Dickkopf-related protein 3 promotes pathogenic stromal remodeling in benign prostatic hyperplasia and prostate cancer
BACKGROUND Compartment‐specific epithelial and stromal expression of the secreted glycoprotein Dickkopf‐related protein (Dkk)‐3 is altered in age‐related proliferative disorders of the human prostate. This study aimed to determine the effect of Dkk‐3 on prostate stromal remodeling that is stromal pr...
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| Veröffentlicht in: | The Prostate 2013-09, Vol.73 (13), p.1441-1452 |
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| creator | Zenzmaier, Christoph Sampson, Natalie Plas, Eugen Berger, Peter |
| description | BACKGROUND
Compartment‐specific epithelial and stromal expression of the secreted glycoprotein Dickkopf‐related protein (Dkk)‐3 is altered in age‐related proliferative disorders of the human prostate. This study aimed to determine the effect of Dkk‐3 on prostate stromal remodeling that is stromal proliferation, fibroblast‐to‐myofibroblast differentiation and expression of angiogenic factors in vitro.
METHODS
Lentiviral‐delivered overexpression and shRNA‐mediated knockdown of DKK3 were applied to primary human prostatic stromal cells (PrSCs). Cellular proliferation was analyzed by BrdU incorporation ELISA. Expression of Dkk‐3, apoptosis‐related genes, cyclin‐dependent kinase inhibitors and angiogenic factors were analyzed by qPCR, Western blot analysis or ELISA. Fibroblast‐to‐myofibroblast differentiation was monitored by smooth muscle cell actin and insulin‐like growth factor binding protein 3 mRNA and protein levels. The relevance of Wnt/β‐catenin and PI3K/AKT signaling pathways was assessed by cytoplasmic/nuclear β‐catenin levels and phosphorylation of AKT.
RESULTS
Knockdown of DKK3 significantly attenuated PrSC proliferation as well as fibroblast‐to‐myofibroblast differentiation and increased the expression of the vessel stabilizing factor angiopoietin‐1. DKK3 knockdown did not affect subcellular localization or levels of β‐catenin but attenuated AKT phosphorylation in PrSCs. Consistently the PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown.
CONCLUSIONS
Dkk‐3 promotes fibroblast proliferation and myofibroblast differentiation and regulates expression of angiopoietin‐1 in prostatic stroma potentially via enhancing PI3K/AKT signaling. Thus, elevated Dkk‐3 in the stroma of the diseased prostate presumably regulates stromal remodeling by enhancing proliferation and differentiation of stromal cells and contributing to the angiogenic switch observed in BPH and PCa. Therefore, Dkk‐3 represents a potential therapeutic target for stromal remodeling in BPH and PCa. Prostate 73: 1441–1452, 2013. © 2013 Wiley‐Liss, Inc. The Prostate published by Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/pros.22691 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3842835</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1426004164</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5521-3a0efe8c466f31132d2374ff182a2ebcc60973736b3d9b9246cca2f8f02da0fe3</originalsourceid><addsrcrecordid>eNp9kU9v1DAQxS0EokvhwgdAkbggpBT_SZzkgoQKFKSKIijs0XKc8a67jh1sB9hvj5ftroADJ488v3l68wahxwSfEYzpiyn4eEYp78gdtCC4a0qMq_ouWmDa4LIirDlBD2K8wTjjmN5HJ5Q1vG4YWaD5tVGbjZ90GcDKBEOR1RIYV7BdNeY6FpNMa78CZ1QRU_6Utggw-gGscasis33urdxuICaZMrbeThAmK6ORhXTDoQOFkk5BeIjuaWkjPLp9T9GXt2-uz9-Vl1cX789fXZaqrikpmcSgoVUV55oRwuiQjVdak5ZKCr1SPC_LGsZ7NnR9RyuulKS61ZgOEmtgp-jlXnea-xEGBS4FacUUzCjDVnhpxN8dZ9Zi5b8L1la0ZXUWeHYrEPy3GWISo4kKrJUO_BwFqSjPYRNeZfTpP-iNn4PL6wnS8BZTTmqeqed7SuVEYgB9NEOw2F1T7KISv6-Z4Sd_2j-ih_NlgOyBH8bC9j9S4uOnq88H0XI_Y2KCn8cZGTaC5zBrsfxwIbpl_bXF9VJcs1_OnrzZ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1768026156</pqid></control><display><type>article</type><title>Dickkopf-related protein 3 promotes pathogenic stromal remodeling in benign prostatic hyperplasia and prostate cancer</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Zenzmaier, Christoph ; Sampson, Natalie ; Plas, Eugen ; Berger, Peter</creator><creatorcontrib>Zenzmaier, Christoph ; Sampson, Natalie ; Plas, Eugen ; Berger, Peter</creatorcontrib><description>BACKGROUND
Compartment‐specific epithelial and stromal expression of the secreted glycoprotein Dickkopf‐related protein (Dkk)‐3 is altered in age‐related proliferative disorders of the human prostate. This study aimed to determine the effect of Dkk‐3 on prostate stromal remodeling that is stromal proliferation, fibroblast‐to‐myofibroblast differentiation and expression of angiogenic factors in vitro.
