Evidence map›Paper›PMID 41188783›Full record

ArticleBMC cancer2025

UHRF1 and NF-κB signaling in prostate cancer progression insights from bioinformatics and experimental validation.

Yan Wang, Jili Wang, Guoping Ren

Abstract read
In one paragraph

Article in BMC cancer, 2025. 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. Article
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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

3 authors.

Yan WangDepartment of Pathology, Zhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, Zhejiang, 310022, China.
Jili WangDepartment of Pathology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, China.
Guoping RenDepartment of Pathology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, China. gpren1999@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence implicates the NF-κB/p65 signaling pathway in the progression of prostate cancer (PC) and the development of resistance to androgen deprivation therapy. This study aimed to investigate the potential role of UHRF1, a key epigenetic regulator, in modulating NF-κB activity, and to evaluate its association with clinicopathological features and clinical outcomes in PC patients.

methodsDifferentially expressed genes (DEGs) were identified using the GSE104749 dataset. UHRF1 expression was validated across TCGA and GEO cohorts and further confirmed in clinical specimens using Western blotting and immunohistochemistry. Survival outcomes were evaluated using Kaplan-Meier and Cox regression analyses. A prognostic model was built incorporating UHRF1, Gleason score, and PSA, with validation via ROC curves and nomogram. Functional studies assessed the impact of UHRF1 silencing or overexpression on cell proliferation, apoptosis, cell cycle, glucose metabolism, and NF-κB signaling. Co-immunoprecipitation was used to assess the physical interaction between UHRF1 and p65.

resultsHigher Gleason scores, advanced clinical stage, lymph node involvement, and distant metastases were all positively connected with UHRF1 expression, which was markedly overexpressed in PC tissues. High UHRF1 expression was associated with shorter overall survival (OS) and disease-free survival (DFS), and independently predicted biochemical recurrence (BCR). A prognostic model incorporating UHRF1 achieved a high predictive accuracy (C-index = 0.752), and the corresponding nomogram demonstrated strong reliability in individualized risk assessment. In vitro, UHRF1 promoted tumor progression by enhancing proliferation, inhibiting apoptosis, driving aerobic glycolysis, and regulating the cell cycle. Mechanistically, UHRF1 bound to p65, promoted its phosphorylation, and activated NF-κB signaling.

conclusionUHRF1 contributes to prostate cancer progression by driving tumor growth, metabolic reprogramming, and NF-κB activation. It holds promise as both a prognostic biomarker and a potential therapeutic target in PC.

Indexed as

CCAAT-Enhancer-Binding ProteinsNF-kappa BProstatic NeoplasmsTranscription Factor RelAUbiquitin-Protein LigasesApoptosisBiomarkers, TumorCell Line, TumorCell ProliferationComputational BiologyDisease ProgressionGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMaleMiddle AgedBiomarkers, TumorCCAAT-Enhancer-Binding ProteinsNF-kappa BTranscription Factor RelAUbiquitin-Protein LigasesUHRF1 protein, human

Identifiers

PMID41188783
PMCPMC12584322

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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.