Evidence map›Paper›PMID 25912421›Full record

ArticleOncotarget2015

A long pentraxin-3-derived pentapeptide for the therapy of FGF8b-driven steroid hormone-regulated cancers.

Arianna Giacomini, Sara Matarazzo, Katiuscia Pagano, Laura Ragona, Sara Rezzola, Michela Corsini, Emanuela Di Salle, Marco Presta, Roberto Ronca

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Role of long pentraxin PTX3 in cancer.Clinical and experimental medicine · 2023
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. [Research progress on the role of pentraxin 3 in polycystic ovary syndrome].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020
    Article
  8. Article
  9. Review
  10. Article
  11. Article
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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 2 institutions in 1 country.

Arianna GiacominiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Sara MatarazzoDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Katiuscia PaganoNMR Laboratory, Istituto per lo Studio delle Macromolecole, CNR, Milan, Italy.
Laura RagonaNMR Laboratory, Istituto per lo Studio delle Macromolecole, CNR, Milan, Italy.
Sara RezzolaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Michela CorsiniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Emanuela Di SalleDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Marco PrestaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Roberto RoncaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
University of Brescia · ITInstitute for Macromolecular Studies · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor-8b (FGF8b) affects the epithelial/stromal compartments of steroid hormone-regulated tumors by exerting an autocrine activity on cancer cells and a paracrine pro-angiogenic function, thus contributing to tumor progression. The FGF8b/FGF receptor (FGFR) system may therefore represent a target for the treatment of steroid hormone-regulated tumors. The soluble pattern recognition receptor long pentraxin-3 (PTX3) binds various FGFs, including FGF2 and FGF8b, thus inhibiting the angiogenic and tumorigenic activity of androgen-regulated tumor cells. Nevertheless, the complex/proteinaceous structure of PTX3 hampers its pharmacological exploitation. In this context, the acetylated pentapeptide Ac-ARPCA-NH2 (ARPCA), corresponding to the N-terminal amino acid sequence PTX3(100-104), was identified as a minimal FGF2-binding peptide able to antagonize the biological activity of FGF2. Here, we demonstrate that ARPCA binds FGF8b and inhibits its capacity to form FGFR1-mediated ternary complexes with heparan sulphate proteoglycans. As a FGF8b antagonist, ARPCA inhibits FGFR1 activation and signalling in endothelial cells, hampering the angiogenic activity exerted in vitro and in vivo by FGF8b. Also, ARPCA suppresses the angiogenic and tumorigenic potential of prototypic androgen/FGF8b-dependent Shionogi 115 mammary carcinoma cells and of androgen/FGF8b/FGF2-dependent TRAMP-C2 prostate cancer cells. In conclusion, ARPCA represents a novel FGF8b antagonist with translational implications for the therapy of steroid hormone-regulated tumors.

Indexed as

AnimalsCell ProliferationChick EmbryoC-Reactive ProteinFibroblast Growth Factor 8HumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred C57BLMice, NudeModels, MolecularNeoplasms, Hormone-DependentNeovascularization, PhysiologicPentraxinsPeptide FragmentsC-Reactive ProteinFibroblast Growth Factor 8PentraxinsPeptide FragmentsSerum Amyloid P-ComponentangiogenesisFGF8hormone-regulated cancerpentraxinpeptide

Identifiers

PMID25912421
PMCPMC4537050
OpenAlexW1552673178

What OpenQuestion holds

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LicenceCC BY
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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.