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Cancer Lett. 2014 Jun 28;348(1-2):1-11. doi: 10.1016/j.canlet.2014.03.010. Epub 2014 Mar 18.

Prostaglandin E3 metabolism and cancer.

Author information

1
Department of General Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, United States. Electronic address: pyang@mdanderson.org.
2
Department of General Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, United States.
3
Department of Molecular Carcinogenesis, The University of Texas, MD Anderson Cancer Center, Houston, TX, United States.

Abstract

The anticancer activity of n-3 fatty acids, especially those derived from fish, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid) (DHA), has been studied for centuries. While there is a growing body of evidence that EPA and DHA may influence cancer initiation and development through targeting multiple events of tumor development, the underlying mechanisms responsible for these activities are still not fully understood. A number of studies have suggested that the anticancer activities of EPA and DHA are associated with their effects on eicosanoid metabolism by which they inhibit prostaglandin E2 (PGE2) production. In contrast to DHA, EPA can function as a substrate for cyclooxygenases (COXs) to synthesize unique 3-series prostaglandin compounds, especially PGE3. With advance technology in mass spectrometry, there is renewed interest in studying the role of PGE3 in EPA elicited anti-proliferative activity in various cancers, with some promising results. Here, we summarize the regulation of PGE3 synthesis in cancer cells and its role in EPA elicited anticancer activity. The development of PGE3 and its metabolites as potential biomarkers for future clinical evaluation of EPA and fish oil in cancer care is discussed.

KEYWORDS:

Cancer cells; Metabolism; PGE(3); Tumor tissues; n-3 Fatty acids

PMID:
24657656
PMCID:
PMC4366418
DOI:
10.1016/j.canlet.2014.03.010
[Indexed for MEDLINE]
Free PMC Article
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