...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Genes & Genetic Systems >Promoter hypermethylation is not the major mechanism for inactivation of the FBXW7 beta-form in human gliomas
【24h】

Promoter hypermethylation is not the major mechanism for inactivation of the FBXW7 beta-form in human gliomas

机译：启动子高甲基化不是人类胶质瘤中FBXW7 beta形式失活的主要机制。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

FBXW7 has been reported to be a candidate tumor suppressor gene on 4q31. Three isoforms (alpha-form, beta-form, and gamma-form) of FBXW7 are produced from mRNAs with distinct 5' exons. Our previous study identified the specific suppression of the mRNA expression of the FBXW7 beta-form in human gliomas. Because this form is the major FBXW7 isoform in the human brain, we elucidated the silencing mechanisms for the FBXW7 beta-form in gliomas. No genetic alterations were found in the whole FBXW7 gene including putative promoter region of the beta-form. Treatments with 5-azacytidine and trichostatin A did not induce re-expression. A sodium bisulfite-modification assay indicated that CpG sequences in the promoter of FBXW7 beta-form were not methylated in glioma cells. Meanwhile we searched for the expression of FBXW7 and the sodium bisulfite sequences in normal human peripheral blood cells, and we surprisingly found that the mRNA expression of the FBXW7 beta-form was highly suppressed and the CpG sequences in the promoter region of the FBXW7 beta-form were heavily methylated. Our data suggest that the inactivation of the FBXW7 beta-form plays an important role in the pathogenesis of gliomas and that an unknown mechanism(s) other than mutation and methylation is the major cause of the suppression of the FBXW7 beta-form in gliomas.
机译：据报道，FBXW7是4q31的候选肿瘤抑制基因。 FBXW7的三种同工型（α形式，β形式和γ形式）由具有不同5'外显子的mRNA产生。我们先前的研究确定了人胶质瘤中FBXW7 beta形式的mRNA表达的特异性抑制。由于这种形式是人脑中主要的FBXW7亚型，因此我们阐明了胶质瘤中FBXW7β形式的沉默机制。在整个FBXW7基因（包括推定的β型启动子区域）中均未发现遗传改变。用5-氮杂胞苷和曲古抑菌素A处理不诱导再表达。亚硫酸氢钠修饰试验表明，在胶质瘤细胞中，FBXW7β-型启动子中的CpG序列未甲基化。同时，我们搜索了正常人外周血细胞中FBXW7的表达和亚硫酸氢钠的序列，我们惊讶地发现FBXW7 beta形式的mRNA表达受到高度抑制，并且FBXW7 beta-启动子区域的CpG序列形式被严重甲基化。我们的数据表明，FBXW7β形式的失活在神经胶质瘤的发病机理中起着重要作用，除了突变和甲基化以外，未知的机制是神经胶质瘤中FBXW7β形式被抑制的主要原因。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号