Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal
Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS). Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor ce...
Gespeichert in:
| Veröffentlicht in: | Journal of neuro-oncology 2008-02, Vol.86 (3), p.285-296 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 296 |
|---|---|
| container_issue | 3 |
| container_start_page | 285 |
| container_title | Journal of neuro-oncology |
| container_volume | 86 |
| creator | Selkirk, Stephen M. Morrow, Jay Barone, Tara A. Hoffer, Alan Lock, Jeffrey DeChant, Anne Mangla, Saisho Plunkett, Robert J. Miller, Robert H. |
| description | Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS). Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor cells. In this study OPN cDNA was cloned into a retroviral vector and used to infect F98 Fischer rat-derived glioma cells and U87 human-derived glioblastoma multiforme (GBM) cells in vitro. Cells expressing high levels of OPN migrated less distance than control cells in vitro. This effect was not RGD mediated, but was reversed in the presence of c-Jun N-terminal kinase (JNK) inhibitor suggesting that JNK1 is an essential component of a negative feedback loop affecting OPN activated signaling cascades. Implantation of tumor cells expressing high levels of OPN into adult Fischer rats and nude rats resulted in morphologically distinct tumors and prolonged host survival relative to controls. We propose that local produced, high level OPN expression limits the malignant character of glioma cells and that the downstream mechanisms involved represent pathways that may have therapeutic value in the treatment of human CNS malignancy. |
| doi_str_mv | 10.1007/s11060-007-9477-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2911624</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20895646</sourcerecordid><originalsourceid>FETCH-LOGICAL-c498t-28c9a111370dd5b3e2fcf651edbc4397c832adc98729c7e37845d547ccb98b983</originalsourceid><addsrcrecordid>eNp1UU2LFDEQDaK44-oP8CLBg7fWVNLd6VwEWdYPWPCi4C2kk-qZLN1Jm3QP7NVfbpoZXRWEkHpUvXqVyiPkObDXwJh8kwFYy6oCK1VLWcEDsoNGikoKKR6SHYNWVo2qv12QJznfMsZqKeAxuQCpeKeadkd-XI94NIuPgcaBxrxgnGNYfKAlj2OmBfXJlHtZp5ioxbEkE7rVYqb9mhwGaoKjc4pTXEour-noj2akyyHFdX8oEYvKwff-15hNhDqfZ0zZjE_Jo8GMGZ-d4yX5-v76y9XH6ubzh09X724qW6tuqXhnlQEAIZlzTS-QD3ZoG0DX21ooaTvBjbOqk1xZiUJ2deOaWlrbq64ccUnennTntZ_QWQxLMqOek59MutPReP13JfiD3sej5gqg5XUReHUWSPH7innRk8_bLiZgXLPmbPvTui3El_8Qb-OaQllOc1BN07WCFRKcSDbFnBMOv18CTG_26pO9eoObvRpKz4s_V7jvOPtZCPxEyKUU9pjuJ_9f9SfZ27RX</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>219558630</pqid></control><display><type>article</type><title>Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Selkirk, Stephen M. ; Morrow, Jay ; Barone, Tara A. ; Hoffer, Alan ; Lock, Jeffrey ; DeChant, Anne ; Mangla, Saisho ; Plunkett, Robert J. ; Miller, Robert H.</creator><creatorcontrib>Selkirk, Stephen M. ; Morrow, Jay ; Barone, Tara A. ; Hoffer, Alan ; Lock, Jeffrey ; DeChant, Anne ; Mangla, Saisho ; Plunkett, Robert J. ; Miller, Robert H.</creatorcontrib><description>Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS). Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor cells. In this study OPN cDNA was cloned into a retroviral vector and used to infect F98 Fischer rat-derived glioma cells and U87 human-derived glioblastoma multiforme (GBM) cells in vitro. Cells expressing high levels of OPN migrated less distance than control cells in vitro. This effect was not RGD mediated, but was reversed in the presence of c-Jun N-terminal kinase (JNK) inhibitor suggesting that JNK1 is an essential component of a negative feedback loop affecting OPN activated signaling cascades. Implantation of tumor cells expressing high levels of OPN into adult Fischer rats and nude rats resulted in morphologically distinct tumors and prolonged host survival relative to controls. We propose that local produced, high level OPN expression limits the malignant character of glioma cells and that the downstream mechanisms involved represent pathways that may have therapeutic value in the treatment of human CNS malignancy.</description><identifier>ISSN: 0167-594X</identifier><identifier>EISSN: 1573-7373</identifier><identifier>DOI: 10.1007/s11060-007-9477-1</identifier><identifier>PMID: 17928956</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Apoptosis - physiology ; Brain Neoplasms - metabolism ; Brain Neoplasms - mortality ; Brain Neoplasms - physiopathology ; Bromodeoxyuridine - metabolism ; Cell Line, Tumor ; Cell Movement - physiology ; Cell Proliferation ; Gene Expression Regulation, Neoplastic - genetics ; Gene Expression Regulation, Neoplastic - physiology ; Glioblastoma - metabolism ; Glioblastoma - mortality ; Glioblastoma - physiopathology ; Glioma - metabolism ; Glioma - mortality ; Glioma - physiopathology ; Green Fluorescent Proteins - metabolism ; Humans ; In Situ Nick-End Labeling ; Lab. Investigation - Human/Animal Tissue ; Medicine ; Medicine & Public Health ; Neurology ; Oncology ; Osteopontin - genetics ; Osteopontin - metabolism ; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism ; Rats ; Survival Analysis ; Time Factors ; Transfection ; Transplants</subject><ispartof>Journal of neuro-oncology, 2008-02, Vol.86 (3), p.285-296</ispartof><rights>Springer Science+Business Media, LLC. 2007</rights><rights>Springer Science+Business Media, LLC. 