Canstatin represses glioma growth by inhibiting formation of VM-like structures

Vasculogenic mimicry (VM) is different from classical tumor angiogenesis and does not depend on endothelial cells. VM is closely related to the prognosis of various cancers. Canstatin was first identified as an endogenous angiogenesis inhibitor. In the present study, the inhibitory effect of canstat...

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Autores principales:	Ma Yuqiang, Wu Tao, Zhou Houjie, He Guilu, Li Yifei, Wang Bocheng, Guo Qiang, Chen Baodong, Li Weiping
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	glioma canstatin vasculogenic mimicry u87 vegf hif-1α Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/56cf1f4e838a44e8a0f2771f6e03528a
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spelling	oai:doaj.org-article:56cf1f4e838a44e8a0f2771f6e03528a2021-12-05T14:11:05ZCanstatin represses glioma growth by inhibiting formation of VM-like structures2081-693610.1515/tnsci-2020-0176https://doaj.org/article/56cf1f4e838a44e8a0f2771f6e03528a2021-08-01T00:00:00Zhttps://doi.org/10.1515/tnsci-2020-0176https://doaj.org/toc/2081-6936Vasculogenic mimicry (VM) is different from classical tumor angiogenesis and does not depend on endothelial cells. VM is closely related to the prognosis of various cancers. Canstatin was first identified as an endogenous angiogenesis inhibitor. In the present study, the inhibitory effect of canstatin on VM formation was evaluated. Human glioblastoma cell lines U87 and U251 were letivirally transduced to overexpress canstatin gene or GFP as control. In vitro assays showed that canstatin overexpression reduced the tube formation of U87 and U251 cells in Matrigel. A xenograft glioma model was created by subcutaneous injection of lentivirally modified U87 cells into nude mice. The results of in vivo experiments showed that canstatin gene introduction inhibited the growth of glioma xenografts. In tumor xenografts overexpressing canstatin, U87-mediated formation of VM-like structures and VM-related VEGF (vascular endothelial growth factor) expression were remarkably reduced. Canstatin overexpression also decreased the phosphorylation of Akt and reduced the expression of Survivin in vitro. In addition, HIF-1α production and MMP-2 secretion were decreased by canstatin overexpression. Therefore, these results suggested a protective role of canstatin during VM-like structure formation of glioma probably via inhibiting signaling pathways inducing vasculogenic mimicry.Ma YuqiangWu TaoZhou HoujieHe GuiluLi YifeiWang BochengGuo QiangChen BaodongLi WeipingDe Gruyterarticlegliomacanstatinvasculogenic mimicryu87vegfhif-1αNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENTranslational Neuroscience, Vol 12, Iss 1, Pp 309-319 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	glioma canstatin vasculogenic mimicry u87 vegf hif-1α Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	glioma canstatin vasculogenic mimicry u87 vegf hif-1α Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Ma Yuqiang Wu Tao Zhou Houjie He Guilu Li Yifei Wang Bocheng Guo Qiang Chen Baodong Li Weiping Canstatin represses glioma growth by inhibiting formation of VM-like structures
description	Vasculogenic mimicry (VM) is different from classical tumor angiogenesis and does not depend on endothelial cells. VM is closely related to the prognosis of various cancers. Canstatin was first identified as an endogenous angiogenesis inhibitor. In the present study, the inhibitory effect of canstatin on VM formation was evaluated. Human glioblastoma cell lines U87 and U251 were letivirally transduced to overexpress canstatin gene or GFP as control. In vitro assays showed that canstatin overexpression reduced the tube formation of U87 and U251 cells in Matrigel. A xenograft glioma model was created by subcutaneous injection of lentivirally modified U87 cells into nude mice. The results of in vivo experiments showed that canstatin gene introduction inhibited the growth of glioma xenografts. In tumor xenografts overexpressing canstatin, U87-mediated formation of VM-like structures and VM-related VEGF (vascular endothelial growth factor) expression were remarkably reduced. Canstatin overexpression also decreased the phosphorylation of Akt and reduced the expression of Survivin in vitro. In addition, HIF-1α production and MMP-2 secretion were decreased by canstatin overexpression. Therefore, these results suggested a protective role of canstatin during VM-like structure formation of glioma probably via inhibiting signaling pathways inducing vasculogenic mimicry.
format	article
author	Ma Yuqiang Wu Tao Zhou Houjie He Guilu Li Yifei Wang Bocheng Guo Qiang Chen Baodong Li Weiping
author_facet	Ma Yuqiang Wu Tao Zhou Houjie He Guilu Li Yifei Wang Bocheng Guo Qiang Chen Baodong Li Weiping
author_sort	Ma Yuqiang
title	Canstatin represses glioma growth by inhibiting formation of VM-like structures
title_short	Canstatin represses glioma growth by inhibiting formation of VM-like structures
title_full	Canstatin represses glioma growth by inhibiting formation of VM-like structures
title_fullStr	Canstatin represses glioma growth by inhibiting formation of VM-like structures
title_full_unstemmed	Canstatin represses glioma growth by inhibiting formation of VM-like structures
title_sort	canstatin represses glioma growth by inhibiting formation of vm-like structures
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/56cf1f4e838a44e8a0f2771f6e03528a
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Canstatin represses glioma growth by inhibiting formation of VM-like structures

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