Activation of BAG3 by Egr-1 in response to FGF-2 in neuroblastoma cells
Activation of BAG3 by Egr-1 in response to FGF-2 in neuroblastoma cells
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DOI：
10.1038/onc.2008.142
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发表时间：
2008-08-28
期刊：
影响因子：
8
通讯作者：
Khalili, K.
中科院分区：
文献类型：
--
作者：
Gentilella, A.;Passiatore, G.;Khalili, K.
属于BAG蛋白家族的共伴侣蛋白BAG 3在不同的肿瘤细胞系中具有确定的抗凋亡功能。在这里，我们证明了治疗的人神经母细胞瘤细胞系，SK-N-MC，与。成纤维细胞生长因子-2（FGF-2）导致BAG 3表达的诱导。FGF-2对BAG 3蛋白的诱导发生在转录水平;它需要细胞外调节激酶1/2途径，并依赖于Egr-1对BAG 3启动子的活性。通过小干扰RNA靶向抑制BAG 3导致细胞周期进程失调，最明显的是在S期和G（2）期，这证实了细胞周期蛋白B1表达水平的降低。这些观察结果表明BAG 3在细胞周期调控中的新作用。
The co-chaperone protein, BAG3, which belongs to the BAG protein family, has an established antiapoptotic function in different tumor cell lines. Here we demonstrated that treatment of the human neuroblastoma cell line, SK-N-MC, with. broblast growth factor-2 (FGF-2) results in induction of BAG3 expression. Induction of BAG3 protein by FGF-2 occurs at the transcriptional level; it requires the extracellular regulated kinase1/2 pathway and is dependent on the activity of Egr-1 upon the BAG3 promoter. Targeted suppression of BAG3 by small-interfering RNA results in dysregulation of cell-cycle progression most notably at S and G(2) phases, which corroborates the decreased level of cyclin B1 expression. These observations suggest a new role for BAG3 in regulation of the cell cycle.