Per2 regulates other molecular and biochemical processes beyond their 
established role in the regulation of the mammalian circadian clock, herein we 
investigated the growth inhibiting potential of Per2 in human K562 leukemia 
cells and the underlying mechanisms. The results showed that over-expression of 
Per2 induced not only cell cycle arrest at G2/M phase but also an increase in 
apoptosis, which was confirmed by characteristic morphological changes, FCM and 
evident DNA fragmentation. Further experiments confirmed both up-regulation of 
P53 and down-regulation of CylinB1and C-myc. On the other hand, while P53 was 
found to be down-regulated. CylinB1 and C-myc were up-regulated. after Per2 
knockdown. In leukemia mice, Per2 transfection was shown to suppress cellular 
proliferation and accelerate apoptosis of K562 cells. Moreover, fewer leukemia 
cells were found to have infiltrated into the livers and spleens of the mice 
from the Per2 transfected group as compared with those from the control group. 
In summary, Per2 displayed a significant anti-tumor effect through cell cycle 
arrest and apoptosis induction in K562 cells. These data further support the 
emerging role of the circadian clock in critical aspects of cancer development 
and thorough research is underway on the mechanism of Per2 in the leukemia.