Abstract
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 ...
Abstract
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.
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