Expression of chicken ovalbumin upstream promoter-transcription factor II enhances invasiveness of human lung carcinoma cells
Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) plays an essential role in angiogenesis and development. It is differentially expressed in tumor cell lines, but its role in carcinogenesis is largely unknown. We demonstrate here that noninvasive human lung cancer cells become...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2004-08, Vol.64 (15), p.5097-5105 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | NAVAB, Roya GONZALEZ-SANTOS, Juana Maria JOHNSTON, Michael R JIANG LIU BRODT, Pnina TSAO, Ming-Sound HU, Jim |
| description | Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) plays an essential role in angiogenesis and development. It is differentially expressed in tumor cell lines, but its role in carcinogenesis is largely unknown. We demonstrate here that noninvasive human lung cancer cells become invasive when COUP-TFII was expressed. The expression of extracellular matrix degrading proteinases, such as matrix metalloproteinase 2 and urokinase-type plasminogen activator, was up-regulated in these cells. This finding was confirmed by transduction of different human lung cancer cell lines with COUP-TFII protein and also by using antisense expression. We observed disorganization of actin filaments and focal adhesion kinase phosphorylation in COUP-TFII-transfected human lung cancer cells in addition to the increase in extracellular metalloproteinase activity. These results suggest that COUP-TFII may be considered as a new target for anticancer therapies. |
| doi_str_mv | 10.1158/0008-5472.CAN-03-1185 |
| format | Article |
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It is differentially expressed in tumor cell lines, but its role in carcinogenesis is largely unknown. We demonstrate here that noninvasive human lung cancer cells become invasive when COUP-TFII was expressed. The expression of extracellular matrix degrading proteinases, such as matrix metalloproteinase 2 and urokinase-type plasminogen activator, was up-regulated in these cells. This finding was confirmed by transduction of different human lung cancer cell lines with COUP-TFII protein and also by using antisense expression. We observed disorganization of actin filaments and focal adhesion kinase phosphorylation in COUP-TFII-transfected human lung cancer cells in addition to the increase in extracellular metalloproteinase activity. These results suggest that COUP-TFII may be considered as a new target for anticancer therapies.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-03-1185</identifier><identifier>PMID: 15289311</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Actins - metabolism ; Antineoplastic agents ; Biological and medical sciences ; Blotting, Western ; COUP Transcription Factor II ; COUP Transcription Factors ; DNA-Binding Proteins - genetics ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Gene Expression Regulation, Neoplastic - physiology ; Humans ; Immunoblotting ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Matrix Metalloproteinase 2 - metabolism ; Medical sciences ; Neoplasm Invasiveness ; Pharmacology. Drug treatments ; Phosphorylation ; Plasmids ; Protein-Tyrosine Kinases - metabolism ; Receptors, Steroid ; Transcription Factors - genetics ; Transfection ; Tumor Cells, Cultured ; Tumors ; Up-Regulation ; Urokinase-Type Plasminogen Activator - metabolism</subject><ispartof>Cancer research (Chicago, Ill.), 2004-08, Vol.64 (15), p.5097-5105</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-a340303a0ddd205fe305cd98bf84ccb6efe93aa48c27081e4939cd67c45b79703</citedby><cites>FETCH-LOGICAL-c447t-a340303a0ddd205fe305cd98bf84ccb6efe93aa48c27081e4939cd67c45b79703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15986088$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15289311$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NAVAB, Roya</creatorcontrib><creatorcontrib>GONZALEZ-SANTOS, Juana Maria</creatorcontrib><creatorcontrib>JOHNSTON, Michael R</creatorcontrib><creatorcontrib>JIANG LIU</creatorcontrib><creatorcontrib>BRODT, Pnina</creatorcontrib><creatorcontrib>TSAO, Ming-Sound</creatorcontrib><creatorcontrib>HU, Jim</creatorcontrib><title>Expression of chicken ovalbumin upstream promoter-transcription factor II enhances invasiveness of human lung carcinoma cells</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) plays an essential role in angiogenesis and development. It is differentially expressed in tumor cell lines, but its role in carcinogenesis is largely unknown. We demonstrate here that noninvasive human lung cancer cells become invasive when COUP-TFII was expressed. The expression of extracellular matrix degrading proteinases, such as matrix metalloproteinase 2 and urokinase-type plasminogen activator, was up-regulated in these cells. This finding was confirmed by transduction of different human lung cancer cell lines with COUP-TFII protein and also by using antisense expression. We observed disorganization of actin filaments and focal adhesion kinase phosphorylation in COUP-TFII-transfected human lung cancer cells in addition to the increase in extracellular metalloproteinase activity. These results suggest that COUP-TFII may be considered as a new target for anticancer therapies.