Evidence map›Paper›PMID 25232946›Full record

ArticlePloS one2014

Endostar, a modified recombinant human endostatin, suppresses angiogenesis through inhibition of Wnt/β-catenin signaling pathway.

Xiaoming Xu, Wei Mao, Qian Chen, Qin Zhuang, Lihui Wang, Jin Dai, Haibing Wang, Zhaoquan Huang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  8. Endothelial Dysfunction in the Context of Blood-Brain Barrier Modeling.Journal of evolutionary biochemistry and physiology · 2022
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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.

Xiaoming XuDepartment of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China.
Wei MaoDepartment of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China.
Qian ChenFirst College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Qin ZhuangFirst College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Lihui WangFirst College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Jin DaiDepartment of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China.
Haibing WangDepartment of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China.
Zhaoquan HuangDepartment of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China.
Zhejiang Provincial Hospital of TCM · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endostar, a novel modified recombinant human endostatin, is now widely studied for the treatment of diseases that are characterized or caused by pathological angiogenesis. However, its molecular mechanism remains unclear. In this study, we investigated the effects of Endostar on the Wnt/β-catenin signaling pathway, which has emerged as an important aspect of angiogenesis. We showed that Endostar significantly inhibited the proliferation, migration, invasion, and capillary-like tube formation of human umbilical vascular endothelial cells in a dose-dependent manner. Using a luciferase reporter assay, we also demonstrated that Endostar suppressed β-catenin-dependent T cell factor transcriptional activity in increasing doses. Moreover, we found that Endostar treatment also restricted the stabilized mutant β-catenin-mediated increase in transcriptional activity, suggesting that Endostar exerts its inhibitory influence on Wnt/β-catenin signaling by targeting β-catenin or its downstream molecules. Western blot and immunofluorescence results revealed that Endostar significantly decreased nuclear and total β-catenin levels. Finally, we discovered that Endostar down-regulated cyclin D1 and VEGF, two proteins that are known as the downstream targets of Wnt/β-catenin signaling and that also play important roles in angiogenesis. Our findings suggested that Endostar inhibits angiogenesis and that the downregulation of the Wnt/β-catenin signaling pathway may be involved in the inhibition of angiogenesis by Endostar. These results support the use of Endostar in further clinical applications.

Indexed as

beta CateninCell LineCell MovementCell ProliferationCell SurvivalCyclin D1EndostatinsHumansHuman Umbilical Vein Endothelial CellsNeovascularization, PathologicRecombinant ProteinsTCF Transcription FactorsTranscription, GeneticVascular Endothelial Growth Factor AWnt ProteinsWnt Signaling Pathwaybeta CateninCyclin D1endostar proteinEndostatinsRecombinant ProteinsTCF Transcription FactorsVascular Endothelial Growth Factor AVEGFA protein, humanWnt Proteins

Identifiers

PMID25232946
PMCPMC4169397
OpenAlexW2008321434

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.