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Table 3 Summary of studies on the role of ferroptosis in the treatment and drug resistance of pancreatic cancer

From: Current understanding of ferroptosis in the progression and treatment of pancreatic cancer

Interventions Mechanism of action Application In vitro/ in vivo Animal model References
NUPR1-LCN2 Reduces iron accumulation and inhibits ROS generation Suppression Both athymic nude female mice [73]
CTSB Activates STING1 to induce ferroptosis Suppression Both NOD-SCID female mice [74]
CRISPR-Cas9 Inhibits the expression of SLC7A11 and reduces the content of GSH Suppression Both female athymic mice [77]
GPX4 Rapamycin and RSL3 enhance anticancer activity by inducing GPX4 protein degradation Suppression Both - [78]
SLC2A1 SLC2A1 promotes glucose uptake and inhibits the expression of PDK4, which induces lipid peroxidation Suppression Both male C57BL/6 J mice [79]
GPX4 depletion or high iron diet Activates TMEM173 to promote TAM infiltration Promotion Both C57BL/6 mice [69]
Erastin Inhibits SLC7A11 to improve sensitivity to gemcitabine and cisplatin Suppression Both female athymic mice [63]
ARF6 Inhibits iron metabolism and improves sensitivity to gemcitabine Suppression In vitro - [57]
NEDD4L Degrades LTF to inhibit ferroptosis Promotion In vitro - [45]
LONP1 inhibitor Activates the Nrf2/Keap1 signalling pathway and upregulates GPX4 expression Promotion In vitro - [61]
  1. “Suppression” indicates that the intervention suppresses pancreatic cancer. “Promotion” indicates that the intervention promotes pancreatic cancer. “In vitro/in vivo” indicates whether the study was performed in vivo, in vitro, or both