Figure 5.

Model of the crosstalk of HO-1 and ROS-mediated tumorigenesis. HO-1 exerts a cytoprotective effect by scavenging ROS to prevent the cell transformation. During tumorigenesis, HO-1 serves as a protector to ameliorate the deteriorated effects of increased-ROS to cancer cells, which supports the proliferation and expansion, as well as the acquiring, of therapeutic resistance. Conversely, excessive activation of HO-1 increases labile Fe²⁺, leading to ROS overload and the death of cancer cells, namely ferroptosis.