ArticleInternational journal of oncology2019
Bile acids promote gastric intestinal metaplasia by upregulating CDX2 and MUC2 expression via the FXR/NF-κB signalling pathway.
Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Meta-Analysis Reveals the Prognostic Relevance of Nuclear and Membrane-Associated Bile Acid Receptors in Gastric Cancer.Clinical and translational gastroenterology · 2021Pooled it
- Endoscopic grading of gastric intestinal metaplasia and microvascular pattern for assessing gastric cancer risk: a prospective study.Annals of medicine · 2026Article
- A TRIM15-CDX2 loop drives bile acid-induced gastric intestinal metaplasia.Molecular medicine (Cambridge, Mass.) · 2026Article
- The dual role of gastric microbiota dysbiosis in gastric cancer progression and therapy.International journal of clinical oncology · 2026Review
- The Farnesoid X receptor-bile acid axis contributes to immune evasion in gastric cancer and its inhibition enhances efficacy of anti-PD-L1 therapy.Biochemistry and biophysics reports · 2026Article
- Gastric intestinal metaplasia: unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention.Cellular and molecular life sciences : CMLS · 2026Review
- Hyodeoxycholic acid relieves neuropathic pain by activating farnesoid X receptor signaling.Journal of advanced research · 2026Article
- A Gut Signature of Microbiome, Bile Acid, and Quorum-Sensing Profiles Is Associated withMicroorganisms · 2026Article
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 2026Review
- Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.Frontiers in immunology · 2026Article
- Integrated microbial and transcriptomic profiling reveals distinct correlations in atrophic gastritis associated with liver cirrhosis.Frontiers in cellular and infection microbiology · 2026Article
- Targetable pathways for drug repurposing in gastric cancer.World journal of gastroenterology · 2025Review
- Multifaceted roles of microbiota-derived deoxycholic acid in gastrointestinal cancers: from barrier disruption to therapeutic implications.Human cell · 2025Review
- Article
- The effects of mechanical stimulation on the morphology and function of spinal ligament cells.BMC musculoskeletal disorders · 2025Article
- Blood metabolites, mitochondrial biofunction, and cervical cancer: a bidirectional Mendelian randomization study.BMC women's health · 2025Article
- Research progress on monocyte/macrophage in the development of gastric cancer.Future oncology (London, England) · 2025Review
- Application of an organoid-based model to exploreFrontiers in cellular and infection microbiology · 2025Article
- Advances in modeling gastric intestinal metaplasia: a comprehensive review of experimental models and mechanistic insights.Frontiers in oncology · 2025Review
- Bile acids affect intestinal barrier function through FXR and TGR5.Frontiers in medicine · 2025Review
17 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bile acids serve a critical role in the induction of gastric intestinal metaplasia (IM) and gastric carcinogenesis. The present study investigated the effects of bile acids on the induction of gastric IM formation. The results demonstrated that the expression levels of caudal‑related homeobox transcription factor 2 (CDX2), mucin 2 (MUC2) and farnesoid X receptor (FXR) were increased in vitro and in vivo following treatment with bile acids, and CDX2 transcriptionally activated MUC2 expression. Furthermore, knockdown of FXR attenuated bile acid‑enhanced CDX2 promoter activity and protein expression. Conversely, the FXR agonist GW4064 synergistically enhanced bile acid‑induced CDX2 promoter activity. Bile acid treatment led to an increase in nuclear factor (NF)‑κB activity and protein expression. Treatment with GW4064 or the FXR antagonist Z‑guggulsterone enhanced or attenuated bile acid‑induced NF‑κB activity, respectively. In addition, quantitative chromatin immunoprecipitation confirmed that bile acids led to enhanced binding of p50 to the CDX2 promoter, whereas this effect was not observed for p65. Treatment with GW4064 or Z‑guggulsterone enhanced and attenuated the binding activity of p50 to the CDX2 promoter, respectively. These results indicated that bile acids may activate the FXR/NF‑κB signalling pathway, thereby upregulating CDX2 and MUC2 expression in normal gastric epithelial cells.
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