Journal
BMC MEDICAL GENOMICS
Volume 12, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12920-018-0469-0
Keywords
T-ALL; Pathogenesis; Cell cycle; Cell proliferation; Feed-forward loops
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Funding
- National Natural Science Foundation of China (NSFC) [31822030, 31801113, 31801154]
- China Postdoctoral Science Foundation [2017 M622455, 2018 M632830]
- Key Research & Development Plan of Shandong Province [2015GSF118031]
- program for HUST Academic Frontier Youth Team
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BackgroundT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy. Aberrant expressed genes contribute to the development and progression of T-ALL. However, the regulation underlying their aberrant expression remains elusive. Dysregulated expression of transcription factors and miRNAs played important regulatory roles in the pathogenesis of T-ALL.MethodsIn this study, we analyzed the alteration of transcriptome profiling and regulatory networks between T-ALL sample and normal T cell samples at transcriptional and post-transcriptional levels.ResultsOur results demonstrated that genes related to cell cycle and cell proliferation processes were significantly upregulated in T-ALL comparing to normal samples. Meanwhile, regulatory network analyses revealed that FOXM1, MYB, SOX4 and miR-21/19b as core regulators played vital roles in the development of T-ALL. FOXM1-miR-21-5p-CDC25A and MYB/SOX4-miR-19b-3p-RBBP8 were identified as important feed-forward loops involved in the oncogenesis of T-ALL. Drug-specific analyses showed that GSK-J4 may be an effective drug, and CDC25A/CAPN2/MCM2 could serve as potential therapeutic targets for T-ALL.ConclusionsThis study may provide novel insights for the regulatory mechanisms underlying the development of T-ALL and potential therapeutic targets.
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