ArticleScientific reports2016
Bile acid receptor TGR5, NADPH Oxidase NOX5-S and CREB Mediate Bile Acid-Induced DNA Damage In Barrett's Esophageal Adenocarcinoma Cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Etiology and Pathophysiology of Barrett's Esophagus/Neoplasia.Digestion · 2026Review
- The cancer microbiome.Advances in clinical chemistry · 2025Review
- ABL1‒YAP1 axis in intestinal stem cell activated by deoxycholic acid contributes to hepatic steatosis.Journal of translational medicine · 2024Article
- Obesity increases genomic instability at DNA repeat-mediated endogenous mutation hotspots.Nature communications · 2024Article
- Structure, regulation, and physiological functions of NADPH oxidase 5 (NOX5).Journal of physiology and biochemistry · 2023Review
- The role of TGR5 as an onco-immunological biomarker in tumor staging and prognosis by encompassing the tumor microenvironment.Frontiers in oncology · 2022Article
- Bile reflux and hypopharyngeal cancer (Review).Oncology reports · 2021Review
- Current research progress in the role of reactive oxygen species in esophageal adenocarcinoma.Translational cancer research · 2021Review
- Sarcopenia Induced by Chronic Liver Disease in Mice Requires the Expression of the Bile Acids Membrane Receptor TGR5.International journal of molecular sciences · 2020Article
- Gut dysbacteriosis and intestinal disease: mechanism and treatment.Journal of applied microbiology · 2020Review
- Update onCancers · 2020Review
- Bile Acid Receptors and Gastrointestinal Functions.Liver research (Beijing, China) · 2019Article
- TGR5 expression in normal kidney and renal neoplasms.Diagnostic pathology · 2018Article
- Organic Solute Transporter α-β Protects Ileal Enterocytes From Bile Acid-Induced Injury.Cellular and molecular gastroenterology and hepatology · 2018Article
- Activation of NADPH oxidases leads to DNA damage in esophageal cells.Scientific reports · 2017Article
- TGR5 expression in benign, preneoplastic and neoplastic lesions of Barrett's esophagus: Case series and findings.World journal of gastroenterology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms whereby bile acid reflux may accelerate the progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA) are not fully understood. In this study we found that bile acid taurodeoxycholic acid (TDCA) significantly increased the tail moment (TM) and histone H2AX phosphorylation in FLO-1 EA cells, an increase which was significantly decreased by knockdown of TGR5. Overexpression of TGR5 significantly increased TDCA-induced TM increase and H2AX phosphorylation. In addition, NADPH oxidase inhibitor diphenylene iodonium significantly inhibited the TDCA-induced increase in TM and H2AX phosphorylation. TDCA-induced increase in TM and H2AX phosphorylation was significantly decreased by knockdown of NOX5-S and overexpression of NOX5-S significantly increased TDCA-induced increase in the tail moment and H2AX phosphorylation. Furthermore, TDCA significantly increased cAMP response element binding protein (CREB) phosphorylation in FLO-1 cells. Knockdown of CREB significantly decreased TDCA-induced increase in NOX5-S mRNA and the tail moment. Conversely, overexpression of CREB significantly increased TDCA-induced TM increase. We conclude that TDCA-induced DNA damage may depend on the activation of TGR5, CREB and NOX5-S. It is possible that in Barrett's patients bile acids may activate NOX5-S and increase reactive oxygen species (ROS) production via activation of TGR5 and CREB. NOX5-S-derived ROS may cause DNA damage, thereby contributing to the progression from BE to EA.
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