Wang Yiwei, Zang Jin, Zhang Dongyong, Sun Zhenxiang, Qiu Bo, Wang Xiaojie
Department of Human Anatomy, Shenyang Medical College, Huanggu District, Shenyang City.
Department of Neurosurgery, First Affiliated Hospital of China Medical University, Heping District, Shenyang City, Liaoning Province, China.
Onco Targets Ther. 2018 Jan 8;11:201-209. doi: 10.2147/OTT.S149833. eCollection 2018.
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.
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.
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.
Taken together, our results revealed that KDM2B might influence gliomas growth and act as a novel therapeutic target for glioma patients.
胶质瘤是人类中枢神经系统中最致命的癌症之一。尽管临床治疗取得了进展，但胶质瘤患者的预后仍然很差。KDM2B是一种组蛋白赖氨酸去甲基化酶，已在多种肿瘤中被观察到。但KDM2B在胶质瘤中的具体作用仍有待进一步阐明。
采用免疫组织化学和蛋白质免疫印迹法检测胶质瘤中KDM2B的表达。此外，在U87和U251胶质瘤细胞系中敲低KDM2B，通过细胞活力测定、克隆形成测定和体外流式细胞术评估增殖能力。采用蛋白质免疫印迹法分析敲低KDM2B后p21、EZH2和细胞周期蛋白D1的变化。
KDM2B在胶质瘤患者组织中上调，且其表达与癌症进展相关。在U87和U251胶质瘤细胞系中下调KDM2B可抑制细胞增殖并使细胞周期停滞在G0/G1期。此外，沉默KDM2B可促进p21的上调，同时降低EZH2和细胞周期蛋白D1的表达。
综上所述，我们的结果表明KDM2B可能影响胶质瘤的生长，并可作为胶质瘤患者的新型治疗靶点。
