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Targeted over-expression of mPGES-1 and elevated PGE2 production is not sufficient for lung tumorigenesis in mice

Stacy A Blaine1, Amy M Meyer, Greg Hurteau

  • 1Department of Pharmacology, University of Colorado Health Science Center, Denver, CO 80262, USA.

Carcinogenesis
|October 9, 2004
PubMed

Insights

Over-expression of microsomal prostaglandin E synthases-1 (mPGES-1) in mice did not lead to increased lung tumor formation. These findings suggest mPGES-1 alone is insufficient to drive lung tumorigenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Arachidonic acid metabolism enzymes and eicosanoids are implicated in cancer, with roles that can be both pro- and anti-tumorigenic.
  • Microsomal prostaglandin E synthase-1 (mPGES-1) is an enzyme in this pathway, and its specific role in lung cancer requires further elucidation.

Purpose of the Study:

  • To investigate the role of microsomal prostaglandin E synthase-1 (mPGES-1) over-expression in the development of lung tumors.
  • To determine if elevated mPGES-1 levels are sufficient to promote lung tumorigenesis.

Main Methods:

  • Generated transgenic mice with targeted over-expression of human mPGES-1 in lung epithelial cells using an SP-C promoter.
  • Exposed mice to urethane (complete carcinogen) or 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT) (initiation/promotion) protocols to induce lung tumors.
  • Assessed tumor incidence, multiplicity, and size at various time points; confirmed mPGES-1 and cyclooxygenase-2 (COX-2) expression via Western blot.

Main Results:

  • Transgenic mice (mPGES-1+) exhibited significantly increased mPGES-1 expression in the lungs, particularly in alveolar type II cells.
  • No significant differences in tumor incidence, multiplicity, or size were observed between mPGES-1+ and control mice following urethane or MCA/BHT treatment.
  • Western blot analysis confirmed elevated mPGES-1 and COX-2 levels in tumors from both groups, with higher overall mPGES-1 expression in the transgenic mice.

Conclusions:

  • Over-expression of microsomal prostaglandin E synthase-1 (mPGES-1) and consequent elevated prostaglandin E2 (PGE2) production are not sufficient to initiate or promote lung tumor formation.
  • The study indicates that other factors likely play a crucial role in mPGES-1's contribution to lung tumorigenesis.

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