The role of GATA2 in lethal prostate cancer aggressiveness
Identifieur interne : 003576 ( Pmc/Corpus ); précédent : 003575; suivant : 003577The role of GATA2 in lethal prostate cancer aggressiveness
Auteurs : Veronica Rodriguez-Bravo ; Marc Carceles-Cordon ; Yujin Hoshida ; Carlos Cordon-Cardo ; Matthew D. Galsky ; Josep Domingo-DomenechSource :
- Nature reviews. Urology [ 1759-4812 ] ; 2016.
Abstract
Advanced prostate cancer is a classic example of the intractability and consequent lethality that characterizes metastatic carcinomas. Novel treatments have improved the survival of men with prostate cancer; however, advanced prostate cancer invariably becomes resistant to these therapies and ultimately progresses to a lethal metastatic stage. Consequently, detailed knowledge of the molecular mechanisms that control prostate cancer cell survival and progression towards this lethal stage of disease will benefit the development of new therapeutics. The transcription factor endothelial transcription factor GATA-2 (GATA2) has been reported to have a key role in driving prostate cancer aggressiveness. In addition to being a pioneer transcription factor that increases androgen receptor (AR) binding and activity, GATA2 regulates a core subset of clinically relevant genes in an AR-independent manner. Functionally, GATA2 overexpression in prostate cancer increases cellular motility and invasiveness, proliferation, tumorigenicity, and resistance to standard therapies. Thus, GATA2 has a multifaceted function in prostate cancer aggressiveness and is a highly attractive target in the development of novel treatments against lethal prostate cancer.
Url:
DOI: 10.1038/nrurol.2016.225
PubMed: 27872477
PubMed Central: 5489122
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PMC:5489122Le document en format XML
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Galsky</name><affiliation><nlm:aff id="A3">Department of Hematology and Oncology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author><author><name sortKey="Domingo Domenech, Josep" sort="Domingo Domenech, Josep" uniqKey="Domingo Domenech J" first="Josep" last="Domingo-Domenech">Josep Domingo-Domenech</name><affiliation><nlm:aff id="A1">Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27872477</idno><idno type="pmc">5489122</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489122</idno><idno type="RBID">PMC:5489122</idno><idno type="doi">10.1038/nrurol.2016.225</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">003576</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003576</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The role of GATA2 in lethal prostate cancer aggressiveness</title><author><name sortKey="Rodriguez Bravo, Veronica" sort="Rodriguez Bravo, Veronica" uniqKey="Rodriguez Bravo V" first="Veronica" last="Rodriguez-Bravo">Veronica Rodriguez-Bravo</name><affiliation><nlm:aff id="A1">Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author><author><name sortKey="Carceles Cordon, Marc" sort="Carceles Cordon, Marc" uniqKey="Carceles Cordon M" first="Marc" last="Carceles-Cordon">Marc Carceles-Cordon</name><affiliation><nlm:aff id="A1">Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author><author><name sortKey="Hoshida, Yujin" sort="Hoshida, Yujin" uniqKey="Hoshida Y" first="Yujin" last="Hoshida">Yujin Hoshida</name><affiliation><nlm:aff id="A2">Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author><author><name sortKey="Cordon Cardo, Carlos" sort="Cordon Cardo, Carlos" uniqKey="Cordon Cardo C" first="Carlos" last="Cordon-Cardo">Carlos Cordon-Cardo</name><affiliation><nlm:aff id="A1">Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author><author><name sortKey="Galsky, Matthew D" sort="Galsky, Matthew D" uniqKey="Galsky M" first="Matthew D." last="Galsky">Matthew D. Galsky</name><affiliation><nlm:aff id="A3">Department of Hematology and Oncology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author><author><name sortKey="Domingo Domenech, Josep" sort="Domingo Domenech, Josep" uniqKey="Domingo Domenech J" first="Josep" last="Domingo-Domenech">Josep Domingo-Domenech</name><affiliation><nlm:aff id="A1">Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Nature reviews. Urology</title><idno type="ISSN">1759-4812</idno><idno type="eISSN">1759-4820</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Advanced prostate cancer is a classic example of the intractability and consequent lethality that characterizes metastatic carcinomas. Novel treatments have improved the survival of men with prostate cancer; however, advanced prostate cancer