ArticleCellular oncology (Dordrecht, Netherlands)2021
Bile acids increase intestinal marker expression via the FXR/SNAI2/miR-1 axis in the stomach.
Article in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- A TRIM15-CDX2 loop drives bile acid-induced gastric intestinal metaplasia.Molecular medicine (Cambridge, Mass.) · 2026Article
- Chronic Pain and Cognitive Dysfunction: Clinical Implement, Mechanism, and Therapeutic Strategy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Single-cell atlas of gastric cancer reveals malignant epithelial evolution and regulatory reprogramming of the tumor microenvironment.PloS one · 2026Article
- Long non-coding RNA PVT1 mediates bile acid-induced gastric intestinal metaplasia via a miR-34b-5p/HNF4α positive feedback loop.Chinese medical journal · 2025Article
- TFF3 initiates gastric intestinal metaplasia by activating JAK2 and STAT3 under high salt conditions.Scientific reports · 2025Article
- GATA4 Forms a Positive Feedback Loop with CDX2 to Transactivate MUC2 in Bile Acids-Induced Gastric Intestinal Metaplasia.Gut and liver · 2024Article
- Gastric intestinal metaplasia: progress and remaining challenges.Journal of gastroenterology · 2024Review
- Bile acids inhibit ferroptosis sensitivity through activating farnesoid X receptor in gastric cancer cells.World journal of gastroenterology · 2024Article
- Identification of miR-1 and miR-499 in chronic atrial fibrillation by bioinformatics analysis and experimental validation.Frontiers in cardiovascular medicine · 2024Article
- Targeting Farnesoid X Receptor in Tumor and the Tumor Microenvironment: Implication for Therapy.International journal of molecular sciences · 2023Review
- Article
- Exploration of gastric carcinogenesis from the relationship between bile acids and intestinal metaplasia and intragastric microorganisms (H. pylori and non-H. pylori).Journal of cancer research and clinical oncology · 2023Review
- Alteration of gastric microbiota and transcriptome in a rat with gastric intestinal metaplasia induced by deoxycholic acid.Frontiers in microbiology · 2023Article
- Inflammatory microenvironment in gastric premalignant lesions: implication and application.Frontiers in immunology · 2023Review
- TCF7/SNAI2/miR-4306 feedback loop promotes hypertrophy of ligamentum flavum.Journal of translational medicine · 2022Article
- Bile Acid-Microbiome Interaction Promotes Gastric Carcinogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Roles and action mechanisms of bile acid-induced gastric intestinal metaplasia: a review.Cell death discovery · 2022Review
- Serum Total Bile Acids in Relation to Gastrointestinal Cancer Risk: A Retrospective Study.Frontiers in oncology · 2022Article
- Identification and Validation of miRNA-TF-mRNA Regulatory Networks in Uterine Fibroids.Frontiers in bioengineering and biotechnology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
purposeIntestinal metaplasia (IM) is a precancerous lesion that increases the risk of subsequent gastric cancer (GC) development. Previously, miR-1 has been shown to play an essential role in the initiation of bile acid (BA)-induced IM. The objective of the present study was to investigate the mechanism underlying miR-1 inhibition by BA in gastric cells.
methodsIngenuity pathway analysis (IPA) was used to identify molecules acting upstream of miR-1. The effects of deoxycholic acid (DCA), FXR and SNAI2 on the expression of intestinal markers were assessed using quantitative real-time PCR (qRT-PCR) and Western blotting. The expression level of major molecules was detected by immunohistochemistry (IHC) in tissue microarrays. The transcriptional regulation of miR-1 was verified using luciferase reporter and chromatin immunoprecipitation (ChIP) assays.
resultsWe found that BA treatment caused aberrant expression of FXR and intestinal markers in gastric cells. Augmented FXR led to transcriptional activation of SNAI2, which in turn suppressed the miR-1 promoter. Moreover, we found that compared with normal tissues, the expression levels of both FXR and SNAI2 were increased and positively correlated with each other in IM tissues. Additionally, their expression showed an inverse correlation with that of miR-1 in IM tissues.
conclusionsOur findings indicate that FXR may be responsible for a series of molecular changes in gastric cells after BA treatment, and that the FXR/SNAI2/miR-1 axis exhibits a crucial role in BA-induced progression of IM. Blocking the FXR-oriented axis may provide a promising approach for IM or even GC treatment.
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