Regular ArticleIs inhibition of cyclooxygenase required for the chemopreventive effect of NSAIDs in colon cancer? A model reconciling the current contradiction☆
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Chemopreventive action of non-steroidal anti-inflammatory drugs on the inflammatory pathways in colon cancer
2016, Biomedicine and PharmacotherapyIncreasing the endogenous NO level causes catalase inactivation and reactivation of intercellular apoptosis signaling specifically in tumor cells
2015, Redox BiologyCitation Excerpt :In addition, the tumorpreventive effect of acetylsalicylic acid, the i. e. the prodrug for salicylic acid, has been demonstrated in multiple studies [114–117]. Salicylic acid-dependent apoptosis induction in tumor cells does not seem to be attributed to inhibition of cyclooxygenase (COX), as salicylic acid also affects COX1- and COX2-deficient tumor cells [118,119] and as certain other nonsteroidal antiinflammatory drugs that inhibit COX as efficiently as salicylic acid do not induce apoptosis [99]. One common feature of salicylic acid- and anthocyanidin-dependent apoptosis induction seems to be the induction of the mitochondrial pathway of apoptosis [102,103,106,109,111] and the provocation of ROS generation [102,105,109].
Mediators of PGE<inf>2</inf> synthesis and signalling downstream of COX-2 represent potential targets for the prevention/treatment of colorectal cancer
2006, Biochimica et Biophysica Acta - Reviews on CancerColorectal Cancer After Start of Nonsteroidal Anti-Inflammatory Drug Use
2006, American Journal of MedicineNonsteroidal anti-inflammatory drugs inhibit the growth of C6 and U138-MG glioma cell lines
2006, European Journal of PharmacologyOxidative stress is responsible for mitochondrial permeability transition induction by salicylate in liver mitochondria
2005, Journal of Biological Chemistry
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Support: NIH CA73298 and CA29502 (Clinical Nutrition Research Unit-New Investigator Award), American Institute for Cancer Research 95B043, and The Arthur and Rochelle Belfer Foundation.