ACOD1 enhances the ferroptosis resistance of tumor-associated macrophages through the KEAP1/NRF2 axis and promotes triple-negative breast cancer progression.
ACOD1 is highly expressed in TNBC TAMs and is driven by TME signals, independent of the classical M2 polarization pathway, and promotes ITA binding to KEAP1, which inhibits the KEAP1-NRF2 interaction and thus activates NRF2-mediated antioxidant and ferroptosis resistance responses in TAMs, promoting TNBC progression.