Systematic analysis of the molecular mechanism of microRNA-124 in hepatoblastoma cells.

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 (SDCBP), Ras homolog family member G (RHOG) and Rho-GDP dissociation inhibitor-α (ARHGDIA). Regulation of actin cytoskeleton, D-glutamine and D-glutamate metabolism, and axon guidance were significant pathways. Axon guidance pathway was associated with neuropilin (NRP1), MET proto-oncogene, receptor tyrosine kinase (MET) and semaphorin 7A, GPI membrane anchor (SEMA7A). Small GTPase-mediated signal transduction, Ras protein signal transduction, regulation of actin cytoskeleton pathway, D-glutamine and D-glutamate metabolism pathway, axon guidance pathway, SDCBP, RHOG, ARHGDIA, NRP1, SEMA7A, and MET may be implicated in the underlying mechanisms of miR-124 overexpression in hepatoblastoma.