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miR-210 inhibits cell migration and invasion by targeting thebrain-derived neurotrophic factor in glioblastoma  期刊论文  

  • 编号:
    7ab69112-c88e-4a0f-b527-40b621bdcdd3
  • 作者:
  • 语种:
    英文
  • 期刊:
    JOURNAL OF CELLULAR BIOCHEMISTRY ISSN:0730-2312 2019 年 120 卷 7 期 (11375 - 11382) ; JUL
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  • 摘要:

    Recently, there is increasing evidence that microRNAs are related to the development, diagnosis, treatment, and prognosis of glioblastoma. microRNA-210 (miR-210) had been identified in many human cancers, but the specific function of miR-210 remains unclear in glioblastoma. The present study mainly focused on exploring its biological role and potential molecular mechanisms in glioblastoma. We found that miR-210 expression was decreased in glioblastoma, and downregulation of miR-210 was related to worse prognosis in glioblastoma patients. In addition, miR-210 overexpression inhibited the migration and invasion of human glioblastoma cells. At the same time, we found that miR-210 directly targets the brain-derived neurotrophic factor (BDNF) and reduces BDNF expression level. Consistently, BDNF silencing had the same effects as miR-210 overexpression in glioblastoma, and upregulation of BDNF counteracted the inhibitory effect of miR-210 in glioblastoma. In conclusion, miR-210 suppressed the migration and invasion of glioblastoma cells by targeting BDNF.

  • 推荐引用方式
    GB/T 7714:
    Liu Shouyue,Jiang Tao,Zhong Yingjie, et al. miR-210 inhibits cell migration and invasion by targeting thebrain-derived neurotrophic factor in glioblastoma [J].JOURNAL OF CELLULAR BIOCHEMISTRY,2019,120(7):11375-11382.
  • APA:
    Liu Shouyue,Jiang Tao,Zhong Yingjie,Yu Yin.(2019).miR-210 inhibits cell migration and invasion by targeting thebrain-derived neurotrophic factor in glioblastoma .JOURNAL OF CELLULAR BIOCHEMISTRY,120(7):11375-11382.
  • MLA:
    Liu Shouyue, et al. "miR-210 inhibits cell migration and invasion by targeting thebrain-derived neurotrophic factor in glioblastoma" .JOURNAL OF CELLULAR BIOCHEMISTRY 120,7(2019):11375-11382.
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