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B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo
Our study was designed to investigate the role of B4GalT1 in glioblastoma, in vitro and in vivo, to detect whether B4GalT1 knockdown could regulate the development of glioblastoma, and further observe the relationship between B4GalT1 knockdown and the apoptosis and autophagy of glioblastoma. To begi...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727053/ https://www.ncbi.nlm.nih.gov/pubmed/33287670 http://dx.doi.org/10.1177/1533033820980104 |
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author | Wang, Pu Li, Xiaolong Xie, Yuan |
author_facet | Wang, Pu Li, Xiaolong Xie, Yuan |
author_sort | Wang, Pu |
collection | PubMed |
description | Our study was designed to investigate the role of B4GalT1 in glioblastoma, in vitro and in vivo, to detect whether B4GalT1 knockdown could regulate the development of glioblastoma, and further observe the relationship between B4GalT1 knockdown and the apoptosis and autophagy of glioblastoma. To begin, we looked at TCGA and GEPIA systems to predict the potential function of B4GalT1. Western blot and RT-PCR were used to analyze the expression, or mRNA level, of B4GalT1 at different tissue or cell lines. Next, the occurrence and development of glioblastoma, in vitro and in vivo, was observed by using B4GalT1 knocked down by lentivirus. Finally, the apoptosis and autophagy of glioblastoma was observed in vitro and in vivo. Results show that B4GalT1 was a highly variable gene, and GEPIA and TCGA systems show B4GalT1 expression in GBM tumor tissue was higher than in normal tissue. Pair-wise gene correlation analysis revealed a probable relationship between B4GalT1 and autophagy related proteins. The B4GalT1 expression and mRNA level were increased in tumor cells, or U87 cells. B4GalT1 knocked down by lentivirus could inhibit glioblastoma development, in vitro and in vivo, by reducing tumor weight and volume, increasing survival, and weakening tumor cells proliferation, migration, invasion. B4GalT1 knockdown could increase apoptosis and autophagy of glioblastoma in vitro and in vivo. Our study demonstrates that B4GalT1 may be able to regulate apoptosis and autophagy of glioblastoma. Bax, Bcl-2, cleaved caspase-3, Beclin-1, and LC3 s may be the downstream target factors of B4GalT1 in apoptosis and autophagy, which may provide a new strategy to reduce glioblastoma development by regulating apoptosis and autophagy. |
format | Online Article Text |
id | pubmed-7727053 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-77270532020-12-18 B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo Wang, Pu Li, Xiaolong Xie, Yuan Technol Cancer Res Treat Original Article Our study was designed to investigate the role of B4GalT1 in glioblastoma, in vitro and in vivo, to detect whether B4GalT1 knockdown could regulate the development of glioblastoma, and further observe the relationship between B4GalT1 knockdown and the apoptosis and autophagy of glioblastoma. To begin, we looked at TCGA and GEPIA systems to predict the potential function of B4GalT1. Western blot and RT-PCR were used to analyze the expression, or mRNA level, of B4GalT1 at different tissue or cell lines. Next, the occurrence and development of glioblastoma, in vitro and in vivo, was observed by using B4GalT1 knocked down by lentivirus. Finally, the apoptosis and autophagy of glioblastoma was observed in vitro and in vivo. Results show that B4GalT1 was a highly variable gene, and GEPIA and TCGA systems show B4GalT1 expression in GBM tumor tissue was higher than in normal tissue. Pair-wise gene correlation analysis revealed a probable relationship between B4GalT1 and autophagy related proteins. The B4GalT1 expression and mRNA level were increased in tumor cells, or U87 cells. B4GalT1 knocked down by lentivirus could inhibit glioblastoma development, in vitro and in vivo, by reducing tumor weight and volume, increasing survival, and weakening tumor cells proliferation, migration, invasion. B4GalT1 knockdown could increase apoptosis and autophagy of glioblastoma in vitro and in vivo. Our study demonstrates that B4GalT1 may be able to regulate apoptosis and autophagy of glioblastoma. Bax, Bcl-2, cleaved caspase-3, Beclin-1, and LC3 s may be the downstream target factors of B4GalT1 in apoptosis and autophagy, which may provide a new strategy to reduce glioblastoma development by regulating apoptosis and autophagy. SAGE Publications 2020-12-08 /pmc/articles/PMC7727053/ /pubmed/33287670 http://dx.doi.org/10.1177/1533033820980104 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Wang, Pu Li, Xiaolong Xie, Yuan B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo |
title | B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo |
title_full | B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo |
title_fullStr | B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo |
title_full_unstemmed | B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo |
title_short | B4GalT1 Regulates Apoptosis and Autophagy of Glioblastoma In Vitro and In Vivo |
title_sort | b4galt1 regulates apoptosis and autophagy of glioblastoma in vitro and in vivo |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727053/ https://www.ncbi.nlm.nih.gov/pubmed/33287670 http://dx.doi.org/10.1177/1533033820980104 |
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