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

ABSTRACT:

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

SUBMITTER: Wu R 

PROVIDER: S-EPMC6390852 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature