The concept that invasive cancer is associated with increased levels of reactive 
oxygen species (ROS) generated by mitochondria is consistent with an 
ROS-mediated signaling mechanism. As a tumor grows, it encounters adverse 
microenvironments, one of which is low oxygen (hypoxia), which selects tumor 
cells with characteristics of increased invasiveness. Hypoxic environments 
select for tumor cells with stabilized HIF1 apha, a transcription factor that 
regulates genes coding for pro-tumor cytokines that signal stromal cells such as 
macrophages and fibroblasts to support an invasive tumor cell phenotype. HIF1 
alpha-mediated switches in the energy production of tumor cells from OXPHOS to 
glycolysis, as well as age-associated decreases in the metabolic rate of the 
host, enhance invasive qualities of tumor cells. An increase in environmental 
oxygen in combination with a mitochondrial targeted catalase mimetic and a 
metabolism booster may be of interest to investigate as a treatment strategy for 
invasive cancer.