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dc.contributor.authorSamanta, Sanjoy
dc.contributor.authorSun, Huayan
dc.contributor.authorGoel, Hira Lal
dc.contributor.authorPursell, Bryan M.
dc.contributor.authorChang, C.
dc.contributor.authorKhan, A.
dc.contributor.authorGreiner, Dale L.
dc.contributor.authorCao, S.
dc.contributor.authorLim, E.
dc.contributor.authorShultz, Leonard 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.issued2015-05-18
dc.date.submitted2015-11-16
dc.identifier.citationSamanta S, Sun H, Goel HL, Pursell B, Chang C, Khan A, Greiner DL, Cao S, Lim E, Shultz LD, Mercurio AM. IMP3 promotes stem-like properties in triple-negative breast cancer by regulating SLUG. Oncogene. 2015 May 18. doi: 10.1038/onc.2015.164. [Epub ahead of print] PubMed PMID: 25982283.
dc.identifier.issn1476-5594
dc.identifier.doi10.1038/onc.2015.164
dc.identifier.pmid25982283
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36529
dc.description.abstractIMP3 (insulin-like growth factor-2 mRNA binding protein 3) is an oncofetal protein whose expression is prognostic for poor outcome in several cancers. Although IMP3 is expressed preferentially in triple-negative breast cancer (TNBC), its function is poorly understood. We observed that IMP3 expression is significantly higher in tumor initiating than in non-tumor initiating breast cancer cells and we demonstrate that IMP3 contributes to self-renewal and tumor initiation, properties associated with cancer stem cells (CSCs). The mechanism by which IMP3 contributes to this phenotype involves its ability to induce the stem cell factor SOX2. IMP3 does not interact with SOX2 mRNA significantly or regulate SOX2 expression directly. We discovered that IMP3 binds avidly to SNAI2 (SLUG) mRNA and regulates its expression by binding to the 5' UTR. This finding is significant because SLUG has been implicated in breast CSCs and TNBC. Moreover, we show that SOX2 is a transcriptional target of SLUG. These data establish a novel mechanism of breast tumor initiation involving IMP3 and they provide a rationale for its association with aggressive disease and poor outcome.
dc.language.isoen_US
dc.publisherNature Publishing Group
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=25982283&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1038/onc.2015.164
dc.subjectCancer Biology
dc.titleIMP3 promotes stem-like properties in triple-negative breast cancer by regulating SLUG
dc.typeJournal Article
dc.source.journaltitleOncogene
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/mccb_pubs/23
dc.identifier.contextkey7846610
html.description.abstract<p>IMP3 (insulin-like growth factor-2 mRNA binding protein 3) is an oncofetal protein whose expression is prognostic for poor outcome in several cancers. Although IMP3 is expressed preferentially in triple-negative breast cancer (TNBC), its function is poorly understood. We observed that IMP3 expression is significantly higher in tumor initiating than in non-tumor initiating breast cancer cells and we demonstrate that IMP3 contributes to self-renewal and tumor initiation, properties associated with cancer stem cells (CSCs). The mechanism by which IMP3 contributes to this phenotype involves its ability to induce the stem cell factor SOX2. IMP3 does not interact with SOX2 mRNA significantly or regulate SOX2 expression directly. We discovered that IMP3 binds avidly to SNAI2 (SLUG) mRNA and regulates its expression by binding to the 5' UTR. This finding is significant because SLUG has been implicated in breast CSCs and TNBC. Moreover, we show that SOX2 is a transcriptional target of SLUG. These data establish a novel mechanism of breast tumor initiation involving IMP3 and they provide a rationale for its association with aggressive disease and poor outcome.</p>
dc.identifier.submissionpathmccb_pubs/23
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology


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