Evidence map›Paper›PMID 41816830›Full record

ArticleHaematologica2026

NSUN2-FOSB reciprocity facilitates leukemogenesis in an m

Bin Zhou, Yigang Yuan, Yue Cai, Jingying Zhou, Liuzhi Shi, Yaqian Qin, Chen Meng, Shixin Zhang, Shirui Yu, Xinyao Chen and 9 more

Abstract read
In one paragraph

Article in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

19 authors.

Bin ZhouMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Yigang YuanMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Yue CaiDepartment of Clinical Medicine, Wenzhou Medical University, Chashan District, Wenzhou, Zhejiang Province.
Jingying ZhouDepartment of Pediatrics, Ningbo First Hospital, Ningbo, Zhejiang, China. 59 Liuting Road, Ningbo, 315000, Zhejiang Province.
Liuzhi ShiDepartment of Clinical Laboratory, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Yaqian QinMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Chen MengMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Shixin ZhangMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Shirui YuMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Xinyao ChenMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Xiaofei HeMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Shanshan WuMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Min LiMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Xuanyu YuMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Yifen ShiDepartment of Hematology, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Chongyun XingDepartment of Hematology, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province.
Chiqi ChenKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai. chenchiqi@sjtu.edu.cn.
Meng ZhaoKey Laboratory of Stem Cells and Tissue Engineering (Ministry of Education), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong Province. zhaom38@mail.sysu.edu.cn.
Shenmeng GaoMedical Research Center, The First Affiliated Hospital of Wenzhou Medical University, 1 Xuefubei Street, Ouhai District, Wenzhou, Zhejiang Province, China; The Key Laboratory of Pediatric Hematology and Oncology Diseases of Wenzhou, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang. gaoshenmeng77@wzhospital.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NOP2/Sun RNA methyltransferase family member 2 (NSUN2) catalyzes 5-methylcytosine (m5C) modifications on RNA to regulate mRNA stability. However, its roles in normal hematopoiesis and leukemogenesis remain poorly understood. Here, we show that NSUN2 is markedly upregulated in primary acute myeloid leukemia (AML) patients' samples compared with normal hematopoietic cells. NSUN2 knockdown impaired AML cell proliferation, induced apoptosis, and reduced colony formation. Genetic ablation of Nsun2 in an MLL-AF9-transformed murine AML model substantially impaired leukemia stem cell self-renewal and prolonged overall survival, while sparing normal hematopoiesis, highlighting NSUN2 as a potential therapeutic target. Notably, wild-type NSUN2, but not catalytically inactive mutants, restored leukemia stem cell function and leukemogenesis in NSUN2-deficient AML cells, indicating that these effects are m⁵C-dependent. Mechanistically, NSUN2 stabilized FosB proto-oncogene (FOSB) mRNA via m⁵C modification at nucleotide 3656 in the 3' untranslated region, thereby upregulating FOSB expression. In turn, FOSB transcriptionally activated NSUN2, forming a feedforward regulatory loop. Furthermore, FOSB promoted expression of the anti-apoptotic regulator B-cell lymphoma-2-like protein 1 (BCL2L1) by directly binding to its promoter. In conclusion, these findings uncover a novel NSUN2-FOSB-BCL2L1 axis that drives AML leukemogenesis in an m5C-dependent manner, suggesting the therapeutic potential of targeting this pathway.

Indexed as

5-MethylcytosineCell Transformation, NeoplasticGene Expression Regulation, LeukemicLeukemia, Myeloid, AcuteMethyltransferasesProto-Oncogene Proteins c-fosAnimalsApoptosisCell ProliferationEpitranscriptomeHumansMiceProto-Oncogene MasRNA Methylation5-MethylcytosineMAS1 protein, humanMethyltransferasesNSUN2 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-fos

Identifiers

PMID41816830
PMCPMC13628030

What Socratic 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 Socratic graph.