Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction complex
Identifieur interne : 000226 ( Pmc/Curation ); précédent : 000225; suivant : 000227Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction complex
Auteurs : Youn-Sang Jung [États-Unis] ; Jae-Il Park [États-Unis]Source :
- Experimental & Molecular Medicine [ 1226-3613 ] ; 2020.
Abstract
Wnt/β-catenin signaling is implicated in many physiological processes, including development, tissue homeostasis, and tissue regeneration. In human cancers, Wnt/β-catenin signaling is highly activated, which has led to the development of various Wnt signaling inhibitors for cancer therapies. Nonetheless, the blockade of Wnt signaling causes side effects such as impairment of tissue homeostasis and regeneration. Recently, several studies have identified cancer-specific Wnt signaling regulators. In this review, we discuss the Wnt inhibitors currently being used in clinical trials and suggest how additional cancer-specific regulators could be utilized to treat Wnt signaling-associated cancer.
Url:
DOI: 10.1038/s12276-020-0380-6
PubMed: 32037398
PubMed Central: 7062731
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institution-id-type="GRID">grid.240145.6</institution-id><institution>Department of Experimental Radiation Oncology, Division of Radiation Oncology,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Houston</wicri:cityArea></affiliation></author><author><name sortKey="Park, Jae Il" sort="Park, Jae Il" uniqKey="Park J" first="Jae-Il" last="Park">Jae-Il Park</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Department of Experimental Radiation Oncology, Division of Radiation Oncology,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Houston</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Graduate School of Biomedical Sciences,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Houston</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Program in Genetics and Epigenetics,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Houston</wicri:cityArea></affiliation></author></analytic><series><title level="j">Experimental & Molecular Medicine</title><idno type="ISSN">1226-3613</idno><idno type="eISSN">2092-6413</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Wnt/β-catenin signaling is implicated in many physiological processes, including development, tissue homeostasis, and tissue regeneration. In human cancers, Wnt/β-catenin signaling is highly activated, which has led to the development of various Wnt signaling inhibitors for cancer therapies. Nonetheless, the blockade of Wnt signaling causes side effects such as impairment of tissue homeostasis and regeneration. Recently, several studies have identified cancer-specific Wnt signaling regulators. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Exp Mol Med</journal-id><journal-id journal-id-type="iso-abbrev">Exp. Mol. Med</journal-id><journal-title-group><journal-title>Experimental & Molecular Medicine</journal-title></journal-title-group><issn pub-type="ppub">1226-3613</issn><issn pub-type="epub">2092-6413</issn><publisher><publisher-name>Nature Publishing Group UK</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32037398</article-id><article-id pub-id-type="pmc">7062731</article-id><article-id pub-id-type="publisher-id">380</article-id><article-id pub-id-type="doi">10.1038/s12276-020-0380-6</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title>Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction complex</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Jung</surname><given-names>Youn-Sang</given-names></name><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0002-0737-2654</contrib-id><name><surname>Park</surname><given-names>Jae-Il</given-names></name><address><email>jaeil@mdanderson.org</email></address><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff2">2</xref><xref ref-type="aff" rid="Aff3">3</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Department of Experimental Radiation Oncology, Division of Radiation Oncology,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</aff><aff id="Aff2"><label>2</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Graduate School of Biomedical Sciences,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</aff><aff id="Aff3"><label>3</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Program in Genetics and Epigenetics,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, TX 77030 USA</aff></contrib-group><pub-date pub-type="epub"><day>10</day><month>2</month><year>2020</year></pub-date><pub-date pub-type="pmc-release"><day>10</day><month>2</month><year>2020</year></pub-date><pub-date pub-type="collection"><month>2</month><year>2020</year></pub-date><volume>52</volume><issue>2</issue><fpage>183</fpage><lpage>191</lpage><history><date date-type="received"><day>15</day><month>10</month><year>2019</year></date><date date-type="rev-recd"><day>20</day><month>12</month><year>2019</year></date><date date-type="accepted"><day>26</day><month>12</month><year>2019</year></date></history><permissions><copyright-statement>© The Author(s) 2020</copyright-statement><license license-type="OpenAccess"><license-p><bold>Open Access</bold> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>.