Open Access

Identification of differentially expressed genes induced by aberrant methylation in acute myeloid leukemia using integrated bioinformatics analyses

  • Authors:
    • Wei-Wen Chen
    • Da-Bin Liu
    • Hong-Xia Xiao
    • Li-Jun Zhou
    • Jia Qu
  • View Affiliations

  • Published online on: September 13, 2022     https://doi.org/10.3892/ol.2022.13503
  • Article Number: 383
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute myeloid leukemia (AML) is a life‑threatening hematological malignant disease. Methylation plays a crucial role in the etiology and pathogenesis of AML. The aim of the present study was to identify the aberrantly methylated differentially expressed genes (DEGs) in AML and determine the underlying mechanisms of tumorigenesis by conducting integrated bioinformatics analyses. Gene expression profiles (GSE109179, GSE142699, GSE49665 and GSE14772) and a gene methylation profile (GSE42042) were analyzed to identify the aberrantly methylated DEGs. Functional enrichment analyses of identified genes were conducted based on the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, and protein‑protein interaction networks were established. Finally, the DEGs were validated by the reverse transcription‑quantitative PCR analysis of patient samples. A total of seven downregulated hypermethylated genes and eight upregulated hypomethylated genes were validated. The differentially methylated DEGs were enriched in GO biological process terms associated with control of the immune response and the KEGG analysis indicated they were involved in AML, ferroptosis, TGF‑β signaling and necroptosis pathways. Additionally, five downregulated hypermethylated genes that were also tumor suppressor genes (TSGs) were identified. In vitro assays revealed that the overexpression of transcription factor 7 (TCF7) and integrin a M (ITGAM) significantly inhibited the proliferation of HL60 cells; by contrast, the knockdown of TCF7 and CAMK4 promoted HL60 cell proliferation. Overall, the present study identified differentially methylated DEGs and pathways associated with AML, which may enhance the understanding of the underlying molecular mechanisms of AML. In the future, abnormally methylated oncogenes and TSGs may function as biomarkers and treatment targets for the diagnosis and treatment of AML.
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November-2022
Volume 24 Issue 5

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Chen W, Liu D, Xiao H, Zhou L and Qu J: Identification of differentially expressed genes induced by aberrant methylation in acute myeloid leukemia using integrated bioinformatics analyses. Oncol Lett 24: 383, 2022
APA
Chen, W., Liu, D., Xiao, H., Zhou, L., & Qu, J. (2022). Identification of differentially expressed genes induced by aberrant methylation in acute myeloid leukemia using integrated bioinformatics analyses. Oncology Letters, 24, 383. https://doi.org/10.3892/ol.2022.13503
MLA
Chen, W., Liu, D., Xiao, H., Zhou, L., Qu, J."Identification of differentially expressed genes induced by aberrant methylation in acute myeloid leukemia using integrated bioinformatics analyses". Oncology Letters 24.5 (2022): 383.
Chicago
Chen, W., Liu, D., Xiao, H., Zhou, L., Qu, J."Identification of differentially expressed genes induced by aberrant methylation in acute myeloid leukemia using integrated bioinformatics analyses". Oncology Letters 24, no. 5 (2022): 383. https://doi.org/10.3892/ol.2022.13503