Evidence map›Paper›PMID 30441765›Full record

ArticleInternational journal of molecular sciences2018

Breast Cancer: An Examination of the Potential of ACKR3 to Modify the Response of CXCR4 to CXCL12.

Irene Del Molino Del Barrio, Georgina C Wilkins, Annette Meeson, Simi Ali, John A Kirby

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Crosstalk between CXCR4/ACKR3 and EGFR Signaling in Breast Cancer Cells.International journal of molecular sciences · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. The extracellular matrix in development.Development (Cambridge, England) · 2020
    Review
  15. Repositioning Lidocaine as an Anticancer Drug: The Role Beyond Anesthesia.Frontiers in cell and developmental biology · 2020
    Review
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Irene Del Molino Del BarrioApplied Immunobiology and Transplantation Group, Institute of Cellular Medicine, Medical School, University of Newcastle Upon Tyne, Newcastle upon Tyne NE2 4HH, UK. irene.delmolinodelbarrio@dpag.ox.ac.uk.
Georgina C WilkinsApplied Immunobiology and Transplantation Group, Institute of Cellular Medicine, Medical School, University of Newcastle Upon Tyne, Newcastle upon Tyne NE2 4HH, UK. G.Wilkins2@newcastle.ac.uk.
Annette MeesonInstitute of Genetic Medicine, International Centre for Life, University of Newcastle Upon Tyne, Newcastle upon Tyne NE1 3BZ, UK. annette.meeson@newcastle.ac.uk.ORCID 0000-0002-5024-5511
Simi AliApplied Immunobiology and Transplantation Group, Institute of Cellular Medicine, Medical School, University of Newcastle Upon Tyne, Newcastle upon Tyne NE2 4HH, UK. simi.ali@newcastle.ac.uk.ORCID 0000-0002-4122-5631
John A KirbyApplied Immunobiology and Transplantation Group, Institute of Cellular Medicine, Medical School, University of Newcastle Upon Tyne, Newcastle upon Tyne NE2 4HH, UK. J.A.Kirby@newcastle.ac.uk.
Newcastle University · GBCentre for Life · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon binding with the chemokine CXCL12, the chemokine receptor CXCR4 has been shown to promote breast cancer progression. This process, however, can be affected by the expression of the atypical chemokine receptor ACKR3. Given ACKR3's ability to form heterodimers with CXCR4, we investigated how dual expression of both receptors differed from their lone expression in terms of their signalling pathways. We created single and double CXCR4 and/or ACKR3 Chinese hamster ovary (CHO) cell transfectants. ERK and Akt phosphorylation after CXCL12 stimulation was assessed and correlated with receptor internalization. Functional consequences in cell migration and proliferation were determined through wound healing assays and calcium flux. Initial experiments showed that CXCR4 and ACKR3 were upregulated in primary breast cancer and that CXCR4 and ACKR3 could form heterodimers in transfected CHO cells. This co-expression modified CXCR4's Akt activation after CXCL12's stimulation but not ERK phosphorylation (

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorChemokine CXCL12CHO CellsCricetinaeCricetulusFemaleHumansMiceReceptors, CXCRReceptors, CXCR4ACKR3 protein, humanChemokine CXCL12CXCR4 protein, humanReceptors, CXCRReceptors, CXCR4ACKR3chemokinesCXCR4CXCR7heterodimerizationmetastasis

Identifiers

PMID30441765
PMCPMC6274818
OpenAlexW2901079642

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.