EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity
The Wilms' tumor 1 gene (WT1) encodes a transcription factor of the zinc-finger family and is homozygously mutated or deleted in a subset of Wilms' tumors. Through alternative mRNA splicing, the gene is expressed as four main polypeptides that differ by a stretch of 17 amino acids just N-t...
Gespeichert in:
| Veröffentlicht in: | Oncogene 2000-02, Vol.19 (6), p.791-800 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 800 |
|---|---|
| container_issue | 6 |
| container_start_page | 791 |
| container_title | Oncogene |
| container_volume | 19 |
| creator | SCHARNHORST, V MENKE, A. L ATTEMA, J HANEVELD, J. K RITECO, N VAN STEENBRUGGE, G. J VAN DER EB, A. J JOCHEMSEN, A. G |
| description | The Wilms' tumor 1 gene (WT1) encodes a transcription factor of the zinc-finger family and is homozygously mutated or deleted in a subset of Wilms' tumors. Through alternative mRNA splicing, the gene is expressed as four main polypeptides that differ by a stretch of 17 amino acids just N-terminal of the four zinc-fingers and three amino acids between zinc fingers 3 and 4. We have previously shown that expression of the WT1(-/-) isoform, lacking both inserts, increases the tumor growth rate of the adenovirus-transformed baby rat kidney (AdBRK) cell line 7C3H2, whereas expression of the WT1(-/+) isoform, lacking the 17aa insert, strongly suppresses the tumorigenic phenotype. In the present study we show that expression of these splice variants does not affect the tumorigenic potential of the similar AdBRK cell line, 7C1T1. In contrast to the 7C3H2 cell line, this AdBRK cell line expresses high endogenous levels of EGR-1 (early growth response-1) protein, a transcription factor structurally related to WT1. Ectopic expression of EGR-1 in the 7C3H2 AdBRK cells significantly increases their in vivo growth rate and nullifies the tumor suppressor activity of the WT1(-/+) protein. Furthermore, we find that EGR-1 levels are elevated in some Wilms' tumors. These data are the first to show that EGR-1 overexpression causes enhanced tumor growth and that WT1 and EGR-1 exert antagonizing effects on growth regulation in baby rat kidney cells, which might reflect the situation in some Wilms' tumors. |
| doi_str_mv | 10.1038/sj.onc.1203390 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70947371</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17480209</sourcerecordid><originalsourceid>FETCH-LOGICAL-c512t-28e26c3b6f0153e6bdc9424a056b8348dffc045f4fd8c817e99c5c253c169d083</originalsourceid><addsrcrecordid>eNqF0c9rFTEQB_AgFvusXj1KUNHTPie_k2MpbRUKhVLxGPKySd8uu5ua7CL97019CxVBPIVkPjNM-CL0hsCWANOfS79Nk98SCowZeIY2hCvZCGH4c7QBI6AxlNFj9LKUHgCUAfoCHROQRnOjNqg_v7xpCA7T3k0-FDwvY8r4Lqef8x67qcVjapfBzY-lfcAhxuBnnOLv2_duGMuntYfguzAFfJ9rg58LTtOh0NXnznfzwyt0FN1Qwuv1PEHfLs5vz740V9eXX89OrxovCJ0bqgOVnu1kBCJYkLvWG065AyF3mnHdxuiBi8hjq70mKhjjhaeCeSJNC5qdoI-HuXWVH0sosx274sMwuCmkpVgFhiumyH8hUVwDBVPh-79gn5Y81U9YKjlhhEgpq3r3T0UVY0CZqGh7QD6nUnKI9j53o8sPloB9TNSW3tZE7ZpobXi7Tl12Y2j_4IcIK_iwAle8G2KuQXblyVFNNdHsFy4Ip8k</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>227330235</pqid></control><display><type>article</type><title>EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>Nature</source><source>EZB Electronic Journals Library</source><creator>SCHARNHORST, V ; MENKE, A. L ; ATTEMA, J ; HANEVELD, J. K ; RITECO, N ; VAN STEENBRUGGE, G. J ; VAN DER EB, A. J ; JOCHEMSEN, A. G</creator><creatorcontrib>SCHARNHORST, V ; MENKE, A. L ; ATTEMA, J ; HANEVELD, J. K ; RITECO, N ; VAN STEENBRUGGE, G. J ; VAN DER EB, A. J ; JOCHEMSEN, A. G</creatorcontrib><description>The Wilms' tumor 1 gene (WT1) encodes a transcription factor of the zinc-finger family and is homozygously mutated or deleted in a subset of Wilms' tumors. Through alternative mRNA splicing, the gene is expressed as four main polypeptides that differ by a stretch of 17 amino acids just N-terminal of the four zinc-fingers and three amino acids between zinc fingers 3 and 4. We have previously shown that expression of the WT1(-/-) isoform, lacking both inserts, increases the tumor growth rate of the adenovirus-transformed baby rat kidney (AdBRK) cell line 7C3H2, whereas expression of the WT1(-/+) isoform, lacking the 17aa insert, strongly suppresses the tumorigenic phenotype. In the present study we show that expression of these splice variants does not affect the tumorigenic potential