ArticleOncotarget2017
Repression of intestinal transporters and FXR-FGF15 signaling explains bile acids dysregulation in experimental colitis-associated colon cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Suppressed intestinal secondary bile acids in moxifloxacin-induced hyperglycemia: studies in normal and diabetic GK rats.Frontiers in pharmacology · 2025Article
- Farnesoid X receptor mediates macrophage-intrinsic responses to suppress colitis-induced colon cancer progression.JCI insight · 2024Article
- Postoperative diarrhea in Crohn's disease: Pathogenesis, diagnosis, and therapy.World journal of clinical cases · 2023Review
- New Insights into Bile Acids Related Signaling Pathways in the Onset of Colorectal Cancer.Nutrients · 2022Review
- Bile acid metabolism dysregulation associates with cancer cachexia: roles of liver and gut microbiome.Journal of cachexia, sarcopenia and muscle · 2021Article
- Targeting Farnesoid X receptor (FXR) for developing novel therapeutics against cancer.Molecular biomedicine · 2021Review
- Deoxycholic Acid-Induced Gut Dysbiosis Disrupts Bile Acid Enterohepatic Circulation and Promotes Intestinal Inflammation.Digestive diseases and sciences · 2021Article
- IBD and Bile Acid Absorption: Focus on Pre-clinical and Clinical Observations.Frontiers in physiology · 2020Review
- Orally Administered Crocin Protects Against Cerebral Ischemia/Reperfusion Injury Through the Metabolic Transformation of Crocetin by Gut Microbiota.Frontiers in pharmacology · 2019Article
- A novel bioluminescence-based method to investigate uptake of bile acids in living cells.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bile acids (BAs) are important endogenous signaling molecules that play vital roles in the pathological development of various diseases including colitis-associated cancer (CAC). BAs were previously found dysregulated under conditions of CAC; however, the exact patterns and underlying molecular mechanisms remain largely elusive. Based on the development of a method for comprehensive analysis of BAs, this study aims to elucidate the dysregulation patterns and involved mechanisms in a typical CAC model induced by azoxymethane (AOM)/dextran sodium sulfate (DSS). CAC mice showed decreased BAs transformation in gut and glucuronidation in colon, leading to accumulation of primary BAs but reduction of secondary BAs in colon. CAC mice were characterized by an accumulation of BAs in various compartments except ileum, which is in line with repressed ileal FXR-FGF15 feedback signaling and the increased expression of hepatic CYP7A1. The compromised ileal FXR-FGF15 signaling was caused in part by the reduced absorption of FXR ligands including free and tauro-conjungated BAs due to the downregulation of various transporters of BAs in the ileum of CAC mice.
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