Evidence map›Paper›PMID 31215106›Full record

ArticleCancer science2019

Vasorin stimulates malignant progression and angiogenesis in glioma.

Weiye Liang, Baoyin Guo, Jiecheng Ye, Hui Liu, Wanying Deng, Chenli Lin, Xueyun Zhong, Lihui Wang

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

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  16. TRIM47 promotes glioma angiogenesis by suppressing Smad4.In vitro cellular & developmental biology. Animal · 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 1 institution in 1 country.

Weiye LiangDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.
Baoyin GuoDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.
Jiecheng YeDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.
Hui LiuDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.
Wanying DengDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.
Chenli LinDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.
Xueyun ZhongDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.ORCID https://orcid.org/0000-0001-9242-2291
Lihui WangDepartment of Pathology, Medical College, Jinan University, Guangzhou, China.ORCID https://orcid.org/0000-0001-9805-2965
Jinan University · CN

Funding

Natural Science Foundation of Guangdong Province 2017A030313117Natural Science Foundation of Guangdong Province 2018A030313301The Fundamental Research Fund for the Central Universities 21616116The Guangzhou Science Technology and Innovation Commission 201804010075The Key Laboratory of Regenerative Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences KLRB201602The Key Laboratory of Regenerative Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences KLRB201711
6 · The paper itself

Abstract

Glioma, the most common human primary brain tumor, is characterized by invasive capabilities and angiogenesis. Vasorin (VASN), a transmembrane protein, is reported to be associated with vascular injury repair and is overexpressed in some human tumors. However, its role in tumor progression and angiogenesis in glioma is unknown. In this study, VASN was shown to be overexpressed in high-grade gliomas, and the expression level correlated with tumor grade and microvessel density in glioma specimens. Glioma patients with high VASN expression had a shorter overall survival time. Knockdown of VASN in glioma cells by shRNA significantly inhibited the malignancy of glioma, including cell proliferation, colony formation, invasion, and sphere formation. Ectopic expression of VASN increased glioma progression in vitro. The expression of VASN correlated with the mesenchymal type of glioblastoma multiforme (GBM) subtyped by gene set enrichment analysis (GSEA). Our results showed that the concentration of VASN was increased in the conditioned medium (CM) from glioma cells with VASN overexpression, and the CM from glioma cells with knockdown or overexpressed VASN inhibited or promoted HUVEC migration and tubulogenesis in vitro, respectively. Glioma growth and angiogenesis were stimulated upon ectopic expression of VASN in vivo. The STAT3 and NOTCH pathways were found to be activated and inhibited by VASN overexpression. Our findings suggest that VASN stimulates tumor progression and angiogenesis in glioma, and, as such, represents a novel therapeutic target for glioma.

Indexed as

AdultBrain NeoplasmsCarrier ProteinsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGlioblastomaGliomaHumansMaleMembrane ProteinsMiddle AgedNeovascularization, PathologicCarrier ProteinsMembrane ProteinsVASN protein, humanangiogenesisgliomaSTAT3tumor progressionVASN

Identifiers

PMID31215106
PMCPMC6676100
OpenAlexW2952563136

What OpenQuestion holds

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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.