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Isthmin inhibits glioma growth through antiangiogenesis in vivo

Among glioma treatment strategies, antiangiogenesis emerges as a meaningful and feasible treatment approach for inducing long-term survival. Isthmin is a gene highly expressed in the isthmus of the midbrain–hindbrain organizer in Xenopus, and has recently been identified as a novel angiogenesis inhi...

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Autores principales: Yuan, Bangqing, Xian, Ronghua, Ma, Jianfang, Chen, Yujian, Lin, Chuangan, Song, Yaoming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432204/
https://www.ncbi.nlm.nih.gov/pubmed/22772605
http://dx.doi.org/10.1007/s11060-012-0910-8
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author Yuan, Bangqing
Xian, Ronghua
Ma, Jianfang
Chen, Yujian
Lin, Chuangan
Song, Yaoming
author_facet Yuan, Bangqing
Xian, Ronghua
Ma, Jianfang
Chen, Yujian
Lin, Chuangan
Song, Yaoming
author_sort Yuan, Bangqing
collection PubMed
description Among glioma treatment strategies, antiangiogenesis emerges as a meaningful and feasible treatment approach for inducing long-term survival. Isthmin is a gene highly expressed in the isthmus of the midbrain–hindbrain organizer in Xenopus, and has recently been identified as a novel angiogenesis inhibitor. However, the potential of isthmin on the glioma angiogenesis has not been well studied. In the present study, we demonstrated that the recombinant adenovirus isthmin (Ad-isthmin) could inhibit VEGF-stimulated endothelial cell proliferation and induce apoptosis through a caspase-dependent pathway. In addition, Ad-isthmin significantly suppressed glioma growth through antiangiogenesis without apparent side effects. Taken together, our results demonstrated that isthmin could act as a novel angiogenesis inhibitor and might be utilized in the glioma antiangiogenesis therapy.
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spelling pubmed-34322042012-09-07 Isthmin inhibits glioma growth through antiangiogenesis in vivo Yuan, Bangqing Xian, Ronghua Ma, Jianfang Chen, Yujian Lin, Chuangan Song, Yaoming J Neurooncol Laboratory Investigation Among glioma treatment strategies, antiangiogenesis emerges as a meaningful and feasible treatment approach for inducing long-term survival. Isthmin is a gene highly expressed in the isthmus of the midbrain–hindbrain organizer in Xenopus, and has recently been identified as a novel angiogenesis inhibitor. However, the potential of isthmin on the glioma angiogenesis has not been well studied. In the present study, we demonstrated that the recombinant adenovirus isthmin (Ad-isthmin) could inhibit VEGF-stimulated endothelial cell proliferation and induce apoptosis through a caspase-dependent pathway. In addition, Ad-isthmin significantly suppressed glioma growth through antiangiogenesis without apparent side effects. Taken together, our results demonstrated that isthmin could act as a novel angiogenesis inhibitor and might be utilized in the glioma antiangiogenesis therapy. Springer US 2012-07-07 2012 /pmc/articles/PMC3432204/ /pubmed/22772605 http://dx.doi.org/10.1007/s11060-012-0910-8 Text en © The Author(s) 2012 https://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Laboratory Investigation
Yuan, Bangqing
Xian, Ronghua
Ma, Jianfang
Chen, Yujian
Lin, Chuangan
Song, Yaoming
Isthmin inhibits glioma growth through antiangiogenesis in vivo
title Isthmin inhibits glioma growth through antiangiogenesis in vivo
title_full Isthmin inhibits glioma growth through antiangiogenesis in vivo
title_fullStr Isthmin inhibits glioma growth through antiangiogenesis in vivo
title_full_unstemmed Isthmin inhibits glioma growth through antiangiogenesis in vivo
title_short Isthmin inhibits glioma growth through antiangiogenesis in vivo
title_sort isthmin inhibits glioma growth through antiangiogenesis in vivo
topic Laboratory Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432204/
https://www.ncbi.nlm.nih.gov/pubmed/22772605
http://dx.doi.org/10.1007/s11060-012-0910-8
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