Evidence map›Paper›PMID 41547814›Full record

ArticleClinical epigenetics2026

HDAC11 interacts with the NuRD (MTA3) complex to transcriptionally suppress TGFβ1 expression and inhibit hepatocellular carcinoma metastasis.

Yang Yang, Jiaoli Wang, Qingqing Wu, Yishan Wang, Hui Meng, Lulu Zeng, Tian Qiu, Haixia Zhao, Qin Hu, Qiaoyou Weng and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Yang Yang *Zhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Jiaoli Wang *Zhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Qingqing WuZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Yishan WangZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Hui MengZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Lulu ZengZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Tian QiuZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Haixia ZhaoZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Qin HuZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Qiaoyou WengZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Meiling LiuZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Minjiang ChenZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China.
Rongfang QiuZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China. qiurongfang2023@wmu.edu.cn.
Jiansong JiZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China. jjstcty@wmu.edu.cn.
Weiqian ChenZhejiang Key Laboratory of Imaging and Interventional Medicine, The Fifth Affliated Hospital of Wenzhou Medical University, Lishui City, 323000, Zhejiang Province, China. ls2119088@126.com.

Funding

Key R&D Program of Lishui City 2025zdyf21Medical and Health Science and Technology Program of Zhejiang Province 2023RC113Medical and Health Science and Technology Program of Zhejiang Province 2025KY486"Pioneer" and "Leading Goose" R&D Program of Zhejiang 2023C03062Provincial and Ministerial Joint Construction of Key Projects WKJ-ZJ-2317
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a leading global health concern, recognized for its complex pathogenesis and high mortality rates. The metastatic progression of HCC, considered the terminal event in tumor development, plays a pivotal role in determining patient prognosis, with metastasis being a key factor in poor survival outcomes.HDAC11 was found to be highly expressed in HCC tissues, with its elevated expression significantly correlating with poor patient survival. Both in vitro and in vivo experiments demonstrated that silencing HDAC11 led to a marked reduction in HCC cell proliferation. Interestingly, HDAC11 knockdown also resulted in a substantial increase in the metastatic potential of HCC cells. Mass spectrometry analysis revealed that HDAC11 interacts with the NuRD (MTA3) complex. Consistently, immunoprecipitation and GST pull-down assays demonstrated that the N-terminal region of HDAC11 directly binds to MTA3. Moreover, transcriptomic analysis indicated that HDAC11 represses TGFB1 transcription, thereby inhibiting HCC metastasis. The enhanced metastatic phenotype induced by HDAC11 silencing was reversed upon concurrent down-regulation of TGFB1. Moreover, nanoparticles encapsulating both HDAC11 and TGF-β1 inhibitors effectively suppressed HCC cell proliferation and metastasis. This research elucidates the molecular mechanism by which HDAC11 inhibits metastasis and provides an effective strategy to mitigate the side effects associated with HDAC11 inhibition, offering novel insights and approaches for the precision treatment of HCC.

Indexed as

Carcinoma, HepatocellularHistone DeacetylasesLiver NeoplasmsMi-2 Nucleosome Remodeling and Deacetylase ComplexTransforming Growth Factor beta1AnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm MetastasisNeoplasm ProteinsRepressor ProteinsHDAC11 protein, humanHistone DeacetylasesMi-2 Nucleosome Remodeling and Deacetylase ComplexMTA3 protein, humanNeoplasm ProteinsRepressor ProteinsTGFB1 protein, humanTransforming Growth Factor beta1EMTHDAC11Hepatocellular carcinomaMetastasisMTA3

Identifiers

PMID41547814
PMCPMC12895668

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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.