Progress in the research of cuproptosis and possible targets for cancer therapy

Figure 1 Effects of excess copper and copper deficiency in cancer. Four copper-related pathways with cancer inhibition effects are described. Elesclomol mediates the entry of Cu²⁺ into the mitochondria and causes reactive oxygen species accumulation. Flavonoids interfere with copper ion oxidation and reduction, inducing mitochondrial apoptosis pathway activation. Copper diethyldithiocarbamate can inhibit proteasome and result in endoplasmic reticulum stress. Copper deficiency can suppress the proliferation and migration of endothelial cells and the formation of connexin, bridling tumor angiogenesis. TCA: Tricarboxylic acid; ROS: Reactive oxygen species; FDX1: Ferredoxin 1; MTF1: Metallothionein; CTR1: Consolidation tumor ratio-1.