Evidence map›Paper›PMID 41935051›Full record

ArticleCell death & disease2026

EBNA1BP2 (EBP2) promotes the progression of hepatocellular carcinoma through upregulating the expression of MCM8 and HMGB1.

Ensi Ma, Hao Xing, Chao Sun, Quanbao Zhang, Conghuan Shen, Yangyang Zhan, Jianhua Li, Li Li, Hongyuan Xue, Ruidong Li and 2 more

Abstract read
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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. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Ensi Ma *Liver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Hao Xing *Liver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-1795-2334
Chao Sun *Liver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Quanbao ZhangLiver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Conghuan ShenLiver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Yangyang ZhanDepartment of Pharmacy, Shanghai Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, China.ORCID http://orcid.org/0000-0003-3394-5070
Jianhua LiLiver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Li LiLiver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Hongyuan XueLiver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China.
Ruidong LiDepartment of Intensive Care Unit, Huashan Hospital, Fudan University, Shanghai, China.
Fei TengDepartment of Liver Surgery and Organ Transplantation, Changzheng Hospital, Naval Medical University, Shanghai, China. tengfei@smmu.edu.cn.ORCID http://orcid.org/0000-0001-9076-8862
Yifeng TaoLiver Transplantation Center, Department of General Surgery, Huashan Hospital & Institute of Organ Transplantation, Fudan University, Shanghai, China. taoyifeng@huashan.org.cn.ORCID http://orcid.org/0009-0003-4586-8735

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary liver cancer ranks among the most prevalent and refractory malignant tumors globally. This investigation delves into the role of Epstein-Barr virus nuclear antigen 2-binding protein (EBP2) in hepatocellular carcinoma (HCC). Significantly, EBP2 exhibits marked overexpression in HCC tissues, a finding that correlates with advanced tumor staging and unfavorable prognostic outcomes. In HCC cells, EBP2 silencing led to attenuated proliferation, enhanced apoptosis, and reduced migratory capacity, coupled with reversal of epithelial-mesenchymal transition (EMT). In vivo studies further demonstrated that EBP2 depletion potently suppressed tumor growth in xenograft models. Mechanistically, EBP2 interacts with CENPA to transcriptionally upregulate minichromosome maintenance protein family member 8 (MCM8), thereby stabilizing the MCM8/MCM9 complex and enhancing homologous recombination-mediated DNA repair. Functional rescue experiments revealed that MCM8 overexpression abrogated the suppressive effects of EBP2 knockdown on HCC cell proliferation and migration. In parallel, EBP2 regulates HMGB1 expression through the CENPA/YY1 transcriptional complex, thereby participating in the progression of HCC. Collectively, these findings highlight EBP2 as a crucial regulator of HCC progression via the dual axes-EBP2-CENPA-MCM8 and EBP2-CENPA/YY1-HMGB1, offering a promising therapeutic target for HCC intervention.

Indexed as

Carcinoma, HepatocellularHMGB1 ProteinLiver NeoplasmsRNA-Binding ProteinsAnimalsApoptosisCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMaleMiceCell Cycle ProteinsHMGB1 ProteinHMGB1 protein, humanMCM8 protein, humanMinichromosome Maintenance ProteinsRNA-Binding Proteins

Identifiers

PMID41935051
PMCPMC13303876

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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.