Evidence map›Paper›PMID 29022893›Full record

ArticleCell death & disease2017

MYCN contributes to the malignant characteristics of erythroleukemia through EZH2-mediated epigenetic repression of p21.

Li Liu, Feng Xu, Chun-Kang Chang, Qi He, Ling-Yun Wu, Zheng Zhang, Xiao Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  2. Review
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  5. Article
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  12. Forkhead Box R2 Knockdown Decreases Chemoresistance to Cisplatin via MYC Pathway in Bladder Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  13. Article
  14. Review
  15. Imidazo[1,2-Molecules (Basel, Switzerland) · 2018
    Article
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

7 authors at 2 institutions in 1 country.

Li LiuDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Feng XuDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Chun-Kang ChangDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Qi HeDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Ling-Yun WuDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Zheng ZhangDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Xiao LiDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai 200233, China.
Shanghai Sixth People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MYC proto-oncogene family including c-myc and n-myc (MYCN) are critical for normal cell development and tumorigenesis. Overexpression of c-myc causes acute erythroleukemia in vivo. However, the role of MYCN in acute erythroleukemia remains poorly understood. In this study, we found that the patients with erythroleukemia showed higher expression of MYCN than normal controls. In vitro experiments, knockdown of MYCN resulted in decreased cell proliferation, elevated autonomously cell apoptosis and increased P21-mediated cell senescence. On the contrary, overexpression of MYCN obviously promoted cell proliferation, and induced erythroid differentiation block and apoptosis resistance to cytotoxic agent. Further gene microarray and functional analysis revealed that EZH2 is a target of MYCN. Knockdown of MYCN inhibited the expression of EZH2, and then activated p21 expression through removal of H3K27me3 at the p21 promoter. Overexpression of ezh2 could antagonize the p21 activation caused by MYCN knockdown. In addition, Aurora inhibitor MLN8237 inhibited the proliferation of erythroleukemia cells through repression of MYCN/EZH2 axis, whereas it minimally affected the normal hematopoietic cells. In conclusion, MYCN contributes to the malignant characteristics of erythroleukemia through EZH2-meidated epigenetic repression of p21. MYCN may serve as a therapy target for the patients with acute erythroleukemia.

Indexed as

ApoptosisAurora KinasesAzepinesCell DifferentiationCell Line, TumorCell ProliferationCellular SenescenceCyclin-Dependent Kinase Inhibitor p21Enhancer of Zeste Homolog 2 ProteinEnzyme ActivationEpigenetic RepressionGene Expression Regulation, NeoplasticHumansLeukemia, Erythroblastic, AcuteN-Myc Proto-Oncogene ProteinPromoter Regions, GeneticAurora KinasesAzepinesCyclin-Dependent Kinase Inhibitor p21Enhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMAS1 protein, humanMLN 8237MYCN protein, humanN-Myc Proto-Oncogene ProteinProto-Oncogene MasPyrimidines

Identifiers

PMID29022893
PMCPMC5682688
OpenAlexW2763263043

What OpenQuestion holds

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LicenceCC BY
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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.