The chicken ovalbumin upstream promoter-transcription factor II negatively regulates the transactivation of androgen receptor in prostate cancer cells
Androgen receptor (AR) is involved in the development and progression of prostate cancers. However, the mechanisms by which this occurs remain incompletely understood. In previous reports, chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II) has been suggested to play a role in t...
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| description | Androgen receptor (AR) is involved in the development and progression of prostate cancers. However, the mechanisms by which this occurs remain incompletely understood. In previous reports, chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II) has been suggested to play a role in the development of cancers. In the present study, we explored a putative role of COUP-TF II in prostate cancers by investigating its effect on cell proliferation and a cross-talk between COUP-TF II and AR. Overexpression of COUP-TF II results in the inhibition of androgen-dependent proliferation of prostate cancer cells. Further studies show that COUP-TF II functions as a corepressor of AR. It represses AR transactivation on target promoters containing the androgen response element (ARE) in a dose-dependent manner. In addition, COUP-TF II interacts physically with AR in vitro and in vivo. It binds to both the DNA binding domain (DBD) and the ligand-binding domain (LBD) of AR and disrupts the N/C terminal interaction of AR. Furthermore, COUP-TF II competes with coactivators such as ARA70, SRC-1, and GRIP1 to modulate AR transactivation as well as inhibiting the recruitment of AR to its ARE-containing target promoter. Taken together, our findings suggest that COUP-TF II is a novel corepressor of AR, and provide an insight into the role of COUP-TF II in prostate cancers. |
| doi_str_mv | 10.1371/journal.pone.0049026 |
| format | Article |
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However, the mechanisms by which this occurs remain incompletely understood. In previous reports, chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II) has been suggested to play a role in the development of cancers. In the present study, we explored a putative role of COUP-TF II in prostate cancers by investigating its effect on cell proliferation and a cross-talk between COUP-TF II and AR. Overexpression of COUP-TF II results in the inhibition of androgen-dependent proliferation of prostate cancer cells. Further studies show that COUP-TF II functions as a corepressor of AR. It represses AR transactivation on target promoters containing the androgen response element (ARE) in a dose-dependent manner. In addition, COUP-TF II interacts physically with AR in vitro and in vivo. It binds to both the DNA binding domain (DBD) and the ligand-binding domain (LBD) of AR and disrupts the N/C terminal interaction of AR. Furthermore, COUP-TF II competes with coactivators such as ARA70, SRC-1, and GRIP1 to modulate AR transactivation as well as inhibiting the recruitment of AR to its ARE-containing target promoter. Taken together, our findings suggest that COUP-TF II is a novel corepressor of AR, and provide an insight into the role of COUP-TF II in prostate cancers.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0049026</identifier><identifier>PMID: 23145053</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Albumin ; Androgen receptors ; Androgens ; Animals ; Binding ; Binding sites ; Biology ; Cancer ; Cancer cells ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Cercopithecus aethiops ; COS Cells ; COUP Transcription Factor II - genetics ; COUP Transcription Factor II - metabolism ; Deoxyribonucleic acid ; Development and progression ; DNA ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Gene expression ; GRIP1 protein ; Inhibition ; Ligands ; Male ; Medicine ; Mice ; Ovalbumin ; Plasmids ; Promoter Regions, Genetic ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Protein Transport ; Proteins ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; Recruitment ; Rodents ; Signal transduction ; Steroid receptor coactivator 1 ; Thyroid gland ; Transcription factors ; Transcription, Genetic ; Transcriptional Activation ; Tumors</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e49026-e49026</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Song et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Song et al 2012 Song