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Nitric oxide induces cyclooxygenase expression and inhibits cell growth in colon cancer cell lines

Qiang Liu1, S T F Chan, Ratha Mahendran

  • 1Department of Surgery, National University Hospital, National University of Singapore, China.

Carcinogenesis
|May 3, 2003
PubMed

Insights

Nitric oxide (NO) donor S-nitrosoglutathione (GSNO) increased prostaglandin E2 (PGE2) and cyclooxygenase (COX) expression in colon cancer cells. Higher GSNO concentrations inhibited cell growth and induced apoptosis, independent of COX-2 levels.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The role of nitric oxide (NO) in colon cancer is debated, with conflicting reports on inducible nitric oxide synthase (iNOS) expression.
  • Cyclooxygenase-2 (COX-2) is implicated in colorectal carcinogenesis, but its interaction with NO in colon cancer is unexplored.

Purpose of the Study:

  • To investigate the effects of the NO donor S-nitrosoglutathione (GSNO) on colon cancer cell lines with varying COX-2 expression.
  • To examine the relationship between NO, prostaglandin E2 (PGE2) production, and COX-1/COX-2 protein expression in colon cancer.

Main Methods:

  • Three human colon cancer cell lines (HCA7, HT29, HCT116) were treated with GSNO (10-500 micro M).
  • Assays included cell growth, PGE2 production, COX-1/COX-2 protein expression, and cell-cycle distribution analysis.

Main Results:

  • GSNO dose- and time-dependently increased PGE2 production and induced COX-1 and COX-2 protein expression.
  • Higher GSNO concentrations inhibited cell growth and induced apoptosis across all cell lines, irrespective of initial COX-2 status.
  • Blocking PGE2 production did not enhance GSNO's inhibitory effects on cell growth.

Conclusions:

  • NO donors like GSNO can modulate COX pathway components in colon cancer cells.
  • GSNO exhibits direct anti-proliferative and pro-apoptotic effects on colon cancer cells, independent of COX-2 expression levels.
  • The findings suggest a complex interplay between NO and COX pathways in colon cancer, with potential therapeutic implications for NO-based strategies.

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