Evidence map›Paper›PMID 24704994›Full record

ArticleEuropean journal of histochemistry : EJH2014

Knockdown of VEGFR2 inhibits proliferation and induces apoptosis in hemangioma-derived endothelial cells.

J M Ou, Z Y Yu, M K Qiu, Y X Dai, Q Dong, J Shen, X F Wang, Y B Liu, Z W Quan, Z W Fei

Open access · goldAbstract read
In one paragraph

Article in European journal of histochemistry : EJH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The interactions between integrin αInternational journal of biological sciences · 2022
    Article
  10. Benign Liver Tumors.Visceral medicine · 2020
    Review
  11. CIZ1 Expression Is Upregulated in Hemangioma of the Tongue.Pathology oncology research : POR · 2019
    Article
  12. Complex Formation between VEGFR2 and the βCell chemical biology · 2019
    Article
  13. Article
  14. Article
  15. Propranolol for the treatment of vascular sarcomas.Journal of experimental pharmacology · 2018
    Review
  16. Article
  17. Is there still room for novelty, in histochemical papers?European journal of histochemistry : EJH · 2016
    Review
  18. Review
  19. 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

10 authors at 2 institutions in 1 country.

J M Ou. zheweifei@163.com.
Z Y Yu
M K Qiu
Y X Dai
Q Dong
J Shen
X F Wang
Y B Liu
Z W Quan
Z W Fei
XinHua Hospital · CNSuzhou Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is a process of development and growth of new capillary blood vessels from pre-existing vessels. Angiogenic growth factors play important roles in the development and maintenance of some malignancies, of which vascular endothelial growth factor (VEGF)/VEGFR2 interactions are involved in proliferation, migration, and survival of many cancer cells. The aim of this study was to investigate the function of VEGFR2 in human hemangiomas (HAs). Using immunohistochemistry assay, we examined the expression levels of VEGF, VEGFR2, Ki-67, glucose transporter-1 (Glut-1), phosphorylated protein kinase B (p-AKT) and p-ERK in different phases of human HAs. Positive expression of VEGF, VEGFR2, Ki-67, Glut-1, p-AKT and p-ERK was significantly increased in proliferating phase HAs, while decreased in involuting phase HAs (P=0.001; P=0.003). In contrast, cell apoptotic indexes were decreased in proliferating phase HAs, but increased in involuting phase HAs (P<0.01). Furthermore, we used small hairpin RNA (shRNA)-mediated VEGFR2 knockdown in primary HA-derived endothelial cells (HemECs) to understand  the  role  of  VEGF/VEGFR2 signaling. Knockdown of VEGFR2 by Lv-shVEGFR2 inhibited cell viability and induced apoptosis in primary HemECs companied with decreased expression of p-AKT, p-ERK, p-p38MAPK and Ki-67 and increased expression of caspase-3 (CAS-3). Overexpression of VEGFR2 promoted cell viability and blocked apoptosis in Lv-VEGFR2-transfected HemECs. Taken together, our findings demonstrate that, increased expression of VEGFR2 is involved in the development of primary HemECs possibly through regulation of the AKT and ERK pathways, suggesting that VEGFR2 may be a potential therapeutic target for HAs.

Indexed as

ApoptosisCell ProliferationCaspase 3Cell Line, TumorEndothelial CellsExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticGene Knockdown TechniquesHemangiomaHumansKi-67 AntigenProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor Receptor-2CASP3 protein, humanCaspase 3Extracellular Signal-Regulated MAP KinasesKDR protein, humanKi-67 AntigenProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID24704994
PMCPMC3980207
OpenAlexW2115378043

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.