ArticleCancer2011
Induction of MUC5AC mucin by conjugated bile acids in the esophagus involves the phosphatidylinositol 3-kinase/protein kinase C/activator protein-1 pathway.
Article in Cancer, 2011. 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, 23 citations in OpenAlex.
- The Role of Mucins in Esophageal Inflammatory Diseases.Journal of personalized medicine · 2026Review
- MiRNA expression analysis from circulating exosomes in Barrett's esophagus patients with visceral obesity.Scientific reports · 2025Article
- Multidimensional mechanisms and therapies underlying gastroesophageal reflux disease: focus on immunity, signaling pathways, and the microbiota-gut-brain axis.Frontiers in immunology · 2025Review
- Bile Acids in Pancreatic Carcinogenesis.Metabolites · 2024Review
- Bile accelerates carcinogenic processes in pancreatic ductal adenocarcinoma cells through the overexpression of MUC4.Scientific reports · 2020Article
- Transcriptomic profiling reveals three molecular phenotypes of adenocarcinoma at the gastroesophageal junction.International journal of cancer · 2019Article
- From genetics to signaling pathways: molecular pathogenesis of esophageal adenocarcinoma.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- A highly integrated precision nanomedicine strategy to target esophageal squamous cell cancer molecularly and physically.Nanomedicine : nanotechnology, biology, and medicine · 2018Article
- Ramifications of secreted mucin MUC5AC in malignant journey: a holistic view.Carcinogenesis · 2018Review
- microRNA involvement in the onset and progression of Barrett's esophagus: a systematic review.Oncotarget · 2018Review
- The Antitumor Effect of Xihuang Pill on Treg Cells Decreased in Tumor Microenvironment of 4T1 Breast Tumor-Bearing Mice by PI3K/AKT~AP-1 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- High mucin 5AC expression predicts adverse postoperative recurrence and survival of patients with clear-cell renal cell carcinoma.Oncotarget · 2017Article
- Bile acids-mediated overexpression of MUC4 via FAK-dependent c-Jun activation in pancreatic cancer.Molecular oncology · 2016Article
- Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction.Cancer biology & therapy · 2013Review
- The role of mucin in GERD and its complications.Nature reviews. Gastroenterology & hepatology · 2011Article
- MUC5AC Expression in Various Tumor Types and Nonneoplastic Tissue: A Tissue Microarray Study on 10 399 Tissue Samples.Technology in cancer research & treatmentArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBile reflux contributes to the development of esophageal injury and neoplasia. The mucin 5AC (MUC5AC) is absent in the normal squamous epithelium of the esophagus but is strongly expressed in Barrett esophagus (BE). The objective of this study was to determine whether and how bile acids influence the expression of MUC5AC in the esophagus.
methodsMUC5AC expression was studied by immunohistochemistry and immunoblotting in human tissues, in tissues from a rat model of BE, and in SKGT-4 cultured esophageal epithelial cells. MUC5AC transcription was studied by real-time polymerase chain reaction and transient transfection assays.
resultsMUC5AC was absent from normal squamous epithelium but was present in 100% of Barrett specimens and in 61.5% of human esophageal adenocarcinoma tissues that were examined. MUC5AC protein expression was induced to a greater degree by conjugated bile acids than by unconjugated bile acids, and this occurred at the transcriptional level. In the rat reflux model, MUC5AC mucin was expressed abundantly in tissues of BE stimulated by duodenoesophageal reflux. Conjugated bile acids induced AKT phosphorylation in SKGT-4 cells but had no effect on extracellular signal-regulated protein kinases 1 and 2, c-Jun N-terminal kinase, or protein-38 kinase phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and a dominant-negative protein kinase C (AKT) construct prevented the induction of MUC5AC by conjugated bile acids. Transactivation of AP-1 by conjugated bile acids coincided with MUC5AC induction, and cotransfection with a dominant-negative activator protein-1 (AP-1) vector decreased MUC5AC transcription and its induction.
conclusionsConjugated bile acids in the bile refluxate contribute to MUC5AC induction in the esophagus. This occurs at the level of transcription and involves activation of the PI3K/AKT/AP-1 pathway.
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