Evidence map›Paper›PMID 27759077›Full record

ArticleScientific reports2016

Down-regulation of β-arrestin2 promotes tumour invasion and indicates poor prognosis of hepatocellular carcinoma.

Wu-Yi Sun, Shan-Shan Hu, Jing-Jing Wu, Qiong Huang, Yang Ma, Qing-Tong Wang, Jing-Yu Chen, Wei Wei

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. β-Arrestin2 is a critical component of the GPCR-eNOS signalosome.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Hedgehog Signal and Genetic Disorders.Frontiers in genetics · 2019
    Review
  20. Review
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.

Wu-Yi SunInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Shan-Shan HuInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Jing-Jing WuInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Qiong HuangInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Yang MaInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Qing-Tong WangInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Jing-Yu ChenInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.
Wei WeiInstitute of Clinical Pharmacology of Anhui Medical University, Hefei 230032, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-arrestins, including β-arrestin1 and β-arrestin2, are multifunctional adaptor proteins. β-arrestins have recently been found to play new roles in regulating intracellular signalling networks associated with malignant cell functions. Altered β-arrestin expression has been reported in many cancers, but its role in hepatocellular carcinoma (HCC) is not clear. We therefore examined the roles of β-arrestins in HCC using an animal model of progressive HCC, HCC patient samples and HCC cell lines with stepwise metastatic potential. We demonstrated that β-arrestin2 level, but not β-arrestin1 level, decreased in conjunction with liver tumourigenesis in a mouse diethylnitrosamine-induced liver tumour model. Furthermore, β-arrestin2 expression was reduced in HCC tissues compared with noncancerous tissues in HCC patients. β-arrestin2 down-regulation in HCC was significantly associated with poor patient prognoses and aggressive pathologic features. In addition, our in vitro study showed that β-arrestin2 overexpression significantly reduced cell migration and invasion in cultured HCC cells. Furthermore, β-arrestin2 overexpression up-regulated E-cadherin expression and inhibited vimentin expression and Akt activation. These results suggest that β-arrestin2 down-regulation increases HCC cell migration and invasion ability. Low β-arrestin2 expression may be indicative of a poor prognosis or early cancer recurrence in patients who have undergone surgery for HCC.

Indexed as

Animalsbeta-Arrestin 2CarcinogenesisCarcinoma, HepatocellularCell Line, TumorCell MovementDiethylnitrosamineDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHumansLiverLiver NeoplasmsMaleMiceMice, Inbred C57BLbeta-Arrestin 2Diethylnitrosamine

Identifiers

PMID27759077
PMCPMC5069669

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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.