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dc.contributor.authorSamanta, Sanjoy
dc.contributor.authorGuru, Santosh
dc.contributor.authorElaimy, Ameer L.
dc.contributor.authorAmante, John J.
dc.contributor.authorOu, Jianhong
dc.contributor.authorYu, Jun
dc.contributor.authorZhu, Lihua Julie
dc.contributor.authorMercurio, Arthur M.
dc.date2022-08-11T08:09:50.000
dc.date.accessioned2022-08-23T16:45:27Z
dc.date.available2022-08-23T16:45:27Z
dc.date.issued2018-05-29
dc.date.submitted2018-07-27
dc.identifier.citation<p>Cell Rep. 2018 May 29;23(9):2559-2567. doi: 10.1016/j.celrep.2018.04.113. <a href="https://doi.org/10.1016/j.celrep.2018.04.113">Link to article on publisher's site</a></p>
dc.identifier.issn2211-1247 (Electronic)
dc.identifier.doi10.1016/j.celrep.2018.04.113
dc.identifier.pmid29847788
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40686
dc.description.abstractInsulin-like growth factor-2 mRNA-binding protein 3 (IMP3) is an oncofetal protein associated with many aggressive cancers and implicated in the function of breast cancer stem cells (CSCs). The mechanisms involved, however, are poorly understood. We observed that IMP3 facilitates the activation of TAZ, a transcriptional co-activator of Hippo signaling that is necessary for the function of breast CSCs. The mechanism by which IMP3 activates TAZ involves both mRNA stability and transcriptional regulation. IMP3 stabilizes the mRNA of an alternative WNT ligand (WNT5B) indirectly by repressing miR145-5p, which targets WNT5B, resulting in TAZ activation by alternative WNT signaling. IMP3 also facilitates the transcription of SLUG, which is necessary for TAZ nuclear localization and activation, by a mechanism that is also mediated by WNT5B. These results demonstrate that TAZ can be regulated by an mRNA-binding protein and that this regulation involves the integration of Hippo and alternative WNT-signaling pathways.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29847788&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsThis is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectRNA-binding protein
dc.subjectTAZ
dc.subjectWnt
dc.subjectbreast cancer
dc.subjectstem cells
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectNeoplasms
dc.titleIMP3 Stabilization of WNT5B mRNA Facilitates TAZ Activation in Breast Cancer
dc.typeJournal Article
dc.source.journaltitleCell reports
dc.source.volume23
dc.source.issue9
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4500&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3489
dc.identifier.contextkey12556173
refterms.dateFOA2022-08-23T16:45:27Z
html.description.abstract<p>Insulin-like growth factor-2 mRNA-binding protein 3 (IMP3) is an oncofetal protein associated with many aggressive cancers and implicated in the function of breast cancer stem cells (CSCs). The mechanisms involved, however, are poorly understood. We observed that IMP3 facilitates the activation of TAZ, a transcriptional co-activator of Hippo signaling that is necessary for the function of breast CSCs. The mechanism by which IMP3 activates TAZ involves both mRNA stability and transcriptional regulation. IMP3 stabilizes the mRNA of an alternative WNT ligand (WNT5B) indirectly by repressing miR145-5p, which targets WNT5B, resulting in TAZ activation by alternative WNT signaling. IMP3 also facilitates the transcription of SLUG, which is necessary for TAZ nuclear localization and activation, by a mechanism that is also mediated by WNT5B. These results demonstrate that TAZ can be regulated by an mRNA-binding protein and that this regulation involves the integration of Hippo and alternative WNT-signaling pathways.</p>
dc.identifier.submissionpathoapubs/3489
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages2559-2567


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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Except where otherwise noted, this item's license is described as This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).