Abstract:
:Nitric oxide donating aspirin (NO-ASA), consisting of a traditional ASA to which a NO-releasing moiety is covalently attached, is a promising chemopreventive agent against colon cancer. Its mechanism of action is not fully delineated. Here we examined its effect on the expression of the nuclear receptor PPARdelta, whose role in colon carcinogenesis remains highly controversial. We studied histochemically the effect of the meta and para positional isomers of NO-ASA on PPARdelta expression in Min (multiple intestinal neoplasia) and wild-type mice, and on cell proliferation and apoptosis. PPARdelta, minimally expressed in wild-type mice, was significantly expressed in Min mice. para NO-ASA inhibited intestinal tumor incidence (59%) and PPARdelta expression (55.3%) more than meta NO-ASA (38 and 41.5%, respectively). Neither isomer affected cell proliferation, but both induced apoptosis in Min mice (para 52.5% for normal mucosa and 70.3% for tumors; meta 31.4 and 21.9%, respectively). The changes in PPARdelta expression correlated significantly with changes in apoptosis. Furthermore, NO-ASA induced areas of necrosis in intestinal tumors are probably resulting from the induction of atypical apoptosis. Our data suggest that NO-ASA suppresses intestinal tumorigenesis possibly in part through its inhibitory effect on PPARdelta, the expression of which may contribute to intestinal carcinogenesis.
journal_name
Carcinogenesisjournal_title
Carcinogenesisauthors
Ouyang N,Williams JL,Rigas Bdoi
10.1093/carcin/bgi221keywords:
subject
Has Abstractpub_date
2006-02-01 00:00:00pages
232-9issue
2eissn
0143-3334issn
1460-2180pii
bgi221journal_volume
27pub_type
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