Circadian gene Clock contributes to cell proliferation and migration of glioma and is directly regulated by tumor-suppressive miR-124

被引：83

作者：

Li, Aihua ^{[1
,2
]}

Lin, Xihua ^{[1
,2
]}

Tan, Xiaochao ^{[1
,2
]}

Yin, Bin ^{[1
,2
]}

Han, Wei ^{[1
,2
]}

Zhao, Jizong ^{[3
]}

Yuan, Jiangang ^{[1
,2
]}

Qiang, Boqin ^{[1
,2
]}

Peng, Xiaozhong ^{[1
,2
]}

机构：

[1] Chinese Acad Med Sci, State Key Lab Med Mol Biol, Dept Mol Biol & Biochem, Inst Basic Med Sci, Beijing 100005, Peoples R China

[2] Peking Union Med Coll, Beijing 100005, Peoples R China

[3] Beijing Tiantan Hosp, Dept Neurosurg, Beijing 100050, Peoples R China

来源：

FEBS LETTERS | 2013年 / 587卷 / 15期

基金：

中国国家自然科学基金;

关键词：

Glioma; CLOCK; miR-124; NF-kappa B; KAPPA-B; DEREGULATED EXPRESSION; IN-VIVO; CANCER; GLIOBLASTOMA; MICRORNAS; DIFFERENTIATION; GLIOMAGENESIS; APOPTOSIS; PER1;

D O I：

10.1016/j.febslet.2013.06.018

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Although the roles of circadian Clock genes and microRNAs in tumorigenesis have been profoundly studied, mechanisms of cross-talk between them in regulation of gliomagenesis are poorly understood. Here we show that the expression level of CLOCK is significantly increased in high-grade human glioma tissues and glioblastoma cell lines. In contrast miR-124 is attenuated in similar samples. Further studies show that Clock is a direct target of miR-124, and either restoration of miR-124 or silencing of CLOCK can reduce the activation of NF-kappa B. In conclusion, we suggest that as a target of glioma suppressor miR-124, CLOCK positively regulates glioma proliferation and migration by reinforcing NF-kappa B activity. (C) 2013 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.

引用

页码：2455 / 2460

页数：6

共 36 条

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