Evidence map›Paper›PMID 28878352›Full record

ArticleLeukemia2018

S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells.

K Vrzalikova, M Ibrahim, M Vockerodt, T Perry, S Margielewska, L Lupino, E Nagy, E Soilleux, D Liebelt, R Hollows and 12 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Leukemia, 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Signal Transduction and Gene Regulation in the Endothelium.Cold Spring Harbor perspectives in medicine · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 7 institutions in 5 countries.

K VrzalikovaInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
M IbrahimInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
M VockerodtInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
T PerryInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
S MargielewskaInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
L LupinoInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
E NagyInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
E SoilleuxDepartment of Cellular Pathology, John Radcliffe Hospital, Oxford, UK.
D LiebeltInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
R HollowsInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
A LastInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
G ReynoldsInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
M AbdullahInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
H CurleyInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
M CareLeeds Institute of Cancer and Pathology, University of Leeds, Leeds, UK.
D KrappmannResearch Unit Cellular Signal Integration, Helmholtz Zentrum München, Neuherberg, Germany.
R ToozeLeeds Institute of Cancer and Pathology, University of Leeds, Leeds, UK.
J AllegoodDepartment of Biochemistry and Molecular Biology and Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
S SpiegelDepartment of Biochemistry and Molecular Biology and Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
W WeiInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
C B J WoodmanInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
P G MurrayInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
University of Birmingham · GBUniversity of Leeds · GBVirginia Commonwealth University · USHelmholtz Zentrum München · DEJohn Radcliffe Hospital · GBPalacký University Olomouc · CZUniversity of Sheffield · GB

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
SPHINGOSINE AS A MODULATOR OF CELLULAR PROLIFERATIONR01GM043880 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 1990 to 2023
$3.8M
Cancer Research UK 10066Cancer Research UK 17723NCI NIH HHS P30 CA016059NIGMS NIH HHS R01 GM043880
6 · The paper itself

Abstract

The Hodgkin/Reed-Sternberg cells of classical Hodgkin lymphoma (HL) are characterised by the aberrant activation of multiple signalling pathways. Here we show that a subset of HL displays altered expression of sphingosine-1-phosphate (S1P) receptors (S1PR)s. S1P activates phosphatidylinositide 3-kinase (PI3-K) in these cells that is mediated by the increased expression of S1PR1 and the decreased expression of S1PR2. We also showed that genes regulated by the PI3-K signalling pathway in HL cell lines significantly overlap with the transcriptional programme of primary HRS cells. Genes upregulated by the PI3-K pathway included the basic leucine zipper transcription factor, ATF-like 3 (BATF3), which is normally associated with the development of dendritic cells. Immunohistochemistry confirmed that BATF3 was expressed in HRS cells of most HL cases. In contrast, in normal lymphoid tissues, BATF3 expression was confined to a small fraction of CD30-positive immunoblasts. Knockdown of BATF3 in HL cell lines revealed that BATF3 contributed to the transcriptional programme of primary HRS cells, including the upregulation of S1PR1. Our data suggest that disruption of this potentially oncogenic feedforward S1P signalling loop could provide novel therapeutic opportunities for patients with HL.

Indexed as

Basic-Leucine Zipper Transcription FactorsCell LineCell Line, TumorGene Expression Regulation, NeoplasticHEK293 CellsHodgkin DiseaseHumansPhosphatidylinositol 3-KinasesReceptors, LysosphingolipidSignal TransductionSphingosine-1-Phosphate ReceptorsTranscription, GeneticTumor Cells, CulturedBasic-Leucine Zipper Transcription FactorsPhosphatidylinositol 3-KinasesReceptors, LysosphingolipidS1PR1 protein, humanSphingosine-1-Phosphate Receptors

Identifiers

PMID28878352
PMCPMC5737877
OpenAlexW2753585708

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.