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      Stromal Expression of Decorin, Semaphorin6D, SPARC, Sprouty1 and Tsukushi in Developing Prostate and Decreased Levels of Decorin in Prostate Cancer

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          Abstract

          Background and Aim

          During prostate development, mesenchymal-epithelial interactions regulate organ growth and differentiation. In adult prostate, stromal-epithelial interactions are important for tissue homeostasis and also play a significant role in prostate cancer. In this study we have identified molecules that show a mesenchymal expression pattern in the developing prostate, and one of these showed reduced expression in prostate cancer stroma.

          Methodology and Principal Findings

          Five candidate molecules identified by transcript profiling of developmental prostate mesenchyme were selected using a wholemount in situ hybridisation screen and studied Decorin (Dcn), Semaphorin6D (Sema6D), SPARC/Osteonectin (SPARC), Sprouty1 (Spry-1) and Tsukushi (Tsku). Expression in rat tissues was evaluated using wholemount in situ hybridisation (postnatal day (P) 0.5) and immunohistochemistry (embryonic day (E) E17.5, E19.5; P0.5; P6; 28 & adult). Four candidates (Decorin, SPARC, Spry-1, Tsukushi) were immunolocalised in human foetal prostate (weeks 14, 16, 19) and expression of Decorin was evaluated on a human prostate cancer tissue microarray. In embryonic and perinatal rats Decorin, Semaphorin6D, SPARC, Spry-1 and Tsukushi were expressed with varying distribution patterns throughout the mesenchyme at E17.5, E19.5, P0.5 and P6.5. In P28 and adult prostates there was either a decrease in the expression (Semaphorin6D) or a switch to epithelial expression of SPARC, and Spry-1, whereas Decorin and Tsukushi were specific to mesenchyme/stroma at all ages. Expression of Decorin, SPARC, Spry-1 and Tsukushi in human foetal prostates paralleled that in rat. Decorin showed mesenchymal and stromal-specific expression at all ages and was further examined in prostate cancer, where stromal expression was significantly reduced compared with non-malignant prostate.

          Conclusion and Significance

          We describe the spatio-temporal expression of Decorin, Semaphorin6D, SPARC, Spry-1 and Tsukushi in developing prostate and observed similar mesenchymal expression patterns in rat and human. Additionally, Decorin showed reduced expression in prostate cancer stroma compared to non-malignant prostate stroma.

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          Autocrine TGF-beta and stromal cell-derived factor-1 (SDF-1) signaling drives the evolution of tumor-promoting mammary stromal myofibroblasts.

          Yasushi Kojima, Ahmet Acar, Elinor Ng Eaton … (2010)
          Much interest is currently focused on the emerging role of tumor-stroma interactions essential for supporting tumor progression. Carcinoma-associated fibroblasts (CAFs), frequently present in the stroma of human breast carcinomas, include a large number of myofibroblasts, a hallmark of activated fibroblasts. These fibroblasts have an ability to substantially promote tumorigenesis. However, the precise cellular origins of CAFs and the molecular mechanisms by which these cells evolve into tumor-promoting myofibroblasts remain unclear. Using a coimplantation breast tumor xenograft model, we show that resident human mammary fibroblasts progressively convert into CAF myofibroblasts during the course of tumor progression. These cells increasingly acquire two autocrine signaling loops, mediated by TGF-β and SDF-1 cytokines, which both act in autostimulatory and cross-communicating fashions. These autocrine-signaling loops initiate and maintain the differentiation of fibroblasts into myofibroblasts and the concurrent tumor-promoting phenotype. Collectively, these findings indicate that the establishment of the self-sustaining TGF-β and SDF-1 autocrine signaling gives rise to tumor-promoting CAF myofibroblasts during tumor progression. This autocrine-signaling mechanism may prove to be an attractive therapeutic target to block the evolution of tumor-promoting CAFs.
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            Carcinoma-associated fibroblasts direct tumor progression of initiated human prostatic epithelium.

