ArticleMicrovascular research2007
Adenoviruses increase endothelial cell proliferation, migration, and tube formation: partial reversal by the focal adhesion kinase inhibitor, FRNK.
Article in Microvascular research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- G Protein α Subunit 14 Mediates Fibroblast Growth Factor 2-Induced Cellular Responses in Human Endothelial Cells.Journal of cellular physiology · 2019Article
- Biallelic CCM3 mutations cause a clonogenic survival advantage and endothelial cell stiffening.Journal of cellular and molecular medicine · 2019Article
- Article
- Molecular mechanism underlying the antiproliferative effect of suppressor of cytokine signaling-1 in non-small-cell lung cancer cells.Cancer science · 2013Article
- BDNF promotes EGF-induced proliferation and migration of human fetal neural stem/progenitor cells via the PI3K/Akt pathway.Molecules (Basel, Switzerland) · 2011Article
- Helper-dependent adenoviral vectors are superior in vitro to first-generation vectors for endothelial cell-targeted gene therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- Mechanical stretch decreases FAK phosphorylation and reduces cell migration through loss of JIP3-induced JNK phosphorylation in airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
During the course of examining the feasibility of using an adenoviral vector to deliver a potential anti-angiogenic agent to endothelial cells, we discovered that adenoviruses, themselves, have pro-angiogenic activities. Thus, an adenoviral vector containing a green fluorescent protein transgene (Ad-GFP) stimulated the growth, migration, tube formation, and phosphorylation of focal adhesion kinase (FAK) of human lung microvascular endothelial cells. However, adenovirus-mediated endothelial cell mitogenesis, tube formation, and FAK phosphorylation were completely reduced and migration was partially reversed by the addition of a Fak-Related Non-Kinase (FRNK) transgene to the vector. Because FRNK inhibits focal adhesion kinase (FAK) activity, this suggests that the adenoviral effects on endothelial cells are in part mediated through FAK. These data, as well as data obtained in other laboratories, suggest that adenoviruses should be used with caution in cancer gene therapy due to potential pro-angiogenic effects. However, some of these untoward effects may be modulated by concurrent use of a FAK inhibitor.
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What OpenQuestion holds
Registered trials
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.