Tenascin-C Signaling in melanoma
Identifieur interne : 000419 ( Pmc/Checkpoint ); précédent : 000418; suivant : 000420Tenascin-C Signaling in melanoma
Auteurs : Hanshuang Shao ; John M. Kirkwood [États-Unis] ; Alan Wells [États-Unis]Source :
- Cell Adhesion & Migration [ 1933-6918 ] ; 2014.
Abstract
Tenascin-C (TNC), a multifunctional matricellular glyco-protein, is highly expressed in the majority of melanoma cell lines and has been implicated in the progression of melanoma. A growing body of evidence has implicated the role of TNC in the process of invasion and metastasis for melanoma. However, the mechanism and individual signaling pathways by which TNC drives melanoma progression have not been illuminated. Herein we provide perspectives from the investigation of TNC in other settings that may hint at the mechanistic role of TNC in this disease.
Url:
DOI: 10.4161/19336918.2014.972781
PubMed: 25482624
PubMed Central: 4422811
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Tenascin-C Signaling in melanoma</title><author><name sortKey="Shao, Hanshuang" sort="Shao, Hanshuang" uniqKey="Shao H" first="Hanshuang" last="Shao">Hanshuang Shao</name><affiliation><nlm:aff id="af0001"><institution>Department of Pathology</institution></nlm:aff></affiliation></author><author><name sortKey="Kirkwood, John M" sort="Kirkwood, John M" uniqKey="Kirkwood J" first="John M" last="Kirkwood">John M. Kirkwood</name><affiliation wicri:level="1"><nlm:aff id="af0002"><institution>Medicine and Dermatology and Translational Science Melanoma Program; University of Pittsburgh Cancer Institute; University of Pittsburgh</institution>; Pittsburgh, PA<country>USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Wells, Alan" sort="Wells, Alan" uniqKey="Wells A" first="Alan" last="Wells">Alan Wells</name><affiliation><nlm:aff id="af0001"><institution>Department of Pathology</institution></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af0003"><institution>Laboratory and Pathology Service; Pittsburgh VA Health System</institution>; Pittsburgh, PA<country>USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25482624</idno><idno type="pmc">4422811</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422811</idno><idno type="RBID">PMC:4422811</idno><idno type="doi">10.4161/19336918.2014.972781</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000210</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000210</idno><idno type="wicri:Area/Pmc/Curation">000210</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000210</idno><idno type="wicri:Area/Pmc/Checkpoint">000419</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000419</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Tenascin-C Signaling in melanoma</title><author><name sortKey="Shao, Hanshuang" sort="Shao, Hanshuang" uniqKey="Shao H" first="Hanshuang" last="Shao">Hanshuang Shao</name><affiliation><nlm:aff id="af0001"><institution>Department of Pathology</institution></nlm:aff></affiliation></author><author><name sortKey="Kirkwood, John M" sort="Kirkwood, John M" uniqKey="Kirkwood J" first="John M" last="Kirkwood">John M. Kirkwood</name><affiliation wicri:level="1"><nlm:aff id="af0002"><institution>Medicine and Dermatology and Translational Science Melanoma Program; University of Pittsburgh Cancer Institute; University of Pittsburgh</institution>; Pittsburgh, PA<country>USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Wells, Alan" sort="Wells, Alan" uniqKey="Wells A" first="Alan" last="Wells">Alan Wells</name><affiliation><nlm:aff id="af0001"><institution>Department of Pathology</institution></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af0003"><institution>Laboratory and Pathology Service; Pittsburgh VA Health System</institution>; Pittsburgh, PA<country>USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cell Adhesion & Migration</title><idno type="ISSN">1933-6918</idno><idno type="eISSN">1933-6926</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Tenascin-C (TNC), a multifunctional matricellular glyco-protein, is highly expressed in
the majority of melanoma cell lines and has been implicated in the progression of
melanoma. A growing body of evidence has implicated the role of TNC in the process of
invasion and metastasis for melanoma. However, the mechanism and individual signaling
pathways by which TNC drives melanoma progression have not been illuminated. Herein we
provide perspectives from the investigation of TNC in other settings that may hint at the
