Evidence map›Paper›PMID 16818645›Full record

ArticleCancer research2006

Sustained expression of early growth response protein-1 blocks angiogenesis and tumor growth.

Markus Lucerna, Jiri Pomyje, Diana Mechtcheriakova, Alexandra Kadl, Florian Gruber, Martin Bilban, Yuri Sobanov, Gernot Schabbauer, Johannes Breuss, Oswald Wagner and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Friend or foe, the role of EGR-1 in cancer.Medical oncology (Northwood, London, England) · 2019
    Review
  5. Article
  6. Evaluation of therapeutic effects ofOncology letters · 2018
    Article
  7. Regulation of Tumor Progression by Programmed Necrosis.Oxidative medicine and cellular longevity · 2018
    Review
  8. Human cytomegalovirus infection downregulates vitamin-D receptor in mammalian cells.The Journal of steroid biochemistry and molecular biology · 2017
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

14 authors at 5 institutions in 3 countries.

Markus LucernaDepartments of Vascular Biology and Thrombosis Research, Ludwig Boltzmann Institute for Clinical and Experimental Oncology, Medical University of Vienna, Lazarettgasse 19, A-1235 Vienna, Austria.
Jiri Pomyje
Diana Mechtcheriakova
Alexandra Kadl
Florian Gruber
Martin Bilban
Yuri Sobanov
Gernot Schabbauer
Johannes Breuss
Oswald Wagner
Markus Bischoff
Matthias Clauss
Bernd R Binder
Erhard Hofer
Medical University of Vienna · ATThrombosis Research Institute · GBCenter for Vascular Biology Research · USLudwig Boltzmann Institute for Experimental and Clinical Traumatology · ATUniversity of Virginia · US

Funding

Austrian Science Fund FWF S 9403
6 · The paper itself

Abstract

Transient induction of the transcription factor early growth response protein-1 (EGR-1) plays a pivotal role in the transcriptional response of endothelial cells to the angiogenic growth factors vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), which are produced by most tumors and are involved in the angiogenic switch. We report here that sustained expression of EGR-1 by recombinant adenoviruses in endothelial cells, however, leads to the specific induction of potent feedback inhibitory mechanisms, including strong up-regulation of transcriptional repressors, negative cell cycle check point effectors, proteins with established antiangiogenic activity, and several proapoptotic genes. Sustained EGR-1 expression consistently leads to an antiangiogenic state characterized by an altered responsiveness to VEGF and bFGF and a striking inhibition of sprouting and tubule formation in vitro. Furthermore, EGR-1-expressing viruses potently inhibit cell invasion and vessel formation in the murine Matrigel model and repress tumor growth in a murine fibrosarcoma model. We propose that gene therapy involving sustained EGR-1 expression may constitute a novel therapeutic principle in the treatment of cancer due to the simultaneous induction of multiple pathways of antiangiogenesis, growth arrest, and apoptosis induction in proliferating cells leading to preferential inhibition of angiogenesis and tumor growth.

Indexed as

AdenoviridaeAnimalsCell Growth ProcessesEarly Growth Response Protein 1Endothelial CellsFibrosarcomaHumansMiceNeovascularization, PathologicRNA, MessengerEarly Growth Response Protein 1EGR1 protein, humanRNA, Messenger

Identifiers

PMID16818645
PMCPMC2882226
OpenAlexW2128516441

What OpenQuestion holds

Textmetadata
LicenceTDM
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.