Figure 2.

(A) Reactive oxygen species (ROS) generated by the mitochondria and/or exogenous sources within a tumor cell affect tumor immunity to promote a more tumorigenic environment. Mitochondrial ROS (mROS) can stimulate differentiation of cancer-associated fibroblasts (CAFs) and ROS produced by the tumor cell can facilitate uptake of exosomes through caveolin-1 inhibition leading to metabolic reprogramming of certain CAFs. ROS can also affect the function of tumor-infiltrating T-cells depending on the level of mROS. Myeloid-derived suppressor cells (MDSCs) and tumor-associated Macrophages (TAMs) also produce ROS that can affect the function of other immune cells and ROS can affect regulatory T-cell function as well. (B) The amount of ROS corresponds to differing effects on biological function. While cytostatic levels of ROS lead to maintenance of biological processes, cytotoxic levels of ROS lead to cell death as well as immune deregulation. Tumor promotion through ROS occurs when ROS reach super-physiological or cytostatic levels while avoiding levels conducive to cell death. As mentioned previously, oxidative stress can arise from tumor cells.