Selective repression of YKL-40 by NF-κB in glioma cell lines involves recruitment of histone deacetylase-1 and-2
Selective repression of YKL-40 by NF-κB in glioma cell lines involves recruitment of histone deacetylase-1 and-2
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DOI：
10.1016/j.febslet.2008.08.010
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发表时间：
2008-09-22
期刊：
影响因子：
3.5
通讯作者：
Aldape, Kenneth D.
中科院分区：
文献类型：
--
作者：
Bhat, Krishna P.;Pelloski, Christopher E.;Aldape, Kenneth D.
在这里，我们表明，与其他类型的癌症相比，肿瘤坏死因子(TNF)-α以核因子-kappa B(NF-kappa B)依赖的方式抑制胶质瘤细胞系中YKL-40的表达。尽管在所有类型的细胞中，肿瘤坏死因子-α都能引起核因子-kappa B的p65和p50亚单位在YKL-40启动子上的募集，但组蛋白脱乙酰酶(HDAC)-1和-2的募集以及随之而来的组蛋白H3在YKL-40启动子上的去乙酰化只在胶质瘤细胞中发生。重要的是，在冷冻的多形性胶质母细胞瘤组织中使用染色质免疫沉淀分析，我们发现YKL-40水平降低与HDAC1募集一致，尽管核p-p65水平较高。本研究提出了一种以严格的细胞类型特异性方式调节其靶标之一的核因子-kappa B的范例。由Elsevier B.V.代表欧洲生化学会联合会出版。
Here we show that in contrast to other cancer types, tumor necrosis factor (TNF)-alpha suppresses YKL-40 expression in glioma cell lines in a nuclear factor kappa B (NF-kappa B) dependent manner. Even though TNF-alpha causes recruitment of p65 and p50 subunits of NF-kappa B to the YKL-40 promoter in all cell types, recruitment of histone deacetylases (HDAC)-1 and -2, and a consequent deacetylation of histone H3 at the YKL-40 promoter occurs only in glioma cells. Importantly, using chromatin immunoprecipitation assays in frozen glioblastoma multiforme tissues, we show that YKL-40 levels decrease consistent with HDAC1 recruitment despite high levels of nuclear p-p65. This study presents a paradigm for NF-kappa B regulation of one of its targets in a strict cell type specific manner. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.