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The chemopreventive NO-donating NSAIDs (NO-NSAIDs; NSAIDs with an NO-releasing moiety) modulate PPAR δ  and offer the opportunity to revisit the controversial role of PPAR δ  in carcinogenesis (several papers report that PPAR δ  either promotes or inhibits cancer). This review summarizes the pharmacology of NO-NSAIDs, PPAR δ  cancer biology, and the relationship between the two. In particular, a study of the chemopreventive effect of two isomers of NO-aspirin on intestinal neoplasia in  Min  mice showed that, compared to wild-type controls, PPAR δ  is overexpressed in the intestinal mucosa of  Min  mice; PPAR δ  responds to   m - and  p -NO-ASA proportionally to their antitumor effect ( p - >  m -). This effect is accompanied by the induction of epithelial cell death, which correlates with the antineoplastic effect of NO-aspirin; and NO-aspirin's effect on PPAR δ  is specific (no changes in PPAR α  or PPAR γ ). Although these data support the notion that PPAR δ  promotes intestinal carcinogenesis and its inhibition could be therapeutically useful, more work is needed before a firm conclusion is reached.

ppar research

NO-Donating NSAIDs, PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>δ</mml:mi></mml:math>, and Cancer: Does PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>δ</mml:mi></mml:math>Contribute to Colon Carcinogenesis?

NO-Donating NSAIDs, PPARδ, and Cancer: Does PPARδContribute to Colon Carcinogenesis?