Down-regulation of miR-106b suppresses the growth of human glioma cells

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• 作者：Anling Zhang (1)
  Jianwei Hao (1)
  Kun Wang (1)
  Qiang Huang (1)
  Kai Yu (1)
  Chunsheng Kang (1)
  Guangxiu Wang (1)
  Zhifan Jia (1)
  Lei Han (1)
  Peiyu Pu (1)
  
• 关键词：Glioma ; miR ; 106b Expression ; miR ; 106b ASON ; RBL2
• 刊名：Journal of Neuro-Oncology
• 出版年：2013
• 出版时间：April 2013
• 年：2013
• 卷：112
• 期：2
• 页码：179-189
• 全文大小：1308KB
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• 作者单位：Anling Zhang (1)
  Jianwei Hao (1)
  Kun Wang (1)
  Qiang Huang (1)
  Kai Yu (1)
  Chunsheng Kang (1)
  Guangxiu Wang (1)
  Zhifan Jia (1)
  Lei Han (1)
  Peiyu Pu (1)
  
  1. Department of Neurosurgery; Tianjin Medical University General Hospital; Tianjin Neurological Institute; Key Laboratory of Post-trauma Neuro-repair and Regeneration of the Central Nervous System, Ministry of Education; Tianjin Key Laboratory of Injuries, Variations and Regeneration of the Nervous System, 154 Anshan Road, Heping District, Tianjin, 300052, People’s Republic of China
  
• ISSN：1573-7373

文摘

Recently, many studies have found that the miR-106b?~25 cluster plays an oncogenic role in tumor progression. However, the precise role of each microRNAs (miRNAs) in the cluster is not yet clear. In the present study, we examined the expression of miR-106b in glioma samples and a tissue microarray by real-time PCR and in situ hybridization (ISH), respectively, finding that miR-106b is overexpressed in the majority of gliomas. Meanwhile, the expression of miR-106b was positively correlated with tumor grade (p?<?0.05). The transfection of a miR-106b anti-sense oligonucleotide (ASON) into three human glioma cell lines (U251, LN229 and TJ905) suppressed the proliferation of these cells. Moreover, the growth of xenograft tumors in nude mice treated with miR-106b ASON was significantly impaired. A bioinformatics analysis predicted that RBL2 may be the target of miR-106b, and dual-luciferase reporter assays identified RBL2, but not RB1 or RBL1, as a target of miR-106b. These results suggest that miR-106b facilitates glioma cell growth by promoting cell cycle progression through the negative regulation of RBL2.