Evidence map›Paper›PMID 22839530›Full record

ArticleJournal of hematology & oncology2012

Correlation of SRSF1 and PRMT1 expression with clinical status of pediatric acute lymphoblastic leukemia.

Limin Zou, Han Zhang, Chaohao Du, Xiao Liu, Shanshan Zhu, Wei Zhang, Zhigang Li, Chao Gao, Xiaoxi Zhao, Mei Mei and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.6field-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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Targeting O-GlcNAcylated METTL3 impedes MDS/AML progression via diminishing SRSF1 mMolecular therapy : the journal of the American Society of Gene Therapy · 2025
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  8. Targeting PRMT1 prevents acute and chronic graft-versus-host disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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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

12 authors at 4 institutions in 1 country.

Limin ZouHematology Oncology Center, Beijing Key Laboratory of Pediatric Hematology Oncology, National Key Discipline of Pediatrics, Beijing Children's Hospital, Capital Medical University, 56 Nanlishi Road, Beijing 100045, China.
Han Zhang
Chaohao Du
Xiao Liu
Shanshan Zhu
Wei Zhang
Zhigang Li
Chao Gao
Xiaoxi Zhao
Mei Mei
Shilai Bao
Huyong Zheng
Capital Medical University · CNBeijing Children’s Hospital · CNChinese Academy of Sciences · CNInstitute of Genetics and Developmental Biology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute lymphoblastic leukemia (ALL) is the most frequently-occurring malignant neoplasm in children, but the pathogenesis of the disease remains unclear. In a microarray assay using samples from 100 children with ALL, SFRS1 was found to be up-regulated. Serine/arginine-rich splicing factor 1 (SRSF1, also termed SF2/ASF), encoded by the SFRS1 gene, had been shown to be a pro-oncoprotein. Our previous study indicated that SRSF1 can be methylated by protein arginine methyltransferase 1 (PRMT1) in vitro; however, the biological function of SRSF1 and PRMT1 in pediatric ALL are presently unknown.

methodsMatched, newly diagnosed (ND), complete remission (CR) and relapse (RE) bone marrow samples from 57 patients were collected in order to evaluate the expression patterns of SRSF1 and PRMT1. The potential oncogenic mechanism of SRSF1 and PRMT1 in leukemogenesis was also investigated.

resultsWe identified significant up-regulation of SRSF1 and PRMT1 in the ND samples. Importantly, the expression of SRSF1 and PRMT1 returned to normal levels after CR, but rebounded in the RE samples. Our observation that SRSF1 could predict disease relapse was of particular interest, although the expression patterns of SRSF1 and PRMT1 were independent of the cytogenetic subtypes. In pre-B-cell lines, both SRSF1 and PRMT1 expression could be efficiently attenuated by the clinical chemotherapy agents arabinoside cytosine (Ara-c) or vincristine (VCR). Moreover, SRSF1 and PRMT1 were associated with each other in leukemia cells in vivo. Knock-down of SRSF1 resulted in an increase in early apoptosis, which could be further induced by chemotherapeutics.

conclusionsOur results indicate that SRSF1 serves as an anti-apoptotic factor and potentially contributes to leukemogenesis in pediatric ALL patients by cooperating with PRMT1.

Indexed as

AdolescentCell Transformation, NeoplasticChildChild, PreschoolFemaleGene Expression Regulation, NeoplasticHumansInfantMaleNuclear ProteinsPrecursor Cell Lymphoblastic Leukemia-LymphomaProtein-Arginine N-MethyltransferasesRepressor ProteinsRNA-Binding ProteinsSerine-Arginine Splicing FactorsUp-RegulationNuclear ProteinsPRMT1 protein, humanProtein-Arginine N-MethyltransferasesRepressor ProteinsRNA-Binding ProteinsSerine-Arginine Splicing Factors

Identifiers

PMID22839530
PMCPMC3459738
OpenAlexW2153916329

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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.