Evidence map›Paper›PMID 26883111›Full record

ArticleOncotarget2016

Targeting endothelial connexin40 inhibits tumor growth by reducing angiogenesis and improving vessel perfusion.

Florian Alonso, Sonia Domingos-Pereira, Loïc Le Gal, Laurent Derré, Paolo Meda, Patrice Jichlinski, Denise Nardelli-Haefliger, Jacques-Antoine Haefliger

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Endothelial Connexins in Developmental and Pathological Angiogenesis.Cold Spring Harbor perspectives in medicine · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Connexins-Therapeutic Targets in Cancers.International journal of molecular sciences · 2020
    Review
  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

8 authors at 2 institutions in 1 country.

Florian AlonsoDepartment of Medicine, Lausanne University Hospital, Lausanne, Switzerland.
Sonia Domingos-PereiraDepartment of Urology, Lausanne University Hospital, Lausanne, Switzerland.
Loïc Le GalDepartment of Medicine, Lausanne University Hospital, Lausanne, Switzerland.
Laurent DerréDepartment of Urology, Lausanne University Hospital, Lausanne, Switzerland.
Paolo MedaDepartment of Cell Physiology and Metabolism, University of Geneva, Medical Center, Geneva, Switzerland.
Patrice JichlinskiDepartment of Urology, Lausanne University Hospital, Lausanne, Switzerland.
Denise Nardelli-HaefligerDepartment of Urology, Lausanne University Hospital, Lausanne, Switzerland.
Jacques-Antoine HaefligerDepartment of Medicine, Lausanne University Hospital, Lausanne, Switzerland.
University of Lausanne · CHUniversity of Geneva · CH

Funding

Gap Junction Mediated Signaling and Vascular ResponsesR01HL064232 · NHLBI · UNIVERSITY OF ARIZONA · PI SIMON, ALEXANDER M · 2001 to 2010
$2.2M
NHLBI NIH HHS R01 HL064232
6 · The paper itself

Abstract

Endothelial connexin40 (Cx40) contributes to regulate the structure and function of vessels. We have examined whether the protein also modulates the altered growth of vessels in tumor models established in control mice (WT), mice lacking Cx40 (Cx40-/-), and mice expressing the protein solely in endothelial cells (Tie2-Cx40). Tumoral angiogenesis and growth were reduced, whereas vessel perfusion, smooth muscle cell (SMC) coverage and animal survival were increased in Cx40-/- but not Tie2-Cx40 mice, revealing a critical involvement of endothelial Cx40 in transformed tissues independently of the hypertensive status of Cx40-/- mice. As a result, Cx40-/- mice bearing tumors survived significantly longer than corresponding controls, including after a cytotoxic administration. Comparable observations were made in WT mice injected with a peptide targeting Cx40, supporting the Cx40 involvement. This involvement was further confirmed in the absence of Cx40 or by peptide-inhibition of this connexin in aorta-sprouting, matrigel plug and SMC migration assays, and associated with a decreased expression of the phosphorylated form of endothelial nitric oxide synthase. The data identify Cx40 as a potential novel target in cancer treatment.

Indexed as

AnimalsAortaApoptosisBiomarkers, TumorBlood VesselsCell ProliferationConnexinsEndothelium, VascularFemaleGap Junction alpha-5 ProteinHumansLung NeoplasmsMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutBiomarkers, TumorConnexinsGap Junction alpha-5 Proteinangiogenesiscell-cell communicationconnexinstransgenic micetumors

Identifiers

PMID26883111
PMCPMC4924695
OpenAlexW2281261884

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.