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Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products

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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). Although multiple studies 2 have shown a strong correlation between elevated L-PGDS (PGD2) metabolites produced by normal prostate stromal cells inhibited tumor cell growth through a peroxisome expression in the male reproductive tract and male fertility proliferator–activated receptor ; (PPAR;)–dependent mech- (14, 16, 17), the mechanistic role L-PGDS plays in normal anism. Enzymatic products of stromal cell L-PGDS included reproductive homeostasis and activity remains unknown. 12,14 In previous studies, we observed that PPARg was highly high levels of PGD2 and 15-deoxy-# -PGD2 but low levels of 12,14 expressed in malignant cells, which promoted selective growth 15-deoxy-# -prostaglandin J . These PGD metabolites 2 2 g activated the PPAR; ligand-binding domain and the peroxi- suppression in tumor cells by PPAR ligands when compared with g some proliferator response element reporter systems. Thus, normal cells that did not express PPAR (18, 19). Because high levels of L-PGDS and PGD2 have been found in normal seminal growth suppression of PPAR;-expressing tumor cells by PGD2 metabolites in the prostate microenvironment is likely to be plasma and reproductive tissue (10), we hypothesized in the g an endogenous mechanism involved in tumor suppression present study that these products stimulate the PPAR expressed that potentially contributes to the indolence and long latency primarily by prostate tumor cells, resulting in specific growth period of this disease. (Cancer Res 2005; 65(14): 6189-98) suppression. As a corollary to this hypothesis, we assumed that normal epithelia not expressing PPARg would remain unaffected by L-PGDS and PGD . To test our hypothesis, we examined the Introduction 2 expression of L-PGDS and its metabolic products in normal Dynamically balanced molecular mechanisms in the prostate prostate cells and their biological effects on normal prostate microenvironment mediate stromal-epithelial function during the epithelial cells and prostate tumor cells. development and homeostatic maintenance of the prostate gland. Perturbation of these molecular dynamics can have a negative or positive influence during prostate carcinogenesis. Materials and Methods Among the many products generated by support tissues in the Cell culture. Normal prostate epithelial cells, prostate stromal cells, and prostate gland, those most likely to profoundly affect the growth of prostate smooth muscle cells isolated from young trauma victims were cancer cells are prostaglandins. Prostaglandins are essential to obtained from Clonetics Corp. (San Diego, CA). The PC-3, LNCaP, and male reproduction (1, 2), and high levels of prostaglandins are DU145 cell lines were obtained from American Type Culture Collection found in semen as products of both prostate and seminal vesicles (Manassas, VA). Control RAW 264.7 cells were provided by Dr. B. Su (3–7). (Department of Immunology, The University of Texas M.D. Anderson Unique among glandular epithelial tissues, the prostate is one Cancer Center, Houston, TX) and HU78 cells by Dr. D. Jones (Department of of the few tissues other than the heart, the brain, and some Hematopathology, The University of Texas M.D. Anderson Cancer Center). adipose tissues that make lipocalin-type prostaglandin D synthase Primary cell cultures were maintained in defined culture medium according to the manufacturer’s instructions as described previously (20). All other cell (L-PGDS), which synthesizes prostaglandin D (PGD ; refs. 8–11). 