Article ID Journal Published Year Pages File Type
10870903 FEBS Letters 2013 6 Pages PDF
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.
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