
CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas
Author(s) -
Liu DaMing,
Wang HongJun,
Han Bo,
Meng XiangQi,
Chen MingHui,
Yang DongBo,
Sun Ying,
Li YongLi,
Jiang ChuanLu
Publication year - 2016
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12531
Subject(s) - methylation , glioma , cancer research , dna methylation , downregulation and upregulation , biology , pyrosequencing , in vitro , immunohistochemistry , gene expression , gene , biochemistry , immunology
Summary Aims To explore the expression, methylation pattern, the prognostic value, and the biological consequences of CAMKK2 in gliomas. Methods The expression and methylation pattern of CAMKK2 was inferred and validated from mRNA expression profile (N = 866) and methylation profile (N = 426) of glioma tissue samples, and independent samples were used for further validation by IHC and pyrosequencing. To explore the function of CAMKK2 in gliomas, in vitro studies, colony formation assays and migration and invasion assays were performed. Results We found the upregulation of CAMKK2 in high‐grade glioma samples was associated with promoter hypomethylation. An elevated expression of CAMKK2 was associated with worse prognosis. By in vitro assays, we demonstrated that CAMKK2 could promote cell migration, invasion, and proliferation. Conclusions The expression level of CAMKK2 could be regulated by promoter methylation. CAMKK2 serves as a prognostic marker in gliomas and could be a potential therapeutic target in gliomas.