Atorvastatin reduces vascular endothelial growth factor (VEGF) expression in human non-small cell lung carcinomas (NSCLCs) via inhibition of reactive oxygen species (ROS) production

摘要: The high metastatic potential of non-small cell lung cancers (NSCLCs) is closely correlated with the elevated expression vascular endothelial growth factor (VEGF) and resultant tumor angiogenesis. However, no effective strategies against VEGF have been available in NSCLCs therapy. This study demonstrated that reactive oxygen species (ROS) levels derived from both mitochondria NADPH oxidase were required for NSCLC cells. Atorvastatin administration could significantly inhibit vitro vivo via inhibition ROS production. inhibited generation partly through suppression Rac1/NADPH activity. Specifically, atorvastatin upregulate activity glutathione peroxidase (GPx) catalase, which are responsible elimination hydrogen peroxide (H(2)O(2)) peroxisomes, respectively. Thus, production by concomitant upregulation GPx catalase contributes critically to atorvastatin-reduced NSCLCs. may be a alternative angiogenesis