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Non-steroid anti-inflammatory drugs, prostaglandins, and cancer

Viola Allaj1, Changxiong Guo1 and Daotai Nie12*

Author Affiliations

1 Department of Medical Microbiology, Immunology, and Cell Biology, Southern Illinois University School of Medicine and Simmons Cancer Institute, Springfield, IL, 62794, USA

2 Department of Medical Microbiology and Immunology, Southern Illinois University School of Medicine, PO Box 19626, Springfield, IL, 62794, USA

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Cell & Bioscience 2013, 3:8  doi:10.1186/2045-3701-3-8

Published: 6 February 2013


Fatty acids are involved in multiple pathways and play a pivotal role in health. Eicosanoids, derived from arachidonic acid, have received extensive attention in the field of cancer research. Following release from the phospholipid membrane, arachidonic acid can be metabolized into different classes of eicosanoids through cyclooxygenases, lipoxygenases, or p450 epoxygenase pathways. Non-steroid anti-inflammatory drugs (NSAIDs) are widely consumed as analgesics to relieve minor aches and pains, as antipyretics to reduce fever, and as anti-inflammatory medications. Most NSAIDs are nonselective inhibitors of cyclooxygenases, the rate limiting enzymes in the formation of prostaglandins. Long term use of some NSAIDs has been linked with reduced incidence and mortality in many cancers. In this review, we appraise the biological activities of prostanoids and their cognate receptors in the context of cancer biology. The existing literature supports that these lipid mediators are involved to a great extent in the occurrence and progression of cancer.