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Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion

Authors Wu R, Yun Q, Zhang JP, Bao J

Received 21 September 2018

Accepted for publication 1 December 2018

Published 22 February 2019 Volume 2019:12 Pages 1509—1520


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr XuYu Yang

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

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