Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylation
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Antigens, CD
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Azacitidine / analogs & derivatives
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Azacitidine / pharmacology
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Cadherins / genetics*
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Cadherins / metabolism
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Cell Line, Tumor
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Chromatin Immunoprecipitation
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Colorectal Neoplasms / enzymology
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Colorectal Neoplasms / genetics*
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Colorectal Neoplasms / metabolism
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DNA Methylation
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DNA Modification Methylases / antagonists & inhibitors
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DNA Modification Methylases / metabolism
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Decitabine
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Enzyme Inhibitors / pharmacology
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Gene Expression Regulation, Neoplastic* / drug effects
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Gene Silencing* / drug effects
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Histone Deacetylase Inhibitors
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Histone Deacetylases / metabolism
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Histones / metabolism*
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Humans
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Hydroxamic Acids / pharmacology
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Polymerase Chain Reaction
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Promoter Regions, Genetic* / drug effects
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RNA, Messenger / metabolism
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Transcription, Genetic* / drug effects
Substances
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Antigens, CD
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CDH1 protein, human
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Cadherins
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Enzyme Inhibitors
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Histone Deacetylase Inhibitors
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Histones
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Hydroxamic Acids
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RNA, Messenger
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trichostatin A
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Decitabine
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DNA Modification Methylases
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Histone Deacetylases
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Azacitidine