Evidence map›Paper›PMID 28400619›Full record

ArticleLeukemia2017

Dysfunction of the WT1-MEG3 signaling promotes AML leukemogenesis via p53-dependent and -independent pathways.

Y Lyu, J Lou, Y Yang, J Feng, Y Hao, S Huang, L Yin, J Xu, D Huang, B Ma and 11 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 125 citations in OpenAlex.

  1. Long non-coding RNA maternally expressed gene 3 (Turkish journal of obstetrics and gynecology · 2026
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  6. MALNC: a new mutant NPM1/IDH2Cancer gene therapy · 2025
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  11. Review
  12. Review
  13. Review
  14. High TCTA expression is an adverse prognostic biomarker in acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2024
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 3 countries.

Y LyuDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
J LouDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
Y YangDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
J FengDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
Y HaoDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
S HuangDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
L YinDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
J XuDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
D HuangDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
B MaDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
D ZouDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
Y WangDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
Y ZhangDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
B ZhangDepartment of Neurosurgery, the Second Affiliated Hospital of Dalian Medical University, Dalian, China.
P ChenDepartment of Obstetrics and Gynecology, the Second Xiangya Hospital, Central South University, Changsha, China.
K YuDepartment of Cellular Biology and Anatomy, Augusta University, Augusta, GA, USA.
E W-F LamDepartment of Surgery and Cancer, Imperial College London, London, UK.
X WangDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
Q LiuDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
J YanDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
B JinDepartment of Hematology, the Second Affiliated Hospital, Institute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, China.
Dalian Medical University · CNSecond Affiliated Hospital of Dalian Medical University · CNAugusta University · USImperial College London · GBSecond Xiangya Hospital of Central South University · CN

Funding

Breast Cancer Now 2012MAYPR070Breast Cancer Now 2012NOVPHD016Cancer Research UK 12011
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) play a pivotal role in tumorigenesis, exemplified by the recent finding that lncRNA maternally expressed gene 3 (MEG3) inhibits tumor growth in a p53-dependent manner. Acute myeloid leukemia (AML) is the most common malignant myeloid disorder in adults, and TP53 mutations or loss are frequently detected in patients with therapy-related AML or AML with complex karyotype. Here, we reveal that MEG3 is significantly downregulated in AML and suppresses leukemogenesis not only in a p53-dependent, but also a p53-independent manner. In addition, MEG3 is proven to be transcriptionally activated by Wilms' tumor 1 (WT1), dysregulation of which by epigenetic silencing or mutations is causally involved in AML. Therefore MEG3 is identified as a novel target of the WT1 molecule. Ten-eleven translocation-2 (TET2) mutations frequently occur in AML and significantly promote leukemogenesis of this disorder. In our study, TET2, acting as a cofactor of WT1, increases MEG3 expression. Taken together, our work demonstrates that TET2 dysregulated WT1-MEG3 axis significantly promotes AML leukemogenesis, paving a new avenue for diagnosis and treatment of AML patients.

Indexed as

Signal TransductionApoptosisCell ProliferationCell Transformation, NeoplasticDioxygenasesDNA-Binding ProteinsDNA MethylationGene Expression Regulation, LeukemicHumansIntronsLeukemia, Myeloid, AcuteProto-Oncogene ProteinsRNA, Long NoncodingTrans-ActivatorsTranscription, GeneticWT1 ProteinsDioxygenasesDNA-Binding ProteinsMEG3 non-coding RNA, humanProto-Oncogene ProteinsRNA, Long NoncodingTET2 protein, humanTrans-ActivatorsWT1 Proteins

Identifiers

PMID28400619
PMCPMC5729340
OpenAlexW2607089824

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.