T antigen transformation reveals Tp53/RB-dependent route to PLAC1 transcription activation in primary fibroblasts.

T antigen transformation reveals Tp53/RB-dependent route to PLAC1 transcription activation in primary fibroblasts.
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DOI:
10.1038/oncsis.2013.31
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发表时间:
2013-09-02
期刊:
影响因子:
6.2
通讯作者:
Nagaraja, R.
Nagaraja, R.
中科院分区:
医学1区
文献类型:
--
作者:
Chen, Y.;Schlessinger, D.;Nagaraja, R.

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PLAC1(胎盘特异性1)是一种胎盘特异性基因,在任何体细胞组织中转录很少。然而,它在许多癌细胞系中表达。为了了解癌细胞如何激活非表达细胞中的基因,我们发现通过SV40 T抗原对正常成纤维细胞的经典转化提供了一个模型。T抗原解除了PLAC1 P1启动子的抑制,Tp53和RB发挥了关键和相反的作用,核受体、维甲酸X受体和肝X受体的表达水平急剧增加。
PLAC1 (placenta-specific 1) is a gene that is placenta specific and transcribed very little, if at all, in any somatic tissue. It is nevertheless expressed in many cancer cell lines. To understand how cancer cells may activate the gene in nonexpressing cells, we found that a model is provided by classical transformation of normal fibroblasts by SV40 T antigen. T antigen derepressed the PLAC1 P1 promoter, with Tp53 and RB exerting critical and opposing actions and nuclear receptors, retinoid X receptor and  liver X receptor, sharply increasing the level of expression.
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