METHODS
Lentiviral‐delivered overexpression and shRNA‐mediated knockdown of DKK3 were applied to primary human prostatic stromal cells (PrSCs). Cellular proliferation was analyzed by BrdU incorporation ELISA. Expression of Dkk‐3, apoptosis‐related genes, cyclin‐dependent kinase inhibitors and angiogenic factors were analyzed by qPCR, Western blot analysis or ELISA. Fibroblast‐to‐myofibroblast differentiation was monitored by smooth muscle cell actin and insulin‐like growth factor binding protein 3 mRNA and protein levels. The relevance of Wnt/β‐catenin and PI3K/AKT signaling pathways was assessed by cytoplasmic/nuclear β‐catenin levels and phosphorylation of AKT.
RESULTS
Knockdown of DKK3 significantly attenuated PrSC proliferation as well as fibroblast‐to‐myofibroblast differentiation and increased the expression of the vessel stabilizing factor angiopoietin‐1. DKK3 knockdown did not affect subcellular localization or levels of β‐catenin but attenuated AKT phosphorylation in PrSCs. Consistently the PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown.
CONCLUSIONS
Dkk‐3 promotes fibroblast proliferation and myofibroblast differentiation and regulates expression of angiopoietin‐1 in prostatic stroma potentially via enhancing PI3K/AKT signaling. Thus, elevated Dkk‐3 in the stroma of the diseased prostate presumably regulates stromal remodeling by enhancing proliferation and differentiation of stromal cells and contributing to the angiogenic switch observed in BPH and PCa. Therefore, Dkk‐3 represents a potential therapeutic target for stromal remodeling in BPH and PCa. Prostate 73: 1441–1452, 2013. © 2013 Wiley‐Liss, Inc. The Prostate published by Wiley Periodicals, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.22691</identifier><identifier>PMID: 23765731</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>angiogenic factors ; angiopoietin ; Angiopoietin-1 - metabolism ; Animals ; beta Catenin - metabolism ; Cell Proliferation ; Cells, Cultured ; Humans ; Insulin-Like Growth Factor Binding Protein 3 - metabolism ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Male ; Mice ; myofibroblast differentiation ; Original ; Phosphorylation ; proliferation ; Prostate - metabolism ; Prostate - pathology ; Prostatic Hyperplasia - genetics ; Prostatic Hyperplasia - metabolism ; Prostatic Hyperplasia - pathology ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Proto-Oncogene Proteins c-akt - metabolism ; RNA, Small Interfering ; Signal Transduction - physiology ; Stromal Cells - metabolism ; Stromal Cells - pathology</subject><ispartof>The Prostate, 2013-09, Vol.73 (13), p.1441-1452</ispartof><rights>2013 Wiley-Liss, Inc.</rights><rights>2013 Wiley Periodicals, Inc.</rights><rights>2013 Wiley Periodicals, Inc. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5521-3a0efe8c466f31132d2374ff182a2ebcc60973736b3d9b9246cca2f8f02da0fe3</citedby><cites>FETCH-LOGICAL-c5521-3a0efe8c466f31132d2374ff182a2ebcc60973736b3d9b9246cca2f8f02da0fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpros.22691$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpros.22691$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23765731$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zenzmaier, Christoph</creatorcontrib><creatorcontrib>Sampson, Natalie</creatorcontrib><creatorcontrib>Plas, Eugen</creatorcontrib><creatorcontrib>Berger, Peter</creatorcontrib><title>Dickkopf-related protein 3 promotes pathogenic stromal remodeling in benign prostatic hyperplasia and prostate cancer</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>BACKGROUND
Compartment‐specific epithelial and stromal expression of the secreted glycoprotein Dickkopf‐related protein (Dkk)‐3 is altered in age‐related proliferative disorders of the human prostate. This study aimed to determine the effect of Dkk‐3 on prostate stromal remodeling that is stromal proliferation, fibroblast‐to‐myofibroblast differentiation and expression of angiogenic factors in vitro.
