Inflammatory Mediators and Nuclear Receptor Signaling in Colorectal Cancer.
From: Department of Medicine, Vanderbilt University Medical Center, and The Vanderbilt-Ingram Cancer Center, Nashville, Tennessee 37232, USA.
Cell cycle (Georgetown, Tex.)
- Publish Date: Mar 2007
- ISSN: 1551-4005
- Volume: 6
- Issue: 6
- Pages: 682-5
- Medium: Internet
- Language: English
- Citation (JAMA): Wang Dingzhi, DuBois Raymond N, et al. Inflammatory Mediators and Nuclear Receptor Signaling in Colorectal Cancer.. Cell Cycle Mar 2007;6:682-5
Abstract
Long-term use of cyclooxygenase (COX) inhibitors (NSAIDs) in humans leads to a 50% reduction in risk for colorectal cancer. However, prolonged use of COX-2 selective inhibitors (coxibs) increases cardiovascular toxicity in some individuals, which highlights the importance of identifying all of the molecular targets that drive progression of colorectal cancer. Colorectal cancer offers a unique model to study the synergistic induction of intestinal neoplasia via dysregulation of multiple signaling pathways. Emerging evidence demonstrates that the peroxisome proliferator-activated receptor delta (PPARdelta) is a focal point of crosstalk between the signaling cascades involved in the progression of colorectal cancer. More importantly, activation of PPARdelta can promote tumor growth by inhibiting epithelial tumor cell apoptosis via a VEGF autocrine signaling loop. These findings may provide a rationale for the development of PPARdelta antagonists for cancer prevention and/or treatment.
Mesh Headings (Keywords): Animals, Antineoplastic Agents, Colorectal Neoplasms, Humans, Inflammation Mediators, Receptors, Cytoplasmic and Nuclear, Signal Transduction
Check for Full Text / PubMed Unique Identifier (PMID): 17374999
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