Arachidonic acid pathway: A molecular target in human testicular cancer (Review)
Recent epidemiological studies and animal experiments have demonstrated that non-steroidal anti-inflammatory drugs (NSAIDs) reduce the incidence of colorectal carcinoma. Cyclooxygenase (COX), the first oxidase in the process of prostaglandin production from arachidonic acid, is the principal target...
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Published in | Molecular medicine reports Vol. 2; no. 4; pp. 527 - 531 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Greece
01.07.2009
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Online Access | Get full text |
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Summary: | Recent epidemiological studies and animal experiments have demonstrated that non-steroidal anti-inflammatory drugs (NSAIDs) reduce the incidence of colorectal carcinoma. Cyclooxygenase (COX), the first oxidase in the process of prostaglandin production from arachidonic acid, is the principal target of NSAIDs. Due to its inhibition by NSAIDs, the COX enzyme may be involved in the initiation and/or promotion of carcinogenesis. Lipoxygenase (LOX) is also an enzyme active in the early stages of the pathway for producing leukotrienes from arachidonic acid, and may, like COX, 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 super-family. PPAR-γ plays a role in both adipocyte differentiation and carcinogenesis, and is a target for the cell growth modulation of NSAIDs. In this review, we report the expression of COX-2, LOX and PPAR-γ in human testicular cancer tissues, as well as the effects of COX-2 and LOX inhibitors and PPAR-γ ligands. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1791-2997 1791-3004 |
DOI: | 10.3892/mmr_00000131 |