ReviewPost screenCyclooxygenase-2 in glioblastoma multiforme

- Current treatment for glioblastoma fails to provide sufficient therapeutic outcomes.
- Overexpressed cyclooxygenase-2 (COX-2) contributes to the glioblastoma progression.
- COX-2 plays complex roles in glioma invasion, angiogenesis, immunosuppression, etc.
- COX-2 inhibitors sensitize glioblastomas to conventional chemo- and radio-therapies.
- 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.