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余瑛, 黄晶, 李荣, 刘联斌, 王琪, 罗德平. δ-三烯生育酚通过上调MicroRNA-34a抑制宫颈癌细胞增殖[J]. 肿瘤防治研究, 2018, 45(12): 965-969. DOI: 10.3971/j.issn.1000-8578.2018.18.0523
引用本文: 余瑛, 黄晶, 李荣, 刘联斌, 王琪, 罗德平. δ-三烯生育酚通过上调MicroRNA-34a抑制宫颈癌细胞增殖[J]. 肿瘤防治研究, 2018, 45(12): 965-969. DOI: 10.3971/j.issn.1000-8578.2018.18.0523
YU Ying, HUANG Jing, LI Rong, LIU Lianbin, WANG Qi, LUO Deping. δ-tocotrienol Inhibits Proliferation of Cervical Carcinoma Cells Through Upregulating MicroRNA-34a[J]. Cancer Research on Prevention and Treatment, 2018, 45(12): 965-969. DOI: 10.3971/j.issn.1000-8578.2018.18.0523
Citation: YU Ying, HUANG Jing, LI Rong, LIU Lianbin, WANG Qi, LUO Deping. δ-tocotrienol Inhibits Proliferation of Cervical Carcinoma Cells Through Upregulating MicroRNA-34a[J]. Cancer Research on Prevention and Treatment, 2018, 45(12): 965-969. DOI: 10.3971/j.issn.1000-8578.2018.18.0523

δ-三烯生育酚通过上调MicroRNA-34a抑制宫颈癌细胞增殖

δ-tocotrienol Inhibits Proliferation of Cervical Carcinoma Cells Through Upregulating MicroRNA-34a

  • 摘要:
    目的 探究δ-三烯生育酚对HeLa宫颈癌细胞增殖的影响以及microRNA-34a(miR-34a)是否介导这一过程。
    方法 用荧光定量PCR
    方法 检测miR-34a和细胞增殖关键基因表达的变化,CCK-8检测细胞活力变化,Western blot检测细胞增殖关键基因蛋白水平的变化,流式细胞术检测细胞周期变化;并利用miR-34a模拟剂和抑制剂,探究其对细胞增殖的影响。
    结果 δ-三烯生育酚处理HeLa宫颈癌细胞36 h显著降低细胞活力并呈剂量依赖效应。用20 μmol/L δ-三烯生育酚处理细胞36 h显著上调miR-34a表达,显著下调细胞周期关键基因CCND1,同时S细胞比例显著下降。细胞转染miR-34a模拟剂后,CCND1表达和细胞活力都下降;而转染miR-34a抑制剂则显著减弱δ-三烯生育酚的增殖抑制作用。
    结论 δ-三烯生育酚通过上调miR-34a抑制宫颈癌细胞增殖。

     

    Abstract:
    Objective To determine the effects of δ-tocotrienol on the proliferation of cervical carcinoma HeLa cells and whether miR-34a is involved in this process.
    Methods The expression of miR-34a and proliferation-related genes, cell viability, the protein levels of proliferation-related genes and cell cycle were examined using Real-time PCR, CCK-8 assay, Western blot and flow cytometry, respectively. miR-34a mimics and inhibitors were used to determine whether miR-34a mediated the effects of δ-tocotrienol on cell proliferation.
    Results δ-tocotrienol treatment for 36h significantly decreased the viability of HeLa cells in a dose-dependent manner. δ-tocotrienol treatment at 20 μmol/L-1 for 36h significantly stimulated miR-34a expression, however, inhibited CCND1 expression; meanwhile, cells proportion in S phase was decreased. Besides, after miR-34a mimics transfection, the cell viability and CCND1 expression were also decreased. Furthermore, miR-34a inhibitor transfection attenuated the inhibitory effects of δ-tocotrienol on cell proliferation.
    Conclusion δ-tocotrienol inhibits the proliferation of cervical carcinoma cells through upregulating miR-34a expression.

     

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