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Originally published online as doi:10.1189/jlb.0406245 on May 30, 2006

Published online before print May 30, 2006
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(Journal of Leukocyte Biology. 2006;80:215-216.)
© 2006 by Society for Leukocyte Biology

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

Hideo Kohka Takahashi*, Gabriele Weitz-Schmidt{dagger}, Hiromi Iwagaki{ddagger}, Tadashi Yoshino§, Noriaki Tanaka{ddagger} and Masahiro Nishibori*,1

* Departments of Pharmacology,
{ddagger} Gastroenterological Surgery, Transplant, and Surgical Oncology, and
§ Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Japan; and
{dagger} Novartis Institutes for Biomedical Research, Basel, Switzerland

1Correspondence: Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. E-mail: mbori{at}md.okayama-u.ac.jp

ABSTRACT

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.

Key Words: statin • cancer






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