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Flurbiprofen Inhibits Glioblastoma Proliferation and Migration by a COX‐Independent Mechanism
Author(s) -
Kohler Missia,
Qadri Yawar J,
Fuller Catherine M,
Benos Dale J
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1168.2
Subject(s) - flurbiprofen , cell growth , cancer research , cyclooxygenase , downregulation and upregulation , glioma , u87 , cell , cell migration , pharmacology , medicine , chemistry , enzyme , biochemistry , gene
Glioblastoma multiformes (GBMs) are primary brain tumors that are difficult to treat. Non Steroidal Anti‐Inflammatory Drugs (NSAIDs) are a promising therapy for colon and prostate cancer. NSAIDs are classically described as non‐selective inhibitors of cyclooxygenase (COX) enzymes, which form prostaglandins that mediate processes such as inflammation and vasoconstriction. While there is evidence that upregulation of COX‐2 in GBMs coincides with a worse prognosis for patients, it is unclear whether NSAIDs affect GBMs through a COX‐mediated mechanism. This study examined whether a NSAID, flurbiprofen, affects GBMs through a COX–dependent mechanism. COX‐1 and COX‐2 were detected in all GBM cell lines using RT‐PCR. Using a tetrazolium‐based cell viability assay, flurbiprofen decreased the proliferation of a GBM cell line in a dose dependent manner. However, this effect was seen at similar doses (≥ 500 μM) with both COX‐active and COX‐inactive enantiomers. GBM cell migration was also measured using an electric cell‐substrate impedance sensing system, and migration was almost completely inhibited by 500 μM flurbiprofen in a non‐enatioselective manner. Ultimately, although COX‐1 and COX‐2 are present in glioblastomas, they do not appear to be involved in the effects of flurbiprofen on glioma migration and proliferation. This study was supported by NIH grant CA101952 and the AMA Foundation.