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Effect of miR-214 on biological function in breast cancer MCF-7 cells
田延锋李 芳刘 擘
河北医科大学第一医院普外科 石家庄 050031
TIAN Yanfeng LI Fang LIU Bo ZHAO Zengren DAI Yongjun WEI Ming
Department of General Surgery,the First Hospital,Hebei Medical University, Shijiazhuang 050031
乳腺癌 微小RNA MCF-7细胞 细胞增殖
breast cancer microRNA MCF-7 cell cell proliferation
目的:探讨微小RNA-214(miR-214)对人乳腺癌MCF-7细胞增殖、凋亡、迁移及周期分布等生物学行为的影响。方法:采用脂质体转染法将miR-214 模拟物转入MCF-7 细胞(实验组),以转入miR-214阴性对照的MCF-7 细胞(阴性对照组)作对照。采用实时荧光定量PCR 法检测miR-214的表达情况; CCK-8法检测细胞增殖能力的改变; 流式细胞仪检测细胞凋亡及细胞周期; 划痕愈合实验检测细胞的迁移。结果:实验组MCF-7细胞miR-214的表达较阴性对照组明显上调; 实验组细胞的增殖能力明显受到抑制; 实验组凋亡细胞所占比例明显高于阴性对照组(P=0.008),G1期细胞数增加,S 期细胞数减少(P<0.05); 划痕愈合实验表明,实验组细胞迁移能力明显受到抑制(P<0.001)。结论:MiR-214可能通过抑制乳腺癌MCF-7细胞增殖及迁移、促进细胞凋亡及影响细胞周期的分布而发挥抑癌作用。
Aim: To explore the effect of microRNA-214(miR-214)on the proliferation, apoptosis, migration and cell cycle distribution of human breast cancer MCF-7 cells.Methods: The miR-214 mimics were transfected into MCF-7 cells(experimental group)through liposome transfection, and the MCF-7 cells transfected by miR-214 negative control were used as control. The expression of miR-214 level was detected by real-time fluorogenic quantitative-PCR. The change of proliferation ability of MCF-7 cells was detected by CCK-8 method. The changes of apoptosis and cell cycle distribution were examined by flow cytometry. The change of migration ability was detected by wound healing assay.Results: After transfection with miR-214 mimics, the expression level of miR-214 in MCF-7 cells was up-regulated.Compared with control, the cell proliferation of MCF-7 cells in experimental group was inhibited, the cell apoptosis rate was elevated(P=0.008)and the proportion of cells at G1 phase increased, and that of cells at S phase decreased(P<0.05),besides, the migration ability was inhibited(P<0.001).Conclusion: MiR-214 may act as a tumor suppressor in MCF-7 cells through inhibiting cell proliferation and migration, promote cell apoptosis and affect cell cycle distribution.


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*河北省科技支撑计划项目 14277755D
更新日期/Last Update: 2017-01-20