| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5520979 | Drug Discovery Today | 2017 | 9 Pages |
â¢Current treatment for glioblastoma fails to provide sufficient therapeutic outcomes.â¢Overexpressed cyclooxygenase-2 (COX-2) contributes to the glioblastoma progression.â¢COX-2 plays complex roles in glioma invasion, angiogenesis, immunosuppression, etc.â¢COX-2 inhibitors sensitize glioblastomas to conventional chemo- and radio-therapies.â¢COX-2 downstream signaling pathways might provide alternative targets for gliomas.
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.
