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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