Cyclooxygenase-2 in glioblastoma multiforme

Drug Discov Today. 2017 Jan;22(1):148-156. doi: 10.1016/j.drudis.2016.09.017. Epub 2016 Sep 28.

Abstract

Glioblastoma multiforme (GBM) represents the most prevalent brain primary tumor, yet there is a lack of effective treatment. With current therapies, fewer than 5% of patients with GBM survive more than 5 years after diagnosis. Mounting evidence from epidemiological studies reveals that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is correlated with reduced incidence of GBM, suggesting that cyclooxygenase-2 (COX-2) and its major product within the brain, prostaglandin E2 (PGE2), are involved in the development and progression of GBM. Here, we highlight our current understanding of COX-2 in GBM proliferation, apoptosis, invasion, angiogenesis, and immunosuppression by focusing on recent in vitro and in vivo experimental data. We also discuss the feasibility of COX-2 as a therapeutic target for GBM in light of the latest human studies.

Publication types

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

MeSH terms

  • Animals
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Brain Neoplasms / drug therapy
  • Brain Neoplasms / enzymology*
  • Cell Proliferation / drug effects
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism*
  • Cyclooxygenase 2 Inhibitors / therapeutic use
  • Dinoprostone / genetics
  • Dinoprostone / metabolism*
  • Glioblastoma / drug therapy
  • Glioblastoma / enzymology*
  • Humans
  • Molecular Targeted Therapy
  • Neovascularization, Pathologic / drug therapy
  • Neovascularization, Pathologic / enzymology*
  • Prostaglandin-E Synthases / antagonists & inhibitors

Substances

  • Antineoplastic Agents
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase 2
  • Prostaglandin-E Synthases
  • Dinoprostone