ArticleCancer research communications2024
Putrescine Supplementation Limits the Expansion of pks+ Escherichia coli and Tumor Development in the Colon.
Article in Cancer research communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Stage-Specific carcinogenic mechanisms and intervention strategies for pksArchives of microbiology · 2026Review
- Harnessing the microbiome for cancer therapy.Nature reviews. Microbiology · 2026Review
- Expansion resistance against genotoxicFrontiers in microbiology · 2026Article
- Surface expression of antitoxin on engineered bacteria neutralizes genotoxic colibactin in the gut.Nature microbiology · 2026Article
- Using Postbiotics from Functional Foods for Managing Colorectal Cancer: Mechanisms, Sources, Therapeutic Potential, and Clinical Perspectives.Microorganisms · 2025Review
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli that harbor the polyketide synthase (pks) genomic island produce colibactin and are associated with sporadic colorectal cancer development. Given the considerable prevalence of pks+ bacteria in healthy individuals, we sought to identify strategies to limit the growth and expansion of pks+ E. coli. We found that culture supernatants of the probiotic strain E. coli Nissle 1917 were able to inhibit the growth of the murine pathogenic strain pks+ E. coli NC101 (EcNC101). We performed a nontargeted analysis of the metabolome in supernatants from several E. coli strains and identified putrescine as a potential postbiotic capable of suppressing EcNC101 growth in vitro. The effect of putrescine supplementation was then evaluated in the azoxymethane/dextran sulfate sodium mouse model of colorectal cancer in mice colonized with EcNC101. Putrescine supplementation inhibited the growth of pks+ E. coli, reduced the number and size of colonic tumors, and downmodulated the release of inflammatory cytokines in the colonic lumen. Additionally, putrescine supplementation led to shifts in the composition and function of gut microbiota, characterized by an increase in the Firmicutes/Bacteroidetes ratio and enhanced acetate production. The effect of putrescine was further confirmed in vitro using a pks+ E. coli strain isolated from a patient with colorectal cancer. These results suggest that probiotic-derived metabolites can be used as an alternative to live bacteria in individuals at risk of developing colorectal cancer due to the presence of pks+ bacteria in their colon. SIGNIFICANCE: Putrescine supplementation inhibits the growth of cancer-promoting bacteria in the gut, lowers inflammation, and reduces colon cancer development. The consumption of healthy foods rich in putrescine may be a potential prophylactic approach for individuals at risk of developing colorectal cancer due to the presence of pks+ bacteria in their colon.
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