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An Immunofluorescent Method for Characterization of Barrett&#8217;s Esophagus Cells
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Examining the connectivity between different cellular processes in the Barrett tissue microenvironment.

J J Phelan1, R Feighery1, O S Eldin2

  • 1Department of Surgery, Institute of Molecular Medicine, Trinity College Dublin, St. James's Hospital, Dublin, Ireland.

Cancer Letters
|December 22, 2015
PubMed
Summary
This summary is machine-generated.

Barrett esophagus tumorigenesis involves early metabolic reprogramming. This study links energy metabolism to hypoxia, inflammation, p53, and obesity in Barrett

Keywords:
Barrett oesophagusGlycolysisHypoxiaInflammationObesityOxidative phosphorylation

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Area of Science:

  • Gastroenterology and Oncology
  • Cellular Metabolism
  • Cancer Biology

Background:

  • Barrett's esophagus (BE) is a precursor to esophageal adenocarcinoma.
  • Metabolic reprogramming, including altered oxidative phosphorylation and glycolysis, is an early event in BE tumorigenesis.
  • The interplay between cellular metabolism and other key processes like hypoxia, inflammation, and tumor suppressor pathways in the BE microenvironment remains unclear.

Purpose of the Study:

  • To investigate the relationship between cellular metabolism (ATP5B/GAPDH) and critical factors in Barrett's esophagus.
  • To explore correlations with hypoxia (HIF1α), inflammation (IL1β/SERPINA3), p53, and obesity status.
  • To elucidate the role of metabolic reprogramming in the context of the BE microenvironment using in-vivo and ex-vivo models.

Main Methods:

  • Utilized in-vivo and ex-vivo models of Barrett's esophagus.
  • Quantified protein levels of key metabolic enzymes (ATP5B, GAPDH), hypoxia markers (HIF1α), inflammatory markers (IL1β, SERPINA3), and p53.
  • Performed correlation analyses to assess relationships between these factors and obesity status.

Main Results:

  • Strong positive correlations were observed between ATP5B and hypoxia (r=0.71), and between ATP5B and IL1β (r=0.8).
  • p53 expression was positively associated with both ATP5B (r=0.53) and hypoxia (r=0.455).
  • Obesity showed a negative association with oxidative phosphorylation (r=-0.6016) and a positive association with glycolysis (r=0.743).

Conclusions:

  • Cellular metabolism is intricately linked with hypoxia, inflammation, p53, and obesity in the Barrett's esophagus microenvironment.
  • These findings highlight the complex interplay of metabolic pathways and cellular signaling in BE progression.
  • Understanding these connections may offer novel therapeutic targets for esophageal adenocarcinoma.