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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Published in:BioMed Research International pp. 1 - 14
Main Authors: Ma, Quanfeng, Wang, Xiuyu, Wang, Hong, Song, Wen, Wang, Qiong, Wang, Jinhuan
Format: pictorial research tables/charts Journal Article
Published: Wiley-Blackwell 5/27/2020
Online Access:View this record in EBSCOhost
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      dt: 5/27/2020
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        143456075
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        10.1155/2020/8610271
        143456075
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      tig:
        atl: HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells.
      aug:
        au:
          Ma, Quanfeng
          Wang, Xiuyu
          Wang, Hong
          Song, Wen
          Wang, Qiong
          Wang, Jinhuan
        affil: Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, China
      sug:
        subj:
          Transcription Factors Metabolism
          Gene Expression
          Glioma Prevention and Control
          Disease Progression Prevention and Control
          Mitogen-Activated Protein Kinases Metabolism
          Protein Kinases Metabolism
          Signal Transduction
          Cell Line, Tumor Metabolism
          Human
          Neoplasm Grading
          Neoplasm Invasiveness
          RNA Metabolism
          Cell Proliferation
          Apoptosis
          Cell Movement
      ab: 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.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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