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Colorectal Neoplasia Goes with the Flow: Prostaglandin Transport and Termination

Author's Affiliation: Department of Medicine and Ireland Cancer Center, Case Western Reserve University School of Medicine and Case Medical Center, Cleveland, Ohio and Howard Hughes Medical Institute, Chevy Chase, Maryland

Requests for reprints: Sanford D. Markowitz, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106. Phone: 216-368-1976; Fax: 216-368-8928; E-mail: sxm10{at}cwru.edu.

Abstract

The past 10 to 15 years have witnessed major advances in our understanding of polyunsaturated fatty acid metabolism involving synthesis, activity, and degradation of prostaglandin (PG), especially prostaglandin E₂ (PGE₂), in neoplasia, in particular colorectal neoplasia. Little is known, however, about the role of PG transport in these processes. The flow of PGs in and out of colorectal cells involves highly coordinated activities of PG transporters that become highly dysregulated in colorectal neoplasia. Recent work by various investigators supports key components of this flow for novel molecular-targeted approaches to prevent or treat colorectal neoplasia.

Key Article

Regulation of Prostaglandin Transporters in Colorectal Neoplasia

Vijaykumar R. Holla, Michael G. Backlund, Peying Yang, Robert A. Newman, and Raymond N. DuBois
Cancer Prevention Research 2008 0: 1940-6207.CAPR-07-0009v1. [Abstract]