Relationship between arachidonic acid pathway and human renal cell carcinoma
Masahide Matsuyama, Rikio Yoshimura
Department of Urology, Osaka City University Graduate School of Medicine, Osaka City University Hospital, Abeno-ku, Osaka, Japan
Abstract: Recent epidemiological studies and animal experiments have demonstrated that nonsteroidal antiinflammatory drugs (NSAIDs) reduce the incidence of colorectal carcinoma. Cyclooxygenase (COX) is the principal target of NSAIDs. COX is the first oxidase in the process of prostaglandin production from arachidonic acid. COX enzyme may be involved in the initiation and/or the promotion of carcinogenesis due to NSAIDs inhibition of COX. Lipoxygenase (LOX) is also an initial enzyme in the pathway for producing leukotrienes from arachidonic acid. Similar to COX, LOX enzyme may also be involved in the initiation and/or promotion of carcinogenesis. Peroxisome proliferator activator-receptor (PPAR)-γ is a ligand-activated transcriptional factor belonging to the steroid receptor superfamily. PPAR-γ plays a role in both adipocyte differentiation and carcinogenesis. PPAR-γ is one target for cell growth modulation of NSAIDs. In this review, we report the expression of COX-2, LOX and PPAR-γ in human renal cell carcinoma tissues as well as the effects of COX-2 and LOX inhibitors and PPAR-γ ligand.
Keywords: cyclooxygenase, lipoxygenase, peroxisome proliferator activator-receptor-γ, renal cell carcinoma
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