Vasorin stimulates malignant progression and angiogenesis in glioma. Issue 8 (23rd July 2019)
- Record Type:
- Journal Article
- Title:
- Vasorin stimulates malignant progression and angiogenesis in glioma. Issue 8 (23rd July 2019)
- Main Title:
- Vasorin stimulates malignant progression and angiogenesis in glioma
- Authors:
- Liang, Weiye
Guo, Baoyin
Ye, Jiecheng
Liu, Hui
Deng, Wanying
Lin, Chenli
Zhong, Xueyun
Wang, Lihui - Abstract:
- 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 progressionAbstract: 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. Abstract : Vasorin stimulates tumor progression and angiogenesis in glioma, and, as such, represents a novel therapeutic target for glioma. … (more)
- Is Part Of:
- Cancer science. Volume 110:Issue 8(2019)
- Journal:
- Cancer science
- Issue:
- Volume 110:Issue 8(2019)
- Issue Display:
- Volume 110, Issue 8 (2019)
- Year:
- 2019
- Volume:
- 110
- Issue:
- 8
- Issue Sort Value:
- 2019-0110-0008-0000
- Page Start:
- 2558
- Page End:
- 2572
- Publication Date:
- 2019-07-23
- Subjects:
- VASN -- glioma -- tumor progression -- angiogenesis -- STAT3
Cancer -- Periodicals
Neoplasms -- Periodicals
Research -- Periodicals
Electronic journals
616.994005 - Journal URLs:
- http://firstsearch.oclc.org ↗
http://firstsearch.oclc.org/journal=1347-9032;screen=info;ECOIP ↗
http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1349-7006 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/cas.14103 ↗
- Languages:
- English
- ISSNs:
- 1347-9032
- Deposit Type:
- Legaldeposit
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- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3046.603000
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