METHODS
Lentiviral‐delivered overexpression and shRNA‐mediated knockdown of DKK3 were applied to primary human prostatic stromal cells (PrSCs). Cellular proliferation was analyzed by BrdU incorporation ELISA. Expression of Dkk‐3, apoptosis‐related genes, cyclin‐dependent kinase inhibitors and angiogenic factors were analyzed by qPCR, Western blot analysis or ELISA. Fibroblast‐to‐myofibroblast differentiation was monitored by smooth muscle cell actin and insulin‐like growth factor binding protein 3 mRNA and protein levels. The relevance of Wnt/β‐catenin and PI3K/AKT signaling pathways was assessed by cytoplasmic/nuclear β‐catenin levels and phosphorylation of AKT.
RESULTS
Knockdown of DKK3 significantly attenuated PrSC proliferation as well as fibroblast‐to‐myofibroblast differentiation and increased the expression of the vessel stabilizing factor angiopoietin‐1. DKK3 knockdown did not affect subcellular localization or levels of β‐catenin but attenuated AKT phosphorylation in PrSCs. Consistently the PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown.
CONCLUSIONS
Dkk‐3 promotes fibroblast proliferation and myofibroblast differentiation and regulates expression of angiopoietin‐1 in prostatic stroma potentially via enhancing PI3K/AKT signaling. Thus, elevated Dkk‐3 in the stroma of the diseased prostate presumably regulates stromal remodeling by enhancing proliferation and differentiation of stromal cells and contributing to the angiogenic switch observed in BPH and PCa. Therefore, Dkk‐3 represents a potential therapeutic target for stromal remodeling in BPH and PCa. Prostate 73: 1441–1452, 2013. © 2013 Wiley‐Liss, Inc. The Prostate published by Wiley Periodicals, Inc.</description><subject>angiogenic factors</subject><subject>angiopoietin</subject><subject>Angiopoietin-1 - metabolism</subject><subject>Animals</subject><subject>beta Catenin - metabolism</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor Binding Protein 3 - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>myofibroblast differentiation</subject><subject>Original</subject><subject>Phosphorylation</subject><subject>proliferation</subject><subject>Prostate - metabolism</subject><subject>Prostate - pathology</subject><subject>Prostatic Hyperplasia - genetics</subject><subject>Prostatic Hyperplasia - metabolism</subject><subject>Prostatic Hyperplasia - pathology</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA, Small Interfering</subject><subject>Signal Transduction - physiology</subject><subject>Stromal Cells - metabolism</subject><subject>Stromal Cells - pathology</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp9kU9v1DAQxS0EokvhwgdAkbggpBT_SZzkgoQKFKSKIijs0XKc8a67jh1sB9hvj5ftroADJ488v3l68wahxwSfEYzpiyn4eEYp78gdtCC4a0qMq_ouWmDa4LIirDlBD2K8wTjjmN5HJ5Q1vG4YWaD5tVGbjZ90GcDKBEOR1RIYV7BdNeY6FpNMa78CZ1QRU_6Utggw-gGscasis33urdxuICaZMrbeThAmK6ORhXTDoQOFkk5BeIjuaWkjPLp9T9GXt2-uz9-Vl1cX789fXZaqrikpmcSgoVUV55oRwuiQjVdak5ZKCr1SPC_LGsZ7NnR9RyuulKS61ZgOEmtgp-jlXnea-xEGBS4FacUUzCjDVnhpxN8dZ9Zi5b8L1la0ZXUWeHYrEPy3GWISo4kKrJUO_BwFqSjPYRNeZfTpP-iNn4PL6wnS8BZTTmqeqed7SuVEYgB9NEOw2F1T7KISv6-Z4Sd_2j-ih_NlgOyBH8bC9j9S4uOnq88H0XI_Y2KCn8cZGTaC5zBrsfxwIbpl_bXF9VJcs1_OnrzZ</recordid><startdate>201309</startdate><enddate>201309</enddate><creator>Zenzmaier, Christoph</creator><creator>Sampson, Natalie</creator><creator>Plas, Eugen</creator><creator>Berger, Peter</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Wiley Periodicals</general><scope>BSCLL</scope><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201309</creationdate><title>Dickkopf-related protein 3 promotes pathogenic stromal remodeling in benign prostatic hyperplasia and prostate cancer</title><author>Zenzmaier, Christoph ; Sampson, Natalie ; Plas, Eugen ; Berger, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5521-3a0efe8c466f31132d2374ff182a2ebcc60973736b3d9b9246cca2f8f02da0fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>angiogenic factors</topic><topic>angiopoietin</topic><topic>Angiopoietin-1 - metabolism</topic><topic>Animals</topic><topic>beta Catenin - metabolism</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Humans</topic><topic>Insulin-Like Growth Factor Binding Protein 3 - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>myofibroblast