Evidence map›Paper›PMID 42031700›Full record

ArticleCell death & disease2026

ASPP2 inhibits hepatocellular carcinoma growth by regulating cuproptosis via mitochondrial protein lipoylation.

Lu Yang, Xuhui Li, Yutong Jiang, Mingzhu Zhang, Tiantian Wu, Peixian Pi, Zhuozhuo Han, Zhiyu Zhang, Fangyuan Kong, Xiuhong Lu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

15 authors.

Lu Yang *Shanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Xuhui Li *Shanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Yutong Jiang *Shanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Mingzhu ZhangShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Tiantian WuShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Peixian PiShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Zhuozhuo HanShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Zhiyu ZhangShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Fangyuan KongShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Xiuhong LuShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Hao YangShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China.ORCID http://orcid.org/0000-0002-3781-7271
Chaohui ZuoResearch Center of Cancer Prevention and Treatment, Translational Medicine Research Center of Liver Cancer, Hunan Provincial Tumor Hospital, affiliated with the Tumor Hospital of Xiangya Medical School of Central South University, Changsha, China.
Gang HuangShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China. huanggang502@sumhs.edu.cn.
Jian ZhaoShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China. zhaoj_24@sumhs.edu.cn.
Beibei LiangShanghai Key Laboratory of Molecular Imaging & Digital and Intelligent Empowerment Biomedical Innovation Center, Pudong Gongli Hospital, Shanghai University of Medicine and Health Sciences, Shanghai, China. liangbb@sumhs.edu.cn.ORCID http://orcid.org/0000-0002-5363-6315

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a metabolically active malignancy. Cuproptosis, a copper-dependent programmed cell death pathway, has been found to be closely associated with tumor progression. Cells with strong oxidative phosphorylation (OXPHOS) capacity exhibit heightened susceptibility to cuproptosis. We demonstrate that the tumor suppressor ASPP2 regulates the key cuproptosis modulator FDX1 by promoting NR2F2 recruitment to the FDX1 promoter in HCC. ASPP2 promotes intracellular copper accumulation through lipoylated protein oligomerization, thereby inducing cuproptosis. Furthermore, ASPP2 facilitates mitochondrial OXPHOS via enhanced tricarboxylic acid (TCA) cycle activity, which sensitizes HCC cells to cuproptosis. In vitro and in vivo experiments confirmed that ASPP2 overexpression suppresses tumor growth and synergizes with copper ionophores. Clinical specimen analysis revealed ASPP2-FDX1 co-expression in 90 HCC cases. A prognostic model incorporating ASPP2 and cuproptosis-related genes demonstrates superior survival prediction in TCGA cohorts. These findings establish the ASPP2-FDX1-NR2F2 axis as a metabolic-cuproptosis link and propose a novel therapeutic strategy for HCC.

Indexed as

Apoptosis Regulatory ProteinsCarcinoma, HepatocellularCopperCuproptosisLiver NeoplasmsMitochondrial ProteinsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMice, NudeMitochondriaOxidative PhosphorylationApoptosis Regulatory ProteinsCopperMitochondrial Proteins

Identifiers

PMID42031700
PMCPMC13443132

What OpenQuestion holds

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LicenceCC BY
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.