Evidence map›Paper›PMID 33037410›Full record

ArticleOncogene2020

SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia.

Yajing Chu, Yangpeng Chen, Huidong Guo, Mengke Li, Bichen Wang, Deyang Shi, Xuelian Cheng, Jinxia Guan, Xiaomin Wang, Chenghai Xue and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
    Review
  6. Review
  7. Modeling the Copy Number of HSATII Repeats in Human Pericentromere.International journal of molecular sciences · 2025
    Article
  8. Article
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  10. Article
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  15. Review
  16. Article
  17. Article
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  19. Review
  20. 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

13 authors at 1 institution in 1 country.

Yajing Chu *State Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China. chuyajing@ihcams.ac.cn.ORCID http://orcid.org/0000-0001-6239-1519
Yangpeng Chen *State Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.ORCID http://orcid.org/0000-0002-4945-3540
Huidong Guo *State Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.ORCID http://orcid.org/0000-0003-3851-3656
Mengke LiState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.
Bichen WangState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.
Deyang ShiState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.
Xuelian ChengState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.
Jinxia GuanMy Health Gene Technology Co., Ltd., Service Centre of Tianjin Chentang Science and Technology Commercial District, 300220, Tianjin, China.
Xiaomin WangState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.
Chenghai XueMy Health Gene Technology Co., Ltd., Service Centre of Tianjin Chentang Science and Technology Commercial District, 300220, Tianjin, China.
Tao ChengState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China.ORCID http://orcid.org/0000-0003-4395-1095
Jun ShiState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China. shijun@ihcams.ac.cn.ORCID http://orcid.org/0000-0002-8531-0483
Weiping YuanState Key Laboratory of Experimental Hematology, National Clinical Research Center for Hematological Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 300020, Tianjin, China. wpyuan@ihcams.ac.cn.ORCID http://orcid.org/0000-0001-8288-5022
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic regulations play crucial roles in leukemogenesis and leukemia progression. SUV39H1 is the dominant H3K9 methyltransferase in the hematopoietic system, and its expression declines with aging. However, the role of SUV39H1 via its-mediated repressive modification H3K9me3 in leukemogenesis/leukemia progression remains to be explored. We found that SUV39H1 was down-regulated in a variety of leukemias, including MLL-r AML, as compared with normal individuals. Decreased levels of Suv39h1 expression and genomic H3K9me3 occupancy were observed in LSCs from MLL-r-induced AML mouse models in comparison with that of hematopoietic stem/progenitor cells. Suv39h1 overexpression increased leukemia latency and decreased the frequency of LSCs in MLL-r AML mouse models, while Suv39h1 knockdown accelerated disease progression with increased number of LSCs. Increased Suv39h1 expression led to the inactivation of Hoxb13 and Six1, as well as reversion of Hoxa9/Meis1 downstream target genes, which in turn decelerated leukemia progression. Interestingly, Hoxb13 expression is up-regulated in MLL-AF9-induced AML cells, while knockdown of Hoxb13 in MLL-AF9 leukemic cells significantly prolonged the survival of leukemic mice with reduced LSC frequencies. Our data revealed that SUV39H1 functions as a tumor suppressor in MLL-AF9-induced AML progression. These findings provide the direct link of SUV39H1 to AML development and progression.

Indexed as

Disease ProgressionAnimalsApoptosisCell Line, TumorCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHematopoietic Stem CellsHistonesHumansLeukemia, Myeloid, AcuteLysineMethylationMethyltransferasesMiceMyeloid-Lymphoid Leukemia ProteinHistonesLysineMethyltransferasesMLL-AF9 fusion protein, humanMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionRepressor ProteinsSUV39H1 protein, human

Identifiers

PMID33037410
PMCPMC7728597
OpenAlexW3092602296

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.