P53-induced microRNA-107 inhibits proliferation of glioma cells and down-regulates the expression of CDK6 and Notch-2

被引：59

作者：

Chen, Lei ^{[1
,2
,3
]}

Zhang, Run ^{[1
,2
,3
]}

Li, Peng ^{[1
,2
,3
]}

Liu, Yi ^{[1
,2
,3
]}

Qin, Kun ^{[1
,2
,3
]}

Fa, Zhi-qiang ^{[1
,2
,3
]}

Liu, Yi-jing ^{[1
,2
,3
]}

Ke, Yi-quan ^{[1
,2
,3
]}

Jiang, Xiao-dan ^{[1
,2
,3
]}

机构：

[1] Southern Med Univ, Dept Neurosurg, Zhujiang Hosp, Guangzhou 510282, Guangdong, Peoples R China

[2] Southern Med Univ, Natl Key Clin Specialty, Guangzhou 510282, Guangdong, Peoples R China

[3] Southern Med Univ, Neurosurg Inst Guangdong Prov, Guangdong Prov Key Lab Brain Funct Repair & Regen, Guangzhou 510282, Guangdong, Peoples R China

来源：

NEUROSCIENCE LETTERS | 2013年 / 534卷

关键词：

Glioma; P53; miR-107; CDK6; Notch-2; MALIGNANT GLIOMAS; CANCER; GLIOBLASTOMA; TEMOZOLOMIDE; TARGETS; MIR-107; GENES; WORLD; LINES; P53;

D O I：

10.1016/j.neulet.2012.11.047

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

MicroRNAs (miRNAs) are small noncoding RNAs that function as tumor suppressors or oncogenes. MicroRNA-107 (miR-107), a transcriptional target of p53, is deregulated in many cancer cell lines. Here, we showed that miR-107 is down-regulated in glioma tissues and cell lines, in particular, p53-mutated U251 and A172. Transfection of wild-type p53 into these cells stimulated miR-107 expression. To investigate the role of miR-107 in tumorigenesis, we constructed a lentiviral vector overexpressing miR-107. Notably, miR-107 inhibited proliferation and arrested the cell cycle at the G0-G1 phase in glioma cells. Transduction of Lenti-GFP-miR-107 into glioma cells inhibited CDK6 and Notch-2 protein expression. Our findings collectively demonstrate that p53-induced miR-107 suppresses brain tumor cell growth and down-regulates CDK6 and Notch-2 expression, supporting its tumor suppressor role and utility as a target for glioma therapy. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

引用

页码：327 / 332

页数：6

共 32 条

[11] miRNAs: Little known mediators of oncogenesis [J].