Evidence map›Paper›PMID 33931742›Full record

ArticleOncogene2021

Targeting protein lysine methyltransferase G9A impairs self-renewal of chronic myelogenous leukemia stem cells via upregulation of SOX6.

Min Zhou, Xiuli Zhang, Chang Liu, Danian Nie, Shuyi Li, Peilong Lai, Yanli Jin

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
    Review
  3. PRMT1 Promotes the Self-renewal of Leukemia Stem Cells by Regulating Protein Synthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. SOX on tumors, a comfort or a constraint?Cell death discovery · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
    Review
  12. Review
  13. Review
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 3 institutions in 1 country.

Min Zhou *Jinan University Institute of Tumor Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China.
Xiuli Zhang *Jinan University Institute of Tumor Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China.
Chang Liu *Jinan University Institute of Tumor Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China.
Danian Nie *Department of Hematology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Shuyi LiJinan University Institute of Tumor Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China.
Peilong LaiDepartment of Hematology, Guangdong General Hospital/Guangdong Academy of Medical Sciences, Guangzhou, China.
Yanli JinJinan University Institute of Tumor Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China. yanlijin2014@jnu.edu.cn.ORCID http://orcid.org/0000-0001-7569-5546
Jinan University · CNGuangdong General Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The application of tyrosine kinase inhibitors (TKIs) in clinic has revolutionized chronic myelogenous leukemia (CML) treatment, but fails to eliminate leukemia stem cells (LSCs), which are considered as roots of drug resistance and disease relapse. Thus, eradication of LSCs may be a promising strategy for curing CML. In this study, we found that protein lysine methyltransferase G9A was overexpressed in CML LSCs. The upregulation of G9A by BCR-ABL was independent on its tyrosine kinase activity. Knockdown of G9A by shRNAs or pharmacological inhibition of G9A by UNC0642 significantly suppressed survival and impaired self-renewal capacity of CML LSCs. Inhibition of G9a eradicated LSCs in CML mice driven by BCR-ABL gene and dramatically prolonged survival of the mice. Ex vivo treatment with G9A inhibitor inhibited long-term engraftment of CML CD34

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmFusion Proteins, bcr-ablHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMice, Inbred C57BLNeoplastic Stem CellsPrimary Cell CultureQuinazolinesAntineoplastic AgentsEHMT2 protein, humanFusion Proteins, bcr-ablHistocompatibility AntigensHistone-Lysine N-MethyltransferaseImatinib MesylateQuinazolinesSOX6 protein, humanSOXD Transcription FactorsUNC0642

Identifiers

PMID33931742
OpenAlexW3158531553

What OpenQuestion holds

Textmetadata
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.