Evidence map›Paper›PMID 36008383›Full record

ArticleCell death & disease2022

Hepatic ARID3A facilitates liver cancer malignancy by cooperating with CEP131 to regulate an embryonic stem cell-like gene signature.

Mengting Shen, Shengli Li, Yiming Zhao, Yizhe Liu, Zhen Liu, Lin Huan, Yejun Qiao, Lu Wang, Leng Han, Zhiao Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
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

21 citing papers in PubMed, 22 citations in OpenAlex.

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  12. Feasibility and mechanism ofAnnals of nuclear medicine · 2025
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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 at 4 institutions in 2 countries.

Mengting Shen *Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Shengli Li *Precision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.ORCID 0000-0001-5430-303X
Yiming Zhao *Department of Hepatic Surgery, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
Yizhe LiuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Zhen LiuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Lin HuanFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.ORCID 0000-0002-5791-4482
Yejun QiaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Lu WangDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China. wangluzl@fudan.edu.cn.ORCID 0000-0002-6856-7084
Leng HanCenter for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX, 77030, USA. leng.han@tamu.edu.ORCID 0000-0002-7380-2640
Zhiao ChenFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China. zachen@fudan.edu.cn.ORCID 0000-0003-4105-8674
Xianghuo HeFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China. xhhe@fudan.edu.cn.ORCID 0000-0001-8872-668X
Fudan University Shanghai Cancer Center · CNFudan University · CNPrevention Institute · USShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver cancer stemness refers to the stem cell-like phenotype of hepatocarcinoma cells and is closely related to a high degree of tumour malignancy. Here, we identified AT-rich interacting domain 3A (ARID3A) as one of the most upregulated stemness-related transcription factors in liver cancer by an in vitro functional screen. ARID3A can promote liver cancer cell viability and metastasis both in vitro and in vivo. Mechanistically, ARID3A interacts with CEP131 and transcriptionally activates KDM3A by co-occupying its promoter element, further upregulating the expression of downstream embryonic stem (ES) signature genes via demethylation of H3K9me2. ARID3A and CEP131 promote an ES cell gene signature through activation of KDM3A and contribute to the poor prognosis of liver cancer patients. Collectively, these results provide evidence highlighting a transcription-dependent mechanism of ARID3A in stemness regulation in liver cancer. The ARID3A/CEP131-KDM3A regulatory circuit could serve as a prognostic indicator and potential therapeutic target for liver cancer.

Indexed as

DNA-Binding ProteinsLiver NeoplasmsCell Cycle ProteinsCytoskeletal ProteinsEmbryonic Stem CellsHumansJumonji Domain-Containing Histone DemethylasesPromoter Regions, GeneticTranscription FactorsARID3A protein, humanCell Cycle ProteinsCEP131 protein, humanCytoskeletal ProteinsDNA-Binding ProteinsJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanTranscription Factors

Identifiers

PMID36008383
PMCPMC9411159
OpenAlexW4293222301

What OpenQuestion holds

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LicenceCC BY
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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.