Non-small cell lung cancer cycloxygenase activity and proliferation are inhibited by non-steroidal antiinflammatory drugs.

The effects of non-steroidal antiinflammatory drugs (NSAIDs) on non-small cell lung cancer (NSCLC) were investigated. Arachidonic acid (AA) was metabolized to prostaglandin E2 (PGE2) in NSCLC cells. NSAIDs such as aspirin or indomethacin reduced PGE2 levels in NCI-H157 and H1264 cells, and the decrease caused by PGE2 was reversed by epidermal growth factor (EGF).

Systemic activation of 15-lipoxygenase in heart, lung, and vascular tissues by hypercholesterolemia: relationship to lipoprotein oxidation and atherogenesis.

There is evidence that oxidized lipoproteins are a major contributing factor in atherosclerosis. 15-Lipoxygenase is the principal mammalian enzyme that can oxidize polysaturated fatty acids present in intact lipoproteins, and in membrane phospholipids in situ. We, and others, have reported previously that levels of the enzyme are increased in aortas of cholesterol-fed and spontaneously atherosclerotic WHHL rabbits.