The Blogs: Mar 31, 2008

Epigenetics and NSAIDs

Kevin Ahern

Is there anything that aspirin-related compounds can’t do? NSAIDs (non-steroidal anti-inflammatory drugs), such as aspirin, inhibit cyclooxygenase enzymes (COX-1 and COX-2) that catalyze formation of prostaglandins from arachidonic acid and they have been widely used for relieving pain, reducing fever and inflammation, “thinning” blood, and slowing the progression of some types of metastatic growth. Aside from their actions to reduce symptoms related to prostaglandins (pain, swelling, inflammation), the molecular basis of action of NSAIDs is not fully understood. Now, however, an explanation has come forward accounting for these compounds’ ability to enhance anti-cancer treatments directed against some types of tumors. In findings published in the most recent issue of Experimental Biology and Medicine, Wen-Chun Hung and colleagues report that one NSAID, known as NS398 (a so-called COX-2 inhibitor) up-regulates several genes known to be involved in negative regulation of cell invasion. Interestingly, the mechanism of NS398 action appears to be by promoter demethylation of these genes (accomplished by inhibition of expression of a methylase), resulting in activation of their gene expression and subsequent inhibition of cell invasion. Promoter methylation/demethylation, like histone acetylation/deacetylation is part of the voodoo known as epigenetics that has taken genetic analysis by storm and looks to do the same for treatments. The latest finding may be the tip of a therapeutic iceberg researchers are standing on, inasmuch as some cancers are known to have pro-apoptotic genes specifically inactivated by methylation. Expect a LOT more research aimed at developing drugs to target methylation/demethylation of specific genes.





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