Heightened expression of cyclooxygenase-2 and peroxisome proliferator-activated receptor-δ human endometrial adenocarcinoma

B. J. Tong, J. Tan, L. Tajeda, S. K. Das, J. A. Chapman, R. N. DuBois, S. K. Dey

    Research output: Contribution to journalArticlepeer-review

    113 Scopus citations

    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 evidences 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 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-PPARδ 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.

    Original languageEnglish (US)
    Pages (from-to)483-490
    Number of pages8
    JournalNeoplasia
    Volume2
    Issue number6
    StatePublished - 2000

    Keywords

    • Cyclooxygenase
    • Endometrial cancer
    • Human
    • Prostaglandins
    • Uterus

    ASJC Scopus subject areas

    • Cancer Research

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