2 2 lines were maintained in DMEM and F-12 low-glucose medium mixed at a Both L-PGDS protein and PGD2 are prominently found in normal ratio of 1:1 (Life Technologies, Bethesda, MD) supplemented with 10% fetal bovine serum. Reverse transcription-PCR. The RNA STAT-60 reagent (Tel-Test, Inc., Requests for reprints: David G. Menter, Department of Clinical Cancer Friendswood, TX) was used to extract the total RNA, which was treated with Prevention, The University of Texas M.D. Anderson Cancer Center, Box 1360, 1515 DNase I before use in a reverse transcription-PCR (RT-PCR) analysis. RNA Holcombe Boulevard, Houston, TX 77030. Phone: 713-792-0626; Fax: 713-794-4403; E-mail: [email protected]. (1 Ag) was reverse transcribed with mouse mammary tumor virus RT (Life I2005 American Association for Cancer Research. Technologies, Inc., Rockville, MD). L-PGDS (600 bp) was amplified by the www.aacrjournals.org 6189 Cancer Res 2005; 65: (14). July 15, 2005 Downloaded from cancerres.aacrjournals.org on September 29, 2021. © 2005 American Association for Cancer Research. Cancer Research primer set 5V-CTGCTCGGCTGCAGGAGAATGGCTACTCATCACAC-3V and Transactivation of the peroxisome proliferator response element. 5V-TGGGGAGTCCTATTGTTCCGTCATGCACTTA-3V, and PGDS (321 bp) PC-3 cells were cotransfected with [acyl-CoA oxidase-peroxisome was amplified by the primer set 5V-CCCAGGTCTCCGTGCAGCCCAACTTC- proliferator response element (PPRE)]-thymidine kinase-luciferase report- CAG-3Vand 5V-TGTACAGCAGGGCGTAGTGGTCGTAGTCA-3Vas described er (250 ng; ref. 27) and hGal cDNA (100 ng); reporter assay analysis previously (21). DP1 receptor (387 bp) was amplified by the primer set 5V- followed as described previously (19). Luciferase activity was normalized GCAACCTCTATGCGATGCAC-3Vand 5V-GAATTGCTGCACCGGCTCCT-3Vas to hGal activity that was cotransfected along with the appropriate described by Sarrazin et al. (22). DP2 receptor (309 bp), otherwise known as reporter. CRTH2 receptor, was amplified by the primer set 5V-CCTCTGT- Peroxisome proliferator–activated receptor ;–specific ligand-bind- GCCCAGAGCCCCACGATGTCGGC-3V and 5V-CACGGCCAAGA- ing domain transactivation. Recombinant pcDNA3 plasmids that AGTAGGTGAAGAAG-3Vas described by Nagata et al. (23). Primer pairs contained cDNA inserts encoding either a fusion protein containing Gal4 (5V-CAGCTCTGGAGAACTGCTG-3Vand 5V-GTGTACTCAGTCTCCACAGA-3V; DNA-binding domain (amino acids 1-147) coupled to a PPARg ligand- ref. 24) were used in RT-PCR analysis to detect 36B4 mRNA (24). The RT- binding domain (LBD; amino acids 174-475) fusion protein or just a Gal4 PCR DNA products were subcloned using a topoisomerase PCR system DNA-binding domain as a control (28) were used to transfect prostate (Invitrogen, Carlsbad, CA) and sequenced by automated sequencing cancer cells in six-well tissue culture plates. Either plasmid (0.5 Ag) plus (SeqWright, Houston, TX) to verify the insert DNA. After sequencing (Gal4UAS)4-thymidine kinase-luciferase reporter plasmid (0.5 Ag; ref. 29) occurred, a 600-bp product was then subcloned into three vectors, a were transfected by using FuGENE 6 (Roche, Indianapolis, IN). Either pIRESNeo2 selectable vector, a pCMVHA-tagged vector, and a pCMVmyc- PPARg ligands (5 Amol/L) dissolved in ethanol or ethanol alone were tagged vector, to yield pLPGDSNeo, pLPGDSHA, and pLPGDSmyc, added 24 hours after the addition of DNA. Luciferase activity was measured respectively. 6 hours after the ligands were added and normalized to the activity of Determination of prostaglandin D2 metabolites in prostate cells. either Renilla luciferase or hGal that was cotransfected with the Various cell lines were plated in 100-mm tissue culture dishes to attain a appropriate normalization reporter at one fifth the concentration of the confluence of 70% to 75%. Cells were then incubated with 10 Amol/L chimeric Gal4/PPARg plasmid. arachidonic acid for 30 minutes and then 1 hour. The culture medium was Construction and transfection with U6-tetO-driven short hairpin collected at each time point, and cells were harvested at 1 hour by RNA plasmids. A tetracycline-inducible version of the human U6 PolIII trypsinization and subjected to PGD2 extraction. promoter construct (U6-tetO) was obtained from Dr. D. Takai (University of Intracellular prostaglandin
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