Asian Pacific Journal of Cancer Prevention

Asian Pacific Journal of Cancer Prevention (아시아태평양암예방학회)
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AntagomiR-27a Targets FOXO3a in Glioblastoma and Suppresses U87 Cell Growth in Vitro and in Vivo

  • Ge, Yun-Fei (Department of Neurosurgery, Wuxi People's Hospital of Nanjing Medical University) ;
  • Sun, Jun (Department of Neurosurgery, Wuxi People's Hospital of Nanjing Medical University) ;
  • Jin, Chun-Jie (Department of Neurosurgery, Beichen Hospital of Tianjin) ;
  • Cao, Bo-Qiang (Department of Neurosurgery, Wuxi People's Hospital of Nanjing Medical University) ;
  • Jiang, Zhi-Feng (Department of Neurosurgery, Jiangyin People's Hospital of Southeast University) ;
  • Shao, Jun-Fei (Department of Neurosurgery, Wuxi People's Hospital of Nanjing Medical University)
  • Published : 2013.02.28
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Abstract

Objective: To study the effect of the antagomiR-27a inhibitor on glioblastoma cells. Methods: The miR-27a expression level in specimens of human glioblastoma and normal human brain tissues excised during decompression for traumatic brain injury was assessed using qRT-PCR; The predicted target gene of miR-27a was screened out through bioinformatics databases, and the predicted gene was verified using genetic report assays; the effect of antagomiR-27a on the invasion and proliferation of glioma cells was analyzed using MTT assays and 5-ethynyl-2'-deoxyuridine (EdU) labeling. A xenograft glioblastoma model in BALB-c nude mice was established to detect the effect of antagomiR-27a on tumour growth. Results: qRT-PCR results showed that miR-27a significantly increased in specimens from glioblastoma comparing with normal human brain tissues. Th miR-27a inhibitor significantly suppressed invasion and proliferation of glioblastoma cells. FOXO3a was verified as a new target of miR-27a by Western blotting and reporter analyzes. Tumor growth in vivo was suppressed by administration of the miR-27a inhibitor. Conclusion: MiR-27a may be up-regulated in human glioblastoma, and antagomiR-27a could inhibit the proliferation and invasion ability of glioblastoma cells.

Keywords

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