ZNF281/ZBP-99: a new player in epithelial–mesenchymal transition, stemness, and cancer
Epithelial–mesenchymal transition (EMT) represents an important mechanism during development and wound healing, and its deregulation has been implicated in metastasis. Recently, the Krüppel-type zinc-finger transcription factor ZNF281 has been characterized as an EMT-inducing transcription factor (E...
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| Veröffentlicht in: | Journal of molecular medicine (Berlin, Germany) Germany), 2014-06, Vol.92 (6), p.571-581 |
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| description | Epithelial–mesenchymal transition (EMT) represents an important mechanism during development and wound healing, and its deregulation has been implicated in metastasis. Recently, the Krüppel-type zinc-finger transcription factor ZNF281 has been characterized as an EMT-inducing transcription factor (EMT-TF). Expression of ZNF281 is induced by the EMT-TF SNAIL and inhibited by the tumor suppressive microRNA miR-34a, which mediates repression of ZNF281 by the p53 tumor suppressor. Therefore, SNAIL, miR-34a and ZNF281 form a feed-forward regulatory loop, which controls EMT. Deregulation of this circuitry by mutational and epigenetic alterations in the p53/miR-34a axis promotes colorectal cancer (CRC) progression and metastasis formation. As ZNF281 physically interacts with the transcription factors NANOG, OCT4, SOX2, and c-MYC, it has been implicated in the regulation of pluripotency, stemness, and cancer. Accordingly, ectopic ZNF281 expression in CRC lines induces the stemness markers LGR5 and CD133 and promotes sphere formation, suggesting that the elevated expression of ZNF281 detected in cancer may enhance tumor stem cell formation and/or function. Here, we review the functional and organismal studies of ZNF281/ZBP-99 and its close relative ZBP-89/ZFP148 reported so far. Taken together, ZNF281 related biology has the potential to be translated into cancer diagnostic, prognostic, and therapeutic approaches. |
| doi_str_mv | 10.1007/s00109-014-1160-3 |
| format | Article |
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Recently, the Krüppel-type zinc-finger transcription factor ZNF281 has been characterized as an EMT-inducing transcription factor (EMT-TF). Expression of ZNF281 is induced by the EMT-TF SNAIL and inhibited by the tumor suppressive microRNA miR-34a, which mediates repression of ZNF281 by the p53 tumor suppressor. Therefore, SNAIL, miR-34a and ZNF281 form a feed-forward regulatory loop, which controls EMT. Deregulation of this circuitry by mutational and epigenetic alterations in the p53/miR-34a axis promotes colorectal cancer (CRC) progression and metastasis formation. As ZNF281 physically interacts with the transcription factors NANOG, OCT4, SOX2, and c-MYC, it has been implicated in the regulation of pluripotency, stemness, and cancer. Accordingly, ectopic ZNF281 expression in CRC lines induces the stemness markers LGR5 and CD133 and promotes sphere formation, suggesting that the elevated expression of ZNF281 detected in cancer may enhance tumor stem cell formation and/or function. Here, we review the functional and organismal studies of ZNF281/ZBP-99 and its close relative ZBP-89/ZFP148 reported so far. Taken together, ZNF281 related biology has the potential to be translated into cancer diagnostic, prognostic, and therapeutic approaches.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s00109-014-1160-3</identifier><identifier>PMID: 24838609</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Epithelial-Mesenchymal Transition - genetics ; Epithelial-Mesenchymal Transition - physiology ; Gene Expression Regulation, Neoplastic - genetics ; Gene Expression Regulation, Neoplastic - physiology ; Human Genetics ; Humans ; Internal Medicine ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Molecular Medicine ; Neoplastic Stem Cells - metabolism ; Review ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2014-06, Vol.92 (6), p.571-581</ispartof><rights>Springer-Verlag Berlin Heidelberg 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-a873b5f78b5d672bd93fd0349a53315ae54ee17f440e66427a9673a628678a9c3</citedby><cites>FETCH-LOGICAL-c372t-a873b5f78b5d672bd93fd0349a53315ae54ee17f440e66427a9673a628678a9c3</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/s00109-014-1160-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00109-014-1160-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27913,27914,41477,42546,51308</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24838609$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hahn, Stefanie</creatorcontrib><creatorcontrib>Hermeking, Heiko</creatorcontrib><title>ZNF281/ZBP-99: a new player in epithelial–mesenchymal transition, stemness, and cancer</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med</addtitle><addtitle>J Mol Med (Berl)</addtitle><description>Epithelial–mesenchymal transition (EMT) represents an important mechanism during development and wound healing, and its deregulation has been implicated in metastasis. Recently, the Krüppel-type zinc-finger transcription factor ZNF281 has been characterized as an EMT-inducing transcription factor (EMT-TF). Expression of ZNF281 is induced by the EMT-TF SNAIL and inhibited by the tumor suppressive microRNA miR-34a, which mediates repression