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NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma
Glioblastoma (GBM) is the most common primary intracranial malignancy. GBM still exhibits high recurrence and mortality rates even following combined treatment with surgery, radiotherapy and chemotherapy, Therefore, the identification of novel therapeutic targets is urgent. Previous research has sho...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6667917/ https://www.ncbi.nlm.nih.gov/pubmed/31322259 http://dx.doi.org/10.3892/or.2019.7227 |
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author | Guo, Qiuyun Han, Na Shi, Lei Yang, Li Zhang, Xiaoxi Zhou, Yangmei Yu, Shiying Zhang, Mengxian |
author_facet | Guo, Qiuyun Han, Na Shi, Lei Yang, Li Zhang, Xiaoxi Zhou, Yangmei Yu, Shiying Zhang, Mengxian |
author_sort | Guo, Qiuyun |
collection | PubMed |
description | Glioblastoma (GBM) is the most common primary intracranial malignancy. GBM still exhibits high recurrence and mortality rates even following combined treatment with surgery, radiotherapy and chemotherapy, Therefore, the identification of novel therapeutic targets is urgent. Previous research has shown that nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in cell metabolism and is closely related to the occurrence and development of many tumor types; yet, little is known concerning its relationship with GBM. Oncomine database analysis showed that the expression of NAMPT in GBM was higher than that in normal tissues; this finding was further confirmed by immunohistochemical staining of a tissue microarray. Data analysis with the R2 platform showed that patients with higher expression of NAMPT had worse prognoses than those with lower NAMPT expression. Using the GBM data in TCGA, four pathways enriched in the high NAMPT expression group were identified by gene set enrichment analysis (GSEA). NAMPT expression was knocked down in U87 and U251 GBM cells by lentiviral vectors carrying a small hairpin RNA (shRNA) targeting NAMPT. CCK-8, colony formation, wound healing, Transwell and apoptosis assays were carried out. The results showed that NAMPT knockdown decreased cell proliferation, migration, and invasion and promoted apoptosis. U87 GBM cells were used in a model of subcutaneous tumorigenesis in nude mice. The results showed that NAMPT knockdown slowed the growth of tumors in vivo. Therefore, we speculate that NAMPT may be a potential prognostic and therapeutic biomarker for glioblastoma. |
format | Online Article Text |
id | pubmed-6667917 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-66679172019-08-08 NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma Guo, Qiuyun Han, Na Shi, Lei Yang, Li Zhang, Xiaoxi Zhou, Yangmei Yu, Shiying Zhang, Mengxian Oncol Rep Articles Glioblastoma (GBM) is the most common primary intracranial malignancy. GBM still exhibits high recurrence and mortality rates even following combined treatment with surgery, radiotherapy and chemotherapy, Therefore, the identification of novel therapeutic targets is urgent. Previous research has shown that nicotinamide phosphoribosyltransferase (NAMPT) plays a key role in cell metabolism and is closely related to the occurrence and development of many tumor types; yet, little is known concerning its relationship with GBM. Oncomine database analysis showed that the expression of NAMPT in GBM was higher than that in normal tissues; this finding was further confirmed by immunohistochemical staining of a tissue microarray. Data analysis with the R2 platform showed that patients with higher expression of NAMPT had worse prognoses than those with lower NAMPT expression. Using the GBM data in TCGA, four pathways enriched in the high NAMPT expression group were identified by gene set enrichment analysis (GSEA). NAMPT expression was knocked down in U87 and U251 GBM cells by lentiviral vectors carrying a small hairpin RNA (shRNA) targeting NAMPT. CCK-8, colony formation, wound healing, Transwell and apoptosis assays were carried out. The results showed that NAMPT knockdown decreased cell proliferation, migration, and invasion and promoted apoptosis. U87 GBM cells were used in a model of subcutaneous tumorigenesis in nude mice. The results showed that NAMPT knockdown slowed the growth of tumors in vivo. Therefore, we speculate that NAMPT may be a potential prognostic and therapeutic biomarker for glioblastoma. D.A. Spandidos 2019-09 2019-07-10 /pmc/articles/PMC6667917/ /pubmed/31322259 http://dx.doi.org/10.3892/or.2019.7227 Text en Copyright: © Guo et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Guo, Qiuyun Han, Na Shi, Lei Yang, Li Zhang, Xiaoxi Zhou, Yangmei Yu, Shiying Zhang, Mengxian NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma |
title | NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma |
title_full | NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma |
title_fullStr | NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma |
title_full_unstemmed | NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma |
title_short | NAMPT: A potential prognostic and therapeutic biomarker in patients with glioblastoma |
title_sort | nampt: a potential prognostic and therapeutic biomarker in patients with glioblastoma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6667917/ https://www.ncbi.nlm.nih.gov/pubmed/31322259 http://dx.doi.org/10.3892/or.2019.7227 |
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