| First Author | Cao Y | Year | 2002 |
| Journal | J Cell Physiol | Volume | 190 |
| Issue | 3 | Pages | 279-86 |
| PubMed ID | 11857443 | Mgi Jnum | J:74307 |
| Mgi Id | MGI:2158045 | Doi | 10.1002/jcp.10068 |
| Citation | Cao Y, et al. (2002) Many actions of cyclooxygenase-2 in cellular dynamics and in cancer. J Cell Physiol 190(3):279-86 |
| abstractText | Cyclooxygenase-2 (COX-2) is the inducible isoform of cyclooxygenase, the enzyme that catalyzes the rate-limiting step in prostaglandin synthesis from arachidonic acid. Various prostaglandins are produced in a cell type-specific manner, and they elicit cellular functions via signaling through G-protein coupled membrane receptors, and in some cases, through the nuclear receptor PPAR. COX-2 utilization of arachidonic acid also perturbs the level of intracellular free arachidonic acid and subsequently affects cellular functions. In a number of cell and animal models, induction of COX-2 has been shown to promote cell growth, inhibit apoptosis and enhance cell motility and adhesion. The mechanisms behind these multiple actions of COX-2 are largely unknown. Compelling evidence from genetic and clinical studies indicates that COX-2 upregulation is a key step in carcinogenesis. Overexpression of COX-2 is sufficient to cause tumorigenesis in animal models and inhibition of the COX-2 pathway results in reduction in tumor incidence and progression. Therefore, the potential for application of non-steroidal anti-inflammatory drugs as well as the recently developed COX-2 specific inhibitors in cancer clinical practice has drawn tremendous attention in the past few years. Inhibition of COX-2 promises to be an effective approach in the prevention and treatment of cancer, especially colorectal cancer. J. Cell. Physiol. 190: 279-286, 2002. |
