BM88/Cend1 is involved in histone deacetylase inhibition-mediated growth arrest and differentiation of neuroblastoma cells

被引:21
|
作者
Politis, Panagiotis K. [1 ]
Akrivou, Sofia [1 ]
Hurel, Catherine [1 ]
Papadodima, Olga [1 ]
Matsas, Rebecca [1 ]
机构
[1] Hellenic Pasteur Inst, Cellular & Mol Neurobiol Lab, Athens 11521, Greece
关键词
transcription; proliferation; trichostatin-A; promoter activation; beta-III-tubulin; acetylation;
D O I
10.1016/j.febslet.2008.01.052
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Histone deacetylase inhibitors arrest the growth of neuroblastoma cells and induce differentiation. Identification of target genes that co-ordinate and mediate these effects is important for understanding the function of this novel class of antitumour drugs. We report here that trichostatin-A (TSA) specifically induces the transcription of Cend1, a neuronal-lineage specific regulator of cell cycle exit and differentiation, in neuroblastoma Neuro2A cells, but not in non-neuronal cells. Furthermore, we show that knockdown of Cend1 alleviates both the anti-proliferative and differentiation effect of TSA. Our findings suggest that Cend1 is an important molecular target for HDAC inhibition. (c) 2008 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:741 / 748
页数:8
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