Evidence map›Paper›PMID 34380537›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

Phosphorylation of NF-κBp65 drives inflammation-mediated hepatocellular carcinogenesis and is a novel therapeutic target.

Xuan Xu, Yiming Lei, Lingjun Chen, Haoxiong Zhou, Huiling Liu, Jie Jiang, Yidong Yang, Bin Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.1field-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

34 citing papers in PubMed, 53 citations in OpenAlex.

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  5. Pharmaceuticals (Basel, Switzerland) · 2026
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  11. Sleep disorders in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025
    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

8 authors at 3 institutions in 1 country.

Xuan Xu *Department of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China.
Yiming Lei *Department of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China.
Lingjun ChenDepartment of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China.
Haoxiong ZhouDepartment of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China.
Huiling LiuDepartment of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China.
Jie JiangDepartment of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China.
Yidong YangDepartment of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China. yangyd6@mail.sysu.edu.cn.
Bin WuDepartment of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, Guangdong Province, China. wubin6@mail.sysu.edu.cn.
Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CNKey Laboratory of Guangdong Province · CN

Funding

National Natural Science Foundation of China 82070574National Natural Science Foundation of China U1501224Natural Science Foundation of Guangdong Province 2018B030312009Science and Technology Planning Project of Guangdong Province 2017B020226003
6 · The paper itself

Abstract

backgroundNuclear factor-κB (NF-κB) plays a vital role in hepatocellular carcinoma (HCC). β-arrestin1 (ARRB1) has been proved to enhance the activity of NF-κBp65, and our previous study indicated that ARRB1 promotes hepatocellular carcinogenesis and development of HCC. However, it remains unknown whether p65 is involved in hepatocellular carcinogenesis through the ARRB1-mediated pathway.

methodsThe levels of NF-κBp65 and NF-κBp65 phosphorylation (p-p65) were assessed in including normal liver, primary HCC and paired paracancerous tissues. Liver-specific p65 knockout mice were used to examine the role of p65 and p-p65 in hepatocarcinogenesis. The mechanism of NF-κBp65 and p-p65 in hepatocarcinogenesis via ARRB1 was also studied both in vitro and in vivo.

resultsPhosphorylation of NF-κBp65 was markedly upregulated in inflammation-related HCC patients and was significantly increased in mouse hepatic inflammation models, which were induced by tetrachloromethane (CCl

conclusionThe data demonstrated that phosphorylation of NF-κBp65 drives hepatocellular carcinogenesis in response to inflammation-mediated ARRB1, and that inhibition of the phosphorylation of NF-κBp65 restrains the hepatocellular carcinogenesis. The results indicate that phosphorylation of NF-κBp65 is a novel therapeutic target for HCC.

Indexed as

AnimalsCarcinoma, HepatocellularHumansInflammation MediatorsLiver NeoplasmsMaleMiceMice, NudeNF-kappa BPhosphorylationInflammation MediatorsNF-kappa BHepatocellular carcinomaInflammationNF-κBp65Phosphorylationβ-arrestin1

Identifiers

PMID34380537
PMCPMC8359590
OpenAlexW3191460655

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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.