Fig. 10

Schematic illustration of the relationship between ROS levels and ACE2 during chemotherapy in breast cancer cells. Left panel: In sensitive breast cancer cells with low ROS levels, ACE2 expression is relatively low; when the cells are stimulated by chemotherapeutic agents, ROS production is induced and phosphorylation of AKT is promoted, which in turn upregulates ACE2 expression by enhancing the expression of HIF-1α. Right panel: ACE2 is expressed at high levels in drug-resistant cells and maintains ROS homeostasis by inhibiting the overproduction of ROS. In drug-resistant cells with knockdown of ACE2, anticancer drugs induced a large increase in ROS levels, which induced apoptosis