Trichostatin A down-regulate DNA methyltransferase 1 in Jurkat T cells

Januchowski, Radosław; Dąbrowski, Mikołaj; Ofori, Harold; Jagodzińśki, Paweł P.

doi:10.1016/j.canlet.2006.03.010

Cited by 59 publications

(42 citation statements)

References 18 publications

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“…This effect was unique to KG-1 cells as TSA was insufficient for p15INK4b reactivation or changes in DNA methylation in AML-193 or KG-1a cells. Although TSA has previously been reported to repress the expression of DNMTs, 33,34 we observed only slight repression of DNMT3a and no alteration in DNMT 1 or 3b protein levels in TSA-treated KG-1 cells (supplemental Figure 10). Combined 5-aza-dC and TSA treatment caused loss of p15INK4b DNA methylation in KG-1 and AML-193 cells.…”

Section: Epigenetic Therapies Induce H3k4me3 At the P15ink4b Promotermentioning

confidence: 47%

“…The unexpected reactivation and demethylation of p15INK4b in KG-1 cells by the treatment with the HDAC inhibitor TSA are consistent with previous reports for E-cadherin and RAR␤2 in HEK 293 cells. 47 Although TSA has been demonstrated to repress the expression of DNMTs, 33,34 we have observed only slight repression of DNMT3a and no alteration of DNMT1 or 3b in KG-1 cells treated with 5-aza-dC or TSA (supplemental Figure 10). The short duration (12 hours) of TSA treatment in our experiments suggests that DNA methylation loss may have occurred through an active process.…”

Section: Discussionmentioning

confidence: 69%

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Signatures of polycomb repression and reduced H3K4 trimethylation are associated with p15INK4b DNA methylation in AML

Paul

Bies

Small

et al. 2010

Blood

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Section: Epigenetic Therapies Induce H3k4me3 At the P15ink4b Promotermentioning

confidence: 47%

Section: Discussionmentioning

confidence: 69%

Signatures of polycomb repression and reduced H3K4 trimethylation are associated with p15INK4b DNA methylation in AML

Paul

Bies

Small

et al. 2010

Blood

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“…Next, the DNA methylation status of the Nestin 5 0 enhancer was assessed in TSA-treated P19 EC cells. TSA can induce not only gene-specific but also global DNA demethylation [26,27]; TSA-induced demethylation has been attributed to Dnmt1 and Dnmt3b downregulation [28,29]. Onset of Nestin 5 0 enhancer demethylation was observed in P19 EC cells after 16 hours of TSA treatment, with a methylation rate of only 30%, which is about twofold lower than that in untreated P19 EC cells and even lower than that in P19 EC cells after 24 hours of 5-aza-dC treatment (Fig.…”

Section: Dna Demethylation Is Not Sufficient To Mediate Activation Ofmentioning

confidence: 99%

Epigenetic Hierarchy Governing Nestin Expression

et al. 2009

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Nestin is an intermediate filament protein expressed specifically in neural stem cells and progenitor cells of the central nervous system. DNA demethylation and histone modifications are two types of epigenetic modifications working in a coordinate or synergistic manner to regulate the expression of various genes. This study investigated and elucidated the epigenetic regulation of Nestin gene expression during embryonic differentiation along the neural cell lineage. Nestin exhibits differential DNA methylation and histone acetylation patterns in Nestin-expressing and nonexpressing cells. In P19 embryonic carcinoma cells, activation of Nestin expression is mediated by both trichostatin A and 5-aza-2 0 -deoxycytidine treatment, concomitant with histone acetylation, but not with DNA demethylation. Nestin transcription is also mediated by treatment with retinoic acid, again in the absence of DNA demethylation. Thus, histone acetylation is sufficient to mediate the activation of Nestin transcription. This study proposed that the regulation of Nestin gene expression can be used as a model to study the epigenetic regulation of gene expression mediated by histone acetylation, but not by DNA demethylation.

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“…In the human colorectal carcinoma cell line, TSA treatment does not affect the DNA methylation status of the CpG islands of two silent genes that were heavily methylated (Cameron et al, 1999). TSA treatment reduces mRNA and protein levels of DNMT3B in human endometrial cells and those of DNMT1 in Jurkat T cells, respectively (Xiong et al, 2005;Januchowski et al, 2007). Therefore, there seems to be in each a dependency between the histone acetylation and DNA methylation.…”

Section: Dna Methylation and Other Histone Modificationsmentioning

confidence: 97%

Interplay between DNA methylation, histone modification and chromatin remodeling in stem cells and during development

Ikegami¹,

Ohgane²,

Tanaka³

et al. 2009

Int. J. Dev. Biol.

106

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Genes constitute only a small proportion of the mammalian genome, the majority of which is composed of non-genic repetitive elements including interspersed repeats and satellites. A unique feature of the mammalian genome is that there are numerous tissue-dependent, differentially methylated regions (T-DMRs) in the non-repetitive sequences, which include genes and their regulatory elements. The epigenetic status of T-DMRs varies from that of repetitive elements and constitutes the DNA methylation profile genome-wide. Since the DNA methylation profile is specific to each cell and tissue type, much like a fingerprint, it can be used as a means of identification. The formation of DNA methylation profiles is the basis for cell differentiation and development in mammals. The epigenetic status of each T-DMR is regulated by the interplay between DNA methyltransferases, histone modification enzymes, histone subtypes, non-histone nuclear proteins and non-coding RNAs. In this review, we will discuss how these epigenetic factors cooperate to establish cell-and tissue-specific DNA methylation profiles. KEY WORDS: epigenetics, DNA methylation, T-DMR, histone modification, chromatin remodeling Epigenetic systems in mammalian developmentIn unicellular organisms, each individual cell uses almost all of the genomic information and displays an essentially identical phenotype. In contrast, in mammals there are at least a few hundred different cell types based on a variety of physiological and morphological criteria. All of these cell types are derived from a single fertilized egg. The differentiation of each cell type is achieved without changes in DNA sequence, but through the coordinated utilization of subsets of genes. In order to achieve the proper temporal and spatial regulation of these genes throughout development, a set of epigenetic mechanisms are employed, which includes histone modifications and DNA methylation (Shiota, 2004;Lieb et al., 2006).In mammals, DNA methylation occurs through DNA methyltransferases (Dnmts) that operate within 5'-CG-3' dinucleInt.

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Trichostatin A down-regulate DNA methyltransferase 1 in Jurkat T cells

Cited by 59 publications

References 18 publications

Signatures of polycomb repression and reduced H3K4 trimethylation are associated with p15INK4b DNA methylation in AML

Signatures of polycomb repression and reduced H3K4 trimethylation are associated with p15INK4b DNA methylation in AML

Epigenetic Hierarchy Governing Nestin Expression

Interplay between DNA methylation, histone modification and chromatin remodeling in stem cells and during development

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