Inhibition of cell motility after nm23 transfection of human and murine tumor cells
Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not y...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1993-05, Vol.53 (9), p.1971-1973 |
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| container_end_page | 1973 |
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| container_issue | 9 |
| container_start_page | 1971 |
| container_title | Cancer research (Chicago, Ill.) |
| container_volume | 53 |
| creator | KANTOR, J. D MCCORMICK, B STEEG, P. S ZETTER, B. R |
| description | Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not yet known. Because cell motility plays an essential role in metastatic dissemination, we have studied whether tumor cells transfected with nm23 complementary DNA have any alterations in their ability to migrate. Our results demonstrate that nm23 transfection inhibits the ability of murine melanoma and human breast carcinoma cells to migrate in response to serum or to defined factors such as platelet derived growth factor or insulin-like growth factor 1. Random, unstimulated cell motility was not depressed in the nm23 transfectants. The results suggest that the nm23 gene product may interact with intracellular molecules that are essential for stimulated cell motility in two different tumor cell systems. |
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D ; MCCORMICK, B ; STEEG, P. S ; ZETTER, B. R</creator><creatorcontrib>KANTOR, J. D ; MCCORMICK, B ; STEEG, P. S ; ZETTER, B. R</creatorcontrib><description>Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not yet known. Because cell motility plays an essential role in metastatic dissemination, we have studied whether tumor cells transfected with nm23 complementary DNA have any alterations in their ability to migrate. Our results demonstrate that nm23 transfection inhibits the ability of murine melanoma and human breast carcinoma cells to migrate in response to serum or to defined factors such as platelet derived growth factor or insulin-like growth factor 1. Random, unstimulated cell motility was not depressed in the nm23 transfectants. The results suggest that the nm23 gene product may interact with intracellular molecules that are essential for stimulated cell motility in two different tumor cell systems.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 8481897</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Biological and medical sciences ; Cell Movement ; Dissemination ; Humans ; Insulin-Like Growth Factor I - pharmacology ; Medical sciences ; Mice ; Monomeric GTP-Binding Proteins ; NM23 Nucleoside Diphosphate Kinases ; Nucleoside-Diphosphate Kinase ; Platelet-Derived Growth Factor - pharmacology ; Proteins - physiology ; Tetradecanoylphorbol Acetate - pharmacology ; Transcription Factors ; Transfection ; Tumor cell ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 1993-05, Vol.53 (9), p.1971-1973</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4709758$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8481897$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KANTOR, J. D</creatorcontrib><creatorcontrib>MCCORMICK, B</creatorcontrib><creatorcontrib>STEEG, P. S</creatorcontrib><creatorcontrib>ZETTER, B. R</creatorcontrib><title>Inhibition of cell motility after nm23 transfection of human and murine tumor cells</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not yet known. Because cell motility plays an essential role in metastatic dissemination, we have studied whether tumor cells transfected with nm23 complementary DNA have any alterations in their ability to migrate. Our results demonstrate that nm23 transfection inhibits the ability of murine melanoma and human breast carcinoma cells to migrate in response to serum or to defined factors such as platelet derived growth factor or insulin-like growth factor 1. Random, unstimulated cell motility was not depressed in the nm23 transfectants. The results suggest that the nm23 gene product may interact with intracellular molecules that are essential for stimulated cell motility in two different tumor cell systems.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Movement</subject><subject>Dissemination</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Monomeric GTP-Binding Proteins</subject><subject>NM23 Nucleoside Diphosphate Kinases</subject><subject>Nucleoside-Diphosphate Kinase</subject><subject>Platelet-Derived Growth Factor - pharmacology</subject><subject>Proteins - physiology</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Transcription Factors</subject><subject>Transfection</subject><subject>Tumor cell</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9j09rxCAUxKW0bNNtP0LBQ68BjbrqsSz9s7DQQ3fPyzNRYolmUXPYb9_Qpj09ht_MPOYKVVQwVUvOxTWqCCGqFlw2t-gu569ZCkrECq0UV1RpWaHPXey98cWPEY8Ot3YYcBiLH3y5YHDFJhxDw3BJELOz7Z-xnwJEDLHDYUo-WlymMKaffL5HNw6GbB-Wu0bH15fD9r3ef7ztts_7um82qtSOW0pbKqQzHQEpQDWONFwZSbTRzAjBZ66MpkTJjQXGwGlmJSGGaCo5W6PH397zZILtTufkA6TLaRk386eFQ25hcPOE1ud_G5__SKHYN2HuWFg</recordid><startdate>19930501</startdate><enddate>19930501</enddate><creator>KANTOR, J. D</creator><creator>MCCORMICK, B</creator><creator>STEEG, P. S</creator><creator>ZETTER, B. R</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></search><sort><creationdate>19930501</creationdate><title>Inhibition of cell motility after nm23 transfection of human and murine tumor cells</title><author>KANTOR, J. D ; MCCORMICK, B ; STEEG, P. S ; ZETTER, B. 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D</creatorcontrib><creatorcontrib>MCCORMICK, B</creatorcontrib><creatorcontrib>STEEG, P. S</creatorcontrib><creatorcontrib>ZETTER, B. R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KANTOR, J. D</au><au>MCCORMICK, B</au><au>STEEG, P. S</au><au>ZETTER, B. R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of cell motility after nm23 transfection of human and murine tumor cells</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1993-05-01</date><risdate>1993</risdate><volume>53</volume><issue>9</issue><spage>1971</spage><epage>1973</epage><pages>1971-1973</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not yet known. Because cell motility plays an essential role in metastatic dissemination, we have studied whether tumor cells transfected with nm23 complementary DNA have any alterations in their ability to migrate. Our results demonstrate that nm23 transfection inhibits the ability of murine melanoma and human breast carcinoma cells to migrate in response to serum or to defined factors such as platelet derived growth factor or insulin-like growth factor 1. Random, unstimulated cell motility was not depressed in the nm23 transfectants. The results suggest that the nm23 gene product may interact with intracellular molecules that are essential for stimulated cell motility in two different tumor cell systems.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>8481897</pmid><tpages>3</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 1993-05, Vol.53 (9), p.1971-1973 |
| issn | 0008-5472 1538-7445 |
| language | eng |
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| source | MEDLINE; American Association for Cancer Research Journals; EZB Electronic Journals Library |
| subjects | Animals Biological and medical sciences Cell Movement Dissemination Humans Insulin-Like Growth Factor I - pharmacology Medical sciences Mice Monomeric GTP-Binding Proteins NM23 Nucleoside Diphosphate Kinases Nucleoside-Diphosphate Kinase Platelet-Derived Growth Factor - pharmacology Proteins - physiology Tetradecanoylphorbol Acetate - pharmacology Transcription Factors Transfection Tumor cell Tumor Cells, Cultured Tumors |
| title | Inhibition of cell motility after nm23 transfection of human and murine tumor cells |
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