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    EED embryonic ectoderm development [ Homo sapiens (human) ]

    Gene ID: 8726, updated on 2-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    EED related overgrowth: First report of multiple members in a single family.

    EED related overgrowth: First report of multiple members in a single family.
    Goel H, O'Donnell S, Edwards M.

    01/12/2024
    The PRC2 molecule EED is a target of epigenetic therapy for neuroblastoma.

    The PRC2 molecule EED is a target of epigenetic therapy for neuroblastoma.
    Shaliman D, Takenobu H, Sugino RP, Ohira M, Kamijo T.

    08/13/2022
    Embryonic Ectoderm Development (EED) as a Novel Target for Cancer Treatment.

    Embryonic Ectoderm Development (EED) as a Novel Target for Cancer Treatment.
    Cook N, Chen J, Zhou J, Wu D.

    02/19/2022
    Methylation of microRNA-338-5p by EED promotes METTL3-mediated translation of oncogene CDCP1 in gastric cancer.

    Methylation of microRNA-338-5p by EED promotes METTL3-mediated translation of oncogene CDCP1 in gastric cancer.
    Zhang F, Yan Y, Cao X, Zhang J, Li Y, Guo C., Free PMC Article

    07/31/2021
    PICOT binding to chromatin-associated EED negatively regulates cyclin D2 expression by increasing H3K27me3 at the CCND2 gene promoter.

    PICOT binding to chromatin-associated EED negatively regulates cyclin D2 expression by increasing H3K27me3 at the CCND2 gene promoter.
    Pandya P, Jethva M, Rubin E, Birnbaum RY, Braiman A, Isakov N., Free PMC Article

    09/26/2020
    BR-001, a potent inhibitor of the EED subunit of the PRC2 complex, suppresses tumor progression by modulating the tumor microenvironment.

    An Allosteric PRC2 Inhibitor Targeting EED Suppresses Tumor Progression by Modulating the Immune Response.
    Dong H, Liu S, Zhang X, Chen S, Kang L, Chen Y, Ma S, Fu X, Liu Y, Zhang H, Zou B.

    05/30/2020
    review the PRC2 complex and clinical syndromes of overgrowth and intellectual disability associated with core components EZH2, EED, and SUZ12

    PRC2-complex related dysfunction in overgrowth syndromes: A review of EZH2, EED, and SUZ12 and their syndromic phenotypes.
    Cyrus S, Burkardt D, Weaver DD, Gibson WT.

    05/9/2020
    Identification of mutations in the PRC2 components EED and SUZ12 in the majority of MPNSTs may imply noncanonical oncogenic activities of the intact component, EZH2, and provide new opportunities for therapeutic intervention.

    Malignant Peripheral Nerve Sheath Tumors: From Epigenome to Bedside.
    Korfhage J, Lombard DB., Free PMC Article

    05/2/2020
    Mutation in the EED gene is associated with Cohen-Gibson syndrome.

    EED and EZH2 constitutive variants: A study to expand the Cohen-Gibson syndrome phenotype and contrast it with Weaver syndrome.
    Griffiths S, Loveday C, Zachariou A, Behan LA, Chandler K, Cole T, D'Arrigo S, Dieckmann A, Foster A, Gibney J, Hunter M, Milani D, Pantaleoni C, Roche E, Sherlock M, Springer A, White SM, Childhood Overgrowth Collaboration, Tatton-Brown K.

    04/25/2020
    PICOT knock-down in Jurkat T cells resulted in a reduced histone H3 lysine 27 trimethylation (H3K27me3) at the PRC2 target gene, myelin transcription factor 1 (MYT1), suggesting that PICOT binding to EED alters PRC2-regulated transcriptional repression, and potentially contributes to the epigenetic regulation of chromatin silencing and remodeling.

    PICOT binding to the polycomb group protein, EED, alters H3K27 methylation at the MYT1 PRC2 target gene.
    Pandya P, Pasvolsky R, Babichev Y, Braiman A, Witte S, Altman A, Isakov N.

    11/2/2019
    Results report that EED presents a direct interaction with androgen receptor (AR). In the context of AR-positive prostate cancer, EED along with EZH2 regulate AR expression levels and its downstream targets.

    Polycomb group proteins EZH2 and EED directly regulate androgen receptor in advanced prostate cancer.
    Liu Q, Wang G, Li Q, Jiang W, Kim JS, Wang R, Zhu S, Wang X, Yan L, Yi Y, Zhang L, Meng Q, Li C, Zhao D, Qiao Y, Li Y, Gursel DB, Chinnaiyan AM, Chen K, Cao Q., Free PMC Article

    11/2/2019
    These findings identify Eed/PRC2 as necessary for maintenance of global gene silencing and terminal differentiation in b cells, and suggest a ''two-hit'' (chromatin and hyperglycemia) model of b cell dedifferentiation.

    The Polycomb-Dependent Epigenome Controls β Cell Dysfunction, Dedifferentiation, and Diabetes.
    Lu TT, Heyne S, Dror E, Casas E, Leonhardt L, Boenke T, Yang CH, Sagar, Arrigoni L, Dalgaard K, Teperino R, Enders L, Selvaraj M, Ruf M, Raja SJ, Xie H, Boenisch U, Orkin SH, Lynn FC, Hoffman BG, Grün D, Vavouri T, Lempradl AM, Pospisilik JA., Free PMC Article

    09/21/2019
    In silico modeling and calculations of the free energy changes resulting from these variants suggested that they not only destabilize the EED protein structure but also adversely affect interactions between EED, EZH2, and/or H3K27me3.