invariably becomes resistant to these therapies and ultimately progresses to a lethal metastatic stage. Consequently, detailed knowledge of the molecular mechanisms that control prostate cancer cell survival and progression towards this lethal stage of disease will benefit the development of new therapeutics. The transcription factor endothelial transcription factor GATA-2 (GATA2) has been reported to have a key role in driving prostate cancer aggressiveness. In addition to being a pioneer transcription factor that increases androgen receptor (AR) binding and activity, GATA2 regulates a core subset of clinically relevant genes in an AR-independent manner. Functionally, GATA2 overexpression in prostate cancer increases cellular motility and invasiveness, proliferation, tumorigenicity, and resistance to standard therapies. Thus, GATA2 has a multifaceted function in prostate cancer aggressiveness and is a highly attractive target in the development of novel treatments against lethal prostate cancer.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101500082</journal-id><journal-id journal-id-type="pubmed-jr-id">35766</journal-id><journal-id journal-id-type="nlm-ta">Nat Rev Urol</journal-id><journal-id journal-id-type="iso-abbrev">Nat Rev Urol</journal-id><journal-title-group><journal-title>Nature reviews. Urology</journal-title></journal-title-group><issn pub-type="ppub">1759-4812</issn><issn pub-type="epub">1759-4820</issn></journal-meta><article-meta><article-id pub-id-type="pmid">27872477</article-id><article-id pub-id-type="pmc">5489122</article-id><article-id pub-id-type="doi">10.1038/nrurol.2016.225</article-id><article-id pub-id-type="manuscript">NIHMS868937</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>The role of GATA2 in lethal prostate cancer aggressiveness</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Rodriguez-Bravo</surname><given-names>Veronica</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Carceles-Cordon</surname><given-names>Marc</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hoshida</surname><given-names>Yujin</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Cordon-Cardo</surname><given-names>Carlos</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Galsky</surname><given-names>Matthew D.</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Domingo-Domenech</surname><given-names>Josep</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</aff><aff id="A2"><label>2</label>Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</aff><aff id="A3"><label>3</label>Department of Hematology and Oncology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA</aff><author-notes><corresp id="FN1">Correspondence to J.D.-D. <email>josep.domingo-domenech@mssm.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>25</day><month>4</month><year>2017</year></pub-date><pub-date pub-type="epub"><day>22</day><month>11</month><year>2016</year></pub-date><pub-date pub-type="ppub"><month>1</month><year>2017</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>7</month><year>2017</year></pub-date><volume>14</volume><issue>1</issue><fpage>38</fpage><lpage>48</lpage><pmc-comment>elocation-id from pubmed: 10.1038/nrurol.2016.225</pmc-comment>
<abstract><p id="P1">Advanced prostate cancer is a classic example of the intractability and consequent lethality that characterizes metastatic carcinomas. Novel treatments have improved the survival of men with prostate cancer; however, advanced prostate cancer invariably becomes resistant to these therapies and ultimately progresses to a lethal metastatic stage. Consequently, detailed knowledge of the molecular mechanisms that control prostate cancer cell survival and progression towards this lethal stage of disease will benefit the development of new therapeutics. The transcription factor endothelial transcription factor GATA-2 (GATA2) has been reported to have a key role in driving prostate cancer aggressiveness. In addition to being a pioneer transcription factor that increases androgen receptor (AR) binding and activity, GATA2 regulates a core subset of clinically relevant genes in an AR-independent manner. Functionally, GATA2 overexpression in prostate cancer increases cellular motility and invasiveness, proliferation, tumorigenicity, and resistance to standard therapies. Thus, GATA2 has a multifaceted function in prostate cancer aggressiveness and is a highly attractive target in the development of novel treatments against lethal prostate cancer.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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