed integrated metagenomic sequencing (Illumina NovaSeq) and immunohistochemistry (targeting CD206+ M2 macrophages) to investigate the linkages between the gut microbiota and the host.
Results:
CRC mice exhibited colonic adenocarcinoma with increased M2 macrophages. Gut microbiota in CRC mice showed enrichment of pro-inflammatory taxa (e.g., Bacteroides massiliensis, Vampirovibrion) and upregulated pathways (carbohydrate metabolism, mucin degradation). Strikingly, the relative abundances of Bacteroides massiliensis and Vampirovibrion showed significant positive correlations with CD206+ M2 macrophage infiltration levels.
Conclusion:
HFD induces microbiota-directed metabolic reprogramming and M2 polarization, synergistically accelerating CRC. Notably, targeting key pro-inflammatory taxa (e.g., B. massiliensis) or glycan hydrolysis pathways (e.g. GH95 enzyme) may provide mechanism-guided anti-CRC strategies.
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