Document Detail

The resistance of esophageal adenocarcinoma to bile salt insult is associated with manganese superoxide dismutase expression.
MedLine Citation:
PMID:  20638682     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Bile acids are implicated as etiologic agents in esophageal cancer. We sought to analyze the impact of bile acid exposure on esophageal epithelial cells, Barrett's metaplastic cells (BE), esophageal adenocarcinoma cells (EAC), and esophageal squamous carcinoma cell (ESC). We sought to determine if cellular resistance is related to manganese superoxide dismutase expression.
METHODS: Cells were exposed to sodium choleate (CA), sodium deoxycholate (DCA), sodium glycocholate (GCA), sodium taurocholate (TCA), or a 1:1 mixture (MIX) of reagents at concentrations in the range 0.2-0.8 mM. Cell viability was evaluated by MTT assay. Manganese superoxide dismutase (MnSOD) expression was analyzed by Western blot. Statistical analysis was performed using SPSS ver. 17.0, SPSS Inc., Chicago, IL.
RESULTS: Bile salt exposure inhibited cell viability in esophageal squamous cells in time- and growth-dependent manner. There was a 50% decrease in cell viability from 4 to 24 h. BE, EAC, and ESC cell lines were more resistant to bile insult. In untreated cell lines, MnSOD expression was significantly decreased in EAC and ESC cell lines compared with esophageal squamous epithelial cells and BE cells (P=0.002). Exposure of ESC cells to bile salt increased MnSOD expression.
CONCLUSION: The confirmation of the role of reactive oxygen species (ROS) and bile acids in esophageal carcinogenesis has interesting implications for chemoprevention in patients with reflux esophagitis and Barrett's esophagus. Further studies are necessary to assess the preventative role of antioxidant supplementation.
Suzanne C Schiffman; Yan Li; Deyi Xiao; Xuanshe Li; Harini S Aiyer; Robert C G Martin
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-05-21
Journal Detail:
Title:  The Journal of surgical research     Volume:  171     ISSN:  1095-8673     ISO Abbreviation:  J. Surg. Res.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-11-14     Completed Date:  2012-01-06     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  623-30     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Department of Surgery, Division of Surgical Oncology, University of Louisville, Louisville, Kentucky 40202, USA.
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MeSH Terms
Adenocarcinoma / metabolism*,  pathology*
Antioxidants / metabolism
Barrett Esophagus / metabolism,  pathology
Bile Acids and Salts / metabolism*,  toxicity
Carcinoma, Squamous Cell / metabolism,  pathology
Cell Line, Transformed
Cell Line, Tumor
Cell Survival / drug effects,  physiology
Esophageal Neoplasms / metabolism*,  pathology*
Oxidative Stress / drug effects,  physiology
Reactive Oxygen Species / metabolism
Superoxide Dismutase / metabolism*
Grant Support
R03 CA137801-01/CA/NCI NIH HHS; R03CA137801/CA/NCI NIH HHS
Reg. No./Substance:
0/Antioxidants; 0/Bile Acids and Salts; 0/Reactive Oxygen Species; EC Dismutase

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