Wang Guiming, Liu Hong, Wei Zhigang, Jia Hongyan, Liu Yu, Liu Jiansheng
Department of Surgery, The First Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Oncol Lett. 2017 Dec;14(6):7161-7170. doi: 10.3892/ol.2017.7131. Epub 2017 Oct 3.
The present study aimed to identify the molecular mechanisms of microRNA-124 (miRNA-124/miR-124) in hepatoblastoma. The GSE6207 microarray dataset, obtained from the Gene Expression Omnibus database, included samples extracted from HepG2 cells transfected with miR-124 duplex (the experimental group) or negative control (the control group) at 4, 8, 16, 24, 32, 72 and 120 h after transfection. Differentially expressed genes (DEGs) were screened between the two groups. miR-124 activity was inferred based on the expression of its target genes. The mRNAs targeted by miR-124 were predicted and a miR-124-target mRNA network was constructed. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed for the target genes. The number of DEGs was highest at 72 h. The experimental group had higher miR-124 activity than that of the control group at 4, 8, 16, 24 and 120 h. Small GTPase-mediated signal transduction and Ras protein signal transduction were significant GO terms enriched with syndecan binding protein (), Ras homolog family member G () and Rho-GDP dissociation inhibitor-α (). Regulation of actin cytoskeleton, D-glutamine and D-glutamate metabolism, and axon guidance were significant pathways. Axon guidance pathway was associated with neuropilin (), MET proto-oncogene, receptor tyrosine kinase and semaphorin 7A, GPI membrane anchor (). Small GTPase-mediated signal transduction, Ras protein signal transduction, regulation of actin cytoskeleton pathway, D-glutamine and D-glutamate metabolism pathway, axon guidance pathway, , and may be implicated in the underlying mechanisms of miR-124 overexpression in hepatoblastoma.
本研究旨在确定微小RNA - 124（miRNA - 124/miR - 124）在肝母细胞瘤中的分子机制。从基因表达综合数据库获得的GSE6207芯片数据集，包括转染miR - 124双链体的HepG2细胞（实验组）或阴性对照（对照组）在转染后4、8、16、24、32、72和120小时提取的样本。筛选两组之间的差异表达基因（DEG）。基于其靶基因的表达推断miR - 124活性。预测miR - 124靶向的mRNA，并构建miR - 124 -靶mRNA网络。对靶基因进行基因本体（GO）和京都基因与基因组百科全书通路富集分析。DEG的数量在72小时时最高。实验组在4、8、16、24和120小时时的miR - 124活性高于对照组。小GTP酶介导的信号转导和Ras蛋白信号转导是富含多配体蛋白聚糖结合蛋白（）、Ras同源家族成员G（）和Rho - GDP解离抑制剂 -α（）的显著GO术语。肌动蛋白细胞骨架调节、D -谷氨酰胺和D -谷氨酸代谢以及轴突导向是显著的通路。轴突导向通路与神经纤毛蛋白（）、原癌基因MET、受体酪氨酸激酶和信号素7A、GPI膜锚定物（）相关。小GTP酶介导的信号转导、Ras蛋白信号转导、肌动蛋白细胞骨架调节通路、D -谷氨酰胺和D -谷氨酸代谢通路、轴突导向通路、以及可能与miR - 124在肝母细胞瘤中过表达的潜在机制有关。
