Open AccessStudy of Arachidonic Acid Pathway in Human Bladder Tumor
Author(s) -
Masahide Matsuyama,
Rikio Yoshimura
Publication year - 2009
Publication title -
substance abuse research and treatment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.027
H-Index - 22
ISSN - 1178-2218
DOI - 10.4137/sart.s2151
Subject(s) - arachidonic acid , carcinogenesis , peroxisome proliferator activated receptor , tumor promotion , cyclooxygenase , cancer research , chemistry , peroxisome proliferator activated receptor gamma , receptor , biology , pharmacology , enzyme , medicine , endocrinology , biochemistry , gene
Recent epidemiological studies and animal experiments have demonstrated that nonsteroidal anti-inflammatory 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 tumorigenesis 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 tumorigenesis. 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 tumorigenesis. 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 bladder tumor tissues as well as the effects of COX-2 and LOX inhibitors and PPAR-γ ligand.
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