Abstract

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.

Highlights

  • Dietary fat is an important energy source

  • Two families with opposing effects belong to this category of fatty acids: linoleic acid and alpha-linolenic acid, which are the precursors of arachidonic acid (AA) and eicosapentanoic acid respectively

  • This paper aims to give a brief overview of the effect of cyclooxygenases and the prostanoid signaling in the initiation, progression and treatment of NSAIDS and COX-2 inhibitors

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Summary

Introduction

Dietary fat is an important energy source. Fatty acids that are produced from catabolism of fats compose an important aspect of a healthy diet. The considerable clinical implication in cancer derives from the fact that DP is expressed on human NK cells and PGD2 mediated activation of this receptor leads to inhibition of the cytotoxic and chemotactic effects as well as decreased accumulation of type 1 cytokine. The same substance has been shown to synergistically augment celecoxib-mediated suppression of PGE2 as well as decrease the amount of the COX-2 inhibitor (celecoxib) necessary for the production of the antitumoral effect [132] Another eicosanod studied as a target for cancer prevention and treatment is the thromboxane A2 formed by the action of thromboxane A2 synthase (TXA2S). More studies are needed to define the involvements of prostanoids in tumor formation and progression and to evaluate the utility of these proostanoid inhibitors in cancer prevention and treatment

Conclusion and perspective
38. Hayaishi O
54. Moncada S
Findings
67. FitzGerald GA
Full Text
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