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

124 Scopus citations


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
Issue number11
StatePublished - 2001

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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