Evidence map›Paper›PMID 26077142›Full record

ArticleNature communications2015

β-Arrestin1 enhances hepatocellular carcinogenesis through inflammation-mediated Akt signalling.

Yidong Yang, Yunwei Guo, Siwei Tan, Bilun Ke, Jin Tao, Huiling Liu, Jie Jiang, Jianning Chen, Guihua Chen, Bin Wu

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026
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  6. Intestinal NF-κB pathway-mediated pyroptosis contributes to endotoxemia-induced intestinal injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  7. Article
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  11. Pharmacological reviews · 2023
    Review
  12. Article
  13. Dual roles of β-arrestin 1 in mediating cell metabolism and proliferation in gastric cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Structural basis and molecular mechanism of biased GPBAR signaling in regulating NSCLC cell growth via YAP activity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
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  20. Article
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

10 authors at 1 institution in 1 country.

Yidong Yang1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Yunwei Guo1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Siwei Tan1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Bilun Ke1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Jin Tao1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Huiling Liu1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Jie Jiang1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.
Jianning ChenDepartment of Pathology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China.
Guihua Chen1] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China [2] Department of Hepatic Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China.
Bin Wu1] Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, 510630, China [2] Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, Guangdong Province, 510630, China.ORCID 000000023284908X
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G-protein-coupled receptors (GPCR) constitute the largest known superfamily for signal transduction and transmission, and they control a variety of physiological and pathological processes. GPCR adaptor β-arrestins (ARRBs) play a role in cancerous proliferation. However, the effect of ARRBs in inflammation-mediated hepatocellular carcinogenesis is unknown. Here we show that ARRB1, but not ARRB2, is upregulated in inflammation-associated hepatocellular carcinoma (HCC) and paracancerous tissues in humans. A genotoxic carcinogen, diethylnitrosamine (DEN), significantly induces hepatic inflammation, TNF-α production and ARRB1 expression. Although ARRB1 deficiency does not affect hepatic inflammation and TNF-α production, it markedly represses hepatocellular carcinogenesis by suppressing malignant proliferation in DEN-treated mice. Furthermore, TNF-α directly induces hepatic ARRB1 expression and enhances ARRB1 interaction with Akt by binding to boost Akt phosphorylation, resulting in malignant proliferation of liver cells. Our data suggest that ARRB1 enhances hepatocellular carcinogenesis by inflammation-mediated Akt signalling and that ARRB1 may be a potential therapeutic target for HCC.

Indexed as

Alkylating AgentsAnimalsArrestinsbeta-Arrestin 1beta-Arrestin 2beta-ArrestinsBlotting, WesternCarcinogenesisCarcinoma, HepatocellularCell Line, TumorDiethylnitrosamineHep G2 CellsHumansImmunohistochemistryInflammationLiver NeoplasmsAlkylating AgentsARRB1 protein, humanArrb1 protein, mouseARRB2 protein, humanArrb2 protein, mouseArrestinsbeta-Arrestin 1beta-Arrestin 2beta-ArrestinsDiethylnitrosamineProto-Oncogene Proteins c-aktRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID26077142
OpenAlexW2206894664

What OpenQuestion holds

Textmetadata
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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.