Evidence map›Paper›PMID 31842402›Full record

ArticleCells2019

Vascular PPARβ/δ Promotes Tumor Angiogenesis and Progression.

Kay-Dietrich Wagner, Siyue Du, Luc Martin, Nathalie Leccia, Jean-François Michiels, Nicole Wagner

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.5field-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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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 1 country.

Kay-Dietrich WagnerUniversité Côte d'Azur, CNRS, INSERM, iBV, 06107 Nice, France.ORCID 0000-0001-5483-7760
Siyue DuUniversité Côte d'Azur, CNRS, INSERM, iBV, 06107 Nice, France.
Luc MartinUniversité Côte d'Azur, CNRS, INSERM, iBV, 06107 Nice, France.
Nathalie LecciaDepartment of Pathology, CHU Nice, 06107 Nice, France.
Jean-François MichielsDepartment of Pathology, CHU Nice, 06107 Nice, France.
Nicole WagnerUniversité Côte d'Azur, CNRS, INSERM, iBV, 06107 Nice, France.ORCID 0000-0002-2746-0707
Centre National de la Recherche Scientifique · FRCentre Hospitalier Universitaire de Nice · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors, which function as transcription factors. Among them, PPARβ/δ is highly expressed in endothelial cells. Pharmacological activation with PPARβ/δ agonists had been shown to increase their angiogenic properties. PPARβ/δ has been suggested to be involved in the regulation of the angiogenic switch in tumor progression. However, until now, it is not clear to what extent the expression of PPARβ/δ in tumor endothelium influences tumor progression and metastasis formation. We addressed this question using transgenic mice with an inducible conditional vascular-specific overexpression of PPARβ/δ. Following specific over-expression of PPARβ/δ in endothelial cells, we induced syngenic tumors. We observed an enhanced tumor growth, a higher vessel density, and enhanced metastasis formation in the tumors of animals with vessel-specific overexpression of PPARβ/δ. In order to identify molecular downstream targets of PPARβ/δ in the tumor endothelium, we sorted endothelial cells from the tumors and performed RNA sequencing. We identified platelet-derived growth factor receptor beta (Pdgfrb), platelet-derived growth factor subunit B (Pdgfb), and the tyrosinkinase KIT (c-Kit) as new PPARβ/δ -dependent molecules. We show here that PPARβ/δ activation, regardless of its action on different cancer cell types, leads to a higher tumor vascularization which favors tumor growth and metastasis formation.

Indexed as

AnimalsCarcinoma, Lewis LungCell Line, TumorDisease ProgressionEndothelial CellsHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsMiceNeovascularization, PathologicPhenolsPPAR-betaPPAR deltaProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor betaSulfhydryl Compounds(4-(((2-(3-fluoro-4-(trifluoromethyl)phenyl)-4-methyl-1,3-thiazol-5-yl)methyl)sulfanyl)-2-methylphenoxy)acetic acidPhenolsPPAR-betaPPAR deltaProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor betaSulfhydryl CompoundsThiazolesendothelial cellsmetastasis formationperoxisome-proliferator activated receptorsRNA sequencingtumor angiogenesistumor progression

Identifiers

PMID31842402
PMCPMC6952835
OpenAlexW2996623836

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.