Abstract:
:Epidemiological studies indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) significantly reduce the risk and mortality from colorectal cancer, in part by inhibiting prostaglandin (PG) synthesis. Cyclooxygenase (COX), the rate-limiting enzyme in PG biosynthesis, exists in two isoforms, COX-1 and COX-2. Genetic and pharmacological evidence suggest that COX-2 is involved in the development of colorectal cancer. We have previously shown that COX-2-derived prostacyclin participates in blastocyst implantation through activation of peroxisome proliferator activated receptor delta (PPARdelta), a member of the nuclear hormone receptor family. Furthermore, our recent studies suggest that a similar pathway is operative during colorectal carcinogenesis. These observations prompted us to examine whether the COX-2-PPARdelta signaling pathway is also involved during development of uterine adenocarcinoma. Here we describe for the first time the heightened expression of COX-2 and PPARdelta, but not COX-1, in uterine endometrial adenocarcinoma.
journal_name
Neoplasiajournal_title
Neoplasia (New York, N.Y.)authors
Tong BJ,Tan J,Tajeda L,Das SK,Chapman JA,DuBois RN,Dey SKdoi
10.1038/sj.neo.7900119keywords:
subject
Has Abstractpub_date
2000-11-01 00:00:00pages
483-90issue
6eissn
1522-8002issn
1476-5586journal_volume
2pub_type
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