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 and other cancers. human tumors (1). COX-2 is undetectable in most normal tissues. However, it is rapidly induced when stimulated in response to mitogens, cytokines, and tumor promoters, which leads to increased accumulation of prostanoids in neoplastic and inflamed tissues (2). COX-2 is highly expressed at high levels in intestinal tumors in rodents and humans (1). For example, more than 80% of all colorectal cancers have been shown to overexpress COX-2 (3-5). Epidemiological studies have shown that regular intake of aspirin or other non-steroidal anti-inflammatory drugs could reduce colorectal cancer mortality by 40-50% compared to those who do not take these drugs (1). A characteristic shared by all these drugs is their ability to inhibit the activity and/or expression of COX (1). Although COX-2 is expressed in 80–90% of human colon carcinoma specimens, not all colorectal cancer cell lines constitutively express COX-2. Constitutive expression of COX-2 has only been detected in a relatively small number of colorectal carcinoma cell lines (6). For example, the human colon adenocarcinoma cell lines, HCT116 and SW480, have been described as COX-2 negative, as they do not express COX-2, either at the mRNA or protein level (7). Prostaglandin E2 derived from COX-2 (PGE2) ...... middle of paper ......te when conditioned medium is collected, with multiple parameters in which not only COX- mRNA and protein will be observed 2, but also PGE2 levels, but also other molecular markers or relevant factors such as those mentioned above. Not only have paradoxical observations of COX-2 expression and functional activity been documented in the human colon cancer cell line, 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 inhibit acute allergic inflammation (56). Therefore, PGE2 can produce both pro- and anti-inflammatory effects (57). More extensive and well-designed experiments are needed to help us unlock the secret of COX-2 expression and functional activity, as well as their role in physiological and pathophysiological conditions..