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PGE(2) is generated by specific COX-2 activity and increases VEGF production in COX-2-expressing human pancreatic

Guido Eibl1, Dennis Bruemmer, Yuji Okada

  • 1Section of Gastrointestinal Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 72-231 CHS, Los Angeles, CA 90095-6904, USA.

Biochemical and Biophysical Research Communications
|June 25, 2003
PubMed

Insights

Cyclooxygenase-2 (COX-2) in pancreatic cancer cells produces prostaglandin E2 (PGE2). This PGE2 stimulates vascular endothelial growth factor (VEGF) secretion, promoting cancer cell growth and migration.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cyclooxygenase (COX) inhibition shows anti-cancer effects in some tumors.
  • The role of COX-derived prostaglandins in pancreatic cancer (PaCa) remains unclear.

Purpose of the Study:

  • To investigate the expression and function of COX enzymes in pancreatic cancer cell lines.
  • To determine the effect of prostaglandin E2 (PGE2) on vascular endothelial growth factor (VEGF) synthesis and endothelial cell migration in PaCa.

Main Methods:

  • Detection of COX-1 and COX-2 expression in PaCa cell lines.
  • Measurement of PGE2 production stimulated by arachidonic acid (AA).
  • Assessment of VEGF synthesis and endothelial cell migration in response to AA, PGE2, and cAMP analogs.

Main Results:

  • COX-2 was detected in a subset of PaCa cell lines, correlating with PGE2 production.
  • PGE2, generated via COX-2 activity, increased VEGF synthesis through the EP2 receptor in a COX-2 dependent manner.
  • AA stimulation of COX-2 expressing PaCa cells enhanced endothelial cell migration, an effect blocked by COX-2 inhibition.

Conclusions:

  • A subset of human pancreatic cancer cell lines express functional COX-2.
  • COX-2-derived PGE2 plays a role in increasing VEGF secretion via an autocrine mechanism.
  • This suggests a potential therapeutic target for pancreatic cancer treatment.

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