Cyclooxygenase-2 (COX-2)-independent anticarcinogenic effects of selective COX-2 inhibitors

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  • Sabine Grösch, Pharmazentrum Frankfurt, ZAFES, Institut für klinische Pharmakologie, Klinikum der Johann Wolfgang Goethe, Universität Frankfurt, Theodor Stern Kai 7, Frankfurt/Main, Germany. groesch@em.uni-frankfurt.de
  • ,
  • Thorsten Maier
  • Susanne Schiffmann
  • ,
  • Gerd Geisslinger

Nonsteroidal antiinflammatory drugs (NSAIDs) appear to reduce the risk of developing cancer. One mechanism through which NSAIDs act to reduce carcinogenesis is to inhibit the activity of cyclooxygenase-2 (COX-2), an enzyme that is overexpressed in various cancer tissues. Overexpression of COX-2 increases cell proliferation and inhibits apoptosis. However, selective COX-2 inhibitors can also act through COX-independent mechanisms. In this review, we describe the COX-2-independent molecular targets of these COX-2 inhibitors and discuss how these targets may be involved in the anticarcinogenic activities of these selective COX-2 inhibitors. We also compare the concentrations of these inhibitors used in in vitro and in vivo experiments and discuss the implications of the in vitro studies for clinical management of cancer with these drugs.

Original languageEnglish
JournalNational Cancer Institute. Journal (Online)
Volume98
Issue11
Pages (from-to)736-47
Number of pages12
ISSN1460-2105
DOIs
Publication statusPublished - 7 Jun 2006

    Research areas

  • Adenomatous Polyposis Coli, Adenomatous Polyposis Coli Protein, Animals, Anti-Inflammatory Agents, Non-Steroidal, Anticarcinogenic Agents, Apoptosis, Cell Cycle, Cell Line, Tumor, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Gene Expression Regulation, Neoplastic, Humans, Lactones, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Pyrazoles, Signal Transduction, Sulfonamides, Sulfones, Tumor Cells, Cultured, beta Catenin

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