Thalidomide and its analogues inhibit lipopolysaccharide-mediated induction of cyclooxygenase-2

Junya Fujita, Juan R. Mestre, Jerome B. Zeldis, Kotha Subbaramaiah, Andrew J. Dannenberg

    Research output: Contribution to journalArticlepeer-review

    126 Scopus citations

    Abstract

    We investigated the effect of thalidomide, a compound with immunomodulatory and antiangiogenic properties, on lipopolysaccharide (LPS)-mediated induction of cyclooxygenase-2 (Cox-2) and prostaglandin (PG) biosynthesis in murine macrophages. Thalidomide caused a dose-dependent inhibition of LPS-mediated induction of PGE2 synthesis in RAW 264.7 cells. The induction of Cox-2 protein and mRNA by LPS was also suppressed by thalidomide. Based on the results of nuclear run-off assays and transient transfections, treatment with LPS stimulated Cox-2 transcription, an effect that was unaffected by thalidomide. Thalidomide decreased the stability of Cox-2 mRNA. A series of structural analogues of thalidomide also inhibited LPS-mediated induction of Cox-2 and PGE2 synthesis. Taken together, these data provide new insights into the antineoplastic and antiinflammatory properties of thalidomide.

    Original languageEnglish (US)
    Pages (from-to)3349-3355
    Number of pages7
    JournalClinical Cancer Research
    Volume7
    Issue number11
    StatePublished - 2001

    ASJC Scopus subject areas

    • General Medicine

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