18799463

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0007102, umls-concept:C0040649, umls-concept:C0334227, umls-concept:C1156197, umls-concept:C1514873
pubmed:issue	46
pubmed:dateCreated	2008-11-10
pubmed:abstractText	15-Lipoxygenase-1 (15-LOX-1) contributes significantly to inflammation regulation and terminal cell differentiation. 15-LOX-1 is transcriptionally silenced in cancer cells, and its transcriptional reactivation (e.g. via histone deacetylase inhibitors (HDACIs)) is essential for restoring terminal cell differentiation to cancer cells. STAT-6 acetylation via the histone acetyltransferase KAT3B has been proposed to be necessary for 15-LOX-1 transcriptional activation. However, the exact mechanism underlying 15-LOX-1 transcriptional reactivation in cancer cells is still undefined, especially in regard to the contribution of 15-LOX-1 promoter histone modifications. We therefore examined the relative mechanistic contributions of 15-LOX-1 promoter histone modifications and STAT-6 to 15-LOX-1 transcriptional reactivation by HDACIs in colon cancer cells. We found that: 1) histone H3 and H4 acetylation in the 15-LOX-1 promoter through KAT3B was critical to 15-LOX-1 transcriptional activation; 2) 15-LOX-1 transcription was activated independently from STAT-6; and 3) dimethyl-histone H3 lysine 9 (H3K9me2) demethylation in the 15-LOX-1 promoter via the histone lysine demethylase KDM3A was an early and specific histone modification and was necessary for activation of transcription. These findings demonstrate that histone modification in the 15-LOX-1 promoter is important to 15-LOX-1 transcriptional silencing in colon cancer cells and that HDACIs can activate gene transcription via KDM3A demethylation of H3K9me2.
pubmed:grant	http://linkedlifedata.com/resource/pubmed/grant/CA104278, http://linkedlifedata.com/resource/pubmed/grant/CA106577, http://linkedlifedata.com/resource/pubmed/grant/R01 CA104278-04, http://linkedlifedata.com/resource/pubmed/grant/R01 CA106577-04
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pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/2985121R
pubmed:citationSubset	IM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Arachidonate 15-Lipoxygenase, http://linkedlifedata.com/resource/pubmed/chemical/Chromatin, http://linkedlifedata.com/resource/pubmed/chemical/Histones, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering, http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor
pubmed:status	MEDLINE
pubmed:month	Nov
pubmed:issn	0021-9258
pubmed:author	pubmed-author:MorrisJeffrey SJS, pubmed-author:ShureiqiImadI, pubmed-author:ZuoXiangshengX
pubmed:issnType	Print
pubmed:day	14
pubmed:volume	283
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	31341-7
pubmed:dateRevised	2011-9-26
pubmed:meshHeading	pubmed-meshheading:18799463-Acetylation, pubmed-meshheading:18799463-Arachidonate 15-Lipoxygenase, pubmed-meshheading:18799463-Cell Line, Tumor, pubmed-meshheading:18799463-Chromatin, pubmed-meshheading:18799463-Colonic Neoplasms, pubmed-meshheading:18799463-Histones, pubmed-meshheading:18799463-Humans, pubmed-meshheading:18799463-Promoter Regions, Genetic, pubmed-meshheading:18799463-RNA, Small Interfering, pubmed-meshheading:18799463-STAT6 Transcription Factor, pubmed-meshheading:18799463-Transcriptional Activation
pubmed:year	2008
pubmed:articleTitle	Chromatin modification requirements for 15-lipoxygenase-1 transcriptional reactivation in colon cancer cells.
pubmed:affiliation	Department of Clinical Cancer Prevention, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't

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