NCOA4 and ferritinophagy in hematological malignancies: a double-edged regulator of iron metabolism and cell fate
Abstract
Ferritinophagy, a selective autophagic process mediated by NCOA4, plays a central role in cellular iron homeostasis by mobilizing iron from ferritin to sustain mitochondrial metabolism and redox balance. In cancer, ferritinophagy's effects vary with context: it can support metabolic fitness in some settings while promoting ferroptotic vulnerability in others. In acute myeloid leukemia (AML), evidence suggests that leukemic stem cells rely more heavily on iron-driven mitochondrial metabolism, making ferritinophagy a potential therapeutic target. This review summarizes current knowledge of NCOA4 regulation and ferritinophagy, discusses their relevance in hematologic malignancies, and highlights therapeutic opportunities and unresolved questions in AML.
Fields of Study & Subjects
Ferroptosis and cancer prognosis
Acute Myeloid Leukemia Research
Iron Metabolism and Disorders
Publication details
- Journal / source
- Frontiers in Oncology
- Publisher
- Frontiers Media SA
- Volume
- 15
- Pages
- 1717435–1717435
- Publication date
- 20 January 2026
- Language
- EN