Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention Susan G. Komen for the Cure-AACR Outstanding Investigator Award for Breast Cancer Research
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[Cancer Research 62, 6817-6819, December 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

5(S)-Hydroxy-6,8,11,14-E,Z,Z,Z-eicosatetraenoate Stimulates PC3 Cell Signaling and Growth by a Receptor-dependent Mechanism1

Joseph T. O’Flaherty2, LeAnn C. Rogers, Brad A. Chadwell, John S. Owen, Anurada Rao, Scott D. Cramer and Larry W. Daniel

Departments of Medicine (J. T. O. and L. C. R.), Cancer Biology (A. R. and S. D. C.), and Biochemistry (J. S. O. and L. W. D.), Wake Forest University School of Medicine and Department of Biology (B. A. C.), Wake Forest University, Winston-Salem, North Carolina 27156

5(S)-Hydroxy-6,8,11,14-E,Z,Z,Z-eicosatetraenoate (5-HETE) causes PC3 cells to grow by an unknown mechanism. We find that it also induces the cells to activate extracellular signal-regulated kinases and Akt. Pertussis toxin inhibits both responses. 5-HETE, 5-oxo-6,8,11,14-E,Z,Z,Z-eicosatetraenoate, and 5-oxo-15-hydroxy-eicosatetraenoate are known to stimulate leukocytes by a receptor coupled to pertussis toxin-sensitive G proteins. Their respective relative potencies in leukocytes are 1, 10, and 3. In PC3 cells, however, these values are 10, 1, and 0. PC3 cells, we propose, express a non-leukocyte-type, G protein-coupled, 5-HETE receptor. This novel receptor and the extracellular signal-regulated kinase and Akt pathways it recruits may contribute to the progression of prostate adenocarcinoma.




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Copyright © 2002 by the American Association for Cancer Research.