Inhibition of canonical WNT signaling attenuates human leiomyoma cell growth
Identifieur interne : 000425 ( Ncbi/Merge ); précédent : 000424; suivant : 000426Inhibition of canonical WNT signaling attenuates human leiomyoma cell growth
Auteurs : Masanori Ono [États-Unis] ; Ping Yin [États-Unis] ; Antonia Navarro [États-Unis] ; Molly B. Moravek [États-Unis] ; John S. Coon V [États-Unis] ; Stacy A. Druschitz [États-Unis] ; Cara J. Gottardi [États-Unis] ; Serdar E. Bulun [États-Unis]Source :
- Fertility and Sterility [ 0015-0282 ] ; 2014.
Abstract
To assess the effect of three WNT/β-catenin pathway inhibitors—inhibitor of β-catenin and TCF4 (ICAT), niclosamide, and XAV939—on the proliferation of primary cultures of human uterine leiomyoma cells.
Prospective study of human leiomyoma cells obtained from myomectomy or hysterectomy.
University research laboratory.
Women (n = 38) aged 27–53 years undergoing surgery.
Adenoviral ICAT overexpression or treatment with varying concentrations of niclosamide or XAV939.
Cell proliferation, cell death, WNT/-catenin target gene expression or reporter gene regulation, β-catenin levels, and cellular localization.
Inhibitor of β-catenin and TCF4, niclosamide, or XAV939 inhibit WNT/β-catenin pathway activation and exert antiproliferative effects in primary cultures of human leiomyoma cells.
Three WNT/-catenin pathway inhibitors specifically block human leiomyoma growth and proliferation, suggesting that the canonical WNT pathway may be a potential therapeutic target for the treatment of uterine leiomyoma. Our findings provide rationale for further preclinical and clinical evaluation of ICAT, niclosamide, and XAV939 as candidate antitumor agents for uterine leiomyoma.
Url:
DOI: 10.1016/j.fertnstert.2014.01.017
PubMed: 24534281
PubMed Central: 4008647
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Moravek</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Coon V, John S" sort="Coon V, John S" uniqKey="Coon V J" first="John S." last="Coon V">John S. Coon V</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Druschitz, Stacy A" sort="Druschitz, Stacy A" uniqKey="Druschitz S" first="Stacy A." last="Druschitz">Stacy A. Druschitz</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Gottardi, Cara J" sort="Gottardi, Cara J" uniqKey="Gottardi C" first="Cara J." last="Gottardi">Cara J. Gottardi</name><affiliation wicri:level="2"><nlm:aff id="aff2">Department of Medicine, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Medicine, Feinberg School of Medicine at Northwestern University, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Bulun, Serdar E" sort="Bulun, Serdar E" uniqKey="Bulun S" first="Serdar E." last="Bulun">Serdar E. Bulun</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago</wicri:cityArea></affiliation></author></analytic><series><title level="j">Fertility and Sterility</title><idno type="ISSN">0015-0282</idno><idno type="eISSN">1556-5653</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Objective</title><p>To assess the effect of three WNT/β-catenin pathway inhibitors—inhibitor of β-catenin and TCF4 (ICAT), niclosamide, and XAV939—on the proliferation of primary cultures of human uterine leiomyoma cells.</p></sec><sec><title>Design</title><p>Prospective study of human leiomyoma cells obtained from myomectomy or hysterectomy.</p></sec><sec><title>Setting</title><p>University research laboratory.</p></sec><sec><title>Patient(s)</title><p>Women (n = 38) aged 27–53 years undergoing surgery.</p></sec><sec><title>Intervention(s)</title><p>Adenoviral ICAT overexpression or treatment with varying concentrations of niclosamide or XAV939.</p></sec><sec><title>Main Outcome Measure(s)</title><p>Cell proliferation, cell death, WNT/-catenin target gene expression or reporter gene regulation, β-catenin levels, and cellular localization.</p></sec><sec><title>Result(s)</title><p>Inhibitor of β-catenin and TCF4, niclosamide, or XAV939 inhibit WNT/β-catenin pathway activation and exert antiproliferative effects in primary cultures of human leiomyoma cells.</p></sec><sec><title>Conclusion(s)</title><p>Three WNT/-catenin pathway inhibitors specifically block human leiomyoma growth and proliferation, suggesting that the canonical WNT pathway may be a potential therapeutic target for the treatment of uterine leiomyoma. 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Reya</name></author><author><name sortKey="Clevers, H" uniqKey="Clevers H">H. Clevers</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Fertil Steril</journal-id><journal-id journal-id-type="iso-abbrev">Fertil. Steril</journal-id><journal-title-group><journal-title>Fertility and Sterility</journal-title></journal-title-group><issn pub-type="ppub">0015-0282</issn><issn pub-type="epub">1556-5653</issn><publisher><publisher-name>Elsevier for the American Society for Reproductive Medicine</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24534281</article-id><article-id pub-id-type="pmc">4008647</article-id><article-id pub-id-type="publisher-id">S0015-0282(14)00048-X</article-id><article-id pub-id-type="doi">10.1016/j.fertnstert.2014.01.017</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Inhibition of canonical WNT signaling attenuates human leiomyoma cell growth</article-title></title-group><contrib-group><contrib contrib-type="author" id="au1"><name><surname>Ono</surname><given-names>Masanori</given-names></name><degrees>M.D., Ph.D.