Fig. 4
Model for PTGS pathway deregulation during colorectal tumorigenesis. Inflammatory processes, including overactivation of PTGS signaling, are present in the colonic mucosae during, and possibly before, tumor development. In the tumor, promoter hypermethylation and other mechanisms contribute to the repression of several prostanoid-specific synthases and membrane receptors. This leads to the prevalence of PGE2 as the major prostanoid in tumor cells, whose downstream actions may include evasion of apoptosis, tumor growth, angiogenesis, and metastasis