Cyclooxygenase-2 in glioblastoma multiforme. Issue 1 (January 2017)

• Record Type: Journal Article
• Authors: Qiu, Jiange; Shi, Zhi; Jiang, Jianxiong
• Is Part Of: Drug discovery today. Volume 22:Issue 1(2017)
• Page Start: 148
• Page End: 156
• Publication Date: 2017-01
• Subjects: Drugs -- Design -- Periodicals; Drugs -- Research -- Periodicals; 615.1
• DOI: 10.1016/j.drudis.2016.09.017
• Languages: English
• ISSNs: 1359-6446

Abstract

Highlights: 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. 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. Abstract : Recent discoveries from animal and human studies reinforce the notion that cyclooxygenases (COXs) play comprehensive roles in glioblastoma development, suggesting that COX inhibitors might be useful adjuvants to treat the deadliest form of brain tumors.