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Int J Clin Exp Pathol 2013;6(5):862-869

Original Article
Knocking down SMC1A inhibits growth and leads to G2/M arrest in human glioma cells

Zengyi Ma, Min Lin, Kui Li, Yuzhi Fu, Xiaodong Liu, Delin Yang, Yao Zhao, Jing Zheng, Bing Sun

Department of Neurosurgery, Shanghai Neurosurgical Center, Huashan Hospital, Fudan University, Shanghai, China; School of Pharmacy,
East China University of Science and Technology, Shanghai, China

Received March 8, 2013; Accepted April 5, 2013; Epub April 15, 2013; Published May 1, 2013

Abstract: 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. (IJCEP1303015).

Keywords: SMC1A, knocking down, human glioma

Address correspondence to: Dr. Bing Sun, Department of Neurosurgery, Shanghai Neurosurgical Center, Huashan Hospital, Fudan
University, Shanghai, China. Phone: +86 21 52887223; E-mail: msunbing@yahoo.com