Evidence map›Paper›PMID 27432059›Full record

ArticleBMC cancer2016

The role of formyl peptide receptor 1 (FPR1) in neuroblastoma tumorigenesis.

Igor Snapkov, Carl Otto Öqvist, Yngve Figenschau, Per Kogner, John Inge Johnsen, Baldur Sveinbjørnsson

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  16. AaTs-1: A Tetrapeptide fromMolecules (Basel, Switzerland) · 2021
    Article
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  19. Phospholipase ACells · 2021
    Review
  20. 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

6 authors at 2 institutions in 2 countries.

Igor SnapkovMolecular Inflammation Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway. igor.v.snapkov@uit.no.
Carl Otto ÖqvistChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Yngve FigenschauEndocrinology Research Group, Department of Clinical Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway.
Per KognerChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
John Inge JohnsenChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Baldur SveinbjørnssonMolecular Inflammation Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway.
Karolinska Institutet · SEUiT The Arctic University of Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFormyl peptide receptor 1 (FPR1) is a G protein-coupled receptor mainly expressed by the cells of myeloid origin, where it mediates the innate immune response to bacterial formylated peptides. High expression of FPR1 has been detected in various cancers but the function of FPR1 in tumorigenesis is poorly understood.

methodsExpression of FPR1 in neuroblastoma cell lines and primary tumors was studied using RT-PCR, western blotting, immunofluorescence and immunohistochemistry. Calcium mobilization assays and western blots with phospho-specific antibodies were used to assess the functional activity of FPR1 in neuroblastoma. The tumorigenic capacity of FPR1 was assessed by xenografting of neuroblastoma cells expressing inducible FPR1 shRNA, FPR1 cDNA or control shRNA in nude mice.

resultsFPR1 is expressed in neuroblastoma primary tumors and cell lines. High expression of FPR1 corresponds with high-risk disease and poor patient survival. Stimulation of FPR1 in neuroblastoma cells using fMLP, a selective FPR1 agonist, induced intracellular calcium mobilization and activation of MAPK/Erk, PI3K/Akt and P38-MAPK signal transduction pathways that were inhibited by using Cyclosporin H, a selective receptor antagonist for FPR1. shRNA knock-down of FPR1 in neuroblastoma cells conferred a delayed xenograft tumor development in nude mice, whereas an ectopic overexpression of FPR1 promoted augmented tumorigenesis in nude mice.

conclusionOur data demonstrate that FPR1 is involved in neuroblastoma development and could represent a therapy option for the treatment of neuroblastoma.

Indexed as

AnimalsCalciumCell ProliferationCell Transformation, NeoplasticChildCyclosporineExtracellular Signal-Regulated MAP KinasesHumansMAP Kinase Signaling SystemMiceMice, NudeNeoplasm TransplantationNeuroblastomap38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPrognosisCalciumCyclosporinecyclosporin HExtracellular Signal-Regulated MAP KinasesFPR1 protein, humanp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Formyl PeptideRNA, Small InterferingFormyl peptide receptor 1FPR1InflammationNeuroblastoma

Identifiers

PMID27432059
PMCPMC4950242
OpenAlexW2477426969

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.