Evidence map›Paper›PMID 42323345›Full record

ArticleScientific reports2026

Deciphering glutamine metabolic reprogramming: a novel therapeutic target ALDH18A1 in triple-negative breast cancer.

Shuixian Li, Shenghan Gao, Jinsong Hu, Shuhan Lyu, Ju Yang, Chenyang Zhang, Chenshuo You, Xiuping Liu, Jigang Wang, Guoyuan Liu

Abstract read
In one paragraph

Article in Scientific reports, 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.

Shuixian Li *Department of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China.
Shenghan Gao *Department of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China.
Jinsong HuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China.
Shuhan LyuDepartment of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90089, USA.
Ju YangDepartment of Pathology, Shanghai Fifth People's Hospital, Fudan University, Shanghai, 200040, China.
Chenyang ZhangDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China.
Chenshuo YouDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China.
Xiuping LiuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China. xpliu1228@fudan.edu.cn.
Jigang WangDepartment of Pathology, The Affiliated Hospital of Qingdao University, No.1677 Wutaishan Road, Qingdao, 266000, Qingdao, Shandong, China. wangjigang@qdu.edu.cn.
Guoyuan LiuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, P.R. China. gyliu@fudan.edu.cn.

Funding

Medical Specialty funded by Minhang, Shanghai No. 2025MWTZB08National Natural Science Foundation of China No. 82172616Natural Science Foundation of Shandong Province No. ZR2021MH097
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) represents the most aggressive breast cancer subtype with limited therapeutic options and poor prognosis, highlighting an urgent need to identify novel metabolic vulnerabilities and prognostic biomarkers to improve patient outcomes. While glutamine metabolism has been implicated in cancer, the specific roles of glutamine metabolism-related genes (GMRGs) in TNBC remain poorly understood. Herein, through an integrating analysis encompassing multi-omics bioinformatics, consensus clustering and tumor microenvironment (TME) analysis, we established a glutamine metabolism-based prognostic classification for TNBC patients, which correlates with distinct survival outcomes and TME features. Furthermore, we identified ALDH18A1, one of the GMRGs that encodes P5CS for proline synthesis, as a novel prognostic biomarker and oncogenic driver. ALDH18A1 is overexpressed in TNBC and associated with larger tumor size, lymph node metastasis and poor survival, as well as an immunosuppressive TME. In vitro experiments confirmed ALDH18A1 activated the AKT/mTOR signaling pathway, promoted the proliferation, migration and invasion of TNBC cells, and increased proline synthesis. Computational drug screening predicted six compounds with potential efficacy against ALDH18A1-high tumors. Collectively, our findings demonstrate that reprogramming of glutamine metabolism plays a crucial role in the malignant progression of TNBC and provide translational insights for precision metabolomic-immunotherapeutic strategies in ALDH18A1-high TNBC.

Indexed as

Aldehyde DehydrogenaseGlutamineTriple Negative Breast NeoplasmsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMetabolic ReprogrammingPrognosisSignal TransductionTOR Serine-Threonine KinasesTumor MicroenvironmentAldehyde DehydrogenaseBiomarkers, TumorGlutamineTOR Serine-Threonine KinasesALDH18A1Drug sensitivity predictionGlutamine metabolismPrognostic biomarkersTriple-negative breast cancerTumor microenvironment

Identifiers

PMID42323345
PMCPMC13562691

What OpenQuestion holds

Textmetadata
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.