Evidence map›Paper›PMID 35803962›Full record

ArticleNature communications2022

PRMT5 activates AKT via methylation to promote tumor metastasis.

Lei Huang, Xiao-Ou Zhang, Esteban J Rozen, Xiaomei Sun, Benjamin Sallis, Odette Verdejo-Torres, Kim Wigglesworth, Daniel Moon, Tingting Huang, John P Cavaretta and 5 more

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

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

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  20. A Further Case for Targeting PRMT5 and the ERK1/2 and PI3K Pathways in CRC.International journal of molecular sciences · 2025
    Article

8 more citing papers are in PubMed but not listed here.

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

15 authors at 4 institutions in 2 countries.

Lei HuangDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Xiao-Ou ZhangProgram in Bioinformatics and Integrative Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Esteban J RozenDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Xiaomei SunDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Benjamin SallisDepartment of Microbiology and Physiological System, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Odette Verdejo-TorresDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Kim WigglesworthDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Daniel MoonDepartment of Biology, Tufts University, Boston, MA, USA.
Tingting HuangDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
John P CavarettaDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Gang WangDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Lei ZhangDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Jason M ShohetDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0001-8059-3771
Mary M LeeSidney Kimmel Medical College, Thomas Jefferson University, Philadephia, PA, USA. mary.lee@nemours.org.ORCID 0000-0003-1985-4594
Qiong WuDepartment of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, USA. joae.wu@umassmed.edu.ORCID 0000-0002-3636-9008
University of Massachusetts Chan Medical School · USThomas Jefferson University · USTongji University · CNTufts University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein arginine methyltransferase 5 (PRMT5) is the primary methyltransferase generating symmetric-dimethyl-arginine marks on histone and non-histone proteins. PRMT5 dysregulation is implicated in multiple oncogenic processes. Here, we report that PRMT5-mediated methylation of protein kinase B (AKT) is required for its subsequent phosphorylation at Thr308 and Ser473. Moreover, pharmacologic or genetic inhibition of PRMT5 abolishes AKT1 arginine 15 methylation, thereby preventing AKT1 translocation to the plasma membrane and subsequent recruitment of its upstream activating kinases PDK1 and mTOR2. We show that PRMT5/AKT signaling controls the expression of the epithelial-mesenchymal-transition transcription factors ZEB1, SNAIL, and TWIST1. PRMT5 inhibition significantly attenuates primary tumor growth and broadly blocks metastasis in multiple organs in xenograft tumor models of high-risk neuroblastoma. Collectively, our results suggest that PRMT5 inhibition augments anti-AKT or other downstream targeted therapeutics in high-risk metastatic cancers.

Indexed as

NeoplasmsProto-Oncogene Proteins c-aktArginineCell Line, TumorHumansMethylationProtein-Arginine N-MethyltransferasesArgininePRMT5 protein, humanProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-akt

Identifiers

PMID35803962
PMCPMC9270419
OpenAlexW4284891916

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.