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Aberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus.

Aberrant promoter DNA-hypermethylation and repressive chromatin constitutes a frequent mechanism of gene inactivation in cancer. There is great interest in dissecting the mechanisms underlying this abnormal silencing. Studies have shown changes in the nuclear organization of chromatin in tumor cells... Full description

Journal Title: Cancer research October 15, 2010, Vol.70(20), pp.8015-8024
Main Author: Easwaran, Hariharan P
Other Authors: Van Neste, Leander , Cope, Leslie , Sen, Subhojit , Mohammad, Helai P , Pageau, Gayle J , Lawrence, Jeanne B , Herman, James G , Schuebel, Kornel E , Baylin, Stephen B
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1538-7445 ; DOI: 10.1158/0008-5472.CAN-10-0765
Link: http://search.proquest.com/docview/758836514/?pq-origsite=primo
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title: Aberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus.
format: Article
creator:
  • Easwaran, Hariharan P
  • Van Neste, Leander
  • Cope, Leslie
  • Sen, Subhojit
  • Mohammad, Helai P
  • Pageau, Gayle J
  • Lawrence, Jeanne B
  • Herman, James G
  • Schuebel, Kornel E
  • Baylin, Stephen B
subjects:
  • Adaptor Proteins, Signal Transducing–Genetics
  • Cell Line, Tumor–Genetics
  • Cell Nucleus–Metabolism
  • Cpg Islands–Genetics
  • DNA Methylation–Genetics
  • Epigenesis, Genetic–Genetics
  • Gene Expression Profiling–Genetics
  • Gene Expression Regulation, Neoplastic–Genetics
  • Gene Silencing–Genetics
  • Genome-Wide Association Study–Genetics
  • Humans–Genetics
  • In Situ Hybridization–Genetics
  • In Situ Hybridization, Fluorescence–Genetics
  • Intercellular Adhesion Molecule-1–Genetics
  • Microsatellite Repeats–Genetics
  • Mutl Protein Homolog 1–Genetics
  • Neoplasms–Genetics
  • Nuclear Proteins–Genetics
  • Proto-Oncogene Proteins–Genetics
  • Reverse Transcriptase Polymerase Chain Reaction–Genetics
  • Adaptor Proteins, Signal Transducing
  • Mlh1 Protein, Human
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Sfrp4 Protein, Human
  • Intercellular Adhesion Molecule-1
  • Mutl Protein Homolog 1
ispartof: Cancer research, October 15, 2010, Vol.70(20), pp.8015-8024
description: Aberrant promoter DNA-hypermethylation and repressive chromatin constitutes a frequent mechanism of gene inactivation in cancer. There is great interest in dissecting the mechanisms underlying this abnormal silencing. Studies have shown changes in the nuclear organization of chromatin in tumor cells as well as the association of aberrant methylation with long-range silencing of neighboring genes. Furthermore, certain tumors show a high incidence of promoter methylation termed as the CpG island methylator phenotype. Here, we have analyzed the role of nuclear chromatin architecture for genes in hypermethylated inactive versus nonmethylated active states and its relation with long-range silencing and CpG island methylator phenotype. Using combined immunostaining for active/repressive chromatin marks and fluorescence in situ hybridization in colorectal cancer cell lines, we show that aberrant silencing of these genes occurs without requirement for their being positioned at heterochromatic domains. Importantly, hypermethylation, even when associated with long-range epigenetic silencing of neighboring genes, occurs independent of their euchromatic or heterochromatic location. Together, these results indicate that, in cancer, extensive changes around promoter chromatin of individual genes or gene clusters could potentially occur locally without preference for nuclear position and/or causing repositioning. These findings have important implications for understanding relationships between nuclear organization and gene expression patterns in cancer. Cancer Res; 70(20); 8015-24. [copy ]2010 AACR.
language: eng
source:
identifier: E-ISSN: 1538-7445 ; DOI: 10.1158/0008-5472.CAN-10-0765
fulltext: fulltext
issn:
  • 15387445
  • 1538-7445
url: Link


