Background Gliomas are one of the most lethal cancers in the human central nervous system. Despite clinical treatment advancements, the prognosis of patients with glioma remains poor. KDM2B is a histone lysine demethylase, which has been observed in multiple tumors. But the concrete role of KDM2B in gliomas remains to be further illustrated. Methods The KDM2B expression in gliomas was detected with immunohistochemistry and Western blot assay. Furthermore, knockdown of KDM2B in U87 and U251 glioma cell lines, the proliferation capacity was evaluated by cell viability assay, colon formation assay and flow cytometry in vitro. Western blot assay was used to analyze the p21, EZH2 and cyclinD1 changes followed by knockdown of KDM2B. Results KDM2B was upregulated in tissues of glioma patients, and the expression was correlated to cancer progression. Downregulation of KDM2B in U87 and U251 glioma cell lines inhibited cell proliferation and arrested cell cycle in G0/G1 phase. In addition, silencing KDM2B promoted the upregulation of p21 while reduced the expression of EZH2 and cyclinD1. Conclusion Taken together, our results revealed that KDM2B might influence gliomas growth and act as a novel therapeutic target for glioma patients.
KDM2B overexpression correlates with poor prognosis and regulates glioma cell growth
Yiwei Wang,Jin Zang,Dongyong Zhang,Zhenxiang Sun,B. Qiu,Xiaojie Wang
Published 2018 in OncoTargets and Therapy
ABSTRACT
PUBLICATION RECORD
- Publication year
2018
- Venue
OncoTargets and Therapy
- Publication date
2018-01-08
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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