Evidence map›Paper›PMID 42764348›Full record

ArticleNature communications2026

A cuproptosis-inducing covalent organic framework synergizes with oncolytic virus for tumor radiotherapy.

Yuan-Tong Liu, Ke-Shan Liu, Han Li, Shuo Wang, Shu-Ying Bie, Ying-Qi Wei, Shan-Shan Gou, Xiang-Bo Wan, Xing-Zhen Li, Liang Zhang and 1 more

Abstract read
In one paragraph

Article in Nature communications, 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

11 authors.

Yuan-Tong Liu *Department of Stomatology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. yuantongdejia@zzu.edu.cn.ORCID http://orcid.org/0000-0001-9341-2626
Ke-Shan Liu *Department of Stomatology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Han Li *State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.
Shuo WangDepartment of Stomatology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Shu-Ying BieState Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.
Ying-Qi WeiState Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.
Shan-Shan GouState Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.
Xiang-Bo WanState Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.
Xing-Zhen LiState Key Laboratory of Precision and Intelligent Chemistry, School of Chemistry and Materials Science, University of Science and Technology of China, Hefei, China. lixingzhen@ustc.edu.cn.ORCID http://orcid.org/0009-0009-2564-4666
Liang ZhangState Key Laboratory of Precision and Intelligent Chemistry, School of Chemistry and Materials Science, University of Science and Technology of China, Hefei, China. zhangliang2025@ustc.edu.cn.ORCID http://orcid.org/0000-0002-5960-8913
Wei HeDepartment of Stomatology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. heweizdyfy@163.com.ORCID http://orcid.org/0000-0002-9722-3264

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82504345
6 · The paper itself

Abstract

Acquired radioresistance limits effective radiotherapy. Cuproptosis is a copper-dependent form of cell death driven by mitochondrial copper accumulation and lipoylated protein aggregation. Building on evidence that radioresistant cancer cells exhibit increased cuproptosis susceptibility, here we combine a radiation-responsive, copper-incorporated covalent organic framework (COF‑Tpy‑Se‑Cu) with an oncolytic adenovirus to target this vulnerability. X-ray irradiation triggers copper release from COF‑Tpy‑Se‑Cu and induces FDX1-dependent cuproptosis, while the oncolytic adenovirus depletes intracellular glutathione and stabilizes FDX1 by limiting its mitochondrial protease-mediated degradation. The combination enhances tumor cell death and remodels the immunosuppressive tumor microenvironment into a T-cell-inflamed state. In models of radioresistant tumors in female mice, this regimen improves tumor control and elicits CD8

Indexed as

CopperCuproptosisNeoplasmsOncolytic VirotherapyOncolytic VirusesAdenoviridaeAnimalsCD8-Positive T-LymphocytesCell Line, TumorFemaleHumansMiceMice, Inbred C57BLTumor MicroenvironmentCopper

Identifiers

PMID42764348
PMCPMC13590516

What OpenQuestion holds

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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.