Integrated analysis of microRNA and transcription factors in the bone marrow of patients with acute monocytic leukemia
| Autor: | Xiao-Cong Lin, Liu-Bo Lan, Hang Ding, Haitao Zhang, Yu-Ming Zhang, Wei-Yu Fu, Ning Li, Qin Yang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Regulation of gene expression Cancer Research microRNA Oncogene Myeloid leukemia Articles sequencing array Computational biology acute monocytic leukemia Biology medicine.disease 03 medical and health sciences Leukemia 030104 developmental biology 0302 clinical medicine Oncology 030220 oncology & carcinogenesis medicine Acute monocytic leukemia Gene Transcription factor transcription factor |
| Zdroj: | Oncology Letters |
| ISSN: | 1792-1082 1792-1074 |
| DOI: | 10.3892/ol.2020.12311 |
| Popis: | Acutemonocytic leukemia (AMoL) is a distinct subtype of acute myeloid leukemia (AML) with poor prognosis. However, the molecular mechanisms and key regulators involved in the global regulation of gene expression levels in AMoL are poorly understood. In order to elucidate the role of microRNAs (miRNAs/miRs) and transcription factors (TFs) in AMoL pathogenesis at the network level, miRNA and TF expression level profiles were systematically analyzed by miRNA sequencing and TF array, respectively; this identified 285 differentially expressed miRNAs and 139 differentially expressed TFs in AMoL samples compared with controls. By combining expression level profile data and bioinformatics tools available for predicting TF and miRNA targets, a comprehensive AMoL-specific miRNA-TF-mediated regulatory network was constructed. A total of 26 miRNAs and 23 TFs were identified as hub nodes in the network. Among these hubs, miR-29b-3p, MYC, TP53 and NFKB1 were determined to be potential AMoL regulators, and were subsequently extracted to construct sub-networks. A hypothetical pathway model was also proposed for miR-29b-3p to reveal the potential co-regulatory mechanisms of miR-29b-3p, MYC, TP53 and NFKB1 in AMoL. The present study provided an effective approach to discover critical regulators via a comprehensive regulatory network in AMoL, in addition to enhancing understanding of the pathogenesis of this disease at the molecular level. |
| Databáze: | OpenAIRE |
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