Inflammatory Mediators and Nuclear Receptor Signaling in Colorectal Cancer

Dingzhi Wang and Raymond N. DuBois

volume 6 | issue 6

15 March 2007
Pages: 682 - 685

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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 δ (PPARδ) is a focal point of crosstalk between the signaling cascades involved in the progression of colorectal cancer. More importantly, activation of PPARδ can promote tumor growth by inhibiting epithelial tumor cell apoptosis by affecting a VEGF autocrine signaling loop. These findings may provide a rationale for the development of PPARδ antagonists for cancer prevention and/or treatment.

Authors

Dingzhi Wang

Vanderbilt University Medical Center and Vanderbilt-Ingram Cancer Center; Nashville, TN USA

Raymond N. DuBois

Vanderbilt University Medical Center and Vanderbilt-Ingram Cancer Center; Nashville, TN USA

We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link: