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Selective repression of YKL‐40 by NF‐κB in glioma cell lines involves recruitment of histone deacetylase‐1 and ‐2
Author(s) -
Bhat Krishna P.,
Pelloski Christopher E.,
Zhang Yujian,
Kim Se Hoon,
deLaCruz Clarissa,
Rehli Michael,
Aldape Kenneth D.
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.08.010
Subject(s) - chromatin immunoprecipitation , hdac1 , histone , cancer research , nf κb , histone deacetylase , acetylation , glioma , tumor necrosis factor alpha , chemistry , chromatin , microbiology and biotechnology , biology , promoter , gene expression , signal transduction , immunology , biochemistry , gene
Here we show that in contrast to other cancer types, tumor necrosis factor (TNF)‐α suppresses YKL‐40 expression in glioma cell lines in a nuclear factor κB (NF‐κB) dependent manner. Even though TNF‐α causes recruitment of p65 and p50 subunits of NF‐κB 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‐κB regulation of one of its targets in a strict cell type specific manner.