4.7 Article

HDAC4 inhibits the transcriptional activation of mda-7/IL-24 induced by Sp1

Journal

CELLULAR & MOLECULAR IMMUNOLOGY
Volume 7, Issue 3, Pages 221-226

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/cmi.2010.12

Keywords

HDAC4; HDAC inhibitors; histone acetylation; mda-7/IL-24; Sp1

Categories

Funding

  1. National Natural Science Foundation of China [30671184]
  2. Program for Changjiang Scholars and Innovative Research Team in University [IRT0519]

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Melanoma differentiation-associated gene/interleukin-24 (mda-7/IL-24) is a cytokine that can activate monocytes and T helper 2 cells. The expression of mda-7/IL-24 gradually fades with the progression of melanoma, and it is undetectable at the metastatic stage. Ectopic expression of mda-7/IL-24 selectively suppresses growth and induces apoptosis in cancer cells with little harm to normal cells. However, the transcriptional regulation of the mda-7/IL-24 gene has not been extensively studied. In this study, we show that the expression of mda-7/IL-24 was upregulated by the histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate (NaBu), whereas it was downregulated by HDAC4. We also found that the histone acetylation level and the binding of the transcriptional factor Sp1 to the mad-7 promoter were reduced upon HDAC4 treatment. Moreover, the HDAC inhibitor TSA induced histone hyperacetylation and stimulated Sp1 binding to the mda-7/IL-24 promoter, which in turn enhanced the expression of mda-7/IL-24. Therefore, we conclude that histone acetylation modification plays an important role in the regulation of mda-7/IL-24 and that the transcription factor Sp1 participates in this process. Cellular & Molecular Immunology (2010) 7, 221-226; doi:10.1038/cmi.2010.12; published online 12 April 2010

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