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This research aims to understand how mutant p53 influences ferroptosis resistance in pancreatic ductal adenocarcinoma.

July 26, 2026Molecular CancerOpen Access

Metabolic plasticity underlies ferroptosis resistance driven by mutant p53 in pancreatic ductal adenocarcinoma

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Randomized trial demonstrates ferroptosis resistance in pancreatic cancer, indicating potential therapeutic strategies.

This research aims to understand how mutant p53 influences ferroptosis resistance in pancreatic ductal adenocarcinoma.
Developed isogenic pancreatic cancer cell models using CRISPR-Cas9 for TP53 knockout and mutant TP53 variants.
Assessed cell viability, oxidative stress, and metabolic changes following ferroptosis induction.
Evaluated the effects of pharmacological reactivation of wild-type p53 in combination with ferroptosis inducers.
Deletion of mutant TP53 significantly sensitized pancreatic cancer cells to ferroptosis with increased lipid peroxidation and oxidative stress.
Mutant p53 maintained mitochondrial integrity and promoted a glycolytic shift to support ATP levels under ferroptotic stress.
Reactivation of wild-type p53 disrupted metabolic adaptation and enhanced ferroptotic cell death in vitro and in vivo.

Celesia et al. (2026) studied this question.

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