Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion
Rile Wu, Qiang Yun, Jianping Zhang, Jingang Bao Department of Neurosurgery, Inner Mongolia People’s Hospital, Hohhot 010017, China Background: Recent evidence indicates that Kruppel-like factor 13 (KLF13) has critical roles in regulating cell differentiation, proliferation and may functi...
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doaj-b7bebcb3254c4854bb7c2652d416149e2020-11-24T23:09:39ZengDove Medical PressOncoTargets and Therapy1178-69302019-02-01Volume 121509152044262Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasionWu RYun QZhang JPBao JRile Wu, Qiang Yun, Jianping Zhang, Jingang Bao Department of Neurosurgery, Inner Mongolia People’s Hospital, Hohhot 010017, China Background: Recent evidence indicates that Kruppel-like factor 13 (KLF13) has critical roles in regulating cell differentiation, proliferation and may function as a tumor suppressor. However, its role in glioma progression is poorly understood. Methods: Public database was used to explore the expression and prognostic value of KLF13 in glioma. Cell proliferation and invasion assays were used to explore the role of KLF13. Bisulfite sequencing and ChIP assay were used to determine the methylation of KLF13 promoter in glioma and the regulation of KLF13 by DNMT1. Results: We found that KLF13 inhibited glioma cell proliferation and invasion, which could be reversed by AKT activation. DNMT1-mediated hypermethylation was responsible for downregulation of KLF13. Knocking down of DNMT1 restored KFL13 expression and inhibited cell proliferation and invasion as well. Patients with high expression of KLF13 might have a better prognosis. Conclusion: KLF13 suppressed glioma aggressiveness and the regulation of KLF13 could be a potential therapeutic target. Keywords: KLF13, DNMT1, AKT, glioma, methylationhttps://www.dovepress.com/downregulation-of-klf13-through-dnmt1-mediated-hypermethylation-promot-peer-reviewed-article-OTTKLF13DNMT1AKTgliomamethylation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Wu R Yun Q Zhang JP Bao J |
spellingShingle |
Wu R Yun Q Zhang JP Bao J Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion OncoTargets and Therapy KLF13 DNMT1 AKT glioma methylation |
author_facet |
Wu R Yun Q Zhang JP Bao J |
author_sort |
Wu R |
title |
Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion |
title_short |
Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion |
title_full |
Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion |
title_fullStr |
Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion |
title_full_unstemmed |
Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion |
title_sort |
downregulation of klf13 through dnmt1-mediated hypermethylation promotes glioma cell proliferation and invasion |
publisher |
Dove Medical Press |
series |
OncoTargets and Therapy |
issn |
1178-6930 |
publishDate |
2019-02-01 |
description |
Rile Wu, Qiang Yun, Jianping Zhang, Jingang Bao Department of Neurosurgery, Inner Mongolia People’s Hospital, Hohhot 010017, China Background: Recent evidence indicates that Kruppel-like factor 13 (KLF13) has critical roles in regulating cell differentiation, proliferation and may function as a tumor suppressor. However, its role in glioma progression is poorly understood. Methods: Public database was used to explore the expression and prognostic value of KLF13 in glioma. Cell proliferation and invasion assays were used to explore the role of KLF13. Bisulfite sequencing and ChIP assay were used to determine the methylation of KLF13 promoter in glioma and the regulation of KLF13 by DNMT1. Results: We found that KLF13 inhibited glioma cell proliferation and invasion, which could be reversed by AKT activation. DNMT1-mediated hypermethylation was responsible for downregulation of KLF13. Knocking down of DNMT1 restored KFL13 expression and inhibited cell proliferation and invasion as well. Patients with high expression of KLF13 might have a better prognosis. Conclusion: KLF13 suppressed glioma aggressiveness and the regulation of KLF13 could be a potential therapeutic target. Keywords: KLF13, DNMT1, AKT, glioma, methylation |
topic |
KLF13 DNMT1 AKT glioma methylation |
url |
https://www.dovepress.com/downregulation-of-klf13-through-dnmt1-mediated-hypermethylation-promot-peer-reviewed-article-OTT |
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