ArticleCancer research2010
Bile acid reflux contributes to development of esophageal adenocarcinoma via activation of phosphatidylinositol-specific phospholipase Cgamma2 and NADPH oxidase NOX5-S.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- PLCG2, A Regulator of Lung Adenocarcinoma Proliferation and Migration Associated with Immune Infiltration.Current cancer drug targets · 2025Article
- Development of a novel oncolytic adenovirus controlled by CDX2 promoter for esophageal adenocarcinoma therapy.Journal of gastroenterology · 2024Article
- In Silico Analysis of Non-Conventional Oxidative Stress-Related Enzymes and Their Potential Relationship with Carcinogenesis.Antioxidants (Basel, Switzerland) · 2024Article
- Taurodeoxycholic acid-YAP1 upregulates OTX1 in promoting gallbladder cancer malignancy through IFITM3-dependent AKT activation.Oncogene · 2023Article
- Elevation of fatty acid desaturase 2 in esophageal adenocarcinoma increases polyunsaturated lipids and may exacerbate bile acid-induced DNA damage.Clinical and translational medicine · 2022Article
- Intestinal Metaplasia in the Esophageal Remnant Is Rare After Ivor Lewis Esophagectomy.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2021Article
- Critical roles of bile acids in regulating intestinal mucosal immune responses.Therapeutic advances in gastroenterology · 2021Review
- Cholic Acid Stimulates MMP-9 in Human Colon Cancer Cells via Activation of MAPK, AP-1, and NF-κB Activity.International journal of molecular sciences · 2020Article
- Phospholipase C.Advances in experimental medicine and biology · 2020Review
- Carcinogenesis and Reactive Oxygen Species Signaling: Interaction of the NADPH Oxidase NOX1-5 and Superoxide Dismutase 1-3 Signal Transduction Pathways.Antioxidants & redox signaling · 2019Review
- Effects of curcumin on canine semen parameters and expression of NOX5 gene in cryopreserved spermatozoa.Veterinary research forum : an international quarterly journal · 2019Article
- NADPH oxidase 5 (NOX5)-induced reactive oxygen signaling modulates normoxic HIF-1α and p27Molecular carcinogenesis · 2017Article
- Endoscopic assessment and management of early esophageal adenocarcinoma.World journal of gastrointestinal oncology · 2014Review
- Regulation of NADPH oxidase 5 by protein kinase C isoforms.PloS one · 2014Article
- Evolution of the ferric reductase domain (FRD) superfamily: modularity, functional diversification, and signature motifs.PloS one · 2013Article
- NOX5 in human spermatozoa: expression, function, and regulation.The Journal of biological chemistry · 2012Article
- Signaling in H2O2-induced increase in cell proliferation in Barrett's esophageal adenocarcinoma cells.The Journal of pharmacology and experimental therapeutics · 2011Article
- Association of NOX5 Expression with Sperm Activity and Motility in Pathospermic Infertile Men.Journal of reproduction & infertilityArticle
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Gastroesophageal reflux disease complicated by Barrett's esophagus (BE) is a major risk factor for esophageal adenocarcinoma (EA). However, the mechanisms of the progression from BE to EA are not fully understood. Besides acid reflux, bile acid reflux may also play an important role in the progression from BE to EA. In this study, we examined the role of phosphatidylinositol-specific phospholipase C (PI-PLC) and a novel NADPH oxidase NOX5-S in bile acid-induced increase in cell proliferation. We found that taurodeoxycholic acid (TDCA) significantly increased NOX5-S expression, hydrogen peroxide (H(2)O(2)) production, and cell proliferation in EA cells. The TDCA-induced increase in cell proliferation was significantly reduced by U73122, an inhibitor of PI-PLC. PI-PLCbeta1, PI-PLCbeta3, PI-PLCbeta4, PI-PLCgamma1, and PI-PLCgamma2, but not PI-PLCbeta2 and PI-PLCdelta1, were detectable in FLO cells by Western blot analysis. Knockdown of PI-PLCgamma2 or extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein (MAP) kinase with small interfering RNAs (siRNA) significantly decreased TDCA-induced NOX5-S expression, H(2)O(2) production, and cell proliferation. In contrast, knockdown of PI-PLCbeta1, PI-PLCbeta3, PI-PLCbeta4, PI-PLCgamma1, or ERK1 MAP kinase had no significant effect. TDCA significantly increased ERK2 phosphorylation, an increase that was reduced by U73122 or PI-PLCgamma2 siRNA. We conclude that TDCA-induced increase in NOX5-S expression and cell proliferation may depend on sequential activation of PI-PLCgamma2 and ERK2 MAP kinase in EA cells. It is possible that bile acid reflux present in patients with BE may increase reactive oxygen species production and cell proliferation via activation of PI-PLCgamma2, ERK2 MAP kinase, and NADPH oxidase NOX5-S, thereby contributing to the development of EA.
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