Park Sung-Won, Do Hyun-Jin, Choi Wonbin, Song Hyuk, Chung Hak-Jae, Kim Jae-Hwan
Department of Biomedical Science, College of Life Science, CHA University, Seongnam-Si, Gyeonggi-Do 13488, Republic of Korea.
Department of Stem Cell & Regenerative Technology, Konkuk Institute of Technology, Konkuk University, Seoul 05030, Republic of Korea.
Biochem Biophys Res Commun. 2017 Jun 3;487(3):532-538. doi: 10.1016/j.bbrc.2017.04.059. Epub 2017 Apr 13.
We demonstrated that ETV4 is a transcriptional activator of the NANOG gene in human embryonic carcinoma NCCIT cells. The endogenous expression of NANOG and ETV4 in naïve cells was significantly down-regulated upon differentiation and by shRNA-mediated knockdown of ETV4. NANOG transcription was significantly upregulated by ETV4 overexpression. A putative ETS binding site (EBS) is present in the region (-285 to -138) of the proximal promoter. Site-directed mutagenesis of the putative EBS (AGGATT) abolished NANOG promoter activity and ETV4 interacted with this putative EBS both in vivo and in vitro. Our data provide the molecular details of ETV4-mediated NANOG gene expression.
我们证明，在人胚胎癌NCCIT细胞中，ETV4是NANOG基因的转录激活因子。在原始细胞中，NANOG和ETV4的内源性表达在分化时以及通过shRNA介导的ETV4敲低后均显著下调。ETV4过表达显著上调了NANOG转录。在近端启动子区域（-285至-138）存在一个假定的ETS结合位点（EBS）。对假定的EBS（AGGATT）进行定点诱变消除了NANOG启动子活性，并且ETV4在体内和体外均与该假定的EBS相互作用。我们的数据提供了ETV4介导的NANOG基因表达的分子细节。