</license-p></license></permissions><abstract id="Abs1"><p id="Par1">Wnt/β-catenin signaling is implicated in many physiological processes, including development, tissue homeostasis, and tissue regeneration. In human cancers, Wnt/β-catenin signaling is highly activated, which has led to the development of various Wnt signaling inhibitors for cancer therapies. Nonetheless, the blockade of Wnt signaling causes side effects such as impairment of tissue homeostasis and regeneration. Recently, several studies have identified cancer-specific Wnt signaling regulators. In this review, we discuss the Wnt inhibitors currently being used in clinical trials and suggest how additional cancer-specific regulators could be utilized to treat Wnt signaling-associated cancer.</p></abstract><abstract id="Abs2" abstract-type="LongSummary"><title>Cancer: A search for safer signaling targets</title><p id="Par2">More effective treatments for cancer could be developed by targeting signaling pathway regulators that are expressed solely in cancer cells. Disruption to a major signaling pathway known as Wnt, which is involved in processes including cell proliferation, tissue homeostasis and tissue regeneration, is now recognized as a significant contributor to the development of certain cancers. Jae-Il Park and Youn-Sang Jung at the University of Texas MD Anderson Cancer Center, Houston, USA, reviewed recent research into Wnt signaling in cancer and possible therapies. Scientists have developed Wnt inhibitors for cancer treatment, but these have detrimental side effects including skeletal degeneration and abdominal pain. New studies suggest there are Wnt signaling regulators that are specifically expressed in cancer cells, which may prove to be more effective drug targets than blocking Wnt signaling as a whole.</p></abstract><kwd-group kwd-group-type="npg-subject"><title>Subject terms</title><kwd>Cancer</kwd><kwd>Drug discovery</kwd></kwd-group><funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100004917</institution-id><institution>Cancer Prevention and Research Institute of Texas (Cancer Prevention Research Institute of Texas)</institution></institution-wrap></funding-source><award-id>RP140563</award-id><principal-award-recipient><name><surname>Park</surname><given-names>Jae-Il</given-names></name></principal-award-recipient></award-group></funding-group><funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100000002</institution-id><institution>U.S. Department of Health & Human Services | National Institutes of Health (NIH)</institution></institution-wrap></funding-source><award-id>R01 CA193297-01</award-id><principal-award-recipient><name><surname>Park</surname><given-names>Jae-Il</given-names></name></principal-award-recipient></award-group></funding-group><funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100000005</institution-id><institution>U.S. Department of Defense (United States Department of Defense)</institution></institution-wrap></funding-source><award-id>W81XWH-15-1-0140</award-id><principal-award-recipient><name><surname>Park</surname><given-names>Jae-Il</given-names></name></principal-award-recipient></award-group></funding-group><funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100007313</institution-id><institution>UT | University of Texas MD Anderson Cancer Center (MD Anderson)</institution></institution-wrap></funding-source><award-id>Institutional Research Grant</award-id><principal-award-recipient><name><surname>Park</surname><given-names>Jae-Il</given-names></name></principal-award-recipient></award-group></funding-group><funding-group><award-group><funding-source><institution>SPORE in endometrial cancer: Specialized Program of Research Excellence in endometrial cancer</institution></funding-source></award-group></funding-group><funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100000043</institution-id><institution>American Association for Cancer Research (American Association for Cancer Research, Inc.)</institution></institution-wrap></funding-source><award-id>19-40-41-Jung</award-id><principal-award-recipient><name><surname>Jung</surname><given-names>Youn-Sang</given-names></name></principal-award-recipient></award-group></funding-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2020</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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