</degrees><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au2"><name><surname>Yin</surname><given-names>Ping</given-names></name><degrees>Ph.D.</degrees><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au3"><name><surname>Navarro</surname><given-names>Antonia</given-names></name><degrees>M.Sc.</degrees><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au4"><name><surname>Moravek</surname><given-names>Molly B.</given-names></name><degrees>M.D.</degrees><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au5"><name><surname>Coon V</surname><given-names>John S.</given-names></name><degrees>M.Sc.</degrees><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au6"><name><surname>Druschitz</surname><given-names>Stacy A.</given-names></name><degrees>B.Sc.</degrees><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au7"><name><surname>Gottardi</surname><given-names>Cara J.</given-names></name><degrees>Ph.D.</degrees><xref rid="aff2" ref-type="aff">b</xref></contrib><contrib contrib-type="author" id="au8"><name><surname>Bulun</surname><given-names>Serdar E.</given-names></name><degrees>M.D.</degrees><email>Sbulun@nmh.org</email><xref rid="aff1" ref-type="aff">a</xref><xref rid="cor1" ref-type="corresp">∗</xref></contrib></contrib-group><aff id="aff1"><label>a</label>Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</aff><aff id="aff2"><label>b</label>Department of Medicine, Feinberg School of Medicine at Northwestern University, Chicago, Illinois</aff><author-notes><corresp id="cor1"><label>∗</label>Reprint requests: Serdar E. Bulun, M.D., Northwestern University, Feinberg School of Medicine, Department of Obstetrics and Gynecology, 303 East Superior St., Ste. 4-123, Chicago, Illinois 60611. <email>Sbulun@nmh.org</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>15</day><month>2</month><year>2014</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>5</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>15</day><month>2</month><year>2014</year></pub-date><volume>101</volume><issue>5</issue><fpage>1441</fpage><lpage>1449.e1</lpage><history><date date-type="received"><day>29</day><month>10</month><year>2013</year></date><date date-type="rev-recd"><day>28</day><month>12</month><year>2013</year></date><date date-type="accepted"><day>13</day><month>1</month><year>2014</year></date></history><permissions><copyright-statement>Copyright © 2014 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>American Society for Reproductive Medicine</copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="abs0010"><sec><title>Objective</title><p>To assess the effect of three WNT/β-catenin pathway inhibitors—inhibitor of β-catenin and TCF4 (ICAT), niclosamide, and XAV939—on the proliferation of primary cultures of human uterine leiomyoma cells.</p></sec><sec><title>Design</title><p>Prospective study of human leiomyoma cells obtained from myomectomy or hysterectomy.</p></sec><sec><title>Setting</title><p>University research laboratory.</p></sec><sec><title>Patient(s)</title><p>Women (n = 38) aged 27–53 years undergoing surgery.</p></sec><sec><title>Intervention(s)</title><p>Adenoviral ICAT overexpression or treatment with varying concentrations of niclosamide or XAV939.</p></sec><sec><title>Main Outcome Measure(s)</title><p>Cell proliferation, cell death, WNT/-catenin target gene expression or reporter gene regulation, β-catenin levels, and cellular localization.</p></sec><sec><title>Result(s)</title><p>Inhibitor of β-catenin and TCF4, niclosamide, or XAV939 inhibit WNT/β-catenin pathway activation and exert antiproliferative effects in primary cultures of human leiomyoma cells.</p></sec><sec><title>Conclusion(s)</title><p>Three WNT/-catenin pathway inhibitors specifically block human leiomyoma growth and proliferation, suggesting that the canonical WNT pathway may be a potential therapeutic target for the treatment of uterine leiomyoma. Our findings provide rationale for further preclinical and clinical evaluation of ICAT, niclosamide, and XAV939 as candidate antitumor agents for uterine leiomyoma.</p></sec></abstract><kwd-group id="kwrds0010"><title>Key Words</title><kwd>Leiomyoma</kwd><kwd>WNT/β-catenin</kwd><kwd>niclosamide</kwd><kwd>XAV939</kwd><kwd>tumor biology</kwd></kwd-group></article-meta></front></pmc><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li></region></list><tree><country name="États-Unis"><region name="Illinois"><name sortKey="Ono, Masanori" sort="Ono, Masanori" uniqKey="Ono M" first="Masanori" last="Ono">Masanori Ono</name></region><name sortKey="Bulun, Serdar E" sort="Bulun, Serdar E" uniqKey="Bulun S" first="Serdar E." last="Bulun">Serdar E. Bulun</name><name sortKey="Coon V, John S" sort="Coon V, John S" uniqKey="Coon V J" first="John S." last="Coon V">John S. Coon V</name><name sortKey="Druschitz, Stacy A" sort="Druschitz, Stacy A" uniqKey="Druschitz S" first="Stacy A." last="Druschitz">Stacy A. Druschitz</name><name sortKey="Gottardi, Cara J" sort="Gottardi, Cara J" uniqKey="Gottardi C" first="Cara J." last="Gottardi">Cara J. Gottardi</name><name sortKey="Moravek, Molly B" sort="Moravek, Molly B" uniqKey="Moravek M" first="Molly B." last="Moravek">Molly B. Moravek</name><name sortKey="Navarro, Antonia" sort="Navarro, Antonia" uniqKey="Navarro A" first="Antonia" last="Navarro">Antonia Navarro</name><name sortKey="Yin, Ping" sort="Yin, Ping" uniqKey="Yin P" first="Ping" last="Yin">Ping Yin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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