Fig. 8

Graphical abstract illustrating the mechanism of SS in treating BC. The SS directly binds to EGFR and ERK2, which may affect the extracellular binding of ligands to EGFR, intracellular phosphorylation of EGFR, phosphorylation of ERK2 by MEK, formation and nuclear translocation of ERK2 dimers to inactivate the ERK2/MAPK signaling pathway, thereby influencing the expression of the transcription factor E-twenty-six-1 (Ets-1) for SLC7A11, resulting in down-regulation of SLC7A11 expression. This subsequently reduces the GSH/GSSG ratio and GPX4 enzyme activity, leading to an increase in lipid peroxidation accumulation, ultimately promoting ferroptosis, and inhibiting BC progression