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

Department of Pathology

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

42 Citations (Scopus)

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
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
Publication status	Published - 2008 Sep 22

Bibliographical 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).

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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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.",

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).",

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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.

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

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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