An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.

Glioblastoma is an extraordinarily aggressive disease that requires more effective therapeutic options. Snail family zinc finger 1, dysregulated in many neoplasms, has been reported to be involved in gliomas. However, the biological mechanisms underlying SNAI1 function in gliomas need further invest...

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Main Authors: Qingsheng Dong, Ning Cai, Tao Tao, Rui Zhang, Wei Yan, Rui Li, Junxia Zhang, Hui Luo, Yan Shi, Wenkang Luan, Yaxuan Zhang, Yongping You, Yingyi Wang, Ning Liu
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4068992?pdf=render
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spelling doaj-99f8a28426c44267967bc88bef5b89be2020-11-25T02:47:03ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0196e9865110.1371/journal.pone.0098651An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.Qingsheng DongNing CaiTao TaoRui ZhangWei YanRui LiJunxia ZhangHui LuoYan ShiWenkang LuanYaxuan ZhangYongping YouYingyi WangNing LiuGlioblastoma is an extraordinarily aggressive disease that requires more effective therapeutic options. Snail family zinc finger 1, dysregulated in many neoplasms, has been reported to be involved in gliomas. However, the biological mechanisms underlying SNAI1 function in gliomas need further investigation.Quantitative real-time PCR was used to measure microRNA-128 (miR-128) expression level and western blot was performed to detect protein expression in U87 and U251 cells and human brain tissues. Cell cycle, CCK-8, transwell and wound-healing assays were performed. Dual-luciferase reporter assay was used for identifying the mechanism of SNAI1 and miR-128b regulation. The mechanism of miR-128 targeting SP1 was also tested by luciferase reporter assay. Immunohistochemistry and in situ hybridisation staining were used for quantifying SNAI1, SP1 and miR-128 expression levels in human glioma samples.The Chinese Glioma Genome Atlas (CGGA) data revealed that SNAI1 was up-regulated in glioma and we confirmed the findings in normal and glioma tissues. SNAI1 depletion by shRNA retarded the cell cycle and suppressed proliferation and invasion in glioma cell lines. The CGGA data showed that the Pearson correlation index between SNAI1 and miR-128 was negatively correlated. SNAI1 suppressed miR-128b expression by binding to the miR-128b specific promoter motif, and miR-128 targeted SP1 via binding to the 3'-untranslated region of SP1. Moreover, introduction of miR-128 anti-sense oligonucleotide alleviated the cell cycle retardation, proliferation and invasion inhibition induced by SNAI1 shRNA. Immunohistochemistry and in situ hybridisation analysis of SNAI1, SP1 and miR-128 unraveled their expression levels and correlations in glioma samples.We propose that the SNAI1/miR-128/SP1 axis, which plays a vital role in glioma progression, may come to be a clinically relevant therapeutic target.http://europepmc.org/articles/PMC4068992?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Qingsheng Dong
Ning Cai
Tao Tao
Rui Zhang
Wei Yan
Rui Li
Junxia Zhang
Hui Luo
Yan Shi
Wenkang Luan
Yaxuan Zhang
Yongping You
Yingyi Wang
Ning Liu
spellingShingle Qingsheng Dong
Ning Cai
Tao Tao
Rui Zhang
Wei Yan
Rui Li
Junxia Zhang
Hui Luo
Yan Shi
Wenkang Luan
Yaxuan Zhang
Yongping You
Yingyi Wang
Ning Liu
An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.
PLoS ONE
author_facet Qingsheng Dong
Ning Cai
Tao Tao
Rui Zhang
Wei Yan
Rui Li
Junxia Zhang
Hui Luo
Yan Shi
Wenkang Luan
Yaxuan Zhang
Yongping You
Yingyi Wang
Ning Liu
author_sort Qingsheng Dong
title An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.
title_short An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.
title_full An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.
title_fullStr An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.
title_full_unstemmed An axis involving SNAI1, microRNA-128 and SP1 modulates glioma progression.
title_sort axis involving snai1, microrna-128 and sp1 modulates glioma progression.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description Glioblastoma is an extraordinarily aggressive disease that requires more effective therapeutic options. Snail family zinc finger 1, dysregulated in many neoplasms, has been reported to be involved in gliomas. However, the biological mechanisms underlying SNAI1 function in gliomas need further investigation.Quantitative real-time PCR was used to measure microRNA-128 (miR-128) expression level and western blot was performed to detect protein expression in U87 and U251 cells and human brain tissues. Cell cycle, CCK-8, transwell and wound-healing assays were performed. Dual-luciferase reporter assay was used for identifying the mechanism of SNAI1 and miR-128b regulation. The mechanism of miR-128 targeting SP1 was also tested by luciferase reporter assay. Immunohistochemistry and in situ hybridisation staining were used for quantifying SNAI1, SP1 and miR-128 expression levels in human glioma samples.The Chinese Glioma Genome Atlas (CGGA) data revealed that SNAI1 was up-regulated in glioma and we confirmed the findings in normal and glioma tissues. SNAI1 depletion by shRNA retarded the cell cycle and suppressed proliferation and invasion in glioma cell lines. The CGGA data showed that the Pearson correlation index between SNAI1 and miR-128 was negatively correlated. SNAI1 suppressed miR-128b expression by binding to the miR-128b specific promoter motif, and miR-128 targeted SP1 via binding to the 3'-untranslated region of SP1. Moreover, introduction of miR-128 anti-sense oligonucleotide alleviated the cell cycle retardation, proliferation and invasion inhibition induced by SNAI1 shRNA. Immunohistochemistry and in situ hybridisation analysis of SNAI1, SP1 and miR-128 unraveled their expression levels and correlations in glioma samples.We propose that the SNAI1/miR-128/SP1 axis, which plays a vital role in glioma progression, may come to be a clinically relevant therapeutic target.
url http://europepmc.org/articles/PMC4068992?pdf=render
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