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International Journal of Cell Biology
Volume 2012, Article ID 723419, 21 pages
Review Article

Prostaglandins in Cancer Cell Adhesion, Migration, and Invasion

1Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
2Department of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA

Received 19 August 2011; Accepted 8 October 2011

Academic Editor: Eok-Soo Oh

Copyright © 2012 David G. Menter and Raymond N. DuBois. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Prostaglandins exert a profound influence over the adhesive, migratory, and invasive behavior of cells during the development and progression of cancer. Cyclooxygenase-2 (COX-2) and microsomal prostaglandin E2 synthase-1 (mPGES-1) are upregulated in inflammation and cancer. This results in the production of prostaglandin E2 (PGE2), which binds to and activates G-protein-coupled prostaglandin E 1 - 4 receptors ( E P 1 - 4 ). Selectively targeting the COX-2/mPGES-1/PGE2/ E P 1 - 4 axis of the prostaglandin pathway can reduce the adhesion, migration, invasion, and angiogenesis. Once stimulated by prostaglandins, cadherin adhesive connections between epithelial or endothelial cells are lost. This enables cells to invade through the underlying basement membrane and extracellular matrix (ECM). Interactions with the ECM are mediated by cell surface integrins by “outside-in signaling” through Src and focal adhesion kinase (FAK) and/or “inside-out signaling” through talins and kindlins. Combining the use of COX-2/mPGES-1/PGE2/ E P 1 - 4 axis-targeted molecules with those targeting cell surface adhesion receptors or their downstream signaling molecules may enhance cancer therapy.