            Thea Tlsty, Scott Carroll, Aria F. Olumi … (1999)
            The present study demonstrates that fibroblasts associated with carcinomas stimulate tumor progression of initiated nontumorigenic epithelial cells both in an in vivo tissue recombination system and in an in vitro coculture system. Human prostatic carcinoma-associated fibroblasts grown with initiated human prostatic epithelial cells dramatically stimulated growth and altered histology of the epithelial population. This effect was not detected when normal prostatic fibroblasts were grown with the initiated epithelial cells under the same experimental conditions. In contrast, carcinoma-associated fibroblasts did not affect growth of normal human prostatic epithelial cells under identical conditions. From these data, we conclude that in this human prostate cancer model, carcinoma-associated fibroblasts stimulate progression of tumorigenesis. Thus, carcinoma-associated fibroblasts can direct tumor progression of an initiated prostate epithelial cell.
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              Negative regulation of transforming growth factor-beta by the proteoglycan decorin.

              Y. Yamaguchi, D Mann, E Ruoslahti (1990)
              Decorin is a small chondroitin-dermatan sulphate proteoglycan consisting of a core protein and a single glycosaminoglycan chain. Eighty per cent of the core protein consists of 10 repeats of a leucin-rich sequence of 24 amino acids. Similar repeats have been found in two other proteoglycans, biglycan and fibromodulin, and in several other proteins including Drosophila morphogenetic proteins. Expression of high levels of decorin in Chinese hamster ovary cells has a dramatic effect on their morphology and growth properties. We now report that this effect is due at least in part to the ability of decorin to bind transforming growth factor-beta, an autocrine factor that stimulates the growth of Chinese hamster ovary cells. As transforming growth factor-beta induces synthesis of decorin in many cell types, our results suggest that decorin may be a component of a feedback system regulating cell growth.
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                Author and article information

                Contributors
                : Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2012
                Publication date (Electronic): 3 August 2012
                Volume: 7
                Issue: 8
                Electronic Location Identifier: e42516
                Affiliations
                [1 ]Medical Research Council, Centre for Reproductive Health, The Queens’s Medical Research Institute, Edinburgh, Scotland, United Kingdom
                [2 ]Edinburgh Urological Cancer Group, Division of Pathology, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom
                IIT Research Institute, United States of America
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                [¤a]

                Current address: Laboratory for Immunotherapy, University Clinic Cologne, Cologne, Germany

                [¤b]

                Current address: Faculty of Health, Life and Social Sciences, Edinburgh Napier University, Edinburgh, United Kingdom

                [¤c]

                Current address: PrimerDesign Ltd, Southampton, Hants, United Kingdom

                [¤d]

                Current address: DestiNA Genomics Ltd, Edinburgh, United Kingdom

                Conceived and designed the experiments: AH GRA AAT. Performed the experiments: AH OCG GRA. Analyzed the data: AH GRA. Contributed reagents/materials/analysis tools: GDS ACPR HY MOD RAA. Wrote the paper: AH RAA AAT. Consenting and operating patients: GDS ACPR.

                Article
                Publisher ID: PONE-D-11-16239
                DOI: 10.1371/journal.pone.0042516
                PMC ID: 3411755
                PubMed ID: 22880013
                SO-VID: 1fbf112e-9cfd-42c1-9d3e-b9ac89ff807b
                Copyright statement: Copyright @ 2012
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 17 August 2011
                Date accepted : 9 July 2012
                Page count
                Pages: 12
                Funding
                The work was funded by the Medical Research Council (WBSe 1276.00.003.00004.01) and the Prostate Cancer Charity ( http://www.prostate-cancer.org.uk/). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Anatomy and Physiology
                Subject: Comparative Anatomy
                Subject: Reproductive System
                Subject: Computational Biology
                Subject: Molecular Genetics
                Subject: Gene Expression
                Subject: Developmental Biology
                Subject: Organism Development
                Subject: Organogenesis
                Subject: Medicine
                Subject: Anatomy and Physiology
                Subject: Comparative Anatomy
                Subject: Reproductive System
                Subject: Urology
                Subject: Prostate Diseases
                Subject: Benign Prostatic Hyperplasia
                Subject: Prostate Cancer

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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