Evidence map›Paper›PMID 41267037›Full record

ArticleMolecular cancer2025

ZNF526 drives tumor growth by enhancing SHMT1-dependent serine metabolism and antioxidant capability in TNBC.

Wenxing Qin, Lujing Shao, Qi Li, Dan Zhang, Xinyan Jia, Chunyan Dong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer, 2025. 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

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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

6 authors.

Wenxing Qin *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, People's Republic of China.
Lujing Shao *Department of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Qi Li *Department of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Dan ZhangDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Xinyan JiaDepartment of Oncology, Shanghai East Hospital, Postgraduate Training Base of Jinzhou Medical University, Shanghai, China.
Chunyan DongDepartment of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China. cy_dong@tongji.edu.cn.

Funding

Chinese Society of Clinical Oncology Foundation Y-2022HER-2AZMS-0349, Y-2023AZMETMS-0077Key Specialty Construction Project of Shanghai Pudong New Area Health Commission PWZzk2022-01Leading Talent Program by Shanghai Municipal Health Commission 2022LJ012National Natural Science Foundation of China 81502260National Natural Science Foundation of China 82073387New Quality Clinical Specialty Program of High-end Medical Disciplinary Construction in Shanghai Pudong New Area 2025-PWXZ-01Shanghai 2023 "Science and Technology Innovation Action Plan" Outstanding Academic/Technical Leader Program 23XD1402800Shanghai Leading Talent Program of Eastern Talent Plan DFYCLJ02Shanghai Pudong New Area Advanced Talent Cultivation Project of Integrated Traditional Chinese and Western Medicine PDZY-2024-0701Shanghai Pudong New Area Traditional Chinese Medicine Inheritance Innovation Development Demonstration Pilot Project Construction YC-2023-0403Shanghai Xuhui District Science and Technology Committee 23XHYD-6the Oriental Talents Program Youth Project (formerly Shanghai Youth Top Talents) of the Organization Department of Shanghai Municipal Party Committee, Shanghai Science and Technology Commission 23Y11909200, 24SF1900200
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive malignancy with limited therapeutic options and poor prognosis. Although the single-nucleotide polymorphism rs3810151 (p.Val94Ala) in ZNF526 has been identified as a breast cancer susceptibility locus, the functional role and mechanistic basis of ZNF526 in TNBC remain unknown. In this study, we observed that ZNF526 is highly expressed in TNBC, and its elevated expression correlates with worse clinical outcomes. Functional assays revealed that ZNF526 overexpression promotes TNBC cell growth, whereas its knockdown suppresses tumor growth. Mechanistically, we discovered that ZNF526 activates SHMT1 expression, which subsequently enhances flux through the serine-glycine-one-carbon (SGOC) metabolic pathway. This metabolic activation increases glutathione (GSH) production, reduces reactive oxygen species (ROS) levels, and strengthens cellular antioxidant defenses, thereby facilitating TNBC progression. Our findings reveal ZNF526 as a novel regulator of redox balance in TNBC through SHMT1-mediated metabolic control, positioning it as a potential therapeutic target for TNBC.

Indexed as

AntioxidantsDNA-Binding ProteinsGlycine HydroxymethyltransferaseSerineTriple Negative Breast NeoplasmsAnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticGlutathioneHumansMiceReactive Oxygen SpeciesAntioxidantsDNA-Binding ProteinsGlutathioneGlycine HydroxymethyltransferaseReactive Oxygen SpeciesSerineSHMT protein, humanGSHSerine metabolismSHMT1TNBCZNF526

Identifiers

PMID41267037
PMCPMC12632037

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Registered trials

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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.