In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type
Altered expression of CCN3 has been observed in a variety of musculoskeletal tumours, including Ewing's sarcoma (ES). Despite its widespread distribution, very little is known about its biological functions and molecular mechanisms of action. We transfected CCN3 gene into a CCN3-negative ES cel...
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| Veröffentlicht in: | Oncogene 2005-06, Vol.24 (27), p.4349-4361 |
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| creator | Benini, Stefania Perbal, Bernard Zambelli, Diana Colombo, Mario Paolo Manara, Maria Cristina Serra, Massimo Parenza, Mariella Martinez, Vincent Picci, Piero Scotlandi, Katia |
| description | Altered expression of CCN3 has been observed in a variety of musculoskeletal tumours, including Ewing's sarcoma (ES). Despite its widespread distribution, very little is known about its biological functions and molecular mechanisms of action. We transfected
CCN3
gene into a CCN3-negative ES cell line and analysed the
in vitro
and
in vivo
behaviours of stably transfected clones. Forced expression of CCN3 significantly reduced cell proliferation
in vitro,
growth in anchorage-independent conditions and tumorigenicity in nude mice. Despite the antiproliferative effect, CCN3-transfected ES cells displayed increased migration and invasion of Matrigel. The decreased expression of α2β1 integrin receptor and the increased amount of cell surface-associated matrix metalloproteinase (MMP)-9 following the expression of CCN3 may be the basis for the increased migratory abilities of transfected cells. Cells lacking α
2
β
1
are less facilitated to have stable anchorage since the predominant collagen extracted from ES tissue is indeed type I collagen and proMMP-9 was recently found to provide a cellular switch between stationary and migratory ES cell phase. Our findings are in line with those recently obtained in glioblastoma. However, the underlying molecular mechanisms appear to be different, further highlighting the importance of the cellular context in the regulation of function of CCN proteins. |
| doi_str_mv | 10.1038/sj.onc.1208620 |
| format | Article |
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CCN3
gene into a CCN3-negative ES cell line and analysed the
in vitro
and
in vivo
behaviours of stably transfected clones. Forced expression of CCN3 significantly reduced cell proliferation
in vitro,
growth in anchorage-independent conditions and tumorigenicity in nude mice. Despite the antiproliferative effect, CCN3-transfected ES cells displayed increased migration and invasion of Matrigel. The decreased expression of α2β1 integrin receptor and the increased amount of cell surface-associated matrix metalloproteinase (MMP)-9 following the expression of CCN3 may be the basis for the increased migratory abilities of transfected cells. Cells lacking α
2
β
1
are less facilitated to have stable anchorage since the predominant collagen extracted from ES tissue is indeed type I collagen and proMMP-9 was recently found to provide a cellular switch between stationary and migratory ES cell phase. Our findings are in line with those recently obtained in glioblastoma. However, the underlying molecular mechanisms appear to be different, further highlighting the importance of the cellular context in the regulation of function of CCN proteins.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1208620</identifier><identifier>PMID: 15824736</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; Bone cancer ; Cell Adhesion ; Cell Biology ; Cell Line ; Cell migration ; Cell Movement ; Cell physiology ; Cell Proliferation ; Cell surface ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Clone Cells - metabolism ; Clone Cells - pathology ; Collagen (type I) ; Connective Tissue Growth Factor ; Diseases of the osteoarticular system ; Ewing's sarcoma ; Ewings sarcoma ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation, Neoplastic ; Genes ; Glioblastoma ; Growth factors ; Human Genetics ; Immediate-Early Proteins - genetics ; Immediate-Early Proteins - metabolism ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Internal Medicine ; Matrix metalloproteinase ; Matrix Metalloproteinases - metabolism ; Medical sciences ; Medicine ; Medicine & Public Health ; Metalloproteinase ; Mice ; Mice, Nude ; Molecular and cellular biology ; Molecular modelling ; Neoplasm Invasiveness ; Nephroblastoma Overexpressed Protein ; Oncology ; original-paper ; Proteins ; Receptor, IGF Type 1 - metabolism ; Receptor, Platelet-Derived Growth Factor alpha - metabolism ; Receptor, Platelet-Derived Growth Factor beta - metabolism ; Sarcoma, Ewing - genetics ; Sarcoma, Ewing - metabolism ; Sarcoma, Ewing - pathology ; Transfection ; Tumorigenicity ; Tumors ; Tumors of striated muscle and skeleton</subject><ispartof>Oncogene, 2005-06, Vol.24 (27), p.4349-4361</ispartof><rights>Springer Nature Limited 2005</rights><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 23, 2005</rights><rights>Nature Publishing Group 2005.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c582t-2d7afc96666e497f4c73580fecdfae908ad6e1857906b9820de0b3a4ea6489533</citedby><cites>FETCH-LOGICAL-c582t-2d7afc96666e497f4c73580fecdfae908ad6e1857906b9820de0b3a4ea6489533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1208620$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1208620$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16907963$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15824736$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Benini, Stefania</creatorcontrib><creatorcontrib>Perbal, Bernard</creatorcontrib><creatorcontrib>Zambelli, Diana</creatorcontrib><creatorcontrib>Colombo, Mario Paolo</creatorcontrib><creatorcontrib>Manara, Maria Cristina</creatorcontrib><creatorcontrib>Serra, Massimo</creatorcontrib><creatorcontrib>Parenza, Mariella</creatorcontrib><creatorcontrib>Martinez, Vincent</creatorcontrib><creatorcontrib>Picci, Piero</creatorcontrib><creatorcontrib>Scotlandi, Katia</creatorcontrib><title>In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Altered expression of CCN3 has been observed in a variety of musculoskeletal tumours, including Ewing's sarcoma (ES). Despite its widespread distribution, very little is known about its biological functions and molecular mechanisms of action. We transfected
CCN3
gene into a CCN3-negative ES cell line and analysed the
in vitro
and
in vivo
behaviours of stably transfected clones. Forced expression of CCN3 significantly reduced cell proliferation
in vitro,
growth in anchorage-independent conditions and tumorigenicity in nude mice. Despite the antiproliferative effect, CCN3-transfected ES cells displayed increased migration and invasion of Matrigel. The decreased expression of α2β1 integrin receptor and the increased amount of cell surface-associated matrix metalloproteinase (MMP)-9 following the expression of CCN3 may be the basis for the increased migratory abilities of transfected cells. Cells lacking α
2
β
1
are less facilitated to have stable anchorage since the predominant collagen extracted from ES tissue is indeed type I collagen and proMMP-9 was recently found to provide a cellular switch between stationary and migratory ES cell phase. Our findings are in line with those recently obtained in glioblastoma. However, the underlying molecular mechanisms appear to be different, further highlighting the importance of the cellular context in the regulation of function of CCN proteins.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Bone cancer</subject><subject>Cell Adhesion</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell physiology</subject><subject>Cell Proliferation</subject><subject>Cell surface</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Clone Cells - metabolism</subject><subject>Clone Cells - pathology</subject><subject>Collagen (type I)</subject><subject>Connective Tissue Growth Factor</subject><subject>Diseases of the osteoarticular system</subject><subject>Ewing's sarcoma</subject><subject>Ewings sarcoma</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Glioblastoma</subject><subject>Growth factors</subject><subject>Human Genetics</subject><subject>Immediate-Early Proteins - genetics</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Internal Medicine</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Molecular and cellular biology</subject><subject>Molecular modelling</subject><subject>Neoplasm Invasiveness</subject><subject>Nephroblastoma Overexpressed Protein</subject><subject>Oncology</subject><subject>original-paper</subject><subject>Proteins</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Receptor, Platelet-Derived Growth Factor alpha - metabolism</subject><subject>Receptor, Platelet-Derived Growth Factor beta - metabolism</subject><subject>Sarcoma, Ewing - genetics</subject><subject>Sarcoma, Ewing - metabolism</subject><subject>Sarcoma, Ewing - pathology</subject><subject>Transfection</subject><subject>Tumorigenicity</subject><subject>Tumors</subject><subject>Tumors of striated muscle and skeleton</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks1rFDEYxgdR7Fq9epRB8esw22TyfSxL1UJpL-o1ZDNvdrPMJNtk1tL_3gwdWJAWk0NI8ns_nuSpqrcYLTEi8izvljHYJW6R5C16Vi0wFbxhTNHn1QIphhrVkvakepXzDiEkFGpfVieYyZYKwhfV_jLUF3c-bD7nOptk42Dq1eqafLm--f219mHr137M9T7F3jtIZvQx1Hdb38N0NsSxhNaD38w3JnQl6I_J0ya6etxCSTtAbaHv6_F-D6-rF870Gd7M62n169vFz9WP5urm--Xq_KqxpbexaTthnFW8DKBKOGoFYRI5sJ0zoJA0HQcsWRHE10q2qAO0JoaC4VQqRshp9ekhb2nz9gB51IPPUxcmQDxkzYXilKD_g1gwohSjBfzwD7iLhxSKCN1yigljVEzU-yeptmgQmOBjqo3pQfvg4piMnerqcyyLJEk5K9TyEarMDgZvYwBXvuHRAJtizgmc3ic_mHSvMdKTXXTe6WIXPdulBLybmz2sB-iO-OyPAnycAZOt6V0ywfp85LgqluLTI549cLlchQ2ko-onSv8Fe9jVeA</recordid><startdate>20050623</startdate><enddate>20050623</enddate><creator>Benini, Stefania</creator><creator>Perbal, Bernard</creator><creator>Zambelli, Diana</creator><creator>Colombo, Mario Paolo</creator><creator>Manara, Maria Cristina</creator><creator>Serra, Massimo</creator><creator>Parenza, Mariella</creator><creator>Martinez, Vincent</creator><creator>Picci, Piero</creator><creator>Scotlandi, Katia</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050623</creationdate><title>In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type</title><author>Benini, Stefania ; Perbal, Bernard ; Zambelli, Diana ; Colombo, Mario Paolo ; Manara, Maria Cristina ; Serra, Massimo ; Parenza, Mariella ; Martinez, Vincent ; Picci, Piero ; Scotlandi, Katia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c582t-2d7afc96666e497f4c73580fecdfae908ad6e1857906b9820de0b3a4ea6489533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Bone cancer</topic><topic>Cell Adhesion</topic><topic>Cell Biology</topic><topic>Cell Line</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell physiology</topic><topic>Cell Proliferation</topic><topic>Cell surface</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Clone Cells - metabolism</topic><topic>Clone Cells - pathology</topic><topic>Collagen (type I)</topic><topic>Connective Tissue Growth Factor</topic><topic>Diseases of the osteoarticular system</topic><topic>Ewing's sarcoma</topic><topic>Ewings sarcoma</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Glioblastoma</topic><topic>Growth factors</topic><topic>Human Genetics</topic><topic>Immediate-Early Proteins - genetics</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Internal Medicine</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Molecular and cellular biology</topic><topic>Molecular modelling</topic><topic>Neoplasm Invasiveness</topic><topic>Nephroblastoma Overexpressed Protein</topic><topic>Oncology</topic><topic>original-paper</topic><topic>Proteins</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Receptor, Platelet-Derived Growth Factor alpha - metabolism</topic><topic>Receptor, Platelet-Derived Growth Factor beta - metabolism</topic><topic>Sarcoma, Ewing - genetics</topic><topic>Sarcoma, Ewing - metabolism</topic><topic>Sarcoma, Ewing - pathology</topic><topic>Transfection</topic><topic>Tumorigenicity</topic><topic>Tumors</topic><topic>Tumors of striated muscle and skeleton</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Benini, Stefania</creatorcontrib><creatorcontrib>Perbal, Bernard</creatorcontrib><creatorcontrib>Zambelli, Diana</creatorcontrib><creatorcontrib>Colombo, Mario Paolo</creatorcontrib><creatorcontrib>Manara, Maria