Abstract
Ferroptosis is a newly identified form of cell death that depends on intracellular iron accumulation and lipid peroxidation. The tumor suppressor p53 is recently demonstrated either positively or negatively regulate ferroptosis, beyond its well-known effects on apoptosis and other non-apoptotic cell death including necroptosis and autophagy. The mechanism of p53 regulating ferroptosis is transcriptional-dependent or transcriptional-independent. On one hand, p53 enhances ferroptosis via inhibition of SLC7A11 (solute carrier family 7 member 11) transcription or enhancing expression of SAT1 (spermidine/spermine N1-acetyltransferase 1) and GLS2 (glutaminase 2). On the other hand, p53 suppresses ferroptosis by inhibiting DPP4 (dipeptidyl peptidase-4) activity or induction of CDKN1A/p21 (cyclin-dependent kinase inhibitor 1 A) expression. The current chapter summarizes the recent discoveries of p53 on ferroptosis.
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