ArticleFrontiers in oncology2022
Swimming Impedes Intestinal Microbiota and Lipid Metabolites of Tumorigenesis in Colitis-Associated Cancer.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Dextran sodium sulfate-induced colitis alters the proportion and composition of replicating gut bacteria.mSphere · 2025Article
- Lactobacillus-based probiotic cocktail inhibits colitis-associated cancer by altering intestinal metabolism.International journal of clinical and experimental pathology · 2025Article
- Peripheral immune and metabolic regulation of Aβ and Tau by exercise in Alzheimer's disease.Frontiers in immunology · 2025Review
- Swimming upregulates APOL3 through regulating macrophage polarization to inhibit glycolysis and the development of melanoma.3 Biotech · 2024Article
- Microbial dysbiosis index for assessing colitis status in mouse models: A systematic review and meta-analysis.iScience · 2024Article
- Effects of fucoidan and synbiotics supplementation during bismuth quadruple therapy ofFrontiers in nutrition · 2024Article
- A Bibliometric Analysis on the Research Trend of Exercise and the Gut Microbiome.Microorganisms · 2023Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Accumulating data support that regular physical activity potentially inhibits chronic colitis, a risk factor for colitis-associated cancer (CAC). However, possible effects of physical activity on CAC and the underlying mechanisms remain poorly understood. Methods: A pretreatment of swimming on azoxymethane/dextran sodium sulfate (AOM/DSS)-induced CAC mice was implemented to determine its protective effect. Inflammation and tumorigenesis were assessed using colorectums from C57BL/6 mice. In order to determine how swimming alters colonic lipid metabolism and gene expression, a comparative analysis was conducted. Meanwhile, alterations in intestinal microbiota and short-chain fatty acids (SCFAs) were detected and analyzed. Finally, an integration analysis of colonic lipid metabolism with gene expression and intestinal microbiota was performed respectively. Result: Swimming pretreatment relieved bowel inflammation and minimized tumor formation. We demonstrated that prostaglandin E2 (PGE2)/PGE2 receptor 2 subtype (EP2) signaling as a potential regulatory target for swimming induces colonic lipid metabolites. Swimming-induced genera, Erysipelatoclostridium, Parabacteroides, Bacteroides, and Rikenellaceae_RC9_gut_group, induced intestinal SCFAs and affected the function of colonic lipid metabolites enriched in glycerophospholipid metabolism and choline metabolism in cancer. Conclusion: According to our experiments, swimming pretreatment can protect mice from CAC by intervention in the possible link between colonic lipid metabolites and PGE2/EP2 signaling. Further, swimming-induced genera and probiotics promoted glycerophospholipid metabolism and choline metabolism in cancer, the major constituents of colonic lipid metabolites, and increased SCFAs, which were also important mechanisms for the anti-inflammatory and anti-tumorigenic effects of swimming.
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