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Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p

Glioblastoma multiform is the most common and malignant primary tumor of the central nervous system in adults, the high recurrence rate and poor prognosis are critical priorities. Pristimerin is a naturally occurring quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae fam...

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Autores principales: Li, Zaiyu, Hu, Cong, Zhen, Yu, Pang, Bo, Yi, Huanfa, Chen, Xianglin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6522714/
https://www.ncbi.nlm.nih.gov/pubmed/31015365
http://dx.doi.org/10.1042/BSR20182389
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author Li, Zaiyu
Hu, Cong
Zhen, Yu
Pang, Bo
Yi, Huanfa
Chen, Xianglin
author_facet Li, Zaiyu
Hu, Cong
Zhen, Yu
Pang, Bo
Yi, Huanfa
Chen, Xianglin
author_sort Li, Zaiyu
collection PubMed
description Glioblastoma multiform is the most common and malignant primary tumor of the central nervous system in adults, the high recurrence rate and poor prognosis are critical priorities. Pristimerin is a naturally occurring quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae families. Its anticancer effects have garnered considerable attention; nonetheless, the mechanisms of action remain unknown. To predict the hub genes of pristimerin, PharmMapper and the Coremine database were used to identify 13 potential protein targets; protein–protein interaction, for which functional enrichment analyses were performed. Compound-target, target-pathway, and compound-target-pathway networks were constructed using Cytoscape. Biological process analysis first revealed that enrichment of these target genes correlated with negative regulation of symbiont growth in the host, and regulation of chronic inflammatory response to antigenic stimulus. Survival analysis in cBioPortal showed that protein tyrosine phosphatase, non-receptor type 1 (PTPN1) and Argonaute 2 (AGO2) might be involved in the carcinogenesis, invasion, or recurrence of diffuse glioma. In addition, we observed that low-dose pristimerin inhibited the viability of glioma cells, while miR-542-5p in vitro; and reduced PTPN1 expression. Notably, high-dose pristimerin induced apoptosis. Furthermore, miR-542-5p silence with siRNA in glioma cells lead to the elevation in AGO2, and decreased PTPN1 level. The effect was obviously post pristimerin treatment and miR-542-5p suppression. In conclusion, pristimerin inhibited glioma progression through AGO2 and PTPN1 expression via a canonical miRNA-mediated mechanism.
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spelling pubmed-65227142019-05-28 Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p Li, Zaiyu Hu, Cong Zhen, Yu Pang, Bo Yi, Huanfa Chen, Xianglin Biosci Rep Research Articles Glioblastoma multiform is the most common and malignant primary tumor of the central nervous system in adults, the high recurrence rate and poor prognosis are critical priorities. Pristimerin is a naturally occurring quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae families. Its anticancer effects have garnered considerable attention; nonetheless, the mechanisms of action remain unknown. To predict the hub genes of pristimerin, PharmMapper and the Coremine database were used to identify 13 potential protein targets; protein–protein interaction, for which functional enrichment analyses were performed. Compound-target, target-pathway, and compound-target-pathway networks were constructed using Cytoscape. Biological process analysis first revealed that enrichment of these target genes correlated with negative regulation of symbiont growth in the host, and regulation of chronic inflammatory response to antigenic stimulus. Survival analysis in cBioPortal showed that protein tyrosine phosphatase, non-receptor type 1 (PTPN1) and Argonaute 2 (AGO2) might be involved in the carcinogenesis, invasion, or recurrence of diffuse glioma. In addition, we observed that low-dose pristimerin inhibited the viability of glioma cells, while miR-542-5p in vitro; and reduced PTPN1 expression. Notably, high-dose pristimerin induced apoptosis. Furthermore, miR-542-5p silence with siRNA in glioma cells lead to the elevation in AGO2, and decreased PTPN1 level. The effect was obviously post pristimerin treatment and miR-542-5p suppression. In conclusion, pristimerin inhibited glioma progression through AGO2 and PTPN1 expression via a canonical miRNA-mediated mechanism. Portland Press Ltd. 2019-05-14 /pmc/articles/PMC6522714/ /pubmed/31015365 http://dx.doi.org/10.1042/BSR20182389 Text en © 2019 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Articles
Li, Zaiyu
Hu, Cong
Zhen, Yu
Pang, Bo
Yi, Huanfa
Chen, Xianglin
Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p
title Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p
title_full Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p
title_fullStr Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p
title_full_unstemmed Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p
title_short Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p
title_sort pristimerin inhibits glioma progression by targeting ago2 and ptpn1 expression via mir-542-5p
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6522714/
https://www.ncbi.nlm.nih.gov/pubmed/31015365
http://dx.doi.org/10.1042/BSR20182389
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