Transcription Factor NFAT5 Promotes Glioblastoma Cell-driven Angiogenesis via SBF2-AS1/miR-338-3p-Mediated EGFL7 Expression Change

Glioblastoma (GBM) is the most aggressive primary intracranial tumor of adults and confers a poor prognosis due to high vascularization. Hence anti-angiogenic therapy has become a promising strategy for GBM treatment. In this study, the transcription factor nuclear factor of activated T-cells 5 (NFA...

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Published inFrontiers in molecular neuroscience Vol. 10; p. 301
Main Authors Yu, Hai, Zheng, Jian, Liu, Xiaobai, Xue, Yixue, Shen, Shuyuan, Zhao, Lini, Li, Zhen, Liu, Yunhui
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 21.09.2017
Frontiers Media S.A
Subjects
Angiogenesis
Antisense RNA
Binding sites
Brain cancer
Brain research
Glioblastoma
glioblastoma angiogenesis
Glioma cells
Growth factors
Hospitals
Laboratories
Liver cancer
long non-coding RNA
Lung cancer
Medical prognosis
MicroRNAs
miR-338-3p
Neuroscience
Neurosciences
Neurosurgery
NFAT5
Non-coding RNA
SBF2-AS1
transcription factor
Transcription factors
Tumors
Vascularization
Xenografts
United States > US
China
NFAT5
glioblastoma angiogenesis
transcription factor
EGFL7
miR-338-3p
long non-coding RNA
SBF2-AS1
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Summary:Glioblastoma (GBM) is the most aggressive primary intracranial tumor of adults and confers a poor prognosis due to high vascularization. Hence anti-angiogenic therapy has become a promising strategy for GBM treatment. In this study, the transcription factor nuclear factor of activated T-cells 5 (NFAT5) was significantly elevated in glioma samples and GBM cell lines, and positively correlated with glioma WHO grades. Knockdown of inhibited GBM cell-driven angiogenesis. Furthermore, long non-coding RNA SBF2 antisense RNA 1 (SBF2-AS1) was upregulated in glioma samples and knockdown of SBF2-AS1 impaired GBM-induced angiogenesis. Downregulation of NFAT5 decreased SBF2-AS1 expression at transcriptional level. In addition, knockdown of repressed GBM cell-driven angiogenesis via enhancing the inhibitory effect of miR-338-3p on EGF like domain multiple 7 (EGFL7). study demonstrated that the combination of knockdown and knockdown produced the smallest xenograft volume and the lowest microvessel density. NFAT5/SBF2-AS1/miR-338-3p/EGFL7 pathway may provide novel targets for glioma anti-angiogenic treatment.
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Reviewed by: Sanjeev Kumar Srivastava, Mitchell Cancer Institute, United States; Yonghe Wu, Deutsches Krebsforschungszentrum (DKFZ), Germany
Edited by: Andrei Surguchov, Kansas University of Medical Center Research Institute, United States
ISSN:1662-5099
1662-5099
DOI:10.3389/fnmol.2017.00301