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IAP regulation of metastasis

dc.contributor.authorMehrotra, Swarna
dc.contributor.authorLanguino, Lucia R.
dc.contributor.authorRaskett, Christopher M.
dc.contributor.authorMercurio, Arthur M.
dc.contributor.authorDohi, Takehiko
dc.contributor.authorAltieri, Dario C.
dc.date2022-08-11T08:08:02.000
dc.date.accessioned2022-08-23T15:39:53Z
dc.date.available2022-08-23T15:39:53Z
dc.date.issued2010-02-05
dc.date.submitted2010-11-07
dc.identifier.citationCancer Cell. 2010 Jan 19;17(1):53-64. <a href="http://dx.doi.org/10.1016/j.ccr.2009.11.021">Link to article on publisher's site</a>
dc.identifier.issn1535-6108 (Linking)
dc.identifier.doi10.1016/j.ccr.2009.11.021
dc.identifier.pmid20129247
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26277
dc.description.abstractInhibitor-of-Apoptosis (IAP) proteins contribute to tumor progression, but the requirements of this pathway are not understood. Here, we show that intermolecular cooperation between XIAP and survivin stimulates tumor cell invasion and promotes metastasis. This pathway is independent of IAP inhibition of cell death. Instead, a survivin-XIAP complex activates NF-kappaB, which in turn leads to increased fibronectin gene expression, signaling by beta1 integrins, and activation of cell motility kinases FAK and Src. Therefore, IAPs are direct metastasis genes, and their antagonists could provide antimetastatic therapies in patients with cancer.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20129247&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.ccr.2009.11.021
dc.subjectAnimals
dc.subjectBlotting, Western
dc.subjectCell Line, Tumor
dc.subjectFemale
dc.subjectHumans
dc.subjectInhibitor of Apoptosis Proteins
dc.subjectMale
dc.subjectMice
dc.subjectMicrotubule-Associated Proteins
dc.subject*Neoplasm Invasiveness
dc.subjectRNA, Small Interfering
dc.subjectSignal Transduction
dc.subjectCancer Biology
dc.subjectNeoplasms
dc.titleIAP regulation of metastasis
dc.typeJournal Article
dc.source.journaltitleCancer cell
dc.source.volume17
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/191
dc.identifier.contextkey1633417
html.description.abstract<p>Inhibitor-of-Apoptosis (IAP) proteins contribute to tumor progression, but the requirements of this pathway are not understood. Here, we show that intermolecular cooperation between XIAP and survivin stimulates tumor cell invasion and promotes metastasis. This pathway is independent of IAP inhibition of cell death. Instead, a survivin-XIAP complex activates NF-kappaB, which in turn leads to increased fibronectin gene expression, signaling by beta1 integrins, and activation of cell motility kinases FAK and Src. Therefore, IAPs are direct metastasis genes, and their antagonists could provide antimetastatic therapies in patients with cancer.</p>
dc.identifier.submissionpathcancerbiology_pp/191
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages53-64


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