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SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling
Serum amyloid A1 (SAA1) is an inflammatory associated high-density lipoprotein. And It is also considered as a predictor and prognostic marker of cancer risk. However, its role and mechanisms in glioblastoma (GBM) still unclear. In this study, we validate that SAA1 is up-regulated in GBM, and its hi...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Ivyspring International Publisher
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040715/ https://www.ncbi.nlm.nih.gov/pubmed/33854635 http://dx.doi.org/10.7150/jca.48419 |
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author | Zhang, Huikai Xu, Yang Deng, Gang Yuan, Fanen Tan, Yinqiu Gao, Lun Sun, Qian Qi, Yangzhi Yang, Kun Geng, Rongxin Jiang, Hongxiang Liu, Baohui Chen, Qianxue |
author_facet | Zhang, Huikai Xu, Yang Deng, Gang Yuan, Fanen Tan, Yinqiu Gao, Lun Sun, Qian Qi, Yangzhi Yang, Kun Geng, Rongxin Jiang, Hongxiang Liu, Baohui Chen, Qianxue |
author_sort | Zhang, Huikai |
collection | PubMed |
description | Serum amyloid A1 (SAA1) is an inflammatory associated high-density lipoprotein. And It is also considered as a predictor and prognostic marker of cancer risk. However, its role and mechanisms in glioblastoma (GBM) still unclear. In this study, we validate that SAA1 is up-regulated in GBM, and its high expression predicts poor prognosis. SAA1 knockdown promotes the apoptosis of GBM cell. Mechanistically, SAA1 knockdown can inhibit serine/threonine protein kinase B (AKT) phosphorylation, thereby regulating the expression of apoptosis-related proteins such as Bcl2 and Bax, leading to GBM cell death. Moreover, Gliomas with low SAA1 expression have increased sensitivity to Temozolomide (TMZ). Low SAA1 expression segregated glioma patients who were treated with Temozolomide (TMZ) or with high MGMT promoter methylation into survival groups in TCGA and CGGA dataset. Our study strongly suggested that SAA1 was a regulator of cells apoptosis and acted not only as a prognostic marker but also a novel biomarker of sensitivity of glioma to TMZ. |
format | Online Article Text |
id | pubmed-8040715 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-80407152021-04-13 SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling Zhang, Huikai Xu, Yang Deng, Gang Yuan, Fanen Tan, Yinqiu Gao, Lun Sun, Qian Qi, Yangzhi Yang, Kun Geng, Rongxin Jiang, Hongxiang Liu, Baohui Chen, Qianxue J Cancer Research Paper Serum amyloid A1 (SAA1) is an inflammatory associated high-density lipoprotein. And It is also considered as a predictor and prognostic marker of cancer risk. However, its role and mechanisms in glioblastoma (GBM) still unclear. In this study, we validate that SAA1 is up-regulated in GBM, and its high expression predicts poor prognosis. SAA1 knockdown promotes the apoptosis of GBM cell. Mechanistically, SAA1 knockdown can inhibit serine/threonine protein kinase B (AKT) phosphorylation, thereby regulating the expression of apoptosis-related proteins such as Bcl2 and Bax, leading to GBM cell death. Moreover, Gliomas with low SAA1 expression have increased sensitivity to Temozolomide (TMZ). Low SAA1 expression segregated glioma patients who were treated with Temozolomide (TMZ) or with high MGMT promoter methylation into survival groups in TCGA and CGGA dataset. Our study strongly suggested that SAA1 was a regulator of cells apoptosis and acted not only as a prognostic marker but also a novel biomarker of sensitivity of glioma to TMZ. Ivyspring International Publisher 2021-03-10 /pmc/articles/PMC8040715/ /pubmed/33854635 http://dx.doi.org/10.7150/jca.48419 Text en © The author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. |
spellingShingle | Research Paper Zhang, Huikai Xu, Yang Deng, Gang Yuan, Fanen Tan, Yinqiu Gao, Lun Sun, Qian Qi, Yangzhi Yang, Kun Geng, Rongxin Jiang, Hongxiang Liu, Baohui Chen, Qianxue SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling |
title | SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling |
title_full | SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling |
title_fullStr | SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling |
title_full_unstemmed | SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling |
title_short | SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling |
title_sort | saa1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of akt signaling |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040715/ https://www.ncbi.nlm.nih.gov/pubmed/33854635 http://dx.doi.org/10.7150/jca.48419 |
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