Effects of cell density and trichostatin A on the expression of HDAC1 and p57Kip2 in Hep 3B cells
Effects of cell density and trichostatin A on the expression of HDAC1 and p57Kip2 in Hep 3B cells
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DOI：
10.1006/bbrc.1998.8449
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发表时间：
1998-04-17
影响因子：
3.1
通讯作者：
Ekström, TJ
中科院分区：
文献类型：
--
作者：
Gray, SG;Ekström, TJ
细胞内乙酰化和去乙酰化活性之间的相互作用被认为是细胞在染色质水平调节基因表达的机制。我们检测了人组蛋白去乙酰化酶基因HDAC 1和细胞周期蛋白依赖性激酶抑制剂p57（Kip 2）在肝癌细胞系Hep 3B中的表达模式。HDAC 1表达在低细胞密度下升高，但一旦达到细胞密度的临界阈值点，表达降低至非常低的水平。研究发现，用组蛋白去乙酰化酶的强效抑制剂--发现TSA下调p57（Kip 2），而上调HDAC 1。发现这些效应是细胞密度依赖性的。结果表明，HDAC 1在其自身的调节中发挥作用，当细胞呈指数增长时，应使用TSA进行研究。(C)北京：科学出版社.
The interplay between the acetylation and deacetylation activities within the cell has been postulated to be a mechanism by which the cell regulates expression from genes at the level of chromatin. We have examined the expression pattern of the human histone deacetylase gene HDAC1 and the cyclin dependent kinase inhibitor p57(Kip2) in the hepatocellular carcinoma cell line Hep 3B. HDAC1 expression was elevated at low cell densities, but once a critical threshold point in cell density was attained, expression was reduced to very low levels. Treatment of the cells with trichostatin A (TSA), a potent inhibitor of histone deacetylases, was found to affect expression. p57(Kip2) was found to be downregulated by TSA, whereas HDAC1 was upregulated. These effects were found to be cell density dependent. The results suggest that HDAC1 plays a role in its own regulation, and that investigations using TSA should be carried out when cells grow exponentially. (C) 1998 Academic Press.