of the similar AdBRK cell line, 7C1T1. In contrast to the 7C3H2 cell line, this AdBRK cell line expresses high endogenous levels of EGR-1 (early growth response-1) protein, a transcription factor structurally related to WT1. Ectopic expression of EGR-1 in the 7C3H2 AdBRK cells significantly increases their in vivo growth rate and nullifies the tumor suppressor activity of the WT1(-/+) protein. Furthermore, we find that EGR-1 levels are elevated in some Wilms' tumors. These data are the first to show that EGR-1 overexpression causes enhanced tumor growth and that WT1 and EGR-1 exert antagonizing effects on growth regulation in baby rat kidney cells, which might reflect the situation in some Wilms' tumors.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1203390</identifier><identifier>PMID: 10698497</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Adenoviridae - physiology ; Alternative splicing ; Amino acids ; Animals ; Biological and medical sciences ; Cell Division ; Cell Line, Transformed ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cell Transformation, Viral ; Cells ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - physiology ; Early Growth Response Protein 1 ; Ectopic expression ; EGR-1 protein ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; Genes ; Genes, Wilms Tumor ; Growth rate ; Immediate-Early Proteins ; Insulin-like growth factors ; Kidney ; Kidney Neoplasms - genetics ; Kidney Neoplasms - pathology ; Kidneys ; Mice ; Mice, Nude ; Molecular and cellular biology ; Neoplasm Proteins - genetics ; Neoplasm Proteins - physiology ; Neoplasm Transplantation ; Phenotypes ; Prostate ; Proteins ; Rats ; RNA Splicing ; Transcription factors ; Transcription Factors - genetics ; Transcription Factors - physiology ; Tumor suppressor genes ; Tumorigenicity ; Tumors ; Wilms Tumor - genetics ; Wilms Tumor - pathology ; Wilms' tumor ; WT1 gene ; WT1 Proteins ; Zinc finger proteins ; Zinc Fingers - genetics</subject><ispartof>Oncogene, 2000-02, Vol.19 (6), p.791-800</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 10, 2000</rights><rights>Macmillan Publishers Limited 2000.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-28e26c3b6f0153e6bdc9424a056b8348dffc045f4fd8c817e99c5c253c169d083</citedby><cites>FETCH-LOGICAL-c512t-28e26c3b6f0153e6bdc9424a056b8348dffc045f4fd8c817e99c5c253c169d083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1282818$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10698497$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SCHARNHORST, V</creatorcontrib><creatorcontrib>MENKE, A. L</creatorcontrib><creatorcontrib>ATTEMA, J</creatorcontrib><creatorcontrib>HANEVELD, J. K</creatorcontrib><creatorcontrib>RITECO, N</creatorcontrib><creatorcontrib>VAN STEENBRUGGE, G. J</creatorcontrib><creatorcontrib>VAN DER EB, A. J</creatorcontrib><creatorcontrib>JOCHEMSEN, A. G</creatorcontrib><title>EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>The Wilms' tumor 1 gene (WT1) encodes a transcription factor of the zinc-finger family and is homozygously mutated or deleted in a subset of Wilms' tumors. Through alternative mRNA splicing, the gene is expressed as four main polypeptides that differ by a stretch of 17 amino acids just N-terminal of the four zinc-fingers and three amino acids between zinc fingers 3 and 4. We have previously shown that expression of the WT1(-/-) isoform, lacking both inserts, increases the tumor growth rate of the adenovirus-transformed baby rat kidney (AdBRK) cell line 7C3H2, whereas expression of the WT1(-/+) isoform, lacking the 17aa insert, strongly suppresses the tumorigenic phenotype. In the present study we show that expression of these splice variants does not affect the tumorigenic potential of the similar AdBRK cell line, 7C1T1. In contrast to the 7C3H2 cell line, this AdBRK cell line expresses high endogenous levels of EGR-1 (early growth response-1) protein, a transcription factor structurally related to WT1. Ectopic expression of EGR-1 in the 7C3H2 AdBRK cells significantly increases their in vivo growth rate and nullifies the tumor suppressor activity of the WT1(-/+) protein. Furthermore, we find that EGR-1 levels are elevated in some Wilms' tumors. These data are the first to show that EGR-1 overexpression causes enhanced tumor growth and that WT1 and EGR-1 exert antagonizing effects on growth regulation in baby rat kidney cells, which might reflect the situation in some Wilms' tumors.