文献类型：期刊文献

英文题名：Chicken CCDC152 shares an NFYB-regulated bidirectional promoter with a growth hormone receptor antisense transcript and inhibits cells proliferation and migration

作者：Lin, Shudai[1,2];Luo, Wei[1,2];Jiang, Mingya[1,2];Luo, Wen[1,2];Abdalla, Bahareldin Ali[1,2];Nie, Qinghua[1,2];Zhang, Li[3];Zhang, Xiquan[1,2]

机构：[1]South China Agr Univ, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Coll Anim Sci, Minist Agr, Guangzhou 510642, Guangdong, Peoples R China;[2]South China Agr Univ, Coll Anim Sci, Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Guangdong, Peoples R China;[3]Guangdong Ocean Univ, Agr Coll, Zhanjiang 524088, Peoples R China

年份：2017

卷号：8

期号：48

起止页码：84039

外文期刊名：ONCOTARGET

收录：SCI-EXPANDED(收录号：WOS:000413030900055)、、WOS

基金：We would like to thank Prof. Yunfeng Wang and Yan Zhao (Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Heilongjiang, China) for donating us LMH cells. This work was supported by the High Technology Research and Development Program of China (2013AA102501), the National Natural Science Foundation (31301958, 31672412), and the China Agriculture Research System (CARS-41-G03).

语种：英文

外文关键词：bidirectional promoter; GHR antisense transcript; coiled-coil domain containing 152; NFYB; cell cycle

外文摘要：The chicken coiled-coil domain-containing protein 152 (CCDC152) recently has been identified as a novel one implicated in cell cycle regulation, cellular proliferation and migration by us. Here we demonstrate that CCDC152 is oriented in a head-to-head configuration with the antisense transcript of growth hormone receptor (GHR) gene. Through serial luciferase reporter assays, we firstly identified a minimal 102 bp intergenic region as a core bidirectional promoter to drive basal transcription in divergent orientations. And site mutation and transient transfected assays showed that nuclear transcription factor Y subunit beta (NFYB) could bind to the CCAAT box and directly transactivate this bidirectional promoter. SiRNA-mediated NFYB depletion could significantly down-regulate the expression of both GHR-AS-I6 and CCDC152. Additionally, the expression of GHR-AS-I6 was significantly up-regulated after CCDC152 overexpression. Overexpression of CCDC152 remarkably reduced cell proliferation and migration through JAK2/STAT signaling pathway. Thus, the GHR-AS-I6-CCDC152 bidirectional transcription unit, as a novel direct target of NFYB, is possibly essential for the accelerated proliferation and motility of different cells.