Abstract
Ibuprofen is a non-steroidal anti-inflammatory drug of generalized use with over-the-counter availability. Population-based studies have provided evidence that its long-term use is associated with a 30-60% decrease in the risk of developing major types of cancer. Initially, the underlying molecular mechanism was thought to be exclusively dependent on its inhibitory effect on cyclooxygenase activity, which is involved in the inflammatory response. However, numerous studies have now shown that the cancer chemopreventive properties of ibuprofen are much more complex and likely involve multiple COX-2-independent effects. Here we review the current knowledge on COX-independent effects of ibuprofen, which affect changes in gene expression or alternative splicing and act through various cell cycle- and apoptosis-regulating pathways, including β-catenin, NF-κB, PPARγ and p53.
Keywords: Cancer chemoprevention, colorectal cancer, cyclooxygenase, ibuprofen, NSAID, tumor growth.
Current Pharmaceutical Design
Title:Beyond Cox-Inhibition: ‘Side-Effects’ of Ibuprofen on Neoplastic Development and Progression
Volume: 21 Issue: 21
Author(s): Paulo Matos and Peter Jordan
Affiliation:
Keywords: Cancer chemoprevention, colorectal cancer, cyclooxygenase, ibuprofen, NSAID, tumor growth.
Abstract: Ibuprofen is a non-steroidal anti-inflammatory drug of generalized use with over-the-counter availability. Population-based studies have provided evidence that its long-term use is associated with a 30-60% decrease in the risk of developing major types of cancer. Initially, the underlying molecular mechanism was thought to be exclusively dependent on its inhibitory effect on cyclooxygenase activity, which is involved in the inflammatory response. However, numerous studies have now shown that the cancer chemopreventive properties of ibuprofen are much more complex and likely involve multiple COX-2-independent effects. Here we review the current knowledge on COX-independent effects of ibuprofen, which affect changes in gene expression or alternative splicing and act through various cell cycle- and apoptosis-regulating pathways, including β-catenin, NF-κB, PPARγ and p53.
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Cite this article as:
Matos Paulo and Jordan Peter, Beyond Cox-Inhibition: ‘Side-Effects’ of Ibuprofen on Neoplastic Development and Progression, Current Pharmaceutical Design 2015; 21 (21) . https://dx.doi.org/10.2174/1381612821666150514104608
DOI https://dx.doi.org/10.2174/1381612821666150514104608 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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