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Acta Pharmacol Sin. 2008 Dec;29(12):1451-8. doi: 10.1111/j.1745-7254.2008.00902.x.

Over-expression of nm23-H1 in HeLa cells provides cells with higher resistance to oxidative stress possibly due to raising intracellular p53 and GPX1.

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1
School of Medicine, Xi'an Jiao-Tong University, Xi'an 710061, China.

Abstract

AIM:

To determine whether the antitumor factor nm23 is related with antioxidation.

METHODS:

Full-length human nm23-H1 was cloned into a mammalianexpressing vector and transiently introduced into HeLa cells.

RESULTS:

A remarkably low level of reactive oxygen species (ROS) was detected in the cells overexpressing 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- regulated gene 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.

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