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MAFF as a Key Transcriptional Regulator of Ferroptosis via Iron Homeostasis and Fatty Acid Synthesis

GSE310349 Homo sapiens Expression profiling by high throughput sequencing 3 samples Submitted 2026/08/05 Platform GPL24676
Summary
Ferroptosis is an iron-dependent form of regulated cell death driven by lipid peroxidation. In this study, we identify the transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene homolog F (MAFF) as a key regulator that promotes breast cancer progression while simultaneously sensitizing tumor cells to ferroptosis. Integrated RNA-sequencing and chromatin immunoprecipitation (ChIP)-sequencing revealed that MAFF directly regulates genes involved in iron and fatty acid metabolism. MAFF enhances intracellular iron availability by transactivating SLC11A2 and NCOA4, expanding the labile iron pool essential for ferroptotic signaling. In parallel, MAFF represses CPT2, FASN, and SCD1, reprogramming lipid metabolism to favor the accumulation of polyunsaturated fatty acids (PUFAs) over monounsaturated fatty acids (MUFAs), thereby increasing lipid peroxidation susceptibility. T
Published in
MAFF regulates ferroptotic sensitivity through iron homeostasis and fatty acid synthesis
Vilaplana Lopera N, Kim J, Lee PJ et al. · Cell death & disease 2026 · PMID 42209456 · doi:10.1038/s41419-026-08885-w
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Also filed as BioProject PRJNA1365799 and SRA study SRP646532. Searching any of these in the dataset finder brings you back here.

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