High levels of copper induce tumor suppressor gene P53 activation, and the activity of P53 may promote cuproptosis by enhancing mitochondrial function, so the mutation or deletion of P53 reduces COX activity as well as mitochondrial respiration.
We showed the mechanism of action of these genes in Cuproptosis. Excess Cu2+ stimulates the activation of ATM which activates SP1 and P53. P53 promotes PRNP, MT1A, MT2A and MT3A to expel Cu2+ out of the cell.
It is also reported that cuproptosis may happen by p53 via regulating the biogenesis of iron‐sulfur clusters and GSH, inhibiting glucose uptake and glycolysis.
