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Targeting the lipids LPA and S1P and their signalling pathways to inhibit tumour progression

Published online by Cambridge University Press:  15 October 2007

Mandi Murph*
Affiliation:
Department of Systems Biology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
Gordon B. Mills
Affiliation:
Department of Systems Biology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
*
*Corresponding author: Mandi Murph, Department of Systems Biology, Unit 950, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA. Tel: +1 713 563 4225; Fax: +1 713 563 4235; E-mail: mmmurph@mdanderson.org

Abstract

The bioactive lipids lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P), the enzymes that generate and degrade them, and the receptors that receive their signals are all potential therapeutic targets in cancer. LPA and S1P signalling pathways can modulate a range of cellular processes that contribute to tumourigenesis, such as proliferation and motility, and components of the signalling pathways often show aberrant expression and altered activity upon malignant transformation. This article reviews LPA- and S1P-mediated activities that might contribute to the aetiology of cancer, and examines the potential of the many antagonists that have been developed to inhibit LPA and S1P signalling pathways. In addition, the outcomes of various clinical trials using LPA- and S1P-associated targets in cancer and other diseases are described, and future directions are discussed.

Type
Review Article
Copyright
Copyright © Cambridge University Press 2007

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References

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Further reading, resources and contacts

Clinical trials can be accessed through the US National Institutes of Health website. The NCT numbers described throughout this review can be searched there. This is a service developed by the National Library of Medicine, which provides regularly updated information on clinical research: