Evidence map›Paper›PMID 41876450›Full record

ArticleCell death & disease2026

AKT1 phosphorylates PRMT7 to promote GLUD1 methylation and gastric cancer progression.

Ziyi Cui, Hongchen Li, Xiaoben Liang, Xinyu Zhao, Kai Xu, Yao Lu, Yan Zhang, Xia Li, Siyao Wu, Zhen Wang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 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

12 authors.

Ziyi Cui *Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Hongchen Li *Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.ORCID http://orcid.org/0000-0003-2639-8726
Xiaoben Liang *Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Xinyu ZhaoTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Kai XuTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Yao LuTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Yan ZhangTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Xia LiTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Siyao WuTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Zhen WangSchool of Medicine, Hebei University of Engineering, Handan, China. wangzhen@hebeu.edu.cn.ORCID http://orcid.org/0000-0002-0308-6562
Lei LvMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China. lvlei@fudan.edu.cn.ORCID http://orcid.org/0000-0003-4820-3125
Yanping XuTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signalling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. yanpingxu@tongji.edu.cn.ORCID http://orcid.org/0000-0003-2750-5466

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172936, 82472850, 82121004, 82372754, 82073128 and 32000918
6 · The paper itself

Abstract

Glutamine metabolism has emerged as an essential metabolic driver of tumor progression. Glutamate dehydrogenase 1 (GLUD1), a key enzyme in glutaminolysis, is frequently overexpressed in malignancies. Post-translational modifications (PTMs) are crucial for regulating protein function and tumor progression. However, the PTMs of GLUD1, particularly arginine methylation, remain unexplored. Here we report that protein arginine methyltransferase 7 (PRMT7) mediates monomethylation of GLUD1 at arginine 76 (R76), enhancing its protein stability by antagonizing ubiquitin-dependent degradation. Moreover, high glucose destabilizes GLUD1 via the PI3K/Akt pathway. Mechanistically, AKT1 phosphorylates PRMT7 at threonine 73 (T73) and promotes its activity to stabilize GLUD1 by increasing its methylation and reducing ubiquitination. Clinical analysis reveals that elevated GLUD1, PRMT7, and meGLUD1(R76) levels correlate with tumor progression in gastric cancer. In xenograft models, PRMT7 inhibitor SGC3027 combined with chemotherapeutic drugs docetaxel (DTX) synergistically suppresses tumor growth. Collectively, this study identifies the AKT1-PRMT7-GLUD1 axis as a key regulatory pathway in gastric cancer, and highlights its potential as a therapeutic target.

Indexed as

Protein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktStomach NeoplasmsAnimalsCell Line, TumorDisease ProgressionHumansMethylationMiceMice, NudePhosphatidylinositol 3-KinasesPhosphorylationSignal TransductionUbiquitinationAKT1 protein, humanPhosphatidylinositol 3-KinasesPRMT7 protein, humanProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-akt

Identifiers

PMID41876450
PMCPMC13040045

What OpenQuestion holds

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LicenceCC BY
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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.