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      The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment.

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          Abstract

          It 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.

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          Author and article information

          Journal
          Carcinogenesis
          Carcinogenesis
          Oxford University Press (OUP)
          1460-2180
          0143-3334
          Mar 2009
          : 30
          : 3
          Affiliations
          [1 ] Department of Cellular and Molecular Medicine, Cancer Research UK Colorectal Tumour Biology Group, University of Bristol, University Walk, Clifton, Bristol, UK.
          Article
          bgp014
          10.1093/carcin/bgp014
          19136477
          850a2bd2-a4fb-4e56-bc87-48ef598f509a
          History

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