期刊
SCIENCE
卷 338, 期 6103, 页码 120-123出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1224820
关键词
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资金
- NIH [T32 DK007737, R01 DK73338, R01 DK47700, R01 CA136887, R01 DK53347-11]
- American Institute for Cancer Research
- UNC University Cancer Research Fund
- New York Presbyterian/Weill Cornell Medical College
- Crohn's and Colitis foundation UK
- NIH Research Specialist Biomedical Research Center in Microbial Disease
- North West Cancer Research Fund UK
- Canadian Institutes of Health Research MOP [114872]
- King Abdulaziz University, through the Saudi Arabian Cultural Bureau in Canada
Inflammation alters host physiology to promote cancer, as seen in colitis-associated colorectal cancer (CRC). Here, we identify the intestinal microbiota as a target of inflammation that affects the progression of CRC. High-throughput sequencing revealed that inflammation modifies gut microbial composition in colitis-susceptible interleukin-10-deficient (Il10(-/-)) mice. Monocolonization with the commensal Escherichia coli NC101 promoted invasive carcinoma in azoxymethane (AOM)-treated Il10(-/-) mice. Deletion of the polyketide synthase (pks) genotoxic island from E. coli NC101 decreased tumor multiplicity and invasion in AOM/Il10(-/-) mice, without altering intestinal inflammation. Mucosa-associated pks(+) E. coli were found in a significantly high percentage of inflammatory bowel disease and CRC patients. This suggests that in mice, colitis can promote tumorigenesis by altering microbial composition and inducing the expansion of microorganisms with genotoxic capabilities.
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