Evidence map›Paper›PMID 28759036›Full record

ArticleOncogene2017

Deficiency in VHR/DUSP3, a suppressor of focal adhesion kinase, reveals its role in regulating cell adhesion and migration.

Y-R Chen, H-C Chou, C-H Yang, H-Y Chen, Y-W Liu, T-Y Lin, C-L Yeh, W-T Chao, H-H Tsou, H-C Chuang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Cancers · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Induction of DUSP14 ubiquitination by PRMT5-mediated arginine methylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  17. 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

11 authors at 2 institutions in 2 countries.

Y-R ChenInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
H-C ChouInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
C-H YangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
H-Y ChenInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
Y-W LiuInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
T-Y LinInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
C-L YehInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
W-T ChaoDepartment of Life Science, Tunghai University, Taichung, Taiwan.
H-H TsouDivision of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan.
H-C ChuangImmunology Research Center, National Health Research Institutes, Zhunan, Taiwan.
T-H TanImmunology Research Center, National Health Research Institutes, Zhunan, Taiwan.
National Health Research Institutes · TWTunghai University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vaccinia H1-related phosphatase (VHR/DUSP3) is a member of the dual-specificity phosphatase family. Deregulation of VHR is observed in various malignant diseases. We identified focal adhesion kinase (FAK) as a VHR-interacting molecule. Over-expression of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation. In vitro assays proved that recombinant VHR directly dephosphorylated FAK and paxillin. VHR-knockout mice did not have obvious abnormality; however, VHR-knockout cells showed decreased expression of integrins and FAK but stronger FAK and paxillin phosphorylation upon attachment to fibronectin. Additionally, VHR-knockout fibroblast and lung epithelial cells had elevated ligand-induced epidermal growth factor receptor (EGFR) phosphorylation. Inducible expression of VHR suppressed directional cell migration, and VHR deficiency resulted in a higher cell migratory ability. VHR-knockout cells have stronger FAK phosphorylation in cell adhesions, long-lasting trailing ends and slower turnover of focal adhesions. These collective data indicate that VHR is a FAK phosphatase and participates in regulating the formation and disassembly of focal adhesions.

Indexed as

Cell AdhesionCell MovementAnimalsCell Line, TumorDual Specificity Phosphatase 3ErbB ReceptorsFocal Adhesion Kinase 1Focal AdhesionsGene Knockout TechniquesHumansIntegrinsMiceMice, Inbred C57BLMice, KnockoutPaxillinPhosphorylationDual Specificity Phosphatase 3DUSP3 protein, humanDusp3 protein, mouseEGFR protein, humanEGFR protein, mouseErbB ReceptorsFocal Adhesion Kinase 1IntegrinsPaxillinPTK2 protein, humanPtk2 protein, mousePXN protein, humanTyrosine

Identifiers

PMID28759036
OpenAlexW2739854793

What OpenQuestion holds

Textmetadata
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.