MiR-212-3p inhibits glioblastoma cell proliferation by targeting SGK3

被引:47
|
作者
Liu, Huailei [1 ,2 ,3 ]
Li, Chenguang [1 ,2 ]
Shen, Chen [1 ,2 ]
Yin, Fei [1 ,2 ]
Wang, Kaikai [1 ,2 ]
Liu, Yaohua [1 ,2 ]
Zheng, Bingjie [1 ,2 ]
Zhang, Weiguang [1 ,2 ]
Hou, Xu [1 ,2 ]
Chen, Xin [1 ,2 ]
Wu, Jianing [1 ,2 ]
Wang, Xiaoxiong [1 ,2 ]
Zhong, Chen [1 ,2 ]
Zhang, Jiakang [1 ,2 ]
Shi, Huaizhang [1 ]
Ai, Jing [3 ]
Zhao, Shiguang [1 ,2 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 1, Dept Neurosurg, Harbin 150001, Heilongjiang Pr, Peoples R China
[2] Harbin Med Univ, Inst Brain Sci, Harbin 150001, Heilongjiang Pr, Peoples R China
[3] Harbin Med Univ, State Prov Key Labs Biomed Pharmaceut China, Dept Pharmacol, Harbin 150081, Heilongjiang Pr, Peoples R China
基金
中国国家自然科学基金;
关键词
MiR-212-3p; Glioblastoma; Serum and glucocorticoid-inducible kinase 3 (SGK3); HUMAN GASTRIC-CANCER; STEM-LIKE CELLS; DOWN-REGULATION; HAIR FOLLICLE; LUNG-CANCER; GLIOMA; AKT; MULTIFORME; MICRORNAS; SERUM;
D O I
10.1007/s11060-015-1736-y
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Glioblastoma multiforme (GBM) is the most malignant brain tumor in humans. Previous studies have demonstrated that microRNA plays important roles in the development and proliferation of GBM cells. Here we defined the mechanism by which miR-212-3p regulated the proliferation of GBM. In this study, we showed that miR-212-3p expression was significantly down-regulated and negatively correlated with serum and glucocorticoid-inducible kinase 3 (SGK3) in GBM. Either over-expression of miR-212-3p or silence of SGK3 decreased viability of GBM cells. Moreover, miR-212-3p directly bound to 3'UTR of SGK3 and inhibited its mRNA and protein expression. And over-expression of SGK3 rescued the decreased proliferation of GBM cells induced by miR-212-3p. Importantly, miR-212-3p also suppressed tumor growth in vivo. Collectively, our results demonstrated that miR-212-3p inhibited proliferation of GBM cells by directly targeting SGK3, and could potentially serve as a new therapeutic target for GBM.
引用
收藏
页码:431 / 439
页数:9
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