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

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

“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

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