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Beyond Cox-Inhibition: 'Side-Effects' of Ibuprofen on Neoplastic Development and Progression
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Orientador(es)
Resumo(s)
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.
Descrição
Palavras-chave
Vias de Transdução de Sinal e Patologias Associadas Cancro Coloretal NSAID Ibuprofen Cell Signalling Rac1b Cancer Chemoprevention Colorectal Cancer Cyclooxygenase Tumor Growth
Contexto Educativo
Citação
Curr Pharm Des. 2015;21(21):2978-82. doi.10.2174/1381612821666150514104608
Editora
Bentham Science Publishers