Cyclooxygenase-2 (COX-2) is a key enzyme in the conversion of arachidonic acid to prostaglandins, which promote cell proliferation, angiogenesis and metastasis, and inhibit apoptosis. Unlike COX-1, which is a constitutively expressed isoform, COX-2 is an inducible isoform of cyclooxygenase and may participate in inflammatory responses and contribute to inflammation and the development of colorectal cancer as well as other human cancers (1). COX-2 is not detectable in most normal tissues. However, it is rapidly induced when stimulated by mitogens, cytokines, and tumor promoters, leading to increased accumulation of prostanoids in neoplastic and inflamed tissues (2). COX-2 is strongly expressed at high levels in intestinal tumors in rodents and humans (1). For example, more than 80% of all colorectal tumors have been shown to overexpress COX-2 (3-5). Epidemiological studies have shown that regular use of aspirin or other nonsteroidal anti-inflammatory drugs could reduce colorectal cancer mortality by 40 to 50% compared to those who do not take these medications (1). A common feature of all of these drugs is their ability to inhibit COX activity and/or expression (1). Although COX-2 is expressed in 80–90% of human colon carcinoma samples, not all colorectal cancer cell lines constitutively express COX-2. 2. Constitutive COX-2 expression has only been detected in a relatively small number of established colorectal carcinoma cell lines (6). For example, human colon adenocarcinoma cell lines, HCT116 and SW480, were described as COX-2 negative, because they did not express COX-2 at either the mRNA or protein level ( 7). COX-2-derived prostaglandin E2 (PGE2)...... middle of paper ......t as well as when the conditioned medium will be collected, with multiple parameters in which not only the mRNA and COX-2 protein as well as PGE2 levels will be observed, but also other relevant molecular markers or factors like those mentioned above. Not only have paradoxical observations of COX-2 expression and functional activity in human colon cancer cell line been documented, but the role of PGE2 on inflammation also appears paradoxical. Although PGE2 is a potent mediator of inflammation (55), it has been suggested that PGE2, the endogenous products of COX, also inhibits acute allergic inflammation (56). Thus, PGE2 can produce both pro- and anti-inflammatory effects (57). More in-depth and well-designed experiments are needed to help us unlock the secret of COX-2 expression and its functional activity as well as their roles in physiological and pathophysiological conditions...