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lüll The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment Greenhough A; Smartt HJ; Moore AE; Roberts HR; Williams AC; Paraskeva C; Kaidi ACarcinogenesis 2009[Mar]; 30 (3): 377-86It is widely accepted that alterations to cyclooxygenase-2 (COX-2) expression and the abundance of its enzymatic product prostaglandin E(2) (PGE(2)) have key roles in influencing the development of colorectal cancer. Deregulation of the COX-2/PGE(2) pathway appears to affect colorectal tumorigenesis via a number of distinct mechanisms: promoting tumour maintenance and progression, encouraging metastatic spread, and perhaps even participating in tumour initiation. Here, we review the role of COX-2/PGE(2) signalling in colorectal tumorigenesis and highlight its ability to influence the hallmarks of cancer--attributes defined by Hanahan and Weinberg as being requisite for tumorigenesis. In addition, we consider components of the COX-prostaglandin pathway emerging as important regulators of tumorigenesis; namely, the prostanoid (EP) receptors, 15-hydroxyprostaglandin dehydrogenase and the prostaglandin transporter. Finally, based on recent findings, we propose a model for the cellular adaptation to the hypoxic tumour microenvironment that encompasses the interplay between COX-2, hypoxia-inducible factor 1 and dynamic switches in beta-catenin function that fine-tune signalling networks to meet the ever-changing demands of a tumour.|Animals[MESH]|Cell Hypoxia[MESH]|Cell Movement/physiology[MESH]|Colorectal Neoplasms/blood supply/*metabolism/pathology[MESH]|Cyclooxygenase 2/*physiology[MESH]|Dinoprostone/*physiology[MESH]|Humans[MESH]|Hydroxyprostaglandin Dehydrogenases/metabolism[MESH]|Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH]|Neovascularization, Pathologic/metabolism[MESH]|Organic Anion Transporters/metabolism[MESH]|Receptors, Prostaglandin E/metabolism[MESH]|Signal Transduction/physiology[MESH]|beta Catenin/metabolism[MESH] |