Evidence map›Paper›PMID 38254216›Full record

ArticleExperimental hematology & oncology2024

ZMIZ2 facilitates hepatocellular carcinoma progression via LEF1 mediated activation of Wnt/β-catenin pathway.

Yang Ding, Yumei Ning, Hui Kang, Yuan Yuan, Kun Lin, Chun Wang, Yun Yi, Jianghua He, Lurao Li, Xingxing He and 1 more

Open access · goldAbstract read
In one paragraph

Article in Experimental hematology & oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  4. Review
  5. Astragalus Polysaccharides Target the Wnt/β-catenin Pathway to Suppress Malignant Behavior in Hepatocellular Carcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
    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

11 authors at 2 institutions in 1 country.

Yang Ding *Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Yumei Ning *Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Hui Kang *Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Yuan YuanDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Kun LinDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Chun WangDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Yun YiDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Jianghua HeDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Lurao LiDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Xingxing HeDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. hexingxing@whu.edu.cn.
Ying ChangDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. changying@whu.edu.cn.
Zhongnan Hospital of Wuhan University · CNWuhan University · CN

Funding

National Nature Science Foundation of China 82172983, 81670554, 82073095Science and technology innovation and cultivation fund of Zhongnan Hospital of Wuhan University CXPY2020042Subjects and platform construction in Zhongnan Hospital of Wuhan University PTMX2020003Wuhan Science and Technology Project 2020020601012208
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the most common malignancies with a high lethality rate. ZMIZ2 is a transcriptional co-activator implicated in various human diseases. However, the role and molecular mechanism of ZMIZ2 in HCC remains to be elucidated.

methodsThe expression and prognostic value of ZMIZ2 in HCC was excavated from public databases and explored by bioinformatic analysis. Then the expression of ZMIZ2 and related genes was further validated by quantitative RT-PCR, western blotting, and immunohistochemistry. Loss and gain-of-function experiments were performed in vitro and in vivo to investigate the function of ZMIZ2 in HCC. In addition, transcriptome sequencing and immunoprecipitation was conducted to explore the potential molecular mechanisms of ZMIZ2.

resultsZMIZ2 was highly expressed in HCC and associated with poor prognosis. Silencing ZMIZ2 significantly inhibited HCC cell proliferation, cell cycle process, migration, and invasion in vitro, and also inhibited the progression of HCC in vivo. Additionally, ZMIZ2 expression was correlated with immune cell infiltration in HCC samples. Somatic mutation analysis showed that ZMIZ2 and TP53 mutations jointly affected the progression of HCC. Mechanistically, ZMIZ2 interacted with LEF1 to regulate malignant progression of HCC by activating the Wnt/β-catenin pathway.

conclusionZMIZ2 was overexpressed in HCC and associated with poor prognosis. The overexpression of ZMIZ2 was corelated with malignant phenotype, and it facilitated HCC progression via LEF1-mediated activation of the Wnt/β-catenin pathway. Furthermore, ZMIZ2 could be served as a prognostic biomarker and a new therapeutic target for HCC.

Indexed as

Hepatocellular carcinomaLEF1PrognosisWnt/β-catenin pathwayZMIZ2

Identifiers

PMID38254216
PMCPMC10802047
OpenAlexW4391098298

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Registered trials

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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.