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

International Journal of Clinical and Experimental Pathology

Delin Yang¹  Bing Sun¹  Kui Li¹  Jing Zheng¹  Min Lin¹  Yao Zhao¹  Yuzhi Fu¹  Xiaodong Liu¹  Zengyi Ma¹ 

关键词: SMC1A;    knocking down;    human glioma;   

DOI  :  

学科分类：生理学与病理学

来源: e-Century Publishing Corporation

【 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.

【 授权许可】

Unknown