Evidence map›Paper›PMID 11821955›Full record

ArticleOncogene2002

Histone deacetylases inhibitors as anti-angiogenic agents altering vascular endothelial growth factor signaling.

Christophe F Deroanne, Karine Bonjean, Sandrine Servotte, Laetitia Devy, Alain Colige, Nathalie Clausse, Sylvia Blacher, Eric Verdin, Jean-Michel Foidart, Betty V Nusgens and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

154 citing papers in PubMed, 396 citations in OpenAlex.

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  7. Carboplatin and Paclitaxel in combination with either vorinostat or placebo for first-line therapy of advanced non-small-cell lung cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2010
    Trial
  8. Phase II study of belinostat (PXD101), a histone deacetylase inhibitor, for second line therapy of advanced malignant pleural mesothelioma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2009
    Trial
  9. Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026
    Review
  10. Review
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  19. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
  20. Article

94 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 2 countries.

Christophe F DeroanneResearch Center in Experimental Cancerology, University of Liège, Sart-Tilman, B-4000 Liège, Belgium. LCTB@ulg.ac.be
Karine Bonjean
Sandrine Servotte
Laetitia Devy
Alain Colige
Nathalie Clausse
Sylvia Blacher
Eric Verdin
Jean-Michel Foidart
Betty V Nusgens
Vincent Castronovo
University of Liège · BEUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is a complex biological process involving the coordinated modulation of many genes. Histone deacetylases (HDAC) are a growing family of enzymes that mediate the availability of chromatin to the transcriptional machinery. Trichostatin-A (TSA) and suberoylanilide hydroxamic acid (SAHA), two HDAC inhibitors known to relieve gene silencing, were evaluated as potential antiangiogenic agents. TSA and SAHA were shown to prevent vascular endothelial growth factor (VEGF)-stimulated human umbilical cord endothelial cells (HUVEC) from invading a type I collagen gel and forming capillary-like structures. SAHA and TSA inhibited the VEGF-induced formation of a CD31-positive capillary-like network in embryoid bodies and inhibited the VEGF-induced angiogenesis in the CAM assay. TSA also prevented, in a dose-response relationship, the sprouting of capillaries from rat aortic rings. TSA inhibited in a dose-dependent and reversible fashion the VEGF-induced expression of VEGF receptors, VEGFR1, VEGFR2, and neuropilin-1. TSA and SAHA upregulated the expression by HUVEC of semaphorin III, a recently described VEGF competitor, at both mRNA and protein levels. This effect was specific to endothelial cells and was not observed in human fibroblasts neither in vascular smooth muscle cells. These observations provide a conspicuous demonstration that HDAC inhibitors are potent anti-angiogenic factors altering VEGF signaling.

Indexed as

Histone Deacetylase InhibitorsSemaphorin-3AAngiogenesis InhibitorsAnimalsAortaBlotting, WesternCarrier ProteinsCells, CulturedChick EmbryoChorionEndothelial Growth FactorsEndothelium, VascularHistone DeacetylasesHumansHydroxamic AcidsLymphokinesAngiogenesis InhibitorsCarrier ProteinsEndothelial Growth FactorsHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsLymphokinesNerve Tissue ProteinsRNA, MessengerRNA, Ribosomal, 28SSEMA3A protein, humanSema3a protein, ratSemaphorin-3Atrichostatin AVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsVorinostat

Identifiers

PMID11821955
OpenAlexW2031671750

What OpenQuestion holds

Textmetadata
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.