Evidence map›Paper›PMID 25975202›Full record

ArticleJournal of experimental & clinical cancer research : CR2015

Decreased expression of ARID1A associates with poor prognosis and promotes metastases of hepatocellular carcinoma.

Fei He, Jie Li, JianFeng Xu, Sheng Zhang, YaPing Xu, WenXiu Zhao, ZhenYu Yin, XiaoMin Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
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  7. Review
  8. A mutational signature and ARID1A mutation associated with outcome in hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. The stage-dependent prognostic role ofTranslational cancer research · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Comprehensive Genomic Profiling IdentifiesJournal of hepatocellular carcinoma · 2023
    Article
  18. Article
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Fei HeFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. hf_xmu@163.com.
Jie LiFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. 444672123@qq.com.
JianFeng XuFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. 584339606@qq.com.
Sheng ZhangFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. zhangshengcmu@163.com.
YaPing XuFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. yaya-xu@qq.com.
WenXiu ZhaoFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. wxzhao@xmu.edu.cn.
ZhenYu YinFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. yinzy@xmu.edu.cn.
XiaoMin WangFujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (based on Xiamen University), Xiamen, Fujian, China. wxm2203@xmu.edu.cn.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is a common malignancy worldwide, which is especially prevalent in Asia. Elucidating the molecular basis of HCC is crucial to develop targeted diagnostic tools and novel therapies. Recent studies have identified AT-rich interactive domain-containing protein 1A (ARID1A) as a broad-spectrum tumor suppressor. We evaluated the clinical implications of decreased ARID1A expression in HCC, and investigated the mechanisms of ARID1A-mediated tumor suppression.

methodsQuantitative PCR, western blotting, immunohistochemical analysis of ARID1A mRNA and protein expression was conducted in 64 paired HCC and adjacent non-tumorous tissues. ARID1A function was evaluated in vitro in MHCC-97H and Huh7 HCC cell lines, and in vivo in a xenografted HCC tumor model.

resultsARID1A mRNA and protein expression were significantly decreased in HCC tissues, and decreased expression was significantly associated with overall metastasis, including local lymph node and distant metastasis, and poor prognosis. ARID1A knockdown promoted HCC cell migration and invasion in vitro, whereas overexpression of ARID1A inhibited migration and invasion. E-cadherin levels were closely correlated with ARID1A expression, suggesting a role in migration and invasion. In addition, ARID1A and E-cadherin (CDH1) expression were found to be regulated in a coordinated fashion in HCC samples. Furthermore, ARID1A knockdown significantly increased HCC tumor growth and lung metastasis in vivo.

conclusionsARID1A served as an important tumor suppressor. Decreased expression of ARID1A was associated with tumor progression, metastasis, and reduced overall survival in mice and humans. ARID1A could represent a promising candidate therapeutic target for HCC.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementDisease Models, AnimalDNA-Binding ProteinsGene Knockdown TechniquesHeterograftsHumansLiver NeoplasmsMiceNeoplasm MetastasisNuclear ProteinsPrognosisRNA SplicingARID1A protein, humanDNA-Binding ProteinsNuclear ProteinsTranscription Factors

Identifiers

PMID25975202
PMCPMC4440314
OpenAlexW2151337762

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.