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Updated: Jun 20, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
The target of arachidonic acid pathway is a new anticancer strategy for human prostate cancer
Masahide Matsuyama1, Rikio Yoshimura
1Department of Urology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Abstract:
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.
Insights
Nonsteroidal anti-inflammatory drugs (NSAIDs) may inhibit cancer by targeting cyclooxygenase (COX) and lipoxygenase (LOX) enzymes. These drugs also modulate peroxisome proliferator activator-receptor gamma (PPAR-gamma), a factor in cell growth and carcinogenesis.
Area of Science:
- Molecular Biology
- Oncology
- Pharmacology
Background:
- Epidemiological and animal studies indicate nonsteroidal anti-inflammatory drugs (NSAIDs) decrease colorectal carcinoma incidence.
- Cyclooxygenase (COX) and lipoxygenase (LOX) are key enzymes in arachidonic acid metabolism, potentially involved in carcinogenesis.
- Peroxisome proliferator activator-receptor gamma (PPAR-gamma) is a nuclear receptor implicated in adipogenesis and cancer development.
Purpose of the Study:
- To review the expression of COX-2, LOX, and PPAR-gamma in human prostate cancer.
- To examine the effects of COX-2 and LOX inhibitors on cancer.
- To investigate the role of PPAR-gamma ligands in cancer modulation.
Main Methods:
- Review of existing epidemiological studies and animal experiments.
- Analysis of expression data for COX-2, LOX, and PPAR-gamma in prostate cancer tissues.
- Evaluation of the impact of specific inhibitors and ligands on cellular processes.
Main Results:
- NSAIDs' inhibition of COX enzymes is a proposed mechanism for cancer risk reduction.
- LOX enzymes, like COX, may contribute to cancer initiation and promotion.
- PPAR-gamma is identified as a target for NSAID-mediated cell growth modulation.
Conclusions:
- COX-2, LOX, and PPAR-gamma are relevant targets in prostate cancer research.
- Inhibitors of COX and LOX, along with PPAR-gamma ligands, show potential in cancer therapy.
- Further research is warranted to elucidate the precise roles of these molecules in carcinogenesis.
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