Evidence map›Paper›PMID 27270428›Full record

ArticleOncogene2017

WNT5A: a motility-promoting factor in Hodgkin lymphoma.

F Linke, S Zaunig, M M Nietert, F von Bonin, S Lutz, C Dullin, P Janovská, T Beissbarth, F Alves, W Klapper and 5 more

Open access · greenAbstract 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. FZD5 prevents epithelial-mesenchymal transition in gastric cancer.Cell communication and signaling : CCS · 2021
    Article
  14. Article
  15. Targeting Casein Kinase 1 (CK1) in Hematological Cancers.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Wnt Signaling in Hematological Malignancies.Progress in molecular biology and translational science · 2018
    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

15 authors at 4 institutions in 2 countries.

F LinkeClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
S ZaunigClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
M M NietertDepartment of Medical Statistics, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
F von BoninClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
S LutzInstitute of Pharmacology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
C DullinInstitute of Diagnostic and Interventional Radiology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
P JanovskáFaculty of Science, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic.
T BeissbarthDepartment of Medical Statistics, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
F AlvesClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
W KlapperSection Hematopathology, UKSH Campus Kiel, Kiel, Germany.
V BryjaFaculty of Science, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic.
T PukropClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
L TrümperClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
J WiltingDepartment of Anatomy and Cell Biology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
D KubeClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
University of Göttingen · DECzech Academy of Sciences, Institute of Biophysics · CZMasaryk University · CZUniversity Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Classical Hodgkin lymphoma (cHL) has a typical clinical manifestation, with dissemination involving functionally neighboring lymph nodes. The factors involved in the spread of lymphoma cells are poorly understood. Here we show that cHL cell lines migrate with higher rates compared with non-Hodgkin lymphoma cell lines. cHL cell migration, invasion and adhesion depend on autocrine WNT signaling as revealed by the inhibition of WNT secretion with the porcupine inhibitors Wnt-C59/IWP-2, but did not affect cell proliferation. While application of recombinant WNT5A or WNT5A overexpression stimulates HL cell migration, neither WNT10A, WNT10B nor WNT16 did so. Time-lapse studies revealed an amoeboid type of cell migration modulated by WNT5A. Reduced migration distances and velocity of cHL cells, as well as altered movement patterns, were observed using porcupine inhibitor or WNT5A antagonist. Knockdown of Frizzled5 and Dishevelled3 disrupted the WNT5A-mediated RHOA activation and cell migration. Overexpression of DVL3-K435M or inhibition of ROCK (Rho-associated protein kinase) by Y-27632/H1152P disrupted cHL cell migration. In addition to these mechanistic insights into the role of WNT5A in vitro, global gene expression data revealed an increased WNT5A expression in primary HL cells in comparison with normal B-cell subsets and other lymphomas. Furthermore, the activity of both porcupine and WNT5A in cHL cells had an impact on lymphoma development in the chick chorionallantoic membrane assay. Massive bleeding of these lymphomas was significantly reduced after inhibition of WNT secretion by Wnt-C59. Therefore, a model is proposed where WNT signaling has an important role in regulating tumor-promoting processes.

Indexed as

AnimalsBiopsyCell AdhesionCell Line, TumorCell MovementCell ProliferationDishevelled ProteinsFrizzled ReceptorsGene ExpressionHodgkin DiseaseHumansModels, BiologicalPorcupinesrhoA GTP-Binding ProteinSignal TransductionTomography, X-Ray ComputedDishevelled ProteinsDVL3 protein, humanFrizzled ReceptorsFZD5 protein, humanrhoA GTP-Binding ProteinWnt-5a Protein

Identifiers

PMID27270428
OpenAlexW2411604270

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.