Evidence map›Paper›PMID 28990104›Full record

ArticleMolecular medicine reports2017

Antiangiogenic properties of caudatin in vitro and in vivo by suppression of VEGF‑VEGFR2‑AKT/FAK signal axis.

Xinzhi Wang, Xiaoting Fu, Shijun Zhao, Xiaoyan Fu, Huifang Zhang, Lurong Shao, Gang Li, Cundong Fan

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Caudatin Inhibits the Proliferation, Invasion, and Glycolysis of Osteosarcoma Cells via the Wnt/Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  5. Molecules (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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.

Xinzhi WangDepartment of Neurosurgery, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Xiaoting FuKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong 271000, P.R. China.
Shijun ZhaoKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong 271000, P.R. China.
Xiaoyan FuKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong 271000, P.R. China.
Huifang ZhangKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong 271000, P.R. China.
Lurong ShaoKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong 271000, P.R. China.
Gang LiDepartment of Neurosurgery, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Cundong FanKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, Shandong 271000, P.R. China.
Taishan Medical University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor angiogenesis provides essential nutrients and oxygen to the tumor microenvironment, which is important in tumor growth, progression and metastasis. Inhibition of tumor angiogenesis represents one of the most promising strategies in tumor therapy. The authors previously demonstrated that caudatin, one species of C‑21 steroidal from Cynanchum auriculatum (C. auriculatum), effectively inhibits human glioma growth in vitro and in vivo through triggering cell cycle arrest and apoptosis. However, little information regarding the antiangiogenic properties of caudatin in human glioma is available. Based on the author's previous study, the antiangiogenic effect of caudatin against human glioma was explored, and the underlying mechanism was investigated. The results suggested that caudatin treatment significantly inhibited HUVEC human umbilical vein endothelial cell proliferation, blocked the HUVECs migration, invasion and capillary‑like tube formation by disturbing the vascular endothelial growth factor (VEGF)‑VEGFR2‑protein kinase B (AKT)/focal adhesion kinase (FAK) signal axis. Notably, caudatin treatment abolished the glioma cell growth by suppression of the in vivo angiogenesis, which involved FAK and AKT dephosphorylation and inhibition of VEGF expression. The findings validated the antiangiogenic potential of caudatin in hunting human glioma.

Indexed as

Angiogenesis InhibitorsCell MovementCell SurvivalFocal Adhesion Protein-Tyrosine KinasesGlycosidesHumansHuman Umbilical Vein Endothelial CellsPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionSteroidsVascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth FactorsAngiogenesis InhibitorscaudatinFocal Adhesion Protein-Tyrosine KinasesGlycosidesProto-Oncogene Proteins c-aktSteroidsVascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factors

Identifiers

PMID28990104
PMCPMC5779977
OpenAlexW2762371242

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.