Yan Sujuan, Deng Yan, Qiang Yong, Xi Qinghua, Liu Rong, Yang Shuyun, Liu Jian, Tang Chunhui, Zhong Jianxin, Wang Yingying
Department of Pathogen Biology, Medical College, Jiangsu Provice Key Laboratory for Information and Molecular Drug Target, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Tumour Biol. 2015 Jun;36(6):4633-42. doi: 10.1007/s13277-015-3111-1. Epub 2015 Jan 28.
SYF2 is reported to be as a cell cycle regulator at the G1/S transition and encodes a nuclear protein that interacts with cyclin-D-type binding protein 1. In our study, we investigated the role of SYF2 in human epithelial ovarian cancer (EOC) progression. Western blot and immunohistochemistry analysis displayed that SYF2 was overexpressed in EOC tissues and EOC cell lines. In addition, the immunoreactivity of SYF2 was positively correlated with tumor grade and Ki-67 expression. In vitro, serum starvation-refeeding experiment and SYF2-siRNA transfection assay demonstrated that the expression of SYF2 was promoted in the proliferative progression of EOC cells, while knockdown of SYF2 expression decreased and inhibited cell growth rate of EOC cells. With all the results, we support that SYF2 might contribute to EOC progression via modulation of proliferation in EOC cells and would provide a novel therapeutic target of human EOC.
据报道,SYF2是一种在G1/S期转换时的细胞周期调节因子,编码一种与细胞周期蛋白D型结合蛋白1相互作用的核蛋白。在我们的研究中,我们调查了SYF2在人上皮性卵巢癌(EOC)进展中的作用。蛋白质印迹法和免疫组织化学分析显示,SYF2在EOC组织和EOC细胞系中过表达。此外,SYF2的免疫反应性与肿瘤分级和Ki-67表达呈正相关。在体外,血清饥饿-再喂养实验和SYF2-siRNA转染试验表明,在EOC细胞的增殖过程中SYF2的表达得到促进,而敲低SYF2表达则降低并抑制了EOC细胞的生长速率。基于所有这些结果,我们支持SYF2可能通过调节EOC细胞的增殖促进EOC进展,并将为人类EOC提供一个新的治疗靶点。