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.
Keywords: CLOCK; Glioma; NF-κB; miR-124.
Copyright © 2013. Published by Elsevier B.V.