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Significance Although it is commonly accepted that p53-mediated cell-cycle arrest, apoptosis, and senescence all serve as major mechanisms of tumor suppression, accumulating evidence indicates that other activities of p53, such as ferroptosis, are also critical for tumor suppression. However, the molecular mechanisms by which p53-mediated ferroptosis operates are not completely understood. In this study, we discovered that p53 can execute ferroptotic cell-death responses by directly activating its target geneSAT1 , coded for the spermidine/spermineN 1 -acetyltransferase 1. These data indicate a regulatory role of p53 in polyamine metabolism and reveal that p53-mediated activation of SAT1 contributes significantly to ferroptotic responses. Thus, p53 may engage multiple metabolic pathways with ferroptotic cell-death responses for tumor suppression.

Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses