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Attention Score in Context
| Title |
Early B-cell factor 3 (EBF3) is a novel tumor suppressor gene with promoter hypermethylation in pediatric acute myeloid leukemia
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|---|---|
| Published in |
Journal of Experimental & Clinical Cancer Research, January 2015
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| DOI | 10.1186/s13046-014-0118-1 |
| Pubmed ID | |
| Authors |
Yan-Fang Tao, Li-Xiao Xu, Jun Lu, Shao-Yan Hu, Fang Fang, Lan Cao, Pei-Fang Xiao, Xiao-Juan Du, Li-Chao Sun, Zhi-Heng Li, Na-Na Wang, Guang-Hao Su, Yan-Hong Li, Gang Li, He Zhao, Yi-Ping Li, Yun-Yun Xu, Hui-Ting Zhou, Yi Wu, Mei-Fang Jin, Lin Liu, Xue-Ming Zhu, Jian Ni, Jian Wang, Feng Xing, Wen-Li Zhao, Jian Pan |
| 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.Results EBF3 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. |
X Demographics
The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| France | 1 | 50% |
| Unknown | 1 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 47 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 47 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 12 | 26% |
| Student > Master | 9 | 19% |
| Researcher | 5 | 11% |
| Student > Bachelor | 4 | 9% |
| Professor | 3 | 6% |
| Other | 8 | 17% |
| Unknown | 6 | 13% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 11 | 23% |
| Biochemistry, Genetics and Molecular Biology | 9 | 19% |
| Agricultural and Biological Sciences | 4 | 9% |
| Psychology | 3 | 6% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 4% |
| Other | 6 | 13% |
| Unknown | 12 | 26% |
Attention Score in Context
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 January 2015.
All research outputs
#16,046,765
of 25,373,627 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#1,011
of 2,378 outputs
Outputs of similar age
#199,997
of 359,647 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#16
of 28 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,378 research outputs from this source. They receive a mean Attention Score of 4.8. This one has gotten more attention than average, scoring higher than 53% of its peers.
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We're also able to compare this research output to 28 others from the same source and published within six weeks on either side of this one. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.