MicroRNA-150-5p对肝细胞癌细胞增殖、凋亡和周期的影响
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Effects of miR-150-5p on proliferation, apoptosis and cell cycle of hepatocellular carcinoma cells
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    目的  研究microRNA-150-5p(miR-150-5p)在人正常肝细胞和肝细胞癌细胞中的表达,及其对肝细胞癌细胞增殖、凋亡和周期的影响及潜在机制。方法  通过实时荧光定量聚合酶链反应(qRT-PCR)检测各处理组细胞中的miR-150-5p的表达水平;MTT法检测miR-150-5p对肝细胞癌细胞增殖的影响;流式细胞术检测miR-150-5p对肝细胞癌细胞凋亡和周期的影响;荧光素酶报告基因实验检测锌指蛋白609是否为miR-150-5p的直接靶基因。结果  miR-150-5p在肝细胞癌细胞系中的表达较人正常肝细胞细胞系降低,miR-150-5p可抑制肝细胞癌细胞的增殖,促进肝细胞癌细胞的凋亡,并阻滞细胞周期于G1期。miR-150-5p在肝细胞癌中发挥肿瘤抑制分子作用的潜在机制为直接靶向抑制ZNF609的表达。结论  miR-150-5p在肝细胞癌细胞中表达降低,并可通过调控ZNF609的表达而调控肝细胞癌细胞增殖、凋亡和周期。

    Abstract:

    Objective To investigate the expression and effect of miR-150-5p on cell proliferation, cell apoptosis and cell cycle in human hepatocellular carcinoma cells. Methods The expression of miR-150-5p in hepatocellular carcinoma cells and normal human liver cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation of hepatocellular carcinoma cells was analyzed by MTT. Cell apoptosis and cell cycle of hepatocellular carcinoma cells were analyzed by flow cytometry. Luciferase assay was performed to detect whether ZNF609 was the direct target of miR-150-5p in the hepatocellular carcinoma cells. Results The expression of miR-150-5p was significantly down regulated in the hepatocellular carcinoma cells compared to the normal human liver cells. Proliferation of the hepatocellular carcinoma cells was significantly inhibited by miR-150-5p, but cell apoptosis was significantly promoted. Cell cycle of the hepatocellular carcinoma cells was arrested at G1 phage after transfection of miR-150-5p mimics. Further investigation proved ZNF609 was the direct target of miR-150-5p in hepatocellular carcinoma cells. Conclusions miR-150-5p may function as tumor suppressor and play important roles in cell proliferation, cell apoptosis and cell cycle in hepatocellular carcinoma cells by directly targeting ZNF609.

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赵月秋,张正宝,郭红霞,詹传飞,鲁皓,钱晓峰. MicroRNA-150-5p对肝细胞癌细胞增殖、凋亡和周期的影响[J].中国现代医学杂志,2017,(4):27-32

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  • 收稿日期:2016-07-13
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  • 在线发布日期: 2017-02-28
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