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    Identification of candidate tumour suppressor genes frequently methylated in renal cell carcinoma.

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    Authors
    Morris, M R
    Ricketts, C
    Gentle, D
    Abdulrahman, M
    Clarke, Noel W
    Brown, Michael D
    Kishida, T
    Yao, M
    Latif, F
    Maher, E R
    Affiliation
    Cancer Research UK Renal Molecular Oncology Group, University of Birmingham, Birmingham, UK.
    Issue Date
    2010-04-08
    
    Metadata
    Show full item record
    Abstract
    Promoter region hyermethylation and transcriptional silencing is a frequent cause of tumour suppressor gene (TSG) inactivation in many types of human cancers. Functional epigenetic studies, in which gene expression is induced by treatment with demethylating agents, may identify novel genes with tumour-specific methylation. We used high-density gene expression microarrays in a functional epigenetic study of 11 renal cell carcinoma (RCC) cell lines. Twenty-eight genes were then selected for analysis of promoter methylation status in cell lines and primary RCC. Eight genes (BNC1, PDLIM4, RPRM, CST6, SFRP1, GREM1, COL14A1 and COL15A1) showed frequent (>30% of RCC tested) tumour-specific promoter region methylation. Hypermethylation was associated with transcriptional silencing. Re-expression of BNC1, CST6, RPRM and SFRP1 suppressed the growth of RCC cell lines and RNA interference knock-down of BNC1, SFRP1 and COL14A1 increased the growth of RCC cell lines. Methylation of BNC1 or COL14A1 was associated with a poorer prognosis independent of tumour size, stage or grade. The identification of these epigenetically inactivated candidate RCC TSGs can provide insights into renal tumourigenesis and a basis for developing novel therapies and biomarkers for prognosis and detection.
    Citation
    Identification of candidate tumour suppressor genes frequently methylated in renal cell carcinoma. 2010, 29 (14):2104-17 Oncogene
    Journal
    Oncogene
    URI
    http://hdl.handle.net/10541/109387
    DOI
    10.1038/onc.2009.493
    PubMed ID
    20154727
    Type
    Article
    Language
    en
    ISSN
    1476-5594
    ae974a485f413a2113503eed53cd6c53
    10.1038/onc.2009.493
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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