ArticleCell death & disease2025
AGR2 suppresses ferroptosis via the p53/FPN1 regulatory axis and drives therapeutic vulnerabilities in pancreatic cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Complementary intra- and extracellular AGR2 activities support epithelial ovarian cancer cell aggressiveness.Oncogene · 2026Article
- ALOX12 suppresses colon cancer progression by promoting p53-mediated ferroptosis through upregulating ROS-induced stress.Translational cancer research · 2026Article
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Authors and funding
14 authors.
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Abstract
Ferroptosis has emerged as a potential therapeutic target in cancer. This study shows the critical role of AGR2 in ferroptosis suppression across pancreatic cancer cell lines and in vivo models. Notably, human pancreatic cancer cells exhibit dose-dependent AGR2 upregulation upon exposure to ferroptosis inducers. Genetic ablation of AGR2 significantly sensitizes cells to ferroptosis through a p53-mediated mechanism, while p53 knockdown effectively rescues ferroptosis resistance. Mechanistic investigations demonstrate that AGR2 deficiency activates p53 signaling, downregulating the iron exporter SLC40A1 (encoding ferroportin/FPN1), inducing intracellular iron overload and consequent ferroptosis. Clinically, we find a positive correlation between AGR2 and FPN1 expression in PDAC specimens, with co-elevation of both markers predicting unfavorable patient prognosis. Therapeutically, administration of an AGR2-targeting peptide synergizes with ferroptosis inducers, significantly enhancing cell death in PDAC models. Our findings not only elucidate a novel AGR2/p53/FPN1 regulatory axis in ferroptosis control but also propose innovative combination strategies for pancreatic cancer treatment.
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