This work was supported by the National Science and Technology Task Force Project (No 2006BAD06A13-2), the National Basic Research Program of China (973 Program) (No 2007CB310505), and National Natural Science Foundation of China (No 30571672, 30500018, and 30771914).
Over-expression of nm23-H1 in HeLa cells provides cells with higher resistance to oxidative stress possibly due to raising intracellular p53 and GPX11
Version of Record online: 14 DEC 2008
© 2008 CPS and SIMM
Acta Pharmacologica Sinica
Volume 29, Issue 12, pages 1451–1458, December 2008
How to Cite
AN, R., CHU, Y.-l., TIAN, C., DAI, X.-x., CHEN, J.-h., SHI, Q., HAN, J. and DONG, X.-p. (2008), Over-expression of nm23-H1 in HeLa cells provides cells with higher resistance to oxidative stress possibly due to raising intracellular p53 and GPX1. Acta Pharmacologica Sinica, 29: 1451–1458. doi: 10.1111/j.1745-7254.2008.00902.x
- Issue online: 14 DEC 2008
- Version of Record online: 14 DEC 2008
- Received 2008-07-08Accepted 2008-09-18
- oxidative stress;
- reactive oxygen species;
- cell viability;
Aim: To determine whether the antitumor factor nm23 is related with antioxidation. Methods: Full-length human nm23-H1 was cloned into a mammalian-expressing vector and transiently introduced into HeLa cells. Results: A remarkably low level of reactive oxygen species (ROS) was detected in the cells over-expressing nm23-H1. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and trypan blue assays found that the cells transfected with a nm23-H1-expressing plasmid had higher viability and stronger resistance to oxidative stress. Immunoprecipitation tests revealed that endogenous nm23-H1 formed a protein complex with p53. Furthermore, the intracellular levels of p53 and p53-regulatedgene GPX1 were obviously increased in the cells overexpressing nm23-H1. The downregulation of p53 in the cells overexpressing nm23-H1 resulted in a higher cellular ROS level and lower cell viability. Conclusion: The findings suggest that nm23-H1 may act as a cellular protector against oxidative stress, possibly triggering the p53-related antioxidative pathway.