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首页> 外文期刊>The FEBS journal >Sp1 and Sp3 are involved in the full transcriptional activity of centromere protein H in human nasopharyngeal carcinoma cells
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Sp1 and Sp3 are involved in the full transcriptional activity of centromere protein H in human nasopharyngeal carcinoma cells

机译：Sp1和Sp3参与着丝粒蛋白H在人鼻咽癌细胞中的全部转录活性

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The overexpression of centromere protein H (CENPH), one of the fundamental components of the human active kinetochore, has been shown to be closely associated with human cancers. However, the mechanism of its transcriptional regulation has not been reported. The aim of the present study was to investigate the regulatory elements for the transcriptional regulation of CENPH in nasopharyngeal carcinoma cells. To characterize the CENPH promoter and identify regulatory elements, we cloned 1015 bp (-975/+40 bp) of the 5'-flanking region of the CENPH gene from immortalized normal nasopharyngeal epithelial cells (Bmi-1/NPEC). Functional analysis established a minimal region (-140/-87 bp) involved in the regulation of human CENPH promoter activity. Through site-directed mutagenesis, a transactivation assay, chromatin immunoprecipitation, and electrophoretic mobility shift assay, we found that the Sp1/Sp3 transcription factors could bind to the CENPH promoter in vitro and in vivo, and that they regulated CENPH promoter activation in human nasopharyngeal carcinoma cells. Furthermore, Sp1 and Sp3 were highly expressed in nasopharyngeal carcinoma cells. Knockdown of Sp1 and Sp3 by small interfering RNA or inhibition of Sp1 and Sp3 activity by mithramycin A decreased CENPH mRNA expression, whereas the exogenous expression of Sp1 and Sp3 upregulated CENPH mRNA expression. Taken together, our results indicate that Sp1 and Sp3 bind to the CENPH minimal promoter and function as a regulator of the transcription of CENPH in human nasopharyngeal carcinomas.
机译：着丝粒蛋白H（CENPH）的过度表达是人类活动动粒的基本组成部分之一，已被证明与人类癌症密切相关。但是，其转录调控的机制尚未见报道。本研究的目的是研究鼻咽癌细胞中CENPH转录调控的调控元件。为了表征CENPH启动子并鉴定调控元件，我们从永生化的正常鼻咽上皮细胞（Bmi-1 / NPEC）中克隆了CENPH基因5'侧翼区域的1015 bp（-975 / + 40 bp）。功能分析建立了涉及人类CENPH启动子活性调节的最小区域（-140 / -87 bp）。通过定点诱变，反式激活测定，染色质免疫沉淀和电泳迁移率迁移测定，我们发现Sp1 / Sp3转录因子可以在体外和体内与CENPH启动子结合，并且它们调节人鼻咽中的CENPH启动子激活。癌细胞。此外，Sp1和Sp3在鼻咽癌细胞中高表达。通过小的干扰RNA抑制Sp1和Sp3或通过光神霉素A抑制Sp1和Sp3活性降低CENPH mRNA表达，而Sp1和Sp3的外源表达上调CENPH mRNA表达。两者合计，我们的结果表明Sp1和Sp3绑定到CENPH最小启动子，并在人类鼻咽癌中充当CENPH转录的调节剂。

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