Evidence map›Paper›PMID 26538215›Full record

ArticleMolecular cancer2015

A20 suppresses hepatocellular carcinoma proliferation and metastasis through inhibition of Twist1 expression.

Haiyang Chen, Liang Hu, Zaili Luo, Jian Zhang, Cunzhen Zhang, Bijun Qiu, Liwei Dong, Yexiong Tan, Jin Ding, Shanhua Tang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

40 citing papers in PubMed, 59 citations in OpenAlex.

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  9. Molecular profiling of core immune-escape genes highlights TNFAIP3 as an immune-related prognostic biomarker in neuroblastoma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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  15. Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023
    Review
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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

13 authors at 5 institutions in 1 country.

Haiyang ChenInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. chenocean@163.com.
Liang HuAnal-Colorectal Surgery Institute, 150th Hospital of PLA, Luoyang, China. lianghudoc@163.com.
Zaili LuoInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. luozaili111@163.com.
Jian ZhangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. zhang_jian032@163.com.
Cunzhen ZhangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. zhangcunzhen87@163.com.
Bijun QiuInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. qiubijun1984@163.com.
Liwei DongInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. liweidongdlw@163.com.
Yexiong TanInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. yxtan1214@163.com.
Jin DingInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. dingjindj2015@163.com.
Shanhua TangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. tangshanhua001@163.com.
Feng ShenInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. shenfengehbh@sina.com.
Zhong LiInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. lizhongsh@yahoo.com.
Hongyang WangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. hywangk@vip.sina.com.
Eastern Hepatobiliary Surgery Hospital · CNSecond Military Medical University · CN82th Hospital of Pla · CNShanghai Cancer Institute · CNShanghai Cell Therapy Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrant expression of A20 has been reported in several human malignancies including hepatocellular carcinoma (HCC). However, its clinical relevance and potential role in HCC remain unknown.

methodsQuantitative PCR, Western blots and immunohistochemistry analyses were used to quantify A20 expression in HCC samples and cell lines. The correlation of A20 expression with clinicopathologic features was analyzed in a cohort containing 143 patients with primary HCC. Kaplan-Meier curves were used to evaluate the association between A20 expression and patient survival. Functional studies were performed to determine the effects of A20 on proliferation and metastasis of HCC cells in vitro and in vivo.

resultsExpression of A20 was increased in HCC tissues and cell lines. Increased expression of A20 was negatively correlated with the tumor size, TNM stage, tumor thrombus formation, capsular invasion and serum AFP levels. Patients with higher A20 expression had a prolonged disease-free survival and overall survival than those with lower A20 expression. Forced expression of A20 significantly inhibited the proliferative and invasive properties of HCC cells both in vitro and in vivo, whereas knockdown of A20 expression showed the opposite effects. Further studies revealed that expression of A20 was inversely correlated with Twist1 levels and NF-κB activity in HCC tissues and cell lines. A20-induced suppression of proliferation and migration of HCC cells were mainly mediated through inhibition of Twist1 expression that was regulated at least partly by A20-induced attenuation of NF-κB activity.

conclusionsOur results demonstrate that A20 plays a negative role in the development and progression of HCC probably through inhibiting Twist1 expression. A20 may serve as a novel prognostic biomarker and potential therapeutic target for HCC patients.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDisease-Free SurvivalDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsLiver NeoplasmsMaleMiceBiomarkers, TumorDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsNF-kappa BNuclear ProteinsTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3TWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID26538215
PMCPMC4634191
OpenAlexW2186810526

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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.