differentiation</topic><topic>Original</topic><topic>Phosphorylation</topic><topic>proliferation</topic><topic>Prostate - metabolism</topic><topic>Prostate - pathology</topic><topic>Prostatic Hyperplasia - genetics</topic><topic>Prostatic Hyperplasia - metabolism</topic><topic>Prostatic Hyperplasia - pathology</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RNA, Small Interfering</topic><topic>Signal Transduction - physiology</topic><topic>Stromal Cells - metabolism</topic><topic>Stromal Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zenzmaier, Christoph</creatorcontrib><creatorcontrib>Sampson, Natalie</creatorcontrib><creatorcontrib>Plas, Eugen</creatorcontrib><creatorcontrib>Berger, Peter</creatorcontrib><collection>Istex</collection><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zenzmaier, Christoph</au><au>Sampson, Natalie</au><au>Plas, Eugen</au><au>Berger, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dickkopf-related protein 3 promotes pathogenic stromal remodeling in benign prostatic hyperplasia and prostate cancer</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2013-09</date><risdate>2013</risdate><volume>73</volume><issue>13</issue><spage>1441</spage><epage>1452</epage><pages>1441-1452</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>BACKGROUND
Compartment‐specific epithelial and stromal expression of the secreted glycoprotein Dickkopf‐related protein (Dkk)‐3 is altered in age‐related proliferative disorders of the human prostate. This study aimed to determine the effect of Dkk‐3 on prostate stromal remodeling that is stromal proliferation, fibroblast‐to‐myofibroblast differentiation and expression of angiogenic factors in vitro.
METHODS
Lentiviral‐delivered overexpression and shRNA‐mediated knockdown of DKK3 were applied to primary human prostatic stromal cells (PrSCs). Cellular proliferation was analyzed by BrdU incorporation ELISA. Expression of Dkk‐3, apoptosis‐related genes, cyclin‐dependent kinase inhibitors and angiogenic factors were analyzed by qPCR, Western blot analysis or ELISA. Fibroblast‐to‐myofibroblast differentiation was monitored by smooth muscle cell actin and insulin‐like growth factor binding protein 3 mRNA and protein levels. The relevance of Wnt/β‐catenin and PI3K/AKT signaling pathways was assessed by cytoplasmic/nuclear β‐catenin levels and phosphorylation of AKT.
RESULTS
Knockdown of DKK3 significantly attenuated PrSC proliferation as well as fibroblast‐to‐myofibroblast differentiation and increased the expression of the vessel stabilizing factor angiopoietin‐1. DKK3 knockdown did not affect subcellular localization or levels of β‐catenin but attenuated AKT phosphorylation in PrSCs. Consistently the PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown.
CONCLUSIONS
Dkk‐3 promotes fibroblast proliferation and myofibroblast differentiation and regulates expression of angiopoietin‐1 in prostatic stroma potentially via enhancing PI3K/AKT signaling. Thus, elevated Dkk‐3 in the stroma of the diseased prostate presumably regulates stromal remodeling by enhancing proliferation and differentiation of stromal cells and contributing to the angiogenic switch observed in BPH and PCa. Therefore, Dkk‐3 represents a potential therapeutic target for stromal remodeling in BPH and PCa. Prostate 73: 1441–1452, 2013. © 2013 Wiley‐Liss, Inc. The Prostate published by Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>23765731</pmid><doi>10.1002/pros.22691</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | angiogenic factors angiopoietin Angiopoietin-1 - metabolism Animals beta Catenin - metabolism Cell Proliferation Cells, Cultured Humans Insulin-Like Growth Factor Binding Protein 3 - metabolism Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Male Mice myofibroblast differentiation Original Phosphorylation proliferation Prostate - metabolism Prostate - pathology Prostatic Hyperplasia - genetics Prostatic Hyperplasia - metabolism Prostatic Hyperplasia - pathology Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Proto-Oncogene Proteins c-akt - metabolism RNA, Small Interfering Signal Transduction - physiology Stromal Cells - metabolism Stromal Cells - pathology |
| title | Dickkopf-related protein 3 promotes pathogenic stromal remodeling in benign prostatic hyperplasia and prostate cancer |
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