ArticleInternational journal of clinical and experimental pathology2017
MicroRNAs and regulated interaction networks reveal differences between adult and pediatric acute myeloid leukemia.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesThe purpose of this study was to identify featured microRNAs and their regulated network between adult and pediatric acute myeloid leukemia (AML) and find potential utility as biomarkers for diagnosis and treatment of pediatric AML.
methodsWe downloaded the microRNA expression dataset GSE35320 from Gene Expression Omnibus database and selected expression chips from bone marrow of 71 pediatric AML samples and 6 adulthood AML samples. Differentially expressed microRNAs were identified by Wilcox test. The target genes of these microRNAs were predicted using an integrative method and their functional enrichment analysis was performed using DAVID. Finally, STRING database and Cytoscape software was used to construct and analyze the interaction network.
resultsA total of 7 differentially expressed microRNAs were identified and the remarkably up-regulated and down-regulated microRNAs were miR-16 and miR-142-5p which included 323 and 22 predicted target genes, respectively. The target genes of 7 microRNAs were most associated with regulation of cell cycle, p53 signaling pathway, Wnt signaling pathway and neurotrophin signaling pathway. The interaction network of miR-16 target genes was constructed among 354 high confidence interaction pairs. The core genes of the network, such as TP53, BCL2, VEGFA, had a role in prognosis of children with AML.
conclusionsThe featured microRNAs and their target genes are significant in the occurrence and development of pediatric AML, which is likely to be important for the identification of therapeutic targets and biomarkers for these patients.
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31966399PMC6965806W3005154149What OpenQuestion holds
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