Prostaglandin E2 Signaling: Alternative Target for Glioblastoma?

Trends Cancer. 2017 Feb;3(2):75-78. doi: 10.1016/j.trecan.2016.12.002. Epub 2017 Jan 11.

Abstract

Elevated cyclooxygenase-2 (COX-2) and the associated inflammation within the brain contribute to glioblastoma development. However, medical use of COX inhibitors in glioblastoma treatment has been limited due to their well-documented vascular toxicity and inconsistent outcomes from recent human studies. Prostaglandin E2 (PGE2) has emerged as a principal mediator for COX-2 cascade-driven gliomagenesis. Are PGE2 terminal synthases and receptors feasible therapeutic targets for glioblastoma?

Keywords: EP receptors; PGE(2); glioblastoma; gliomagenesis; mPGES-1; neuroinflammation.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 Inhibitors / adverse effects
  • Dinoprostone / antagonists & inhibitors*
  • Dinoprostone / genetics
  • Glioblastoma / drug therapy*
  • Glioblastoma / genetics
  • Glioblastoma / pathology
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Inflammation / pathology
  • Molecular Targeted Therapy*
  • Signal Transduction

Substances

  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase 2
  • Dinoprostone