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dc.contributor.authorChang, Cheng
dc.contributor.authorGoel, Hira Lal
dc.contributor.authorGao, Huijie
dc.contributor.authorPursell, Bryan M.
dc.contributor.authorShultz, Leonard D.
dc.contributor.authorGreiner, Dale L.
dc.contributor.authorIngerpuu, Sulev
dc.contributor.authorPatarroyo, Manuel
dc.contributor.authorCao, Shiliang
dc.contributor.authorLim, Elgene
dc.contributor.authorMao, Junhao
dc.contributor.authorMcKee, Karen Kulju.
dc.contributor.authorYurchenco, Peter D.
dc.contributor.authorMercurio, Arthur M.
dc.date2022-08-11T08:09:19.000
dc.date.accessioned2022-08-23T16:26:16Z
dc.date.available2022-08-23T16:26:16Z
dc.date.issued2015-01-01
dc.date.submitted2015-04-24
dc.identifier.citation<p>Genes Dev. 2015 Jan 1;29(1):1-6. doi: 10.1101/gad.253682.114. <a href="http://dx.doi.org/10.1101/gad.253682.114">Link to article on publisher's site</a></p>
dc.identifier.issn0890-9369 (Linking)
dc.identifier.doi10.1101/gad.253682.114
dc.identifier.pmid25561492
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36528
dc.description.abstractUnderstanding how the extracellular matrix impacts the function of cancer stem cells (CSCs) is a significant but poorly understood problem. We report that breast CSCs produce a laminin (LM) 511 matrix that promotes self-renewal and tumor initiation by engaging the alpha6Bbeta1 integrin and activating the Hippo transducer TAZ. Although TAZ is important for the function of breast CSCs, the mechanism is unknown. We observed that TAZ regulates the transcription of the alpha5 subunit of LM511 and the formation of a LM511 matrix. These data establish a positive feedback loop involving TAZ and LM511 that contributes to stemness in breast cancer.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=25561492&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttp://dx.doi.org/10.1101/gad.253682.114
dc.rights<p>© 2015 Chang et al.; Published by Cold Spring Harbor Laboratory Press</p> <p id="x-x-x-x-x-x-x-p-3">This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see<a href="http://genesdev.cshlp.org/site/misc/terms.xhtml"> http://genesdev.cshlp.org/site/misc/terms.xhtml</a>). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at <a href="http://creativecommons.org/licenses/by-nc/4.0/">http://creativecommons.org/licenses/by-nc/4.0/</a>.</p>
dc.subjectBreast Neoplasms
dc.subjectExtracellular Matrix
dc.subjectFemale
dc.subjectHumans
dc.subjectIntegrin alpha6beta1
dc.subjectLaminin
dc.subjectLigands
dc.subjectNeoplastic Stem Cells
dc.subjectTranscription Factors
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectCells
dc.subjectDevelopmental Biology
dc.subjectMolecular Biology
dc.titleA laminin 511 matrix is regulated by TAZ and functions as the ligand for the alpha6Bbeta1 integrin to sustain breast cancer stem cells
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume29
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1021&amp;context=mccb_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/mccb_pubs/22
dc.identifier.contextkey7027668
refterms.dateFOA2022-08-23T16:26:16Z
html.description.abstract<p>Understanding how the extracellular matrix impacts the function of cancer stem cells (CSCs) is a significant but poorly understood problem. We report that breast CSCs produce a laminin (LM) 511 matrix that promotes self-renewal and tumor initiation by engaging the alpha6Bbeta1 integrin and activating the Hippo transducer TAZ. Although TAZ is important for the function of breast CSCs, the mechanism is unknown. We observed that TAZ regulates the transcription of the alpha5 subunit of LM511 and the formation of a LM511 matrix. These data establish a positive feedback loop involving TAZ and LM511 that contributes to stemness in breast cancer.</p>
dc.identifier.submissionpathmccb_pubs/22
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages1-6


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