of ZNF281 by the p53 tumor suppressor. Therefore, SNAIL, miR-34a and ZNF281 form a feed-forward regulatory loop, which controls EMT. Deregulation of this circuitry by mutational and epigenetic alterations in the p53/miR-34a axis promotes colorectal cancer (CRC) progression and metastasis formation. As ZNF281 physically interacts with the transcription factors NANOG, OCT4, SOX2, and c-MYC, it has been implicated in the regulation of pluripotency, stemness, and cancer. Accordingly, ectopic ZNF281 expression in CRC lines induces the stemness markers LGR5 and CD133 and promotes sphere formation, suggesting that the elevated expression of ZNF281 detected in cancer may enhance tumor stem cell formation and/or function. Here, we review the functional and organismal studies of ZNF281/ZBP-99 and its close relative ZBP-89/ZFP148 reported so far. Taken together, ZNF281 related biology has the potential to be translated into cancer diagnostic, prognostic, and therapeutic approaches.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Epithelial-Mesenchymal Transition - physiology</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Molecular Medicine</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Review</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>0946-2716</issn><issn>1432-1440</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kM9O3DAQhy1UBAvlAbhUlnrpAYPHdvynN0BQkFDbQyuhvVjeZFKCEmexs6r2xjvwhjxJs9oFoUqc5jDf_GbmI-QQ-DFwbk4y58Ad46AYgOZMbpEJKCkYKMU_kAl3SjNhQO-SvZzvR9oUTu2QXaGstJq7Cbmdfr8UFk6mZz-Zc19poBH_0nkblphoEynOm-EO2ya0z49PHWaM5d2yCy0dUoi5GZo-HtE8YBcx5yMaYkXLEEtMH8l2HdqMB5u6T35fXvw6v2I3P75dn5_esFIaMbBgjZwVtbGzotJGzCon64pL5UIhJRQBC4UIph4fQq2VMMFpI4MWVhsbXCn3yZd17jz1DwvMg--aXGLbhoj9InsohJHC2MKO6Of_0Pt-keJ43YrSwC3oFQVrqkx9zglrP09NF9LSA_cr7X6t3Y_a_Uq7l-PMp03yYtZh9Trx4nkExBrIYyv-wfRm9bup_wCEiYrf</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Hahn, Stefanie</creator><creator>Hermeking, Heiko</creator><general>Springer Berlin Heidelberg</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>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>7X8</scope></search><sort><creationdate>20140601</creationdate><title>ZNF281/ZBP-99: a new player in epithelial–mesenchymal transition, stemness, and cancer</title><author>Hahn, Stefanie ; Hermeking, Heiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-a873b5f78b5d672bd93fd0349a53315ae54ee17f440e66427a9673a628678a9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Epithelial-Mesenchymal Transition - physiology</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Molecular Medicine</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Review</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hahn, Stefanie</creatorcontrib><creatorcontrib>Hermeking, Heiko</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</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>MEDLINE - Academic</collection><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hahn, Stefanie</au><au>Hermeking, Heiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ZNF281/ZBP-99: a new player in epithelial–mesenchymal transition, stemness, and cancer</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><stitle>J Mol Med</stitle><addtitle>J Mol Med (Berl)</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>92</volume><issue>6</issue><spage>571</spage><epage>581</epage><pages>571-581</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><abstract>Epithelial–mesenchymal transition (EMT) represents an important mechanism during development and wound healing, and its deregulation has been implicated in metastasis. Recently, the Krüppel-type zinc-finger transcription factor ZNF281 has been characterized as an EMT-inducing transcription factor (EMT-TF). Expression of ZNF281 is induced by the EMT-TF SNAIL and inhibited by the tumor suppressive microRNA miR-34a, which mediates repression of ZNF281 by the p53 tumor suppressor. Therefore, SNAIL, miR-34a and ZNF281 form a feed-forward regulatory loop, which controls EMT. Deregulation of this circuitry by mutational and epigenetic alterations in the p53/miR-34a axis promotes colorectal cancer (CRC) progression and metastasis formation. As ZNF281 physically interacts with the transcription factors NANOG, OCT4, SOX2, and c-MYC, it has been implicated in the regulation of pluripotency, stemness, and cancer. Accordingly, ectopic ZNF281 expression in CRC lines induces the stemness markers LGR5 and CD133 and promotes sphere formation, suggesting that the elevated expression of ZNF281 detected in cancer may enhance tumor stem cell formation and/or function. 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| subjects | Biomedical and Life Sciences Biomedicine DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Epithelial-Mesenchymal Transition - genetics Epithelial-Mesenchymal Transition - physiology Gene Expression Regulation, Neoplastic - genetics Gene Expression Regulation, Neoplastic - physiology Human Genetics Humans Internal Medicine MicroRNAs - genetics MicroRNAs - metabolism Molecular Medicine Neoplastic Stem Cells - metabolism Review Trans-Activators - genetics Trans-Activators - metabolism Transcription Factors - genetics Transcription Factors - metabolism |
| title | ZNF281/ZBP-99: a new player in epithelial–mesenchymal transition, stemness, and cancer |
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