Apigenin inhibits glioma cell growth through promoting microRNA-16 and suppression of BCL-2 and nuclear factor-B/MMP-9
Apigenin inhibits glioma cell growth through promoting microRNA-16 and suppression of BCL-2 and nuclear factor-B/MMP-9
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DOI：
10.3892/mmr.2016.5460
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发表时间：
2016-09-01
影响因子：
3.4
通讯作者：
You, Jin
中科院分区：
文献类型：
--
作者：
Chen, Xin-Jun;Wu, Mian-Yun;You, Jin
本研究旨在观察芹菜素对胶质瘤细胞的作用，并探讨其可能的作用机制。在本研究中使用了用芹菜素处理的U87人胶质瘤细胞。采用Cell Counting Kit-8溶液和Annexin V-异硫氰酸荧光素/碘化丙啶细胞凋亡检测试剂盒分析芹菜素对U87细胞活力和凋亡细胞死亡的影响。逆转录-定量聚合酶链反应分析也用于确定microRNA-16（miR-16）和MMP-9基因表达水平。核因子-B（NF-B）和B-细胞CLL/淋巴瘤2（BCL 2）蛋白表达水平测定使用蛋白质印迹分析。构建抗miR-16质粒并转染U87细胞。目前的研究表明，芹菜素显着降低细胞活力，诱导U87细胞凋亡的细胞死亡的剂量依赖性方式。此外，研究表明芹菜素显著增加了U87细胞中miR-16水平，抑制了BCL 2蛋白表达，并抑制了NF-B/MMP 9信号通路。此外，使用anti-miR-16质粒下调miR-16逆转了芹菜素对U87细胞中细胞活力、BCL 2蛋白表达和NF-B/MMP-9通路的影响。本研究结果表明芹菜素通过促进miR-16和抑制BCL 2和NF-B/MMP-9抑制胶质瘤细胞生长。总之，本研究证实了芹菜素对胶质瘤细胞的潜在抗癌作用。
The present study aimed to investigate the effect of apigenin on glioma cells and to explore its potential mechanism. U87 human glioma cells treated with apigenin were used in the current study. Cell Counting Kit-8 solution and Annexin V-fluorescein isothiocyanate/propidium iodide Apoptosis Detection kit were used to analyze the effect of apigenin on U87 cell viability and apoptotic cell death. Reverse transcription-quantitative polymerase chain reaction analysis was also used to determine microRNA-16 (miR-16) and MMP-9 gene expression levels. Nuclear factor-B (NF-B) and B-cell CLL/lymphoma 2 (BCL2) protein expression levels were determined using western blot analysis. An anti-miR-16 plasmid was constructed and transfected into U87 cells. The current study demonstrated that apigenin significantly decreased cell viability and induced apoptotic cell death of U87 cells in a dose-dependent manner. Additionally, it was demonstrated that apigenin significantly increased miR-16 levels, suppressed BCL2 protein expression and suppressed the NF-B/MMP9 signaling pathway in U87 cells. Furthermore, downregulation of miR-16 using the anti-miR-16 plasmid reversed the effect of apigenin on cell viability, BCL2 protein expression and the NF-B/MMP-9 pathway in U87 cells. The results of the present study suggested that apigenin inhibits glioma cell growth through promoting miR-16 and suppression of BCL2 and NF-B/MMP-9. In conclusion, the present study demonstrated the potential anticancer effects of apigenin on glioma cells.