2009
DOI: 10.1038/onc.2009.122
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DNA methyltransferase-mediated transcriptional silencing in malignant glioma: a combined whole-genome microarray and promoter array analysis

Abstract: Epigenetic inactivation of tumor suppressor genes is a common feature in human cancer. Promoter hypermethylation and histone deacetylation are reversible epigenetic mechanisms associated with transcriptional regulation. DNA methyltransferases (DNMT1 and DNMT3b) regulate and maintain promoter methylation and are overexpressed in human cancer. We performed whole-genome microarray analysis to identify genes with altered expression after RNAi-induced suppression of DNMT in a glioblastoma multiforme (GBM) cell line… Show more

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Cited by 48 publications
(40 citation statements)
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“…In concordance with this suggestion is the classification of common and distinct promoter groups identified after RNA interference-mediated suppression of DNMT1 and DNMT3B. 56 Interestingly, whereas the expression levels of DNMT1 and DNMT3A remained unchanged in the UHRF1 knockdown clones, there was a significant increase of DNMT3B expression in the absence of any methylation change of its promoter. The reasons behind the increase of DNMT3B expression upon UHRF1 knockdown are not currently clear.…”
Section: Discussionmentioning
confidence: 59%
“…In concordance with this suggestion is the classification of common and distinct promoter groups identified after RNA interference-mediated suppression of DNMT1 and DNMT3B. 56 Interestingly, whereas the expression levels of DNMT1 and DNMT3A remained unchanged in the UHRF1 knockdown clones, there was a significant increase of DNMT3B expression in the absence of any methylation change of its promoter. The reasons behind the increase of DNMT3B expression upon UHRF1 knockdown are not currently clear.…”
Section: Discussionmentioning
confidence: 59%
“…In this study, we found that the upregulation of DNMT1 expression associated with gliomas malignancy is observed in gliomas specimens. Selective depletion of DNMT1 has been shown to induce demethylation of promoters and re-expression of the silenced genes, including tumor suppressor genes or tumor suppressive miRNAs, due to hypermethylation (31,32). Here, we demonstrated that knockdown of DNMT1 inhibited the growth of glioma cells and induced apoptosis of glioma cells, and reversed the methylation of MEG promoter and subsequently restored MEG3 expression.…”
Section: Discussionmentioning
confidence: 72%
“…Although it has been accepted that miR-29s could restore the expression of tumor suppressors by silencing DNMT3A/3B [4,18,[23][24][25][26], the real mechanisms are still controversial. For example, Foltz et al found the re-expression of tumor suppressors in glioma cells after DNMT silencing was not associated with promoter demethylation, but rather with the changes of histone methylation and chromatin conformation [27]. This implies that the anti-glioma effects of the miR-29s/DNMTs pathway deserve further study.…”
Section: Discussionmentioning
confidence: 99%