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Differentiation of human neuroblastoma recapitulates neural crest development.In our whole genome DNA methylation screening of tissue-specific differentiallymethylated regions (T-DMRs) and developmental stage specific differentially methylatedregions (DS-DMRs) we reported that the exon 5 CpG island (CpGi) of Zfp206 (human:ZNF206), which was required to maintain embryonic stem cells in a pluripotentstate, was one of potent brain and testis-specific T-DMRs in mice. In this studymethylation level of the CpG sites at Zfp206-exon 5 CpGi in mouse brain samplesat three different developmental stages (15-day-old embryo; E15, new born; NB,12-week adult; AD) were quantitatively analyzed and it was identified that Zfp206-exon5 CpGi was the DS-DMRs in mouse brain. In AD brains, Zfp206-exon 5 CpGi was significantlyhypomethylated and Zfp206 expression was repressed, compared with E15 and NB brains.Hence, methylation level of human 5'-end of CpGi at ZNF206-exon 5, which is homologousCpGi to mice, was analyzed in neuroblastomas. Although all four adrenal samplesshowed complete methylation at the homologous region, we found the hypomethylationin 7 out of 26 neuroblastomas and a significant association between the hypomethylationand poor prognosis. In neuroblastoma cell lines and specimens, the hypomethylationwas also associated with ZNF206 expression. These data indicated that the changesin DNA methylation levels at the Zfp206-exon 5 might be one of the important factorsduring neuronal development in mice and that the hypomethylation of the homologousregion induced ZNF206 expression in humans and was associated with human neuroblastomagenesis.Even though the function of ZNF206 and its expression regulation in neuroblastomaremain elusive, ZNF206 might be a candidate differentiation suppressor and prognosismarker in neuroblastoma.

DNA hypomethylation at the ZNF206-exon 5 CpG island associated with neuronal differentiation in mice and development of neuroblastoma in humans