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Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway

Canstatin, the non-collagenous domain of collagen type IV α-chains, belongs to a series of collagen-derived angiogenic inhibitors. In this study, the inhibitory effect of recombinant canstatin on tumour growth was investigated using a gastric cancer xenograft model. The volume and weight of tumours...

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Detalles Bibliográficos
Autores principales: Xing, Ya-Nan, Deng, Peng, Xu, Hui-Mian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999450/
https://www.ncbi.nlm.nih.gov/pubmed/27919040
http://dx.doi.org/10.1042/BSR20140012
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author Xing, Ya-Nan
Deng, Peng
Xu, Hui-Mian
author_facet Xing, Ya-Nan
Deng, Peng
Xu, Hui-Mian
author_sort Xing, Ya-Nan
collection PubMed
description Canstatin, the non-collagenous domain of collagen type IV α-chains, belongs to a series of collagen-derived angiogenic inhibitors. In this study, the inhibitory effect of recombinant canstatin on tumour growth was investigated using a gastric cancer xenograft model. The volume and weight of tumours in mice treated with canstatin were lower than that in mice treated with PBS. Accordingly, the survival rate of these mice was significantly higher than that of mice bearing tumours treated with PBS. Moreover, valuable insight into the mechanisms mediated by canstatin was obtained.
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spelling pubmed-39994502014-04-30 Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway Xing, Ya-Nan Deng, Peng Xu, Hui-Mian Biosci Rep Original Paper Canstatin, the non-collagenous domain of collagen type IV α-chains, belongs to a series of collagen-derived angiogenic inhibitors. In this study, the inhibitory effect of recombinant canstatin on tumour growth was investigated using a gastric cancer xenograft model. The volume and weight of tumours in mice treated with canstatin were lower than that in mice treated with PBS. Accordingly, the survival rate of these mice was significantly higher than that of mice bearing tumours treated with PBS. Moreover, valuable insight into the mechanisms mediated by canstatin was obtained. Portland Press Ltd. 2014-04-25 /pmc/articles/PMC3999450/ /pubmed/27919040 http://dx.doi.org/10.1042/BSR20140012 Text en © 2014 The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Licence (CC-BY)(http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence (CC-BY) (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Paper
Xing, Ya-Nan
Deng, Peng
Xu, Hui-Mian
Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
title Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
title_full Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
title_fullStr Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
title_full_unstemmed Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
title_short Canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
title_sort canstatin induces apoptosis in gastric cancer xenograft growth in mice through the mitochondrial apoptotic pathway
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999450/
https://www.ncbi.nlm.nih.gov/pubmed/27919040
http://dx.doi.org/10.1042/BSR20140012
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