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程艳香, 杨潇, 陈干涛. miR-216b通过靶向调控Beclin-1的表达抑制宫颈癌细胞自噬[J]. 肿瘤防治研究, 2016, 43(11): 954-958. DOI: 10.3971/j.issn.1000-8578.2016.11.007
引用本文: 程艳香, 杨潇, 陈干涛. miR-216b通过靶向调控Beclin-1的表达抑制宫颈癌细胞自噬[J]. 肿瘤防治研究, 2016, 43(11): 954-958. DOI: 10.3971/j.issn.1000-8578.2016.11.007
Cheng Yanxiang, Yang Xiao, Chen Gantao. miR-216b Inhibits Cervical Cancer Cells Autophagy by Regulating Beclin-1 Expression[J]. Cancer Research on Prevention and Treatment, 2016, 43(11): 954-958. DOI: 10.3971/j.issn.1000-8578.2016.11.007
Citation: Cheng Yanxiang, Yang Xiao, Chen Gantao. miR-216b Inhibits Cervical Cancer Cells Autophagy by Regulating Beclin-1 Expression[J]. Cancer Research on Prevention and Treatment, 2016, 43(11): 954-958. DOI: 10.3971/j.issn.1000-8578.2016.11.007

miR-216b通过靶向调控Beclin-1的表达抑制宫颈癌细胞自噬

miR-216b Inhibits Cervical Cancer Cells Autophagy by Regulating Beclin-1 Expression

  • 摘要:
    目的 研究miR-216b影响宫颈癌HeLa细胞自噬的作用机制。
    方法 转染miR-216b及应用其抑制剂后,利用GFP-LC3 shRNA转染等方法检测HeLa细胞的自噬水平,Western blot检测自噬相关基因Beclin-1和LC3-Ⅱ的表达变化。
    结果 HeLa细胞转染miR-216b后,HeLa细胞中自噬相关基因Beclin-1受到抑制,LC3-Ⅱ的表达增加,细胞自噬受抑,而抑制miR-216b的表达,自噬水平升高。进一步研究发现,miR-216b能够通过靶结合Beclin-1 3’UTR抑制Beclin-1表达从而抑制细胞自噬的发生。
    结论 miR-216b能够抑制宫颈癌HeLa细胞发生自噬,为宫颈癌的临床治疗提供了的理论基础。

     

    Abstract:
    Objective To investigate the effect of miR-216b on autophagy in cervical cancer HeLa cells.
    Methods After the transfection of miR-216b and the application of their inhibitors,we used GFP-LC3 shRNA transfection to test the autophagy levels of HeLa cells and Western blot to test the expression changes of autophagy-related genes Beclin-1 and LC3-Ⅱ.
    Results After transfected with miR-216b,autophagy related gene Beclin-1 was inhibited in HeLa cells,the expression of LC3-Ⅱ was increased,and autophagy was inhibited; however,the level of autophagy was increased when the expression of miR-216b was inhibited. Further,miR-216b can inhibit the occurrence of autophagy by inhibiting the expression of Beclin-1 by targeting Beclin-1 3’UTR.
    Conclusion  miR-216b could inhibit HeLa cells autophagy,which provides a theoretical basis for the clinical treatment of cervical cancer.

     

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