Evidence map›Paper›PMID 39668478›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

PRMT1 Promotes the Self-renewal of Leukemia Stem Cells by Regulating Protein Synthesis.

Min Zhou, Yi Huang, Ping Xu, Shuyi Li, Chen Duan, Xiaoying Lin, Shilai Bao, Waiyi Zou, Jingxuan Pan, Chang Liu and 1 more

Abstract read
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In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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  11. PRMT1 Promotes the Self-renewal of Leukemia Stem Cells by Regulating Protein Synthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

11 authors.

Min ZhouState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Yi HuangState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Ping XuState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Shuyi LiState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Chen DuanState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Xiaoying LinState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Shilai BaoState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, 100101, China.
Waiyi ZouDepartment of Hematology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Jingxuan PanState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, 510060, China.
Chang LiuState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
Yanli JinState Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.ORCID https://orcid.org/0000-0001-7569-5546

Funding

Basic and Applied Basic Research Project of Guangzhou Basic Research Program 2024A03J0451Basic and Applied Basic Research Project of Guangzhou Basic Research Program 2024A04J3325National Natural Science Foundation of China 81922069National Natural Science Foundation of China 81974505National Natural Science Foundation of China 82003778National Natural Science Foundation of China 82373897
6 · The paper itself

Abstract

The application of tyrosine kinase inhibitors (TKIs) has revolutionized the management of chronic myeloid leukemia (CML). However, disease relapse and progression particularly due to persistent leukemia stem cells (LSCs) remain a big challenge in the clinic. Therefore, validation of the therapeutic vulnerability in LSCs is urgently needed. This study verifies the critical role of protein arginine methyltransferase 1 (PRMT1) in the maintenance of CML LSCs. It is found that PRMT1 promotes the survival and serially plating abilities of human primary CML LSCs. Genetic deletion of Prmt1 significantly delays the leukemogenesis and impairs the self-renewal of LSCs in BCR-ABL-driven CML mice. PRMT1 regulates LSCs and leukemia development depending on its methyltransferase activity. Pharmacological inhibition of PRMT1 activity by MS023 remarkably eliminates LSCs and prolongs the survival of CML mice. Mechanistical studies reveal that PRMT1 promotes transcriptional activation of ribosomal protein L29 (RPL29) via catalyzing asymmetric dimethylation of histone H4R3 (H4R3me2a) at its gene promoter region. PRMT1 augments the global protein synthesis via RPL29 in CML LSCs. Taken together, the findings provide new evidence that histone arginine methylation modification regulates protein synthesis in LSCs and highlight PRMT1 as a valuable druggable target for patients with CML.

Indexed as

Cell Self RenewalLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsProtein-Arginine N-MethyltransferasesProtein BiosynthesisRepressor ProteinsAnimalsHumansMicePRMT1 protein, humanPrmt1 protein, mouseProtein-Arginine N-MethyltransferasesRepressor ProteinsCMLleukemia stem cellsPRMT1protein synthesisRPL29self‐renewal

Identifiers

PMID39668478
PMCPMC11791931

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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.