Targeted inhibition of the transcription factor YY1 in an embryonal carcinoma cell line results in retarded cell growth, elevated levels of p53 but no increase in apoptotic cell death
Targeted inhibition of the transcription factor YY1 in an embryonal carcinoma cell line results in retarded cell growth, elevated levels of p53 but no increase in apoptotic cell death
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DOI：
10.1016/j.ejcb.2004.12.024
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发表时间：
2005-06-01
影响因子：
6.6
通讯作者：
Sinclair, J
中科院分区：
文献类型：
--
作者：
Bain, M;Sinclair, J
普遍存在的细胞转录因子Yin Yang-1（YY 1）参与许多细胞和病毒基因的转录调控。已知其在非允许性T2细胞中与人巨细胞病毒（HCMV）的主要立即早期启动子结合并抑制其活性。因此，YY 1至少部分地负责这些细胞的生产性裂解感染的缺乏。在这项研究中，我们已经使用短干扰RNA（siRNA）特异性敲低YY 1在T2细胞中的表达。我们希望评估去除这种负作用因子是否会使这些通常不允许感染的细胞允许感染。我们表明，我们可以有效地抑制YY 1的表达，但这种敲低对细胞的正常生物学有显着的影响。特别是，我们注意到生长迟缓，形态改变和p53水平增加。然而，细胞不经历凋亡，不被诱导分化，不表现出过度水平的DNA损伤，并且正常合成DNA。(c)2005年Elsevier GmbH。All rights reserved.
The ubiquitous cellular transcription factor Yin Yang-1 (YY1) is involved in the transcriptional regulation of many cellular and viral genes. It is known to bind to, and repress the activity of, the major immediate-early promoter of human cytomegalovirus (HCMV) in non-permissive T2 cells. Thus, YY1 is at least partly responsible for the lack of productive lytic infection of these cells. In this study, we have used short interfering RNA (siRNA) to specifically knock down YY1 expression in T2 cells. We wished to assess whether the removal of this negatively acting factor would render these ordinarily non-permissive cells permissive for infection. We show that we can potently inhibit YY1 expression but that this knock down has dramatic effects on the normal biology of the cells. In particular, we noted growth retardation, altered morphology and increased levels of p53. However, the cells do not undergo apoptosis, are not induced to differentiate, do not exhibit excessive levels of DNA damage, and synthesise DNA normally. (c) 2005 Elsevier GmbH. All rights reserved.