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 journalArticlepeer-review

39 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 languageEnglish
Pages (from-to)3193-3200
Number of pages8
JournalFEBS Letters
Volume582
Issue number21-22
DOIs
Publication statusPublished - 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

Fingerprint

Dive into the research topics of 'Selective repression of YKL-40 by NF-κB in glioma cell lines involves recruitment of histone deacetylase-1 and -2'. Together they form a unique fingerprint.

Cite this