Cristina</creatorcontrib><creatorcontrib>Serra, Massimo</creatorcontrib><creatorcontrib>Parenza, Mariella</creatorcontrib><creatorcontrib>Martinez, Vincent</creatorcontrib><creatorcontrib>Picci, Piero</creatorcontrib><creatorcontrib>Scotlandi, Katia</creatorcontrib><collection>Pascal-Francis</collection><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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</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 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Benini, Stefania</au><au>Perbal, Bernard</au><au>Zambelli, Diana</au><au>Colombo, Mario Paolo</au><au>Manara, Maria Cristina</au><au>Serra, Massimo</au><au>Parenza, Mariella</au><au>Martinez, Vincent</au><au>Picci, Piero</au><au>Scotlandi, Katia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2005-06-23</date><risdate>2005</risdate><volume>24</volume><issue>27</issue><spage>4349</spage><epage>4361</epage><pages>4349-4361</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Altered expression of CCN3 has been observed in a variety of musculoskeletal tumours, including Ewing's sarcoma (ES). Despite its widespread distribution, very little is known about its biological functions and molecular mechanisms of action. We transfected
CCN3
gene into a CCN3-negative ES cell line and analysed the
in vitro
and
in vivo
behaviours of stably transfected clones. Forced expression of CCN3 significantly reduced cell proliferation
in vitro,
growth in anchorage-independent conditions and tumorigenicity in nude mice. Despite the antiproliferative effect, CCN3-transfected ES cells displayed increased migration and invasion of Matrigel. The decreased expression of α2β1 integrin receptor and the increased amount of cell surface-associated matrix metalloproteinase (MMP)-9 following the expression of CCN3 may be the basis for the increased migratory abilities of transfected cells. Cells lacking α
2
β
1
are less facilitated to have stable anchorage since the predominant collagen extracted from ES tissue is indeed type I collagen and proMMP-9 was recently found to provide a cellular switch between stationary and migratory ES cell phase. Our findings are in line with those recently obtained in glioblastoma. However, the underlying molecular mechanisms appear to be different, further highlighting the importance of the cellular context in the regulation of function of CCN proteins.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15824736</pmid><doi>10.1038/sj.onc.1208620</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2005-06, Vol.24 (27), p.4349-4361 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67964303 |
| source | MEDLINE; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | Animals Apoptosis Biological and medical sciences Bone cancer Cell Adhesion Cell Biology Cell Line Cell migration Cell Movement Cell physiology Cell Proliferation Cell surface Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Clone Cells - metabolism Clone Cells - pathology Collagen (type I) Connective Tissue Growth Factor Diseases of the osteoarticular system Ewing's sarcoma Ewings sarcoma Female Fundamental and applied biological sciences. Psychology Gene Expression Regulation, Neoplastic Genes Glioblastoma Growth factors Human Genetics Immediate-Early Proteins - genetics Immediate-Early Proteins - metabolism Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Internal Medicine Matrix metalloproteinase Matrix Metalloproteinases - metabolism Medical sciences Medicine Medicine & Public Health Metalloproteinase Mice Mice, Nude Molecular and cellular biology Molecular modelling Neoplasm Invasiveness Nephroblastoma Overexpressed Protein Oncology original-paper Proteins Receptor, IGF Type 1 - metabolism Receptor, Platelet-Derived Growth Factor alpha - metabolism Receptor, Platelet-Derived Growth Factor beta - metabolism Sarcoma, Ewing - genetics Sarcoma, Ewing - metabolism Sarcoma, Ewing - pathology Transfection Tumorigenicity Tumors Tumors of striated muscle and skeleton |
| title | In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type |
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