Evidence map›Paper›PMID 36351894›Full record

ArticleCell death & disease2022

PRMT3 drives glioblastoma progression by enhancing HIF1A and glycolytic metabolism.

Yunfei Liao, Zaili Luo, Yifeng Lin, Huiyao Chen, Tong Chen, Lingli Xu, Sean Orgurek, Kalen Berry, Monika Dzieciatkowska, Julie A Reisz and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  17. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
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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

13 authors at 3 institutions in 2 countries.

Yunfei Liao *Key Laboratory of Birth Defects, Children's Hospital, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zaili Luo *Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.ORCID 0000-0002-8773-604X
Yifeng Lin *Key Laboratory of Birth Defects, Children's Hospital, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Huiyao ChenKey Laboratory of Birth Defects, Children's Hospital, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Tong ChenKey Laboratory of Birth Defects, Children's Hospital, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Lingli XuBrain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Sean OrgurekBrain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Kalen BerryBrain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Monika DzieciatkowskaUniversity of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
Julie A ReiszUniversity of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
Angelo D'AlessandroUniversity of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
Wenhao ZhouKey Laboratory of Birth Defects, Children's Hospital, Institutes of Biomedical Sciences, Fudan University, Shanghai, China. zhouwenhao@fudan.edu.cn.ORCID 0000-0001-8956-7238
Q Richard LuBrain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA. richard.lu@cchmc.org.ORCID 0000-0001-6846-9014
Cincinnati Children's Hospital Medical Center · USChildren's Hospital of Fudan University · CNUniversity of Colorado Anschutz Medical Campus · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common and aggressive primary brain tumor, but the mechanisms underlying tumor growth and progression remain unclear. The protein arginine methyltransferases (PRMTs) regulate a variety of biological processes, however, their roles in GBM growth and progression are not fully understood. In this study, our functional analysis of gene expression networks revealed that among the PRMT family expression of PRMT3 was most significantly enriched in both GBM and low-grade gliomas. Higher PRMT3 expression predicted poorer overall survival rate in patients with gliomas. Knockdown of PRMT3 markedly reduced the proliferation and migration of GBM cell lines and patient-derived glioblastoma stem cells (GSC) in cell culture, while its over-expression increased the proliferative capacity of GSC cells by promoting cell cycle progression. Consistently, stable PRMT3 knockdown strongly inhibited tumor growth in xenograft mouse models, along with a significant decrease in cell proliferation as well as an increase in apoptosis. We further found that PRMT3 reprogrammed metabolic pathways to promote GSC growth via increasing glycolysis and its critical transcriptional regulator HIF1α. In addition, pharmacological inhibition of PRMT3 with a PRMT3-specific inhibitor SGC707 impaired the growth of GBM cells. Thus, our study demonstrates that PRMT3 promotes GBM progression by enhancing HIF1A-mediated glycolysis and metabolic rewiring, presenting a point of metabolic vulnerability for therapeutic targeting in malignant gliomas.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsApoptosisCell Line, TumorCell ProliferationGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitMiceProtein-Arginine N-MethyltransferasesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitPRMT3 protein, humanPRMT3 protein, mouseProtein-Arginine N-Methyltransferases

Identifiers

PMID36351894
PMCPMC9646854
OpenAlexW4308735240

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.