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Clinical Cancer Research Vol. 7, 3349-3355, November 2001
© 2001 American Association for Cancer Research

Advances in Brief

Thalidomide and Its Analogues Inhibit Lipopolysaccharide-mediated Induction of Cyclooxygenase-21

Junya Fujita, Juan R. Mestre, Jerome B. Zeldis, Kotha Subbaramaiah and Andrew J. Dannenberg2

Departments of Surgery [J. F., J. R. M.] and Medicine [K. S., A. J. D.], New York Presbyterian Hospital and Weill Medical College of Cornell University, New York, New York 10021; Strang Cancer Prevention Center, New York, New York 10021 [K. S., A. J. D.]; and Celgene Corporation, Warren, New Jersey 07059 [J. B. Z.]

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 anti-inflammatory properties of thalidomide.


Commentary

Thalidomide, Cyclooxygenase-2, and Angiogenesis: Potential for Therapy
Amir Onn, Jennifer E. Tseng, and Roy S. Herbst
Clin. Cancer Res. 2001 7: 3311-3313. [Full Text] [PDF]



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Copyright © 2001 by the American Association for Cancer Research.