ArticleNucleic acids research2002
Heterogeneity in the modification and involvement of chromatin components of the CpG island of the silenced human CDH1 gene in cancer cells.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 74 citations in OpenAlex.
- DNA methylation in pulmonary fibrosis and lung cancer.Expert review of respiratory medicine · 2022Review
- Epigenetic mechanisms and the hallmarks of cancer: an intimate affair.American journal of cancer research · 2020Review
- Epigenetics in cancer stem cells.Molecular cancer · 2017Review
- Article
- Epigenetic regulation of epithelial-mesenchymal transition.Cellular and molecular life sciences : CMLS · 2016Review
- A novel MeCP2 acetylation site regulates interaction with ATRX and HDAC1.Genes & cancer · 2015Article
- Regulation of breast cancer stem cell features.Contemporary oncology (Poznan, Poland) · 2015Review
- Epigenetic alterations involved in cancer stem cell reprogramming.Molecular oncology · 2012Review
- The SRA protein UHRF1 promotes epigenetic crosstalks and is involved in prostate cancer progression.Oncogene · 2012Article
- Article
- Methyl-H3K9-binding protein MPP8 mediates E-cadherin gene silencing and promotes tumour cell motility and invasion.The EMBO journal · 2010Article
- Involvement of members of the cadherin superfamily in cancer.Cold Spring Harbor perspectives in biology · 2009Review
- Expression of EphA2 and E-cadherin in gastric cancer: correlated with tumor progression and lymphogenous metastasis.Pathology oncology research : POR · 2009Article
- Unmasking of epigenetically silenced candidate tumor suppressor genes by removal of methyl-CpG-binding domain proteins.Oncogene · 2008Article
- Enhancer of zeste homolog 2 downregulates E-cadherin by mediating histone H3 methylation in gastric cancer cells.Cancer science · 2008Article
- The impact of MECP2 mutations in the expression patterns of Rett syndrome patients.Human genetics · 2005Article
- Methyl-CpG binding proteins identify novel sites of epigenetic inactivation in human cancer.The EMBO journal · 2003Article
- Wnt-cadherin connections in normal and neoplastic mammary epithelium.Journal of mammary gland biology and neoplasia · 2003Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The structural alteration of chromatin has a key role in regulating gene expression. The alteration of chromatin is mediated by modification of its components. Detailed understanding of the relationship between these modifications, notably, methylation of the full-length CpG island, the association of methyl-CpG binding proteins (MBPs), and the acetylation and methylation of histones in gene silencing is vitally important. Currently, however, the manner in which chromatin components, associated with a specific gene, are modified is poorly understood. Here we provide in vivo evidence in cancer cells of the differential association between CpG methylation, MBPs, and histone modification in the entire CpG island of the human E-cadherin (CDH1) gene. Of the cell lines with CDH1 transcriptional repression, the distribution of methyl-CpGs in the CpG island differed markedly. In a cell line with gene silencing, the promoter region was almost methylation-free. Chromatin immunoprecipitation analysis revealed that the acetylation status of histone H4 differed between cell lines. However, deacetylated histone H3 was associated with the CpG island in all silenced cell lines. Binding of MeCP2 was also detected in all silenced cell lines. Additional binding of MBD1 protein was detected in a cell line in which the promoter region was poorly methylated and only histone H3 was deacetylated. Binding of MBD2 protein was detected in all other silenced cell lines. Histone H3 lysine 9 was methylated in all silenced cells, while histone H3 lysine 4 was methylated in some silenced cell lines. These results demonstrate that chromatin components associated with inactive CDH1 chromatin is heterogeneously modified and suggests the presence of multiple pathways for the formation of inactive chromatin.
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