Growing evidence shows that the deregulation of the circadian clock plays an important role in the development of malignant tumors, including gliomas. However, the molecular mecha- The expression of clock in highgrade gliomas was significantly higher than that of the lowgrade gliomas and non-glioma. Therefore, we suggest that disturbances in clock expression may result in the disruption of the control of normal circadian rhythm, thus benefiting the survival of glioma cells and promoting carcinogenesis.
The Clock gene, an indispensable component of the circadian clock, not only modulates circadian oscillations but also regulates organismal function. We examined whether silencing the expression of the human Clock gene in glioma cells influences cell growth and induces apoptosis after irradiation. Silencing the expression of Clock in a human glioma cell line (U87MG), but not in a control glioma cell line, resulted in increased apoptosis and cell cycle arrest. Moreover, silencing Clock expression altered the expression of apoptosis-related genes. The protein levels of c-Myc and Cyclin B1 were downregulated, but those of p53 were upregulated, in human Clock-silenced U87MG cells compared with control cells. Our results suggest that the circadian gene human Clock may play an important role in carcinogenesis by inhibiting apoptotic cell death via attenuating proapoptotic signaling.
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