Review Series 10.1172/JCI97953

Role of prostanoids in gastrointestinal cancer

Dingzhi Wang1 and Raymond N. DuBois1,2

1Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, USA.

2Department of Research and Division of Gastroenterology, Mayo Clinic, Scottsdale, Arizona, USA.

Address correspondence to: Raymond N. DuBois, 601 Clinical Science Building, 96 Jonathan Lucas Street, Suite 601, Charleston, South Carolina 29425, USA. Phone: 843.792.2842; Email: duboisrn@musc.edu.

Find articles by Wang, D. in: JCI | PubMed | Google Scholar

1Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, USA.

2Department of Research and Division of Gastroenterology, Mayo Clinic, Scottsdale, Arizona, USA.

Address correspondence to: Raymond N. DuBois, 601 Clinical Science Building, 96 Jonathan Lucas Street, Suite 601, Charleston, South Carolina 29425, USA. Phone: 843.792.2842; Email: duboisrn@musc.edu.

Find articles by DuBois, R. in: JCI | PubMed | Google Scholar

First published May 7, 2018 - More info

Published in Volume 128, Issue 7 on July 2, 2018
J Clin Invest. 2018;128(7):2732–2742. https://doi.org/10.1172/JCI97953.
Copyright © 2018, American Society for Clinical Investigation

First published May 7, 2018 - Version history

Chronic inflammation is a risk factor for gastrointestinal cancer and other diseases. Most studies have focused on cytokines and chemokines as mediators connecting chronic inflammation to cancer, whereas the involvement of lipid mediators, including prostanoids, has not been extensively investigated. Prostanoids are among the earliest signaling molecules released in response to inflammation. Multiple lines of evidence suggest that prostanoids are involved in gastrointestinal cancer. In this Review, we discuss how prostanoids impact gastrointestinal cancer development. In particular, we highlight recent advances in our understanding of how prostaglandin E2 induces the immunosuppressive microenvironment in gastrointestinal cancers.

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