Exploratory experiment designed to discover new patterns targeting PPARγ, GPX4, NCOA4 in TNBC cell lines. Primary outcome: Ferroptosis induction markers (lipid peroxidation, Fe²+ levels)
Mechanistic studies investigating how S-equol induces ferroptosis in triple negative breast cancer cells through modulation of the PI3K/AKT/mTOR signaling pathway. The experiments examined the effects of S-equol on lipid peroxidation levels, intracellular Fe²+ concentrations, and key ferroptosis regulators including PPARγ, GPX4, and NCOA4. The study utilized specific agonists for PPARγ and STAT3, as well as autophagy inhibitor ULK101, to validate the proposed mechanism. Additionally, NCOA4 knockdown and PPARγ overexpression experiments were performed to further confirm the molecular pathways involved in S-equol-mediated ferroptosis induction.
Lipid peroxidation assays, iron level measurement, gene knockdown/overexpression, pharmacological inhibition
Increased lipid peroxidation and Fe²+ levels, decreased GPX4 activity
Significant changes in ferroptosis markers upon S-equol treatment
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