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[Cancer Research 65, 1822-1829, March 1, 2005]
© 2005 American Association for Cancer Research

Cell and Tumor Biology

Prostaglandin E2 Enhances Intestinal Adenoma Growth via Activation of the Ras-Mitogen-Activated Protein Kinase Cascade

Dingzhi Wang1, F. Gregory Buchanan1, Haibin Wang2, Sudhansu K. Dey2,3,4 and Raymond N. DuBois1,3,4

Departments of 1 Medicine, 2 Pediatrics, 3 Cancer Biology, and 4 Cell and Developmental and Biology, Vanderbilt University Medical Center and Vanderbilt-Ingram Cancer Center, Nashville, Tennessee

Requests for reprints: Raymond N. DuBois, Vanderbilt-Ingram Cancer Center, Room 694, Preston Research Building, 2300 Pierce Avenue, Nashville, TN 37232-6838. Phone: 615-343-0527; Fax: 615-936-2697; E-mail: raymond.dubois{at}vanderbilt.edu.

A large body of clinical, genetic, and biochemical evidence indicates that cyclooxygenase-2 (COX-2), a key enzyme for prostanoid biosynthesis, contributes to the promotion of colorectal cancer. COX-2-derived prostaglandin E2 (PGE2) is the most abundant prostaglandin found in several gastrointestinal malignancies. Although PGE2 enhances intestinal adenoma growth in Apcmin mice, the mechanism(s) by which it accelerates tumor growth is not completely understood. Here we investigated how PGE2 promotes intestinal tumor growth and the signaling pathways responsible for its effects. We observed that PGE2 treatment leads to increased epithelial cell proliferation and induces COX-2 expression in intestinal adenomas. Furthermore, we show that PGE2 regulation of COX-2 expression is mediated by activation of a Ras-mitogen-activated protein kinase signaling cascade. One intriguing finding is that COX-2-derived PGE2 mimics the effects of constitutively active Ras through a self-amplifying loop that allows for a distinct growth advantage.




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