Heightened expression of cyclooxygenase-2 and peroxisome proliferator-activated receptor-delta in human endometrial adenocarcinoma.
Heightened expression of cyclooxygenase-2 and peroxisome proliferator-activated receptor-delta in human endometrial adenocarcinoma.
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人类子宫内膜腺癌中环氧合酶 2 和过氧化物酶体增殖物激活受体 δ 的表达升高。
DOI:
10.1038/sj.neo.7900119
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发表时间:
2000
期刊:
影响因子:
--
通讯作者:
Dey,SK
中科院分区:
文献类型:
--
作者:
Tong,BJ;Tan,J;Tajeda,L;Das,SK;Chapman,JA;DuBois,RN;Dey,SK
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 evidences suggest that COX-2 is involved in the development of colorectal cancer. We have previously shown that COX-2derived prostacyclin participates in blastocyst implantation through activation of peroxisome proliferator activated receptor δ (PPARδ), 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-PPAR6 signaling pathway is also involved during development of uterine adenocarcinoma. Here we describe for the first time the heightened expression of COX-2 and PPARδ, but not COX-1, in uterine endometrial adenocarcinoma.