    Three additional patients with EED-associated overgrowth: potential mutation hotspots identified?
    Spellicy CJ, Peng Y, Olewiler L, Cathey SS, Rogers RC, Bartholomew D, Johnson J, Alexov E, Lee JA, Friez MJ, Jones JR.

    09/7/2019
    we present a patient with a clinical diagnosis of Weaver syndrome and novel de novo sequence variant in EED. Our observation together with previous reports [2, 3, 5] suggests that EED gene testing is warranted in patients with the overgrowth syndrome features and suspicion of Weaver syndrome with normal results for EZH2 gene sequencing.

    Novel de novo mutation affecting two adjacent aminoacids in the EED gene in a patient with Weaver syndrome.
    Smigiel R, Biernacka A, Biela M, Murcia-Pienkowski V, Szmida E, Gasperowicz P, Kosinska J, Kostrzewa G, Koppolu AA, Walczak A, Wawrzuta D, Rydzanicz M, Sasiadek M, Ploski R.

    09/8/2018
    Data suggest the polycomb repressive complex 2 subunits EZH2, SUZ12, and EED protein axis as promising therapeutic target for treating sarcoma.

    Prognostic implications of polycomb proteins ezh2, suz12, and eed1 and histone modification by H3K27me3 in sarcoma.
    Cho YJ, Kim SH, Kim EK, Han JW, Shin KH, Hu H, Kim KS, Choi YD, Kim S, Lee YH, Suh JS, Ahn JB, Chung HC, Noh SH, Rha SY, Jung ST, Kim HS., Free PMC Article

    08/25/2018
    we analyzed eight probands with clinically suspected Weaver syndrome by whole-exome sequencing and identified three mutations: a 25.4-kb deletion partially involving EZH2 and CUL1 ,a missense mutation , and a missense mutation in SUZ12 inherited from her father .In vitro functional analyses demonstrated that the identified EED and SUZ12 missense mutations cause decreased decreased trimethylation of lysine 27 of H3

    Mutations in genes encoding polycomb repressive complex 2 subunits cause Weaver syndrome.
    Imagawa E, Higashimoto K, Sakai Y, Numakura C, Okamoto N, Matsunaga S, Ryo A, Sato Y, Sanefuji M, Ihara K, Takada Y, Nishimura G, Saitsu H, Mizuguchi T, Miyatake S, Nakashima M, Miyake N, Soejima H, Matsumoto N.

    02/24/2018
    These findings support that Weaver syndrome is a disorder with locus heterogeneity and can be due to pathogenic variants in either EZH2 or EED. This case highlights the utility of exome sequencing as a clinical diagnostic tool for novel gene discovery as well as the importance of re-examination of exome data as new information about gene-disease associations becomes available.

    Novel EED mutation in patient with Weaver syndrome.
    Cooney E, Bi W, Schlesinger AE, Vinson S, Potocki L.

    10/28/2017
    we have found two unrelated families of different ethnicities, with a similar rare phenotype, both associated with de novo mutations in this member of the PRC2 complex, we are confident that EED is indeed a novel overgrowth gene.

    EED-associated overgrowth in a second male patient.
    Cohen AS, Gibson WT.

    04/8/2017
    Mutations of SUZ12 and EED are reported to have tumor suppressive functions. (Review)

    Mutations and deletions of PRC2 in prostate cancer.
    Jain P, Di Croce L.

    01/14/2017
    These results suggest that the SNPs of the EED gene might not be associated with susceptibility to CRC.

    EED gene polymorphism in patients with colorectal cancer.
    Seo GS, Yu JI, Chae SC, Park WC, Shin SR, Yoo ST, Choi SC, Lee SH.

    09/3/2016
    An integral role for EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2, is reported.

    The central role of EED in the orchestration of polycomb group complexes.
    Cao Q, Wang X, Zhao M, Yang R, Malik R, Qiao Y, Poliakov A, Yocum AK, Li Y, Chen W, Cao X, Jiang X, Dahiya A, Harris C, Feng FY, Kalantry S, Qin ZS, Dhanasekaran SM, Chinnaiyan AM., Free PMC Article

    10/31/2015
    Data show that overall enhancer of zeste 2 (EZH2), embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12) expression in the colorectal cancer (CRC) tissues was significantly increased than in the non-cancerous tissue.

    Expression and clinicopathological significance of EED, SUZ12 and EZH2 mRNA in colorectal cancer.
    Liu YL, Gao X, Jiang Y, Zhang G, Sun ZC, Cui BB, Yang YM.

    06/20/2015
    EED, a component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in epithelial-mesenchymal transition (EMT) of cancer cells induced by Transforming Growth Factor-beta (TGF-beta).

    EED regulates epithelial-mesenchymal transition of cancer cells induced by TGF-β.
    Oktyabri D, Tange S, Terashima M, Ishimura A, Suzuki T.

    02/14/2015
    Polycomb repressive complex 2 is recurrently inactivated through EED or SUZ12 loss in malignant peripheral nerve sheath tumors.

    PRC2 is recurrently inactivated through EED or SUZ12 loss in malignant peripheral nerve sheath tumors.
    Lee W, Teckie S, Wiesner T, Ran L, Prieto Granada CN, Lin M, Zhu S, Cao Z, Liang Y, Sboner A, Tap WD, Fletcher JA, Huberman KH, Qin LX, Viale A, Singer S, Zheng D, Berger MF, Chen Y, Antonescu CR, Chi P., Free PMC Article

    01/24/2015
    EZH2-EED is necessary and sufficient for binding to the lncRNA HOTAIR.

    Binding interactions between long noncoding RNA HOTAIR and PRC2 proteins.
    Wu L, Murat P, Matak-Vinkovic D, Murrell A, Balasubramanian S., Free PMC Article

    03/8/2014
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