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Vol. 301, Issue 3, 1126-1131, June 2002
Laboratory of Molecular Carcinogenesis, National Institute of
Environmental Health Sciences, National Institutes of Health, Research
Triangle Park, North Carolina
Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used drugs for
the treatment of inflammatory disease and have a chemopreventive effect
on colorectal cancer. NSAIDs inhibit cyclooxygenase (COX)-1 and/or
COX-2 activity, but the chemopreventive effect may be, in part,
independent of prostaglandin inhibition. NSAID-activated gene (NAG-1)
was previously identified as a gene induced by some NSAIDs in cells
devoid of COX activity. NAG-1 has proapoptotic and antitumorigenic
activity in vitro and in vivo. To determine whether the induction of
NAG-1 by NSAIDs is influenced by COX expression, we developed COX-1-
and COX-2-overexpressing HCT-116 cells. COX expression did not affect
NSAID-induced NAG-1 expression as assessed by transient and stable
transfection. Also, NAG-1 expression was not affected by
PGE2 and arachidonic acid, suggesting that NAG-1 induction
by NSAIDs occurs by a prostanoid-independent manner. We also report
that indomethacin increased NAG-1 expression in a number of cells from
tissues other than colorectal. In conclusion, NSAIDs have dual
function, induction of NAG-1 expression and inhibition of COX activity
that occurs in a variety of cell lines.
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