Heightened expression of cyclooxygenase-2 and peroxisome proliferator-activated receptor-delta in human endometrial adenocarcinoma.

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

Neoplasia

authors

Tong BJ,Tan J,Tajeda L,Das SK,Chapman JA,DuBois RN,Dey SK

doi

10.1038/sj.neo.7900119

keywords:

subject

Has Abstract

pub_date

2000-11-01 00:00:00

pages

483-90

issue

6

eissn

1522-8002

issn

1476-5586

journal_volume

2

pub_type

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