HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells

HMGN5 regulates biological function and molecular transcription via combining with a nucleosome. There has been growing evidence that aberrant expression of HMGN5 is associated with malignant neoplasm development and progression. In the present study, we found that the expression of HMGN5 is signifi...

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Main Authors: Quanfeng Ma, Xiuyu Wang, Hong Wang, Wen Song, Qiong Wang, Jinhuan Wang
Format: Article
Language:English
Published: Hindawi Limited 2020-01-01
Series:BioMed Research International
Online Access:http://dx.doi.org/10.1155/2020/8610271
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spelling doaj-24b4bb9eb1474be480e5a4290c3d65a92020-11-25T03:27:49ZengHindawi LimitedBioMed Research International2314-61332314-61412020-01-01202010.1155/2020/86102718610271HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma CellsQuanfeng Ma0Xiuyu Wang1Hong Wang2Wen Song3Qiong Wang4Jinhuan Wang5Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, ChinaDepartment of Neurosurgery, Tianjin First Center Hospital, Tianjin 300192, ChinaTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, ChinaThe Graduate School, Tianjin Medical University, Tianjin 300070, ChinaTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, ChinaTianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, ChinaHMGN5 regulates biological function and molecular transcription via combining with a nucleosome. There has been growing evidence that aberrant expression of HMGN5 is associated with malignant neoplasm development and progression. In the present study, we found that the expression of HMGN5 is significantly higher in high-grade glioblastoma tissues than in low-grade samples. To clarify the function of HMGN5 in glioblastoma, we knocked down HMGN5 in U87 and U251 glioblastoma cells via siRNA. The results demonstrated that HMGN5 was involved in the regulation of proliferation and apoptosis, migration, and invasion of glioblastoma cells. These outcomes also indicated that silencing HMGN5 possibly suppressed the expression of p-AKT and p-ERK1/2. Taken together, our research reveals that HMGN5 might be an efficient target for glioblastoma-targeted therapy.http://dx.doi.org/10.1155/2020/8610271
collection DOAJ
language English
format Article
sources DOAJ
author Quanfeng Ma
Xiuyu Wang
Hong Wang
Wen Song
Qiong Wang
Jinhuan Wang
spellingShingle Quanfeng Ma
Xiuyu Wang
Hong Wang
Wen Song
Qiong Wang
Jinhuan Wang
HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells
BioMed Research International
author_facet Quanfeng Ma
Xiuyu Wang
Hong Wang
Wen Song
Qiong Wang
Jinhuan Wang
author_sort Quanfeng Ma
title HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells
title_short HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells
title_full HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells
title_fullStr HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells
title_full_unstemmed HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells
title_sort hmgn5 silencing suppresses cell biological progression via akt/mapk pathway in human glioblastoma cells
publisher Hindawi Limited
series BioMed Research International
issn 2314-6133
2314-6141
publishDate 2020-01-01
description HMGN5 regulates biological function and molecular transcription via combining with a nucleosome. There has been growing evidence that aberrant expression of HMGN5 is associated with malignant neoplasm development and progression. In the present study, we found that the expression of HMGN5 is significantly higher in high-grade glioblastoma tissues than in low-grade samples. To clarify the function of HMGN5 in glioblastoma, we knocked down HMGN5 in U87 and U251 glioblastoma cells via siRNA. The results demonstrated that HMGN5 was involved in the regulation of proliferation and apoptosis, migration, and invasion of glioblastoma cells. These outcomes also indicated that silencing HMGN5 possibly suppressed the expression of p-AKT and p-ERK1/2. Taken together, our research reveals that HMGN5 might be an efficient target for glioblastoma-targeted therapy.
url http://dx.doi.org/10.1155/2020/8610271
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