Department of Animal Biotechnology, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, People's Republic of China.
BMB Rep. 2012 Jan;45(1):20-5. doi: 10.5483/bmbrep.2012.45.1.20.
The present study aimed to investigate the function of translationally controlled tumor protein (TCTP) in the regulation of Oct4 in mouse embryonic carcinoma P19 cells and mouse J1 embryonic stem (ES) cells. The mRNA level of endogenous TCTP in somatic cells was 2-4 folds higher than that in pluripotent P19 and J1 ES cells. Overexpression of TCTP in mouse pluripotent cells not only reduced the level of Oct4 transcription, but also decreased the pluripotency of stem cells. The N-terminal end of TCTP (amino acids 1-60) played an important role in suppressing the Oct4 promoter. Moreover, overexpression of TCTP in P19 cells suppressed the Oct4 promoter activity in a dose- and a time-dependent manner. In addition, knockdown of TCTP by small interfering RNA increased the expression of Oct4. Our study indicates that TCTP downregulates the Oct4 expression by binding the Sf1 site of Oct4 promoter in mouse pluripotent cells.
本研究旨在探讨翻译控制肿瘤蛋白（TCTP）在调节小鼠胚胎癌细胞 P19 细胞和小鼠 J1 胚胎干细胞（ES 细胞）中的 Oct4 功能。体细胞中内源性 TCTP 的 mRNA 水平比多能性 P19 和 J1 ES 细胞高 2-4 倍。TCTP 在小鼠多能性细胞中的过表达不仅降低了 Oct4 转录水平，而且降低了干细胞的多能性。TCTP 的 N 端（氨基酸 1-60）在抑制 Oct4 启动子中起重要作用。此外，TCTP 在 P19 细胞中的过表达以剂量和时间依赖的方式抑制 Oct4 启动子活性。此外，通过小干扰 RNA 敲低 TCTP 增加了 Oct4 的表达。我们的研究表明，TCTP 通过结合小鼠多能细胞中 Oct4 启动子的 Sf1 位点下调 Oct4 的表达。
