Evidence map›Paper›PMID 39747898›Full record

ArticleNature communications2025

Positive feedback between arginine methylation of YAP and methionine transporter SLC43A2 drives anticancer drug resistance.

Xia-Lu Hong, Chen-Kai Huang, Hui Qian, Chen-Hong Ding, Fang Liu, Huan-Yu Hong, Shu-Qing Liu, Si-Han Wu, Xin Zhang, Wei-Fen Xie

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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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

10 authors.

Xia-Lu Hong *Department of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Chen-Kai Huang *Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Hui Qian *Department of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Chen-Hong DingDepartment of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Fang LiuDepartment of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Huan-Yu HongDepartment of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Shu-Qing LiuDepartment of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Si-Han WuDepartment of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Xin ZhangDepartment of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China. zhang68@hotmail.com.
Wei-Fen XieDepartment of Gastroenterology, Changzheng Hospital, Naval Medical University, Shanghai, China. weifenxie@medmail.com.cn.ORCID 0000-0002-7137-112X

Funding

National Natural Science Foundation of China (National Science Foundation of China) grant 82072641
6 · The paper itself

Abstract

Yes-associated protein (YAP) activation confers resistance to chemotherapy and targeted therapy. Methionine participates in cellular processes by converting to methyl donor for the methylation of DNA, RNA and protein. However, it remains unclear whether methionine affects drug resistance by influencing YAP activity. In this study, we report that methionine deprivation remarkably suppresses the transcriptional activity of YAP-TEAD in cancer cells. Methionine promotes PRMT1-catalyzed asymmetric dimethylation at R124 of YAP (YAP R124me2a). Mimicking of YAP methylation abolishes the reduction effect of methionine-restricted diet on YAP-induced drug resistance. YAP activates the transcription of SLC43A2, the methionine transporter, to increase methionine uptake in cancer cells. Knockdown of SLC43A2 decreases the level of YAP R124me2a. BCH, the inhibitor of SLC43A2, sensitizes tumors to anticancer drugs. Thus, our results unravel the positive feedback between YAP R124 methylation and SLC43A2 that contributes to anticancer drug resistance. Disrupting this positive feedback could be a potential strategy for cancer therapy.

Indexed as

Adaptor Proteins, Signal TransducingAntineoplastic AgentsArginineDrug Resistance, NeoplasmMethionineProtein-Arginine N-MethyltransferasesTranscription FactorsYAP-Signaling ProteinsAnimalsCell Line, TumorFeedback, PhysiologicalGene Expression Regulation, NeoplasticHumansMethylationMiceMice, NudeAdaptor Proteins, Signal TransducingAntineoplastic AgentsArginineMethioninePhosphoproteinsPRMT1 protein, humanProtein-Arginine N-MethyltransferasesRepressor ProteinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID39747898
PMCPMC11697449

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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.