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dc.contributor.authorValastyan, Scott John
dc.contributor.authorReinhardt, Ferenc
dc.contributor.authorBenaich, Nathan
dc.contributor.authorCalogrias, Diana
dc.contributor.authorSzász, Attila M.
dc.contributor.authorWang, Zhigang C.
dc.contributor.authorBrock, Jane E.
dc.contributor.authorRichardson, Andrea L.
dc.contributor.authorNathan Benaich
dc.contributor.authorWeinberg, Robert A
dc.date.accessioned2015-03-26T20:31:15Z
dc.date.available2015-03-26T20:31:15Z
dc.date.issued2009-06
dc.date.submitted2009-01
dc.identifier.issn00928674
dc.identifier.urihttp://hdl.handle.net/1721.1/96204
dc.description.abstractMicroRNAs are well suited to regulate tumor metastasis because of their capacity to coordinately repress numerous target genes, thereby potentially enabling their intervention at multiple steps of the invasion-metastasis cascade. We identify a microRNA exemplifying these attributes, miR-31, whose expression correlates inversely with metastasis in human breast cancer patients. Overexpression of miR-31 in otherwise-aggressive breast tumor cells suppresses metastasis. We deploy a stable microRNA sponge strategy to inhibit miR-31 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize. These phenotypes do not involve confounding influences on primary tumor development and are specifically attributable to miR-31-mediated inhibition of several steps of metastasis, including local invasion, extravasation or initial survival at a distant site, and metastatic colonization. Such pleiotropy is achieved via coordinate repression of a cohort of metastasis-promoting genes, including RhoA. Indeed, RhoA re-expression partially reverses miR-31-imposed metastasis suppression. These findings indicate that miR-31 uses multiple mechanisms to oppose metastasis.en_US
dc.description.sponsorshipMassachusetts Institute of Technology (Daniel K. Ludwig Foundation Cancer Research Professor)en_US
dc.description.sponsorshipAmerican Cancer Society (ACS Research Professor)en_US
dc.description.sponsorshipUnited States. Dept. of Defense (Breast Cancer Research Program Predoctoral Fellow)en_US
dc.description.sponsorshipUnited States. Dept. of Defense (Breast Cancer Research Program, DoD BCRP Idea Award))en_US
dc.description.sponsorshipHarvard University (Harvard Breast Cancer SPORE)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (RO1 CA078461)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (PO1 CA080111)en_US
dc.language.isoen_US
dc.publisherElsevier B.V.en_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.cell.2009.03.047en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceElsevieren_US
dc.titleA Pleiotropically Acting MicroRNA, miR-31, Inhibits Breast Cancer Metastasisen_US
dc.typeArticleen_US
dc.identifier.citationValastyan, Scott, Ferenc Reinhardt, Nathan Benaich, Diana Calogrias, Attila M. Szász, Zhigang C. Wang, Jane E. Brock, Andrea L. Richardson, and Robert A. Weinberg. “A Pleiotropically Acting MicroRNA, miR-31, Inhibits Breast Cancer Metastasis.” Cell 137, no. 6 (June 2009): 1032–1046. © 2009 Elsevier Inc.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentWhitehead Institute for Biomedical Researchen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.contributor.mitauthorValastyan, Scott Johnen_US
dc.contributor.mitauthorReinhardt, Ferencen_US
dc.contributor.mitauthorNathan Benaichen_US
dc.contributor.mitauthorWeinberg, Robert A.en_US
dc.relation.journalCellen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsValastyan, Scott; Reinhardt, Ferenc; Benaich, Nathan; Calogrias, Diana; Szász, Attila M.; Wang, Zhigang C.; Brock, Jane E.; Richardson, Andrea L.; Weinberg, Robert A.en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-0895-3557
mit.licensePUBLISHER_POLICYen_US


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