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急性B淋巴细胞白血病的差异microRNA综合调控网络的生物信息学分析
OBJECTIVE: To reveal the involvement of molecules in the pathogenesis of B-cell acute lymphoblastic leukemia (B-ALL) by bioinformatics analyses. METHODS: The microarray data of B-ALL were downloaded from the Gene Expression Omnibus (GEO) database and Qlucore Omics Explorer software was used to scree...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
Publicado: |
Editorial office of Chinese Journal of Hematology
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365002/ https://www.ncbi.nlm.nih.gov/pubmed/27535859 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2016.07.009 |
Sumario: | OBJECTIVE: To reveal the involvement of molecules in the pathogenesis of B-cell acute lymphoblastic leukemia (B-ALL) by bioinformatics analyses. METHODS: The microarray data of B-ALL were downloaded from the Gene Expression Omnibus (GEO) database and Qlucore Omics Explorer software was used to screen differentially expressed miRNA. Based on the differentially expressed miRNAs, we predicted the target genes, long non-coding RNAs (lncRNA) and transcription factors (TFs). Then we constructed the miRNAs-centered comprehensive regulatory network. In addition, we performed functional enrichment analysis to analyze the functions of target genes. RESULTS: Of all the 15 differentially expressed miRNAs, 7 miRNAs were of overexpression, 8 miRNAs underexpressed. From the miRNAs comprehensive regulatory network, we found that hsa-miR-486-3p and hsa-miR-126 regulated a large number of target genes, hsa-miR-126 including target genes MYC. The hsa-miR-29a, hsa-miR-130a and hsa-miR-181c regu-lated a lot of lncRNAs containing X-inactive-specific transcript (XIST). The hsa-miR-181a-2, hsa-miR-181b-2 and hsa-miR-663 were regulated by a host of TFs including caudal-related homeobox transcription fact2 (CDX2). Additionally, the target genes of has-miR-126 were enriched in Wnt pathways. CONCLUSION: The expression of hsa-miR-29a, hsa-miR-126 and has-miR-181 family were significantly different in B-ALL. Target gene of MYC, TFs of CDX2 and lncRNA of XIST may play important roles in the development of B-ALL, serving as a potential therapeutic target. |
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