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

Zhaodi Gu, Kenichi Inomata, Hidetoshi Mitsui, Akira Horii

研究成果: Article査読

7 被引用数 (Scopus)

抄録

FBXW7 has been reported to be a candidate tumor suppressor gene on 4q31. Three isoforms (α-form, β-form, and γ-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 β-form in human gliomas. Because this form is the major FBXW7 isoform in the human brain, we elucidated the silencing mechanisms for the FBXW7 β-form in gliomas. No genetic alterations were found in the whole FBXW7 gene including putative promoter region of the β-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 β-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 β-form was highly suppressed and the CpG sequences in the promoter region of the FBXW7 β-form were heavily methylated. Our data suggest that the inactivation of the FBXW7 β-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 β-form in gliomas.

本文言語English
ページ(範囲)347-352
ページ数6
ジャーナルGenes and Genetic Systems
83
4
DOI
出版ステータスPublished - 2008
外部発表はい

ASJC Scopus subject areas

  • 分子生物学
  • 遺伝学

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