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Overexpression of the fragile histidine triad (FHIT) gene in inflammatory bowel disease

P M Wierzbicki1, K Adrych, D Kartanowicz

  • 1Department of Histology, Medical University of Gdansk, Gdansk, Poland. pwierzb@amg.gda.pl

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society
|January 20, 2010
PubMed
Abstract

Insights

The FHIT gene is overexpressed in active ulcerative colitis (UC), suggesting a protective role against inflammation and DNA damage in this inflammatory bowel disease (IBD). This finding highlights FHIT

Area of Science:

  • Molecular biology
  • Gastroenterology
  • Oncology

Background:

  • The FHIT gene encodes a human diadenosine triphosphate hydrolase.
  • FHIT is implicated in cell cycle regulation and nucleotide metabolism.
  • FHIT is a candidate tumor suppressor gene.

Purpose of the Study:

  • Investigate FHIT gene expression at mRNA and protein levels in sporadic inflammatory bowel disease (IBD).
  • Determine if FHIT expression differs between ulcerative colitis (UC) and Crohn's disease (CD).

Main Methods:

  • FHIT mRNA quantified using quantitative real-time PCR (QPCR).
  • FHIT protein detected by immunohistochemistry (IHC).
  • Analysis performed on mucosal biopsies from 139 UC patients, 19 CD patients, and 37 controls.

Main Results:

  • Significant FHIT gene overexpression observed in 78% of active UC patients.
  • No significant FHIT overexpression found in Crohn's disease (CD) patients.
  • Immunohistochemistry results correlated with QPCR findings.

Conclusions:

  • Local up-regulation of FHIT gene and protein in active UC may be a response to inflammatory challenges.
  • Increased FHIT expression might protect epithelial cell homeostasis.
  • FHIT up-regulation could guard against DNA damage and cell cycle disturbances in UC.

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