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dc.contributor.authorBernard, D
dc.contributor.authorMartinez-Leal, JF
dc.contributor.authorRizzo, S
dc.contributor.authorMartinez, D
dc.contributor.authorHudson, D
dc.contributor.authorVisakorpi, T
dc.contributor.authorPeters, G
dc.contributor.authorCarnero, A
dc.contributor.authorBeach, D
dc.contributor.authorGil, J
dc.date.accessioned2018-09-06T13:02:59Z
dc.date.issued2005-08-25
dc.identifier36
dc.identifier.citationONCOGENE, 2005, 24 pp. 5543 - 5551
dc.identifier.issn0950-9232
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2570
dc.identifier.doi10.1038/sj.onc.1208735
dc.description.abstractControl of cell proliferation by Polycomb group proteins (PcG) is an important facet of cellular homeostasis and its disruption can promote tumorigenesis. We recently described CBX7 as a novel PcG protein controlling the growth of normal cells. In an attempt to identify a putative role of CBX7 in tumorigenesis, we analysed CBX7 expression in a panel of cancer cell lines and primary tissues. CBX7 was highly expressed in three different prostate cancer cell lines and present at elevated levels in normal prostate. Ablation of CBX7 expression using short hairpin RNAs (shRNA) resulted in upregulation of p16(Ink4a) and p14(Arf) in both LNCaP and PC-3 prostate cell lines. CBX7 knockdown caused an impairment of cell growth that was dependent on the status of the p14(Arf)/p53 and p16(Ink4a)/Rb pathways in both normal and cancer prostate cells. CBX7 overexpression in LNCaP cells resulted in a slight growth advantage in both androgen-dependent and independent conditions. Moreover, CBX7 expression cooperated with c-Myc in rendering LNCaP cells insensitive to growth arrest by androgen receptor inhibition. Together, these data suggest that CBX7 represses p16(Ink4a) and p14(Arf) expression in normal and tumor-derived prostate cells, affecting their growth depending on the status of the p16(Ink4a)/Rb and the p14(Arf)/p53 pathways.
dc.format.extent5543 - 5551
dc.languageeng
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.titleCBX7 controls the growth of normal and tumor-derived prostate cells by repressing the Ink4a/Arf locus
dc.typeJournal Article
rioxxterms.versionofrecord10.1038/sj.onc.1208735
rioxxterms.licenseref.startdate2005-08-25
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfONCOGENE
pubs.notesaffiliation: Gil, J (Reprint Author), London Res Inst, Canc Res UK, Mol Oncol Lab, 44 Lincolns Inn Fields, London WC2A 3PX, England. London Res Inst, Canc Res UK, Mol Oncol Lab, London WC2A 3PX, England. Free Univ Brussels, Fac Med, Mol Virol Lab, Brussels, Belgium. Ctr Nacl Invest Oncol, Expt Therapeut Program, Madrid 28029, Spain. Inst Canc Res, Prostate Stem Cell Lab, Sutton SM2 5NG, Surrey, England. UCL, Wolfson Inst Biomed Res, London WC1E 6BT, England. Tampere Univ, Inst Med Technol, FIN-33014 Tampere, Finland. Tampere Univ Hosp, FIN-33014 Tampere, Finland. Ctr Cutaneous Biol, Inst Cell & Mol Sci, London E1 2AT, England. keywords: polycomb; prostate; CBX7; transformation keywords-plus: POLYCOMB-GROUP PROTEINS; MOLECULAR-GENETICS; STEM-CELLS; CANCER; EZH2; GENES; BMI-1; TRANSFORMATION; METHYLATION; MECHANISMS 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: Bernard, David/D-6265-2018 Gil, Jesus/C-7739-2012 IBIS, CANCER/P-3323-2015 Martinez Leal, Juan/N-6328-2013 orcid-numbers: Bernard, David/0000-0002-1557-2074 Gil, Jesus/0000-0002-4303-6260 Martinez Leal, Juan/0000-0002-7538-0875 Visakorpi, Tapio/0000-0002-5004-0364 Carnero, Amancio/0000-0003-4357-3979 number-of-cited-references: 43 times-cited: 88 usage-count-last-180-days: 0 usage-count-since-2013: 12 journal-iso: Oncogene doc-delivery-number: 956JN unique-id: ISI:000231296100002 oa: gold_or_bronze da: 2018-09-06
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR
pubs.volume24
pubs.embargo.termsNot known
dc.contributor.icrauthorHudson, Daviden


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