The target of arachidonic acid pathway is a new anticancer strategy for human prostate cancer
Author(s) -
Masahide Matsuyama
Publication year - 2008
Publication title -
biologics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 38
eISSN - 1177-5491
pISSN - 1177-5475
DOI - 10.2147/btt.s3151
Subject(s) - arachidonic acid , peroxisome proliferator activated receptor , carcinogenesis , cancer research , cyclooxygenase , tumor promotion , chemistry , biology , receptor , cancer , pharmacology , enzyme , medicine , endocrinology , biochemistry
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 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)-gamma is a ligand-activated transcriptional factor belonging to the steroid receptor superfamily. PPAR-gamma plays a role in both adipocyte differentiation and carcinogenesis. PPAR-gamma is one target for cell growth modulation of NSAIDs. In this review, we report the expression of COX-2, LOX and PPAR-gamma in human prostate cancer tissues as well as the effects of COX-2 and LOX inhibitors and PPAR-gamma ligand.
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