Liu Yingxiang, Wei Xing, Zhang Caixia, Liu Jingya, Yu Mengying, Feng Peiwen, Guo Zekun
Orthopedic Oncology Institute, Department of Orthopedic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an 710000, China.
College of Veterinary Medicine, Northwest A&F University, Yangling 712100, China.
Acta Biochim Biophys Sin (Shanghai). 2025 Mar 12. doi: 10.3724/abbs.2025035.
Primordial germ cell 7 (PGC7) is prominently expressed in primordial germ cells (PGCs) and embryonic stem cells (ESCs), serving as a pivotal marker for discerning stem cell pluripotency. However, the role of PGC7 in regulating core pluripotency factors remains unclear. In this study, the expression dynamics of PGC7 and pluripotency- associated proteins are systematically evaluated by quantitative reverse transcription PCR (RT-qPCR) and western blot analysis. Complementary experimental approaches including confocal immunofluorescence and Co- immunoprecipitation (Co-IP) assays are subsequently employed to establish subcellular colocalization patterns and elucidate the molecular mechanisms associated with PGC7 function. The results show that PGC7 is closely associated with the pluripotency status of F9 embryonal carcinoma (EC) cells. Notably, PGC7 can counteract the decrease in pluripotency induced by retinoic acid (RA). Ectopic expression of PGC7 in F9 EC cells enhances the translation of Nanog. Mechanistic analysis reveal that PGC7 activates Y-box binding protein 1 (YBX1) phosphorylation by enhancing the interaction between YBX1 and AKT1. The subsequent phosphorylation of YBX1 reduces its binding to Nanog mRNA and promotes the translation of Nanog. These results shed light on a previously unknown role of PGC7 in supporting the translation of Nanog, offering valuable insights into the functions of PGC7 in F9 EC cells.
原始生殖细胞7（PGC7）在原始生殖细胞（PGC）和胚胎干细胞（ESC）中显著表达，是识别干细胞多能性的关键标志物。然而，PGC7在调节核心多能性因子中的作用仍不清楚。在本研究中，通过定量逆转录PCR（RT-qPCR）和蛋白质免疫印迹分析系统评估了PGC7和多能性相关蛋白的表达动态。随后采用包括共聚焦免疫荧光和免疫共沉淀（Co-IP）分析在内的补充实验方法来建立亚细胞共定位模式，并阐明与PGC7功能相关的分子机制。结果表明，PGC7与F9胚胎癌细胞的多能性状态密切相关。值得注意的是，PGC7可以抵消视黄酸（RA）诱导的多能性降低。PGC7在F9胚胎癌细胞中的异位表达增强了Nanog的翻译。机制分析表明，PGC7通过增强Y盒结合蛋白1（YBX1）与AKT1之间的相互作用来激活YBX1磷酸化。YBX1随后的磷酸化减少了其与Nanog mRNA的结合，并促进了Nanog的翻译。这些结果揭示了PGC7在支持Nanog翻译方面以前未知的作用，为PGC7在F9胚胎癌细胞中的功能提供了有价值的见解。
