Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products
Research Article Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products Jeri Kim,1 Peiying Yang,2 Milind Suraokar,3 Anita L. Sabichi,3 Norma D. Llansa,3 Gabriela Mendoza,3 Vemparalla Subbarayan,3 Christopher J. Logothetis,1 Robert A. Newman,2 Scott M. Lippman,3 and David G. Menter3 Departments of 1Genitourinary Medical Oncology, 2Experimental Therapeutics, and 3Clinical Cancer Prevention, The University of Texas M.D. Anderson Cancer Center, Houston, Texas Abstract seminal fluid (10). Once PGD2 is made, it forms derivative Stromal-epithelial interactions and the bioactive molecules compounds, most of which can transactivate the peroxisome g g produced by these interactions maintain tissue homeostasis proliferator–activated receptor (PPAR ). One PGD2 derivative, 15-deoxy-D12,14-prostaglandin J (15-d-PGJ ), can slow the growth and influence carcinogenesis. Bioactive prostaglandins pro- 2 2 duced by prostaglandin synthases and secreted by the prostate and induce the partial differentiation of selected cancer cells (12). D12,14 into seminal plasma are thought to support reproduction, but Another PGD2 derivative, 15-deoxy- -PGD2 (15-d-PGD2), has g their endogenous effects on cancer formation remain unre- also been shown to stimulate PPAR transactivation in RAW 264.7 solved. No studies to date have examined prostaglandin cell macrophage cultures as effectively as 15-d-PGJ2 (13). L-PGDS enzyme production or prostaglandin metabolism in normal also binds tritiated testosterone and may play a role in androgen prostate stromal cells. Our results show that lipocalin-type transport (14). In castrated rats, testosterone proprionate induces prostaglandin D synthase (L-PGDS) and prostaglandin D L-PGDS synthesis in the epididymis (15).
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