Evidence map›Paper›PMID 25373734›Full record

ArticleOncotarget2014

Angiostatic, tumor inflammatory and anti-tumor effects of CXCL4(47-70) and CXCL4L1(47-70) in an EGF-dependent breast cancer model.

Katrien Van Raemdonck, Nele Berghmans, Vincent Vanheule, Antonella Bugatti, Paul Proost, Ghislain Opdenakker, Marco Presta, Jo Van Damme, Sofie Struyf

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. The role of CXC chemokines and receptors in breast cancer.Clinical and experimental medicine · 2025
    Review
  2. Review
  3. Article
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  6. Article
  7. Review
  8. Cancer management and research · 2019
    Article
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  13. Observational
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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

9 authors at 3 institutions in 2 countries.

Katrien Van RaemdonckLaboratory of Molecular Immunology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Nele BerghmansLaboratory of Molecular Immunology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Vincent VanheuleLaboratory of Molecular Immunology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Antonella BugattiLaboratory of Experimental Oncology and Immunology, University of Brescia, Department of Molecular and Translational Medicine Brescia, Italy.
Paul ProostLaboratory of Molecular Immunology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Ghislain OpdenakkerLaboratory of Immunobiology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Marco PrestaLaboratory of Experimental Oncology and Immunology, University of Brescia, Department of Molecular and Translational Medicine Brescia, Italy.
Jo Van DammeLaboratory of Molecular Immunology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Sofie StruyfLaboratory of Molecular Immunology, KU Leuven - University of Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium.
Rega Institute for Medical Research · BEKU Leuven · BEUniversity of Brescia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CXCL4 and CXCL4L1, platelet-derived CXC chemokines, and their carboxy-terminal peptides CXCL4(47-70) and CXCL4L1(47-70) previously displayed angiostatic and anti-tumoral activity in a melanoma model. Here, we found CXCL4(47-70) and CXCL4L1(47-70) to inhibit lymphatic endothelial cell proliferation in vitro. Furthermore, the angiostatic potential of CXCL4(47-70) and CXCL4L1(47-70) was tested against different angiogenic stimuli (FGF1, FGF2, FGF8, EGF and VEGF). Besides reducing FGF2-induced vascular endothelial cell growth, CXCL4(47-70) and CXCL4L1(47-70) efficiently counteracted EGF. Consequently, we considered their anti-tumoral potential in EGF-dependent MDA-MB-231 breast tumors. In tumor-bearing mice, CXCL4(47-70) reduced tumor growth better than CXCL4L1(47-70). In CXCL4(47-70)-treated tumors significantly more intratumoral monocytes/macrophages and dendritic cells were present and higher expression levels of CCL5 and IFN- γ were detected by qPCR on tumor lysates. Because neither peptide was able to specifically bind CXCR3A or CXCR3B, differential glycosaminoglycan binding and direct interaction with cytokines (EGF and CCL5) might explain any differences in anti-tumoral effects. Notably, CCL5-induced monocyte chemotaxis in vitro was increased by addition of CXCL4(47-70) or CXCL4L1(47-70). Finally, CXCL4(47-70) and CXCL4L1(47-70) inhibited proliferation of MDA-MB-231 cells. Our results suggest a tumor type-dependent responsiveness to either CXCL4(47-70) or CXCL4L1(47-70) treatment, defined by anti-proliferative, angiostatic and inflammatory actions, and substantiate their therapeutic potential.

Indexed as

Platelet Factor 4Angiostatic ProteinsAnimalsAntineoplastic AgentsApoptosisBlotting, WesternBreast NeoplasmsCattleCell ProliferationCells, CulturedChemotaxisCoagulantsCytokinesDisease Models, AnimalEndothelial CellsEndothelium, VascularAngiostatic ProteinsAntineoplastic AgentsCoagulantsCytokinesEpidermal Growth FactorInflammation MediatorsPeptide FragmentsPF4V1 protein, humanPlatelet Factor 4

Identifiers

PMID25373734
PMCPMC4279419
OpenAlexW2146744250

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.