The Roles of ROS in Cancer Heterogeneity and Therapy

Figure 1

Quiescent and/or self-renewing stem cells display low levels of ROS due to their basal metabolism associated to an efficient antioxidant machinery. ROS can result from increased metabolism associated with dysfunctional mitochondria, oncogene activation, or cytokine/growth factor signaling that triggers ROS-producing enzymes: NADPH oxidases, cycloxygenases (COX), and lipoxygenases (LOX). ROS-induced Wnt/β-catenin signal in cancer stem-like cells. The exposure to oxidative stress activates Wnt pathway and upregulates c-Myc. In CSCs, c-Myc expression level varies from cell-to-cell contributing to cancer heterogeneity. Wnt activate downstream signaling molecules that promote the stabilization and accumulation of the β-catenin in the nucleus and leading to EMT, a hallmark of cancer.