文献类型：期刊文献

英文题名：Knocking down SMC1A inhibits growth and leads to G2/M arrest in human glioma cells

作者：Ma, Zengyi[1];Lin, Min[2];Li, Kui[2];Fu, Yuzhi[2];Liu, Xiaodong[1];Yang, Delin[1];Zhao, Yao[1];Zheng, Jing[2];Sun, Bing[1]

机构：[1]Fudan Univ, Dept Neurosurg, Shanghai Neurosurg Ctr, Huashan Hosp, Shanghai 200433, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Shanghai 200237, Peoples R China

年份：2013

卷号：6

期号：5

起止页码：862

外文期刊名：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000318573200006)】；

基金：This work was supported by grants from the National Natural Science Foundation of China (No.30600577).

语种：英文

外文关键词：SMC1A; knocking down; human glioma

摘要：Cohesin, a multiunit complex of SMC1A, SMC3 and Rad21, associates with chromatin after mitosis and holds sister chromatids together following DNA replication. It has been reported that SMC1A is mutated in some cancer types, leading to genomic instability and abnormal cell growth. In this study, we investigated the role of SMC1A in human glioma. We found that SMC1A was expressed at abnormally high levels in human glioma tissue and in cultured U251 glioma cells. Knocking down SMC1A expression in U251 cells with SMC1A-targeted interfering RNAs inhibited cell growth and induced G2/M cell cycle arrest. Furthermore, expression of the cell cycle associated gene CCNB1IP1 was dramatically increased, whereas expression of Cyclin B1 was decreased in SMC1A-deficienct U251 cells. These results suggest that SMC1A upregulation is involved in the pathogenesis of glioma.