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-28c9a111370dd5b3e2fcf651edbc4397c832adc98729c7e37845d547ccb98b983</citedby><cites>FETCH-LOGICAL-c498t-28c9a111370dd5b3e2fcf651edbc4397c832adc98729c7e37845d547ccb98b983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11060-007-9477-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11060-007-9477-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17928956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Selkirk, Stephen M.</creatorcontrib><creatorcontrib>Morrow, Jay</creatorcontrib><creatorcontrib>Barone, Tara A.</creatorcontrib><creatorcontrib>Hoffer, Alan</creatorcontrib><creatorcontrib>Lock, Jeffrey</creatorcontrib><creatorcontrib>DeChant, Anne</creatorcontrib><creatorcontrib>Mangla, Saisho</creatorcontrib><creatorcontrib>Plunkett, Robert J.</creatorcontrib><creatorcontrib>Miller, Robert H.</creatorcontrib><title>Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal</title><title>Journal of neuro-oncology</title><addtitle>J Neurooncol</addtitle><addtitle>J Neurooncol</addtitle><description>Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS). Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor cells. In this study OPN cDNA was cloned into a retroviral vector and used to infect F98 Fischer rat-derived glioma cells and U87 human-derived glioblastoma multiforme (GBM) cells in vitro. Cells expressing high levels of OPN migrated less distance than control cells in vitro. This effect was not RGD mediated, but was reversed in the presence of c-Jun N-terminal kinase (JNK) inhibitor suggesting that JNK1 is an essential component of a negative feedback loop affecting OPN activated signaling cascades. Implantation of tumor cells expressing high levels of OPN into adult Fischer rats and nude rats resulted in morphologically distinct tumors and prolonged host survival relative to controls. We propose that local produced, high level OPN expression limits the malignant character of glioma cells and that the downstream mechanisms involved represent pathways that may have therapeutic value in the treatment of human CNS malignancy.</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - mortality</subject><subject>Brain Neoplasms - physiopathology</subject><subject>Bromodeoxyuridine - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - physiology</subject><subject>Cell Proliferation</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Glioblastoma - metabolism</subject><subject>Glioblastoma - mortality</subject><subject>Glioblastoma - physiopathology</subject><subject>Glioma - metabolism</subject><subject>Glioma - mortality</subject><subject>Glioma - physiopathology</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Humans</subject><subject>In Situ Nick-End Labeling</subject><subject>Lab. Investigation - Human/Animal Tissue</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Osteopontin - genetics</subject><subject>Osteopontin - metabolism</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</subject><subject>Rats</subject><subject>Survival Analysis</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Transplants</subject><issn>0167-594X</issn><issn>1573-7373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1UU2LFDEQDaK44-oP8CLBg7fWVNLd6VwEWdYPWPCi4C2kk-qZLN1Jm3QP7NVfbpoZXRWEkHpUvXqVyiPkObDXwJh8kwFYy6oCK1VLWcEDsoNGikoKKR6SHYNWVo2qv12QJznfMsZqKeAxuQCpeKeadkd-XI94NIuPgcaBxrxgnGNYfKAlj2OmBfXJlHtZp5ioxbEkE7rVYqb9mhwGaoKjc4pTXEour-noj2akyyHFdX8oEYvKwff-15hNhDqfZ0zZjE_Jo8GMGZ-d4yX5-v76y9XH6ubzh09X724qW6tuqXhnlQEAIZlzTS-QD3ZoG0DX21ooaTvBjbOqk1xZiUJ2deOaWlrbq64ccUnennTntZ_QWQxLMqOek59MutPReP13JfiD3sej5gqg5XUReHUWSPH7innRk8_bLiZgXLPmbPvTui3El_8Qb-OaQllOc1BN07WCFRKcSDbFnBMOv18CTG_26pO9eoObvRpKz4s_V7jvOPtZCPxEyKUU9pjuJ_9f9SfZ27RX</recordid><startdate>20080201</startdate><enddate>20080201</enddate><creator>Selkirk, Stephen M.</creator><creator>Morrow, Jay</creator><creator>Barone, Tara A.</creator><creator>Hoffer, Alan</creator><creator>Lock, Jeffrey</creator><creator>DeChant, Anne</creator><creator>Mangla, Saisho</creator><creator>Plunkett, Robert J.</creator><creator>Miller, Robert H.