CRM1 敲低抑制丝氨酸 10 磷酸化的 p27(Kip1)的核输出，并在卵巢上皮性癌的发病机制中发挥作用。
Knockdown of CRM1 inhibits the nuclear export of p27(Kip1) phosphorylated at serine 10 and plays a role in the pathogenesis of epithelial ovarian cancer.
机构信息
Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, PR China; Department of Obstetrics and Gynecology, Wuxi Maternal and Child Health Hospital, Nanjing Medical University, Wuxi 214000, PR China.
Department of Obstetrics and Gynecology, Nantong University Cancer Hospital, Nantong University, Nantong 226001, Jiangsu, PR China.
出版信息
Cancer Lett. 2014 Feb 1;343(1):6-13. doi: 10.1016/j.canlet.2013.09.002. Epub 2013 Sep 7.
In a previous study, the nuclear export protein chromosomal region maintenance (CRM1) was correlated with p27(Kip1) in glioma. The aims of the present study were to investigate the expression of CRM1 and pSer10p27 and their functional roles in epithelial ovarian cancer (EOC) tissues. Using immunohistochemical analysis, CRM1 and pSer10p27 expression levels were shown to be associated with histologic stage and grade (P<0.05). High CRM1 and pSer10p27 expression levels were prognostic indicators of overall survival (P<0.05). Knockdown of CRM1 and pSer10p27 expression arrested cell cycle progression and inhibited the proliferation of SKOV3 cells both in vitro and in vivo. These data support the idea that pSer10p27 and CRM1 play cooperative roles in EOC.
在之前的研究中，核输出蛋白染色体区域维持（CRM1）与神经胶质瘤中的 p27(Kip1) 相关。本研究旨在探讨 CRM1 和 pSer10p27 的表达及其在卵巢上皮性癌（EOC）组织中的功能作用。采用免疫组织化学分析，CRM1 和 pSer10p27 的表达水平与组织学分期和分级相关（P<0.05）。高 CRM1 和 pSer10p27 表达水平是总生存期的预后指标（P<0.05）。CRM1 和 pSer10p27 表达的敲低可阻止细胞周期进程，并抑制 SKOV3 细胞在体外和体内的增殖。这些数据支持 pSer10p27 和 CRM1 在 EOC 中发挥协同作用的观点。
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