The Role of Cyclooxygenase-2 in Signaling Pathways Promoting Colorectal Cancer

Colorectal cancer is one of the most common cancers in the world. Various factors are involved in the development and progression of this disease. One of these agents is cyclooxygenase-2 (COX-2). COX-2 is a product of the PTGS2 gene and converts free arachidonic acid to prostaglandins. COX-2 is not naturally expressed in most normal cells. Noticeably, the increased expression of COX-2 has been observed in chronic inflammatory diseases and various cancers. COX-2 promotes colorectal cancer through various signaling pathways. COX-2 plays its role in colorectal cancer by induction of Bcl-2 expression, and β-catenin pathway activation, and leads to translocate of the NF-κB from the cytoplasm to the nucleus. NF-κB transcription factor plays an important role in physiological processes such as cell proliferation, cell death, and inflammation. Deregulation of NF-κB and its impact on the signaling pathway play a critical role in the development and progression of colorectal cancer. Another factor that plays a role in the development and progression of colorectal cancer is the β-catenin gene. Mutations in the β-catenin gene have been found in more than half of colorectal cancer patients. Bcl-2 is also known as an anti-apoptotic factor in all types of cancers. COX-2 controls all these pathways. Therefore, targeting COX-2 can be proposed as a therapeutic strategy for the treatment of colorectal cancer. The purpose of this review is to investigate the signaling pathways related to COX-2 in colorectal cancer