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titleAberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus.
creatorEaswaran, Hariharan P ; Van Neste, Leander ; Cope, Leslie ; Sen, Subhojit ; Mohammad, Helai P ; Pageau, Gayle J ; Lawrence, Jeanne B ; Herman, James G ; Schuebel, Kornel E ; Baylin, Stephen B
contributorEaswaran, Hariharan P (correspondence author) ; Easwaran, Hariharan P (record owner)
ispartofCancer research, October 15, 2010, Vol.70(20), pp.8015-8024
identifierE-ISSN: 1538-7445 ; DOI: 10.1158/0008-5472.CAN-10-0765
subjectAdaptor Proteins, Signal Transducing–Genetics ; Cell Line, Tumor–Genetics ; Cell Nucleus–Metabolism ; Cpg Islands–Genetics ; DNA Methylation–Genetics ; Epigenesis, Genetic–Genetics ; Gene Expression Profiling–Genetics ; Gene Expression Regulation, Neoplastic–Genetics ; Gene Silencing–Genetics ; Genome-Wide Association Study–Genetics ; Humans–Genetics ; In Situ Hybridization–Genetics ; In Situ Hybridization, Fluorescence–Genetics ; Intercellular Adhesion Molecule-1–Genetics ; Microsatellite Repeats–Genetics ; Mutl Protein Homolog 1–Genetics ; Neoplasms–Genetics ; Nuclear Proteins–Genetics ; Proto-Oncogene Proteins–Genetics ; Reverse Transcriptase Polymerase Chain Reaction–Genetics ; Adaptor Proteins, Signal Transducing ; Mlh1 Protein, Human ; Nuclear Proteins ; Proto-Oncogene Proteins ; Sfrp4 Protein, Human ; Intercellular Adhesion Molecule-1 ; Mutl Protein Homolog 1
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descriptionAberrant promoter DNA-hypermethylation and repressive chromatin constitutes a frequent mechanism of gene inactivation in cancer. There is great interest in dissecting the mechanisms underlying this abnormal silencing. Studies have shown changes in the nuclear organization of chromatin in tumor cells as well as the association of aberrant methylation with long-range silencing of neighboring genes. Furthermore, certain tumors show a high incidence of promoter methylation termed as the CpG island methylator phenotype. Here, we have analyzed the role of nuclear chromatin architecture for genes in hypermethylated inactive versus nonmethylated active states and its relation with long-range silencing and CpG island methylator phenotype. Using combined immunostaining for active/repressive chromatin marks and fluorescence in situ hybridization in colorectal cancer cell lines, we show that aberrant silencing of these genes occurs without requirement for their being positioned at heterochromatic domains. Importantly, hypermethylation, even when associated with long-range epigenetic silencing of neighboring genes, occurs independent of their euchromatic or heterochromatic location. Together, these results indicate that, in cancer, extensive changes around promoter chromatin of individual genes or gene clusters could potentially occur locally without preference for nuclear position and/or causing repositioning. These findings have important implications for understanding relationships between nuclear organization and gene expression patterns in cancer. Cancer Res; 70(20); 8015-24. [copy ]2010 AACR.
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8Schuebel, Kornel E
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titleAberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus.
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11In Situ Hybridization–Genetics
12In Situ Hybridization, Fluorescence–Genetics
13Intercellular Adhesion Molecule-1–Genetics
14Microsatellite Repeats–Genetics
15Mutl Protein Homolog 1–Genetics
16Neoplasms–Genetics
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18Proto-Oncogene Proteins–Genetics
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titleAberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus.
authorEaswaran, Hariharan P ; Van Neste, Leander ; Cope, Leslie ; Sen, Subhojit ; Mohammad, Helai P ; Pageau, Gayle J ; Lawrence, Jeanne B ; Herman, James G ; Schuebel, Kornel E ; Baylin, Stephen B
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2Cell Nucleus–Metabolism
3Cpg Islands–Genetics
4DNA Methylation–Genetics
5Epigenesis, Genetic–Genetics
6Gene Expression Profiling–Genetics
7Gene Expression Regulation, Neoplastic–Genetics
8Gene Silencing–Genetics
9Genome-Wide Association Study–Genetics
10Humans–Genetics
11In Situ Hybridization–Genetics
12In Situ Hybridization, Fluorescence–Genetics
13Intercellular Adhesion Molecule-1–Genetics
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15Mutl Protein Homolog 1–Genetics
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19Reverse Transcriptase Polymerase Chain Reaction–Genetics
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23Proto-Oncogene Proteins
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