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首页> 外文期刊>Journal of cellular biochemistry. >Signal transducer and activator of transcription 1 (Stat1) maintains basal mRNA expression of pro-survival stat3-target genes in glioma C6 cells.
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Signal transducer and activator of transcription 1 (Stat1) maintains basal mRNA expression of pro-survival stat3-target genes in glioma C6 cells.

机译：信号转导和转录激活因子1（Stat1）维持神经胶质瘤C6细胞中生存前stat3目标基因的基础mRNA表达。

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摘要

The STAT proteins (signal transducers and activators of transcription) are transcription factors mediating cytokine/growth factor signaling, which play important role in controlling cell cycle progression and apoptosis. In many cancer cell lines and tumors (including gliomas) the STAT proteins (in particular Stats 1, 3, and 5) are persistently activated. In this study, we employed DNA decoys, siRNAs, and protein overexpression, to elucidate the role of Stat1 and Stat3 in regulation of expression of endogenous Stat3-target genes (Bcl2l1, Myc, Ccnd1) and a Stat-driven reporter plasmid, in rat C6 glioma cells. The results obtained with the decoys and siRNA suggest that in proliferating C6 cells, Stat1 supports the basal expression of Bcl2l1, while the decoy and chromatin immunoprecipitation results suggest it also plays a similar role for Myc. In the Stat-driven reporter system, overexpression of Stat1 stimulated, while overexpression of Stat3 inhibited the reporter gene expression. The level of Stat1 phosphorylation observed under basal conditions in proliferating glioma C6 cells is very low. Therefore, we speculate that it is the activity of the unphosphorylated Stat1 that is inhibited by Stat1 decoy or Stat1 siRNA. Taken together, our results demonstrate that it is Stat1 not Stat3 that maintains the expression of Bcl2l1 and possibly Myc in proliferating glioma C6 cells. An established paradigm is that Stat3 exerts a pro-survival and potentially oncogenic effects, while Stat1 is mainly associated with the immune response. Our results add to a number of reports that challenge this paradigm.
机译：STAT蛋白（信号转导和转录激活剂）是介导细胞因子/生长因子信号传导的转录因子，在控制细胞周期进程和凋亡中起重要作用。在许多癌细胞系和肿瘤（包括神经胶质瘤）中，STAT蛋白（特别是Stats 1、3和5）被持续激活。在这项研究中，我们采用了DNA诱饵，siRNA和蛋白质过表达，以阐明Stat1和Stat3在调节内源性Stat3靶基因（Bcl2l1，Myc，Ccnd1）和一个Stat驱动的报告质粒表达中的作用C6胶质瘤细胞。诱饵和siRNA获得的结果表明，在C6细胞增殖中，Stat1支持Bcl2l1的基础表达，而诱饵和染色质的免疫沉淀结果表明，它对Myc也起类似的作用。在Stat驱动的报告系统中，Stat1的过表达被刺激，而Stat3的过表达则抑制了报告基因的表达。在基础条件下，在增殖的神经胶质瘤C6细胞中观察到的Stat1磷酸化水平非常低。因此，我们推测是Stat1诱饵或Stat1 siRNA抑制了未磷酸化Stat1的活性。两者合计，我们的结果表明，在增殖性神经胶质瘤C6细胞中，Bcl2l1可能还有Myc的表达不是Stat1，而是Stat3。既定的范例是Stat3发挥促生存作用和潜在的致癌作用，而Stat1主要与免疫反应相关。我们的结果增加了许多挑战这一范式的报告。

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