Selective repression of YKL-40 by NF-κB in glioma cell lines involves recruitment of histone deacetylase-1 and-2

被引:39
作者
Bhat, Krishna P. [1 ,2 ]
Pelloski, Christopher E. [1 ,2 ,3 ]
Zhang, Yujian [2 ,4 ]
Kim, Se Hoon [1 ,2 ]
deLaCruz, Clarissa [1 ,2 ]
Rehli, Michael [5 ,6 ]
Aldape, Kenneth D. [1 ,2 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Unit 85, Houston, TX 77030 USA
[2] Univ Texas MD Anderson Canc Ctr, Brain Tumor Ctr, Houston, TX 77030 USA
[3] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA
[4] Univ Texas MD Anderson Canc Ctr, Dept Neurosurg, Houston, TX 77030 USA
[5] Univ Regensburg, Dept Hematol & Oncol, D-93042 Regensburg, Germany
[6] Yonsei Univ, Coll Med, Dept Pathol, Seoul, South Korea
关键词
YKL-40; NF-kappa B; glioma; HDAC;
D O I
10.1016/j.febslet.2008.08.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
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.
引用
收藏
页码:3193 / 3200
页数:8
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