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

Figure 2 General molecular biological process of cuproptosis. Copper can be transported into cells through the action of consolidation tumor ratio-1 and elesclomol encapsulation. When Cu²⁺ encapsulated by elesclomol enter the mitochondria, it gains an electron from ferrodoxin 1 (FDX1) (FDX1 expression can be promoted by metallothionein) and converts into Cu⁺. Concurrently, proteins responsible for dehydrogenation and acyl transfer (dihydrolipoamide transacetylase, dihydrolipoamide S-succinyltransferase, dihydrolipoamide dehydrogenase, pyruvate dehydrogenase α1, and pyruvate dehydrogenase β) undergo electron loss and are liporated by lipoic acid synthase. Subsequently, Cu⁺ promotes the oligomerization of liporated proteins. This cascade of events leads to a series of phenomena, including reactive oxygen species accumulation, mitochondrial dysfunction, and tricarboxylic acid inhibition, ultimately culminating in cuproptosis. CTR1: Consolidation tumor ratio-1; (Cu (DDC)2): Copper diethyldithiocarbamate; FDX1: Ferrodoxin 1.