Significant Reduction of WT1 Gene Expression, Possibly Due to Epigenetic Alteration in Wilms' Tumor

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  • Satoh Yuji
    Division of Molecular Biology and Genetics, Department of Biomolecular Sciences, Saga Medical School Department of Urology, Saga Medical School
  • Nakagawachi Tetsuji
    Division of Molecular Biology and Genetics, Department of Biomolecular Sciences, Saga Medical School
  • Nakadate Hisaya
    Department of Pediatrics, Kitasato University Hospital
  • Kaneko Yasuhiko
    Department of Cancer Chemotherapy, Saitama Cancer Center Hospital
  • Masaki Zenjiro
    Department of Urology, Saga Medical School
  • Mukai Tsunehiro
    Division of Molecular Biology and Genetics, Department of Biomolecular Sciences, Saga Medical School
  • Soejima Hidenobu
    Division of Molecular Biology and Genetics, Department of Biomolecular Sciences, Saga Medical School

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  • Significant Reduction of <i>WT1</i> Gene Expression, Possibly Due to Epigenetic Alteration in Wilms' Tumor

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WT1 at 11p13 is a tumor suppressor gene, an aberration of which causes Wilms' tumor (WT). Since WT1 expression is reduced in a certain poroportion of WTs and its mutation is found only in 10-20% of WTs, we examined WT1 gene silencing due to epigenetic alteration in a total of 22 WTs. WT1 expression was significantly reduced in half of WTs without any mutation in the WT1 gene itself, suggesting that the reduction of expression was possibly epigenetic. We found promoter hypermethylation in one WT with loss of heterozygosity (LOH) and showed that promoter methylation reduced reporter gene activity by a reporter assay. These data suggested that methylation was an epigenetic mechanism leading to WT1 silencing and that the expression-reduced allele by hypermethylation combined with LOH was consistent with the revised twohit model. In addition, as the β-catenin mutation is frequently associated with the WT1 mutation, the association of WT1 silencing with the β-catenin mutation was also investigated. β-catenin mutated in only one WT without WT1 silencing, suggesting that the β-catenin mutation was not associated with the reduction of WT1 expression.

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