Circadian gene Clock contributes to cell proliferation and migration of glioma and is directly regulated by tumor‐suppressive miR‐124. Issue 15 (19th June 2013)

• Record Type: Journal Article
• Authors: Li, Aihua; Lin, Xihua; Tan, Xiaochao; Yin, Bin; Han, Wei; Zhao, Jizong; Yuan, Jiangang; Qiang, Boqin; Peng, Xiaozhong
• Is Part Of: FEBS letters. Volume 587:Issue 15(2013)
• Page Start: 2455
• Page End: 2460
• Publication Date: 2013-06-19
• Subjects: Glioma -- CLOCK -- miR-124 -- NF-κB; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2013.06.018
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : 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‐κB. In conclusion, we suggest that as a target of glioma suppressor miR‐124, CLOCK positively regulates glioma proliferation and migration by reinforcing NF‐κB activity. Abstract : CLOCK expression is upregulated in high‐grade glioma tissues vs. low‐grade or normal tissues. MiR‐124 can directly target and repress Clock. The upregulation of CLOCK is likely a consequence of the downregulation of miR‐124 in gliomas. CLOCK can positively regulate glioma proliferation and migration. The effects of CLOCK on tumorigenesis are likely the result of enhanced NF‐κB signaling.