We are analyzing https://link.springer.com/article/10.1007/s11060-010-0520-2.

Title:
Epigenetic regulation of DNA methyltransferases: DNMT1 and DNMT3B in gliomas | Journal of Neuro-Oncology
Description:
The role of epigenetics and significance of aberrant gene regulation in etiology of cancer is a well-established phenomenon. The hallmark of cancer epigenetics is aberrant DNA methylation consisting of global hypomethylation and regional hypermethylation of tumor suppressor genes (TSGs) by DNA methyltransferases (DNMTs). In mammals, DNA methylation is catalyzed by DNMTs encoded by DNMT1, DNMT3A, and DNMT3B. Interestingly, little is known about variation in the methylation status of epigenetic regulators themselves in gliomas. Here, we report significant overexpression of DNMT1 and DNMT3B. A study of the methylation status and histone modifications at the promoter region of DNA methyltransferase I (DNMT1) gene revealed an unmethylated DNA promoter, similar to that detected in normal brain tissues. However, a differential histone code with distinct euchromatin marks—AcH3, AcH4, and H3k4me2—was specifically detected in tumors, unlike in normal brain tissues, which were found predominantly enriched with heterochromatin marks such as H3K9me2 and H3K27me3. In contrast, a differential methylation pattern of DNMT3B gene promoter occurred in glioma tumors, wherein it was found hypomethylated. Transcriptional silencing by CpG island methylation is a prevalent mechanism for inactivation of TSGs. Inhibiting DNMTs by 5-azacytidine (DNMT inhibitor) treatment led to significant inhibition of expression of DNMT1 and DNMT3B and enhanced expression of TSGs such as PTEN and p21 analyzed in this study. Our studies have identified effects of increased presence of DNMTs on inhibition of tumor suppressors that are epigenetically silenced in gliomas, thereby leading to aberrant regulation of cell cycle progression and failure to maintain genomic stability.
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Keywords {🔍}

article, google, scholar, pubmed, cas, cancer, dna, methylation, human, res, dnmt, expression, cell, dnmtb, tumor, gene, genes, histone, methyltransferases, gliomas, methyltransferase, cells, baylin, promoter, content, epigenetic, dnmts, brain, stem, privacy, cookies, journal, regulation, shiras, hypermethylation, suppressor, dnmta, tumors, cpg, access, biol, novo, herman, india, analysis, data, information, publish, research, search,

Topics {✒️}

s1 q-rt-pcr expression month download article/chapter s2 qrt-pcr analyses covalent histone modifications—miswritten multiple tumor-related genes c-met autocrine activation peri-centromeric satellite regions tumor suppressor genes distinct euchromatin marks—ach3 tumor suppressor micrornas histone acetylation patterns polycomb target genes full article pdf human gapdh controls faint pcr product neuro-oncology aims neural stem cells de novo methylation privacy choices/manage cookies cancer stem cells anjali shiras dna methylation machinery dna methylation errors stepwise dna methylation abnormal dna methylation human cell lines hemimethylated target sites chip data cell cycle progression cancer cell survival electronic supplementary material aberrant gene regulation papillary glioneuronal tumor unmethylated dna promoter differential methylation pattern concordant methylation behaviours cpg island methylation nih 3t3 cells differential histone code san miguel jf hamilton sr acetylated histone h3 histone h3 lysine 4 entamoeba histolytica dna human dna methyltransferases human cancer cells poorer tumor differentiation histone modifications high-grade gliomas trna methyltransferase dnmt2

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         headline:Epigenetic regulation of DNA methyltransferases: DNMT1 and DNMT3B in gliomas
         description:The role of epigenetics and significance of aberrant gene regulation in etiology of cancer is a well-established phenomenon. The hallmark of cancer epigenetics is aberrant DNA methylation consisting of global hypomethylation and regional hypermethylation of tumor suppressor genes (TSGs) by DNA methyltransferases (DNMTs). In mammals, DNA methylation is catalyzed by DNMTs encoded by DNMT1, DNMT3A, and DNMT3B. Interestingly, little is known about variation in the methylation status of epigenetic regulators themselves in gliomas. Here, we report significant overexpression of DNMT1 and DNMT3B. A study of the methylation status and histone modifications at the promoter region of DNA methyltransferase I (DNMT1) gene revealed an unmethylated DNA promoter, similar to that detected in normal brain tissues. However, a differential histone code with distinct euchromatin marks—AcH3, AcH4, and H3k4me2—was specifically detected in tumors, unlike in normal brain tissues, which were found predominantly enriched with heterochromatin marks such as H3K9me2 and H3K27me3. In contrast, a differential methylation pattern of DNMT3B gene promoter occurred in glioma tumors, wherein it was found hypomethylated. Transcriptional silencing by CpG island methylation is a prevalent mechanism for inactivation of TSGs. Inhibiting DNMTs by 5-azacytidine (DNMT inhibitor) treatment led to significant inhibition of expression of DNMT1 and DNMT3B and enhanced expression of TSGs such as PTEN and p21 analyzed in this study. Our studies have identified effects of increased presence of DNMTs on inhibition of tumor suppressors that are epigenetically silenced in gliomas, thereby leading to aberrant regulation of cell cycle progression and failure to maintain genomic stability.
         datePublished:2011-01-13T00:00:00Z
         dateModified:2011-01-13T00:00:00Z
         pageStart:483
         pageEnd:494
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            Histone modifications
            Acetylation
            DNA methylation
            MS-PCR
            ChIP assay
            Oncology
            Neurology
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      headline:Epigenetic regulation of DNA methyltransferases: DNMT1 and DNMT3B in gliomas
      description:The role of epigenetics and significance of aberrant gene regulation in etiology of cancer is a well-established phenomenon. The hallmark of cancer epigenetics is aberrant DNA methylation consisting of global hypomethylation and regional hypermethylation of tumor suppressor genes (TSGs) by DNA methyltransferases (DNMTs). In mammals, DNA methylation is catalyzed by DNMTs encoded by DNMT1, DNMT3A, and DNMT3B. Interestingly, little is known about variation in the methylation status of epigenetic regulators themselves in gliomas. Here, we report significant overexpression of DNMT1 and DNMT3B. A study of the methylation status and histone modifications at the promoter region of DNA methyltransferase I (DNMT1) gene revealed an unmethylated DNA promoter, similar to that detected in normal brain tissues. However, a differential histone code with distinct euchromatin marks—AcH3, AcH4, and H3k4me2—was specifically detected in tumors, unlike in normal brain tissues, which were found predominantly enriched with heterochromatin marks such as H3K9me2 and H3K27me3. In contrast, a differential methylation pattern of DNMT3B gene promoter occurred in glioma tumors, wherein it was found hypomethylated. Transcriptional silencing by CpG island methylation is a prevalent mechanism for inactivation of TSGs. Inhibiting DNMTs by 5-azacytidine (DNMT inhibitor) treatment led to significant inhibition of expression of DNMT1 and DNMT3B and enhanced expression of TSGs such as PTEN and p21 analyzed in this study. Our studies have identified effects of increased presence of DNMTs on inhibition of tumor suppressors that are epigenetically silenced in gliomas, thereby leading to aberrant regulation of cell cycle progression and failure to maintain genomic stability.
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      dateModified:2011-01-13T00:00:00Z
      pageStart:483
      pageEnd:494
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         Tumor suppressor genes
         Histone modifications
         Acetylation
         DNA methylation
         MS-PCR
         ChIP assay
         Oncology
         Neurology
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