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Loss of the retinoblastoma binding protein 2 (RBP2) histone demethylase suppresses tumorigenesis in mice lacking Rb1 or Men1

dc.contributor.authorLin, Wenchu
dc.contributor.authorCao, Jian
dc.contributor.authorLiu, Jiayun
dc.contributor.authorBeshiri, Michael L.
dc.contributor.authorFujiwara, Yuko
dc.contributor.authorFrancis, Joshua M.
dc.contributor.authorCherniack, Andrew D.
dc.contributor.authorGeisen, Christoph
dc.contributor.authorBlair, Lauren P.
dc.contributor.authorZou, Mike R.
dc.contributor.authorShen, Xiaohua
dc.contributor.authorLiu, Zongzhi
dc.contributor.authorGrisanzio, Chiara
dc.contributor.authorWatanabe, Hideo
dc.contributor.authorMinamishima, Yoji Andrew
dc.contributor.authorZhang, Qing
dc.contributor.authorKulkarni, Rohit N.
dc.contributor.authorSignoretti, Sabina
dc.contributor.authorRodig, Scott J.
dc.contributor.authorBronson, Roderick T.
dc.contributor.authorOrkin, Stuart H.
dc.contributor.authorTuck, David P.
dc.contributor.authorBenevolenskaya, Elizaveta V.
dc.contributor.authorKawamori, Dan
dc.contributor.authorMeyerson, Matthew L.
dc.contributor.authorKaelin Jr., William G.
dc.contributor.authorQin, Yan
dc.date.accessioned2012-04-20T15:34:27Z
dc.date.available2012-04-20T15:34:27Z
dc.date.issued2011-08
dc.date.submitted2011-05
dc.identifier.issn0027-8424
dc.identifier.issn1091-6490
dc.identifier.urihttp://hdl.handle.net/1721.1/70074
dc.description.abstractAberrations in epigenetic processes, such as histone methylation, can cause cancer. Retinoblastoma binding protein 2 (RBP2; also called JARID1A or KDM5A) can demethylate tri- and dimethylated lysine 4 in histone H3, which are epigenetic marks for transcriptionally active chromatin, whereas the multiple endocrine neoplasia type 1 (MEN1) tumor suppressor promotes H3K4 methylation. Previous studies suggested that inhibition of RBP2 contributed to tumor suppression by the retinoblastoma protein (pRB). Here, we show that genetic ablation of Rbp2 decreases tumor formation and prolongs survival in Rb1+/− mice and Men1-defective mice. These studies link RBP2 histone demethylase activity to tumorigenesis and nominate RBP2 as a potential target for cancer therapy.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant CA138631)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant CA076120)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant CA16359)en_US
dc.description.sponsorshipRaymond and Beverley Sackler Foundation (Fund for the Arts and Sciences)en_US
dc.description.sponsorshipCaring for Carcinoid Foundationen_US
dc.description.sponsorshipV Foundation for Cancer Research (V Scholar Award)en_US
dc.description.sponsorshipHoward Hughes Medical Institute (Investigator)en_US
dc.description.sponsorshipDoris Duke Charitable Foundationen_US
dc.description.sponsorshipBreast Cancer Allianceen_US
dc.description.sponsorshipAlexander and Margaret Stewart Trusten_US
dc.language.isoen_US
dc.publisherNational Academy of Sciences (U.S.)en_US
dc.relation.isversionofhttp://dx.doi.org/10.1073/pnas.1110104108en_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.sourcePNASen_US
dc.titleLoss of the retinoblastoma binding protein 2 (RBP2) histone demethylase suppresses tumorigenesis in mice lacking Rb1 or Men1en_US
dc.typeArticleen_US
dc.identifier.citationLin, W. et al. “Loss of the Retinoblastoma Binding Protein 2 (RBP2) Histone Demethylase Suppresses Tumorigenesis in Mice Lacking Rb1 or Men1.” Proceedings of the National Academy of Sciences 108.33 (2011): 13379–13386. Web.en_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technologyen_US
dc.contributor.approverMeyerson, Matthew L.
dc.contributor.mitauthorMeyerson, Matthew L.
dc.relation.journalProceedings of the National Academy of Sciences of the United States of Americaen_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.orderedauthorsLin, W.; Cao, J.; Liu, J.; Beshiri, M. L.; Fujiwara, Y.; Francis, J.; Cherniack, A. D.; Geisen, C.; Blair, L. P.; Zou, M. R.; Shen, X.; Kawamori, D.; Liu, Z.; Grisanzio, C.; Watanabe, H.; Minamishima, Y. A.; Zhang, Q.; Kulkarni, R. N.; Signoretti, S.; Rodig, S. J.; Bronson, R. T.; Orkin, S. H.; Tuck, D. P.; Benevolenskaya, E. V.; Meyerson, M.; Kaelin, W. G.; Yan, Q.en
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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