Hypothesis: The antitumor activities of statins may be mediated by IL-18

Hideo Kohka Takahashi, Gabriele Weitz-Schmidt, Hiromi Iwagaki, Tadashi Yoshino, Noriaki Tanaka, Masahiro Nishibori

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)


Statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase, are thought to reduce the risk of cancer through the inhibition of Ras farnesylation and serum lipid level. A pleiotropic proinflammatory cytokine, interleukin-18 (IL-18), is reported to exhibit significant antitumor activities through the activation of cytotoxic T lymphocytes and natural killer cells and the inhibition of angiogenesis. Previously, we found that pravastatin, fluvastatin, and simvastatin induced the production of IL-18 in human monocytes. The addition of mevalonate abolished the IL-18 production induced by pravastatin, fluvastatin, and simvastatin, indicating that the IL-18 production might be a result of the inhibition of HMG-CoA reductase. We present a new hypothesis that the production of IL-18 might play roles in the action of statins on cancer.

Original languageEnglish
Pages (from-to)215-216
Number of pages2
JournalJournal of Leukocyte Biology
Issue number2
Publication statusPublished - Aug 2006


  • Cancer
  • Statin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology


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