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dc.contributor.authorBernard, D
dc.contributor.authorGil, J
dc.contributor.authorDumont, P
dc.contributor.authorRizzo, S
dc.contributor.authorMonte, D
dc.contributor.authorQuatannens, B
dc.contributor.authorHudson, D
dc.contributor.authorVisakorpi, T
dc.contributor.authorFuks, F
dc.contributor.authorde Launoit, Y
dc.date.accessioned2018-09-04T11:58:51Z
dc.date.issued2006-03-02
dc.identifier9
dc.identifier.citationONCOGENE, 2006, 25 pp. 1358 - 1366
dc.identifier.issn0950-9232
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2547
dc.identifier.doi10.1038/sj.onc.1209179
dc.description.abstractThe incidence of prostate cancer is increasing in western countries because of population aging. Prostate cancer begins as an androgen-dependent disease, but it can become androgen independent at a later stage or in tumors recurring after an antihormonal treatment. Although many genetic events have been described to be involved in androgen-dependent and/or -independent prostate cancer growth, little is known about the contribution of epigenetic events. Here we have examined the possibility that the methyl-CpG-binding protein MECP2 might play a role in controlling the growth of prostate cancer cells. Inhibition of MECP2 expression by stable short hairpin RNA stopped the growth of both normal and cancer human prostate cells. In addition, ectopic expression of the MECP2 conferred a growth advantage to human prostate cancer cells. More importantly, this expression allowed androgen-dependent cells to grow independently of androgen stimulation and to retain tumorigenic properties in androgen-depleted conditions. Analysis of signaling pathways showed that this effect is independent of androgen receptor signaling. Instead, MECP2 appears to act by maintaining a constant c-myc level during antihormonal treatment. We further show that MECP2-expressing cells possess a functional p53 pathway and are still responsive to chemotherapeutic drugs.
dc.format.extent1358 - 1366
dc.languageeng
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.titleThe methyl-CpG- binding protein MECP2 is required for prostate cancer cell growth
dc.typeJournal Article
rioxxterms.versionofrecord10.1038/sj.onc.1209179
rioxxterms.licenseref.startdate2006-03-02
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfONCOGENE
pubs.notesaffiliation: Bernard, D (Reprint Author), ULB, Fac Med, Lab Virol Mol, CP 614,808 Route Lennik, B-1070 Brussels, Belgium. ULB, Fac Med, Lab Virol Mol, B-1070 Brussels, Belgium. Imperial Coll Sch Med, MRC Clin Sci Ctr, London, England. Univ Sci & Technol, CNRS, UMR 8117, Inst Pasteur Lille,Inst Biol, Lille, France. Inst Canc Res, Prostate Stem Cell Lab, Sutton, Surrey, England. Tampere Univ Hosp, Tampere, Finland. keywords: methyl-CpG-binding protein; epigenetic; cancer; prostate; growth keywords-plus: ANDROGEN DEPRIVATION THERAPY; HISTONE DEACETYLASE COMPLEX; DNA METHYLATION; NEUROENDOCRINE DIFFERENTIATION; MOLECULAR-GENETICS; C-MYC; EXPRESSION; CARCINOMA; RECEPTOR; METHYLTRANSFERASE research-areas: Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity web-of-science-categories: Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity author-email: [email protected] researcherid-numbers: Gil, Jesus/C-7739-2012 Bernard, David/D-6265-2018 orcid-numbers: Gil, Jesus/0000-0002-4303-6260 Bernard, David/0000-0002-1557-2074 Visakorpi, Tapio/0000-0002-5004-0364 monte, didier/0000-0002-0613-6203 funding-acknowledgement: Medical Research Council [MC_U120085810] number-of-cited-references: 52 times-cited: 34 usage-count-last-180-days: 0 usage-count-since-2013: 2 journal-iso: Oncogene doc-delivery-number: 017QN unique-id: ISI:000235708200009 oa: gold_or_bronze da: 2018-09-04
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR
pubs.volume25
pubs.embargo.termsNot known
dc.contributor.icrauthorHudson, Daviden


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