Evidence map›Paper›PMID 42733934›Full record

ArticleiScience2026

Integrating proteomics and metabolomics to reveal MAT2A for metabolic reprogramming in non-small cell lung cancer cells.

Yimin Chen, Yuxi Liu, Zhenyun Zhu, Anqi Ding, Yuying Suo, Cheng Wang, Xiongjun Wang, Hu Zhou, Qiyu Fang, Qian Liu

Abstract read
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yimin ChenAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Yuxi LiuAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Zhenyun ZhuAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Anqi DingAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Yuying SuoAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Cheng WangSchool of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Xiongjun WangSchool of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Hu ZhouAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Qiyu FangDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, School of Medicine, Tongji University, Shanghai 200433, China.
Qian LiuAnalytical Research Center for Organic and Biological Molecules, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methionine adenosyltransferase 2A (MAT2A) links metabolic reprogramming to epigenetic regulation via S-adenosylmethionine (SAM) production, but its role in non-small cell lung cancer (NSCLC) remains unclear, and current inhibitors require combination strategies. Using proteomics and metabolomics in NSCLC cells treated with MAT2A-targeting siRNA or the inhibitor AG-270, we characterized MAT2A-driven metabolic rewiring. In fatty acid biosynthesis, MAT2A regulates FASN and SCD; exogenous palmitic acid reverses AG-270-induced growth inhibition, supporting combination with the FASN inhibitor TVB-2640. In cholesterol metabolism, MAT2A modulates biosynthesis and efflux, and an LXR agonist promoting cholesterol efflux enhances AG-270 efficacy. In energy metabolism, MAT2A governs glycolysis via HIF1A, and a GLUT1 inhibitor synergizes with AG-270. In the transsulfuration pathway, MAT2A transcriptionally regulates CBS and shows synergy with inhibitors of PHGDH (producing serine for cysteine biosynthesis) and SLC7A11 (mediating cysteine uptake). Collectively, our findings establish MAT2A as a central metabolic regulator in NSCLC and propose rational combination strategies.

Indexed as

MAT2Ametabolic reprogrammingmetabolomicsnon-small cell lung cancerproteomics

Identifiers

PMID42733934
PMCPMC13571943

What OpenQuestion holds

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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.