ArticleJournal of experimental & clinical cancer research : CR2015
Early B-cell factor 3 (EBF3) is a novel tumor suppressor gene with promoter hypermethylation in pediatric acute myeloid leukemia.
Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 34 citations in OpenAlex.
- Tumor suppressor-like mutations mark a dosage-constrained dependency in leukemia.bioRxiv : the preprint server for biology · 2026Article
- MiR-301b-3p targets and regulates EBF3 to impact the stem-like phenotype of breast cancer cells through glycolysis.Journal of clinical biochemistry and nutrition · 2025Article
- Aberrant DNA methylation distorts developmental trajectories in atypical teratoid/rhabdoid tumors.Life science alliance · 2024Article
- Construction of a Prognostic Model for Hepatocellular Carcinoma Based on Macrophage Polarization-Related Genes.Journal of hepatocellular carcinoma · 2024Article
- Circadian clock protein Bmal1 accelerates acute myeloid leukemia by inhibiting ferroptosis through the EBF3/ALOX15 axis.Cancer science · 2023Article
- Epigenome-wide association study of serum folate in maternal peripheral blood leukocytes.Epigenomics · 2023Article
- Gliosarcoma: The Distinct Genomic Alterations Identified by Comprehensive Analysis of Copy Number Variations.Analytical cellular pathology (Amsterdam) · 2022Article
- A novel 10-gene ferroptosis-related prognostic signature in acute myeloid leukemia.Frontiers in oncology · 2022Article
- Identification and validation of prognosis-related DLX5 methylation as an epigenetic driver in myeloid neoplasms.Clinical and translational medicine · 2020Article
- miR-216a-mediated upregulation of TSPAN1 contributes to pancreatic cancer progression via transcriptional regulation of ITGA2.American journal of cancer research · 2020Article
- DNA methylation of a NF-κB binding site in the aquaporin 5 promoter impacts on mortality in sepsis.Scientific reports · 2019Article
- CRISPR-Cas9 genome editing induces megabase-scale chromosomal truncations.Nature communications · 2019Article
- Rare Variant, Gene-Based Association Study of Hereditary Melanoma Using Whole-Exome Sequencing.Journal of the National Cancer Institute · 2017Article
- De novo variants inCold Spring Harbor molecular case studies · 2017Article
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27 authors at 4 institutions in 1 country.
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Abstract
backgroundPediatric acute myeloid leukemia (AML) comprises up to 20% of all childhood leukemia. Recent research shows that aberrant DNA methylation patterning may play a role in leukemogenesis. The epigenetic silencing of the EBF3 locus is very frequent in glioblastoma. However, the expression profiles and molecular function of EBF3 in pediatric AML is still unclear.
methodsTwelve human acute leukemia cell lines, 105 pediatric AML samples and 30 normal bone marrow/idiopathic thrombocytopenic purpura (NBM/ITP) control samples were analyzed. Transcriptional level of EBF3 was evaluated by semi-quantitative and real-time PCR. EBF3 methylation status was determined by methylation specific PCR (MSP) and bisulfite genomic sequencing (BGS). The molecular mechanism of EBF3 was investigated by apoptosis assays and PCR array analysis.
resultsEBF3 promoter was hypermethylated in 10/12 leukemia cell lines. Aberrant EBF3 methylation was observed in 42.9% (45/105) of the pediatric AML samples using MSP analysis, and the BGS results confirmed promoter methylation. EBF3 expression was decreased in the AML samples compared with control. Methylated samples revealed similar survival outcomes by Kaplan-Meier survival analysis. EBF3 overexpression significantly inhibited cell proliferation and increased apoptosis. Real-time PCR array analysis revealed 93 dysregulated genes possibly implicated in the apoptosis of EBF3-induced AML cells.
conclusionIn this study, we firstly identified epigenetic inactivation of EBF3 in both AML cell lines and pediatric AML samples for the first time. Our findings also showed for the first time that transcriptional overexpression of EBF3 could inhibit proliferation and induce apoptosis in AML cells. We identified 93 dysregulated apoptosis-related genes in EBF3-overexpressing, including DCC, AIFM2 and DAPK1. Most of these genes have never been related with EBF3 over expression. These results may provide new insights into the molecular mechanism of EBF3-induced apoptosis; however, further research will be required to determine the underlying details. Our findings suggest that EBF3 may act as a putative tumor suppressor gene in pediatric AML.
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