Evidence map›Paper›PMID 41854933›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

CircBARD1 suppresses tumor progression driven by H3K18 lactylation-CCNA2 axis in human bladder cancer.

Zhenghui Hu, Nan Jiang, Bo Xie, Jiatong Zhou, Juntao Lin, Xianwu Chen, Xuejian Zhou, Yan Zhang, Mengjing Fan, Ning He and 2 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 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

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

12 authors.

Zhenghui Hu *Department of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, R.P. China.
Nan Jiang *Department of Urology, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310006, R.P. China.
Bo Xie *Department of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, R.P. China.
Jiatong ZhouDepartment of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, R.P. China.
Juntao LinDepartment of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, R.P. China.
Xianwu ChenDepartment of Urology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, R.P. China.
Xuejian ZhouDepartment of Urology, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, 200025, China.
Yan ZhangDepartment of Urology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310009, R.P. China.
Mengjing FanDepartment of Pathology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310016, R.P. China.
Ning HeDepartment of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, R.P. China.
Xiaodong JinDepartment of Urology, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310006, R.P. China. 20233003@zcmu.edu.cn.
Feifan WangDepartment of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, R.P. China. 1322083@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBladder cancer (BCa) represents the fourth most prevalent malignancy worldwide, characterized by unfavorable clinical outcomes. The functional significance and molecular mechanisms underlying circular RNAs in BCa pathogenesis require further investigation. This study reveals that circBARD1 suppresses histone lactylation-driven tumor progression by modulating ENO1 protein stability in bladder cancer.

methodsFunctional characterization of circBARD1 was performed through gain-of-function experiments in T24 and TCCSUP cell lines. RNA immunoprecipitation (RIP) and immunoprecipitation assays were employed to investigate circBARD1-ENO1 interactions. CUT&Tag and chromatin immunoprecipitation (ChIP) assays were conducted to examine H3K18 lactylation-mediated transcriptional regulation of CCNA2.

resultsCircBARD1 expression was significantly downregulated in bladder cancer tissues. Ectopic expression of circBARD1 inhibited malignant proliferation and migration capacities in BCa cell lines. Furthermore, circBARD1 demonstrated negative regulation of glycolytic flux and intracellular lactate accumulation. Mechanistic studies revealed that circBARD1 physically interacts with ENO1 protein, facilitating its ubiquitination-mediated proteasomal degradation mediated by FBXW7. This circBARD1/ENO1 regulatory axis attenuates tumor progression through suppression of H3K18 lactylation and subsequent downregulation of CCNA2 transcription.

conclusionsOur findings establish that circBARD1 functions as a tumor suppressor in bladder cancer by promoting ENO1 ubiquitination and degradation, thereby inhibiting histone lactylation-mediated oncogenesis. This study provides new insights into therapeutic targets for clinical management of bladder cancer.

Indexed as

Disease ProgressionHistonesRNA, CircularUrinary Bladder NeoplasmsCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansPhosphopyruvate HydrataseTumor Suppressor ProteinsUbiquitinationDNA-Binding ProteinsENO1 protein, humanHistonesPhosphopyruvate HydrataseRNA, CircularTumor Suppressor ProteinsBladder cancercircBARD1Histone lactylationTumor progression

Identifiers

PMID41854933
PMCPMC13003086

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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.