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

Krishna P. Bhat; Christopher E. Pelloski; Yujian Zhang; Se Hoon Kim; Clarissa deLaCruz; Michael Rehli; Kenneth D. Aldape

doi:10.1016/j.febslet.2008.08.010

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

Krishna P. Bhat, Christopher E. Pelloski, Yujian Zhang, Se Hoon Kim, Clarissa deLaCruz, Michael Rehli, Kenneth D. Aldape

Research output: Contribution to journal › Article › peer-review

43 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	3193-3200
Number of pages	8
Journal	FEBS Letters
Volume	582
Issue number	21-22
DOIs	https://doi.org/10.1016/j.febslet.2008.08.010
State	Published - Sep 22 2008

Keywords

Glioma
HDAC
NF-κB
YKL-40

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2008.08.010

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

abstract = "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.",

keywords = "Glioma, HDAC, NF-κB, YKL-40",

author = "Bhat, {Krishna P.} and Pelloski, {Christopher E.} and Yujian Zhang and Kim, {Se Hoon} and Clarissa deLaCruz and Michael Rehli and Aldape, {Kenneth D.}",

note = "Funding Information: This work was supported by a Grant from the American Brain Tumor Association (to K.P. Bhat), and an Odyssey Fellowship sponsored by the Theodore N. Law Award for scientific achievement (to K.P. Bhat).",

year = "2008",

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doi = "10.1016/j.febslet.2008.08.010",

language = "English (US)",

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T1 - Selective repression of YKL-40 by NF-κB in glioma cell lines involves recruitment of histone deacetylase-1 and -2

AU - Bhat, Krishna P.

AU - Pelloski, Christopher E.

AU - Zhang, Yujian

AU - Kim, Se Hoon

AU - deLaCruz, Clarissa

AU - Rehli, Michael

AU - Aldape, Kenneth D.

N1 - Funding Information: This work was supported by a Grant from the American Brain Tumor Association (to K.P. Bhat), and an Odyssey Fellowship sponsored by the Theodore N. Law Award for scientific achievement (to K.P. Bhat).

PY - 2008/9/22

Y1 - 2008/9/22

N2 - 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.

AB - 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.

KW - Glioma

KW - HDAC

KW - NF-κB

KW - YKL-40

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JO - FEBS Letters

JF - FEBS Letters

IS - 21-22

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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