</description><subject>Adenoviridae - physiology</subject><subject>Alternative splicing</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Division</subject><subject>Cell Line, Transformed</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cell Transformation, Viral</subject><subject>Cells</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Early Growth Response Protein 1</subject><subject>Ectopic expression</subject><subject>EGR-1 protein</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Deletion</subject><subject>Genes</subject><subject>Genes, Wilms Tumor</subject><subject>Growth rate</subject><subject>Immediate-Early Proteins</subject><subject>Insulin-like growth factors</subject><subject>Kidney</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - pathology</subject><subject>Kidneys</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Molecular and cellular biology</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - physiology</subject><subject>Neoplasm Transplantation</subject><subject>Phenotypes</subject><subject>Prostate</subject><subject>Proteins</subject><subject>Rats</subject><subject>RNA Splicing</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><subject>Tumor suppressor genes</subject><subject>Tumorigenicity</subject><subject>Tumors</subject><subject>Wilms Tumor - genetics</subject><subject>Wilms Tumor - pathology</subject><subject>Wilms' tumor</subject><subject>WT1 gene</subject><subject>WT1 Proteins</subject><subject>Zinc finger proteins</subject><subject>Zinc Fingers - genetics</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0c9rFTEQB_AgFvusXj1KUNHTPie_k2MpbRUKhVLxGPKySd8uu5ua7CL97019CxVBPIVkPjNM-CL0hsCWANOfS79Nk98SCowZeIY2hCvZCGH4c7QBI6AxlNFj9LKUHgCUAfoCHROQRnOjNqg_v7xpCA7T3k0-FDwvY8r4Lqef8x67qcVjapfBzY-lfcAhxuBnnOLv2_duGMuntYfguzAFfJ9rg58LTtOh0NXnznfzwyt0FN1Qwuv1PEHfLs5vz740V9eXX89OrxovCJ0bqgOVnu1kBCJYkLvWG065AyF3mnHdxuiBi8hjq70mKhjjhaeCeSJNC5qdoI-HuXWVH0sosx274sMwuCmkpVgFhiumyH8hUVwDBVPh-79gn5Y81U9YKjlhhEgpq3r3T0UVY0CZqGh7QD6nUnKI9j53o8sPloB9TNSW3tZE7ZpobXi7Tl12Y2j_4IcIK_iwAle8G2KuQXblyVFNNdHsFy4Ip8k</recordid><startdate>20000210</startdate><enddate>20000210</enddate><creator>SCHARNHORST, V</creator><creator>MENKE, A. L</creator><creator>ATTEMA, J</creator><creator>HANEVELD, J. K</creator><creator>RITECO, N</creator><creator>VAN STEENBRUGGE, G. J</creator><creator>VAN DER EB, A. J</creator><creator>JOCHEMSEN, A. G</creator><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>20000210</creationdate><title>EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity</title><author>SCHARNHORST, V ; MENKE, A. L ; ATTEMA, J ; HANEVELD, J. K ; RITECO, N ; VAN STEENBRUGGE, G. J ; VAN DER EB, A. J ; JOCHEMSEN, A. G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-28e26c3b6f0153e6bdc9424a056b8348dffc045f4fd8c817e99c5c253c169d083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenoviridae - physiology</topic><topic>Alternative splicing</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Division</topic><topic>Cell Line, Transformed</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cell Transformation, Viral</topic><topic>Cells</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Early Growth Response Protein 1</topic><topic>Ectopic expression</topic><topic>EGR-1 protein</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Deletion</topic><topic>Genes</topic><topic>Genes, Wilms Tumor</topic><topic>Growth rate</topic><topic>Immediate-Early Proteins</topic><topic>Insulin-like growth factors</topic><topic>Kidney</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - pathology</topic><topic>Kidneys</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Molecular and cellular biology</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - physiology</topic><topic>Neoplasm Transplantation</topic><topic>Phenotypes</topic><topic>Prostate</topic><topic>Proteins</topic><topic>Rats</topic><topic>RNA Splicing</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - physiology</topic><topic>Tumor suppressor genes</topic><topic>Tumorigenicity</topic><topic>Tumors</topic><topic>Wilms Tumor - genetics</topic><topic>Wilms Tumor - pathology</topic><topic>Wilms' tumor</topic><topic>WT1 gene</topic><topic>WT1 Proteins</topic><topic>Zinc finger proteins</topic><topic>Zinc Fingers - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SCHARNHORST, V</creatorcontrib><creatorcontrib>MENKE, A. L</creatorcontrib><creatorcontrib>ATTEMA, J</creatorcontrib><creatorcontrib>HANEVELD, J. K</creatorcontrib><creatorcontrib>RITECO, N</creatorcontrib><creatorcontrib>VAN STEENBRUGGE, G. J</creatorcontrib><creatorcontrib>VAN DER EB, A. J</creatorcontrib><creatorcontrib>JOCHEMSEN, A. G</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>ProQuest - Health & Medical Complete保健、医学与药学数据库</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)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest 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>SCHARNHORST, V</au><au>MENKE, A. L</au><au>ATTEMA, J</au><au>HANEVELD, J. K</au><au>RITECO, N</au><au>VAN STEENBRUGGE, G. J</au><au>VAN DER EB, A. J</au><au>JOCHEMSEN, A. G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2000-02-10</date><risdate>2000</risdate><volume>19</volume><issue>6</issue><spage>791</spage><epage>800</epage><pages>791-800</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The Wilms' tumor 1 gene (WT1) encodes a transcription factor of the zinc-finger family and is homozygously mutated or deleted in a subset of Wilms' tumors. Through alternative mRNA splicing, the gene is expressed as four main polypeptides that differ by a stretch of 17 amino acids just N-terminal of the four zinc-fingers and three amino acids between zinc fingers 3 and 4. We have previously shown that expression of the WT1(-/-) isoform, lacking both inserts, increases the tumor growth rate of the adenovirus-transformed baby rat kidney (AdBRK) cell line 7C3H2, whereas expression of the WT1(-/+) isoform, lacking the 17aa insert, strongly suppresses the tumorigenic phenotype. In the present study we show that expression of these splice variants does not affect the tumorigenic potential of the similar AdBRK cell line, 7C1T1. In contrast to the 7C3H2 cell line, this AdBRK cell line expresses high endogenous levels of EGR-1 (early growth response-1) protein, a transcription factor structurally related to WT1. Ectopic expression of EGR-1 in the 7C3H2 AdBRK cells significantly increases their in vivo growth rate and nullifies the tumor suppressor activity of the WT1(-/+) protein. Furthermore, we find that EGR-1 levels are elevated in some Wilms' tumors. These data are the first to show that EGR-1 overexpression causes enhanced tumor growth and that WT1 and EGR-1 exert antagonizing effects on growth regulation in baby rat kidney cells, which might reflect the situation in some Wilms' tumors.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>10698497</pmid><doi>10.1038/sj.onc.1203390</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2000-02, Vol.19 (6), p.791-800 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70947371 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature; EZB Electronic Journals Library |
| subjects | Adenoviridae - physiology Alternative splicing Amino acids Animals Biological and medical sciences Cell Division Cell Line, Transformed Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Viral Cells DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Early Growth Response Protein 1 Ectopic expression EGR-1 protein Female Fundamental and applied biological sciences. Psychology Gene Deletion Genes Genes, Wilms Tumor Growth rate Immediate-Early Proteins Insulin-like growth factors Kidney Kidney Neoplasms - genetics Kidney Neoplasms - pathology Kidneys Mice Mice, Nude Molecular and cellular biology Neoplasm Proteins - genetics Neoplasm Proteins - physiology Neoplasm Transplantation Phenotypes Prostate Proteins Rats RNA Splicing Transcription factors Transcription Factors - genetics Transcription Factors - physiology Tumor suppressor genes Tumorigenicity Tumors Wilms Tumor - genetics Wilms Tumor - pathology Wilms' tumor WT1 gene WT1 Proteins Zinc finger proteins Zinc Fingers - genetics |
| title | EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T14%3A33%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=EGR-1%20enhances%20tumor%20growth%20and%20modulates%20the%20effect%20of%20the%20Wilms'%20tumor%201%20gene%20products%20on%20tumorigenicity&rft.jtitle=Oncogene&rft.au=SCHARNHORST,%20V&rft.date=2000-02-10&rft.volume=19&rft.issue=6&rft.spage=791&rft.epage=800&rft.pages=791-800&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/sj.onc.1203390&rft_dat=%3Cproquest_cross%3E17480209%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=227330235&rft_id=info:pmid/10698497&rfr_iscdi=true |