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An Orthotopic Bladder Tumor Model and the Evaluation of Intravesical saRNA Treatment
Published on: July 28, 2012
Study of arachidonic Acid pathway in human bladder tumor
Masahide Matsuyama1, Rikio Yoshimura1
1Department of Urology, Osaka City University Graduate School of Medicine, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, 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 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.
Insights
Nonsteroidal anti-inflammatory drugs (NSAIDs) may inhibit tumor growth by targeting cyclooxygenase (COX), lipoxygenase (LOX), and peroxisome proliferator activator-receptor gamma (PPAR-γ). This review explores their expression in bladder cancer.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to reduce colorectal cancer incidence.
- Cyclooxygenase (COX) and lipoxygenase (LOX) are key enzymes in inflammatory pathways and may be involved in tumorigenesis.
- Peroxisome proliferator activator-receptor gamma (PPAR-γ) is implicated in adipocyte differentiation and cancer development.
Purpose of the Study:
- To review the expression of COX-2, LOX, and PPAR-γ in human bladder tumor tissues.
- To examine the effects of COX-2 and LOX inhibitors on bladder tumors.
- To investigate the impact of PPAR-γ ligands on bladder cancer.
Main Methods:
- Review of epidemiological studies and animal experiments on NSAIDs and cancer.
- Analysis of gene and protein expression data for COX-2, LOX, and PPAR-γ in bladder tumors.
- Evaluation of studies using COX-2/LOX inhibitors and PPAR-γ ligands in cancer models.
Main Results:
- NSAIDs' inhibition of COX may play a role in cancer initiation and promotion.
- LOX enzymes, similar to COX, might contribute to tumorigenesis.
- PPAR-γ is a target for NSAIDs in modulating cell growth and is expressed in bladder tumors.
Conclusions:
- COX-2, LOX, and PPAR-γ are relevant targets in bladder cancer research.
- Inhibitors of COX and LOX, along with PPAR-γ ligands, show potential in modulating bladder tumor progression.
- Further research is warranted to elucidate the precise roles and therapeutic applications.
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