</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7U9</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20080201</creationdate><title>Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal</title><author>Selkirk, Stephen M. ; Morrow, Jay ; Barone, Tara A. ; Hoffer, Alan ; Lock, Jeffrey ; DeChant, Anne ; Mangla, Saisho ; Plunkett, Robert J. ; Miller, Robert H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-28c9a111370dd5b3e2fcf651edbc4397c832adc98729c7e37845d547ccb98b983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain Neoplasms - mortality</topic><topic>Brain Neoplasms - physiopathology</topic><topic>Bromodeoxyuridine - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - physiology</topic><topic>Cell Proliferation</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Glioblastoma - metabolism</topic><topic>Glioblastoma - mortality</topic><topic>Glioblastoma - physiopathology</topic><topic>Glioma - metabolism</topic><topic>Glioma - mortality</topic><topic>Glioma - physiopathology</topic><topic>Green Fluorescent Proteins - metabolism</topic><topic>Humans</topic><topic>In Situ Nick-End Labeling</topic><topic>Lab. Investigation - Human/Animal Tissue</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Osteopontin - genetics</topic><topic>Osteopontin - metabolism</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</topic><topic>Rats</topic><topic>Survival Analysis</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Transplants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Selkirk, Stephen M.</creatorcontrib><creatorcontrib>Morrow, Jay</creatorcontrib><creatorcontrib>Barone, Tara A.</creatorcontrib><creatorcontrib>Hoffer, Alan</creatorcontrib><creatorcontrib>Lock, Jeffrey</creatorcontrib><creatorcontrib>DeChant, Anne</creatorcontrib><creatorcontrib>Mangla, Saisho</creatorcontrib><creatorcontrib>Plunkett, Robert J.</creatorcontrib><creatorcontrib>Miller, Robert H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health and Medical</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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuro-oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Selkirk, Stephen M.</au><au>Morrow, Jay</au><au>Barone, Tara A.</au><au>Hoffer, Alan</au><au>Lock, Jeffrey</au><au>DeChant, Anne</au><au>Mangla, Saisho</au><au>Plunkett, Robert J.</au><au>Miller, Robert H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal</atitle><jtitle>Journal of neuro-oncology</jtitle><stitle>J Neurooncol</stitle><addtitle>J Neurooncol</addtitle><date>2008-02-01</date><risdate>2008</risdate><volume>86</volume><issue>3</issue><spage>285</spage><epage>296</epage><pages>285-296</pages><issn>0167-594X</issn><eissn>1573-7373</eissn><abstract>Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS). Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor cells. In this study OPN cDNA was cloned into a retroviral vector and used to infect F98 Fischer rat-derived glioma cells and U87 human-derived glioblastoma multiforme (GBM) cells in vitro. Cells expressing high levels of OPN migrated less distance than control cells in vitro. This effect was not RGD mediated, but was reversed in the presence of c-Jun N-terminal kinase (JNK) inhibitor suggesting that JNK1 is an essential component of a negative feedback loop affecting OPN activated signaling cascades. Implantation of tumor cells expressing high levels of OPN into adult Fischer rats and nude rats resulted in morphologically distinct tumors and prolonged host survival relative to controls. We propose that local produced, high level OPN expression limits the malignant character of glioma cells and that the downstream mechanisms involved represent pathways that may have therapeutic value in the treatment of human CNS malignancy.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>17928956</pmid><doi>10.1007/s11060-007-9477-1</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0167-594X |
| ispartof | Journal of neuro-oncology, 2008-02, Vol.86 (3), p.285-296 |
| issn | 0167-594X 1573-7373 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2911624 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Animals Apoptosis - physiology Brain Neoplasms - metabolism Brain Neoplasms - mortality Brain Neoplasms - physiopathology Bromodeoxyuridine - metabolism Cell Line, Tumor Cell Movement - physiology Cell Proliferation Gene Expression Regulation, Neoplastic - genetics Gene Expression Regulation, Neoplastic - physiology Glioblastoma - metabolism Glioblastoma - mortality Glioblastoma - physiopathology Glioma - metabolism Glioma - mortality Glioma - physiopathology Green Fluorescent Proteins - metabolism Humans In Situ Nick-End Labeling Lab. Investigation - Human/Animal Tissue Medicine Medicine & Public Health Neurology Oncology Osteopontin - genetics Osteopontin - metabolism Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Rats Survival Analysis Time Factors Transfection Transplants |
| title | Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T11%3A50%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Elevation%20of%20osteopontin%20levels%20in%20brain%20tumor%20cells%20reduces%20burden%20and%20promotes%20survival%20through%20the%20inhibition%20of%20cell%20dispersal&rft.jtitle=Journal%20of%20neuro-oncology&rft.au=Selkirk,%20Stephen%20M.&rft.date=2008-02-01&rft.volume=86&rft.issue=3&rft.spage=285&rft.epage=296&rft.pages=285-296&rft.issn=0167-594X&rft.eissn=1573-7373&rft_id=info:doi/10.1007/s11060-007-9477-1&rft_dat=%3Cproquest_pubme%3E20895646%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=219558630&rft_id=info:pmid/17928956&rfr_iscdi=true |