Source:http://linkedlifedata.com/resource/pubmed/id/11280805
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2001-3-30
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| pubmed:abstractText |
We hypothesize that elevation of Nm23-H1 expression in micrometastatic breast cancer cells may inhibit their metastatic colonization and further invasion, and induce differentiation, thus resulting in a clinical benefit. The current study investigated the possible contribution of DNA methylation to the regulation of Nm23-H1 expression, based on the observation that two CpG islands are present in its promoter. 5-Aza-2'-deoxycytidine (5-Aza-CdR), a DNA methylation inhibitor, increased the Nm23-H1 expression of 5 of 11 human breast carcinoma cell lines in vitro, including 3 of 3 metastatically competent lines. Increased Nm23-H1 expression was accompanied by a reduction in motility in vitro, with minimal effect on proliferation. Both increased Nm23-H1 expression and decreased motility were observed using low (75 nM) concentrations of 5-Aza-CdR. Array analysis of MDA-MB-231 breast carcinoma cells treated with 5-Aza-CdR confirmed the elevation of nm23-H1 mRNA, whereas relatively few other genes exhibited altered expression. Bisulfite sequencing of the two CpG islands in a panel of cell lines and in 20 infiltrating ductal carcinomas revealed that one island (-3090 bp to -3922 bp) exhibited infrequent differential methylation. The data indicate that DNA methylation inhibitors can directly or indirectly cause both elevation of Nm23-H1 expression and decreased function in one aspect of metastasis, motility.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antimetabolites, Antineoplastic,
http://linkedlifedata.com/resource/pubmed/chemical/Azacitidine,
http://linkedlifedata.com/resource/pubmed/chemical/Monomeric GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NM23 Nucleoside Diphosphate Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/NME1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nucleoside-Diphosphate Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/decitabine
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| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
0008-5472
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
61
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2320-7
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:11280805-Antimetabolites, Antineoplastic,
pubmed-meshheading:11280805-Azacitidine,
pubmed-meshheading:11280805-Breast Neoplasms,
pubmed-meshheading:11280805-Carcinoma, Ductal, Breast,
pubmed-meshheading:11280805-Cell Movement,
pubmed-meshheading:11280805-CpG Islands,
pubmed-meshheading:11280805-DNA Methylation,
pubmed-meshheading:11280805-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:11280805-Genes, Tumor Suppressor,
pubmed-meshheading:11280805-Humans,
pubmed-meshheading:11280805-Monomeric GTP-Binding Proteins,
pubmed-meshheading:11280805-NM23 Nucleoside Diphosphate Kinases,
pubmed-meshheading:11280805-Neoplasm Metastasis,
pubmed-meshheading:11280805-Nucleoside-Diphosphate Kinase,
pubmed-meshheading:11280805-Promoter Regions, Genetic,
pubmed-meshheading:11280805-Transcription Factors,
pubmed-meshheading:11280805-Transfection,
pubmed-meshheading:11280805-Tumor Cells, Cultured
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| pubmed:year |
2001
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| pubmed:articleTitle |
Elevation of breast carcinoma Nm23-H1 metastasis suppressor gene expression and reduced motility by DNA methylation inhibition.
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| pubmed:affiliation |
Division of Clinical Sciences, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. hartso@box-h.nih.gov
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| pubmed:publicationType |
Journal Article
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