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Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma
Glioblastoma multiforme (GBM) is a highly vascularized malignant brain tumor. Our previous study showed that prostate-specific membrane antigen (PSMA) promotes angiogenesis of GBM. However, the specific mechanism underlying GBM-induced PSMA upregulation remains unclear. In this study, we demonstrate...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10160226/ https://www.ncbi.nlm.nih.gov/pubmed/36305723 http://dx.doi.org/10.3724/abbs.2022157 |
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author | Tu, Wenjing Zheng, Hui Li, Liangdong Zhou, Changshuai Feng, Mingtao Chen, Lei Li, Deheng Chen, Xin Hao, Bin Sun, Huaping Cao, Yiqun Gao, Yang |
author_facet | Tu, Wenjing Zheng, Hui Li, Liangdong Zhou, Changshuai Feng, Mingtao Chen, Lei Li, Deheng Chen, Xin Hao, Bin Sun, Huaping Cao, Yiqun Gao, Yang |
author_sort | Tu, Wenjing |
collection | PubMed |
description | Glioblastoma multiforme (GBM) is a highly vascularized malignant brain tumor. Our previous study showed that prostate-specific membrane antigen (PSMA) promotes angiogenesis of GBM. However, the specific mechanism underlying GBM-induced PSMA upregulation remains unclear. In this study, we demonstrate that the GBM-secreted cytokine phosphoprotein 1 (SPP1) can regulate the expression of PSMA in human umbilical vein endothelial cells (HUVECs). Our mechanistic study further reveals that SPP1 regulates the expression of PSMA through the transcription factor HIF1α. Moreover, SPP1 promotes HUVEC migration and tube formation. In addition, HIF1α knockdown reduces the expression of PSMA in HUVECs and blocks the ability of SPP1 to promote HUVEC migration and tube formation. We further confirm that SPP1 is abundantly expressed in GBM, is associated with poor prognosis, and has high clinical diagnostic value with considerable sensitivity and specificity. Collectively, our findings identify that the GBM-secreted cytokine SPP1 upregulates PSMA expression in endothelial cells via the transcription factor HIF1α, providing insight into the angiogenic process and promising candidates for targeted GBM therapy. |
format | Online Article Text |
id | pubmed-10160226 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-101602262023-05-06 Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma Tu, Wenjing Zheng, Hui Li, Liangdong Zhou, Changshuai Feng, Mingtao Chen, Lei Li, Deheng Chen, Xin Hao, Bin Sun, Huaping Cao, Yiqun Gao, Yang Acta Biochim Biophys Sin (Shanghai) Research Article Glioblastoma multiforme (GBM) is a highly vascularized malignant brain tumor. Our previous study showed that prostate-specific membrane antigen (PSMA) promotes angiogenesis of GBM. However, the specific mechanism underlying GBM-induced PSMA upregulation remains unclear. In this study, we demonstrate that the GBM-secreted cytokine phosphoprotein 1 (SPP1) can regulate the expression of PSMA in human umbilical vein endothelial cells (HUVECs). Our mechanistic study further reveals that SPP1 regulates the expression of PSMA through the transcription factor HIF1α. Moreover, SPP1 promotes HUVEC migration and tube formation. In addition, HIF1α knockdown reduces the expression of PSMA in HUVECs and blocks the ability of SPP1 to promote HUVEC migration and tube formation. We further confirm that SPP1 is abundantly expressed in GBM, is associated with poor prognosis, and has high clinical diagnostic value with considerable sensitivity and specificity. Collectively, our findings identify that the GBM-secreted cytokine SPP1 upregulates PSMA expression in endothelial cells via the transcription factor HIF1α, providing insight into the angiogenic process and promising candidates for targeted GBM therapy. Oxford University Press 2022-10-26 /pmc/articles/PMC10160226/ /pubmed/36305723 http://dx.doi.org/10.3724/abbs.2022157 Text en © The Author(s) 2021. 0 https://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/). |
spellingShingle | Research Article Tu, Wenjing Zheng, Hui Li, Liangdong Zhou, Changshuai Feng, Mingtao Chen, Lei Li, Deheng Chen, Xin Hao, Bin Sun, Huaping Cao, Yiqun Gao, Yang Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma |
title | Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma |
title_full | Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma |
title_fullStr | Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma |
title_full_unstemmed | Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma |
title_short | Secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating PSMA expression via transcription factor HIF1α: SPP1 promotes angiogenesis of glioblastoma |
title_sort | secreted phosphoprotein 1 promotes angiogenesis of glioblastoma through upregulating psma expression via transcription factor hif1α: spp1 promotes angiogenesis of glioblastoma |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10160226/ https://www.ncbi.nlm.nih.gov/pubmed/36305723 http://dx.doi.org/10.3724/abbs.2022157 |
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