Oncotarget

Research Papers:

The pharmacological role of histone demethylase JMJD3 inhibitor GSK-J4 on glioma cells

Aixia Sui, Yongbing Xu, Yitong Li, Qilu Hu, Zeyang Wang, Hongtao Zhang, Junjie Yang, Xiaoqiang Guo and Wenqing Zhao _

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Oncotarget. 2017; 8:68591-68598. https://doi.org/10.18632/oncotarget.19793

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Abstract

Aixia Sui1,2, Yongbing Xu2, Yitong Li2, Qilu Hu2, Zeyang Wang2, Hongtao Zhang2, Junjie Yang2, Xiaoqiang Guo4,5 and Wenqing Zhao1,3

1Faculty of Graduate Studies, Hebei Medical University, Shijiazhuang 050081, Hebei, China

2Department of Oncology, Hebei General Hospital, Shijiazhuang 050051, Hebei, China

3Department of Neurosurgery, Hebei General Hospital, Shijiazhuang 050051, Hebei, China

4State Engineering Laboratory of Medical Key Technologies Application of Synthetic Biology, Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, The First Affliated Hospital of Shenzhen University, Shenzhen 518035, Guangdong, China

5Department of Urology, Peking University Shenzhen Hospital, Institute of Urology of Shenzhen PKU-HKUST Medical Center, Shenzhen 518036, Guangdong, China

Correspondence to:

Wenqing Zhao, email: hbghwenqingzhao@126.com

Xiaoqiang Guo, email: xiaoqiangguo123@163.com

Keywords: glioma, histone demethylase, JMJD3, inhibitor, GSK-J4

Abbreviations: JMJD3: jumonji domain-containing protein 3; KDM6B: lysine-specific demethylase 6B; CCK-8: Cell Counting Kit-8; K27M: lysine (K) 27 to methionine (M) mutation

Received: March 31, 2017     Accepted: June 28, 2017     Published: August 02, 2017

ABSTRACT

Glioma is regarded as the most prevalent malignant carcinoma of the central nervous system, and lack of effective treatment. Thus, the development of new therapeutic strategies targeting glioma is of significant clinical importance. In the present study, histone H3K27 demethylase jumonji domain-containing protein 3 (JMJD3) was investigated as target for glioma treatment. The mRNA of JMJD3 was overexpressed in glioblastoma tissues compared to normal brain tissues (P<0.05). The content of JMJD3 was also higher in glioma cells than in human brain microvascular endothelial cell (hCMEC), and the corresponding level of H3K27me3 was decreased (P<0.05). The treatment with JMJD3 specific inhibitor GSK-J4 can increase the content of H3K27me3 in glioma cells, which means the activity of JMJD3 was inhibited. GSK-J4 can inhibit glioma cell proliferation in a concentration dependent and time-dependent manner (P<0.05). GSK-J4 also induced glioma cell apoptosis and inhibited cell migration (P<0.05). But there was no obvious effect of GSK-J4 on hCMEC cells. All together, these data suggest that GSK-J4 has important potential in the gliomas treatment.


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