et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-fdd3320447e0f7658413e4cea2661017f5d7deaab7801651e5476fa3e5c77b283</citedby><cites>FETCH-LOGICAL-c692t-fdd3320447e0f7658413e4cea2661017f5d7deaab7801651e5476fa3e5c77b283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492188/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492188/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23849,27907,27908,53774,53776,79351,79352</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23145053$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Roemer, Klaus</contributor><creatorcontrib>Song, Chin-Hee</creatorcontrib><creatorcontrib>Lee, Hyun Joo</creatorcontrib><creatorcontrib>Park, Eunsook</creatorcontrib><creatorcontrib>Lee, Keesook</creatorcontrib><title>The chicken ovalbumin upstream promoter-transcription factor II negatively regulates the transactivation of androgen receptor in prostate cancer cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Androgen receptor (AR) is involved in the development and progression of prostate cancers. However, the mechanisms by which this occurs remain incompletely understood. In previous reports, chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II) has been suggested to play a role in the development of cancers. In the present study, we explored a putative role of COUP-TF II in prostate cancers by investigating its effect on cell proliferation and a cross-talk between COUP-TF II and AR. Overexpression of COUP-TF II results in the inhibition of androgen-dependent proliferation of prostate cancer cells. Further studies show that COUP-TF II functions as a corepressor of AR. It represses AR transactivation on target promoters containing the androgen response element (ARE) in a dose-dependent manner. In addition, COUP-TF II interacts physically with AR in vitro and in vivo. It binds to both the DNA binding domain (DBD) and the ligand-binding domain (LBD) of AR and disrupts the N/C terminal interaction of AR. Furthermore, COUP-TF II competes with coactivators such as ARA70, SRC-1, and GRIP1 to modulate AR transactivation as well as inhibiting the recruitment of AR to its ARE-containing target promoter. Taken together, our findings suggest that COUP-TF II is a novel corepressor of AR, and provide an insight into the role of COUP-TF II in prostate cancers.</description><subject>Albumin</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Animals</subject><subject>Binding</subject><subject>Binding sites</subject><subject>Biology</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cercopithecus aethiops</subject><subject>COS Cells</subject><subject>COUP Transcription Factor II - genetics</subject><subject>COUP Transcription Factor II - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Gene expression</subject><subject>GRIP1 protein</subject><subject>Inhibition</subject><subject>Ligands</subject><subject>Male</subject><subject>Medicine</subject><subject>Mice</subject><subject>Ovalbumin</subject><subject>Plasmids</subject><subject>Promoter Regions, Genetic</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>Recruitment</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Steroid receptor coactivator 1</subject><subject>Thyroid gland</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><subject>Transcriptional Activation</subject><subject>Tumors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkJw0eJvNzdI08RHpUmTYHBruc5J6pLYme1U7I_we3G2bmrRLlAuHNvP-x77-JyieInRHFOJP2z8GJzu5oN3MEeIVYiIR8UxriiZCYLo473_o-JZjBuEOF0I8bQ4IhQznmfHxZ_LNZRmbc0vcKXf6m419taV4xBTAN2XQ_C9TxBmKWgXTbBDst6VjTbJh3K5LB20OtktdNdlgHbsdIJYpmx6I8iY3eobiW9K7erg2xwogIFhMsihcoSYsqo02hkIpYGui8-LJ43uIrzYjSfFj8-fLs--zs4vvizPTs9nRlQkzZq6ppQgxiSgRgq-YJgCM6CJEBhh2fBa1qD1Si4QFhwDZ1I0mgI3Uq7Igp4Ur299h85HtUtpVJgSISkVBGdieUvUXm_UEGyvw7Xy2qqbBR9apUOypgNlcC00Z3UDEjHcIM04EL7SgtewqrjJXh930cZVD7UBl5PUHZge7ji7Vq3fKsoqghfTcd_tDIK_GiEm1ds4JUw78GM-N-a4yq_OSUbf_IM-fLsd1ep8Aesan-OayVSdMilRhYWsMjV_gMpfDb01uf4am9cPBO8PBJlJ8Du1eoxRLb9_-3_24uch-3aPXYPu0jr6bpwKLB6C7BY0ubpigOY-yRipqX3usqGm9lG79smyV_sPdC-66xf6F3dWGP4</recordid><startdate>20121107</startdate><enddate>20121107</enddate><creator>Song, Chin-Hee</creator><creator>Lee, Hyun Joo</creator><creator>Park, Eunsook</creator><creator>Lee, Keesook</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121107</creationdate><title>The chicken ovalbumin upstream promoter-transcription factor II negatively regulates the transactivation of androgen receptor in prostate cancer cells</title><author>Song, Chin-Hee ; Lee, Hyun Joo ; Park, Eunsook ; Lee, Keesook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-fdd3320447e0f7658413e4cea2661017f5d7deaab7801651e5476fa3e5c77b283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Albumin</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Animals</topic><topic>Binding</topic><topic>Binding sites</topic><topic>Biology</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cercopithecus aethiops</topic><topic>COS Cells</topic><topic>COUP Transcription Factor II - genetics</topic><topic>COUP Transcription Factor II - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>DNA</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Gene expression</topic><topic>GRIP1 protein</topic><topic>Inhibition</topic><topic>Ligands</topic><topic>Male</topic><topic>Medicine</topic><topic>Mice</topic><topic>Ovalbumin</topic><topic>Plasmids</topic><topic>Promoter Regions, Genetic</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Protein Transport</topic><topic>Proteins</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Androgen - metabolism</topic><topic>Recruitment</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Steroid receptor coactivator 1</topic><topic>Thyroid gland</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><topic>Transcriptional Activation</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Chin-Hee</creatorcontrib><creatorcontrib>Lee, Hyun Joo</creatorcontrib><creatorcontrib>Park, Eunsook</creatorcontrib><creatorcontrib>Lee, Keesook</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Chin-Hee</au><au>Lee, Hyun Joo</au><au>Park, Eunsook</au><au>Lee, Keesook</au><au>Roemer, Klaus</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The chicken ovalbumin upstream promoter-transcription factor II negatively regulates the transactivation of androgen receptor in prostate cancer cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-11-07</date><risdate>2012</risdate><volume>7</volume><issue>11</issue><spage>e49026</spage><epage>e49026</epage><pages>e49026-e49026</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Androgen receptor (AR) is involved in the development and progression of prostate cancers. However, the mechanisms by which this occurs remain incompletely understood. In previous reports, chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II) has been suggested to play a role in the development of cancers. In the present study, we explored a putative role of COUP-TF II in prostate cancers by investigating its effect on cell proliferation and a cross-talk between COUP-TF II and AR. Overexpression of COUP-TF II results in the inhibition of androgen-dependent proliferation of prostate cancer cells. Further studies show that COUP-TF II functions as a corepressor of AR. It represses AR transactivation on target promoters containing the androgen response element (ARE) in a dose-dependent manner. In addition, COUP-TF II interacts physically with AR in vitro and in vivo. It binds to both the DNA binding domain (DBD) and the ligand-binding domain (LBD) of AR and disrupts the N/C terminal interaction of AR. Furthermore, COUP-TF II competes with coactivators such as ARA70, SRC-1, and GRIP1 to modulate AR transactivation as well as inhibiting the recruitment of AR to its ARE-containing target promoter. Taken together, our findings suggest that COUP-TF II is a novel corepressor of AR, and provide an insight into the role of COUP-TF II in prostate cancers.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23145053</pmid><doi>10.1371/journal.pone.0049026</doi><tpages>e49026</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Albumin Androgen receptors Androgens Animals Binding Binding sites Biology Cancer Cancer cells Cell cycle Cell growth Cell Line, Tumor Cell Proliferation Cercopithecus aethiops COS Cells COUP Transcription Factor II - genetics COUP Transcription Factor II - metabolism Deoxyribonucleic acid Development and progression DNA DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Gene expression GRIP1 protein Inhibition Ligands Male Medicine Mice Ovalbumin Plasmids Promoter Regions, Genetic Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Protein Transport Proteins Receptors, Androgen - genetics Receptors, Androgen - metabolism Recruitment Rodents Signal transduction Steroid receptor coactivator 1 Thyroid gland Transcription factors Transcription, Genetic Transcriptional Activation Tumors |
| title | The chicken ovalbumin upstream promoter-transcription factor II negatively regulates the transactivation of androgen receptor in prostate cancer cells |
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