mechanistic role of TNC in this disease.</p></div></front></TEI><pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Adh Migr</journal-id><journal-id journal-id-type="iso-abbrev">Cell Adh Migr</journal-id><journal-id journal-id-type="pmc">KCAM</journal-id><journal-title-group><journal-title>Cell Adhesion & Migration</journal-title></journal-title-group><issn pub-type="ppub">1933-6918</issn><issn pub-type="epub">1933-6926</issn><publisher><publisher-name>Taylor & Francis</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25482624</article-id><article-id pub-id-type="pmc">4422811</article-id><article-id pub-id-type="publisher-id">972781</article-id><article-id pub-id-type="doi">10.4161/19336918.2014.972781</article-id><article-categories><subj-group subj-group-type="heading"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>Tenascin-C Signaling in melanoma</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Shao</surname><given-names>Hanshuang</given-names></name><xref ref-type="aff" rid="af0001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kirkwood</surname><given-names>John M</given-names></name><xref ref-type="aff" rid="af0002"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wells</surname><given-names>Alan</given-names></name><xref ref-type="aff" rid="af0001"><sup>1</sup></xref><xref ref-type="aff" rid="af0003"><sup>3</sup></xref><xref ref-type="corresp" rid="an0001"><sup>*</sup></xref></contrib><aff id="af0001"><label>1</label><institution>Department of Pathology</institution></aff><aff id="af0002"><label>2</label><institution>Medicine and Dermatology and Translational Science Melanoma Program; University of Pittsburgh Cancer Institute; University of Pittsburgh</institution>; Pittsburgh, PA<country>USA</country></aff><aff id="af0003"><label>3</label><institution>Laboratory and Pathology Service; Pittsburgh VA Health System</institution>; Pittsburgh, PA<country>USA</country></aff></contrib-group><author-notes><corresp id="an0001"><label>*</label>Correspondence to: Alan Wells; Email: <email xlink:href="wellsa@upmc.edu">wellsa@upmc.edu</email></corresp></author-notes><pub-date pub-type="collection"><season>Jan-Apr</season><year>2015</year></pub-date><pub-date pub-type="epub"><day>30</day><month>10</month><year>2014</year></pub-date><volume>9</volume><issue>1-2</issue><issue-title>Tenascins: Defining Their Role in Tissue Homeostasis and Cancer</issue-title><fpage seq="12">125</fpage><lpage>130</lpage><history><date date-type="received"><day>1</day><month>7</month><year>2014</year></date><date date-type="rev-recd"><day>8</day><month>10</month><year>2014</year></date><date date-type="accepted"><day>10</day><month>9</month><year>2014</year></date></history><permissions><copyright-statement>© 2015 Taylor & Francis Group, LLC</copyright-statement><copyright-year>2015</copyright-year><copyright-holder>Taylor & Francis Group, LLC</copyright-holder></permissions><self-uri content-type="pdf" xlink:href="kcam-09-125.pdf"></self-uri><abstract><p>Tenascin-C (TNC), a multifunctional matricellular glyco-protein, is highly expressed in
the majority of melanoma cell lines and has been implicated in the progression of
melanoma. A growing body of evidence has implicated the role of TNC in the process of
invasion and metastasis for melanoma. However, the mechanism and individual signaling
pathways by which TNC drives melanoma progression have not been illuminated. Herein we
provide perspectives from the investigation of TNC in other settings that may hint at the
mechanistic role of TNC in this disease.</p></abstract><kwd-group kwd-group-type="author"><title>Keywords</title><kwd>invasion</kwd><kwd>melanoma</kwd><kwd>survival</kwd><kwd>Tenascin-C</kwd></kwd-group><counts><fig-count count="3"></fig-count><table-count count="0"></table-count><ref-count count="53"></ref-count><page-count count="6"></page-count></counts></article-meta></front></pmc><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Shao, Hanshuang" sort="Shao, Hanshuang" uniqKey="Shao H" first="Hanshuang" last="Shao">Hanshuang Shao</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Kirkwood, John M" sort="Kirkwood, John M" uniqKey="Kirkwood J" first="John M" last="Kirkwood">John M. Kirkwood</name></noRegion><name sortKey="Wells, Alan" sort="Wells, Alan" uniqKey="Wells A" first="Alan" last="Wells">Alan Wells</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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