Evidence map›Paper›PMID 32273578›Full record

ArticleScientific reports2020

Fasentin diminishes endothelial cell proliferation, differentiation and invasion in a glucose metabolism-independent manner.

Mª Carmen Ocaña, Beatriz Martínez-Poveda, Manuel Marí-Beffa, Ana R Quesada, Miguel Ángel Medina

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. In Vitro and In Vivo Effects of Ulvan Polysaccharides fromPharmaceuticals (Basel, Switzerland) · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Cancer cell metabolic plasticity in migration and metastasis.Clinical & experimental metastasis · 2021
    Review
  20. Review
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

5 authors at 4 institutions in 1 country.

Mª Carmen OcañaUniversidad de Málaga, Andalucía Tech, Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, E-29071, Málaga, Spain.
Beatriz Martínez-PovedaUniversidad de Málaga, Andalucía Tech, Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, E-29071, Málaga, Spain.
Manuel Marí-BeffaUniversidad de Málaga, Andalucía Tech, Departamento de Biología Celular, Genética y Fisiología, Facultad de Ciencias, E-29071, Málaga, Spain.
Ana R QuesadaUniversidad de Málaga, Andalucía Tech, Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, E-29071, Málaga, Spain.ORCID http://orcid.org/0000-0002-6419-8867
Miguel Ángel MedinaUniversidad de Málaga, Andalucía Tech, Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, E-29071, Málaga, Spain. medina@uma.es.ORCID http://orcid.org/0000-0001-7275-6462
Instituto de Investigación Biomédica de Málaga · ESCentre for Biomedical Network Research on Rare Diseases · ESCentro de Investigación en Red en Enfermedades Cardiovasculares · ESUniversidad de Málaga · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The synthetic compound fasentin has been described as a modulator of GLUT-1 and GLUT-4 transporters, thus inhibiting glucose uptake in some cancer cells. Endothelial glucose metabolism has been recently connected to angiogenesis and it is now an emerging topic in scientific research. Indeed, certain compounds with a known effect on glucose metabolism have also been shown to inhibit angiogenesis. In this work we tested the capability of fasentin to modulate angiogenesis in vitro and in vivo. We show that fasentin inhibited tube formation in endothelial cells by a mechanism that involves a negative effect on endothelial cell proliferation and invasion, without affecting other steps related to the angiogenic process. However, fasentin barely decreased glucose uptake in human dermal microvascular endothelial cells and the GLUT-1 inhibitor STF-31 failed to inhibit tube formation in these cells. Therefore, this modulatory capacity on endothelial cells function exerted by fasentin is most likely independent of a modulation of glucose metabolism. Taken together, our results show a novel biological activity of fasentin, which could be evaluated for its utility in cancer and other angiogenesis-dependent diseases.

Indexed as

Cell DifferentiationCell MovementCell ProliferationAnilidesAnimalsCattleCells, CulturedChick EmbryoGlucoseHeLa CellsHumansHuman Umbilical Vein Endothelial CellsMCF-7 CellsNeovascularization, PhysiologicPyridinesAnilidesfasentinGlucosePyridinesSTF-31

Identifiers

PMID32273578
PMCPMC7145862
OpenAlexW3015867366

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.