Figure 3.

Potential therapeutic pathways in cancer targeting abnormal iron metabolism. [A] Iron chelators limit the available amount of iron in tumor cells. Chelators and other drugs can be delivered through a TfR1-mediated drug delivery. [B] Inhibiting TfR1 by antibodies and gene silencing can lower iron import, depriving the cell of its desired iron content. [C] Inhibition of HIFs and their target genes can ultimately limit the amount of iron available for cells and hinder the ability of cancer cells to proliferate. [D] Inhibition of hepcidin-FPN axis can increase cellular iron export depriving the cell of iron. [E] Inhibition of cellular antioxidant defenses such as system xC- and GPX4 renders the cell prone to ROS accumulation from iron metabolism, leading to lipid peroxidation and ferroptosis. TfR1: transferrin receptor; HIFs: hypoxia-inducible factors; FPN: ferroportin; xC-: cystine-glutamate antiporter; GPX4: glutathione peroxidase 4; ROS: reactive oxygen species. Created with BioRender.com