Abstract

BackgroundEsophageal reflux and Barrett's esophagus represent two major risk factors for the development of esophageal adenocarcinoma. Previous studies have shown that brief exposure of the Barrett's-associated adenocarcinoma cell line, SEG-1, or primary cultures of Barrett's esophageal tissues to acid or bile results in changes consistent with cell proliferation. In this study, we determined whether similar exposure to acid or bile salts results in gene expression changes that provide insights into malignant transformation.MethodsUsing previously published methods, Barrett's-associated esophageal adenocarcinoma cell lines and primary cultures of Barrett's esophageal tissue were exposed to short pulses of acid or bile salts followed by incubation in culture media at pH 7.4. A genome-wide assessment of gene expression was then determined for the samples using cDNA microarrays. Subsequent analysis evaluated for statistical differences in gene expression with and without treatment.ResultsThe SEG-1 cell line showed changes in gene expression that was dependent on the length of exposure to pH 3.5. Further analysis using the Gene Ontology, however, showed that representation by genes associated with cell proliferation is not enhanced by acid exposure. The changes in gene expression also did not involve genes known to be differentially expressed in esophageal adenocarcinoma. Similar experiments using short-term primary cultures of Barrett's esophagus also did not result in detectable changes in gene expression with either acid or bile salt exposure.ConclusionShort-term exposure of esophageal adenocarcinoma SEG-1 cells or primary cultures of Barrett's esophagus does not result in gene expression changes that are consistent with enhanced cell proliferation. Thus other model systems are needed that may reflect the impact of acid and bile salt exposure on the esophagus in vivo.

Highlights

  • Esophageal reflux and Barrett's esophagus represent two major risk factors for the development of esophageal adenocarcinoma

  • The major risk factor for esophageal adenocarcinoma is the presence of Barrett's esophagus, a premalignant neoplastic lesion that is characterized by intestinal metaplasia replacing the normal squamous esophageal epithelia[2]

  • Primary cultures of Barrett's esophageal tissues exposed to short pulses of acid or bile salts show increased immunocytochemical staining for proliferating cell nuclear antigen (PCNA) or [3H]thymidine uptake, which serve as markers for cell proliferation [8,9,10]

Read more

Summary

Introduction

Esophageal reflux and Barrett's esophagus represent two major risk factors for the development of esophageal adenocarcinoma. Previous studies have shown that brief exposure of the Barrett's-associated adenocarcinoma cell line, SEG-1, or primary cultures of Barrett's esophageal tissues to acid or bile results in changes consistent with cell proliferation. Clinical studies have identified esophageal acid reflux as a risk factor for Barrett's esophagus and adenocarcinoma[3]. In vitro experiments using adenocarcionoma and non-neoplastic Barrett's esophageal cell lines established that short-term exposure to an acidic environment results in increase cell proliferation [5,6,7]. Primary cultures of Barrett's esophageal tissues exposed to short pulses of acid or bile salts show increased immunocytochemical staining for PCNA or [3H]thymidine uptake, which serve as markers for cell proliferation [8,9,10]

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.