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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2008-6-27
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pubmed:abstractText |
Epigenetic parameters linked to E-cadherin gene were investigated in 5 human colorectal cancer cell lines. Treatment with trichostatin A led to enhanced acetylation of histone H3-K9 with concurrent induction of E-cadherin mRNA in 3 E-cadherin low/negative cell lines that are not DNA methylated. Co-treatment with 5-aza-2'-deoxycytidine and trichostatin A resulted in additive/synergic induction of E-cadherin mRNA in all 5 cell lines with concomitant enhancement of histone H3-K9 acetylation in 4 E-cadherin low/negative cell lines. Our results suggest that histone H3-K9 deacetylation appears to play a crucial role in transcriptional repression of E-cadherin in colorectal cancers.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Azacitidine,
http://linkedlifedata.com/resource/pubmed/chemical/CDH1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Modification Methylases,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylases,
http://linkedlifedata.com/resource/pubmed/chemical/Histones,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxamic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/decitabine,
http://linkedlifedata.com/resource/pubmed/chemical/trichostatin A
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1532-4192
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
575-82
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18584348-Acetylation,
pubmed-meshheading:18584348-Azacitidine,
pubmed-meshheading:18584348-Cadherins,
pubmed-meshheading:18584348-Cell Line, Tumor,
pubmed-meshheading:18584348-Chromatin Immunoprecipitation,
pubmed-meshheading:18584348-Colorectal Neoplasms,
pubmed-meshheading:18584348-DNA Methylation,
pubmed-meshheading:18584348-DNA Modification Methylases,
pubmed-meshheading:18584348-Enzyme Inhibitors,
pubmed-meshheading:18584348-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:18584348-Gene Silencing,
pubmed-meshheading:18584348-Histone Deacetylase Inhibitors,
pubmed-meshheading:18584348-Histone Deacetylases,
pubmed-meshheading:18584348-Histones,
pubmed-meshheading:18584348-Humans,
pubmed-meshheading:18584348-Hydroxamic Acids,
pubmed-meshheading:18584348-Polymerase Chain Reaction,
pubmed-meshheading:18584348-Promoter Regions, Genetic,
pubmed-meshheading:18584348-RNA, Messenger,
pubmed-meshheading:18584348-Transcription, Genetic
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pubmed:year |
2008
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pubmed:articleTitle |
Histone H3 (lys-9) deacetylation is associated with transcriptional silencing of E-cadherin in colorectal cancer cell lines.
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pubmed:affiliation |
Department of Colorectal Surgery, Singapore General Hospital, Singapore. liu.yan.qun@sgh.com.sg
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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