</description><subject>Actins - metabolism</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>COUP Transcription Factor II</subject><subject>COUP Transcription Factors</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Focal Adhesion Kinase 1</subject><subject>Focal Adhesion Protein-Tyrosine Kinases</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Medical sciences</subject><subject>Neoplasm Invasiveness</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Plasmids</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Receptors, Steroid</subject><subject>Transcription Factors - genetics</subject><subject>Transfection</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Up-Regulation</subject><subject>Urokinase-Type Plasminogen Activator - metabolism</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMFu1DAQhi0EokvbR6DyBW4pdmxvnGO1amGlCi5wtiaTCWtInNROVuXAu-NoV8DJY-n7_7E_xt5KcSulsR-EELYwuipvd3efC6EKKa15wTbSKFtUWpuXbPOXuWBvUvqRr0YK85pdSFPaWkm5Yb_vn6dIKfkx8LHjePD4k_J4hL5ZBh_4MqU5Egx8iuMwzhSLOUJIGP00r6EOcB4j3-85hQMEpMR9OELyRwq5dy09LAME3i_hO0eI6MM4AEfq-3TFXnXQJ7o-n5fs28P9192n4vHLx_3u7rFArau5AKWFEgpE27alMB0pYbCtbdNZjdhsqaNaAWiLZSWsJF2rGttthdo0VV0Jdcnen3rzJ54WSrMbfFpfAIHGJTlpRamkrjJoTiDGMaVInZuiHyD-clK41btbnbrVqcvenVBu9Z5zN-cFSzNQ-y91Fp2Bd2cAEkLfZYfo039cbbfCWvUH9PWOfw</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>NAVAB, Roya</creator><creator>GONZALEZ-SANTOS, Juana Maria</creator><creator>JOHNSTON, Michael R</creator><creator>JIANG LIU</creator><creator>BRODT, Pnina</creator><creator>TSAO, Ming-Sound</creator><creator>HU, Jim</creator><general>American Association for Cancer Research</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>7TM</scope></search><sort><creationdate>20040801</creationdate><title>Expression of chicken ovalbumin upstream promoter-transcription factor II enhances invasiveness of human lung carcinoma cells</title><author>NAVAB, Roya ; GONZALEZ-SANTOS, Juana Maria ; JOHNSTON, Michael R ; JIANG LIU ; BRODT, Pnina ; TSAO, Ming-Sound ; HU, Jim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-a340303a0ddd205fe305cd98bf84ccb6efe93aa48c27081e4939cd67c45b79703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Actins - metabolism</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>COUP Transcription Factor II</topic><topic>COUP Transcription Factors</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Focal Adhesion Kinase 1</topic><topic>Focal Adhesion Protein-Tyrosine Kinases</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Medical sciences</topic><topic>Neoplasm Invasiveness</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation</topic><topic>Plasmids</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Receptors, Steroid</topic><topic>Transcription Factors - genetics</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Up-Regulation</topic><topic>Urokinase-Type Plasminogen Activator - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAVAB, Roya</creatorcontrib><creatorcontrib>GONZALEZ-SANTOS, Juana Maria</creatorcontrib><creatorcontrib>JOHNSTON, Michael R</creatorcontrib><creatorcontrib>JIANG LIU</creatorcontrib><creatorcontrib>BRODT, Pnina</creatorcontrib><creatorcontrib>TSAO, Ming-Sound</creatorcontrib><creatorcontrib>HU, Jim</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>Nucleic Acids Abstracts</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAVAB, Roya</au><au>GONZALEZ-SANTOS, Juana Maria</au><au>JOHNSTON, Michael R</au><au>JIANG LIU</au><au>BRODT, Pnina</au><au>TSAO, Ming-Sound</au><au>HU, Jim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of chicken ovalbumin upstream promoter-transcription factor II enhances invasiveness of human lung carcinoma cells</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>64</volume><issue>15</issue><spage>5097</spage><epage>5105</epage><pages>5097-5105</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) plays an essential role in angiogenesis and development. It is differentially expressed in tumor cell lines, but its role in carcinogenesis is largely unknown. We demonstrate here that noninvasive human lung cancer cells become invasive when COUP-TFII was expressed. The expression of extracellular matrix degrading proteinases, such as matrix metalloproteinase 2 and urokinase-type plasminogen activator, was up-regulated in these cells. This finding was confirmed by transduction of different human lung cancer cell lines with COUP-TFII protein and also by using antisense expression. We observed disorganization of actin filaments and focal adhesion kinase phosphorylation in COUP-TFII-transfected human lung cancer cells in addition to the increase in extracellular metalloproteinase activity. 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| subjects | Actins - metabolism Antineoplastic agents Biological and medical sciences Blotting, Western COUP Transcription Factor II COUP Transcription Factors DNA-Binding Proteins - genetics Focal Adhesion Kinase 1 Focal Adhesion Protein-Tyrosine Kinases Gene Expression Regulation, Neoplastic - physiology Humans Immunoblotting Lung Neoplasms - metabolism Lung Neoplasms - pathology Matrix Metalloproteinase 2 - metabolism Medical sciences Neoplasm Invasiveness Pharmacology. Drug treatments Phosphorylation Plasmids Protein-Tyrosine Kinases - metabolism Receptors, Steroid Transcription Factors - genetics Transfection Tumor Cells, Cultured Tumors Up-Regulation Urokinase-Type Plasminogen Activator - metabolism |
| title | Expression of chicken ovalbumin upstream promoter-transcription factor II enhances invasiveness of human lung carcinoma cells |
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