What are cyclooxygenases and lipoxygenases doing in the driver's seat of carcinogenesis?
Article first published online: 18 AUG 2006
Copyright © 2006 Wiley-Liss, Inc.
International Journal of Cancer
Volume 119, Issue 10, pages 2247–2254, 15 November 2006
How to Cite
Fürstenberger, G., Krieg, P., Müller-Decker, K. and Habenicht, A.J.R. (2006), What are cyclooxygenases and lipoxygenases doing in the driver's seat of carcinogenesis?. Int. J. Cancer, 119: 2247–2254. doi: 10.1002/ijc.22153
- Issue published online: 26 SEP 2006
- Article first published online: 18 AUG 2006
- Manuscript Accepted: 10 MAY 2006
- Manuscript Received: 6 MAR 2006
- arachidonic acid
Substantial evidence supports a functional role for cyclooxygenase- and lipoxygenase-catalyzed arachidonic and linoleic acid metabolism in cancer development. Genetic intervention studies firmly established cause-effect relations for cyclooxygenase-2, but cyclooxygenase-1 may also be involved. In addition, pharmacologic cyclooxygenase inhibition was found to suppress carcinogenesis in both experimental mouse models and several cancers in humans. Arachidonic acid-derived eicosanoid or linoleic acid-derived hydro[peroxy]fatty acid signaling are likely to be involved impacting fundamental biologic phenomina as diverse as cell growth, cell survival, angiogenesis, cell invasion, metastatic potential and immunomodulation. However, long chain unsaturated fatty acid oxidation reactions indicate antipodal functions of distinct lipoxygenase isoforms in carcinogenesis, i.e., the 5- and platelet-type 12-lipoxygenase exhibit procarcinogenic activities, while 15-lipoxygenase-1 and 15-lipoxygenase-2 may suppress carcinogenesis. © 2006 Wiley-Liss, Inc.