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Iron transporter DMT1 regulates endosome‐mitochondria dynamics, mitochondrial metabolism and invasive migration in breast cancer cells

Iron is essential to support tumor initiation, growth and metastasis. Mitochondria are the ultimate cellular iron sink, where iron can be either used for iron‐sulfur cluster and heme synthesis or stored in mitochondrial ferritin. Recently, mitochondrial morphology, dynamics and function have been shown to be regulated by interaction with other organelles, such as ER and endosomes. We have shown that interaction between early endosomes (EE) and mitochondria regulates iron translocation into the mitochondria in epithelial cells. Furthermore, blocking iron release has been shown to prolong EE‐mitochondria interactions and increase endosomal dynamics. Divalent metal transporter 1 (DMT1) modulates iron transport from endosomes into mitochondria and has been suggested as a regulator of endosome‐mitochondria interactions. We have evaluated the role of DMT1 in EE‐mitochondria interactions, EE dynamics and its relationship with cancer‐related processes.