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Significance The p53 tumor suppressor protein is a critical stress response mediator. Polymorphisms in the human TP53 gene can alter protein function. We investigated an African-centric variant affecting codon 47 (P47S). Compared with those with the P47 variant, cells and mice expressing the serine 47 (S47) variant exhibit increased levels of coenzyme A (CoA) and glutathione (GSH). These molecules inhibit the induction of ferroptosis in S47 cells and mice. Elevated levels of CoA and GSH feedback on the p53 protein to negatively regulate the structure and function of this tumor suppressor protein. We identify CoA as a regulator of ferroptosis and show that the control of cell fate in response to certain ferroptosis inducers and p53 is reversible by altering the redox environment.

Mechanistic basis for impaired ferroptosis in cells expressing the African-centric S47 variant of p53