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Selective cyclooxygenase-2 inhibition suppresses basic fibroblast growth factor expression in human esophageal

Mark Baguma-Nibasheka1, Christie Barclay, Audrey W Li

  • 1Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.

Molecular Carcinogenesis
|May 5, 2007
PubMed

Insights

Selective cyclooxygenase (COX)-2 inhibitors suppress esophageal adenocarcinoma growth by reducing basic fibroblast growth factor (FGF-2). This suggests COX-2 is a potential therapeutic target and biomarker for EADC, impacting patient outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cyclooxygenase (COX)-2 inhibition shows potential against human esophageal adenocarcinoma (EADC).
  • The exact biological mechanism of COX-2 inhibitors in EADC is not fully understood.
  • Basic fibroblast growth factor (FGF-2) is overexpressed in EADC and may be involved in tumor growth.

Purpose of the Study:

  • To investigate if COX-2 inhibitors' antitumor activity in EADC involves modulating FGF-2.
  • To evaluate the effects of a selective COX-2 inhibitor (NS-398) on FGF-2 expression and EADC cell proliferation.
  • To correlate COX-2 and FGF-2 expression with clinical findings and patient outcomes in EADC.

Main Methods:

  • Utilized EADC cell lines with and without COX-2 expression (Seg-1 and Bic-1).
  • Treated cells with NS-398 (selective COX-2 inhibitor) and assessed FGF-2 levels and proliferation.
  • Administered exogenous FGF-2 and anti-FGF-2 antibodies to evaluate their impact on cell growth and apoptosis.
  • Analyzed COX-2 and FGF-2 expression in patient tumor tissues and correlated with clinical data.

Main Results:

  • NS-398 significantly inhibited proliferation and induced apoptosis in COX-2-expressing EADC cells (Seg-1).
  • NS-398 treatment reduced FGF-2 levels in Seg-1 cells; FGF-2 levels rebounded upon drug removal.
  • The antitumor effects of NS-398 were diminished by exogenous FGF-2, and enhanced by anti-FGF-2 antibodies.
  • NS-398 had no effect on EADC cells lacking COX-2 expression (Bic-1).
  • COX-2 was highly expressed in 46% of EADC tissues, showing a trend towards reduced disease-free survival.

Conclusions:

  • The antitumor effects of COX-2 inhibition in EADC are likely mediated through the suppression of FGF-2.
  • COX-2 plays a significant role in EADC cell proliferation and survival.
  • COX-2 may serve as a clinically relevant molecular marker for managing human EADC.
  • Targeting COX-2 offers a potential therapeutic strategy for EADC, possibly in conjunction with FGF-2 modulation.

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