Evidence map›Paper›PMID 24874473›Full record

ArticleBritish journal of cancer2014

A novel decoy receptor fusion protein for FGF-2 potently inhibits tumour growth.

D Li, X Wei, K Xie, K Chen, J Li, J Fang

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Article
  3. Heparan Sulfate Proteoglycans: Key Mediators of Stem Cell Function.Frontiers in cell and developmental biology · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Specific Antibody Fragment Ligand Traps Blocking FGF1 Activity.International journal of molecular sciences · 2018
    Article
  8. Article
  9. Review
  10. Molecular Pathways: Receptor Ectodomain Shedding in Treatment, Resistance, and Monitoring of Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Review
  11. Article
  12. Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells.International journal of molecular sciences · 2016
    Review
  13. Review
  14. Anti-angiogenic alternatives to VEGF blockade.Clinical & experimental metastasis · 2016
    Review
  15. Article
  16. miRNA-646 suppresses osteosarcoma cell metastasis by downregulating fibroblast growth factor 2 (FGF2).Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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 1 institution in 1 country.

D LiSchool of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
X WeiSchool of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
K XieSchool of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
K ChenSchool of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
J LiSchool of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
J FangSchool of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAntiangiogenic therapies have been proven effective in cancer treatment. Fibroblast growth factor-2 (FGF-2) has been functionally implicated in tumour angiogenesis and is an important target of antiangiogenic therapies. The aim of this work was to develop a novel FGF-2 inhibitor for cancer therapy.

methodsEleven fusion proteins were developed by fusing various truncated extracellular regions of FGFR1 with the Fc region of IgG1. The optimal decoy receptor fusion protein with the highest binding affinity for FGF-2 was identified by an FGF-2-binding assay and its potential antitumour effects were investigated.

resultsWe obtained a soluble decoy receptor fusion protein with the highest binding activity for FGF-2, named FGF-Trap. Fibroblast growth factor-Trap significantly abolished FGF-2-stimulated activation of FGF signalling as demonstrated by its suppression of FGF-2-mediated phosphorylation of Erk1/2 and Akt, upregulation of cyclins D1 and E and the increase in mRNA levels of vascular endothelial growth factor R1 and R2 (VEGFR1 and VEGFR2). Furthermore, FGF-Trap effectively suppressed FGF-2-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs) in vitro. Most importantly, FGF-Trap potently inhibited tumour growth and angiogenesis in Caki-1 and A549 xenograft models in vivo.

conclusionsFibroblast growth factor-Trap potently inhibits tumour growth by blocking FGF-2 signalling pathways and could be an effective therapeutic agent for cancer patients.

Indexed as

Angiogenesis InhibitorsAnimalsCell Growth ProcessesCHO CellsCricetinaeCricetulusFemaleFibroblast Growth Factor 2HumansImmunoglobulin GMiceMice, Inbred BALB CMice, NudeNeoplasmsPhosphorylationReceptor, Fibroblast Growth Factor, Type 1Angiogenesis InhibitorsFGFR1 protein, humanFibroblast Growth Factor 2Immunoglobulin GReceptor, Fibroblast Growth Factor, Type 1Recombinant Fusion Proteins

Identifiers

PMID24874473
PMCPMC4090743
OpenAlexW2029464256

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.