Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the cyclooxygenase (COX) enzyme and suppress PG synthesis which are used commonly as anti-inflammatory, anti-pyretic and analgestic agents. Though NSAIDs is known to suppress incidence and progression of cancer especially colorectal cancer, the precise mechanism of their protective effect remain unknown. A wide range of mechanism about anti-tumor effect of NSAIDs have been reported. Some of them are unrelated to the inhibition of COX activity and subsequent PG formation. However, recent result from by using knockout mice and selective antagonists indicated that prostanoid receptor, especially PGE2 enhances angiogenesis and tumor growth. Here, we summarize significant of PGE2 signaling via EP3 receptors which exists on the stroma but on tumor cells. An EP3 receptor antagonist may be a candidate of chemopreventive agents for malignant tumor.
